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Traumatic Brain Injury Dayna Ryan, PT, DPT Winter 2012 TRAUMATIC BRAIN INJURY • Lesion: Brain • ~ 5 million persons living with TBI • ~$60 billion in the United States in 2000 TBI INCIDENCE (March 2010 CDC data) • ~ 1. 7 million TBI occur in the US annually • TBI rates among individuals younger than 65 y. o. – Male : Females = 1.4 : 1 ~ 80% of TBI treated & released TBI INCIDENCE BY AGE (March 2010 CDC data) Highest incidence among ages 0-4 (children), 15-19 (teens), 65+ (elderly) ~ 90% ER visits by children aged 0-14 y. o. Highest rates of TBI-related hospitalizations & deaths occur in adults aged > 75 y. o. CAUSE OF TBI (March 2010 CDC data) Falls are #1 cause of TBI among all age groups Highest rates of fall-related TBI in children 0-4 y.o. & adults > 75 y.o. Highest rates of motor vehicle & assault-related TBI among adults aged 20-24 y.o. Alcohol involved in >50% of cases RISK FACTORS Young (average age of TBI = 29 y. o.) Male Risk taking behaviors (age 15-24 y. o.) Low income inner city dwellers Substance abuse (50% hospitalizations by TBI due to alcohol intoxication) Availability of firearm Previous TBI (e.g. sports-related concussions) Old age (more susceptible to tearing of blood vessels, declines in cerebrovascular circulation, slower reaction time, movements & gait) CLASSIFICATION OF TBI (BY MECHANISM) Open meninges have been breached, brain is exposed Closed no skull fracture or laceration of the brain coup-contrecoup Primary injury at impact 2nd injury at the opposite side Blast Blast wave from explosion hits the body Air-filled organ or brain surrounded by fluid are particularly at risks of blast injuries Coup-Countercoup Injury CLASSIFICATION OF TBI - BY TYPES OF INJURIES • Primary vs. Secondary (Biomolecular response to injury) – Primary = direct injury to the brain – Secondary = damage after the traumatic event, caused by brain hypotension, hypoxia, or herniation • Focal vs. Diffuse or a Combination of the Two – Focal = localized trauma (gun shot) – Diffuse = trauma over a large area (swelling) CLINICAL CLASSIFICATION OF TBI - BY SEVERITY OF DAMAGE Mild (i.e. concussion): ~ 75% of TBI * Moderate Severe Classification Criteria & Prognosis Types Mild (Concussion) Moderate Severe Loss of Glasgow Memory Consciousness Coma Loss (LOC) Scale < 30 min > 30 min < 24 hr > 24 hr 13-15 8-12 <8 < 24 hr Prognosis Good Most recover completely > 24 hr < 7 days Good Learn to manage problems resulting from TBI > 7 days Most impossible to recover completely Physical and/or cognitive disability (* Centers for Disease Control and Prevention (CDC), National Center for Injury Prevention and Control. Report to Congress on mild traumatic brain injury in the United States: steps to prevent a serious public health problem. Atlanta (GA): Centers for Disease Control and Prevention; 2003. ) SPECIFIC INJURIES Concussion (= mild TBI) Diffuse axonal injury Contusion Skull fracture Intracerebral hematoma Subdural hematoma Epidural hematoma Subarachnoid hemorrhage Patient: MILD T.B.I. (Concussion) COMMON SYMPTOMS headache dizziness irritability decreased memory &concentration depression/anxiety fatigue sleep disturbance pain THESE SYMPTOMS ARE ALSO COMMON IN THE GENERAL POPULATION AND AMONG CHRONIC PAIN PATIENTS CONCUSSION (MILD TBI) Most common head injury Alteration of consciousness & memory Non-penetrating (non-opened) injury CT or MRI usually normal Good prognosis Cumulative effects of repeated concussion can cause chronic dementia 50-100% mortality rate in second impact syndrome seen in athletes a 2nd TBI while the 1st is NOT yet resolved Post-Concussion Syndrome Characterized by: dizziness, disorientation, nausea, headache, fatigue Also see decreased control of emotions and personality changes Attention deficit usually present **If concussion lasts >2 minutes, patient should be kept under observation DIFFUSE AXON INJURY (DAI) Severe and fatal head injuries Widespread axonal damage As a result of shear and tensile forces within the brain Coma and decerebrate posturing Poor prognosis CT or MRI usually unremarkable CONTUSION Coup-countercoup injuries Can involve a small (mild) or large (severe) area Most common in the frontal & temporal lobes Lesion often enlarge during the first week after injuries HEMORRHAGE • • • • Intracerebral hematoma Subdural hematoma Subarachnoid hemorrhage Epidural hematoma • Intracerebral hematoma – In brain parenchyma – hematoma may enlarge during the