Download Anatomical Variations of the Accessory Nerve and Resultant Clinical

Research Project
Entitled
Anatomical Variations of the Accessory Nerve and Resultant Clinical Implications:
A Literature Review with Cadaveric Dissection
By:
Casey Waller
Submitted in partial fulfillment of the requirements for graduation as an Honor Scholar at Point Loma
Nazarene University, San Diego, California, May 7, 2016
Approved by ___________________________________
Leon Kugler, Mentor
April 16, 2016
Committee Members:
______________________________________
Rebecca Flietstra
______________________________________
Brandon Sawyer
Abstract:
The accessory nerve (CNXI) is often injured through extreme stretch, blunt trauma, or radical
neck dissection (RND) and can present with insidious symptoms including motor deficits of the
sternocleidomastoid (SCM) and trapezius, as well as possible sensory deficits. Due to the level of
variation in the structure of the accessory nerve, it is critical that differential diagnosis takes into
account the variance in susceptibility of each variation to different mechanisms of injury as well
as resulting symptoms in order to increase evaluative accuracy and treatment strategies.
Accessory nerve (CNXI) damage can manifest in impaired ability to rotate, flex, and laterally
flex the cervical spine, as well as elevation, retraction, depression, upward and downward
rotation of the scapula. Symptoms depend on the location and severity of injury as well as the
level of external nerve involvement. In cadaveric study, the path of the spinal root of the
accessory nerve (SAN) and the cranial root of the accessory nerve (CAN) from the jugular
foramen to the SCM and trapezius were identified and studied in order to determine the level of
external nerve involvement, which can result in varying symptoms following injury. It was
concluded that improved knowledge of the relationship between the accessory nerve and the
cervical plexus can assist clinicians in evaluation, prognosis assessment, and treatment strategies.
Key Words: Accessory nerve (CNXI), sternocleidomastoid (SCM), trapezius
2
Key Acronyms
SAN: Spinal root of the Accessory Nerve
CAN: Cranial root of the Accessory Nerve
IJV: Internal Jugular Vein
JF: Jugular Foramen
SCM: Sternocleidomastoid
CNX: Vagus Nerve
CNXI: Accessory Nerve
EMG: Electromyography
C2: Cervical nerve root 2
C3: Cervical nerve root 3
C4: Cervical nerve root 4
SANP: Spinal Accessory Nerve Palsy
3
Introduction
The structure of the accessory nerve (CNXI) has considerable variation in its path from
the cranial origin to each target muscle, namely the trapezius and the sternocleidomastoid (SCM)
muscles. As a result, a study was performed to elucidate the implications of CNXI variations on
diagnosis, rehabilitation, and surgical techniques. It is hoped that improvement in accuracy and
speed of diagnosis can result in improved outcomes for patients with the panoply of deficits
associated with all the variations and etiological factors of CNXI pathology.
The accessory nerve (CNXI) has been described as having spinal and cranial roots
traveling through the middle compartment of the jugular foramen (JF).1,2,3 The spinal portion is
formed from cervical spinal cord nerve roots as inferior as C6 originating from the anterior rami,
which ultimately form a nerve trunk that runs superolaterally along the posterior cranial fossa in
order to pass through the posterolateral dural perforation of the jugular foramen.3 (See Figure 3)
The cranial portion arises from up to five nerve roots from the post-olivary groove of the
posterolateral medulla anterior to the rootlets of the vagus nerve (CNX). It is generally accepted
that previous to entering, as well as inside the jugular foramen, there are branching connections
between the cranial and spinal portions of CNXI. Inside the JF, the vagus nerve (CNX) often
shares a fibrous sheath with CNXI and co-mingling of nerve fibers. The vagus nerve originates
from the post-olivary sulcus of the medulla, anterior to the glossopharyngeal nerve (CNIX), and
then crosses the basal cistern to enter the pars vascularis of the jugular foramen in order to meet
the accessory nerve. (See Figure 4) Inside the JF, the spinal accessory nerve lies posterior to
CNX and anteromedial to the internal jugular vein (IJV) in its own connective sheath.3 Inside the
JF, CNX expands into its inferior ganglion, and upon exiting the JF, it travels inferior along the
4
carotid space in the posterior groove between the IJV and the internal carotid, and ultimately
common carotid arteries.4 (See Figure 5)
Upon exit from the JF, CNXI passes anterior to the IJV to the SCM. Here it pierces the
upper third of the muscle belly, where a portion of CNXI innervates the muscle and another
portion of the nerve continues through the SCM and travels to the trapezius as depicted below
and in cadaveric study.5 (See Figure 1) The structure of the spinal root of the accessory nerve
(SAN) apart from the cranial root of the accessory nerve (CAN) exhibits many variations as
reported in the literature. These variations include positioning in the JF, the path outside of the
JF, its positioning in regards to the anterior and posterior triangle, as well as the level of cervical
nerve root involvement both before and after the innervation of the SCM and trapezius.
