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Keys to Understanding Common Nerve Entrapments Course Description: This course utilizes the text: Orthopedic Clinical Advisor by Derrick Sueki, PT, DPT, GCPT, OCS and Jacklyn Brechter, PhD, PT. This course will help you access the information you need to confidently handle multiple orthopedic conditions. Essential clinical reference information provides up-to-date diagnostic and therapeutic information on common nerve entrapments conditions in a bulleted, quick-reference format ideal for both students and practitioners. Content is written entirely by orthopedic physical therapists and is logically organized to promote accurate, efficient differential diagnosis and intervention. Nerve Entrapments covered are: Axillary Nerve Entrapment Brachial Plexus Nerve Entrapment Common Fibular Nerve Entrapment Deep Fibular Nerve Entrapment Femoral Nerve Entrapment Interosseous Nerve Entrapment Lateral Femoral Cutaneous Nerve Entrapment Long Thoracic Nerve Pathology Median Nerve Entrapment Neurogenic Thoracic Outlet Syndrome Obturator Nerve Entrapment Plantar Nerve Entrapment Radial Nerve Entrapment Saphenous Nerve Entrapment Sciatic Nerve Entrapment Suprascapular Nerve Entrapment Sural Nerve Entrapment Tibial Nerve Entrapment Vascular Thoracic Outlet Syndrome Ulnar Nerve Entrapment Each diagnosis covers: Definition Synonyms Optimal Number of Visits/Maximal Number of Visits Etiology Epidemiology and Demographics 1 of 57 Mechanism of Injury Common Signs and Symptoms Aggravating Activities Easing Activities 24-Hour Symptom Pattern Past History for the Region Physical Examination Important Objective Tests Differential Diagnosis Contributing Factors Treatment Surgical Options Rehabilitation Prognosis Signs and Symptoms Indicating Referral to Physician Methods of Instruction: Online course available via internet Target Audience: Physical Therapists, Physical Therapist Assistants, Occupational Therapists, Occupational Therapist Assistants and Athletic Trainers Educational Level: Intermediate Prerequisites: None Course Goals and Objectives: At the completion of this course, participants should be able to: 1. Identify areas of injury for Axillary Nerve Entrapment 2. Recognize the signs/symptoms of Brachial Nerve Entrapment 3. Identify the sensory distribution for Common Fibular Nerve Entrapment 4. Identify aggravating activities of Deep Fibular Nerve Entrapment 5. Recognize contributing factors of Femoral Nerve Entrapment 6. Recognize the differential diagnosis for Interosseous Nerve Entrapment 7. Identify the signs/symptoms of Lateral Femoral Cutaneous Nerve Entrapment 8. Recognize the most common complaint of Long Thoracic Nerve Pathology 9. Identify the demographics of Median Nerve Entrapment 10. Recognize the synonyms for Neurogenic Thoracic Outlet Syndrome 11. Recognize the signs/symptoms for physician referral of Obturator Nerve Entrapment 12. Identify the components of a physical examination for Plantar Nerve Entrapment 13. Differentiate between the classifications of nerve injury for Radial Nerve Entrapment 14. Identify the signs/symptoms of Saphenous Nerve Entrapment 15. Recognize the differential diagnosis for Suprascapular Nerve Entrapment Criteria for Obtaining Continuing Education Credits: A score of 70% or greater on the written post-test 2 of 57 DIRECTIONS FOR COMPLETING THE COURSE: 1. 2. 3. 4. 5. 6. 7. 8. 9. This course is offered in conjunction with and with written permission of Elsevier Science Publishing. Review the goals and objectives for the module. Review the course material. We strongly suggest printing out a hard copy of the test. Mark your answers as you go along and then transfer them to the actual test. A printable test can be found when clicking on “View/Take Test” in your “My Account”. After reading the course material, when you are ready to take the test, go back to your “My Account” and click on “View/Take Test”. A grade of 70% or higher on the test is considered passing. If you have not scored 70% or higher, this indicates that the material was not fully comprehended. To obtain your completion certificate, please re-read the material and take the test again. After passing the test, you will be required to fill out a short survey. After the survey, your certificate of completion will immediately appear. We suggest that you save a copy of your certificate to your computer and print a hard copy for your records. You have up to one year to complete this course from the date of purchase. If we can help in any way, please don’t hesitate to contact us utilizing our live chat, via email at [email protected] or by phone at 405-974-0164. 3 of 57 CHAPTER 16 Axillary Nerve Entrapment Nerve BASIC INFORMATION DEFINITION • Axillary nerve entrapment pathologies encompass any injury that interrupts the function of the axillary nerve at any point along its course. • The axillary nerve is particularly vulnerable to injury at the following: Surgical neck of the humerus Inferior aspect of the glenohumeral joint Quadrilateral space Deltoid muscle • The loss of function results in muscle weakness, pain, or sensory dysfunction. SYNONYMS Quadrilateral space syndrome ICD-9CM CODES 354 Mononeuritis of upper limb and mononeuritis multiplex 354.8 Other mononeuritis of upper limb 354.9 Mononeuritis of upper limb unspecified 6 MAXIMAL NUMBER OF VISITS 20 • The axillary nerve is the smaller of the terminal branches of the posterior cord and the shortest of the major terminal branches of the brachial plexus. It is a mixed motor and sensory nerve derived from the C5 and 6 nerve roots that originates from the anterior aspect of the subscapularis muscle, passes laterally toward the inferior aspect of the shoulder joint, passes inferiorly to the head of the humerus, above the tendons of latissimus dorsi and teres major, and passes through the quadrilateral space, which is bounded medially by the humerus, laterally by the long head of the triceps muscle, superiorly by teres minor (which it supplies), and inferiorly by teres major. • It then wraps horizontally around the posterior aspect of the surgical neck of the humerus and enters the deltoid muscle as three branches: an anterior branch to the middle and anterior aspects of the deltoid, a posterior branch to the posterior deltoid, and the upper lateral brachial cutaneous nerve branch to the skin in the area of the deltoid tuberosity • The axillary nerve may be affected at any point along its course by direct 4 of 57 EPIDEMIOLOGY AND DEMOGRAPHICS • Axillary nerve injury is the most common nerve injury associated with the shoulder, particularly in relation to trauma such as fracture and dislocation. • Quadrilateral space syndrome is an uncommon pathology seen in throwing athletes, as well as in sports with repetitive cocking action such as tennis or volleyball. The cocking action involves end-range shoulder abduction, extension, and external rotation followed by rapid flexion and internal rotation. MECHANISM OF INJURY • Mechanisms of injury for the axillary nerve are described in relation to their location, as follows: Direct trauma in the form of a humeral neck fracture causing damage to the nerve Dislocation of the glenohumeral joint in which the nerve is stretched across the humeral neck by an anterior dislocation Operative procedures at the inferior aspect of the shoulder such as capsular shift involving a deltoid-splitting incision that directly injures the nerve Blunt injury such as a heavy fall onto the lateral aspect of the shoulder compressing the nerve within the deltoid muscle Overuse syndromes from repeated scapular motions, leading to compression of the posterior humeral circumflex artery and the axillary nerve within the quadrilateral space by fibrous bands. The size of the quadrilateral space is reduced in positions of abduction and external rotation. Overuse syndrome occasionally occurs after general anesthesia or sleeping prone with the arms raised above the head. COMMON SIGNS AND SYMPTOMS • Poorly localized posterior shoulder pain • Paraesthesia over the lateral aspect of the shoulder and arm • Weakness of deltoid and teres minor resulting in difficulty abducting the arm • External rotation may be mildly weaker. • Patient may describe shoulder weakness. • Atrophy of the deltoid may be evident. AGGRAVATING ACTIVITIES • Activities that involve shoulder abduction ORTHOPEDIC PATHOLOGY ETIOLOGY repair damage incurred but produce adhesions to the nerve, limiting their glide and increasing anoxia. Section III OPTIMAL NUMBER OF VISITS trauma or compression entrapment, causing nerve tissue hypoxia.The insult to the nerve can be mechanical, thermal, chemical, or ischemic; however, the axillary nerve is most commonly injured by glenohumeral fractures and dislocations. • Axillary nerve entrapment is usually related to trauma; nevertheless, pathology can occur in a number of ways, as follows: Direct trauma in the form of a humeral neck fracture Dislocation of the glenohumeral joint in which the nerve is stretched across the humeral neck by an anterior dislocation Operative procedures at the inferior aspect of the shoulder such as capsular shift involving a deltoid-splitting incision Blunt injury such as a heavy fall onto the lateral aspect of the shoulder Overuse syndromes from repeated scapular motions, leading to compression of the posterior humeral circumflex artery and the axillary nerve within the quadrilateral space by fibrous bands. The size of the quadrilateral space is reduced in positions of abduction and external rotation. • Nerve injury is classified according to the severity of the injury and its potential for reversibility. • Neurapraxia (first-degree injury) is a distortion of the myelin about the nodes of Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance, which produces temporary loss of nerve conduction. • Axonotmesis (second-degree injury) is an interruption of the axon with secondary wallerian degeneration.The supporting tissue surrounding the axon is preserved, and the recovery period depends on the distance between the site of injury and the end organs. • Neurotmesis is a complete disruption of the nerve and its supporting structures. Neurotmesis has been further divided into the following three subcategories: Third-degree nerve injury: Endoneurium is disrupted with intact perineurium and epineurium. Fourth-degree nerve injury: All neural elements sparing the epineurium are disrupted. Fifth-degree nerve injury: Complete transaction and discontinuity of the nerve with no capacity for regeneration • Physiologically, there is disruption to any part of the nerve responsible for conduction. In repetitive-type nerve entrapment, it is proposed that repetitive work or static postures produce an inflammatory process and fibroblasts appear to 739 740 Axillary Nerve Entrapment • Repetitive shoulder internal and/or external rotation occurs particularly when the shoulder is in an abducted position. EASING ACTIVITIES Rest and/or modification of aggravating activities CHAPTER 16 • NERVE tors, such as posture and patterning, that will assist with rehabilitation and activity modification. In the case of the axillary nerve, the patient often demonstrates trick movements to accomplish shoulder abduction through use of the rotator cuff and proximal scapular and cervical muscles. 24-HOUR SYMPTOM PATTERN IMPORTANT OBJECTIVE TESTS • Generally, the symptoms are related to activity and do not follow a typical 24-hour pattern unless there is a strong inflammatory component, which may be seen in repetitive tasks. • If there is an inflammatory component, there may be worsening of symptoms with use toward the end of the day, as well as morning stiffness. • Electromyography (EMG) may reveal delayed conduction velocity and fibrillation potentials. • Needle EMG should assist with determination of specific muscle involvement and provide differential diagnosis from the other shoulder neuropathies and cervical radiculopathies. • If quadrilateral space syndrome is suspected, there will be concomitant posterior humeral circumflex artery compression, and therefore a subclavian arteriogram can provide diagnostic information. PAST HISTORY FOR THE REGION • History of trauma, fracture, or dislocation of the glenohumeral joint • Repetitive overuse of the shoulder in occupation or sports • Generalized hypermobility PHYSICAL EXAMINATION • Examine the shoulder for signs of atrophy of the deltoid muscle. • Manual muscle testing (MMT) may reveal weakness in the following muscles: Deltoid: Tested in shoulder flexion, abduction, and extension for each of the portions of the deltoid; however, weakness is usually demonstrated in pure abduction. Teres minor: Tested in external rotation; however, the infraspinatus muscle is a stronger external rotator and is likely to compensate for the loss of the teres minor muscle. • Sensation testing should be performed. The cutaneous branch of the axillary nerve supplies the lateral aspect of the shoulder overlying the deltoid muscle and tuberosity. Sensation testing should include pinprick, two-point discrimination, and tuning fork tests and compared for asymmetry with the unaffected side (where available). • Physical examination should also exclude pathology in other areas, particularly performing active range of motion (AROM) and passive ROM (PROM) at the neck and shoulder, which may reveal restrictions, other shoulder pathology, and/or central involvement of the nerve. • Physical examination should also include movement analysis to determine the movement patterns that the patient adopts when performing the aggravating activities. Movement analysis can be done visually or with the assistance of a video camera. The analysis should give some clues as to predisposing fac- TREATMENT SURGICAL OPTIONS • Surgery may be considered after a failure of conservative management. • Surgery involves nerve grafting techniques and a rotational transfer of deltoid removing the denervated portion. REHABILITATION • Lesion to the posterior cord of the brachial plexus • C5 or C6 radiculopathy • Suprascapular neuropathy produces a similar pattern of weak arm abduction and external rotation but no sensory loss. • Rotator cuff tears • Rotator cuff tendinopathies • Adhesive capsulitis • Shoulder instability • Degenerative joint disease at the glenohumeral or acromioclavicular (AC) joints • Underlying neuropathic disease • Neuralgic amyotrophy • Muscular dystrophy • Tumors or space-occupying lesions • Upper motor neuron lesion in the cerebrum • The goal of rehabilitation should be pain reduction to encourage pain-free exercise and to provide task or sports reeducation and interventions leading to reacquisition of fine motor and sporting skills. • Manual therapy Pain reduction can be achieved through the use of ice and electrotherapeutic modalities. Soft tissue release may assist with restoration of muscle balance around the scapula, which is useful if compensations have occurred in other muscles to make up for the loss of the deltoid and teres minor muscles. • Functional rehabilitation Reeducation of movement patterns, particularly proximal control of the trunk and neck, to provide a stable foundation for scapular stability Scapular position education initially with isometric hold and then the addition of controlled functional movement patterns Prevention of aberrant movement patterns and contractures with ROM and gentle stretch techniques Specific muscle strengthening gradually increasing in intensity to restore full power to the deltoid and teres minor muscles Integration of functional exercise and strength work into sport- or task-specific skills Graduated return to full strength, speed, and power CONTRIBUTING FACTORS PROGNOSIS • Trauma is the most common contributing factory for axillary nerve injuries; however, for any nerve entrapments that are nontraumatic, there is often an element of repetitive activity involving the affected limb. • Typically in the case of the axillary nerve, the repetitive action involves shoulder abduction and external glenohumeral rotation. • Postural factors may be involved, particularly with repetitive work or sporting activities with reduction in proximal stability and control, leading to an overuse of more distal muscle groups to perform a task. • Prognosis depends entirely on the extent of damage to the nerve. • Neurapraxia should resolve rapidly and lead to a complete restoration of function, usually within 2 to 3 months. • If the injury is a more severe axonotmesis, the recovery time depends on the distance from the site of injury to the denervated tissue. • Peripheral nerves have been reported to recover at an approximate rate of 1 to 4 mm per day and may not result in a complete restoration of function. • If there has been a complete sectioning of the nerve (neurapraxia), then the nerve will not fully recover. DIFFERENTIAL DIAGNOSIS 5 of 57 Axillary Nerve Entrapment CHAPTER 16 • NERVE • The results of treating neurapraxia even with surgical intervention are generally not satisfactory. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN If axillary nerve entrapment is suspected, all cases should be referred to a physician for appropriate investigation. SUGGESTED READINGS Aldridge JW, Bruno RJ, Strauch RJ, Rosenwasser MP. Nerve entrapment in athletes. Clin Sports Med. 2001;20(1):95. Goslin KL, Krivickas LS. Proximal neuropathies of the upper extremity. Neurol Clin. 1999;17(3). Kibler WB, Murrell GAC. Shoulder pain. In: Brukner P, Khan K, eds. Clinical Sports Medicine. 3rd ed. Australia: McGraw-Hill Book Company; 2006:243–288. 741 Leffert RD. Nerve lesions about the shoulder. Orthop Clin North Am. 2000;31(2). AUTHOR: JOSEPHINE LOUISE COULTER Section III ORTHOPEDIC PATHOLOGY 6 of 57 Brachial Plexus Nerve Entrapment 742 BASIC INFORMATION DEFINITION • The brachial plexus, composed of the posterior cord (formed from the posterior divisions of the upper trunk from C5 and C6 nerve roots, the middle trunk from C7, and the lower trunk from C8 and T1), the lateral cord (formed from the anterior divisions of the upper and middle trunks), and the medial cord (formed from the anterior division of the lower trunk), communicates the nerve supply between the cervical roots and the upper limb, passing through the scalene muscles and sternocleidomastoid, and under the clavicle. • It may be subject to the following injuries: Traction injury during birth if the head is pulled away from the shoulder (Erb’s palsy in which the arm is held in adduction and internal rotation with forearm pronation and wrist and hand flexion, or Klumpke’s palsy with Horner’s syndrome consisting of meiosis, ptosis, and anhydrosis) Traction injury from a traumatic event Compression injury from trauma to the cervical spine, clavicle, humerus, or pectoral girdle; impact on Erb’s point; or poor postures Compression injury from narrowing of the neural foramen with cervical hyperextension and ipsilateral rotation Compression injury from anatomical variations in the cervical spine, clavicle, first rib, pectoral girdle, or posterior triangle SYNONYMS • • • • • • • • • • Brachial plexus injury Cervical rib syndrome Cervical pinch syndrome Costoclavicular syndrome Scalenus anticus syndrome Hyperabduction syndrome Thoracic outlet syndrome Stinger Burner syndrome Chronic burner syndrome ICD-9CM CODES 353.0 Brachial plexus lesions 953.4 Injury to brachial plexus OPTIMAL NUMBER OF VISITS Recovery normally occurs between 24 hours and 2 to 3 weeks. MAXIMAL NUMBER OF VISITS Symptoms persisting for more than 2 to 3 weeks, together with worsening neurological signs, warrant further clinical investigation. CHAPTER 16 • NERVE ETIOLOGY • Insult to the nerve may be mechanical, thermal, chemical, or ischemic. In entrapment syndromes, compression or direct trauma leads to nerve tissue hypoxia. • The brachial plexus may be compressed from trauma to the cervical spine, shoulder, pectoral girdle, clavicle, or rib; from postural issues, with direct pressure on Erb’s point (punctum nervosum at the union between C5 and C6 nerve roots on the lateral cord 2 to 3 cm above the clavicle); or from narrowing of the neural foramen with cervical hyperextension and ipsilateral rotation. Specific anatomical features of entrapment in the upper limb are described by Pratt. • In entrapments, nerve trauma occurs because the size of the neural structure exceeds the anatomical space available for it, resulting in increased pressure that in turn leads to impaired blood flow and subsequent hypoxia of the tissue and disruption to the axonal transport system. Nerve injury is classified according to severity of the injury and potential for reversibility. • Original classifications described previously remain in current use, as follows: First-degree neurapraxia involves distortion of myelin about the nodes of Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance, resulting in temporary loss of nerve conduction. Recovery is usually rapid and complete. Second-degree axonotmesis involves interruption of the axon with secondary wallerian degeneration, but the supporting tissue around the axon is preserved. Recovery may be complete but takes longer to occur and depends on the distance between the site of injury and the end structure (denervated muscle). Third-degree neurotmesis involves extensive disruption of the nerve and its supporting structures, but while the endoneurium is disrupted, the perineurium and epineurium remain intact. Fourth-degree neurotmesis involves disruption of all neural components except the epineurium. Fifth-degree neurotmesis involves complete transaction and discontinuity of the nerve, with no capacity for regeneration. Neurotmesis rarely occurs from entrapment, but when continuity has been disrupted, complete recovery is not possible, even with surgical techniques, and the eventual outcome depends on individual circumstances. A comprehensive overview of neurobiology, nerve injury, and nerve repair is provided by Dahlin. 7 of 57 • Double-crush syndrome refers to the fairly common phenomenon of nerve entrapment and radiculopathy occurring in combination, although the syndrome is considered controversial. Compression or irritation of the nerve roots at the cervical level is thought to increase sensitivity to compression or movement restrictions more distally in the structure. • As noted, increasing pressure on the nerve causes impaired blood flow, tissue hypoxia, and disruption to the anterograde and retrograde intercellular transport of materials within axons, eventually disturbing depolarization within the nerve. In brachial plexus compression, the pressure may result directly from anatomical structures, direct trauma, or from the associated phenomena of edema, glenohumeral dislocation, or clavicular fracture. Mechanisms and patterns of injury are discussed by Moran et al. EPIDEMIOLOGY AND DEMOGRAPHICS • In adults, compression injury of the brachial plexus tends to occur most commonly from an accident or sportsrelated trauma to the cervical spine, shoulder, pectoral girdle, and upper quadrant, particularly sports involving high impact such as contact sports and gymnastics. • It may also occur from the presence of a cervical rib arising from C7 vertebra (cervical rib syndrome), narrowing of the costoclavicular space between the clavicle and the first rib as a result of bony anomaly or combined depression and retraction of the shoulder as occurs when carrying a rucksack (costoclavicular syndrome), compression at the coracoid process when the upper limb is held in hyperabduction (hyperabduction syndrome), or compression between the anterior and medial scalenes (scalenus anticus syndrome). • Pathology related to trauma tends to occur in younger people predominantly because of the type of activity usually associated with the injury. Pathology related to anatomical anomalies and variation may occur across a broader spectrum of the population. MECHANISM OF INJURY • Brachial plexus injury is discussed by Mannan and Carlstedt and Bishop et al. Impact trauma resulting in clavicular fracture, glenohumeral dislocation, or edema around the shoulder may result in direct pressure on the brachial plexus as it passes under the clavicle or at Erb’s point (burner syndrome). • The presence of a cervical rib reduces the space between the scalenes, making Brachial Plexus Nerve Entrapment CHAPTER 16 • NERVE compression more likely in the region of the posterior triangle (cervical rib syndrome). • Bony anomaly or combined depression and retraction of the shoulder reduces the space between the clavicle and first rib, making compression more likely at this site (costoclavicular syndrome). • Anatomical variations in the posterior triangle and scalene muscles, particularly if combined with other associated elements, may produce compression at this site (scalenus anticus syndrome). • Compression at the coracoid process and pectoralis minor muscle may occur with sustained overhead arm postures. COMMON SIGNS AND SYMPTOMS • Activities and postures that involve impact through the upper quadrant • Cervical extension and ipsilateral rotation • Poor posture with “drooping” shoulders • Loading through the shoulder (particularly into depression and retraction) such as carrying a rucksack or a heavy object in the hand with the arm at the side • Activities involving sustained periods with the arm overhead, such as painting EASING ACTIVITIES Adaptations in posture and reduction in loading reduce the stress on the brachial plexus, as described in Aggravating Activities. 24-HOUR SYMPTOM PATTERN • In general, symptoms are more likely to be associated with trauma, posture, and activity rather than time. However, when symptoms are aggravated by cervical spine or overhead arm positions, there may be an increase in symptoms • Presence of anatomical anomalies • Impact trauma producing clavicular fracture • Glenohumeral dislocation • Edema around the shoulder • Hyperextension and ipsilateral rotation of the cervical spine PHYSICAL EXAMINATION • Clinical assessment in brachial plexus injuries is summarized by Mannan and Carlstedt. Physical findings in brachial plexus compression may include the following: Shoulder pain, radiating up into the neck and down into the upper limb, combined with weakness or paralysis of the biceps brachii, deltoid, brachialis, brachioradialis, and coracobrachialis muscles and muscles supplied by the axillary, musculocutaneous, and radial nerves, together with associated paraesthesia and numbness Bony anomalies may be detected. Erb’s point may be tender on palpation. Grip strength may be reduced. The upper limb may be held in adduction and medial rotation with forearm pronation and wrist and hand flexion (“waiter’s tip” position). Individuals may describe sensation of burning in the neck, weakness, cold, “heaviness,” or “dead arm” and complain of clumsiness. IMPORTANT OBJECTIVE TESTS • Diagnostic accuracy of neurological upper limb examination employing a battery of standard test procedures has been found to be reproducible and reliable. • For brachial plexus injuries, initial assessment must focus on neurological function, cervical spine fracture, and spinal cord injury before further testing is performed. • Radiography, ultrasound, and magnetic resonance imaging (MRI) techniques and neurophysiology and EMG testing may be helpful in identifying underlying anatomical or traumatic issues and clarifying clinical diagnosis. • Spurling test: Brachial plexus symptoms are reproduced with cervical extension, ipsilateral rotation, and axial loading for a positive result. • Erb’s point palpation:Tenderness is elicited for a positive result. • Costoclavicular maneuver: Brachial plexus symptoms and a reduction in 8 of 57 DIFFERENTIAL DIAGNOSIS • Cervical spine injuries, including spinal cord injury, bony trauma, soft tissue injury, radiculopathy, and discogenic trauma • Glenohumeral dislocation • AC joint injury • Shoulder impingement syndrome • Thoracic outlet syndrome • Peripheral neuropathies • Vascular pathology • Cardiac pathology • Pulmonary pathology • Pancoast’s syndrome • Tobias or Ciuffini-Pancoast-Tobias syndrome • Breast carcinoma • Mesothelioma, plasmacytoma • Lymphoma • Metastatic carcinoma CONTRIBUTING FACTORS Traumatic injury is often a factor in brachial plexus compression, but the presence of anatomical anomalies in the cervical spine, clavicle, and posterior triangle may predispose an individual to the pathology. TREATMENT SURGICAL OPTIONS • An overview of basic neurosurgical techniques is provided by Dahlin.When compression is due to cervical or first rib abnormalities, surgical resection of the rib may be required if conservative methods have failed to produce resolution. Division of fibrous bands, release techniques for relevant soft tissues, and correction, reduction, or fixation after traumatic injury may also be appropriate, depending on the underlying cause of the pathology. When severe and violent trauma has occurred, specialist neurosurgery may be required, including nerve transfers, nerve grafts, and neurolysis of scar tissue at the brachial plexus. ORTHOPEDIC PATHOLOGY AGGRAVATING ACTIVITIES PAST HISTORY FOR THE REGION radial pulse are reproduced in the upper limb with shoulder depression and retraction in individuals with costoclavicular syndrome. • Adson’s test (scalene test): Brachial plexus symptoms and a reduction in radial pulse are reproduced with cervical extension and ipsilateral rotation while sustaining a deep inspiration for a positive result. • Wright’s test: Brachial plexus symptoms and a reduction in radial pulse are reproduced with hyperabduction in sitting and supine lying for a positive result. Section III • Shoulder pain, radiating up into the neck and down into the upper limb • Weakness or paralysis of the biceps brachii, deltoid, brachialis, brachioradialis, and coracobrachialis muscles and muscles supplied by the axillary, musculocutaneous, and radial nerves, together with associated paraesthesia and numbness • The upper limb may be held in adduction and medial rotation with forearm pronation and wrist and hand flexion (“waiter’s tip” position). • Individuals may describe a sensation of weakness, cold, “heaviness,” or “dead arm” and complain of clumsiness. • Pain may be referred up into the neck, throughout the shoulder, and down into the upper limb. • Sensory and motor symptoms may occur throughout the upper limb. nocturnally as a consequence of sleeping postures. • Increases in nocturnal pain are also reported in which deafferentation pain is present. 743 744 Brachial Plexus Nerve Entrapment • Very few presentations require surgical intervention, but in common with other neural entrapments affecting the upper limb, surgery produces a good outcome in approximately 90% of cases. • Traumatic injuries requiring correction, reduction, or fixation may need early surgical intervention. Otherwise, surgery is indicated only in those cases in which response to conservative management has been poor. REHABILITATION • In the acute stage, treatment is focused on pain relief, antiinflammatory therapy, and early mobilization. • During the subacute stages, active exercise therapy aims to regain normal movement, strength, posture, and functional control, with particular emphasis on support for the injured neural structures. • In the late recovery stages, further progression aims to return the individual to preinjury fitness. • Physiotherapy involves a comprehensive management program composed of manual mobilization and soft tissue techniques, electrotherapy modalities, biomechanical analysis, postural reeducation and control, and functional movement, strength, and stability work. Appropriate aids to support the neck and affected structures may be advisable to prevent further injury during recovery. PROGNOSIS • Presence of anatomical anomalies in the cervical spine, clavicle, pectoral girdle, and posterior triangle, combined with a past history of trauma in these regions CHAPTER 16 • NERVE and participation in high-impact contact sports or high-loading activities with or without sustained postures, predispose an individual to brachial plexus trauma and compression. • Complications include chronic burner syndrome, contractures, scoliosis, glenohumeral dislocation, and, rarely, upper limb agnosia and deafferentation pain, but the majority of cases show complete resolution with conservative management. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN Indications for further medical evaluation include evidence of underlying trauma, worsening neurological function or symptoms, failure to respond to conservative management, suspicion or presence of underlying disease, and unexplained symptoms inconsistent with the pathology. SUGGESTED READINGS Bishop AT, Spinner RJ, Shin AY. Brachial plexus injuries in adults. Hand Clin. 2005; 21(1):ix–x. Dahlin LB. Mini-symposium: hand trauma (ii) nerve injuries. Curr Orthop. 2008;22(1):9–16. Hall TM, Elvey RL. Nerve trunk pain: physical diagnosis and treatment. Man Ther. 1999;4(2):63–73. Hassan S, Kay S. Brachial plexus injury. Surgery. 2003;21(10):262–264. Jepsen JR, Laursen LH, Hagert C-G, Kreiner S, Larsen AI. Diagnostic accuracy of the neurological upper limb examination I: interrelater reproducibility of selected findings and patterns. BMC Neurol. 2006;6(8). Jepsen JR, Laursen LH, Hagert C-G, Kreiner S, Larsen AI. Diagnostic accuracy of the 9 of 57 neurological upper limb examination II: relations to symptoms of patterns of findings. BMC Neurol. 2006;6(10). Kinlaw D. Pre-/postoperative therapy for adult plexus injury. Hand Clin. 2005;21(1): 103–108. Levitz CL, Reilly PJ, Torg JS. The pathomechanics of chronic, recurrent cervical nerve root neuropraxia. The chronic burner syndrome. Am J Sports Med. 1997;25(1):73–76. Mannan K, Carlstedt T. Injuries to the brachial plexus. Surgery. 2006;24(12):415–420. Markey KL, Di Benedetto M, Curl WW. Upper trunk brachial plexopathy. The stinger syndrome. Am J Sports Med. 1993;21(5): 650–655. Moran SL, Steinmann SP, Shin AY. Adult brachial plexus injuries: mechanism, patterns of injury, and physical diagnosis. Hand Clin. 2005;21(1):13–24. Nithi K. Physiology of the peripheral nervous system. Surgery. 2003;21(10):264a–264e. Pratt N. Anatomy of nerve entrapment sites in the upper quarter. J Hand Ther. 2005;18(2):216–219. Reid S, Trent V. Brachial plexus injuries—report of two cases presenting to a sports medicine practice. Phys Ther Sport. 2002;3(4): 175–182. Seddon HJ. Surgical Disorders of the Peripheral Nerves. 2nd ed. Edinburgh: Churchill Livingstone; 1975. Shin AY, Spinner RJ, Steinmann SP, Bishop AT. Adult traumatic brachial plexus injuries. J Am Acad Orthop Surg. 2005;13:382–396. Sunderland S. Nerve and Nerve Injuries. 2nd ed. Edinburgh: Churchill Livingstone; 1978. Weinberg J, Rokito S, Silber JS. Etiology, treatment, and prevention of athletic stingers. Clin Sports Med. 2003;22(3):493–500. Wilbourn AJ, Gilliat RW. Double crush syndrome: a critical analysis. Neurology. 1997; 49:21–29. AUTHOR: SARAH GRAHAM Common Fibular Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Common fibular nerve entrapment is a mononeuropathy that results from compression or restricted movement of the nerve usually found around the fibular head or in the popliteal space behind the knee. SYNONYMS • Common peroneal nerve entrapment • Strawberry picker’s knee • Slimmer’s paralysis ICD-9CM CODES 355.7 Other mononeuritis of lower limb OPTIMAL NUMBER OF VISITS 6 or fewer MAXIMAL NUMBER OF VISITS 16 ETIOLOGY EPIDEMIOLOGY AND DEMOGRAPHICS This condition is the most common nerve entrapment syndrome in the lower extremity after trauma. Certain jobs or activities where repetitive or prolonged knee flexion is required may cause more fibular nerve compression and develop into this pathology. No gender or age differences were noted in the incidence of common fibular nerve entrapment. MECHANISM OF INJURY COMMON SIGNS AND SYMPTOMS • The most identifiable symptom is weakness in the ankle dorsiflexors, which tends to alter the normal gait pattern. This symptom is usually the most concerning for the patient since it may lead to tripping, loss of balance, and even falls from inadequate foot clearance. 