first few days after injury • Subdural hematoma – Beneath the dura – Acute or chronic (>2 wk) – Laceration of bridging cortical veins during sudden head deceleration – A feature of shaken baby syndrome • Subarachnoid hemorrhage – Poor prognosis if bleeding into ventricular system – Need to r/o aneurysm • Epidural hematoma – In epidural space – Between dura mater & skull – Acute bleeding – Common in temporal bone fracture Severe TBI Assess severity of brain injury Acute surgical care: expanding mass lesion from increasing ICP Address life-threatening injuries (ABC – airway, breathing, circulation) Prevent complications Preventative Rehab interventions GENERAL SYMPTOMS & SIGNS Altered Level of Consciousness Cognitive & Behavioral Deficits Cranial Nerve Damages Motor Deficits Sensory Deficits Altered Level of Consciousness Reduction in response to stimuli Due to diffuse bilateral cerebral hemispheric damage or a lesion in the brainstem Arousal is associated with wakefulness and depends on an intact reticular formation and upper brainstem Coma rarely last > 4 wks Coma is used to determine current status and prognosis Altered Level of Consciousness Coma: state of unresponsiveness; not opening eyes Persistent vegetative state or stupor: no evident cerebral cortical function; eye opening with sleepwake cycles Obtundity: decreased interest in the environment; slowed responses to stimulation; sleep more than normal; drowsiness between sleep states Lethargy: severe drowsiness; aroused by moderate stimuli & then drift back to sleep Confusion: disorientation, bewilderment, and difficulty following commands Clouding: inattention & reduced wakefulness COGNITIVE IMPAIRMENT Difficulties in: Attention, concentration Learning, memory Abstract thinking, information processing Problem solving Initiation, executive functions Inaccurate perception (leaning) Deficits often remain despite a full return of consciousness MEMORY DEFICITS IN TBI Retrograde amnesia Loss of memory of events immediately preceding the injury Post-traumatic amnesia (PTA) (impaired anterograde memory) (50 first dates) Unable to recall events that occur after the injury Inability to form new memory No carryover or tasks requiring memory / learning Duration of PTA indicates the severity of injury BEHAVIORAL IMPAIRMENT Mood disturbances including depression and anxiety Symptoms depending on brain area involved Inappropriate, excessive social behaviors Inappropriate sexual behaviors Irritability; rage; refuse to cooperate Euphoria; involuntary laughing or crying Apathy; indifference Motor, sensory, verbal perserveration CRANIAL NERVE DAMAGE Usually occur following focal damage in the brainstem or herniation Disturbances in CN function e.g. gaze and tracking deficits, diplopia, ptosis, facial sensory deficits, absent corneal reflex, hearing & vestibular dysfunction, cardiac irregularities, dysphagia, loss of gag reflex CN dysfunction reflects level of lesion Normal pupillary reflex (to light) indicates a lesion rostral to the midbrain MOTOR DEFICITS Usually flaccid at onset Increased tone, spasticity and rigidity develop gradually Decortical posturing Hyperactive UE flexors Hyperactive LE extensors Decerebrate posturing Hyperactive UE & LE extensors A. Decerebrate posturing seen in cerebral hemisphere/white matter, internal capsule and thalamic lesions B. Decortical posturing seen with midbrain lesions/compression; also with cerebellar and posteria fossa lesions MOTOR DEFICITS Monoplegia, hemiplegia Abnormal reflexes (e.g. palmar grasp & Babinski reflex) Abnormal balance reactions Cerebellar and BG dysfunction: e.g. ataxia, dysmetria, tremor, bradykinesia SENSORY DEFICITS Somatosensory dysfunction is determined by the brain area involved COMPLICATIONS • • Increased intracranial pressure (ICP) Heterotoptic ossification: • • • • • osteoclast destroy bone, so increase od Ca in blood, form boney spurs at joint. DVT Spasticity / Contracture Decubitus ulcer (tuberosity) Seizure INCREASED INTRACRANIAL PRESSURE (ICP) Secondary complications develop over hours or days after the primary injury Cause: swelling, fluid build-up in the brain & hematomas Increased ICP compresses the brain within the rigid skull Serious, life-threatening ICP monitoring: Medications Fluid management Decompressive craniectomy Lynda Yang http://www-personal.umich.edu/~chronis/ICP.html Cycle of Primary and Secondary Injury Cerebral Perfusion Pressure = Mean Arterial Pressure - Intracranial Pressure HETEROTOPIC