Figure 1. The path of the Accessory Cranial Nerve (CNXI)
5
Structural Variations
Multiple variations in the structure of the accessory nerve upon leaving the jugular
foramen (JF) are documented. In a study of 34 cadaveric dissections, the SAN passed laterally to
the IJV in only 56% of specimen, while passing medial in 44% of specimen.6 A study with a
sample size of 84 subjects found the SAN traveled anteromedial to the IJV in 87% of necks
inside the JF, crossing anteriorly (80%) or posteriorly (19%) to the IJV, and ultimately lateral to
the IJV in 67% after exiting the JF as depicted below.7 (See Figure 2) As a result, clear,
significant variance is shown in the extra-cranial path of the SAN.
Figure 2. Variations in the path of CNXI
Other less common variations have been reported including cases of the SAN branching
proximal to the SCM resulting in the superior branch innervating the SCM and the inferior
innervating the trapezius.8 This is notably different from the common path where the nerve
pierces through the SCM and continues on to the trapezius. (See Figure 5) A more rare
occurrence involves the bifurcation of the IJV inside the anterior triangle creating a hiatus for the
6
SAN to traverse through the vein.9 In a study involving 192 neck dissections, this anomaly was
found in 4 (2.1%) dissections.9 This is referred to as the fenestration of the IJV, where the SAN
passed medially to the anterior portion and laterally to the posterior portion.9
The nerve has been found to exit the SCM from the posterior border at the mid-portion as
well as at the junction of the middle and upper third of the SCM with equal variance.1 From here,
the SAN travels inside the posterior triangle which is made up of the SCM, Trapezius, and
clavicle, where it becomes most superficial. In a fetal cadaveric study of bilateral differences
between the paths traveled by the SAN, significant differences were found between the mean
angle that the nerve takes upon exit from the SCM and nerve angle into the trapezius inside the
posterior triangle. Investigators found the mean angle that the SAN took upon exit from the SCM
was 73.3 degrees on the right side and 60.5 degrees on the left side.10 Additionally, upon entry to
the trapezius an average angle of 41.4 degrees and 62.2 degrees were found on the right and left
side respectively.10 Although, this is a fetal model, possible left side vulnerability is suggested
since the SAN travels further inferior and has an average of .3 cm longer distance inside the
posterior triangle. Since this is the point where the nerve is most superficial, possible increased
vulnerability to both frontal plane stretch pathologies as well as blunt trauma may be present on
the left side. CNXI then passes obliquely on the border of levator scapulae, and ultimately passes
deep to the anterior border of the trapezius.1,11 At this point the nerve is surrounded by
superficial cervical lymph nodes, putting it at risk of iatrogenic injury during radical neck
dissection.4,11 (See Figure 7)
In regards to the cranial portion of CNXI (CAN), it originates at the nucleus ambiguus
and emerges as up to five rootlets just inferior to the vagus nerve on the medulla oblongata. 12 The
CAN then branches off of the main trunk and connects to the vagus nerve at approximately the
7
upper border of the transverse process of C1 (axis).3 In a cadaveric study, three courses of the
CAN were found upon connection to the vagus nerve and exit from the JF.12 These branches
include the pharyngeal branch, descending branch, and the recurrent laryngeal nerve (RLN); all
of which travel along the vagus nerve with complex connection.12 The pharyngeal branch is
composed primarily of the CAN, and controls motor function of the pharynx. 12 The descending
branch, with vagus contribution, provides parasympathetic innervation to the abdominal and
thoracic viscera.12 The laryngeal distribution of the internal branch and vagus nerve was
confirmed in the posterior cricoarytenoid, lateral cricoarytenoid, and thyroarytenoid muscles
resulting in motor function of the trachea and esophagus.4,12 It was determined that although the
origin of the two nerves is different, the path and function of the vagus and CAN are the same.12
Cadaveric studies promote the idea of both the spinal and cranial roots traveling without