10 of 57 AGGRAVATING ACTIVITIES • • • • Prolonged kneeling or squatting Prolonged exercise Wearing a tight knee brace or cast Any activity that increases the local pressure around the nerve, thus increasing the compression and therefore the symptoms. Prolonged exercise, such as running, in which the fibularis longus is continually used may lead to more local trauma and swelling. EASING ACTIVITIES • Rest • Ice and local modalities • Avoiding aggravating activities 24-HOUR SYMPTOM PATTERN No specific pattern of symptoms is noted. However, if there is a significant inflammatory component to the problem the patient may experience night symptoms or have increased symptoms in the morning that resolve slightly after about 30 minutes of light activity. PAST HISTORY Past history might include previous bouts of the same condition, local trauma, or previous lumbar spine or nerve disorder. PHYSICAL EXAMINATION • As mentioned, the most prominent sign in this condition is ankle dorsiflexion weakness and gait difficulties. They may manifest with a steppage gait pattern where compensations, such as increased knee flexion and hip flexion, occur during swing phase to clear the foot. If considerable weakness is present without compensations, the patient may complain of tripping caused by inadequate toe clearance. A foot slap or absent heel strike may also be present. • Weakness of the tibialis anterior, extensor hallucis longus, and extensor digitorum longus should be noted on MMT. • Sensation changes over the fibular head, anterolateral leg, and dorsum of the foot may be present. If the lesion or compression site is below the fibular neck, the sensation on the lateral calf may be spared, while still having changes on the dorsum of the foot. ORTHOPEDIC PATHOLOGY The common fibular nerve entrapment may occur after traumatic events such as the following: • Direct trauma • Lacerations • Femur or fibular fracture • Gun shot wounds • Local surgery Open reduction and internal fixation (ORIF) Tibial osteotomy Total knee replacement • Knee dislocations • Other factors that may lead to entrapment: Habitual leg crossing Compression against bed railing or hard mattress in debilitated patients Prolonged immobilization Improperly fitting cast or brace Intraneural or extraneural ganglia Schwannoma Desmoid tumor Angioma Neuroma Baker’s cyst Chondromatosis Exostosis Well-developed muscles in the athletic population • Sensory loss and paresthesias are noted in the distribution of the common fibular nerve, which includes the lateral leg over the fibular head, anterolateral lower leg/calf region, and the dorsum of the foot. • Although pain is less likely in this condition, it may be present if significant soft tissue swelling and inflammation accompany the entrapment. Section III • Originating from the sciatic nerve in the middle distal third of the thigh, the common fibular nerve descends to the popliteal fossa along the lateral aspect of the distal thigh under the long and short head of the biceps femoris to the fibular head. The nerve then courses around the fibular neck through an opening near the superficial head of the fibularis longus. Here, the common fibular nerve divides into the superficial and deep fibular nerves. • Motor innervation of the common fibular nerve is as follows: Short head of the biceps femoris Fibularis longus and brevis (via superficial fibular nerve) Tibialis anterior, extensor hallucis longus, extensor digitorum longus, and fibularis tertius (via deep fibular nerve) • Sensory distribution of the common fibular nerve is as follows: The common fibular nerve innervates the anterolateral leg and the dorsum of the foot through the superficial and deep branches. The common fibular nerve itself innervates a portion of the lateral leg, over the head of the fibula. • Typical entrapment sites of the common fibular nerve are as follows: In the fibroosseous opening below the fibular head and near the superficial head of the fibularis longus the nerve passes through at a very acute angle. Here, the connective tissue may be tough since it helps secure the nerve to the proximal portion of the fibula. These factors make this a common area for entrapment. Repeated stress or injury to the lateral aspect of the knee may lead to entrapment of either the superficial or deep branch of the common fibular nerve. The superficial branch passes through the deep fascia and junction between the middle and distal third of the leg. Here, the fascia may be tough or restricted, limiting mobility of the nerve. 745 746 Common Fibular Nerve Entrapment IMPORTANT OBJECTIVE TESTS • Gait analysis: Gait changes as noted are more obvious when there is significant or long-standing compression of the common fibular nerve. • Tinel’s sign: Tapping around the fibular head and head of the fibularis longus may reproduce symptoms into the distribution of the nerve. • MMT and myotomal testing should reveal weakness of the extensor hallucis longus, tibialis anterior, and possibly fibularis brevis. • Sensory testing is important to confirm that changes are occurring in only a peripheral nerve distribution related to the common fibular nerve. If symptoms are in a more dermatomal distribution, other proximal causes should be considered, such as lumbar spine radiculopathy. • Neurodynamic testing may implicate a neurogenic source of symptoms. • Lumbar ROM testing, accessory mobility testing, and palpation DIFFERENTIAL DIAGNOSIS • • • • • Lumbar spine radiculopathy (L4) Local fracture Local tumor or space-occupying lesion Compartment syndrome Infection CONTRIBUTING FACTORS • Excessive weight loss may contribute to this condition since it can lead to a decrease in the fat pad over the fibular head. This lack of protection may leave the nerve more vulnerable to local compression. • Bulky lower extremity muscles, may also increase the pressure on the common fibular nerve, especially if combined with repetitive lower extremity activities such as running. • Jobs or activities with repetitive knee flexion or kneeling may lead to more compression on the nerve. • Hyperthyroidism, diabetes mellitus, vascular disorders, and leprosy have all been shown to have some effect on lower extremity nerve entrapment. CHAPTER 16 • NERVE TREATMENT PROGNOSIS MEDICAL/SURGICAL OPTIONS • Spontaneous recovery is noted in many cases of this condition, so nonoperative management is recommended for 3 to 4 months. However, if anterior compartment syndrome (ACS) is suspected, an immediate referral to physician, urgent care, or emergency department is needed because this is an emergency situation in which a fasciotomy needs to be performed as soon as possible to relieve pressure on the nerve and surrounding structures. • For common fibular nerve entrapment, a surgical decompression may be performed, especially in the case of spaceoccupying lesions. • Nonsteroidal antiinflammatory drugs (NSAIDs), oral corticosteroids, or local injections may help alleviate symptoms if there is significant pain or inflammation. REHABILITATION • The first goal of rehabilitation is to identify and remove the cause of the nerve compression if possible. • If significant weakness and gait deviations occur, bracing such as an ankle-foot orthotic (AFO), splint, or orthopedic shoes may help to normalize gait patterns. A lightweight rigid AFO or a hinged AFO with dorsiflexion assist may be appropriate. • If the patient has significant pain or if an inflammatory component is suspected, local modalities, such as ice, ultrasound, interferential current, phonophoresis, or massage, may help manage symptoms. • In the presence of positive neurodynamic findings and suspected restricted nerve mobility without significant compression, soft tissue mobilization along with neurodynamic mobilizations may be warranted. Butler suggests techniques that attempt to glide, slide, or put tension on the nervous system to free up local adhesions that may be restricting movement and preventing normal signal transmission. 11 of 57 • In a number of cases, spontaneous recovery has been noted in patients with this condition. This also depends on the cause of the lesion because a transient compression will have much better results with therapy compared to a space-occupying lesion, such as a tumor, or internal factors such as a hardware used to fixate a fibular fracture. • Wheeless noted that for partial fibular nerve palsy, >80% of patients recover completely and for complete nerve palsy <40% of patients have complete recovery. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Constant, unrelenting pain may indicate tumor or infection needing further medical management or workup. • Symptoms not following the normal common fibular nerve distribution may indicate a different pathology that may require further physical therapy or medical evaluation. • Increased pain or pressure in the anterior shin with tibialis anterior weakness may indicate ACS; immediate treatment by fasciotomy is needed to relieve the buildup of internal fluid and pressure. SUGGESTED READINGS Butler DS. The Sensitive Nervous System. Adelaide, Australia: Noigroup Publications; 2000. Butler DS. Mobilisation of the Nervous System. New York: Churchill Livingston; 1991. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. http://www.wheelessonline.com/ortho/ peroneal_nerve AUTHOR: CHRIS IZU Deep Fibular Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Deep fibular nerve entrapment is a mononeuropathy caused by compression or restriction of movement of the nerve in the anterior compartment of the lower leg or in the lateral ankle. SYNONYMS • Deep peroneal nerve entrapment • Anterior tarsal tunnel syndrome (ATTS) • Ski-boot syndrome ICD-9CM CODES 355.7 Other mononeuritis of lower limb laterally, the interosseous membrane posteriorly, and the anterior fascia anteriorly. The deep fibular nerve may also be entrapped at the anterior tarsal tunnel, which is formed by the talotibial joint, the talonavicular joint, and the extensor retinaculum. Here, the nerve and the dorsalis pedis artery pass beneath the retinaculum. Repeated mechanical irritation beneath the retinaculum is the most common form of tarsal tunnel syndrome. The deep fibular nerve may also be compressed in the tunnel by osteophytes, exostosis, bony prominences, or space-occupying lesions such as ganglia. decreased dorsiflexion in swing may be noted. • Loss of sensation in the web space of the first and second digits is common, as this is main sensory distribution of the nerve. AGGRAVATING ACTIVITIES • • • • • • • • EPIDEMIOLOGY AND DEMOGRAPHICS OPTIMAL NUMBER OF VISITS Wearing tight shoes Wearing boots or athletic wear Walking Prolonged standing Ascending or descending stairs Sitting with foot in plantar flexion Sleeping with feet under the covers Some of the previous activities and external pressure on the foot may compress the nerve. Other activities with increased plantar flexion may place a stretch on the nerve, shortening its diameter. EASING ACTIVITIES 16 No reports on the incidence of this pathology were found. Clinically, it is commonly seen along with other injuries such as ACS or localized trauma to the anterior shin. ETIOLOGY MECHANISM OF INJURY 24-HOUR SYMPTOM PATTERN • Branching off the common fibular nerve just distal to the fibular head, the deep fibular nerve enters the anterior compartment in the front of the leg near the interosseus membrane. It then courses distally lateral to the tibialis anterior muscle near the extensor digitorum longus, where it eventually goes under the extensor hallucis just above the ankle mortise. Passing in front of the ankle, the deep fibular nerve goes under the extensor retinaculum, where it divides into the lateral and medial branches. • Sensory distribution of the deep fibular nerve: The nerve supplies sensation to the web space of the first and second toes, the adjacent metatarso phalangeal joint, and the nearby interphalangeal joints. • Motor distribution of the deep fibular nerve:The lateral branch of the deep fibular nerve supplies the tibialis anterior, extensor digitorum brevis, extensor hallucis brevis, the adjacent tarsal and tarsometatarsal joints, and sometimes the second and third dorsal interossei. The medial branch innervates the extensor hallucis longus tendon and the extensor hallucis brevis muscle. • Typical areas for deep fibular nerve entrapment are as follows: With repeated stress or injury to surrounding musculature or fascia, fibrotic scarring may occur and entrap the deep fibular nerve. The nerve is commonly trapped within either the anterior compartment or the anterior tarsal tunnel. The anterior compartment is formed by the tibia medially, the fibula • Direct trauma, such as snake bites or a blunt force, may cause injury to this area. • Other common injuries leading to possible nerve entrapment include muscle inflammation secondary to prolonged exercise and local arterial bleeding. • Forced or uncontrolled plantar flexion and inversion of the ankle can place this region under lots of stress. • It is thought that repeated ankle sprains may be a contributing factor to fibular nerve entrapment in this area. • Postural changes in the lower extremity that alter biomechanics may place more stress on the deep fibular nerve. • Footwear that has a tight strap over the anterior part of the ankle can add external compression. • Prolonged sitting with the foot in plantarflexion may also place strain on the deep fibular nerve. Since activities such as prolonged walking or standing are aggravating activities, more pain might be noted later in the day. Pain also could occur at night with plantar flexion of the foot under the covers or in the case of a strong inflammatory component to the condition. Associated pain in the morning might also be present. 6 or fewer MAXIMAL NUMBER OF VISITS 12 of 57 Properly fitting footwear Sitting Rest Modalities PAST HISTORY No specific past history is noted in the literature, but it seems feasible that repetitive trauma or past injury to the front of the shin or ankle may predispose an individual to this problem. Repetitive injury or poor healing from another injury may lead to fibrotic scarring around surrounding nerve fascia. PHYSICAL EXAMINATION • Sensory changes within the web space of the first and second digit are commonly present with deep fibular nerve entrapment. • Antalgic gait or gait with limited dorsiflexion or toe extension may also be present. IMPORTANT OBJECTIVE TESTS • Lower quarter neurological examination Sensory examination may find sensory changes as noted previously. Motor examination should be normal with myotomal testing, but pain may be present with dorsiflexion or slight weakness with toe extension Reflexes should be normal since this neuropathy is below the level of the patellar tendon reflex and a different ORTHOPEDIC PATHOLOGY • The most common complaint is a vague pain, burning, or cramping over the dorsum of the foot, usually with pain within the web space of the first and second digit. • Weakness in the toe extension may be present as the deep fibular nerve provides motor input to both the extensor digitorum brevis and the extensor hallucis brevis. • Because of weakness and pain in the foot, the patient may complain of gait difficulties. If the proximal component of the nerve (common fibular nerve) is involved, footdrop or foot slap with • • • • Section III COMMON SIGNS AND SYMPTOMS 747 748 Deep Fibular Nerve Entrapment branch of the sciatic nerve that does not innervate the Achilles tendon. • The following tests may also help to rule out possible proximal causes such as lumbar radiculopathy: Tinel’s test:Tapping at the anterior tarsal tunnel may reproduce more distal symptoms. Palpation: Palpation of surrounding musculature in the anterior compartment or anterior surface of the ankle may also reproduce symptomatic complaints. Neurodynamic examination: Using the straight leg raise (SLR) with plantar flexion and inversion, the clinician may be able to differentiate between neurogenic (deep fibular nerve) and nonneurogenic (local muscles or tendons). DIFFERENTIAL DIAGNOSIS • • • • • • • Bony impingement Cystic masses Lumbar spine radiculopathy Common fibular nerve entrapment Sciatic nerve entrapment ACS Shin splints CONTRIBUTING FACTORS • Improper footwear • Abnormal foot positioning: Pes planus or cavus • Thyroid dysfunction • Diabetes TREATMENT SURGICAL OPTIONS • If there is significant increase in pressure within the anterior compartment (ACS), a fasciotomy, in which a small incision is made in the anterior fascia, is necessary to reduce building pressure. This situation can be a medical CHAPTER 16 • NERVE emergency, and failure to do such a procedure may result in permanent damage to the local and distal structure of the lower extremity. • Surgical release of the deep fibular nerves may also be performed. This has been reported to produce immediate relief of symptoms and requires an excision of the nerve from the perceived entrapment site. • Removal of osteophytes or space-occupying lesions are an important part of surgical management. REHABILITATION • The first goal of rehabilitation is to reduce symptoms and associated inflammation sensitizing the nerve. • Modalities, such as ultrasound, phonophoresis, iontophoresis, interferential current therapy, ice, and compression, are theorized to help during more acute or inflammatory stages. • Addressing postural faults and foot positioning may help to take stress off the deep fibular nerve. Taping and orthotic prescription may assist in this task. • Once symptoms are alleviated, other techniques, such as soft tissue mobilization, may help free the nerve from surrounding fibrotic tissue. • Neurodynamic techniques to help slide, glide, or place the nerve under tension may be warranted at this time to help restore the normal mobility of the nervous system. • Other biomechanical faults or impairments that are hypothesized to place more stress on the deep fibular nerve must also be addressed before the rehabilitation program can be considered complete. PROGNOSIS No data were found at this time for the long-term outcomes of deep fibular nerve entrapment. Wheeless noted that for partial fibular nerve palsy >80% of patients 13 of 57 recover completely and for complete nerve palsy <40% of patients have complete recovery. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Severe unrelenting pain occurring through the anterior shin may indicate ACS and worsening compression on the nerve. A fasciotomy must be done as soon as possible to release this pressure. • Unrelenting symptoms, especially combined with worse pain at night, may indicate a local tumor. • Lack of improvement within the expected time frame or symptoms that are not affected by physical therapy in a few visits should be referred back to the physician because a space-occupying lesion may be present. • A recent history of trauma with suspected fracture may warrant further imaging before continuing physical therapy. • Impaired circulation or vascular compromise may also warrant more medical management. SUGGESTED READINGS Butler DS. Mobilisation of the Nervous System. New York: Churchill Livingston; 1991. Butler DS. The Sensitive Nervous System. Adelaide, Australia: Noigroup Publications; 2000. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. http://www.wheelessonline.com/ortho/ peroneal_nerve AUTHOR: CHRIS IZU Femoral Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Femoral nerve entrapment is a mononeuropathy that results from compression or restriction of movement of the nerve, usually in the anterior abdominal wall as it passes through the femoral triangle under the inguinal ligament. ICD-9CM CODES 355.2 Other lesion of femoral nerve OPTIMAL NUMBER OF VISITS 6 or fewer MAXIMAL NUMBER OF VISITS 16 ETIOLOGY • The femoral nerve may become injured or entrapped from local trauma to the anterior hip or thigh such as a contusion or repetitive strain. • It may also be injured or compressed during stressful abduction or external rotation activities such as during birth (vaginal deliveries). • Intrapelvic injury and injury to the inguinal region have also been documented to lead to nerve entrapment. • Common traumatic events include the following: Gunshot wounds Knife wounds Puncture wounds Pelvic surgeries Total hip replacement (anterior approach) Pelvic fractures • Other noted factors that can lead to compression include the following: Pelvic radiation therapy Appendical or renal abscess Tumors Compartment-like compression COMMON SIGNS AND SYMPTOMS AGGRAVATING ACTIVITIES • Walking or standing may aggravate symptoms secondary to a stretch on the femoral nerve with hip extension, especially during trailing limb posture in gait. • Walking may also be difficult if significant quadriceps weakness is present. EASING ACTIVITIES EPIDEMIOLOGY AND DEMOGRAPHICS One reference stated that this entrapment syndrome is thought to be a rare occurrence and that earlier reported cases may have been mislabeled as femoral nerve neuropathies instead of other proximal causes. • • • • Sitting Hip flexion or external rotation Rest Local modalities 24-HOUR SYMPTOM PATTERN No specific pattern of symptoms is noted. However, if there is a significant inflam- 14 of 57 PAST HISTORY • Prior history of surgery in the pelvic region (i.e., hernia, cesarean section, or hysterectomy) • Past history of a patient with this condition may include previous trauma to the area, repetitive stress injuries, or other lumbopelvic problems. • Prior history of prostate or uterine pathology PHYSICAL EXAMINATION • Weakness with hip flexion and knee extension are the most common symptoms associated with femoral nerve entrapment. Gait deviations may be noted to compensate for quadriceps weakness, and a quadriceps avoidance pattern of limited knee flex during loading response may be present. • A diminished patellar tendon reflex is most likely present secondary to impaired nerve conduction. • Sensory deficits are likely present in the anteromedial aspect of the thigh and may be in the medial aspect of the leg because of the saphenous branch of the femoral nerve. • Pain may be noted with resisted hip flexion from the possible involvement of the psoas muscle and with stretching into combined hip extension and knee flexion. • Palpation around the lateral portion of the femoral triangle, psoas, or iliacus muscle may be painful compared to the unaffected side and may reproduce symptoms down into the anteromedial aspect of the thigh or knee. IMPORTANT OBJECTIVE TESTS • Strength testing Motor deficits in hip flexion and knee extension might be the most obvious signs of femoral nerve compression. However, weakness in the area alone should not be considered diagnostic because an L3 radiculopathy may produce the same result. • Lower quarter neurological examination To make sure symptoms are only the result of an isolated peripheral nerve problem, a full lower quadrant neurological examination is warranted. Symptoms that follow along a more dermatomal or myotomal pattern indicate a more proximal problem. Symptoms that cross one or more dermatomes or peripheral nerve regions may be the result of a polyneuropathy. ORTHOPEDIC PATHOLOGY • Weakness in knee extension is common because of the motor input of the femoral nerve to the large quadriceps muscles. Hip flexion may also be difficult from the contribution of the rectus femoris. • Gait difficulties or functional activities like squatting may become more difficult because of the weakness in knee extension. • Sensation loss in the anterior aspect of the thigh may be present if the anterior cutaneous branch of the femoral nerve is affected.An individual with this condition may also have sensation loss to the medial aspect of the knee from involvement of the saphenous branch. • Pain may be present in the inguinal region from the cause of the compression. matory component to the problem, one may experience night symptoms or may have increased symptoms in the morning that resolve slightly after about 30 minutes of light activity. Section III • The femoral nerve originates from the ventral rami of L2, L3, and L4 near the psoas major and travels inferiorly in the intermuscular groove between the psoas and the iliacus muscle. From there, it passes under the inguinal ligament in the femoral triangle lateral to the femoral artery and vein. It then divides into both sensory and motor branches. • The cutaneous sensory branches of the nerve innervate the proximal upper and anterior thigh. • The femoral nerve sends branches to the large quadriceps muscles. • Because of the location of the femoral nerve, there is a multitude of factors that can cause femoral nerve entrapment.The most common entrapment area occurs underneath the inguinal ligament. • It also may be entrapped or compressed more inferiorly where the nerve is close to the humeral head and attachments of the vastus intermedius and psoas tendons. Problems with those tendons or muscles may cause femoral nerve restrictions or irritation. • Local tumors, psoas abscesses, lymph node enlargement, hematomas, and penetrating trauma are some of the most commonly documented causes of internal compression of the femoral nerve. • Tissue healing after trauma or surgery has also been hypothesized to lay down scar tissue that may restrict the mobility of the femoral nerve within its neural container. MECHANISM OF INJURY 749 750 Femoral Nerve Entrapment • Slump knee bend test Performing this test in sidelying, according to Butler, with cervical flexion and extension as a sensitizing maneuver may help determine if neurogenic symptoms are present, as in the case of femoral nerve entrapment. • Lumbar ROM testing, accessory mobility testing, and palpation may help differentiate a lumbar spine problem from an isolated femoral nerve entrapment. DIFFERENTIAL DIAGNOSIS • Lumbar radiculopathy (L3 most likely) • Local muscular strain • Pelvic fracture • Hip fracture • Hip joint pathology • Appendical or renal abscess • Tumors CONTRIBUTING FACTORS • • • • Diabetes mellitus Thyroid problems Poor posture Impaired trunk and motor control TREATMENT SURGICAL OPTIONS Microsurgical nerve decompression CHAPTER 16 • NERVE REHABILITATION • The initial goals of rehabilitation are to reduce the pain and inflammation in the present state of the condition. • Modalities, such as ultrasound, phonophoresis, iontophoresis, interferential current therapy, light massage, and cold, may help to accomplish this. • If there are any external compression factors such as tight clothes, modification of attire is necessary. • After symptoms have calmed, rehabilitation may focus on improving the health and mobility of the nerve. • Soft tissue mobilization directed at fibrotic scarring around the nerve may be beneficial. • Neurodynamic mobilizations aimed at sliding, gliding, or placing tension on the nerve may also be warranted to restore normal mobility to the nervous system. • A complete rehabilitation program will also work to address any other biomechanical faults or impairments that might be leading to stress or strain on the femoral nerve. PROGNOSIS One study reported up to 70% improvement of symptoms in this population, although improvement may take up to a year. If there is severe axonal loss, it is thought that there will be some recovery of function, although not complete. 15 of 57 SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Unrelenting pain not related to biomechanical factors • Weight loss • Bowel or bladder dysfunction • Saddle paresthesias • Gait disturbances: Clumsiness or ataxic gait • Bilateral glove or sock numbness • Symptoms that do not initially improve with symptoms SUGGESTED READINGS Butler DS. The Sensitive Nervous System. Adelaide, Australia: Noigroup Publications; 2000. Butler DS. Mobilisation of the Nervous System. New York: Churchill Livingston; 1991. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. http://www.emedicine.com/Or thoped/ topic422.htm AUTHOR: CHRIS IZU Interosseous Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Compression of the posterior interosseous nerve (which arises from the radial nerve) at the tendinous margin of the extensor carpi radialis brevis, fibrous bands anterior to the head of the radius, radial recurrent blood vessels, or between the two supinator heads in the arcade of Frohse, which is a fibrous arch occurring in 30% of the population. SYNONYMS • Radial tunnel syndrome • Posterior interosseous nerve syndrome ICD-9CM CODES 955.3 Injury to radial nerve OPTIMAL NUMBER OF VISITS Conservative management should produce some reduction in symptoms within 3 to 6 weeks. MAXIMAL NUMBER OF VISITS ETIOLOGY EPIDEMIOLOGY AND DEMOGRAPHICS • Posterior interosseous nerve entrapment is an uncommon cause of lateral elbow and forearm symptoms. • Since the causes for this pathology are so diverse, it occurs across a broad spectrum of the population. MECHANISM OF INJURY • The nerve entrapment may be caused by local edema from irritation of the neighboring tissues or volume changes 16 of 57 COMMON SIGNS AND SYMPTOMS • Posterior interosseous nerve entrapment commonly manifests with pain in the extensor region of the lateral forearm. The pain is most intense over the supinator, sometimes extending to the wrist and proximal humerus. It can be combined with pain on resisted supination when the elbow is flexed and resisted extension of the middle finger when the elbow is extended, weakness in wrist and finger extension, and paraesthesias in the hand and lateral forearm, although this is disputed by some authors. • Clinical signs and symptoms for radial tunnel syndrome and posterior interosseous compression, with indications and options for surgical treatment, are presented by Markiewitz and Merryman. • The typical referral pattern for posterior interosseous nerve entrapment is local pain at the elbow and lateral forearm, extending to the wrist and upper regions of the humerus. AGGRAVATING ACTIVITIES • Repetitive forearm rotation • Resisted supination from pronation with wrist flexion • Full-range pronation • Elbow extension • These movement patterns occur with a range of activities but are prevalent in office workers, manual workers, musicians, and athletes. EASING ACTIVITIES • Reducing load • Avoiding the aggravating movement patterns • Positioning • Rest (absolute or relative with the aid of splinting or taping) 24-HOUR SYMPTOM PATTERN Symptoms worsen with aggravating activities, but pain may also increase nocturnally, which is similar to many entrapment neuropathies. ORTHOPEDIC PATHOLOGY • The insult to the nerve may be mechanical, thermal, chemical, or ischemic. • In entrapment syndromes, compression or direct trauma leads to nerve tissue hypoxia. • Posterior interosseous nerve entrapment pathology may occur with repetitive or overuse movement patterns involving supination and pronation of the forearm, trauma, surgery, underlying rheumatoid disease, ganglions, and tumors. • In entrapments, nerve trauma occurs because the size of the neural structure exceeds the anatomical space available for it, resulting in increased pressure, which in turn leads to impaired blood flow and subsequent hypoxia of the tissue and disruption of the axonal transport system. • Nerve injury is classified according to severity of the injury and potential for reversibility. Original classifications described previously remain in current use. First-degree neuropraxia involves distortion of myelin about the nodes of Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance, resulting in temporary loss of nerve conduction. Recovery is rapid and complete in most cases. Second-degree axonotmesis involves interruption of the axon with second- in surrounding tissues generated by mechanical overload via repetitive activity or impact trauma, specifically in supinator and extensor carpi radialis brevis. • Posterior interosseous nerve entrapment may be compounded by the presence of certain anatomical features: Fibrous bands anterior to the radial head or within the supinator arch (the arcade of Frohse) and the specific location of the radial recurrent blood vessels. • Other causes include fractures, inappropriately positioned surgical fixings and plates, surgical trauma, rheumatoid synovitis, ganglions, and tumors. Section III If there is little or no response to conservative management after 12 weeks, a surgical opinion should be obtained. ary wallerian degeneration, but the supporting tissue around the axon is preserved. Recovery may be complete but takes longer to occur and depends on the distance between the site of injury and the end structure (denervated muscle). Third-degree neurotmesis involves extensive disruption of the nerve and its supporting structures, but while the endoneurium is disrupted, the perineurium and epineurium remain intact. Fourth-degree neurotmesis involves disruption of all neural components except the epineurium. Fifth-degree neurotmesis involves complete transaction and discontinuity of the nerve with no capacity for regeneration. • Neurotmesis rarely occurs from entrapment, but where continuity has been disrupted, complete recovery is not possible, even with surgical techniques, and the eventual outcome depends on individual circumstances. • Double-crush syndrome refers to the fairly common phenomenon of nerve entrapment and radiculopathy occurring in combination, although the syndrome is considered controversial. Compression or irritation of the nerve roots at the cervical level is thought to increase sensitivity to compression or movement restrictions more distally in the structure. • As noted earlier, increasing pressure on the nerve causes impaired blood flow, tissue hypoxia, and disruption to the anterograde and retrograde intercellular transport of materials within axons, eventually disturbing depolarization within the nerve. In overuse-type entrapments, it is proposed that repetitive work or static postures produce an inflammatory response. Fibroblasts appear to repair the damage incurred but generate adhesions that limit neural glide and subsequently increase anoxia. Other studies have found that cortical dedifferentiation may occur from repetitive motion activities and nerve injuries. This may result in reinforced poor posturing and use of aberrant motor pathways. 