OSSIFICATION • Abnormal bone growth around a joint • Most commonly in hips, elbows, shoulders and knees • Onset 4-12 wk after injury • Diagnostic test – X-ray – Bone scan with increased uptake – Elevation of alkaline phospatase • Symptoms and signs – loss of ROM, tenderness, palpable mass, redness, swelling, pain with movement DIAGNOSIS OF TBI • • • • History Clinical exam Imaging Functional capacity HISTORY • Magnitude of injury • Altered consciousness and memory – witnessed – self-report • Duration of coma correlates with severity of injury CLINICAL EXAM • • • • Evidence of trauma Glasgow Coma Scale Ranchos Los Amigos Cognitive Scale Post-traumatic amnesia GLASGOW COMA SCALE EYE OPENINGSCORE spontaneous to speech to pain none E4 E3 E2 E1 GLASGOW COMA SCALE VERBAL RESPONSE SCORE appropriate confused, disoriented inappropriate words unintelligible none V5 V4 V3 V2 V1 GLASGOW COMA SCALE MOTOR RESPONSE Follows commands Localized (to pain) Generalized (to pain) Decorticate posturing (flexion) Decerebrate posturing (extension) None SCORE M6 M5 M4 M3 M2 M1 GLASGOW COMA SCALE Most accurate early in course >12 = Mild 9-12 = Moderate <8 for longer than 6 hours = severe 3 = Dead RANCHO LOS AMIGOS COGNITIVE SCALE I. no response V. II. generalized response VI. confused, appropriate III. localized response IV. confused, agitated confused, inappropriate VII. automatic, appropriate VIII. purposeful, appropriate Diagnostic Imaging CT MRI DTI SPECT PET Computed Tomography Anatomic 1st line of imaging studies Bone & brain tissue Can see damage to gray matter Rapid (< 1 min for whole brain) Less costly Accessible (even with monitor, life-support equipment, or combative patient) Best for skull fx, hemorrhage vs. edema, & intracerebral hemorrhage Computed Tomography Abnormal findings in ~ 18% of patients without neurologic deficits Severity of findings correlates with outcome Not sensitive enough in detecting mild TBI (concussion) May underestimate non-hemorrhagic lesion May not show non-hemorrhagic parenchymal (neurons and glial cell) injuries M.R.I. Anatomic Most sensitive 24-48 hours after injury Higher resolution than CT Better for hemorrhagic contusions (after first 24 hours) More sensitive than CT to diffuse axon injury Scans > 6 months post-injury correlate with outcome Disadvantage compared to CT Duration of scan time, more costly Not for combative patients Diffusion Tensor Imaging Neuroimaging that builds on MRI technology Study movement of fluid in the brain Detect damage in the white matter (axons) Axons are colored according to orientation Single Photon Emission Computed Tomography (S.P.E.C.T.) Injection of a small amount of short-lived radioactive particles into the blood Image of regional blood flow More sensitive than MRI Limited value in acute stage Abnormal in many patients with normal neurologic exam, CT, and MRI Poor image resolution Not readily available Positron Emission Tomography Study metabolic activity and function Used in mild TBI NEUROPSYCHOLOGICAL TESTING Standardized measure to assess Memory Concentration Attention Motor control Processing / Decision making Use testing findings to Plan and implement treatment Monitor progress Return to work ACUTE TBI MEDICAL AND SURGICAL MANAGEMENT Surgery (e.g. for hemorrhage; reduce ICP) Monitor intracranial pressure (ICP) Cerebral vasoconstrictive agents to decrease cerebral blood volume Mannitol Barbiturates Etomidate Proprofol SUBACUTE AND CRHONIC TBI MEDICAL AND SURGICAL MANAGEMENT Spasticity medications Seizure control Bacolfen Diazepam Dantrolene Depakote Depression Non-tricyclic antidepressants CONDITONS PREDICTING POOR PROGNOSIS IN TBI Loss of pupillary light reflexes Oculomotor deficits Significant damage to brainstem Midline shift of brain structures Acute hemispheric swelling with extra-cerebral hematoma Multiple small hemorrhages Skull is fractured Subarachnoid hemorrhage Diffuse axon injury Rigidity persists Epilepsy develops within first 7 days of injury Long duration of post-traumatic amnesia FUNCTIONAL CONSIDERATIONS If with NG tube is in place Head of bed > 30º to avoid aspiration If chest tubes are in place Drainage tube should be kept below level of chest at all times PRECAUTIONS AND CONTRAINDICATIONS In presence of increased intracranial pressure Pulmonary PT (percussion and vibration) may be contraindicated Hetertopic ossification developed 4-12 weeks following TBI Palpable tenderness and mass by a joint from abnormal bone growth Can decrease ROM