751 752 Interosseous Nerve Entrapment PAST HISTORY FOR THE REGION • Previous history of trauma, surgery, or overuse-type injury at the elbow, forearm, or wrist • History of rheumatoid disease PHYSICAL EXAMINATION • Pain over the anterolateral forearm with referral as described previously. • Maximum tenderness is approximately 6 to 8 cm distal to the lateral epicondyle, over the supinator. • Pain is provoked or worsened with resisted supination, elbow extension with pronation, and extension of the middle finger. • Depending on the site of compression, weakness may also be present in wrist extension (extensor carpi ulnaris and extensor digitorum communis are affected), finger extension (extensor digiti quinti, extensor digitorum communis, and extensor indicis proprius are affected), and thumb movement (abductor pollicis longus, extensor pollicis longus, and brevis are affected). IMPORTANT OBJECTIVE TESTS • Radiography and MRI facilitate detection of underlying factors such as fractures, ganglions, tumors, or other tissue abnormality. • Local injection at the lateral epicondyle may distinguish between lateral epicondylitis (when it is usually much more effective) and radial tunnel syndrome (when it has little or no effect). • EMG and nerve conduction studies may be inconclusive, so clinical findings previously described, in conjunction with neural tension techniques, may provide the most reliable aid to diagnosis. • Diagnostic accuracy of neurological upper limb examination employing a battery of standard test procedures has been found to be reproducible and reliable. DIFFERENTIAL DIAGNOSIS • Cervical radiculopathy (C7 pathology affects triceps brachii and wrist flexors) • Lateral epicondylitis (maximal tenderness is at the lateral epicondyle rather than distal to it) • Trigger finger (passive, as well as active, movement is affected) • Extensor tendon rupture (fingers fail to extend on passive wrist flexion) • Adverse neural tension CONTRIBUTING FACTORS • • • • Anatomical arrangement Presence of other underlying disease Past history of trauma or surgery Lifestyle activities involving elbow or forearm movement patterns CHAPTER 16 • NERVE TREATMENT PROGNOSIS SURGICAL OPTIONS • An overview of basic neurosurgical techniques is provided by Dahlin. Individuals who fail to respond to conservative management may require decompression surgery. • Two main techniques, anterolateral and posterior, may be employed. The anterolateral technique is preferred because it allows greater access to more of the entrapment sites, facilitating release at the supinator, arcade of Frohse, fibrous margin of extensor carpi radialis brevis, distal fascia, and dissection of the nerve from scar tissue posttrauma. • If symptoms are arising from fixation devices, corrective surgery will be required. • If compression is due to ganglion or tumor, surgical technique will obviously depend on precise location. • In addition to the standard risks associated with any surgery, there is a risk of further damage to the nerve during the procedure. However, success rates of 90% have been reported for neurapraxic injuries, with fast recovery to full normal function. • Individuals who have failed to respond to conservative management after a period of 8 to 12 weeks should be considered for surgical opinion. In addition, any worsening of neurological function despite intervention should be evaluated (Cravens and Kline). REHABILITATION • Cleary provided an overview of concepts and evidence for conservative management in radial tunnel syndrome but notes that definitive clinical evidence is scarce. • Conservative treatment consists of manual techniques consisting of soft tissue release work, myofascial release work, and neural stretching or mobilizing techniques. • Depending on the underlying cause of the pathology, antiinflammatory modalities may also be useful, combined with offloading the stressed structures. • The effectiveness of antiinflammatory medication is disputed, although many authors recommend including these in the management regimen since they produce benefit in some cases. • It may be appropriate to teach individuals stretching or mobilizing techniques to be applied between treatment sessions. • If abhorrent movement patterns are the result of other muscle imbalance or recruitment issues, it may be appropriate to address these issues as part of the rehabilitative process. 17 of 57 • As previously noted, factors that contribute or predispose an individual to the pathology include anatomical arrangement, presence of other underlying disease, past history of trauma or surgery, or lifestyle activities involving elbow and forearm movement patterns. • Prognosis for full recovery is good, with almost all cases responding to either conservative or surgical management. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Worsening neurological function or symptoms • Failure to respond to conservative management • Suspicion or presence of underlying disease • Unexplained symptoms inconsistent with the pathology SUGGESTED READINGS Brukner P, Khan K. Clinical Sports Medicine. 3rd ed. New York: McGraw-Hill; 2006. Cleary CK. Management of radial tunnel syndrome: a therapist’s clinical perspective. J Hand Ther. 2006;9(2):166–191. Cravens G,Kline DG.Posterior interosseous nerve palsies. Neurosurgery. 1990;27(3):397–402. Dahlin LB. Mini-symposium: hand trauma (ii) nerve injuries. Curr Orthop. 2008; 22(1):9–16. Hall TM, Elvey RL. Nerve trunk pain: physical diagnosis and treatment. Man Ther. 1999; 4(2):63–73. Jepsen JR, Laursen LH, Hagert C-G, Kreiner S, Larsen AI. Diagnostic accuracy of the neurological upper limb examination I: interrelater reproducibility of selected findings and patterns. BMC Neurol. 2006;6(8). Jepsen JR, Laursen LH, Hagert C-G, Kreiner S, Larsen AI. Diagnostic accuracy of the neurological upper limb examination II: relations to symptoms of patterns of findings. BMC Neurol. 2006;6(10). Magee DJ. Orthopaedic Physical Assessment. 5th ed. Philadelphia: Saunders; 2008. Markiewitz AD, Merryman J. Radial nerve compression in the upper extremity. J Am Soc Surg Hand. 2005;5(2):87–99. Pratt N. Anatomy of nerve entrapment sites in the upper quarter. J Hand Ther. 2005; 18(2):216–219. Seddon HJ. Surgical Disorders of the Peripheral Nerves. 2nd ed. Edinburgh: Churchill Livingstone; 1975. Sunderland S. Nerve and Nerve Injuries. 2nd ed. Edinburgh: Churchill Livingstone; 1978. Wilbourn AJ, Gilliat RW. Double crush syndrome: a critical analysis. Neurology. 1997;49:21–29. AUTHOR: SARAH GRAHAM Lateral Femoral Cutaneous Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Lateral femoral cutaneous nerve (LFCN) entrapment is a mononeuropathy that results from either compression or restriction of movement of the nerve, most likely as it passes under the inguinal ligament near the anterior superior iliac spine. SYNONYMS Meralgia paresthetica ICD-9CM CODES 355.1 Meralgia paresthetica OPTIMAL NUMBER OF VISITS 6 or fewer MAXIMAL NUMBER OF VISITS 12 ETIOLOGY • As the incidence of rapid weight gain increases in those who are middle-aged, so does the incidence of entrapment of the LFCN. • Construction workers, mechanics, or other professionals, whose jobs require Direct trauma, stretch injuries, and is chemi a are the most likely culprits, which would lead to compromise of the LFCN. Some documented traumatic events that have led to this condition include seatbelt injuries in motor vehicle accidents (MVAs), pelvic fractures, and surgical procedures. It has also been noted that LFCN entrapment may occur after lying in the fetal position for a long period of time. COMMON SIGNS AND SYMPTOMS • Most important to note is that there is likely no motor deficit with this condition since the LFCN is purely sensory. Some local muscle guarding may appear as a result of pain and muscle inhibition in both hip flexion and extension as the nerve is either further compressed or stretched. • The hallmark of LFCN entrapment is altered sensation over the lateral aspect of the mid-thigh. This may include numbness, tingling, or even a burning pain, a dull ache, or itching. • Symptoms are usually unilateral, although they may be bilateral in cases of rapid weight gain that affect the body symmetrically. AGGRAVATING ACTIVITIES • Walking or prolonged standing • Wearing tight clothes or accessories • Activities that include sustained or repetitive hip extension or flexion • Tight clothing and garments add external compression to the superficial region of the nerve, whereas hip extension activities may place stretch on surrounding structures that would in turn increase the local pressure around the nerve. Hip extension may also place the LFCN under more tensile stress. EASING ACTIVITIES • • • • Sitting or rest Removal of tight clothing Avoiding excessive hip extension Once the external compression is removed, improved axonal flow and neuronal blood flow should help alleviate some of the symptoms. 24-HOUR SYMPTOM PATTERN Current research has not addressed a 24-hour pattern of symptoms of this disorder. However, if there is a significant inflammatory component of the disorder, symptoms may be worse in the 18 of 57 PAST HISTORY Previous trauma to the area or incidence of the same condition may predispose a person to LFCN entrapment. PHYSICAL EXAMINATION • Altered sensation is the hallmark of the condition and should manifest as numbness, paresthesias, or pain in the anterolateral thigh. • Motor examination or MMT of lower extremity myotomes should be normal since the LFCN is purely sensory. The patient may have pain with hip flexion or knee extension secondary to local attachment near the dysfunctional area, but strength should be symmetrical. IMPORTANT OBJECTIVE TESTS • Sensation testing It is important to map out the specific area or distribution of symptoms to differentiate the cause from a potential more proximal lumbar spine cause. Symptoms that occur more distally than the anterolateral thigh, such as down to the lateral leg or foot, suggest further lumbar spine testing. One suggestion has been to use a marker or pen to accurately draw the area on the patient’s leg. • Tinel’s test With tapping over the superficial region over the nerve (over the lateral and upper part of the inguinal ligament), symptoms should be reproduced. • LFCN test This test is performed as a variation of the slump knee bend test. Butler (2000) added adduction and internal rotation of the hip to stress the LFCN and to help determine if the symptoms are neurogenic by using cervical extension and flexion as a sensitizing maneuver. • Lumbar ROM testing, accessory mobility testing, and palpation Because of the chance that a more upper lumbar spine problem may refer symptoms distally into this region, it is important to rule out that area as a potential source of symptoms. DIFFERENTIAL DIAGNOSIS • Lumbar spine referral Disc dysfunction Somatic referred pain Nerve root irritation • Muscle strain • Pelvic fracture • Pelvic neoplasm ORTHOPEDIC PATHOLOGY EPIDEMIOLOGY AND DEMOGRAPHICS MECHANISM OF INJURY morning or may even cause wakening in the night. Section III • The nerve originates from the lumbar plexus and travels distally through the pelvis near the psoas major muscle and eventually through a tunnel formed by the lateral attachment on the inguinal ligament and the anterior superior iliac spine (ASIS). The nerve travels superficially to supply the skin about 10 cm distal to the inguinal ligament. Here, the nerve has less protection than it does more proximally in the pelvis. • Both internal and external factors can compromise the LFCN. Research and case studies have pointed toward tight clothing, such as jeans, underwear, or a belt, as possible external factors that could lead to nerve compression. Internal factors could include a pendulous abdomen, rapid increase in weight, or space-occupying lesions as potential causes of LFCN entrapment. Examples may include contained iliopsoas hemorrhage or neoplasm. • Another hypothesis of the cause of nerve entrapment is that the surrounding tissues that form the neural container may restrict or limit its ability to slide or glide as a result of dysfunction of nearby fascial layers. These tissues may leave the nerve bound to adjacent structures after trauma and healing have taken place such as in abdominal surgery or recent pelvic fracture. them to wear tight or heavy attire around their waists, have a higher incidence of this condition. • There is no difference in incidence between right and left sides of the body, and symptoms may also appear intermittently. 753 754 Lateral Femoral Cutaneous Nerve Entrapment • Polyneuropathy • Retroperitoneal hemorrhage CONTRIBUTING FACTORS • Diabetes can affect the health of the nervous system and predispose a person to nerve entrapment syndromes. • Obesity and especially rapid weight gain can increase the pressure or compression on the superficial region of the LFCN. • Pregnancy is a common contributing factor for the same reason as rapid weight gain. • Occupational requirements that include tight attire around the waste such as tight pants or work belts TREATMENT SURGICAL OPTIONS • If conservative measures fail, surgical decompression may be considered. Successful predictors of good outcomes after surgery include a positive Tinel’s test, abnormal electrodiagnostic findings (that do not suggest other potential causes), and immediate relief of symptoms after local nerve block. • In very rare instances, the nerve can be surgically transected.The long-term outcomes are suspect, and since the nerve has no motor function, which may lead to more serious disability, this option is not recommended. • A physician may be able to do a focal nerve block near the inguinal ligament using a combination of lidocaine and corticosteroids.This is a good treatment option if the pain is severe and may provide relief for several days to weeks. REHABILITATION • The most important factor in treatment is to remove the cause of the problem. Patient education on avoidance of tight clothing or accessories usually helps resolve the symptoms. If obesity or rapid gain is thought to be at fault, those factors also need to be addressed. • Concurrent rehabilitation may include modalities, such as ultrasound, interferential current therapy, and phonophoresis, to reduce swelling and inflammation. • It is also important to address other contributing factors such as the following: Ergonomics Postural changes and adaptations General fitness level, including stretching • If positive neurodynamic testing suggests nerve entrapment from restricted nerve mobility, other methods of treatment may include local soft tissue mobilization followed by nerve gliding with respect to irritability of symptoms. • Neurogenic pain medications, such as carbamazepine or gabapentin, have been shown to have some effect on symptoms in select patients, but the effects are usually minimal. PROGNOSIS Because of the pure sensory function of the LFCN, it is not typical for this condition to lead to severe functional loss or disability. Research shows that it is not associated with mortality or significant morbidity. Typically, the paresthesias resolve slowly over time, but numbness in the peripheral nerve distribution may persist. Removal of the cause of the nerve compression usually results in good outcomes. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Constant or unrelenting deep, boring pain may be a sign of a space-occupying lesion causing the nerve entrapment. These symptoms are even more of a 19 of 57 CHAPTER 16 • NERVE • • • • concern if not in the distribution of the LFCN such as the back, pelvis, or anterior hip. Pain or symptoms that do not change with treatment or removal of the hypothesized cause of the nerve compression may also point toward infection or tumor. Symptoms associated with trauma that has not been screened with radiographs or other imaging studies may be caused by concurrent pelvic fracture. Any other neurological signs, such as myotomal weakness or dermatomal sensory changes, may require further work-up or diagnostics, to rule out more proximal causes of symptoms. Severe pain preventing the patient from participating in therapy may require nerve block or other management before continuing. SUGGESTED READINGS Butler DS. Mobilisation of the Nervous System. New York: Churchill Livingston; 1991. Butler DS. The Sensitive Nervous System. Adelaide, Australia: Noigroup Publications; 2000. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. http://www.emedicine.com/Or thoped/ topic422.htm AUTHOR: CHRIS IZU Long Thoracic Nerve Pathology CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Long thoracic nerve pathologies encompass any injury that interrupts the function of the long thoracic nerve at any point along its course. The loss of function results in serratus anterior muscle dysfunction and often pain. SYNONYMS • Long thoracic nerve palsy • Serratus anterior muscle palsy • Rucksack palsy ICD-9CM CODES 354 Mononeuritis of upper limb and mononeuritis complex 354.8 Other mononeuritis of upper limb 354.9 Mononeuritis of upper limb unspecified OPTIMAL NUMBER OF VISITS 6 MAXIMAL NUMBER OF VISITS ETIOLOGY EPIDEMIOLOGY AND DEMOGRAPHICS The prevalence of long thoracic nerve injury has not been reported in the literature, but it is generally believed to be uncommon; no age groups have been reported as more prone to damage to the nerve and no gender specificity has been reported in the literature. MECHANISM OF INJURY • The long thoracic nerve is most susceptible to acute or recurrent trauma caused by traction or pressure. • Nontraumatic pressure on the nerve can result at a number of sites along its path, by the following: Within musculature (seen commonly in the scalene medius muscle) and inflamed bursa in the shoulder region Between the first two ribs and the clavicle or between the coracoid process and the first or second ribs In the axillary region from the presence of an axillary mass, excessive or poor use of old-style crutches, and overly tight bandage or plaster applications. • Traction trauma to the long thoracic nerve can occur in the following ways: Repetitive isolated stretch with cervical flexion, lateral flexion, and rotation away, combined with ipsilateral 20 of 57 COMMON SIGNS AND SYMPTOMS • The most common complaint is an insidious onset of shoulder girdle weakness with or without pain. • Pain can often be present in the first few days to weeks followed by weakness with overhead activities. • The patient may report decreased active shoulder ROM, particularly into forward flexion. This is accompanied by scapular winging, especially when pushing forward against resistance. • The pain is often described as a burning, aching, or sharp pain in the shoulder, which may radiate to the scapula, arm, or scalene muscle region. AGGRAVATING ACTIVITIES • Aggravating activities involve repetitive positions that place stress on the nerve (cervical flexion, lateral flexion, and rotation away, combined with ipsilateral arm flexion) such as throwing (baseball, javelin, or football), serving in tennis, spiking or serving in volleyball, and driving a golf ball. • Patients may also report symptom aggravation and reduced ability to pull and/or carry heavy objects, overhead lifting, tackling, and wrestling. ORTHOPEDIC PATHOLOGY • The anatomy of the nerve is as follows: Motor nerve that is 22 to 24 cm long with a superficial course Comprises the ventral rami of the C5 to C7 nerve roots (also the C8 nerve roots and intercostal nerves in some) C5 and C6 roots merge and pierce the scalene medius muscle, while the C7 root travels between the anterior and middle scalene muscles. The C5, C6, and C7 roots join to form the long thoracic nerve sitting anteriorly to the posterior scalene muscle. The nerve travels between the clavicle and first rib, laterally toward the midaxillary line, and here it sends out branches and innervates the serratus anterior muscle. • Physiologically there is disruption to any part of the nerve responsible for conduction. • In repetitive nerve injury, it is proposed that repetitive work or static postures produce an inflammatory process, fibroblasts appear to repair the damage incurred but produce adhesions to the nerve, limiting their glide and increasing anoxia. • Lacerations generally result in neurotmesis injury.The pathology is essentially an injury to the long thoracic nerve. Nerve injury can be classified according to the severity of the injury and its potential for reversibility. arm flexion. The cervical movement places an anterior, medial, and superior pull on the proximal portion of the nerve with the scalenus medius muscle, while the distal nerve segment is tensioned with the overhead arm position in a posterior, lateral, and inferior direction with the serratus anterior muscle. The scalenus medius and serratus anterior muscles act as points of fixation, resulting in excessive elongation of the nerve.This position of stretch is commonly seen with throwing in baseball, javelin, and football; serving in tennis; spiking or serving in volleyball; and driving a golf ball. Additionally, tackling, wrestling, and lifting heavy weights overhead may also traction the nerve. Repetitive bow-stringing of the nerve over a fascial band in shoulder abduction and external rotation. Repetitive carrying of heavy loads or an injury involving sudden forced scapular depression • Direct trauma to the nerve as it sits superficially in the supraclavicular fossa or chest may also occur with MVAs, falls, and strong massage. • Iatrogenic injury to the nerve is also common during first rib resection and heart or breast surgery. • Neuralgic amyotrophy, vaccinations, or infections may also affect the long thoracic nerve, either selectively or with other nerve involvement. Section III 20 • The following is a basic overview of the Sunderland classification of nerve injury, which describes five degrees of nerve pathology (an expansion of Seddon’s three-tier classification of neurapraxia, axonotmesis, and neurotmesis). Neurapraxia (first-degree injury): Distortion of the myelin around the nodes of Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance produces temporary loss of nerve conduction. Axonotmesis (second-degree injury): Interruption of the axon with secondary wallerian degeneration; the supporting tissue surrounding the axon is preserved and the recovery period depends on the distance between the site of injury and the end-organs. Neurotmesis: Complete disruption of the nerve and its supporting structures. • Neurotmesis has been further divided into the following three subcategories: Third-degree nerve injury: Endoneurium is disrupted with intact perineurium and epineurium. Fourth-degree nerve injury: All neural elements sparing the epineurium are disrupted. Fifth-degree nerve injury: Complete transaction and discontinuity of the nerve with no capacity for regeneration 755 756 Long Thoracic Nerve Pathology • Positions that cause overstretching of the serratus anterior muscle will also aggravate the pathology. These include forward flexion movements and arm weight-bearing positions that create excessive scapular winging. EASING ACTIVITIES • Rest and/or modification of aggravating activities • Placing the neck, arm, and scapula in a neutral, supported position that does not tension the nerve. 24-HOUR SYMPTOM PATTERN Generally, the symptoms are related to activity and do not follow a typical 24-hour pattern unless there is a strong inflammatory component such as may be seen in repetitive strain. If there is an inflammatory component, there may be worsening of symptoms with use toward the end of the day, pain at night, and morning stiffness with ache. PAST HISTORY FOR THE REGION • The patient commonly reports a history of the following: Vigorous and/or repetitive overhead activity, including throwing in baseball, javelin, or football; serving in tennis; spiking or serving in volleyball; driving a golf ball, tackling, or wrestling. Repetitive carrying of heavy loads Injury involving sudden forced scapular depression Excessive or poor use of old-style crutches and overly tight bandage or plaster applications into the axilla Direct trauma to the supraclavicular region or chest, including MVAs, falls, and strong massage First rib resection and heart or breast surgery Vaccinations or infections PHYSICAL EXAMINATION • Inferior scapular winging at rest • Reduced active shoulder flexion range and/or strength • Scapular winging inferiorly and medially with active shoulder flexion and/or pressing against a wall or doing push-ups (as the forward arm movement places a posteriorly directed force on the medial border of the scapula, which is unopposed with a weak serratus anterior muscle) • Weakened active shoulder abduction (with minimal loss of range as the lower trapezius can compensate for the lack of serratus anterior to upwardly rotate the scapula) • MMT reveals weakness in the serratus anterior muscle. • Poor scapulohumeral rhythm with active shoulder movements caused by CHAPTER 16 • NERVE impaired scapular rotation (with possible resultant positive impingement signs) • Visible atrophy of the serratus anterior muscle • Possible reduction of range and/or reproduction of pain on cervical lateral flexion away • Upper limb neurodynamic testing may reveal adverse neurodynamics and elicit symptoms. IMPORTANT OBJECTIVE TESTS • It is important to confirm the diagnosis of long thoracic nerve neuropathy with electrodiagnostic evaluation. Needle examination testing is the most reliable test to evaluate the severity of long thoracic nerve damage and can be used to monitor progress of the condition. Nerve conduction studies, however, have been deemed unreliable to test for long thoracic nerve trauma, although they can be used for differential diagnosis of other brachial plexus lesions. • A plain radiograph is also useful to assess for the presence of a cervical rib and for calcifications, although most often results are normal. • MRI of the cervical spine and brachial plexus can also be used to exclude cervical or brachial pathologies. DIFFERENTIAL DIAGNOSIS • Cervical Cervical spondylosis Cervical disc disease Cervical nerve root syndrome • Shoulder Shoulder impingement Malunion of scapular fracture Rotator cuff tear or tendinopathy Adhesive capsulitis Instability of the glenohumeral or acromioclavicular joints Degenerative arthritis of the glenohumeral or acromioclavicular joints Scapulothoracic or scapulohumeral bursitis syndromes • Nerve Spinal accessory nerve or trapezius palsy Dorsal scapular nerve or rhomboid palsy Suprascapular nerve palsy Thoracic outlet syndrome Brachial plexus neuropathy (ParsonageTurner syndrome) Quadrilateral space syndrome • Other Polymyositis Diffuse peripheral neuropathy Osteochondroma Muscular dystrophy 21 of 57 CONTRIBUTING FACTORS • For any nerve pathology that is nontraumatic, there is often an element of repetitive activity involving the affected limb. Typically, in the case of the long thoracic nerve, the repetitive action that may create a traction or compressive neuropathy involves cervical flexion, lateral flexion, and rotation away, combined with ipsilateral arm flexion. Individuals involved in overhead sporting or occupational activity are therefore more at risk. • Other repetitive tasks or activities, such as carrying loads in heavy manual work, weight lifting, tackling, and wrestling, may also predispose to long thoracic nerve injury. • Postural factors may be involved, particularly with repetitive work or sporting activities, with reduction in proximal stability and scapular control leading to increased strain on the nerve. TREATMENT SURGICAL OPTIONS • Safran reviewed literature pertaining to surgical options and found the most favorable results from the surgical transfer of the sternal head of the pectoralis major to replace serratus anterior function. The author felt that this particular transfer allowed the most similar muscle activity to that of the serratus anterior as a result of the orientation of the fibers and similar excursion levels. The semitendinosus-gracilis graft was also favored for its strength, low morbidity, and harvest efficiency. The pectoralis minor, rhomboid, and teres minor muscles have also been used for muscle transfers. • Supraclavicular neurolysis of the long thoracic nerve and nerve transfers using the thoracodorsal or medial pectoral nerves have also been reported. • Nath et al advocate the use of microneurolysis with supraclavicular decompression with patients who have a history pertaining to injury of the long thoracic nerve in the scalene musculature. • Scapulothoracic fusion has also been used to stabilize the scapula in more extreme cases and if previous surgery has failed. • Safran reported very good results with outcome measures such as function, pain, and scapular winging for pectoralis major transfer surgery. • A significant loss of range of elevation is expected with scapulothoracic fusion, and this outcome should be considered for determining if this type of surgery is appropriate. • Nath et al also reported very good outcomes after microneurolysis with supraclavicular decompression in Long Thoracic Nerve Pathology CHAPTER 16 • NERVE patients with a history of long thoracic nerve injury occurring in the scalene musculature. • Surgery may be indicated if the patient has not responded to conservative management after 1 to 2 years and if no improvement has been seen on EMG testing. REHABILITATION PROGNOSIS 22 of 57 SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN All patients with suspected long thoracic nerve pathology should be referred to a physician for appropriate investigation. SUGGESTED READINGS Cleary CK. Management of radial tunnel syndrome: a therapist’s clinical perspective. J Hand Ther. 2006;9(2):166–191. Dumestre G. Long thoracic nerve palsy. J Man Manipulative Ther. 1995;3(2):44–49. Goslin KL, Krivickas LS. Proximal neuropathies of the upper extremity. Neurol Clin. 1999;17(3):525–548. Hermann DN, Logigian EL. Electrodiagnostic approach to the patient with suspected mononeuropathy of the upper extremity. Neurol Clin. 2002;20(2):451–478. Kendall FP, McCreary EK, Provance PG, Rodgers MM,RomaniWA.Muscles Testing and Function with Posture and Pain. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2005. Nath RK, Lyons AB, Bietz G. Microneurolysis and decompression of long thoracic nerve injury are effective in reversing scapular winging: Long term results in 50 cases. BMC Musculoskelet Disord. 2007;8:25. Pecina MM, Krmpotic-Nemanic J, Markiewitz AP. Tunnel Syndromes: Peripheral Nerve Compression Syndromes. 3rd ed. CRC Press; 2001. Safran MR. Nerve injuries about the shoulder in athletes, Part 2: long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med. 2007;32(4). Seddon HJ. Surgical Disorders of the Peripheral Nerves. Edinburgh: Churchill; 1975. Sunderland S. Nerve and Nerve Injuries. 2nd ed. Edinburgh: Churchill Livingstone; 1978. Sunderland S. Nerve Injuries and Their. Repair. A Critical Appraisal. Edinburgh: Churchill Livingstone; 1991. AUTHOR: KATINA DIMOPOULOS ORTHOPEDIC PATHOLOGY • Most cases of nontraumatic long thoracic nerve pathology resolve within a year, with improvements seen for up to 2 years. However, as with all peripheral nerve pathologies, the prognosis depends on the extent of damage to the nerve. • Neurapraxia should resolve rapidly and lead to a complete restoration of function, usually within several months. If the injury is a more severe axonotmesis, the recovery time depends on the distance from the site of injury to the denervated tissue. Peripheral nerves have been reported to recover at an approximate rate of between 1 and 4 mm per day but recovery may not result in a complete restoration of function. The extensive length of the long thoracic nerve results in a longer reinnervation distance, thus a longer recovery time (up to 2 years). • If there has been a complete sectioning of the nerve (neurotmesis), then a full recovery will not occur. The results of treating neurotmesis will depend on surgical outcome. Section III • The aim of rehabilitation is to promote healing of the nerve and denervated muscles.This can be achieved by reducing symptoms, encouraging pain-free exercise, and providing task or sports reeducation and interventions leading to reacquisition of function. • Manual therapy Symptom reduction can be achieved through use of ice, electrotherapeutic modalities, and relative rest (forward elevation of the arm should be avoided). Scapular taping and bracing have been described in the literature to reduce overstretch of the serratus anterior muscle and to add proprioception to the area. Stretching, soft tissue release, and trigger point therapy of the periscapular muscles may also help alleviate the associated hypertonicity and/or pain caused by muscle compensations for the loss of the serratus anterior muscle and help restore muscle balance around the scapula. Joint mobilization to the cervical and thoracic spine, as well as to the ribs, scapula, and acromioclavicular and glenohumeral joints, may also be useful to increase mobility and alleviate pain. Muscle energy techniques may also be necessary to increase mobility and alleviate pain in the upper and middle rib cage (because of serratus anterior muscle attachments). • Gentle active-assisted shoulder ROM exercises should be started early to prevent joint contracture. • Scapular position education initially with active-assisted exercise and isometric hold and then the addition of controlled functional movement patterns • Periscapular muscle strengthening as required may help optimize scapular position and stability, starting in neutral, unloaded positions. • Neuromuscular electrical stimulation (NMES) can be used if the patient demonstrates some activity in the serratus anterior muscle. It can be used to reduce atrophy by applying the electrodes to motor points and stimulating the muscle at rest or during an active exercise. • Nerve gliding exercises have been purported to disperse intraneural edema, increase blood flow, optimize axonal transport, and lengthen nerve adhesions. Neural mobilization can be achieved using scapular mobilization both actively and passively into elevation, depression, protraction, and retraction. • Functional rehabilitation should include the following: Reeducation of movement patterns, particularly proximal control of the trunk and neck, to provide a stable foundation for scapular stability Specific muscle strengthening by gradually increasing intensity to restore full power to the serratus anterior Integration of functional exercise and strength work into sport- or task-specific skills Graduated return to full strength, speed, and power 757 Median Nerve Entrapment 758 BASIC INFORMATION DEFINITION The median nerve may be compressed or entrapped at several places in the arm. It can be entrapped proximal (pronator syndrome) or distal (anterior interosseous nerve syndrome, or Kiloh-Nevin syndrome) to the anterior interosseous branch as it passes between the two heads of the pronator teres. It can also be entrapped as it passes under the ligament of Struthers (found in 1% of the population) that runs between an abnormal process on the shaft of the humerus to its medial epicondyle (humerus supracondylar process syndrome). Entrapment can occur as the lacertus fibrosis is tensioned on pronation at the bicipital tuberosity of the radius. The median nerve can also be entrapped at the carpal tunnel between the flexor tendons, the carpal bones, and the transverse carpal ligament (carpal tunnel syndrome). SYNONYMS • • • • • Anterior interosseous syndrome Kiloh-Nevin syndrome Pronator teres compression syndrome Pronator syndrome Humerus supracondylar process syndrome • Carpal tunnel syndrome ICD-9CM CODES 955.1 Injury to median nerve 354.0 Carpal tunnel syndrome OPTIMAL AND MAXIMAL NUMBER OF VISITS For anterior interosseous syndrome, surgical intervention should be considered after 8 to 12 weeks if response to conservative management is poor. For other pathologies, the number of visits depends on progression. Mild-to-moderate presentations may be successfully treated or managed with conservative intervention. If the underlying cause involves biomechanical issues associated with lifestyle, such interventions may need to continue for protracted time periods. More severe presentations and unrelenting, unresponsive, or worsening symptoms may warrant earlier medical or surgical intervention. ETIOLOGY • Insult to the nerve may be mechanical, thermal, chemical or ischemic. • In entrapment syndromes, compression or direct trauma leads to nerve tissue hypoxia. • Median nerve entrapment pathology may occur with repetitive or overuse CHAPTER 16 • NERVE movement patterns involving the elbow, wrist and hand, vibration injuries, trauma, pregnancy, menopause, obesity, underlying disease and medical issues (diabetes mellitus, thyroid myxedema, osteoarthritis, acromegaly, amyloidosis, renal dialysis, or alcoholism), space-occupying entities (neurofibroma, lipoma, aneurysm, hemangioma, ganglion, or xanthoma), presence of anatomical anomalies, and psychological stress. Some authors have also reported possible inherited predisposition. While all of these factors have been linked to median nerve entrapments, many cases are described as idiopathic, and it is likely that most are multifactorial. • In entrapments, nerve trauma occurs because the size of the neural structure exceeds the anatomical space available for it, resulting in increased pressure, which in turn leads to impaired blood flow and subsequent hypoxia of the tissue and disruption to the axonal transport system. • Nerve injury is classified according to severity of the injury and potential for reversibility. Original classifications described previously remain in current use, as follows: First-degree neurapraxia involves distortion of myelin around the nodes of Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance, resulting in temporary loss of nerve conduction. Recovery is rapid and complete in most cases. Second-degree axonotmesis involves interruption of the axon with secondary wallerian degeneration, but the supporting tissue around the axon is preserved. Recovery may be complete but takes longer to occur and depends on the distance between the site of injury and the end-structure (denervated muscle). Third-degree neurotmesis involves extensive disruption of the nerve and its supporting structures, but while the endoneurium is disrupted, the perineurium and epineurium remain intact. Fourth-degree neurotmesis involves disruption of all neural components except the epineurium. Fifth-degree neurotmesis involves complete transaction and discontinuity of the nerve with no capacity for regeneration. Neurotmesis rarely occurs from entrapment, but where continuity has been disrupted, complete recovery is not possible, even with surgical techniques, and the eventual outcome depends on individual circumstances. A comprehensive overview of neurobiology, nerve injury, and nerve repair is provided by Dahlin. 23 of 57 • Double-crush syndrome refers to the fairly common phenomenon of nerve entrapment and radiculopathy occurring in combination, although the syndrome is considered controversial. Compression or irritation of the nerve roots at the cervical level is thought to increase sensitivity to compression or movement restrictions more distally in the structure. • In overuse-type entrapments, it is proposed that repetitive work or static postures produce an inflammatory response. Fibroblasts appear to repair the damage incurred but generate adhesions that limit neural glide and subsequently increase anoxia. Other studies found that cortical dedifferentiation may occur from repetitive motion activities and nerve injuries. This may result in reinforced poor posturing and use of aberrant motor pathways. EPIDEMIOLOGY AND DEMOGRAPHICS • Carpal tunnel syndrome is among the most commonly reported nerve entrapments, anterior interosseous syndrome and pronator syndrome occur much less frequently, and humerus supracondylar process syndrome is rare. • Anterior interosseous syndrome, pronator syndrome, and humerus supracondylar process syndrome tend to be linked to specific activity, trauma, disease, or anatomical makeup rather than associated with a particular age group. • Carpal tunnel syndrome presentations tend to be more than twice as common in females compared to males, and most commonly occur between 45 and 54 years of age, although the syndrome also occurs quite frequently during pregnancy. • Median nerve entrapments occur more frequently among office workers, manual workers, and individuals who engage in repetitive movement pattern activities such as musicians, artists, and sports participants. MECHANISM OF INJURY • Specific anatomical sites for entrapment in the upper limbs are described by Pratt. Anterior interosseous nerve syndrome may occur when the nerve is compressed at the tendinous origin of the deep head of pronator teres (most common presentation) or as it passes between the two heads of pronator teres, by impingement from a bicipital tendon bursa or radial and ulnar artery abnormalities in the forearm, by fascial bands at the origin of flexor digitorum superficialis, or by anatomical anomalies within the deep palmar compartment involving flexor pollicis longus or palmaris profundus. A review of compression Median Nerve Entrapment CHAPTER 16 • NERVE • • • • COMMON SIGNS AND SYMPTOMS • • • AGGRAVATING ACTIVITIES • Repetitive movement patterns at the elbow, wrist, and hand, particularly repetitive pronation and supination, tend to exacerbate the symptoms. • The pathology may be worsened with sustained postures, especially those involving the wrist, head, and neck and activities that increase the volume of structures, which may be implicated in entrapment such as those that may lead to pronator hypertrophy. EASING ACTIVITIES • Relative or absolute rest may assist in alleviating symptoms in cases where the pathology has been caused by overuse or repetitive movement patterns. 24 of 57 • Adapting movement strategies and altering or correcting posture may reduce loading on irritated structures where absolute rest is not possible. • Use of splints to maintain more neutral positions and thus reduce neural tension, either during activity or overnight, may also be helpful. 24-HOUR SYMPTOM PATTERN • Symptoms are worsened with aggravating activities but also tend to increase nocturnally, particularly paraesthesia and numbness. • In females, symptoms may show hormonal variation; in individuals in whom the presentation is related to another medical condition, symptoms may vary according to physiological balance associated with the underlying condition. PAST HISTORY FOR THE REGION • Median nerve entrapment can occur from a broad spectrum of associated causative factors; consequently, past history for the pathology may vary widely between individuals. • Anatomical anomalies involving bony structures (supracondylar process on humerus and the presence of the ligament of Struthers and form and alignment of carpal bones), vascular structures (radial, ulnar, and median arteries), and connective tissue (fascia) may predispose individuals to the pathology, together with the presence of underlying disease and medical issues (diabetes mellitus, thyroid myxedema, osteoarthritis, obesity, pregnancy, menopause, space-occupying entities such as neurofibroma or lipoma, aneurysm, hemangioma, ganglion, xanthoma, acromegaly, amyloidosis, renal dialysis, or alcoholism). • Trauma history may include work or leisure activities involving repetitive movement patterns or vibration exposure (all median nerve entrapment pathologies), partial rupture at the musculotendinous junction of biceps brachii (lacertus fibrosis tension), fractures of the upper limb, particularly Colles’ fracture, or fracture or subluxation and dislocation injuries, particularly those involving the carpal bones (carpal tunnel syndrome). PHYSICAL EXAMINATION • Anterior interosseous syndrome commonly presents with weakness and difficulty moving the index and middle fingers (flexor digitorum profundus), combined with weakness in the thumb (flexor pollicis longus), making pinch grip difficult from loss of flexion in the fingers and thumb as the distal phalanges remain extended or hyperextended. • Variations in innervation for the hand mean that the presentation for ORTHOPEDIC PATHOLOGY • Anterior interosseous syndrome commonly presents with weakness and difficulty moving the index and middle fingers (flexor digitorum profundus, combined with weakness in the thumb (flexor pollicis longus), making pinch grip difficult. • However, variations in innervation for the hand, particularly the Martin Gruber anastomosis (in which the motor nerve crosses over from the median nerve to the ulnar nerve, present in 10% to 15% of the population), mean that the presentation for entrapment may vary significantly and could involve flexor pollicis brevis, adductor pollicis, abductor pollicis brevis, lumbrical, and abductor digiti minimi muscles, or even the entire hand. • Pronator syndrome commonly manifests with pain in the forearm and wrist, combined with weakness and atrophy of the thenar muscles. Flexor carpi radialis, palmaris longus, and flexor digitorum muscles are affected, with or without the addition of those muscles usually supplied by the anterior interosseous nerve—flexor pollicis longus, flexor digitorum profundus, and pronator quadratus muscles. However, the tendency for variation in muscle innervation patterns in the hand should be remembered. • Paraesthesia in median nerve distribution may occur with repetitive pronation • and supination, and individuals may experience early fatigue in muscles of the forearm, particularly with excessive pronation. Lacertus fibrosis tension produces pain radiating from the elbow to the forearm with pronation or resisted supination with the forearm in flexion, combined with localized symptoms around the fibrous arcade at the origin of flexor digitorum superficialis with resisted middle-finger flexion. Humerus supracondylar process syndrome may manifest with pain and paraesthesia in median nerve distribution, combined with weakness in the muscles as described for pronator syndrome but with the addition of pronator teres. Individuals may report weak grip and pronation and may exhibit forearm atrophy. Carpal tunnel syndrome commonly manifests with progressively worsening pain (classically described as aching and burning in nature) and paraesthesia in the thumb, forefinger, middle finger, hand, and wrist, which may extend to the forearm, elbow, shoulder, and neck. Symptoms are often worse nocturnally. Individuals may complain of problems with grip and weakness in the wrist and hand. Anterior interosseous syndrome produces weakness in the thumb, forefinger, and middle finger, although other regions of the hand may be affected. Pronator syndrome produces pain in the forearm and wrist, combined with paraesthesia and weakness in the thumb, fingers, and wrist. Lacertus fibrosis tension produces pain radiating from the elbow to the forearm. Humerus supracondylar process syndrome produces pain, paraesthesia, and weakness in the elbow, wrist, and hand. Carpal tunnel syndrome produces pain and significant paraesthesia in the hand and wrist, which may extend to the forearm, elbow, shoulder, and neck. Section III syndromes in the median nerve is given by Koo and Szabo. Pronator syndrome refers to median nerve compression between the two pronator teres heads before it branches to form the anterior interosseous nerve. Lacertus fibrosis (bicipital aponeurosis) tension may cause median nerve compression as it is pulled across the nerve with pronation as the bicipital tuberosity of radius passes posteriorly or when the forearm is maintained in resisted supination and flexion. Humerus supracondylar process syndrome may occur when the median nerve is compressed above the elbow as it passes under the ligament of Struthers in individuals in whom the structure is present. Carpal tunnel syndrome refers to compression of the median nerve as it passes, together with the tendons of flexor digitorum profundus, flexor digitorum superficialis, flexor pollicis longus, and flexor carpi radialis, through the enclosure created by trapezoid, capitate, the flexor retinaculum (transverse carpal ligament) and its attachments to the scaphoid tubercle, trapezium, hook of hamate, and pisiform. 759 760 Median Nerve Entrapment • • • • • entrapment may vary significantly and could involve the flexor pollicis brevis, adductor pollicis, abductor pollicis brevis, lumbrical, and abductor digiti minimi muscles or even the entire hand. Individuals with pronator syndrome may exhibit weakness and atrophy of the thenar muscles. Flexor carpi radialis, palmaris longus, and flexor digitorum muscles are affected with or without the addition of the muscles usually supplied by the anterior interosseous nerve— flexor pollicis longus, flexor digitorum profundus, and pronator quadratus. Paraesthesia in median nerve distribution may occur with repetitive pronation and supination, and individuals may experience early fatigue in muscles of the forearm, particularly with excessive pronation. Tinel’s sign may be positive in the mid to proximal forearm rather than at the wrist. Lacertus fibrosis tension produces pain radiating from the elbow to the forearm with pronation or resisted supination with the forearm in flexion, combined with localized symptoms around the fibrous arcade at the origin of flexor digitorum superficialis with resisted middle-finger flexion. Past trauma history may also indicate this syndrome. Individuals with humerus supracondylar process syndrome may report pain and paraesthesia in median nerve distribution. In addition to the weakness and atrophy patterns observed in the hand with more distal compression, there may also be evidence of forearm atrophy with weakness noted in both grip and pronation. Individuals with carpal tunnel syndrome present with significant paraesthesia and numbness in the hand and wrist. Additionally, atrophy of abductor pollicis brevis may be noted and Tinel’s sign (at the wrist), Phalen’s test, and wrist flexion provocation tests may be positive. IMPORTANT OBJECTIVE TESTS • Diagnostic accuracy of neurological upper limb examination employing a battery of standard test procedures has been found to be reproducible and reliable. • Neurophysiology and EMGs may produce positive findings, particularly for carpal tunnel syndrome. Results are often inconclusive for anterior interosseous syndrome because of the deep location of the structures. If pronator syndrome is suspected, an initial negative test accompanied by a strong suggestive history should be repeated after approximately 6 weeks. Radiographic, ultrasound, and MRI may identify anatomical anomalies, and vas- CHAPTER 16 • NERVE • • • • • • cular tests may be helpful in differential diagnosis. Pinch test (precision grip): Individuals with anterior interosseous syndrome are unable to flex the distal phalanges of the thumb, forefinger, and middle finger so that contact can only be made through the pads rather than the tips of the digits. Tinel’s sign: Tapping over the median nerve distribution reproduces sensory symptoms distal to the test site.This test is positive at the proximal to mid-forearm rather than at the wrist in pronator syndrome and positive at the wrist over the carpal tunnel in carpal tunnel syndrome. Phalen’s test: Maximal wrist flexion either with gravity or pressure applied by the examiner reproduces sensory symptoms in the thumb, forefinger, and middle finger. (Normal subjects may experience similar symptoms after 1 minute.) A variation of this is the reverse Phalen’s test where the subject grips the examiner’s hand as the wrist is extended and direct pressure is applied over the carpal tunnel for 1 minute. A positive test reproduces the same symptoms. Wrist flexion provocative test: Constant digital pressure over the median nerve at the carpal tunnel with elbow extended and forearm supinated reproduces paraesthesia and numbness within 30 seconds for a positive test. Durkan compression test (carpal compression test): With the wrist in neutral and forearm supinated, carpal compression is applied either manually or with a pressure-sensitive instrument. A positive test is recorded if sensory symptoms occur within 30 seconds. Sensory discrimination tests may also be helpful in defining the affected area. DIFFERENTIAL DIAGNOSIS • Anterior interosseous syndrome: Cervical radiculopathy (C8), pronator syndrome, carpal tunnel syndrome, lacertus fibrosis tension, humerus supracondylar process syndrome, lateral cord lesion, ulnar neuropathy, flexor digitorum profundus tendon rupture or avulsion, or flexor pollicis longus rupture • Pronator syndrome: Cervical radiculopathy (C6 to C7), lacertus fibrosis tension, flexor superficialis syndrome, humerus supracondylar process syndrome, anterior interosseous syndrome, carpal tunnel syndrome, soft tissue overuse syndromes, vascular pathologies, or cardiac pathologies • Lacertus fibrosis tension: Cervical radiculopathy (C6 to C7), pronator syndrome, 25 of 57 humerus supracondylar process syndrome, anterior interosseous syndrome, carpal tunnel syndrome, soft tissue overuse pathologies, or cardiac pathologies • Humerus supracondylar process syndrome: Cervical radiculopathy (C6/ C7), anterior interosseous syndrome, pronator syndrome, lacertus fibrosis tension, carpal tunnel syndrome, soft tissue overuse syndromes, or vascular pathologies • Carpal tunnel syndrome: Cervical radiculopathy (C6/C7, T1), thoracic outlet syndrome, anterior interosseous syndrome, pronator syndrome, lacertus fibrosis tension, humerus supracondylar process syndrome, ulnar neuropathy, vascular pathologies, soft tissue overuse syndromes, carpometacarpal arthritis, shoulder bursitis, transient ischemic attack, or myocardial ischemia CONTRIBUTING FACTORS • Presence of anatomical anomalies • Underlying disease or medical condition • Repetitive work or leisure activities • Past trauma history • Psychological stress • Genetic predisposition TREATMENT SURGICAL OPTIONS • An overview of basic neurosurgical techniques is provided by Dahlin. Anterior interosseous syndrome: Decompression at pronator heads, fascial release at flexor digitorum superficialis or the deep palmar compartment, exploration techniques to release pressure generated by bursa or vascular abnormalities Pronator syndrome: Release of the humeral head of pronator teres combined with fascial release at flexor digitorum superficialis Lacertus fibrosis tension: Release of lacertus fibrosis, possibly with associated repair for biceps brachii Humerus supracondylar process syndrome: Release at the bony process and ligament of Struthers Carpal tunnel syndrome: Open or endoscopic release techniques to divide the transverse carpal ligament, restore neural glide, relieve adhesions, and where the condition results from compression caused by some form of space-occupying lesion, appropriate techniques to address the specific lesion. • When accurate diagnosis has been made, surgical intervention produces good results for all the pathologies described, with success rates around 90% and low recurrence rate. Recovery depends on Median Nerve Entrapment CHAPTER 16 • NERVE level of nerve injury, with neurapraxias showing the fastest and most complete return to function. • Surgery may be indicated for individuals with severe, worsening, or unrelenting symptoms that are nonresponsive to conservative management involving antiinflammatory medication, splinting, and manual and electrotherapy physiotherapy modalities and addressing of ergonomic issues. Early surgical intervention (within 8 to 12 weeks) is generally recommended for anterior interosseous syndrome to achieve the best outcome. REHABILITATION • Factors that contribute to median nerve entrapment pathology include the presence of anatomical anomalies, an underlying disease or medical condition, repetitive work or leisure activities, past trauma history, psychological stress, and genetic predisposition. • Systematic review found inconclusive evidence for conservative management of carpal tunnel syndrome, but as noted • Severe or worsening neurological function or symptoms • Failure to respond to conservative management • Suspicion or presence of underlying disease • Unexplained symptoms inconsistent with the pathology SUGGESTED READINGS Akalin E, El O, Peker O, et al. Treatment of carpal tunnel syndrome with nerve and tendon gliding exercises. Am J Phys Med Rehabil. 2002;81(2):108–113. Chin DHCL, Meals R. Anterior interosseous nerve syndrome. J Am Soc Surg Hand. 2001;1(4):249–257. Cleary CK. Management of radial tunnel syndrome: a therapist’s clinical perspective. J Hand Therapy. 2006;9(2):166–191. Dahlin LB. Mini-symposium: hand trauma (ii) nerve injuries. Curr Orthop. 2008;22(1):9–16. Freedman J. Acupuncture for carpal tunnel syndrome. Acupunct Med. 2002;20(1):39–40. Gomes I, Becker J, Ehlers JA, Nora DB. Prediction of the neurophysiological diagnosis of carpal tunnel syndrome from the demographic and clinical data. Clin Neurophysiol. 2006;117(5):964–971. Hall TM, Elvey RL. Nerve trunk pain: physical diagnosis and treatment. Man Ther. 1999;4(2):63–73. Jepsen JR, Laursen LH, Hagert C-G, Kreiner S, Larsen AI. Diagnostic accuracy of the neurological upper limb examination I: inter- 26 of 57 AUTHOR: SARAH GRAHAM ORTHOPEDIC PATHOLOGY PROGNOSIS SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN relater reproducibility of selected findings and patterns. BMC Neurol. 2006;6(8). Jepsen JR, Laursen LH, Hagert C-G, Kreiner S, Larsen AI. Diagnostic accuracy of the neurological upper limb examination II: relations to symptoms of patterns of findings. BMC Neurol. 2006;6(10). Koo JT, Szabo RM. Compression neuropathies of the median nerve. J Am Soc Surg Hand. 2004;4(3):156–175. Latinovic R, Gulliford MC, Hughes RA. Incidence of common compressive neuropathies in primary care. J Neurol Neurosurg Psychiatry. 2006;77(2):263–265. Magee DJ. Orthopaedic Physical Assessment. 5th ed. Philadelphia: Saunders; 2008. Naeser MA, Hahn KA, Lieberman BE, Branco KF. Carpal tunnel syndrome treated with low level laser and microamperes transcutaneous electric nerve stimulation: a controlled study. Arch Phys Med Rehabil. 2002;83(7):978–988. Nithi K. Physiology of the peripheral nervous system. Surgery. 2003;21(10):264a–264e. Piazzini DB, Aprile I, Ferrara PE, et al. A systematic review of conservative treatment of carpal tunnel syndrome. Clin Rehabil. 2007;21(4):299–314. Pratt N. Anatomy of nerve entrapment sites in the upper quarter. J Hand Ther. 2005;18(2):216–219. Premoselli S, Sioli P, Grossi A, Cerri C. Neutral wrist splinting in carpal tunnel syndrome: a 3 and 6 months clinical and neurophysiologic follow up evaluation of nightonly splinting therapy. Eura Medicophys. 2006;42(2):121–126. Seddon HJ. Surgical Disorders of the Peripheral Nerves. Edinburgh: Churchill Livingstone; 1975. Seitz WH, Matsuoka H, McAdoo J, Sherman G, Stickney DP.Acute compression of the median nerve at the elbow by the lacertus fibrosis. J Shoulder Elbow Surg. 2007;16(1):91–94. Sunderland S. Nerve and Nerve Injuries. 2nd ed. Edinburgh: Churchill Livingstone; 1978. Tetro AM, Bradley EA, Hollstien SB, Gelberman RH. A new provocative test for carpal tunnel syndrome. Assessment of the wrist and nerve compression. J Bone Joint Surg. 1998;80(3):493–498. Wilbourn AJ, Gilliat RW. Double crush syndrome: a critical analysis. Neurology. 1997;49:21–29. Section III • Rehabilitation may focus on two goals: Addressing the underlying causative factors and reducing the symptoms. In cases where repetitive movement patterns or exposure to vibration trauma feature in the development of the pathology, a detailed ergonomic assessment may be helpful in identifying areas in which loading stress may be reduced by changes in behavior, activity, or posture or through use of appropriate braces. • Therapeutic techniques to alleviate symptoms may include soft tissue manual techniques, neural mobilizing techniques, massage, acupuncture, and electrotherapy techniques to address pain, inflammation, and loss of movement and function. When psychological stress is considered a significant factor, individuals may benefit from more general therapeutic exercise programs. by other researchers, definitive statements regarding prognosis are difficult because differential diagnosis is not always achieved. Mild-to-moderate presentations of median nerve entrapments may be effectively treated or well-controlled with conservative intervention. In individuals with more severe presentations or who have failed to respond to conservative measures, surgical procedures generally have a good outcome in terms of symptom relief and functional outcome. 761 Neurogenic Thoracic Outlet Syndrome 762 BASIC INFORMATION CHAPTER 16 • NERVE OPTIMAL NUMBER OF VISITS 10 DEFINITION MAXIMAL NUMBER OF VISITS • Thoracic outlet syndrome (TOS) encompasses numerous scenarios of compression (neurological and vascular) in the thoracic outlet region of the shoulder girdle. Although vascular and neurological classifications exist, it must be noted that these conditions can also be observed together. • Neurogenic TOS involves compression of various portions of the brachial plexus and is the most common form of TOS (over 90% of cases).The brachial plexus is formed by the C5 to T1 nerve roots, although the most caudal root or “lower plexus” (C8 and T1) is most commonly affected. The “upper plexus” may also be involved, and this affects the C5, C6, or C7 nerves, or in rare cases may be involved in combination with the lower plexus. • Defining the syndrome has been fraught with difficulty in the literature because of its variable etiology and presentation and often minimal clinical findings. • Two main neurogenic TOS classifications exist as a result of the following variable clinical presentations: True neurogenic TOS, where patients present with a typical clinical presentation with positive neurological findings on examination Nonspecific neurogenic or “classic” TOS, in which pain is a predominant feature with minimal neurological findings on examination.This subcategory comprises most TOS presentations. 30 SYNONYMS • • • • • • • • • • • • • • • Cervical rib syndrome First rib syndrome Scalenus anticus syndrome Costoclavicular syndrome First thoracic rib syndrome Hyperabduction syndrome Scalenus medius syndrome Pectoralis minor syndrome Subcoracoid-pectoralis minor syndrome Brachiocephalic syndrome Nocturnal paresthetic brachialgia Rucksack palsy Droopy shoulder syndrome Fractured clavicle-rib syndrome Motor type neurogenic TOS ICD-9CM CODES 353 Nerve root and plexus disorders 354 Mononeuritis of upper limb and mononeuritis complex 354.8 Other mononeuritis of upper limb 354.9 Mononeuritis of upper limb unspecified ETIOLOGY • The current belief of the cause of TOS is the underlying existence of bony or fibromuscular anomalies with overlying injury and/or spasm in the thoracic outlet region causing compromise.The anatomical anomalies are generally seen as predisposing factors. • The pathology involves compression of portions of the brachial plexus in the thoracic outlet region as a result of underlying bony or fibromuscular anomalies with overlying muscle injury and/or spasm. • Local spasm in the thoracic outlet region can result in muscle swelling and place the local neural structures under strain or traction, resulting in nerve edema. As the condition becomes more chronic, scarring and fibrosis of the nerve can take place. • Bony anomalies can be congenital, traumatic, or posttraumatic and include the presence of a cervical rib, elongated C7 transverse process, first rib deformity, displaced first rib fracture, excessive callus formation after first rib fracture, rib hemangioma, fractured or subluxed clavicle, and pseudarthroses. Cervical ribs are known to exist in approximately 0.5% of the population, with 10% to 20% resulting in symptoms, although this depends on their size. • Soft tissue anomalies can also be congenital, traumatic, or posttraumatic and include altered scalene muscle insertions and origins, presence of scalenus minimus or scalenus pleuralis muscle, hypertrophy or injury of scalene muscles, presence of congenital fibromuscular bands (classified into types 1 to 10) or dense fibrous sheaths, cervical ligaments and bands, and pectoralis minor shortening. • Anatomical variations of the passage of the brachial plexus through the thoracic outlet, the adherence of the nerves to the scalene muscles, can also predispose to TOS. • The superimposed injury involved in causing TOS symptoms may include whiplash, direct or indirect blow to the shoulder, repetitive strain through prolonged upper limb activity, accessory breathing, and/or poor posture. • The following three spaces in the thoracic outlet region have been identified as potential areas of brachial plexus compression (Atasoy): Interscalene space or triangle is bordered anteriorly by the anterior sca- 27 of 57 lene muscle, posteriorly by the middle scalene muscle, and inferiorly by the first rib. The brachial plexus passes posteriorly to the anterior scalene muscle here, in close relation and directly superior to the subclavian artery. Costoclavicular space is bordered anteriorly by the medial aspect of the clavicle, subclavian muscle and tendon, and costocoracoid ligament. The posterolateral border is formed by the upper border of the scapula and the posteromedial border by the first rib anterior and middle scalene muscle insertions. Here, the brachial plexus travels with the subclavian vein and artery under the clavicle and subclavius muscle toward the subpectoralis minor space. Subpectoralis minor space is located inferior to the coracoid process and posterior to the pectoralis minor muscle insertion. Here, the brachial plexus continues to travel with the subclavian vein and artery beneath the pectoralis muscle toward the axilla. The interscalene and costoclavicular spaces are equally common sites of compression in neurogenic TOS, while compression in the subpectoralis minor space is much less common. • Hypertrophy, degeneration, and fibrosis of the anterior scalene muscle caused from a previous single traumatic incident or repeated trauma is believed to be the current overlying cause of compressive symptoms. Various studies have demonstrated histological abnormalities in the anterior scalene muscles, including type 1 muscle fiber proliferation, reduction of type 2 muscle fibers, and increased connective tissue content and muscle scarring. • Physiologically, there is disruption to the underlying nerve of the brachial plexus, which is responsible for conduction. • Neurogenic TOS involves a continuum of damage from periodic nerve ischemia to chronic ischemia resulting in segmental demyelination (neurapraxic injury). This may progress to axonotmesis injury (in more severe cases of continued nerve compression) in which interruption of the axon with secondary wallerian degeneration will occur. EPIDEMIOLOGY AND DEMOGRAPHICS • Nonspecific neurogenic TOS is fairly common, although its prevalence is difficult to estimate because diagnosis is difficult. It can be missed or overdiagnosed. • True neurogenic TOS is uncommon. • Young and middle-aged adults are the most susceptible to nonspecific neurogenic TOS. Neurogenic Thoracic Outlet Syndrome CHAPTER 16 • NERVE • True neurogenic TOS symptom onset is most common in teenagers and young adults. • Females are at least three times as likely to develop nonspecific neurogenic TOS as males. • True neurogenic TOS mainly affects females. MECHANISM OF INJURY • The superimposed injury involved in causing TOS symptoms may include whiplash, direct or indirect blow to the shoulder, repetitive strain through prolonged upper limb activity, and/or poor posture. • Positions and postures that place increased strain on the thoracic outlet include the following: Prolonged writing or use of keyboard or telephone Assembly line works Poor posture (i.e., droopy shoulders) Prolonged overhead or reaching activity such as styling hair, painting, playing musical instruments (e.g., violin or flute), and swimming Excessive carrying of heavy objects such as suitcases and shopping bags Prolonged carrying of a heavy backpack AGGRAVATING ACTIVITIES • Overhead arm or hand positions or arm elevated repetitive activities. These commonly include styling hair, painting, working overhead, playing musical instruments (e.g., violin or flute), and swimming. • Carrying heavy objects such as suitcases and shopping bags • Prolonged use of arm as in writing and typing • Cervical contralateral rotation and/ or lateral flexion can often aggravate symptoms resulting from upper plexus involvement. • Symptoms may be delayed until after arm activity in some cases. EASING ACTIVITIES • Rest from aggravating activities • Arm adduction and flexion across body • Shoulder girdle support by using an arm rest, placing hand in pocket, or using a sling 24-HOUR SYMPTOM PATTERN • Morning Stiffness and ache depends on inflammatory component • Daytime Depends on arm activity • Nighttime Entire arm may feel numb or weak during the night, especially if patient sleeps on the ipsilateral side with the arm overhead and elbow flexed May often wake from pain, especially if patient has engaged in repetitive arm activity during the day. PAST HISTORY FOR THE REGION • The patient may report a previous history of whiplash injury or a direct or indirect blow to the shoulder resulting in first rib, muscular, or clavicular trauma. Symptoms generally develop from 1 month up to several months after whiplash injury. 28 of 57 PHYSICAL EXAMINATION • Nonspecific neurogenic TOS Poor posture (including downwardly rotated and protracted scapula, large breasts and/or obesity, forward head posture) Exaggerated upper chest or accessory breathing Neurological tests negative Altered neurodynamics on upper limb neurodynamic tests and/or brachial plexus tension tests Reproduction of arm symptoms and/ or local discomfort on palpation over the brachial plexus (also known as pressure provocation test or Spurling maneuver) Positive Tinel’s sign for reproduction of arm pain and/or paraesthesias or symptoms over brachial plexus Muscle spasm, tenderness, and/or shortening of anterior scalene muscle on palpation and length testing Muscle spasm, tenderness, and/or shortening of pectoralis minor muscle on palpation and length testing Ipsilateral elevated first rib Positive Roos, Adson’s, Halsted’s, and Wright’s hyperabduction tests: Increased arm pain and paraesthesias Hypomobility of the lower cervical and upper thoracic spinal levels • Lower and upper plexus involvement: The following objective findings are more specific to which part of the plexus is involved. Although rare, mixed plexus TOS also exists. As implied, it manifests with a combination of upper and lower plexus TOS symptoms. Lower plexus involvement (most common) Weakened interossei, flexor carpi ulnaris, thenar, and hypothenar muscles (patients may present with weakness of various C8/T1 innervated muscles). Slightly reduced triceps muscle strength (triceps partially supplied by C8) Reduced sensation on light touch and pinprick testing in the medial arm and medial one-and-a-half fingers (ulnar nerve distribution). Tinel’s test performed over the lower brachial plexus is positive for local discomfort and reproduction of referred pain. Pressure provocation test positive over the lower brachial plexus Lower brachial plexus tension test is positive for reproduction of medial arm symptoms, with the arm at 90 degrees, and the elbow and wrist extended and supinated. ORTHOPEDIC PATHOLOGY • Nonspecific neurogenic TOS. • Pain generally involves the neck, head, chest, scapula, shoulder, arm, and hand (area of pain depends on which part of the brachial plexus is involved). • Numbness or paresthesias of the arm and hand (area depends on which part of the brachial plexus is involved). • Coldness of the hand and increased sensitivity to cold exposure • Whole arm numbness and heaviness with arm elevation • Clumsiness with fine hand activities and weakness on gripping • True neurogenic TOS Pain absent Clumsiness with fine hand activities and weakness on gripping If the lower plexus (C8 or T1 nerves) is involved, the patient may present with the following: Ipsilateral anterior or posterior shoulder pain extending to the medial arm, forearm, and hand Ipsilateral paresthesias into the ring and small fingers (in the sensory distribution of the ulnar nerve) Ipsilateral pain in the clavicular region extending to the occipital region and mastoid (headaches can be quite severe) Ipsilateral anterior chest pain • If the upper plexus (C5, C6, or C7 nerves) is involved, the patient may present with the following: • The onset of symptoms may also be insidious but may reveal increased or unaccustomed prolonged or repetitive upper limb activity. Section III COMMON SIGNS AND SYMPTOMS Ipsilateral cervical pain with radiation to the ear, face, and head (mandibular, temporal, and occipital regions) Ipsilateral “stuffy” ear Ipsilateral pain in the medial scapular, anterior clavicular, upper chest, and lateral shoulder and arm pain (in the sensory distribution of C5 or C6 nerve roots) Ipsilateral sympathetic-mediated swelling of the face, night vision difficulties, and rarely, an eyelid droop Dizziness, vertigo, blurred vision 763 764 Neurogenic Thoracic Outlet Syndrome • Upper plexus involvement Weakness of the deltoid, biceps, and triceps (C5-C7) Reduced sensation on light touch and pinprick testing in the lateral shoulder and arm extending to the thumb, index, and middle finger Tinel’s test performed over the upper brachial plexus is positive for local discomfort and reproduction of referred pain. Pressure provocation test positive over the upper brachial plexus Upper brachial plexus tension test positive for reproduction of lateral arm symptoms with arm in exaggerated waiter’s tip posture. • True neurogenic TOS The distinguishing feature of this TOS category is that neurological tests are always positive (reduced strength and sensation: The muscles and areas of skin affected depend on which part of the brachial plexus is involved). In more severe cases, atrophy of the hand is evident. Reflexes, however, are normal. • • IMPORTANT OBJECTIVE TESTS • Four tests (Adson’s, Halsted’s, Wright’s hyperabduction, and Roos) have traditionally been used to diagnose TOS. These tests have been extensively discussed, criticized, and “modified” in the literature as a result of poor sensitivity and specificity. • First, since the Adson’s, Halsted’s, and Wright’s tests monitor the radial pulse, they should be considered tests for arterial TOS rather than neurogenic TOS. More recently, these tests are generally considered provocative tests for pain or paraesthesias in neurogenic TOS, although they remain invalidated. • Furthermore, if these tests are used to provoke pain from brachial plexus compression, then only one site of nerve compression should be provoked. None of these tests is specific enough to exclude other pathology. Thus various authors have postulated new or modified tests to diagnose neurogenic TOS. • The Roos test (or elevated arm stress test) is generally described as the most reliable test for all types of TOS. As described, the reproduction of cervical, shoulder, and arm pain and paresthesias is seen as a positive test. If a patient is unable to complete the test because of symptoms, it can also reflect the severity of their condition. Because of its lack of specificity, Novak et al, as cited by Mackinnon and Novak, have suggested the use of a modified test, which was shown to be positive in 95% of a patient group with TOS in their study. • • • • • CHAPTER 16 • NERVE The patient places both arms into elevation with elbows extended and forearms in neutral (pronation/supination). With the wrists in neutral, they maintain this position for 1 minute. The test is positive for neurogenic TOS if there is a reproduction of cervical, shoulder, and arm pain and paresthesias. Furthermore, when using this modified Roos test, the authors found that when they applied sustained direct pressure over the brachial plexus, they reproduced symptoms in their TOS patients. Thus a combination of a provocative test with compression of the entrapment site may also be used to help diagnose TOS and other nerve entrapment neuropathies. Vibration or pressure threshold testing was also shown to be abnormal in a study of patients with neurogenic TOS, with arm elevation and sustained pressure over the brachial plexus. Twopoint discrimination was found to be normal, however, except in cases of coexisting carpal and cubital tunnel syndrome. Tinel’s sign has more recently been found to be quite useful in assessing nerves that are subject to irritation rather than just assessing for nerve regeneration. The median, ulnar, and radial nerves should be tested because double-crush syndromes exist in up to 50% of cases. An extensive neurological examination should also be performed to differentiate true and nonspecific neurogenic TOS and to rule out a cervical nerve root disorder. Cervical spine, shoulder, and chest x-rays are necessary to identify bony abnormalities and/or degenerative changes in the thoracic outlet region. MRI and/or MRI neurograms may also be necessary to identify soft tissue abnormalities in the thoracic outlet region. It is, however, more useful in excluding the presence of cervical nerve root or thoracic pathology. Computed tomography (CT) is indicated for suspected bony abnormalities (rib or pulmonary) especially in true neurogenic TOS. Nerve conduction studies (motor and sensory) and EMG tests may be useful to diagnose true neurogenic TOS (may find evidence of demyelination and axonal loss) but have difficulties in application and interpretation. These tests, however, are very useful to rule out other nerve pathologies (such as the median and ulnar nerve) that commonly coexist with this condition.They are of little use for the diagnosis of nonspecific neurogenic TOS (low specificity and sensitivity) because a negative result does not exclude the possibility of the presence of this condition. 29 of 57 • Anterior scalene blocks can be used to test if symptoms are being caused by scalene spasm but do not provide information about other underlying anatomical causes. DIFFERENTIAL DIAGNOSIS • Shoulder pathologies Glenohumeral instabilities Subacromial or subcoracoid impingement Subacromial bursitis Glenohumeral labral tears Rotator cuff tendinopathies Biceps tendinopathy Adhesive capsulitis Degenerative arthritis of the glenohumeral or AC joints Myofascial pain from scapulohumeral musculature • Cervical or thoracic pathologies Cervical spondylosis Cervical degenerative disc disease Cervical nerve root syndrome Cervical spine stenosis Thoracic facet syndrome T4 syndrome Rib dysfunction • Peripheral nerve entrapments Ulnar nerve entrapment (cubital tunnel/Guyon’s canal) Median nerve entrapment (carpal tunnel/pronator teres) Radial nerve entrapment (forearm) Multiple crush syndrome • Other Muscular dystrophy Polymyositis Complex regional pain syndrome (CRPS) Diffuse peripheral neuropathy Angina and other cardiac conditions Rheumatoid arthritis (RA) Lupus Pancoast’s tumor Multiple sclerosis Spinal cord lesion Hypothyroidism Pleuritis and other pulmonary conditions Raynaud’s phenomenon Head, neck, or upper quadrant tumors Lymphedema CONTRIBUTING FACTORS • Underlying existence of bony or fibromuscular anomalies in the thoracic outlet region (always found in true neurogenic TOS) • Previous history of whiplash injury or a direct or indirect blow to the shoulder resulting in first rib, muscular, or clavicular trauma. • Exposure to increased or unaccustomed prolonged or repetitive upper limb Neurogenic Thoracic Outlet Syndrome CHAPTER 16 • NERVE • • • • • • activity (e.g., overhead sport, occupation, or playing a musical instrument) Large breasts, breast implants, radical mastectomy surgery, pregnancy, and/or obesity Poor posture (e.g., downwardly rotated scapula, forward head posture) Accessory or upper chest breathing patterns Generalized low muscle tone Anterior shoulder instabilities Overdeveloped neck, trapezius, or pectoralis musculature as seen in weight lifters, swimmers, tennis players, and baseball pitchers. TREATMENT SURGICAL OPTIONS REHABILITATION 30 of 57 PROGNOSIS • Patients generally respond very well to conservative treatment, with most studies reporting positive outcomes in 60% to 90% of cases. • Prognosis strongly depends on the extent of damage to the brachial plexus and compliance to conservative treatment. Favorable outcomes are seen in those who comply with exercise programs and modify their behavior at work and home. Obesity, double-crush syndrome, psychosocial issues, and more severe and long-standing symptoms are seen as negative prognostic factors. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • The following presentations should be referred to a physician for appropriate investigation: • No response to conservative treatment after several weeks ORTHOPEDIC PATHOLOGY • The main goal of treatment is to reduce the compression on the brachial plexus to alleviate symptoms. Additionally, restoration of ideal neurodynamics, posture, breathing, and movement patterns is necessary for successful rehabilitation. • Initially, pain and symptom relief is paramount. In latter stages, improving functional stability and preventing recurrence becomes the priority. • Pain therapy or behavior modification Pain medication, including NSAIDs and muscle relaxants Electrotherapeutic modalities, including TENS, interferential current therapy, or ultrasound Ice or heat packs • Education Rest from aggravating activities, including heavy lifting Postural or ergonomic advice: Arms should remain supported in sustained activities, and correct lumbopelvic posture allows and assists maintenance of cervicoscapular neutral positioning. Standing: Hands may be placed in pockets initially to reduce the drag on shoulders. Sleeping position: Patient should lie supine or on the unaffected side with an extra pillow to support the affected arm in front of the body. Patients who sleep in a supine position may need to place a wedge under the shoulder and flex the elbow to unload neural structures. • Manual or soft tissue therapy Mobilization of the cervical and thoracic spine (including ribs); sternoclavicular, AC, and glenohumeral joints; and scapula may help unload the region. Cervical traction may also help reduce symptoms. Anterior accessory mobilizations of the lower cervical spine and first and second ribs are also very useful techniques, although low grades should initially be employed. Caudal mobilizations and muscle energy techniques (MET)for the first rib may also be effective, especially if the patient presents with an elevated first rib. Soft tissue therapy may include a combination of trigger point therapy, soft tissue release, or myofascial or positional release techniques to reduce tension associated with the production of symptoms and poor posture. The main muscles requiring treatment include the scalenes, levator scapulae, sternocleidomastoid, suboccipital, upper trapezius, rhomboids, and pectoralis major and minor. Additionally, the outer abdominal muscle unit (external and internal oblique and rectus abdominis muscles) may need releasing to allow more optimal breathing patterns into the lower rib cage. • Exercise therapy Lateral costal with diaphragmatic breathing in supine followed by a variety of functional positions Cervical ROM exercises maintaining good alignment Neurodynamic gliding exercises emphasizing upper or lower brachial plexus or involved nerves Motor control and stability functional rehabilitation exercises for proximal muscles of the trunk, neck, and shoulder include deep cervical flexor strengthening in supine, ensuring that the superficial cervical musculature remains relaxed. Stretching of tight muscles, particularly pectoralis minor and major, levator scapulae, and scalenes, to reduce fibrous bands and adhesions in muscles compressing the brachial plexus. Care should be taken not to reproduce symptoms. Gradual introduction of strengthening exercises for any muscles that have been subjected to motor loss, including fine motor and dexterity skills reacquisition. Progressive cardiovascular training program, especially for those in poor aerobic condition.Weight loss programs will also be necessary for obese patients. Section III • The following is a simplified summary of current surgical approaches for neurogenic TOS: Transaxillary first rib resection (approach used for lower plexus neurogenic TOS) Supraclavicular first rib resection (approach used for upper or lower plexus neurogenic TOS) Anterior and middle scalenectomy (used for obese patients in whom rib resection is difficult and for upper plexus neurogenic TOS) Combined rib resection and scalenectomy (combined approach most commonly used now, especially because of the lower rate of success of a secondary operation) Comprehensive supraclavicular decompression with scalenectomy Epineurectomy with anterior scalenectomy • Success rates for most of the current surgical techniques range from 70% to over 90%. Poor outcomes, however, are seen on reoperation (15% rate of success). Failure is often attributed to poor patient compliance to postoperative therapy or recurrent injury. Transaxillary first rib resection surgery has been found to have lower success rates for upper plexus neurogenic TOS. Lower rates of success with surgery have also been seen with patients who suffer from work-related TOS than from MVAs. • Surgical indicators include the following: Failure of conservative treatment after 3 to 6 months (ongoing pain and dysfunction) Worsening neurological status Presence of significant muscle atrophy with cervical rib (true neurogenic TOS) All differential diagnoses have been treated or excluded. Since TOS patients often suffer from coexisting nerve entrapments (especially at the carpal tunnel and cubital tunnel), it is important to consider surgery on these areas, possibly before consideration of TOS surgery because alleviation of pressure distally can affect and relieve TOS symptoms. 765 766 Neurogenic Thoracic Outlet Syndrome • Worsening neurological status • Atypical symptoms • Vascular symptoms (see the section on Vascular TOS) • Presence of significant muscle atrophy with cervical rib (true neurogenic TOS) • Red flags (e.g., unexplained weight loss). SUGGESTED READINGS Atasoy E. Thoracic outlet syndrome: anatomy. Hand Clin. 2004;20(1):7–14. Ault J, Suutala K. Thoracic outlet syndrome. J Man Manipulative Ther. 1998;6(3): 118–129. Brantigan CO, Roos DB, David B. Etiology of neurogenic thoracic outlet syndrome. Hand Clin. 2004a;20(1):17–22. Brantigan CO, Roos DB. Diagnosing thoracic outlet syndrome. Hand Clin. 2004b;20(1): 27–36. Crosby CA, Wehbe MA. Conservative treatment for thoracic outlet syndrome. 2004;20(1): 43–49. Dawson DM, Hallett M, Milender LH. Entrapment Neuropathies. 2nd ed. Boston: Little, Brown; 1990. CHAPTER 16 • NERVE Demondian X, Herbinet P, Van Sint Jan S, Boutry N, Chantelot C, Cotton A. Imaging assessment of thoracic outlet syndrome. Radiographics. 2006;26:1735–1750. Edgelow PL. 2003:Neurovascular consequences of cumulative trauma disorders affecting the thoracic outlet: A patient-centred treatment approach. In: Donatelli RA, ed. Physical Therapy of the Shoulder. Philadelphia: Churchill Livingstone;. Mackinnon SE, Novak CB. Thoracic outlet syndrome. Curr Probl Surg. 2002;39(11):1070–1145. Novak CB, Mackinnon SE, Patterson GA. Evaluation of patients with thoracic outlet syndrome. J Hand Surg. 1993;18A:292–299. Pecina MM, Krmpotic-Nemanic J, Markiewitz AP. Tunnel Syndromes: Peripheral Nerve Compression Syndromes. 3rd ed. Boca Raton, FL: CRC Press; 2001. Safran MR. Nerve injuries about the shoulder in athletes, Part 2: Long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med. 2007;32(4):1063–1076. Sanders RJ, Hammond MD. Etiology and pathology. Hand Clin. 2004;20(1):23–26. 31 of 57 Sanders RJ, Hammond SL. Supraclavicular first rib resection and total scalenectomy: technique and results. Hand Clin. 2004;20(1): 61–70. Urschel Jr HC, Kourlis Jr H. Thoracic outlet syndrome: A 50-year experience at Baylor University Medical Center. Baylor Univ Med Cent Proc. 2007;20(2):125–135. Urschel Jr HC, Razzuk MA. Neurovascular compression in the thoracic outlet. Changing management over 50 years. Ann Surg. 1998;228(4):609–617. Vanti C, et al. Conservative treatment of thoracic outlet syndrome: A review of the literature. Eura Medicophys. 2007;43(1):55–70. Wehbe MA. Thoracic outlet syndrome. Guest editor. Hand Clin. 2004;20(1). Whitenack SH, Hunter JM, Read RL. Thoracic outlet syndrome: a brachial plexopathy. In: Mackin EJ, Schneider LH, Callahan AD, et al., eds. Rehabilitation of the Hand and Upper Extremity. 5th ed. St Louis: Mosby; 2002. AUTHOR: KATINA DIMOPOULOS Obturator Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION COMMON SIGNS AND SYMPTOMS DEFINITION • Pain in the groin region, near the inguinal ligament, is common. • Gait changes or problems may occur because of the instability or weakness of the hip adductors. • Sensory changes or numbness might be noted in the medial portion of the thigh. • Exercise-induced symptoms may be present in athletes with a decreased performance in jumping or running. • If the condition becomes more severe, the patient might have more severe loss of internal rotation, adduction, or abduction. Obturator nerve entrapment is a rare mononeuropathy that results from compression or restriction of movement of the obturator nerve through the obturator foramen as it passes by the obturator externus. SYNONYMS None currently used ICD-9CM CODES 355.7 Other mononeuritis of lower limb OPTIMAL NUMBER OF VISITS 6 or fewer MAXIMAL NUMBER OF VISITS AGGRAVATING ACTIVITIES • • • • • Walking Prolonged standing Running Jumping Stretching of the hip into adduction or abduction 16 EASING ACTIVITIES ETIOLOGY • Rest • Sitting • Modalities No specific data were found on the incidence of this condition; however, some authors have stated that this condition is not very common. MECHANISM OF INJURY • Most injuries are associated with acute trauma such as the following: Childbirth: The head of the fetus may compress the nerve against the bony structures of the pelvis Pelvic fracture Postsurgical, after total hip replacement Malpositioning of the lower limb for prolonged periods Contusion or strain of the adductor muscles No studies on a particular pattern of symptoms were found for obturator nerve entrapment. Increased symptoms at night or lasting symptoms in the morning may point to a strong inflammatory component to the symptoms. This may also suggest a space-occupying lesion, such as a tumor, so careful attention should be paid to other factors and the progression of symptoms. PAST HISTORY Previous similar injuries or repetitive injuries in a similar area might be found in a patient’s history that may predispose them to such a nerve entrapment. PHYSICAL EXAMINATION • Antalgic or unsteady gait is probably one of the most common features of this condition because of the innervation of the adductor muscles and their importance during gait. • If the condition has been prolonged, the patient may present with atrophy or wasting of the adductor muscles. • Sensation changes may be present in the middle portion of the medial thigh. Pain or paresthesias may also be found in the same distribution. • Passive movements of the hip are likely to be guarded, and full internal rotation or adduction may increase the compression and be symptomatic. Abduction may also be uncomfortable because the tissues around the nerve or the nerve itself is put on tension. 32 of 57 • Sensation testing in the medial lower extremity may help confirm obturator nerve involvement and differentiate between more proximal lumbar or sacral pathology. • MMT of the adductors may also help to confirm weakness or pain in those muscles. • Palpation of the adductor muscles and surrounding structures may reproduce symptoms into the nerve distribution. • Neurodynamic testing (Butler, 2000) may also help differentiate between a neurogenic and nonneurogenic source of symptoms. A variation of the slump knee bend test with cervical extension and flexion as a sensitizing maneuver may be performed. DIFFERENTIAL DIAGNOSIS • • • • • • • Adductor muscle strain Osteitis pubis Stress fracture Inguinal ligament enthesopathy Femoral nerve entrapment Inguinal hernia Lumbar plexopathy or sacral plexopathy CONTRIBUTING FACTORS • • • • Diabetes mellitus Thyroid problems Poor posture Impaired trunk and motor control TREATMENT SURGICAL OPTIONS In athletes, surgery may be the preferred treatment for neuropathy. The surgery may involve dividing the fascia over the pectineus and adductor longus muscle. To reveal the anterior branch of the nerve from the fascia, it may require dissecting the space between these two muscles. REHABILITATION • Addressing irritable symptoms with modalities, such as ultrasound, interferential current therapy, phonophoresis, or ice and to address pain and inflammation may be the first step of treatment. • In the case of antalgic gait or poor gait mechanics, an assistive device, such as a single-point cane, may be warranted to decrease the mechanical stress on the nerve and adductors during walking. • Soft tissue mobilization can be a beneficial technique to help address both pain and fibrotic scarring of surrounding fascia that may be restricting the nerve. • If it is hypothesized that abnormal neurodynamic movement exists, then ORTHOPEDIC PATHOLOGY EPIDEMIOLOGY AND DEMOGRAPHICS 24-HOUR SYMPTOM PATTERN IMPORTANT OBJECTIVE TESTS Section III • Arising from the anterior branches of L2, L3, and L4, the obturator nerve follows the medial border of the psoas distally to the lateral wall of the lesser pelvis through the obturator foramen. It then divides into the anterior branch, which descends between the adductor longus and brevis, and the posterior branch, which descends between the adductor magnus and brevis. • The obturator nerve innervates the adductor, the obturator externus, the gracilis, and the pectineus muscles. • The obturator nerve supplies the middle portion of the medial thigh. • Entrapment of the obturator nerve usually happens within the obturator foramen or nearby the proximal portion of the adductor muscles.The nerve may be compressed by external factors or also entrapped by fibrosis of surrounding fascia. 767 768 Obturator Nerve Entrapment neurodynamic techniques described by Butler (1991) that attempt to slide, glide, and put tension on the nervous system can be beneficial. • Any other biomechanical faults or impairments that may lead to putting more stress on the adductors or hip should also be assessed. PROGNOSIS Because of the rarity of this condition, no literature has been found on long-term prognosis. However, it most likely follows patterns of other nerve entrapment syndromes that have good outcomes if discovered early and proper management is implemented. CHAPTER 16 • NERVE SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Unrelenting pain not related to biomechanical factors • Weight loss • Bowel or bladder dysfunction • Saddle paresthesias • Gait disturbances: Clumsiness or ataxic gait • Bilateral glove or sock numbness • Symptoms that do not initially improve with symptoms SUGGESTED READINGS Butler DS. The Sensitive Nervous System. Adelaide,Australia: Noigroup Publications; 2000. 33 of 57 Butler DS. Mobilisation of the Nervous System. New York: Churchill Livingstone; 1991. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. AUTHOR: CHRIS IZU Plantar Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION EPIDEMIOLOGY AND DEMOGRAPHICS DEFINITION • The incidence of true plantar nerve pathology is difficult to distinguish since it is often grouped with distal tibial nerve entrapment (proximal tarsal tunnel syndrome) because the clinical picture and management may be very similar. • It is thought that there may be a slight female predominance, and the age range has been stated from 14 to 80 years of age. • Medial plantar nerve entrapment has been noted to occur commonly in athletes or runners, thus the term “jogger’s foot.” Plantar nerve entrapment is a neuropathy from compression or restriction of movement of the medial or lateral plantar nerve most commonly under the deep fascia of the plantar surface of the foot. SYNONYMS • Distal tarsal tunnel syndrome • Jogger’s foot ICD-9CM CODES 355.5 Tarsal tunnel syndrome OPTIMAL NUMBER OF VISITS 8 or fewer MAXIMAL NUMBER OF VISITS 16 ETIOLOGY • Traction injuries from repetitive motions of the foot and ankle • Direct blow or trauma to foot • Space-occupying lesions • Constant pressure (e.g., improper fitting orthotic) • More often the onset is insidious or gradually builds up over time. COMMON SIGNS AND SYMPTOMS AGGRAVATING ACTIVITIES • • • • Prolonged standing Walking Running Wearing high heels or walking without shoes • Any activity with increased weight bearing usually aggravates the symptoms of plantar nerve entrapment because of local pressure or stretching of the nerve. If the symptoms are less irritable, it may take prolonged running or even jumping to bring on symptoms. EASING ACTIVITIES • • • • Rest Sitting Wearing proper fitting shoes Modalities for pain or inflammation 24-HOUR SYMPTOM PATTERN • One author suggested that there may be more pain at night that is eased with standing and walking. • Intuitively, it would seem that the pain may be worse later in the day if the 34 of 57 PAST HISTORY No specific history of symptoms has been documented in this population. However, a history of previous trauma to the foot and ankle would make sense as they may develop fibrosis of the surrounding muscle fascia. A previous history of similar nerve entrapment syndromes may also be noted in their history. PHYSICAL EXAMINATION • Pain and dysesthesias in the plantar surface of the foot are the most common findings in this population. • Antalgic gait and pain with increased weight bearing may also be noted. A rapid pronation may be noted during the initial stance phase of gait or a lack of supination may be noted during the terminal stance phase. • Balance activities may be slightly more difficult or painful on the affected side, caused by the activation of the abductor hallucis and quadratus during these activities. • Pain on palpation may also be a key finding. IMPORTANT OBJECTIVE TESTS • Lower quarter neurological testing Sensory testing should reveal altered symptoms within the plantar surface of the foot. Using Semmes-Weinstein monofilaments may help with increasing sensitivity of the examination. Motor testing should be normal, except for possible pain-inhibited weakness with repetitive plantarflexion in standing. Reflexes: The Achilles and the patellar tendon should be normal secondary to the lesion below the level of tested reflexes. • Palpating the surrounding fascia and muscles may reproduce pain into the distribution of the medial or lateral plantar nerve. • Neurodynamic testing: Using the slump or SLR test with sensitizing maneuvers may help to distinguish neurogenic (plantar nerves) from nonneurogenic (surrounding musculature) as a source of symptoms. The addition of forefoot inversion to the SLR test may add more tension to the medial plantar nerve, while forefoot eversion may add more tension to the lateral plantar nerve. DIFFERENTIAL DIAGNOSIS • Heel spur • Plantar fasciitis • Polyneuropathy ORTHOPEDIC PATHOLOGY • Patients typically complain of vague, diffuse pain in the plantar surface of the foot.They may also note chronic, intractable heel pain if more of the calcaneal branches are involved. • Gait or balance problems may be noted as difficulties with the foot’s intrinsic muscles may occur. • It may be difficult to run, jog, or perform repetitive lower extremity exercises or activities. patient is required or chooses to do a lot of standing or walking. Section III • The medial plantar nerve is the larger branch of the tibial nerve that passes distally between the abductor hallucis and the flexor digitorum brevis. It then divides into both cutaneous and muscular branches. • The lateral plantar nerve is the smaller branch of the tibial nerve that passes laterally underneath the foot between the quadratus plantae and flexor digitorum brevis. From there it divides into superficial and deep branches. • The medial plantar nerve supplies the medial side of the sole of the foot and sides of the first three digits. • The lateral plantar nerve supplies the skin on the sole of the lateral side of the foot, which can be delineated by a line that splits the fourth digit. • The medial plantar nerve innervates the abductor hallucis, flexor digitorum brevis, flexor hallucis brevis, and the first lumbrical. • The lateral plantar nerve innervates the quadratus plantae, abductor digiti minimi brevis, plantar interossei, dorsal interossei, lateral three lumbricals, and abductor hallucis. • The medial plantar nerve is commonly entrapped in the area of the master knot of Henry, which is a fibrous slip between the flexor hallucis longus and the flexor digitorum longus that binds the medial plantar surface. • The lateral plantar nerve is usually entrapped beneath the deep fascia of the abductor hallucis or the quadratus plantae. It is theorized that this entrapment may result from repeated stretching and tethering of the nerve caused by abnormal forces at the foot such as excessive valgus, external rotation, or pronation. MECHANISM OF INJURY 769 770 Plantar Nerve Entrapment • Systemic disorders • Lumbar spine radiculopathy CONTRIBUTING FACTORS • • • • • • • • • • • Tenosynovitis of adjacent tendons Partial or complete rupture of tendons Obesity Ankylosing spondylitis Acromegaly Talocalcaneal coalition Diabetes mellitus RA Abnormal foot positioning Alcoholism Thyroid disease TREATMENT SURGICAL OPTIONS • Surgical release of the surrounding tissue may help with relief of compression on the nerve. In most cases, a full release of both the posterior tibial nerve and the lateral plantar nerve is recommended. • If a space-occupying lesion is noted to have a significant effect on the nerve,then removal by surgery is recommended. REHABILITATION • Initially rehabilitation should focus on reduction of symptoms, finding easing activities, and managing inflammation. • Modalities, such as ultrasound, phonophoresis, iontophoresis, ice massage, and interferential current therapy, may help to manage initial symptoms. • Taping or orthotic prescription to control abnormal foot motions or support CHAPTER 16 • NERVE the medial longitudinal arch may also help reduce symptoms by decreasing abnormal strain. • During less irritable conditions, more vigorous treatment, such as soft tissue mobilization, may help free fibrotic scarring or fascial thickening around the nerve sheath. • Neurodynamic mobilization, using techniques to slide, glide, or place tension on the nerve, may help restore more normal mobility to neural structures. Alterations of the slump test or SLR test may be good places to start when dealing with plantar nerve mobility. • Exercises should address lower extremity impairments or biomechanical faults that may place further stress on the plantar nerve. Common activities include improving forefoot, rearfoot, or entire lower extremity control with attempts to decrease abnormal or rapid pronation. PROGNOSIS • After surgical release procedures, one study reported good-to-excellent results in about 84% of patients. • Although no data were found, clinical observations of plantar nerve entrapment have shown good response to conservative rehabilitation when few contributing factors are present. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • If suspected worsening compression on the nerve is suspected from a compartment syndrome, immediate referral to 35 of 57 • • • • a physician is warranted. A fasciotomy may be done to release this pressure. Unrelenting symptoms, especially combined with worse pain at night, may indicate a local tumor. Lack of improvement within the expected time frame or symptoms that are not affected by physical therapy in a few visits should be referred back to the physician because a space-occupying lesion may be present. A recent history of trauma with suspected fracture may warrant further imaging done before continuing physical therapy. Impaired circulation or vascular compromise may also warrant more medical management. SUGGESTED READINGS Butler DS. The Sensitive Nervous System. Adelaide, Australia: Noigroup Publications; 2000. Butler DS. Mobilisation of the Nervous System. New York: Churchill Livingstone; 1991. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. AUTHOR: CHRIS IZU Radial Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Radial nerve entrapment pathologies encompass any injury that interrupts the function of the radial nerve at any point along its course. The loss of function results in muscle weakness, pain, or sensory dysfunction. SYNONYMS • Saturday night palsy or syndrome • Radial tunnel syndrome (RTS) • Posterior interosseous nerve (PIN) syndrome ICD-9CM CODES 354 Mononeuritis of upper limb and mononeuritis multiplex 354.3 Lesion of radial nerve OPTIMAL NUMBER OF VISITS 6 MAXIMAL NUMBER OF VISITS 20 36 of 57 EPIDEMIOLOGY AND DEMOGRAPHICS • Of the three major nerves in the upper limb, entrapment of the radial nerve is least common. • The most common site for entrapment and injury is the spiral groove of the humerus related to humeral fracture. ORTHOPEDIC PATHOLOGY • The radial nerve is derived from C5-C8 nerve roots with an additional sensory component from T1. • The radial nerve is the larger terminal branch of the posterior cord of the brachial plexus. • It arises proximal to the lower border of subscapularis, then runs posterolaterally inferior to latissimus dorsi and teres major at their attachment to the humerus. • It descends obliquely across the posterior portion of the midshaft of the humerus in the spiral/radial groove between the medial and lateral heads of the triceps brachii muscle. • While in the groove, it is accompanied by the deep brachial vessels, the groove ends just distal to the deltoid tuberosity, and at that point the nerve enters the anterior compartment of the arm through the fibrous intermuscular septum in a deep position between the brachialis and brachioradialis muscles. • It continues to descend to supply extensor carpi radialis longus and brevis superficially and deeply to the lateral elbow capsule and the radial tunnel. • The superficial branch continues through the forearm deep to the brachioradialis and provides cutaneous innervation to the dorsolateral hand. • The deep branch (posterior interosseous nerve) curves around the neck of the radius between the two layers of the supinator muscle, emerging as multiple tive pronation and supination tasks in sport or occupation Compression between the tendons of the brachioradialis and extensor carpi radialis longus muscles and through the antebrachial fascia again seen in repetitive pronation, supination, pinching, grasping, or heavy pushing and pulling tasks Compression of the superficial branch over the lateral aspect of the forearm by direct trauma or by straps, watches, and wrist bands • Nerve injury is classified according to the severity of the injury and its potential for reversibility as follows: Neurapraxia (first-degree injury): Distortion of the myelin around the nodes of Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance produces temporary loss of nerve conduction. Axonotmesis (second-degree injury): Interruption of the axon with secondary wallerian degeneration. The supporting tissue surrounding the axon is preserved, and the recovery period depends on the distance between the site of injury and the end-organs. Neurotmesis: Complete disruption of the nerve and its supporting structures • Neurotmesis has been further divided into the following three subcategories: Third-degree nerve injury: Endoneurium is disrupted with intact perineurium and epineurium Fourth-degree nerve injury: All neural elements sparing the epineurium are disrupted. Fifth-degree nerve injury: Complete transaction and discontinuity of the nerve with no capacity for regeneration • Physiologically, there is disruption to any part of the nerve responsible for conduction. • In repetitive-type nerve entrapment, it is proposed that repetitive work or static postures produce an inflammatory response, and fibroblasts appear to repair damage incurred but produce adhesions to the nerve, limiting their glide and increasing anoxia. • Other studies found that cortical dedifferentiation can result from repetitive motion activities and nerve injuries.This may result in reinforced poor posturing and use of aberrant motor pathways. Section III ETIOLOGY branches that supply the deep posterior muscles of the forearm and wrist joint. • The radial nerve is vulnerable to injury at several points along its course, as follows: Proximally at the axilla Along the shaft of the humerus while in the spiral groove By the lateral heads of triceps and as it passes through the fibrous intermuscular septum While in the radial tunnel by a fibrous band at the level of the radial head, by the radial recurrent artery, or by the tendinous edge of extensor carpi radialis brevis Within the arcade of Frohse Within the supinator or by the distal edge of the supinator Between the tendons of the brachioradialis and extensor carpi radialis longus muscles and through the antebrachial fascia Superficially over the lateral aspect of the forearm • The radial nerve may be affected at any point along its course by direct trauma or compression entrapment causing nerve tissue hypoxia. The insult to the nerve can be mechanical, thermal, chemical, and ischemic. • This pathology can occur in of the following ways: Through compression at the axilla such as occurs when falling asleep with the arm over the back of a chair (Saturday night palsy) or with the use of shoulder crutches By direct damage to the nerve during a humeral shaft fracture or from compression against callus formation along the spiral groove after a traumatic humeral injury Compression by the lateral head of the triceps and as the nerve passes through the fibrous intermuscular septum sometimes seen in weight lifting or other activity that involves heavy repetitive triceps activation Compression in the radial tunnel by a fibrous band at the level of the radial head or by the radial recurrent artery (leash of Henry) in which the tunnel does not provide adequate space for the course of the nerve Compression by the tendinous edge of extensor carpi radialis brevis when subjected to repetitive wrist and finger extension activity such as in some factory and office-based tasks Compression within the arcade of Frohse by a space-occupying lesion or simply by anatomical restriction of the arcade space Compression within the supinator muscle or by the distal edge of the supinator that may occur with repeti- 771 772 Radial Nerve Entrapment • Work-related entrapments are becoming more common, in particular with computer use and seated postures. • RTS has a very small incidence (1% to 2%) of upper extremity entrapments. RTS most commonly involves patients in the fourth to sixth decade of life without significant gender predilection. MECHANISM OF INJURY • There are a number of mechanisms of injury for the radial nerve that will be described in relation to their location: Through compression at axilla such as falling asleep with the arm over the back of a chair (Saturday night palsy) or with the use of shoulder crutches By direct damage to the nerve during a humeral shaft fracture or from compression against callus formation along the spiral groove after a traumatic humeral injury Compression by the lateral head of the triceps and as the nerve passes through the fibrous intermuscular septum as sometimes seen in weight lifting or other activity that involves heavy repetitive triceps activation Compression in the radial tunnel by a fibrous band at the level of the radial head or by the radial recurrent artery (leash of Henry) where the tunnel does not provide adequate space for the course of the nerve. Compression by the tendinous edge of extensor carpi radialis brevis when subjected to repetitive wrist and finger extension activity such as found in some factory and office-based tasks. Compression within the arcade of Frohse by a space-occupying lesion or simply by anatomical restriction of the arcade space. Compression within the supinator muscle or by the distal edge of the supinator that may occur with repetitive pronation and supination tasks in sport or occupation Compression between the tendons of the brachioradialis and extensor carpi radialis longus muscles and through the antebrachial fascia again seen in repetitive pronation, supination, pinching, grasping, or heavy pushing and pulling tasks Compression of the superficial branch over the lateral aspect of the forearm by direct trauma or by straps, watches, and wrist bands. COMMON SIGNS AND SYMPTOMS • High radial nerve palsies Weakness of the elbow extension (triceps) Mild weakness of elbow flexion (brachioradialis) CHAPTER 16 • NERVE Mild weakness of wrist and finger extension There may be variable loss of sensation over the posterior arm forearm and hand. Triceps and brachioradialis reflexes are lost or reduced. Often result in a characteristic posture of wrist drop with slight flaccid flexion, the hand pronated and thumb adducted (waiter’s tip position). Generally, this is an injury to the entire lower brachial plexus not just the radial nerve so the medial and ulnar branches may also be involved and must be assessed. Spiral groove lesions are similar to high radial nerve palsies, but the triceps power and reflexes are spared. Posterior interosseous neuropathies are generally motor; pain may be present but is not the major symptom. There is a resultant finger drop with variable weakness of wrist extension. When wrist extension is attempted, there may be weak dorsoradial deviation caused by the preservation of the radial wrist extensors. • RTS Deep, dull lateral elbow pain Pain over the extensor mass Wrist aching Middle or upper third humeral pain Increased pain on resisted supination of the forearm Increased pain with middle-finger extension (also evident in extensor tendinopathies) Paraesthesias (tingling and numbness) over the dorsal hand and lateral forearm Neural tension tests may reproduce the symptoms. To distinguish between RTS and extensor tendinopathies the location of the pain is less localized to the lateral epicondyle and more likely to be over the extensor mass and supinator. The pain of RTS is more achy and produces more muscle fatigue. RTS appears to be more related to repetitive pronation and supination rather than repeated wrist extension for extensor tendinopathy. RTS and extensor tendinopathy occur together in 5% of cases. • Superficial branch of the radial nerve results in sensory loss over the dorsum of the hand, most commonly of the dorsal thumb, index, and middle fingers; occasionally the dorsolateral half of the ring finger is also involved. This type of nerve compression can cause poorly localized pain in this distribution and above. • For all levels of radial nerve injury, there may have been loss of nerve 37 of 57 representation of the nerve injured area on the somatosensory cortex. AGGRAVATING ACTIVITIES • Any repeated actions of the forearm extensors, supination, or pronation. • Repetitive, forceful pushing and pulling, bending the wrist, gripping and pinching • Screwdriver motion • Work tasks involving repetitive finger work such as typing or mouse work • Higher radial nerve injuries may be provoked by repetitive elbow extension activating the triceps such as weight lifting. • Sports involving gripping, pronation, supination, or wrist and finger extension. EASING ACTIVITIES Rest and/or modification of aggravating activities 24-HOUR SYMPTOM PATTERN • Generally the symptoms are related to activity and do not follow a typical 24-hour pattern unless there is a strong inflammatory component such as may be seen in occupational repetitive tasks. • If there is an inflammatory component, there may be worsening of symptoms with use toward the end of the day and morning stiffness. PAST HISTORY FOR THE REGION • History of trauma, fracture, dislocation, or blow to the radial nerve distribution. • Repeated activity involving pushing, pulling, gripping, supination, or pronation • Work tasks involving exertions of greater than 1 kg of force more than 10 times an hour, static pinching or squeezing objects or tools, working with the elbow extended, and maintaining positioning of the forearm in pronation or supination. • Racquet sports: Repetitive pronation and supination, gripping and wrist extension • When the superficial branch is involved the patient should be questioned about any straps, watches, or wristbands worn. • Working with hand tools or power tools (vibration) PHYSICAL EXAMINATION • Examine the limb for signs of autonomic dysfunction trophic changes such as edema, inflammation, and alteration in skin texture • Reflex testing, paying particular attention to limb asymmetries of the triceps and brachioradialis reflexes Radial Nerve Entrapment CHAPTER 16 • NERVE • Needle EMG is valuable for evaluating the extent of motor fiber loss within a nerve territory. EMG assists with determining the location of the injury and to monitor progression over time. • X-ray of the humerus may reveal an undiagnosed fracture of the humeral shaft or callus formation from a previous injury. • MRI is increasingly being used in the assessment of peripheral nerve injuries to rule out cervical nerve root involvement and determine the presence of edema, space restriction, or space-occupying lesion along the course of the radial nerve. DIFFERENTIAL DIAGNOSIS • • • • • • • • • Forearm extensor tendinopathy Underlying neuropathic disease Idiopathic brachial neuritis Myopathies Muscular dystrophy Isolated neuropathy in the diabetic Tumors or space-occupying lesions C6 or C7 cervical radiculopathy Upper motor neuron lesion in the cerebrum • De Quervain’s tenosynovitis CONTRIBUTING FACTORS TREATMENT IMPORTANT OBJECTIVE TESTS • The earliest electrodiagnostic sign of entrapment is a loss of the nerve action potential seen during a nerve conduction study. To isolate the specific location of the conduction block, serial stimulations are delivered to the nerve above and below the suspected lesion. SURGICAL OPTIONS • Surgery is generally considered a last resort if conservative management fails. • Nerve palsy after a closed fracture of the humerus is generally observed over 6 to 12 weeks to determine the effect of the swelling subsiding. However, if the 38 of 57 REHABILITATION • Current best evidence for the conservative management of RTS consists primarily of expert opinion and inferences taken from studies on other nerve compressions. • The goal of rehabilitation should be to reduce pain, to encourage pain-free exercise, to provide ergonomic education and interventions, and if the neuropathy has been prolonged, to introduce cortical reorganization activities. • Splinting should be used to provide immobilization to allow the reduction in swelling and inflammation. Functional splinting can also be employed to prevent contracture and facilitate normal movement patterns (e.g., for a high radial nerve palsy the use of a static wrist extension splint with dynamic extension apparatus for the proximal phalanges). • Elimination of aggravating tasks by avoiding or modifying those tasks to prevent further damage • Use of ice to reduce inflammation and prevent secondary cell damage • Theoretically, ultrasound may be helpful to promote nerve regeneration, improve profusion to the healing nerve, and decrease inflammation. • Direct low-intensity electrical stimulation has been found to increase the number of vasa nervorum and nerve fiber density in rats. • Steroid injection is often advocated to reduce inflammation particularly in RTS. • Iontophoresis with dexamethasone and lidocaine • Nerve gliding exercise, have been purported to disperse intraneural edema, increase blood flow, optimize axonal transport, and lengthen nerve adhesions. Neural mobilization can be assessed using the brachial plexus provocation test positions to identify symptom reproduction and these positions and movements can also be used both actively and passively for a treatment technique. • Use of soft tissue mobilization and muscle stretching techniques to reduce fibrous bands and adhesions in muscles surrounding the radial nerve. Stretches must not produce tingling or discomfort because this may indicate ORTHOPEDIC PATHOLOGY • For any nerve entrapments that are nontraumatic, there is often an element of repetitive activity involving the affected limb. Typically, in the case of the radial nerve, the repetitive action involves, elbow extension, forearm pronation, supination, gripping, forceful pushing and pulling, and/or wrist and finger extension. • Postural factors may be involved, particularly with repetitive work or sporting activities with reduction in proximal stability and control leading to an overuse of more distal muscle groups to perform a task. • Excessive loads, such as in heavy manual work or sports, involving weight lifting can overload the capacity of the muscles to adapt, thus creating inflammation and subsequent nerve compression. • The use of tight wristbands, cuffs, or other strapping across the wrist may contribute to superficial radial nerve compression. palsy continues, then surgical intervention is indicated. • The goal of surgical intervention would be to relieve pressure or entrapment along the course of the nerve, (e.g., surgical release of the superficial head of supinator and division of the ligament of Frohse to expand the available space in the radial tunnel). Section III • MMT may reveal weakness in any of the following muscles: Triceps (C7, C8): Extend elbow against resistance Brachioradialis (C5, C6): Flex elbow with forearm half way between pronation and supination Extensor carpi radialis longus (C6, C7): Extend wrist to the radial side with fingers extended Supinator (C5, C6): Arm by side resist hand pronation. Extensor digitorum (C7, C8): Maintain finger extension at the MCP joints Extensor carpi ulnaris(C7, C8): Extend wrist to ulnar side Abductor pollicis longus (C7, C8): Abduct thumb to 90degrees to palm Extensor pollicis brevis (C7, C8): Extend thumb at MCP Extensor pollicis longus (C7, C8): Resist thumb flexion at IP joint • Sensation: The cutaneous branches of the radial nerve supply the dorsal aspect of the forearm from below the elbow down over the lateral part of the hand to include the thumb to the interphalangeal joint and the fingers distal to the interphalangeal joint, including index and middle fingers but not the little finger. Sensation testing should include pinprick, two-point discrimination, tuning fork, and joint position sense and compared for asymmetry with the unaffected side (where available). • Tinel’s sign may be positive over the anatomical snuff box. • Physical examination should also exclude pathology in other areas, particularly performing AROM and PROM at the neck and shoulder, which may reveal restrictions and central involvement of the nerve. • Upper limb neural tissue provocation testing may reveal changes in nerve mobility and elicit symptoms. • Physical examination should also include movement analysis to determine the movement patterns that the patient adopts when performing the aggravating activities. Movement analysis can be done visually or with the assistance of a video camera. The analysis should give some clues as to predisposing factors, such as posture and patterning, that will assist with rehabilitation and activity modification. 773 774 Radial Nerve Entrapment • • • • • decreased blood flow to the already stressed nerve. Motor control and stability functional rehabilitation exercise for proximal muscles of the trunk, neck, and shoulder. Gradual introduction of strengthening exercises for any muscles that have been subjected to motor loss Ergonomic interventions, workplace assessment, provision of ergonomic aides such as tilted keyboards or altered mouse shape Cortical reorganization techniques such as use of mirror box Reacquisition of fine motor and dexterity skills PROGNOSIS • Prognosis depends entirely on the extent of damage to the nerve. • Neurapraxia should resolve rapidly and lead to a complete restoration of function, usually within 2 to 3 months. CHAPTER 16 • NERVE • If the injury is a more severe axonotmesis, the recovery time depend on the distance from the site of injury to the denervated tissue. • Peripheral nerves have been reported to recover at an approximate rate of between 1 and 4 mm per day, but complete function might not be restored. • If there has been a complete sectioning of the nerve (neurapraxia), then a full recovery will not occur. • The results of treating neurapraxia even with surgical intervention are generally not satisfactory. SUGGESTED READINGS Bencardino JT, Rosenberg ZS. Entrapment neuropathies of the shoulder and elbow in the athlete. Clin Sports Med. 2006;25:465–487. Cleary CK. Management of radial tunnel syndrome: A therapist’s clinical perspective. J Hand Ther. 2006;19(2):186–191. Pratt N. Anatomy of nerve entrapment sites in the upper quarter. J Hand Ther. 2005;18(2):216–229. Roquelaure Y, Raimbeau G, Dano X. Occupational risk factors for radial tunnel syndrome in industrial workers. Scand J Work Environ Health. 2000;26:507–513. AUTHOR: JOSEPHINE LOUISE COULTER SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN If radial nerve entrapment is suspected, all cases should be referred to a physician for appropriate investigation. 39 of 57 Saphenous Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Saphenous nerve entrapment is a mononeuropathy that results from compression or restriction of movement of the saphenous nerve in the distal thigh as it passes through the adductor canal. SYNONYMS None currently used ICD-9CM CODES 355.7 Other mononeuritis of lower limb OPTIMAL NUMBER OF VISITS 6 or fewer MAXIMAL NUMBER OF VISITS • • • • • Pes anserine bursitis Postsurgical vein operations Medial knee arthrotomies Postsurgical meniscal repairs Improperly protected leg during surgery COMMON SIGNS AND SYMPTOMS • The most common complaint of saphenous nerve entrapment is medial knee pain. Usually, it is described as a dull, aching sensation in the knee, but the patient may also have discomfort in the medial thigh. • Paresthesias may be found in the cutaneous distribution of the saphenous nerve, which includes the medial knee and medial region of the lower leg down into the medial ankle and foot. • It is important to note that since the nerve is purely sensory, no motor deficits or gait abnormalities should be part of the symptoms. 20 ETIOLOGY EASING ACTIVITIES • Rest and avoiding aggravating activities • Antiinflammatories 24-HOUR SYMPTOM PATTERN If there is a significant inflammatory component to the symptoms or a space-occupying lesion, more night symptoms may be expected. Following this, symptoms may also be worse in the morning. One study has noted that two thirds of the patients with saphenous nerve entrapment in their study had increased symptoms at night. PAST HISTORY It is believed that this condition, as well as peroneal nerve entrapment, is the most common form of lower extremity nerve entrapment syndrome. As a result of the traumatic or repetitive stress injury causes of saphenous nerve entrapment, there may be no significant items noted on their history. Since fibrosis of the surrounding tissues may be a contributing factor to this nerve entrapment, a previous history of trauma may be found. MECHANISM OF INJURY PHYSICAL EXAMINATION • Direct trauma • Entrapment by femoral vessels • Usually, sensory deficits and pain are the only presentation of this condition. EPIDEMIOLOGY AND DEMOGRAPHICS 40 of 57 IMPORTANT OBJECTIVE TESTS • Sensation testing: Light touch, pinprick, or sharp/dull testing should reveal altered sensation in the saphenous nerve distribution. • Lower quarter neurological examination should be performed to help rule out more proximal causes of the symptoms such as lumbar spine radiculopathy. Again, no motor or reflex deficits should be found on examination. • Palpation should be done along the path of the nerve, especially at the superior to the medial epicondyle where the nerve passes through the dense connective tissue. • Tinel’s test: Tapping along the path of the nerve, especially where it is more superficial because it is above or below the medial epicondyle, may reproduce symptoms. • Slump knee bend test, as described by Butler, may help to determine a neurogenic cause of symptoms. Similar to testing the femoral nerve in sidelying, using the sensitizing maneuver of cervical extension and flexion may help to differentiate between neurogenic (saphenous nerve) and nonneurogenic (local muscle or other knee pathology) source of symptoms. • Lumbar ROM, accessory mobility testing, and palpation All three of these examinations may help to differentiate a lumbar spine problem from an isolated saphenous nerve entrapment. DIFFERENTIAL DIAGNOSIS • • • • • • • • • Lumbar spine radiculopathy Lumbar spine stenosis Lumbar spine somatic referral Femoral or tibial fracture Medial collateral ligament injury Meniscal pathology Osteoarthritis Patellofemoral pain Pes anserine bursitis CONTRIBUTING FACTORS • Increased age (over 40 years of age) • Increased thigh obesity • Genu varum, with or without tibial torsion ORTHOPEDIC PATHOLOGY • Repetitive knee motions that place stress on the surrounding fascia or muscles may cause increased symptoms such as running or biking. • Prolonged standing or walking • Stair climbing • It is believed that active knee extension may place more stress or tension on the involved nerve. Therefore any activities, such as standing, walking, or stair climbing, that require knee extension may be symptomatic. • Gait and functional testing may be painful, but no motor deficits should be noted with MMT. • Avoidance with knee extension might be noted but should not be thought of as diagnostic since many other competing conditions will also have pain with or limited knee extension. Section III • The saphenous nerve (from L3 and L4) arises off the femoral nerve slightly distal to the inguinal ligament and courses down the medial thigh. Between the sartorius and gracilis muscles, about 10 cm proximal to the medial epicondyle, the nerve pierces the connective tissue toward the medial knee and continues down the medial side of the lower leg. • The saphenous nerve is purely sensory and does not innervate the muscle in the lower leg. • Its cutaneous branches supply the skin of the anteromedial knee, the medial side of the lower leg, and the medial side of the foot distally (sometimes as far as the first metatarso phalangeal joint). • Most commonly, the nerve is entrapped where it pierces the connective tissue (referred to as Hunter’s canal) and may be irritated by repetitive contraction and relaxation of the surrounding musculature; this may be caused by the angulation of the saphenous nerve as it enters the canal traction to the nerve.The nerve may also undergo compression around the top of the calf region from external pressure such as tight garments. AGGRAVATING ACTIVITIES 775 776 Saphenous Nerve Entrapment TREATMENT SURGICAL OPTIONS After conservative measures of treatment have failed, a surgical decompression may be considered. Other possible methods may be surgical removal of the nerve or neurolysis. REHABILITATION • Initially, the goals of physical therapy are management of the symptoms and patient education regarding the dysfunction. • Modalities, such as interferential current therapy, ultrasound, phonophoresis, iontophoresis, ice, or compression, may help address any symptoms more related to an inflammatory component. • Soft tissue massage dealing with the location of hypothesized nerve entrapment may help the fibrosis or scarring of surrounding fascia. • After soft tissue treatments, neural mobilization techniques that help slide, glide, or place tension on the nervous system CHAPTER 16 • NERVE could be used to help restore more normal movement the saphenous nerve. • Addressing other biomechanical factors, such as foot or lower extremity alignment, is also necessary for a comprehensive rehabilitation program. PROGNOSIS In general, the prognosis for this condition is good. It is not associated with mortality or high rates of morbidity. Conservative treatment methods have been shown to be successful, and surgical options have few postoperative complications because of the pure sensory function of the nerve. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Night pain and unrelenting symptoms may indicate a local tumor. • Symptoms that do not improve within the expected time or that are not affected by physical therapy in a few visits should be referred back to the 41 of 57 physician since a space-occupying lesion may be present. • A recent history of trauma with suspected fracture may need imaging studies done before starting treatment. • Impaired circulation or vascular compromise may also warrant more medical management. SUGGESTED READINGS Butler DS. The Sensitive Nervous System. Adelaide,Australia: Noigroup Publications; 2000. Butler DS. Mobilisation of the Nervous System. New York: Churchill Livingstone; 1991. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. http://www.emedicine.com/Orthoped/topic422. htm AUTHOR: CHRIS IZU Sciatic Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Sciatic nerve entrapment is a neuropathy that results from compression or restriction of movement of the sciatic nerve, usually found in the posterior gluteal region near the piriformis muscle. SYNONYMS Piriformis syndrome ICD-9CM CODES 355.0 Lesion of sciatic nerve OPTIMAL NUMBER OF VISITS 8 or fewer MAXIMAL NUMBER OF VISITS 20 ETIOLOGY • The prevalence of this condition is difficult to assess secondary to the lack of agreement of its diagnosis and its close • Blunt injury may cause scarring of the surrounding structures. • Prolonged pressure, such as sitting, may cause compression. • Postsurgical complications (e.g., total hip replacement) • After vigorous activity, causing strain on the piriformis muscle or surrounding structures • The onset of symptoms from sciatic nerve entrapment can be sudden after trauma as noted or gradual overtime. In overuse injuries or gradual buildup of stress over time on the affected areas, symptoms may take time to come on or become problematic enough to seek medical attention. COMMON SIGNS AND SYMPTOMS • Pain originating in the gluteal region that progresses down into the posterior thigh and lower leg is the most common complaint in patients with this condition. In certain cases, pain is felt more distally in the lower extremity and less in the gluteal region. • Weakness may be present in the lower extremity muscles that control the foot and ankle along with knee flex. • Gait is almost always affected, and patients usually complain of pain with bearing weight on the affected leg. AGGRAVATING ACTIVITIES • Walking • Prolonged standing • Sitting, with pressure on the affected area • Sitting cross-legged • Sleeping or lying with the hip in a flexed or adducted position • Driving, especially when the right lower extremity is affected • Walking or standing may cause an overuse of the piriformis, especially as it may attempt to assist with pelvic and hip stability during gait. Other activities that add local compression or place the piriformis on stretch may also irritate the symptoms. EASING ACTIVITIES • Rest • Ice or modalities to reduce inflammation 42 of 57 24-HOUR SYMPTOM PATTERN No specific pattern has been reported in the literature. A presence of more nighttime symptoms or increased pain the morning or after resting may be more related to an inflammatory component of the disorder. It may also suggest another underlying pathology, such as a tumor, compressing the sciatic nerve. PAST HISTORY Previous similar symptoms, low back injuries, or other lower extremity injuries that may predispose someone to sciatic nerve entrapment may be found in the patient’s history. PHYSICAL EXAMINATION • This condition is often very painful and usually leads to an antalgic gait pattern, in which less time is spent in single-leg stance on the affected leg and with an ipsilateral trunk lean. It is also common to see external rotation of the affected extremity. • Sciatic nerve entrapment may have few distinguishing factors from that of a lumbar spine radiculopathy, stenosis, or discogenic dysfunction. Patients may also present with pain in the lumbar spine. • Patients may assume a posture in sitting or standing in which less pressure is placed through the affected lower extremity. • Weakness is most likely noted with resisted hamstring testing, either to the result of pain or decreased nerve conduction from sciatic nerve compression. Other lower extremity muscles below the knee may also be weak because of the sciatic nerve’s contribution to the tibial and common fibular nerve. • Assessing neurodynamics is also important if sciatic nerve entrapment is suspected because it may help to differentiate between a neurogenic source of pain (the sciatic nerve itself) and an nonneurogenic source (hamstrings). IMPORTANT OBJECTIVE TESTS • Palpation is often helpful in differentiating between symptoms of the lumbar spine, sacroiliac, and local muscles. Deep palpation of the piriformis muscle proximally in the posterior gluteal ORTHOPEDIC PATHOLOGY EPIDEMIOLOGY AND DEMOGRAPHICS MECHANISM OF INJURY • Heat to relax local musculature • Frequently changing positions, either from sitting or from sitting to standing • Sitting with legs apart • Sleeping or lying with a pillow between legs • Either decreasing the abnormal pressure on the piriformis by removing compressive forces or placing it in a resting position should help to alleviate symptoms. Section III • The large sciatic nerve originates from the sacral plexus (L4 to S3) and enters the gluteal region through the greater sciatic foramen near the piriformis muscle. It then descends along the posterior aspect of the thigh, dividing into the tibial and common peroneal nerve. • The sciatic nerve innervates all of the hamstring with the exception of the short head of the biceps. Because it branches into the tibial and common peroneal nerves, it sends motor input to the entire lower part of the leg. • The sciatic nerve branches off into the tibial and common peroneal nerves, which supply the superficial area of the entire lower leg except for the medial side of the leg and ankle (saphenous nerve). • The most common cause of sciatic nerve entrapment is irritation of the piriformis muscle. It is reported that 10% to 20% of individuals actually have a sciatic nerve that courses through the piriformis muscle instead of anterior to it. • Two different theories in which the sciatic nerve could become entrapped by the piriformis muscle are as follows: By a spasm of the muscle that becomes tight around the nerve By irritation of the muscle if the muscle is long and weak • Other causes of nerve entrapment include the following: Muscle anomalies Fibrosis caused by trauma Myositis ossificans relationship to lumbar spine pathology when the lumbar plexus is involved. Some report that the condition may be very rare (6% of sciatica cases), whereas others note that when looking at the incidence of low back pain with the inclusion of lower extremity symptoms, it may be more common than reported. • There seems to be a higher female prevalence with sciatic nerve entrapment and some estimates are as high as 6:1. 777 778 Sciatic Nerve Entrapment • • • • region and along the length of the sciatic nerve down in the posterior thigh should reproduce symptoms. Freiberg’s test: Forced internal rotation of the hip with the hip in extension may reproduce the symptoms by placing the piriformis and other deep hip external rotators on stretch. Combining this motion with abduction and external rotation of the hip while in hip flexion (Beatty maneuver) may help increase the sensitivity of testing. FAIR test: The patient is positioned in the sidelying position, with the patient’s affected leg placed in flexion, adduction, and internal rotation. A positive test will reproduce the patient’s symptoms in the buttock and leg. A full lower quarter neurological examination is also necessary to help differentiate a possible sciatic nerve entrapment from a lumbar spine radiculopathy or disc problem. Slump or SLR tests to assess neurodynamic mobility also help differentiate or implicate neural structures. DIFFERENTIAL DIAGNOSIS • • • • • • Lumbar spine radiculopathy Lumbar spine stenosis Lumbar spine discogenic dysfunction Hamstring strain or tear Ischial tuberosity bursitis Sciatica CONTRIBUTING FACTORS • Diabetes mellitus • Leg length discrepancy • Morton’s foot: Prominent second metatarsal head and changing gait pattern TREATMENT SURGICAL OPTIONS Surgical treatment of this condition is considered a last resort.The piriformis muscle could be resected or could be released CHAPTER 16 • NERVE near its insertion at the superior aspect of the greater trochanter. Although these surgical procedures have been noted with some success and, one author stated, are not associated with postoperative disability, one should be skeptical. There should be certainty that symptoms are not arising from the lumbar spine or other structure and postoperative management of appropriate tissue healing should be worked out before surgery is attempted. REHABILITATION • With the lack of clinical trials supporting treatment efficacy, most evidence comes from clinical practice. • Modalities that help reduce pain and inflammation, such as ultrasound, interferential current therapy, or cold pack, should be considered acutely and during highly irritable states, suggesting an inflammatory response. • In the case of extremely irritable symptoms and antalgic gait, assistive devices, such as a single-point cane, can be used to decrease weight bearing on the affected leg and the strain on muscles, such as the piriformis, to help stabilize the pelvis during walking. • Activity modification to avoid situations where prolonged sitting or standing, especially in known aggravating conditions like a very firm chair, is an important part of the patient education process. • Soft tissue mobilization and hip joint mobilization should also be considered to help improve the mobility of surrounding structures. Care should be taken to match the appropriate soft tissue technique and vigor to the area secondary to the possible irritability or altered pain processing damage to neural structures. • Other manual techniques, such as contract-relax, positional release, or straincounterstrain, have been suggested to treat the piriformis. • Treating the functional biomechanical deficits is also important to have successful outcomes. Stretching tight 43 of 57 muscles that may alter normal movement is important. Strengthening the hip abductors and external rotators is a common beneficial addition to a treatment program to decrease strain on the piriformis. PROGNOSIS This condition is not life-threatening but can be associated with significant morbidity caused by pain and weakness. It is generally believed that if it is recognized early, the treatment outcomes are relatively good. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Unrelenting pain not related to biomechanical factors • Weight loss • Bowel or bladder dysfunction • Saddle paresthesias • Gait disturbances: Clumsiness or ataxic gait • Bilateral glove or sock numbness • Symptoms that do not initially improve SUGGESTED READINGS Butler DS. The Sensitive Nervous System. Adelaide, Australia: Noigroup Publications; 2000. Butler DS. Mobilisation of the Nervous System. New York: Churchill Livingstone; 1991. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. http://www.emedicine.com/Orthoped/topic422. htm AUTHOR: CHRIS IZU Suprascapular Nerve Entrapment CHAPTER 16 • NERVE BASIC INFORMATION DEFINITION Suprascapular nerve entrapment pathologies encompass any injury that interrupts the function of the suprascapular nerve at any point along its course. The loss of function results in muscle weakness, pain, or sensory dysfunction. SYNONYMS Bra strap palsy ICD-9CM CODES 354 Mononeuritis of upper limb and mononeuritis multiplex 354.8 Other mononeuritis of upper limb 354.9 Mononeuritis of upper limb unspecified OPTIMAL NUMBER OF VISITS 6 MAXIMAL NUMBER OF VISITS 20 44 of 57 EPIDEMIOLOGY AND DEMOGRAPHICS • Relatively rare entrapment is seen in sports with repetitive cocking action such as tennis or volleyball. • The cocking action involves end-range shoulder abduction, extension, and external rotation followed by rapid flexion and internal rotation. • Suprascapular nerve injuries are often related to degenerative changes in the glenohumeral joint, and the incidence of entrapment increases with increasing age of the patient and with capsular laxity. • Also seen in occupations involving carrying heavy objects on the shoulder such as a camera operator and furniture mover. MECHANISM OF INJURY • There are a number of mechanisms of injury for the suprascapular nerve that will be described in relation to their location: Direct trauma in the form of a blow to the base of the neck or posterior shoulder Shoulder dislocation leading to tractioning of the nerve, particularly if the shoulder is forced into end-range external rotation Scapular fracture that distorts the bony confines of the suprascapular or spinoglenoid notches The nerve may be stretched or kinked by extremes of scapular motion associated with the throwing action. Kinking of the nerve can be exaggerated by a resting position of depression or forward rotation of the shoulder girdle. Compression entrapment within the suprascapular notch through hypertrophy of the transverse scapular ligament, an anatomically narrow suprascapular notch, or presence of a ganglion cyst. Compression at either notch from a tumor or varicosities Compression of the nerve in the spinoglenoid notch by a ganglion cyst arising from the glenohumeral joint. Ganglion cysts may be formed as a result of degenerative shoulder conditions and also after acute glenoid labral lesions such as SLAP lesions. Overuse syndromes from repeated scapular motions leading to compression of the nerve may occur in sports with repetitive overhead throwing action such as volleyball, serving in tennis, or baseball. ORTHOPEDIC PATHOLOGY • The suprascapular nerve is derived from the upper trunk of the brachial plexus formed by the C5 and 6 nerve roots; however, up to 50% receive contributions from the C4 nerve root. • The suprascapular nerve is a mixed sensory and motor nerve that descends along the posterior neck triangle, beneath the anterior border of trapezius, to the superior border of the scapula. • The nerve passes into the supraspinous fossa through the suprascapular notch, and the roof is formed by the transverse scapular ligament. • It supplies the supraspinatus, as well as receiving sensory articular branches from the glenohumeral and AC joints. • The nerve then curves around the lateral edge of the base of the spine of the scapula by the spinoglenoid notch (in close proximity to the glenohumeral joint) to innervate the infraspinatus in the infraspinatus fossa. • The nerve has no cutaneous component. • The suprascapular nerve is particularly vulnerable to injury at the following two points along its course: The suprascapular notch The spinoglenoid notch • The suprascapular nerve may be affected at any point along its course by direct trauma or compression entrapment, leading to nerve tissue hypoxia. • The insult to the nerve can be mechanical, thermal, chemical, or ischemic. process, fibroblasts appear to repair damage incurred but produce adhesions to the nerve limiting their glide and increasing anoxia. Section III ETIOLOGY • The suprascapular nerve is most commonly entrapped at the suprascapular and spinoglenoid notches. • The pathophysiology of suprascapular nerve entrapment is usually related to a compressive lesion of the nerve; nevertheless, pathology can occur in a number of ways as follows: Direct trauma in the form of a blow to the base of the neck or posterior shoulder Shoulder dislocation leading to tractioning of the nerve Scapular fracture Compression entrapment within the suprascapular notch through hypertrophy of the transverse scapular ligament, a narrow suprascapular notch, or presence of a ganglion cyst Compression of the nerve in the spinoglenoid notch by a ganglion cyst arising from the glenohumeral joint. Ganglion cysts may be formed as a result of degenerative shoulder conditions and also after acute glenoid labral lesions such as superior labrum from anterior to posterior (SLAP) lesions. Overuse syndromes from repeated scapular motions leading to compression of the nerve • Nerve injury is classified according to the severity of the injury and its potential for reversibility, as follows: Neurapraxia (first-degree injury): Distortion of the myelin about the nodes of Ranvier caused by ischemia, mechanical compression, or electrolyte imbalance produces temporary loss of nerve conduction. Axonotmesis (second-degree injury): Interruption of the axon with secondary wallerian degeneration. The supporting tissue surrounding the axon is preserved, and the recovery period depends on the distance between the site of injury and the end-organs. Neurotmesis: Complete disruption of the nerve and its supporting structures. • Neurotmesis has been further divided into the following three subcategories: Third-degree nerve injury: Endoneurium is disrupted with intact perineurium and epineurium. Fourth-degree nerve injury: All neural elements sparing the epineurium are disrupted. Fifth-degree nerve injury: Complete transection and discontinuity of the nerve with no capacity for regeneration. • Physiologically, there is disruption to any part of the nerve responsible for conduction. • In repetitive-type nerve entrapment, it is proposed that repetitive work or static posture produces an inflammatory 779 780 Suprascapular Nerve Entrapment Compression of the nerve by weighted objects being carried repeatedly on the shoulder such as may occur with a barbell in weight lifting, camera work, backpacking, furniture removals, or other load-carrying occupations. COMMON SIGNS AND SYMPTOMS • Pain that is deep and poorly localized, often felt posterior and lateral in the shoulder or referred to the arm, neck, or anterior chest wall. • Patients may describe shoulder weakness. • Wasting of the supraspinatus and/or infraspinatus • Weakness of abduction and external rotation • May have tenderness over the suprascapular notch • If there is combined supraspinatus and infraspinatus weakness, the entrapment is most likely to be at the suprascapular notch. • Isolated infraspinatus weakness may occur when the nerve is compressed in the spinoglenoid notch and the motor branch to the supraspinatus is spared. • Occasionally, deltoid muscle atrophy accompanies the injury because of disuse. AGGRAVATING ACTIVITIES • Activities that involve repetitive shoulder internal and/or external rotation, particularly when the shoulder is in an abducted position • Activities that involve horizontal adduction of the arm, such as reaching across the chest, can exacerbate the pain • Carrying loads on the top of the shoulder EASING ACTIVITIES Rest and/or modification of aggravating activities 24-HOUR SYMPTOM PATTERN • Generally, the symptoms are related to activity and do not follow a typical 24-hour pattern unless there is a strong inflammatory component such as may be seen in repetitive tasks. • If there is an inflammatory component, there may be worsening of symptoms with use toward the end of the day and morning stiffness. PAST HISTORY FOR THE REGION • History of trauma, fracture, or dislocation of the glenohumeral joint • History of forceful scapular depression such as a fall onto the point of the shoulder • Repetitive overuse of the shoulder in occupation or sports • Generalized hypermobility CHAPTER 16 • NERVE PHYSICAL EXAMINATION • Examine the shoulder for signs of atrophy around the shoulder blade, particularly in the supraspinatus and infraspinatus fossae. • MMT may reveal weakness in the following muscles: Supraspinatus: Weakness of glenohumeral abduction can be assessed using the scaption position in which the shoulder arm is resisted in 90 degrees of flexion in the plane of the scapular. Infraspinatus: Weakness of external rotation at the glenohumeral joint, particularly biased toward infraspinatus when external rotation is resisted in 90 degrees of shoulder abduction. • There may be loss of fine proprioceptive control of the glenohumeral and AC joints due to the loss of afferent conduction. Therefore the therapist may notice an alteration in the control of those joints during functional movement patterns. • Physical examination should also exclude pathology in other areas, particularly when performing AROM and PROM at the neck and shoulder, which may reveal restrictions, other shoulder pathology, and/or central involvement of the nerve. • Physical examination should also include movement analysis to determine the movement patterns that the patient adopts when performing the aggravating activities. Movement analysis can be done visually or with the assistance of a video camera. The analysis should give some clues to predisposing factors, such as posture and patterning, that assist with rehabilitation and activity modification. IMPORTANT OBJECTIVE TESTS • EMG may reveal delayed conduction velocity and fibrillation potentials; however, EMGs are often reported as normal, and therefore a negative EMG does not rule out the diagnosis of suprascapular nerve entrapment. • MRI is considered to be the most effective study for suprascapular nerve entrapment since it can reveal lesions to the glenoid labrum and the presence of a ganglion cyst in the region of the nerve. DIFFERENTIAL DIAGNOSIS • • • • • Rotator cuff tears Rotator cuff tendinopathies Subacromial bursitis Adhesive capsulitis Shoulder instability 45 of 57 • Degenerative joint disease at the glenohumeral or AC joints • Underlying neuropathic disease • Neuralgic amyotrophy • Muscular dystrophy • Isolated neuropathy in the diabetic • Tumors or space-occupying lesions • C4, C5, or C6 cervical radiculopathy • Upper motor neuron lesion in the cerebrum CONTRIBUTING FACTORS • For any nerve entrapments that are nontraumatic, there is often an element of repetitive activity involving the affected limb. • Typically, in the case of the suprascapular nerve, the repetitive action will involve shoulder abduction and repetitive internal and external glenohumeral rotation. • Other repetitive tasks involving crossbody adduction, such as polishing or reaching repeatedly across the body, may create a traction neuropathy. • Postural factors may be involved, particularly in repetitive work or sporting activities with reduction in proximal stability and control leading to an overuse of more distal muscle groups to perform a task. • Excessive loads, such as in heavy manual work or sports involving weight lifting, can create compression of the nerve, particularly when the load is carried over the trapezius muscle. TREATMENT SURGICAL OPTIONS • Surgery will be considered after a failure of conservative management. • There are a number of surgical approaches to achieve decompression of the suprascapular nerve, involving enlargement of the suprascapular notch, as follows: Anterior approach Posterior trapezius splitting approach Posterior trapezius elevating approach Superior cranial approach • When there is entrapment at the spinoglenoid notch,a different approach is required because generally there is an underlying shoulder pathology leading to the formation of a ganglionic cyst that compresses the nerve. • Therefore, shoulder arthroscopy initially is performed to examine for a SLAP lesion, followed by debridement and repair if required. At the time of arthroscopy, the cyst can be evacuated and decompressed. REHABILITATION • The goal of rehabilitation should be pain reduction to encourage pain-free exercise and to provide task or sports Suprascapular Nerve Entrapment CHAPTER 16 • NERVE reeducation and interventions leading to reacquisition of fine motor and sporting skills. • Manual therapy Pain reduction can be achieved through the use of ice and electrotherapeutic modalities. Soft tissue release may assist with restoration of muscle balance around the scapula, which will be useful if compensations have occurred in other muscles to make up for the loss of rotator cuff control. Nerve gliding exercises have been purported to disperse intraneural edema, increase blood flow, optimize axonal transport, and lengthen nerve adhesions. Neural mobilization can be achieved using scapular mobilization, both actively and passively into elevation, depression, protraction, and retraction • Functional rehabilitation Reeducation of movement patterns, particularly proximal control of the trunk and neck to provide a stable foundation for scapular stability Scapular position education initially, with isometric hold and then the addi- tion of controlled functional movement patterns Specific muscle strengthening gradually increasing intensity to restore full power to the rotator cuff Integration of functional exercise and strength work into sport- or taskspecific skills Graduated return to full strength, speed, and power. 781 • The results of treating neurapraxia even with surgical intervention are generally not satisfactory. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN If suprascapular nerve entrapment is suspected, all cases should be referred to a physician for appropriate investigation. PROGNOSIS SUGGESTED READINGS • Prognosis depends entirely on the extent of damage to the nerve. • Neurapraxia should resolve rapidly and lead to a complete restoration of function usually within 2 to 3 months. • If the injury is a more severe axonotmesis, the recovery time will depend on the distance from the site of injury to the denervated tissue. Peripheral nerves have been reported to recover at an approximate rate of between 1 and 4 mm per day, but complete function might not be restored. • If there has been a complete sectioning of the nerve (neurapraxia), a full recovery will not occur. Aldridge JW, Bruno RJ, Strauch RJ, Rosenwasser MP. Nerve entrapment in athletes. Clin Sports Med. 2001;20(1):95. Goslin KL, Krivickas LS. Proximal neuropathies of the upper extremity. Neurol Clin. 1999;17(3). Kibler WB, Murrell GAC. Shoulder pain. In: Brukner P, Khan K, eds. Clinical Sports Medicine. 3rd ed. Australia: McGraw-Hill; 2006:243–288. Leffert RD. Nerve lesions about the shoulder. Orthop Clin North Am. 2000;31(2). Moore TP, Hunter RE. Suprascapular nerve entrapment. Oper Tech Sports Med. 1996;4(1):8–14. AUTHOR: JOSEPHINE LOUISE COULTER Section III ORTHOPEDIC PATHOLOGY 46 of 57 782 Sural Nerve Entrapment BASIC INFORMATION DEFINITION Sural nerve entrapment is a mononeuropathy that results from compression or restriction of movement of the sural nerve, usually at the deep fascia of the leg in the calf and lateral lower leg region. SYNONYMS None currently used CHAPTER 16 • NERVE MECHANISM OF INJURY • Fractures: Fifth metatarsal, cuboid, calcaneus, fibula • Lateral ankle sprains • Peroneal tendon rupture • Engorged lesser saphenous veins: Chronic venous insufficiency • Ganglions • Hematomas • Postsurgical scarring • Improper fitting boots COMMON SIGNS AND SYMPTOMS ICD-9CM CODES 355.7 Other mononeuritis of lower limb OPTIMAL NUMBER OF VISITS 6 or fewer • Pain and dysesthesias in the sural nerve distribution, especially around the lateral ankle, are the most common sensory complaint. • Gait deviations from pain with ankle or foot motions might also be noted in the present history. MAXIMAL NUMBER OF VISITS AGGRAVATING ACTIVITIES 20 • • • • • • • • ETIOLOGY • Arising from branches off the tibial nerve, the sural nerve descends between the two heads of the gastrocnemius and becomes superficial at the middle of the leg. It descends along side the saphenous vein and passes inferior to the lateral malleolus to the lateral side of the foot. • The sural nerve supplies the skin on the posterior and lateral aspects of the lower leg and lateral side of the foot up to the base of the fifth metatarsal. • The sural nerve is believed to be purely sensory and has very little if any motor involvement. A few recent cadaver and clinical studies have found some motor fibers within the sural nerve. Still, the nerve is viewed primarily as a sensory nerve. • Since the sural nerve becomes more superficial in the lower leg, it is believed to be more at risk of compression. Internal compression, such as a ganglion cyst or tumor, has been noted to compress the nerve. Stretch injuries may also create strain on the nerve and repetitive injuries or trauma may be the catalyst for more fibrotic scarring of the surrounding fascia that may entrap the nerve. EPIDEMIOLOGY AND DEMOGRAPHICS • This condition is thought to be relatively rare; although a small number of studies stated that it is a common syndrome in athletes. • A gender difference has not been strictly reported, but one study of 13 patients with sural nerve entrapment noted that 11 were male and 2 were female. Physical exertion with lower extremities Heel raises or going up on toes Prolonged standing Walking Running Cycling Wearing tight boots or hockey skates Calf stretches EASING ACTIVITIES • Rest • Ice or modalities for inflammation • Massage 24-HOUR SYMPTOM PATTERN No writings on a particular pattern of symptoms were found for sural nerve entrapment. Increased symptoms at night or lasting symptoms in the morning may point to a strong inflammatory component to the symptoms. This may also suggest space-occupying lesion, such as a tumor, so careful attention should be paid to other factors and the progression of symptoms. PAST HISTORY No typical past history has been noted for sural nerve entrapment. One study’s review of their participants noted that the leg of one subject, before onset of this problem, had been run over by a truck, possibly contributing to fibrotic scarring around the nerve sheath. Following this theory, one might find a previous incident, trauma, or overuse that may have led to neurodynamic restrictions and internal changes in the nerve connective tissue or nerve itself. PHYSICAL EXAMINATION • The most common physical finding is altered sensation in the sural nerve’s 47 of 57 sensory distribution in the lateral lower part of the leg, calf, and lateral ankle. • Gait deviations might be noted and associated with changed mechanics caused by pain. • It is important to note that normal muscle strength should be tested since this nerve is purely sensory. If weakness is found, another peripheral nerve or more proximal lesions, such as on the lumbar spine, must be examined. IMPORTANT OBJECTIVE TESTS • Lower quarter neurological examination is as follows: Sensory examination: Light touch, pinprick, or sharp/dull may be used to determine altered sensation in a specific distribution. Motor examination: No myotomal weakness should be noted with examination. However, pain may be noted with contracting muscle surrounding the nerve such as the gastrocnemius. No reflexive changes should be noted. Tinel’s test: Tapping on the superficial regions of the nerve may reproduce symptoms into the specific nerve distribution. Palpation: Muscles around the nerve, especially gastrocnemius, may reproduce symptoms or may have noted soft tissue restrictions that possibly indicate fibrotic scarring around the nerve. SLR test (or slump test) • A neurodynamic examination helps differentiate neurogenic (sural nerve) from nonneurogenic (gastrocnemius or peroneals) sources of symptoms. DIFFERENTIAL DIAGNOSIS • • • • • • • • Local muscle strain Knee ligamentous strain Meniscal pathology Osteoarthritis Deep vein thrombosis Lumbar spine radiculopathy Lumbar spine stenosis Polyneuropathy CONTRIBUTING FACTORS • Running and overuse of the lower extremity muscles • Poor lower quarter alignment • Poor trunk or lower extremity • Diabetes mellitus • Alcoholism TREATMENT SURGICAL OPTIONS • Surgical decompression may be recommended to release the nerve from surrounding fibrotic connective tissues. Sural Nerve Entrapment CHAPTER 16 • NERVE • Surgical neurolysis is not recommended but may be done when the condition is unresponsive to other measures. REHABILITATION • The first goal of rehabilitation should be to decrease any inflammation or irritation around the nerve, thereby decreasing symptoms. • Modalities, such as ultrasound, phonophoresis, iontophoresis, ice, interferential current therapy, or light massage techniques, may assist in decreasing symptoms. • Taping, bracing, or footwear modification have also been suggested, which may help decrease strain on the affected region. • If fibrotic scarring is one of the hypothesized mechanisms for sural nerve entrapment, then more vigorous massage techniques to free up the nerve may be beneficial. This could be followed up with neurodynamic techniques that attempt to glide, slide, or place tension on the nerve to restore normal mobility. • It is also important to address any biomechanical faults that may be contributing to stress or strain on the sural nerve. PROGNOSIS No specific data on long-term outcomes were found after sural nerve entrapment. Because of the pure sensory function of the sural nerve, it is most likely not associated with high rates of morbidity. One author did suggest that return of sensation may take up to a year after surgery. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN • Unrelenting pain not related to biomechanical factors • Weight loss • Bowel or bladder dysfunction • Saddle paresthesias • Gait disturbances: Clumsiness or ataxic gait 783 • Bilateral glove or sock numbness • Symptoms that do not initially improve with symptoms SUGGESTED READINGS Butler DS. Mobilisation of the Nervous System. New York: Churchill Livingston; 1991. Butler DS. The Sensitive Nervous System. Adelaide, Australia: Noigroup Publications; 2000. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. http://www.emedicine.com/Orthoped/topic422. htm AUTHOR: CHRIS IZU Section III ORTHOPEDIC PATHOLOGY 48 of 57 784 Tibial Nerve Entrapment BASIC INFORMATION DEFINITION Tibial nerve entrapment syndrome is a mononeuropathy that results from compression or restriction of movement of the tibial nerve, usually through the tarsal tunnel in the ankle. SYNONYMS Tarsal tunnel syndrome: Sometimes referred to as proximal tarsal tunnel syndrome since the distal tarsal tunnel may be used to describe the region in which the distal plantar branches of the tibial nerve may become entrapped. ICD-9CM CODES 355.5 Tarsal tunnel syndrome OPTIMAL NUMBER OF VISITS 6 or fewer MAXIMAL NUMBER OF VISITS 20 ETIOLOGY • The tibial nerve is a branch of the large sciatic nerve in the posterior leg that runs distally between the heads of the gastrocnemius muscle deep to the soleus muscle. It usually lies between the flexor digitorum longus and the tibialis posterior muscle. Traveling distally and posterior to the medial malleolus, it continues through the tarsal tunnel, where it eventually divides into the medial and lateral plantar nerves. • The tibial nerve may become entrapped anywhere along its pathway, such as the popliteal fossa, but is most likely affected in the tarsal tunnel. The tunnel is formed by the medial surface of the talus, the inferomedial navicular, the sustentaculum tali, and the medial surface of calcaneus and the flexor retinaculum. The deep and superficial aponeuroses of the leg help form the flexor retinaculum, which is closely attached to the surrounding muscle sheaths. • Compression of the tibial nerve can be from space-occupying lesions such as neuromas, ganglion cysts, lipomas, osteochondromas, tumors, or abnormal varicosities. • Limited space within the tarsal tunnel may also be caused by tenosynovitis or rupture of adjacent tendons. • Biomechanical factors have also been proposed as a cause of tibial nerve entrapment since it has been noted that pressure within the tarsal tunnel increases with full dorsiflexion/eversion of the foot and ankle and also full CHAPTER 16 • NERVE inversion. Abnormal standing postures or gait may continually put stress on the tarsal tunnel. • Because of the network of fibrous connective tissue around the tarsal tunnel and surrounding musculature, it has also been suggested that limited mobility of the nerve may come from tethering of the nerve sheath to adjacent structures. EPIDEMIOLOGY AND DEMOGRAPHICS Of the nerves in the foot and ankle, the tibial nerve is the most likely to be entrapped. Some studies point to a slight female predominance, and in general the age ranges from about 14 to 80 years of age with a peak in the 50 to 60 years age range. It is common in nonathletes but also has been noted in distance runners. MECHANISM OF INJURY • A gradual or insidious onset is most commonly seen in this condition as space-occupying lesions continue to add compression to the area or biomechanical factors continue to strain local tissues. • Types of injuries that may lead to tibial nerve entrapment include the following: Direct blunt trauma Traction injury Repeated ankle sprains Fractures of the surrounding bones COMMON SIGNS AND SYMPTOMS • Common symptoms of this condition are pain, burning, and paresthesias in the distribution of the tibial nerve on the plantar surface of the foot. • Symptoms are generally unilateral but may be on both sides. • Symptoms occasionally radiate more proximally into the medial leg. AGGRAVATING ACTIVITIES • • • • Prolonged standing or walking Extreme dorsiflexion Increased weight-bearing activities Wearing nonsupportive shoes or sandals EASING ACTIVITIES • • • • Rest and relief of weight-bearing activities Sitting Massage Ice or antiinflammatories 24-HOUR SYMPTOM PATTERN • If there is a significant inflammatory component to the symptoms or a space-occupying lesion, more nighttime symptoms may be expected. Following this, symptoms may also be worse in the morning. • Often, there is less pain in the morning after rest, but there may be pain on the first step when getting out of bed. 49 of 57 PAST HISTORY Patients may note previous bouts with the same condition. They may also report previous lower extremity or lumbar spine injuries, which in turn might have affected lower quarter biomechanics. Patients may have a previous history of other space-occupying lesions, such as a Baker’s cyst. PHYSICAL EXAMINATION • Abnormal foot or lower extremity alignment, such as a pes planus or pes cavus, may be noted. Looking from the more proximal view, it may be associated with tibial or femoral internal or external rotation. From the posterior view, the calcaneal position may also be altered. • An examination of gait may also reveal a corresponding deviation with abnormal pronation or supination of the foot during the loading response to terminal stance phases. • Palpation of the local areas most likely reproduce the patient’s symptoms into the heel or foot. • A sensory examination usually reveals abnormal sensation in the distribution of the tibial nerve. • Neurodynamic testing most likely helps differentiate a neurogenic source of symptoms from other local or referred sources. IMPORTANT OBJECTIVE TESTS • Tinel’s test: Tapping on the tarsal tunnel most likely reproduces the patient’s symptoms in a tibial nerve distribution. • Sensory examination: Using SemmesWeinstein monofilaments, an area of altered or diminished sensation should be noted in the same distribution distal to the side of the lesion. • Manual compression: Sustained pressure at the tarsal tunnel may also reproduce symptoms and help confirm diagnosis. • Motor examination: Weakness might be found in plantar flexion of the ankle or in knee flexion. • Gait examination: Contributing biomechanical factors during walking, jogging, or running need to be assessed since these may be impairments that could be addressed in rehabilitation. Neurodynamic Lower quarter neurological exam Lumbar spine ROM Lumbar spine palpation Lumbar spine accessory motion: These tests are important to help determine contribution of proximal sources to the symptoms in the case of lumbar spine radiculopathy or double-crush. Tibial Nerve Entrapment CHAPTER 16 • NERVE DIFFERENTIAL DIAGNOSIS • • • • • • • • Lumbar spine radiculopathy Exostosis Malunions Osteochondromas Fractures Tibialis posterior tendinitis Plantar fasciitis Heel spur CONTRIBUTING FACTORS • • • • • • • • • • Obesity Ankylosing spondylitis Acromegaly Talocalcaneal coalition Diabetes RA: Proliferative synovitis Foot deformities Varicose veins Alcoholism Thyroid disease • • • • • TREATMENT • SURGICAL OPTIONS • Rehabilitation of this condition should focus not only on alleviating the 50 of 57 • If suspected worsening compression on the nerve is suspected from a compartment syndrome, immediate referral to a physician is warranted. A fasciotomy may be done to release this pressure. • Night pain and unrelenting symptoms may indicate a local tumor. • Symptoms that do not improve within the expected time or that are not affected by physical therapy in a few visits should be referred to the physician because a space-occupying lesion may be present. • A recent history of trauma with suspected fracture may need imaging studies done before starting treatment. • Impaired circulation or vascular compromise may also warrant more medical management. SUGGESTED READINGS Butler DS. Mobilisation of the Nervous System. New York, NY: Churchill Livingston; 1991. Butler DS. The Sensitive Nervous System. Adelaide, Australia: Noigroup Publications; 2000. Dawson DM, Hallett M, Wilbourn AJ, eds. Entrapment Neuropathies. Philadelphia: Lippincott-Raven; 1999. Moore KL, Dalley AF. Clinical Oriented Anatomy. 4th ed. Philadelphia: Lippincott Williams & Wilkins; 1999. Placzek JD, Boyce DA, eds. Orthopedic Physical Therapy Secrets. 2nd ed. Philadelphia: Elsevier; 2006. Shacklock M. Clinical Neurodynamics. Philadelphia: Elsevier; 2005. AUTHOR: CHRIS IZU ORTHOPEDIC PATHOLOGY REHABILITATION PROGNOSIS Another study following postoperative patients after tarsal tunnel release showed good-to-excellent results in 84% of cases. No statistics were found regarding improvement with conservative measures; however, clinically it is thought that with proper management of contributing factors, in the absence of a space-occupying lesion or marked fixed-foot deformity, outcomes are relatively good. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN Section III • Tarsal tunnel decompression has been shown to be fairly successful for shortterm relief of symptoms. Some authors noted that 1 month after surgery, 24 out of 26 patients had good outcomes. • In the case of cystic lesions, aspiration might also provide relief of pressure within the tarsal tunnel and reduce symptoms. • A surgical release of the flexor retinaculum or removal of the space-occupying lesion are common procedures to address tarsal tunnel syndrome. • From a clinician’s perspective, it is important to follow surgery by addressing any biomechanical contributing factors that may have led to the condition. symptoms but also on the underlying cause of compression. NSAIDs and relative rest, ice, compression, and elevation (RRICE) should initially be implemented in acute or inflammatory stages to help relieve symptoms. In more severe cases, individuals with tibial nerve entrapment may benefit from immobilization, such as using a walking boot or cast or splint, and limiting weight bearing with use of assistive devices. Other modalities, such as ultrasound, interferential current therapy, or phonophoresis, may be administered to help with local symptoms. Taping and use of orthoses have clinically shown to be effective when addressing abnormal foot mechanics and positioning. If neurodynamic restriction is suspected, soft tissue mobilization and techniques to slide, glide, and place tension on the nerve as described by Butler may be warranted. More complete rehabilitation should also address other lower extremity or trunk impairments or motor control problems that may lead to increased pressure at the tarsal tunnel. For example, inadequate timing or force production of the gluteus medius during gait may influence the pronation component of the foot, leading to increased strain of the medial ankle structures. 785 Vascular Thoracic Outlet Syndrome 786 BASIC INFORMATION DEFINITION • TOS encompasses numerous scenarios of compression (neurological and vascular) in the thoracic outlet region of the shoulder girdle. Although vascular and neurological classifications exist, it must be noted that these conditions can also be observed together. It is also believed that in 98% of TOS cases, the resultant symptoms are neurogenic. Defining the syndrome has been difficult in the literature because of its variable etiology and presentation and often minimal clinical findings. • The following vascular TOS classifications exist: Arterial TOS is caused by compression of the subclavian and/or axillary artery and is very uncommon, occurring in only 3% to 4% of cases. Venous TOS is caused by compression of the subclavian and/or axillary vein and occurs in only 6% to 7% of cases. • The subclavian vein and artery receive new nomenclature as the axillary vein and artery, once they pass the first rib). SYNONYMS • • • • • • • • • • • • • • • Cervical rib syndrome First rib syndrome Scalenus anticus syndrome Costoclavicular syndrome First thoracic rib syndrome Hyperabduction syndrome Scalenus medius syndrome Pectoralis minor syndrome Subcoracoid-pectoralis minor syndrome Brachiocephalic syndrome Paget-Schroetter syndrome (effort vein thrombosis of subclavian vein) Nocturnal paresthetic brachialgia Rucksack palsy Droopy shoulder syndrome Fractured clavicle-rib syndrome ICD-9CM CODES 353 Nerve root and plexus disorders 442.82 Aneurysm of subclavian artery OPTIMAL NUMBER OF VISITS Not applicable MAXIMAL NUMBER OF VISITS Not applicable ETIOLOGY • Current belief of the cause of TOS is the underlying existence of bony or fibromuscular anomalies with overlying injury and/or spasm in the thoracic outlet region causing compromise.The anatomical anomalies are generally seen as predisposing factors. CHAPTER 16 • NERVE • Bony anomalies can be congenital, traumatic, or posttraumatic and include the presence of: a cervical rib, elongated C7 transverse process, first rib deformity, displaced first rib fracture, excessive callus formation after first rib fracture, rib hemangioma, fractured or subluxed clavicle, and pseudarthroses. • Cervical ribs are known to exist in approximately 0.5% of the population, with 10% to 20% resulting in symptoms, although this depends on their size. • Soft tissue anomalies can also be congenital, traumatic, or posttraumatic and include altered scalene muscle insertions and origins, presence of scalenus minimus or scalenus pleuralis muscle, hypertrophy or injury of scalene muscles, presence of congenital fibromuscular bands (classified as type 1 to 10) or dense fibrous sheaths, cervical ligaments and band, and pectoralis minor shortening. • The following three spaces in the thoracic outlet region have been identified as potential areas of vascular compression: Interscalene space or triangle is bordered anteriorly by the anterior scalene muscle, posteriorly by the middle scalene muscle, and inferiorly by the first rib. Here the subclavian artery passes posterior to the anterior scalene muscle (in close relation with the brachial plexus), then superior to the first rib. The subclavian vein bypasses this space by traveling anteromedial to the anterior scalene muscle. Costoclavicular space is bordered anteriorly by the medial aspect of the clavicle, subclavian muscle and tendon, and costocoracoid ligament. The posterolateral border is formed by the upper scapula, and the first rib and the anterior and middle scalene muscle insertions create the posteromedial border. Here the subclavian vein and artery travel with the brachial plexus under the clavicle and subclavius muscle toward the subpectoralis minor space. Subpectoralis minor space is located inferior to the coracoid process and posterior to the pectoralis minor muscle insertion. Here the subclavian vein and artery continue to travel with the brachial plexus beneath the pectoralis muscle toward the axilla. A further region involved in vascular TOS has also been described at the head of humerus, where the axillary artery gives off posterior humeral circumflex branches. This area is often not involved in vascular TOS but is commonly seen. • Arterial TOS Compression of the subclavian artery in TOS can be acute or chronic and 51 of 57 can occur in the interscalene triangle, costoclavicular space, or subpectoralis minor space.This occurs as a result of underlying bony or fibromuscular anomalies with overlying muscle injury and/or spasm. In most cases of arterial TOS, compression is caused by the tip of the cervical rib or an elongated C7 transverse process. Compression in the subpectoralis space is less common and is referred to as hyperabduction syndrome. This is in reference to the arm position during which the neurovascular structures are compromised. Additionally, vascular compression has been reported to occur at the humeral head. Here the axillary artery may be tethered via its circumflex branches, as a result of excessive movement of the head of humerus. Although rare, chronic compression can lead to occlusive and aneurysmal disease. The subclavian artery sustains chronic intimal damage, which can result in either thrombosis or occlusion. Poststenotic dilations may also develop. If the rate of occlusion is slow, the body is able to develop sufficient collateral circulation, so the patient may only feel symptoms with excessive arm use. Rapid occlusion creates more obvious claudication symptoms, as well as symptoms with minimal arm activity or at rest. Damage to the full thickness of the subclavian artery wall (aneurysmal disease) can also produce debris, which may dislodge and create distal emboli in the arm, hand, or fingers. • Venous TOS Compression of the subclavian vein in the thoracic outlet region can have an acute onset (generally known as effort thrombosis or Paget-Schroetter syndrome) or an insidious one. The most common pathological cause of this syndrome is a congenital anomaly of the costoclavicular ligament combined with anterior scalene muscle hypertrophy, resulting in venous compression and occlusion. Thromboses may also occur from subclavian venous catheters (intravenous [IV] therapy), dialysis treatment, and the presence of abnormalities in blood factors, antibodies, and proteins. Chronic compression of the subclavian vein produces an inflammatory reaction, endothelial damage, and venous stasis. EPIDEMIOLOGY AND DEMOGRAPHICS • Arterial TOS is very rare. • Arterial TOS occurs more often in the younger, active population. Vascular Thoracic Outlet Syndrome CHAPTER 16 • NERVE • Carrying heavy objects such as suitcases and shopping bags • Arterial TOS occurs equally among males and females. • Venous TOS is quite rare. • Venous TOS occurs more often in the younger population. • Venous TOS occurs most often in young males. EASING ACTIVITIES MECHANISM OF INJURY Unknown, not applicable, and not related to activity. • Note that despite the following classifications, some patients also demonstrate neurogenic TOS symptoms. • Arterial TOS Arm coldness, heaviness, pulselessness, pallor, loss of strength or fatigue with exercise (i.e., true arm claudication during activity, particularly overhead activity) Weakened grip and reduced finger function (difficulty gripping and carrying bags) • Venous TOS Swelling, edema, cyanosis, and arm discomfort with activity If the subclavian vein has thrombosed, the patient presents with a sudden onset of edema in the arm with associated discomfort and cyanosis. Symptoms usually develop in the dominant arm AGGRAVATING ACTIVITIES • Overhead arm and hand positions or arm elevated repetitive activities. These commonly include styling hair, painting, working overhead, pitching or throwing a ball, playing musical instruments (e.g., violin or flute), and swimming. 24-HOUR SYMPTOM PATTERN PAST HISTORY FOR THE REGION • Arterial The onset of symptoms usually reveals increased or unaccustomed prolonged or repetitive upper limb activity (i.e., pitching in baseball but may also be insidious in nature). The patient may report a previous history of whiplash injury or a direct or indirect blow to the shoulder resulting in first rib, muscular, or clavicular trauma. • Venous The onset of symptoms usually reveals increased or unaccustomed prolonged or repetitive upper limb activity but may also be insidious in nature. Recent use of a subclavian venous catheter (intravenous therapy) and dialysis treatment. The patient may report a previous history of whiplash injury or a direct or indirect blow to the shoulder resulting in first rib, muscular, or clavicular trauma. PHYSICAL EXAMINATION • Arterial TOS Loss or reduction of radial pulse with arm activity Difference of blood pressure between the arms of >20 mm Hg Positive Roos, Adson’s, Halsted’s, and Wright’s hyperabduction tests Loss of radial pulse and arm discomfort and/or development of arm pallor during the Roos test with subsequent hyperemia after lowering the arm Coldness of hand and fingers Trophic changes in fingernails or skin Gangrene of finger tips (in extreme cases of peripheral embolization) Pulsatile mass palpable in the supraclavicular fossa (not common but indicative of a subclavian aneurysm) • Venous TOS Superficial vein distention in upper limb and chest Edema of the upper limb (measurement of limb girth) Discoloration of the limb Arm discomfort with activity Positive Roos test: Development of cyanosis and arm swelling during test • Any of the following physical findings of neurogenic TOS may also be present: Poor posture (including downwardly rotated and protracted scapula, large 52 of 57 IMPORTANT OBJECTIVE TESTS • Observation of the affected arm is important in the diagnosis of vascular TOS. Arm size, color, temperature, and pulses must be compared to the normal side at rest, during overhead activity, and after activity. • Palpation of the supraclavicular fossa is important for detection of aneurysms. • Three tests (Adson’s, Halsted’s, and Wright’s hyperabduction tests) have traditionally been used to diagnose TOS because they monitor the radial pulse. These tests have been extensively discussed, criticized, and “modified” in the literature because of the high level of false positives and false negatives (many asymptomatic people demonstrate pulse changes during these tests). • Roos test (elevated arm stress test), however, is described as the most reliable test for all types of TOS. If a patient is unable to complete the test because of their symptoms, it can also reflect the severity of their arterial or venous compromise. • Patients may also demonstrate a bruit in the subclavian artery on auscultation during these tests indicating arterial TOS. • Arterial TOS Doppler studies Arteriography in provocative positions and followed to digits to pick-up embolus Magnetic resonance angiograms (MRAs) • Venous TOS Doppler studies Positional venography Coagulation studies DIFFERENTIAL DIAGNOSIS • Shoulder pathologies Glenohumeral instabilities ORTHOPEDIC PATHOLOGY COMMON SIGNS AND SYMPTOMS Rest from aggravating activities breasts and/or obesity, or forward head posture) Exaggerated upper chest or accessory breathing Neurological tests negative Altered neurodynamics on upper limb neurodynamic tests Reproduction of arm pain or symptoms on palpation over brachial plexus Positive Tinel’s sign for reproduction of arm pain or symptoms over brachial plexus Muscle spasm and/or shortening of anterior scalene muscle on palpation and length testing Muscle spasm and/or shortening of pectoralis minor muscle on palpation and length testing Ipsilateral elevated first rib Section III • The most common cause of vascular TOS is repetitive strain through prolonged or vigorous upper limb activity. Other causes may include a history of whiplash and direct or indirect blows to the shoulder. • The superimposed injury involved in causing TOS symptoms may include whiplash, direct or indirect blow to the shoulder, repetitive strain through prolonged upper limb activity, accessory breathing, and/or poor posture. • Positions or postures that place increased strain on the vascular structures of the thoracic outlet include the following: Prolonged writing or use of keyboard or telephone Assembly line workers Poor posture (i.e., droopy shoulders) Prolonged overhead or reaching activity such as styling hair, painting, playing musical instruments (e.g., violin or flute), swimming, playing tennis, and pitching. Excessive carrying of heavy objects such as suitcases and shopping bags Prolonged carrying of a heavy backpack 787 788 Vascular Thoracic Outlet Syndrome Subacromial or subcoracoid impingement Subacromial bursitis Glenohumeral labral tears Rotator cuff tendinopathies • Cervical or thoracic pathologies Cervical spondylosis Cervical degenerative disc disease Cervical nerve root syndrome Cervical spine stenosis Thoracic facet syndrome T4 syndrome Rib dysfunction • Peripheral nerve entrapments Ulnar nerve entrapment (cubital tunnel/Guyon’s canal) Median nerve entrapment (carpal tunnel/pronator teres) Radial nerve entrapment (forearm) • Other Muscular dystrophy Polymyositis CRPS Diffuse peripheral neuropathy Angina and other cardiac conditions RA Lupus Pancoast’s tumor Multiple sclerosis Spinal cord lesion Hypothyroidism Pleuritis and other pulmonary conditions Raynaud’s phenomenon Head, neck, or upper quadrant tumors Lymphedema CONTRIBUTING FACTORS • Underlying existence of bony or fibromuscular anomalies in the thoracic outlet region • Previous history of whiplash injury or a direct or indirect blow to the shoulder resulting in first rib, muscular, or clavicular trauma. • Exposure to increased or unaccustomed prolonged or repetitive upper limb activity (e.g., overhead sport, occupation, playing a musical instrument) • Presence of glenohumeral instability or hypertrophy of the humeral head or local muscular hypertrophy (arterial) • Exposure to cold temperatures combined with trauma (venous) • Presence of blood clotting factors (venous) • The use of a subclavian venous catheter (IV therapy) and dialysis treatment (venous) TREATMENT SURGICAL OPTIONS • The following is a list of current surgical techniques that are used alone or in combination to treat vascular TOS. The surgical techniques chosen depend on the degree of damage to the vessel, his- CHAPTER 16 • NERVE tory of symptoms, and degree of compression in the thoracic outlet region. • Arterial TOS Rib resection (transaxillary approach) Aneurysm resection with graft Thrombectomy Embolectomy Artery reconstruction or replacement Dorsal sympathectomy • Venous TOS Rib resection (transaxillary approach) Scalenectomy Fibrous band or adhesion resection Thrombectomy (limited use) Claviculectomy SURGICAL OUTCOMES • Arterial TOS Good results are generally seen with surgery, although outcomes are less favorable with delayed diagnosis and surgery, and the presence of distal embolism (Durham et al 1995). • Venous TOS The combination of a prompt diagnosis, contrast venography with catheter-directed thrombolytic therapy, and consequent TOS decompressive surgery has shown very good results. Delayed thrombolytic therapy with surgery (>3 months from onset of condition) also had a less positive outcome. SURGICAL INDICATORS • Arterial TOS Presence of arterial aneurysm, occlusion, or thrombosis Persistence of symptoms • Venous TOS Presence of thrombosis Persistence of symptoms Positive venogram exhibiting compression at rest or during provocative testing. REHABILITATION • Surgical intervention is the mainstay of treatment of vascular TOS, although its use is more controversial in less serious cases. A patient is therefore more likely to present for postsurgical rehabilitation on the request of the vascular surgeon. • The following rehabilitation guidelines are based on the principles of reducing ongoing trauma to the subclavian vessels in the thoracic outlet region, relieving symptoms, restoring upper limb function, and improving cardiovascular health. The guidelines are not meant to be used as a definitive postsurgical rehabilitation program. • Refer to the neurogenic TOS section for additional rehabilitation techniques for patients who present with combined neurogenic and vascular TOS symptoms. 53 of 57 • Arterial TOS Rest from aggravating activities Postural or ergonomic advice Lateral costal combined with diaphragmatic breathing techniques Motor control and stability functional rehabilitation exercises for trunk, scapula, neck, and shoulder (especially in cases of axillary artery injury that present with an unstable head of humerus) Gradual return to overhead arm activity Progressive cardiovascular training program, especially for those in poor aerobic condition • Venous TOS Edema control (e.g., compression sleeves, bandages, and gloves and supported elevation) Massage of upper limb to promote drainage of edema Gentle exercises of upper limb to promote drainage of edema Rest from aggravating activities Postural or ergonomic advice Lateral costal combined with diaphragmatic breathing techniques Motor control and stability functional rehabilitation exercises for trunk, scapula, neck, and shoulder Gradual return to overhead arm activity Progressive cardiovascular training program, especially for those in poor aerobic condition PROGNOSIS • Arterial TOS Since most cases of arterial TOS require surgery, the prognosis depends on surgical outcomes. Good results are generally seen with surgery, although outcomes are less favorable with delayed diagnosis and surgery and the presence of distal embolism. • Venous TOS Since most cases of venous TOS require surgery, the prognosis depends on surgical outcomes. The combination of a prompt diagnosis, contrast venography with catheter-directed thrombolytic therapy, and consequent TOS decompressive surgery has shown very good results. Delayed thrombolytic therapy with surgery (>3 months from onset of condition) had a less positive outcome. Conservative treatment tends to demonstrate the poorest outcomes. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN If vascular TOS is suspected, all cases should immediately be referred to a physician for prompt investigation and medical intervention. Vascular Thoracic Outlet Syndrome CHAPTER 16 • NERVE SUGGESTED READINGS Atasoy E. Thoracic outlet syndrome: anatomy. Hand Clin. 2004;20(1):7–14. Ault J, Suutala K. Thoracic outlet syndrome. J Man Manipulative Ther. 1998;6(3): 118–129. Brantigan CO, Roos DB, David B. Etiology of neurogenic thoracic outlet syndrome. Hand Clin. 2004a;20(1):17–22. Brantigan CO, Roos DB. Diagnosing thoracic outlet syndrome. Hand Clin. 2004b;20(1): 27–36. Crosby CA, Wehbé MA. Conservative treatment for thoracic outlet syndrome. Hand Clin. 2004 Feb;20(1):43–49, vi. Dawson DM, Hallett M, Milender LH. Entrapment Neuropathies. 2nd ed. Boston: Little, Brown; 1990. Demondian X, Herbinet P, Van Sint Jan S, Boutry N, Chantelot C, Cotton A. Imaging assessment of thoracic outlet syndrome. Radiographics. 2006;26:1735–1750. Durham JR, Yao JST, Pearce WH, Nuber G, Mc Carthy WJ.Arterial injuries in the thoracic outlet syndrome. J Vasc Surg. 1995;21:57–70. Edgelow PL. Chapter 7 Neurovascular consequences of cumulative trauma disorders affecting the thoracic outlet: a patient-centred treatment approach. In: Donatelli RA. Physical Therapy of the Shoulder. Philadelphia: Churchill Livingstone; 2003. Mackinnon SE, Novak CB. Thoracic outlet syndrome. Curr Probl Surg. 2002;39(11): 1070–1145. Pecina MM, Krmpotic-Nemanic J, Markiewitz AP. Tunnel Syndromes: Peripheral Nerve Compression Syndromes. 3rd ed. Boca Raton, FL: CRC Press; 2001. Safran MR. Nerve injuries about the shoulder in athletes, Part 2: long thoracic nerve, spinal accessory nerve, burners/stingers, thoracic outlet syndrome. Am J Sports Med. 2007;32(4):1063–1076. Sanders RJ, Hammond MD. Etiology and pathology. Hand Clin. 2004;20(1):23–26. Sanders RJ, Hammond SL. Supraclavicular first rib resection and total scalenectomy: technique and results. Hand Clin. 2004;20(1):61–70. Shebel ND, Marin A. Effort thrombosis (PagetSchroetter Syndrome) in active young adults: 789 Current concepts in diagnosis and treatment. J Vasc Nurs. 2006;24:116–126. Urschel Jr HC, Kourlis Jr H. Thoracic outlet syndrome: A 50-year experience at Baylor University Medical Center. Baylor Univ Med Cen Proc. 2007;20(2):125–135. Urschel Jr HC, Razzuk MA. Neurovascular compression in the thoracic outlet. changing management over 50 years. Ann Surg. 1998;228(4):609–617. Vanti C, Natalini L, Romeo A, Tosarelli D, Pillastrini P. Conservative treatment of thoracic outlet syndrome: A review of the literature. Eura Medicophys. 2007;43(1):55–70. Wehbe MA. Thoracic outlet syndrome. Hand Clin. 2004;20(1). Guest Editor. Whitenack SH, Hunter JM, Read RL. Thoracic outlet syndrome: a brachial plexopathy. In: Mackin EJ, Callahan AD, Skirven TM, Schneider LH, Osterman AL, eds. Rehabilitation of the Hand and Upper Extremity. 5th ed. St Louis: Mosby; 2002. AUTHOR: KATINA DIMOPOULOS Section III ORTHOPEDIC PATHOLOGY 54 of 57 Ulnar Nerve Entrapment 790 BASIC INFORMATION DEFINITION Ulnar nerve entrapment pathologies encompass any injury that interrupts the function of the ulnar nerve at any point along its course. The loss of function results in muscle weakness, pain, or sensory dysfunction. SYNONYMS • Cubital tunnel syndrome • Ulnar nerve palsy ICD-9CM CODES 354 Mononeuritis of upper limb and mononeuritis multiplex 354.2 Lesion of ulnar nerve OPTIMAL NUMBER OF VISITS 6 MAXIMAL NUMBER OF VISITS 20 ETIOLOGY • The ulnar nerve is a mixed sensory and motor nerve derived from C8 and T1 nerve roots. • It comes from the terminal branch of the medial cord of the brachial plexus. • It travels within the axillary sheath posterior to pectoralis minor and continues medially to the axillary artery and the brachial artery to the middle of the arm. • It becomes the ulnar nerve after piercing the intermuscular septum and follows the medial head of the triceps to the groove between the medial epicondyle and the olecranon. • It then crosses the elbow, giving off articular branches to the elbow and motor branches to the flexor carpi ulnaris and the medial half of flexor digitorum profundus. • It gives off a large dorsal sensory branch proximal to the wrist that supplies the skin of the dorsal wrist and ulnar side of the hand and continues into the hand via Guyon’s canal, then splits into superficial and deep branches. Guyon’s canal is bounded proximally and distally by the pisiform bone and the hook of hamate; it is covered by the volar carpal ligament and the palmaris brevis muscle. • Superficial branch supplies the palmaris brevis, the skin of the hypothenar eminence, and digital nerves to the fifth and ulnar side of the fourth fingers. • Deep branch passes between the abductor digiti minimi and flexor digiti minimi brevis with the deep branch of the ulnar artery. CHAPTER 16 • NERVE • It perforates the opponens digiti quinti and follows the deep volar arch across the interossei and supplies the three small muscles of the fifth finger, third and fourth lumbricales, the volar and dorsal interossei, the adductor pollicis, and the deep head of flexor pollicis brevis • The ulnar nerve is vulnerable to injury at several points along its course: Proximally at the axilla At the myofascial band, called the arcade of Struthers, proximal to the medial epicondyle The medial head of triceps muscle In the area of the medial epicondyle Within the ulnar groove of the medial epicondyle Within the cubital tunnel formed distal to the medial epicondyle as the nerve passes between the two heads of the flexor carpi ulnaris At the flexor-pronator aponeurosis Within Guyon’s canal • The ulnar nerve may be affected at any point along its course by direct trauma or compression entrapment leading to tissue hypoxia. The insult to the nerve can be mechanical, thermal, chemical, and ischemic. • Nerve injury is classified according to the severity of the injury and its potential for reversibility: Neurapraxia (first-degree injury): Distortion of the myelin about the nodes of Ranvier, caused by ischemia, mechanical compression, or electrolyte imbalance, produces temporary loss of nerve conduction. Axonotmesis (second-degree injury): Interruption of the axon with secondary wallerian degeneration. The supporting tissue surrounding the axon is preserved, and the recovery period depends on the distance between the site of injury and the end-organs. Neurotmesis: Complete disruption of the nerve and its supporting structures. • Neurotmesis has been further divided into the following three subcategories: Third-degree nerve injury: Endoneurium is disrupted with intact perineurium and epineurium. Fourth-degree nerve injury: All neural elements sparing the epineurium are disrupted. Fifth-degree nerve injury: Complete transaction and discontinuity of the nerve with no capacity for regeneration • Physiologically, there is disruption to any part of the nerve responsible for conduction. • In repetitive-type nerve entrapment, it is proposed that repetitive work or static postures produce an inflammatory process, fibroblasts appear to repair damage 55 of 57 incurred but produce adhesions to the nerve, limiting their glide and increasing anoxia. EPIDEMIOLOGY AND DEMOGRAPHICS • The ulnar nerve is the most commonly compressed nerve in the elbow region and is the second most common compressive neuropathy of the upper extremity. • Males develop perioperative neuropathies of the ulnar nerve at the elbow more frequently than females possibly because females have more fat content in the medial elbow overlying the tubercle of the ulnar coronoid process (Berman). • Most commonly seen in the throwing athlete but also seen in skiing, weight lifting, and racquet sports. MECHANISM OF INJURY • A number of mechanisms of injury for the ulnar nerve are described in relation to their location. • Direct trauma at any point along the course of the nerve • Proximally at the axilla through direct trauma or compression often sustained when the arm lies across a firm object such as a chair back for a sustained period of time or through the use of axillary crutches • Compression beneath the arcade of Struthers, proximal to the medial epicondyle • Compression from the medial head of triceps muscle, which, when hypertrophied, can snap over the medial epicondyle, causing friction neuritis. • In the area of the medial epicondyle, a fracture callus or valgus deformity can chronically stretch the ulnar nerve. • Frictional neuritis within the ulnar groove of the medial epicondyle if the groove is congenitally shallow or has a torn fibrous roof, allowing the nerve to sublux. • Superficial compression at the elbow from repeated leaning on elbows or a direct blow. • Compression within the ulnar groove by fracture fragments, spurs, soft tissue ganglia, or other space-occupying lesions. • Compression within the cubital tunnel during elbow flexion as the tunnel flattens, causing pressure to increase around the nerve. For example, in the throwing athlete, the position of elbow flexion with wrist extension creates a threefold increase in pressure in the cubital tunnel; this increases to six times the resting pressure during the cocking position of a throw. Therefore repetitive pressure and stress on the nerve at this point can create cubital tunnel syndrome. Ulnar Nerve Entrapment CHAPTER 16 • NERVE • Compression at the flexor-pronator aponeurosis as the nerve exits the flexor carpi ulnaris to perforate the fascial layer between flexor digitorum superficialis and flexor digitorum profundus. • Compression within Guyon’s canal by a fractured hook of hamate or ganglion COMMON SIGNS AND SYMPTOMS • Tasks involving repetitive fine hand motions may reveal fatigue and weakness. • Sports involving repetitive throwing actions with forceful elbow flexion and rapid extension • Occupational tasks involving sustained elbow flexion such as computer work or assembly line tasks • Leaning on elbows, particularly on hard surfaces EASING ACTIVITIES Rest and/or modification of aggravating activities PAST HISTORY FOR THE REGION • History of trauma, fracture, dislocation, or blow to the ulnar nerve distribution. • Repeated activity repetitive elbow flexion and extension such as may occur in forceful throwing activities such as pitching in baseball • Occupations involving sustained elbow flexion PHYSICAL EXAMINATION • Examine the limb for signs of autonomic dysfunction trophic changes such as edema, inflammation, and alteration in skin texture • Examine the limb for any characteristic posturing of the hand; with chronic ulnar neuropathy the hand may develop a claw appearance, with the fourth and fifth digits flexed. • The clinician may note wasting of the hand intrinsics. • Froment sign: The patient is unable to tightly grasp a piece of paper between the index finger and thumb because of weakness of the adductor pollicis and first dorsal interosseous muscles. The thumb also may flex at the interphalangeal joint because the flexor pollicis longus activates in an attempt to compensate for the weakness. • MMT may reveal weakness in any of the following muscles: Dorsal interossei Volar interossei Abductor digiti minimi Flexor digitorum profundus Flexor carpi ulnaris • To measure flexor carpi ulnaris and flexor digitorum profundus strength, ask the patient to cross the third finger over the fourth finger • If the neuropathy occurs at the wrist, there will be weakness of hand intrinsics with the forearm flexors spared, which generally implies that the compression has occurred at Guyon’s canal. • Intrinsic weakness with no sensory loss would imply that the deep branch has been compressed after the bifurcation from the superficial sensory branch. • Sensation: The cutaneous branch of the ulnar nerve supplies the fifth finger and the ulnar side of the fourth digit. Sensation testing should include pinprick, two-point discrimination, tuning 56 of 57 • • • • fork, and joint position sense and should be compared for asymmetry with the unaffected side (where available). Tinel’s sign may be positive at the elbow in the ulnar groove or over the cubital tunnel. Physical examination should also exclude pathology in other areas, particularly performing AROM and PROM at the neck and shoulder, which may reveal restrictions and central involvement of the nerve. Upper limb neural tissue provocation testing may reveal changes in nerve mobility and elicit symptoms. Physical examination should also include movement analysis to determine the movement patterns that the patient adopts when performing the aggravating activities. Movement analysis can be done visually or with the assistance of a video camera. The analysis should give some clues to predisposing factors, such as posture and patterning, that will assist with rehabilitation and activity modification. IMPORTANT OBJECTIVE TESTS • The earliest electrodiagnostic sign of entrapment is a loss of the nerve action potential seen during a nerve conduction study. • To isolate the specific location of the conduction block, serial stimulations are delivered to the nerve above and below the suspected lesion. • Needle EMG is valuable for evaluating the extent of motor fiber loss within a nerve territory. EMG assists with determining the location of the injury and monitoring progression over time. • MRI is increasingly being used in the assessment of peripheral nerve injuries to rule out cervical nerve root involvement and to determine the presence of edema, space restriction, or a spaceoccupying lesion along the course of the ulnar nerve. • Ultrasonography can detect cysts in Guyon’s canal. DIFFERENTIAL DIAGNOSIS • Medial epicondylitis • Thoracic outlet syndrome • Ulnar artery aneurysms or thrombosis at the wrist • Underlying neuropathic disease • Idiopathic brachial neuritis • Myopathies • Muscular dystrophy • Isolated neuropathy in the diabetic • Tumors or space-occupying lesions • Cervical radiculopathy • Upper motor neuron lesion in the cerebrum ORTHOPEDIC PATHOLOGY AGGRAVATING ACTIVITIES • Generally, the symptoms are related to activity and do not follow a typical 24-hour pattern unless there is a strong inflammatory component such as may be seen in an occupational repetitive task. • If there is an inflammatory component, there may be worsening of symptoms with use toward the end of the day and morning stiffness. Section III • Ulnar neuropathies often result in the following: Sensory changes in the fourth and fifth digits: Feelings of tingling, numbness, or burning Pain rarely occurs in the hand. Pain tends to be felt farther up the arm toward the elbow. Patients rarely notice the specific muscular atrophy, but it may be noticed by the clinician. Wartenberg sign: Patient complains that the little finger gets caught on the edge of trouser pockets when attempting to put hands in pockets (patient cannot pull the fifth finger tightly against the fourth). Patient may complain that their grip is weak. Pincer grip may also be weak. Difficulty opening jars or doors Early fatigue or weakness if work requires repetitive hand motions. Numbness and paraesthesias when resting on elbows • Cubital tunnel syndrome generallymanifests as follows: Medial elbow pain Paraesthesia of the fifth digit and ulnar side of the fourth digit Reduced fine motor control and weak grip • Neural tension tests may reproduce the symptoms. • The severity of complaints can vary from mild transient paresthesias in the fourth and fifth fingers to clawing of these digits, severe intrinsic muscle atrophy, and severe pain at the elbow and wrist with radiation into the hand or up into the shoulder and neck. 24-HOUR SYMPTOM PATTERN 791 792 Ulnar Nerve Entrapment CHAPTER 16 • NERVE CONTRIBUTING FACTORS • Fracture or dislocation of the elbow, particularly if it results in increasing valgus deformity of the forearm away from the midline. • Repetitive throwing action • Occupations requiring significant elbow flexion throughout the day such as typing, computer work, or assembly line work • Repeatedly leaning heavily on the elbows, particularly on hard surfaces • Nerve compressions are more common in people with arthritis, diabetes, thyroid problems, and alcoholism. TREATMENT • • • • • • SURGICAL OPTIONS • Indications for surgery include the following: No improvement in the presenting symptoms after 6 to 12 weeks of conservative treatment Progressive palsy or paralysis Clinical evidence of long-standing lesion: Clawing of fourth and fifth digits and muscle wasting • Several surgical options have been reported to relieve ulnar nerve compression, including the following: In situ decompression Medial epicondylectomy with or without decompression Anterior transposition Intramuscular transposition REHABILITATION • The goals of rehabilitation should be pain reduction to encourage pain-free exercise, to provide ergonomic education and interventions, and if the neuropathy has been prolonged, to introduce cortical reorganization activities. • Splinting should be used to provide immobilization to allow the reduction in swelling and inflammation. Night splinting in 45 degrees of elbow flexion • • • • • • with a neutrally rotated forearm can be used. Avoid leaning on the elbows. Eliminate aggravating tasks by avoiding or modifying those tasks to prevent further damage. Use ice to reduce inflammation and prevent secondary cell damage. Theoretically, ultrasound may help promote nerve regeneration, improve profusion to the healing nerve, and decrease inflammation. Direct low-intensity electrical stimulation has been found to increase the number of vasa nervorum and nerve fiber density in rats. Nerve-gliding exercises have been purported to disperse intraneural edema, increase blood flow, optimize axonal transport, and lengthen nerve adhesions. Neural mobilization can be assessed using the brachial plexus provocation test positions to identify symptom reproduction, and these positions and movements can also be used both actively and passively for a treatment technique. Use of soft tissue mobilization and muscle stretching techniques to reduce fibrous bands and adhesions in muscles surrounding the ulnar nerve. Stretches must not produce tingling or discomfort because this may indicate decreased blood flow to the already stressed nerve. Motor control and stability functional rehabilitation exercise for proximal muscles of the trunk, neck, and shoulder Gradual introduction of strengthening exercises for any muscles that have been subjected to motor loss Ergonomic interventions, work place assessment, or provision of ergonomic aids, such as tilted keyboards or altered mouse shape Cortical reorganization techniques such as use of mirror box Reacquisition of fine motor and dexterity skills 57 of 57 PROGNOSIS • Prognosis depends entirely on the extent of damage to the nerve. • Neurapraxia should resolve rapidly and lead to a complete restoration of function, usually within 2 to 3 months. • If the injury is a more severe axonotmesis, the recovery time depends on the distance from the site of injury to the denervated tissue. • Peripheral nerves have been reported to recover at an approximate rate of between 1 and 4 mm per day, and recovery may not result in a complete restoration of function. • If there has been a complete sectioning of the nerve (neurapraxia), a full recovery will not occur.The results of treating neurapraxia, even with surgical intervention, are generally not satisfactory. • In chronic palsy, surgical outcome is less certain and improvement may be limited. SIGNS AND SYMPTOMS INDICATING REFERRAL TO PHYSICIAN If ulnar nerve entrapment is suspected, then all cases should be referred to a physician for appropriate investigation. SUGGESTED READINGS Bencardino JT, Rosenberg ZS. Entrapment neuropathies of the shoulder and elbow in the athlete. Clin Sports Med. 2006;25:465–487. Berman SA. Ulnar neuropathy. Emedicine. www.emedicine.com/neuro/topic387.html; 2007. Izzi J, Dennison D, Noerdlinger M, Dasilva M, Akelman E. Nerve injuries of the elbow, wrist, and hand in athletes. Clin Sports Med. 2001;20(1). Pratt N. Anatomy of nerve entrapment sites in the upper quarter. J Hand Ther. 2005;18(2):216–229. Stern M. Ulnar nerve entrapment. Emedicine. www.emedicine.com/Orthoped/topic574. html; 2004. AUTHOR: JOSEPHINE LOUISE COULTER