connection through the JF. In a cadaveric study, none of the 15 specimens had a distinct cranial
portion. This suggests that the traditional view of the spinal and cranial roots of CNXI sharing
fibers in the JF is a rare variation, and not typically present. 2 A separate follow-up study found
similar results as Lachman et al in 11 of 12 specimens.3 The small connection found in one
specimen passed between the cranial and spinal roots at an oblique angle just distal to the jugular
foramen. However, even this variation is different from the traditionally accepted “typical”
anatomical description of the two roots joining at the entrance of the jugular foramen.3
Functional Implications
In regards to function, many cases of cervical plexus contributions to the SAN are
documented in the literature. In one cadaveric study, 96% of neck dissections exhibited SCM
innervation involving the cervical plexus, including C3 in 72% of subjects. 13 In an intra-operative
study of the 20 necks, 20% of subjects had cervical nerve root contributions which were
8
determined with electromyography (EMG) to recruit motor units following SAN excision
proximal to contribution.14 Electromyography was administered, and it was found that when the
SAN was excised with no cervical nerve root contribution, no motor units (MU’s) were recruited
with stimulation. However, when cervical roots were found, MU’s were found to be recruited
irrespective to SAN excision as long as cervical contributions were distal to the location of
excision.14
In an intraoperative study involving 34 patients during radical neck dissection (RND),
electroneurography was used to detect muscle innervations through electrical stimulation of
nervous tissue with the SAN intact and results are depicted below.15 (See Table 1)
Table 1. Cervical Nerve Root Contributions to the Three Portions of the Trapezius
Nerve Root
Upper Trapezius
Middle Trapezius
Lower Trapezius
C2
15
13
14
C3
18
21
15
C4
5
19
20
In one case, C2 innervated all three portions of the trapezius, and in two others both the
upper and middle trapezius. However, innervation was only through co-mingling with the SAN.
Innervation of lower and middle trapezius via C3 and C4 nerve roots occurred directly, separate
from the SAN.15 (See Figure 5) Therefore, it was determined that in the majority of cases,
cervical nerve roots contribute to the innervations of the trapezius both by co-mingling with the
SAN and directly from the spinal cord.15
9
When CNXI was severed superior to cervical contribution, C3 and C4 were able to
maintain lower trapezius innervation (68%), middle trapezius (59%), and upper trapezius
(53%).15 However, when severed below, the upper trapezius was completely lost, but lower and
middle trapezius innervations remained constant from C3 and C4.15 As a result, it is proposed
that loss of upper trapezius innervation may be used to differentiate between the location the
SAN excision.
Following excision of the SAN, function of all three portions of the trapezius remained if
the SAN was damaged superior to the cervical branches in 62% of subjects, while two subjects
maintained lower and middle trapezius innervations, and one subject maintained solely the lower
trapezius.15 In addition, following complete SAN excision, C2 was no longer able to elicit
trapezius contraction in any of the subjects, and C3 and C4 were able to innervate the middle
trapezius (59%, 53% respectively) and the lower trapezius (38%, 56% respectively).15 This level
of reported cervical involvement supports the notion that the SAN does not act alone in
performing its traditional motor function of SCM and trapezius innervations.
Histochemical staining in the above study also reported mixed cervical contributions,
where both motor and sensory axons innervated the trapezius.15 A separate 18 subject
intraoperative study reported a motor cervical branch to the trapezius in 39% of subjects at the
level of C3.16 However, it was determined through electromyography that all motor contributions
solely innervated the upper trapezius.16 This further validates the use of manual muscle testing of
scapular elevation as a test of motor capacity.
Other contributions to the SAN have been reported in the literature. In a study of intraoperative RND patients, the contribution of the great auricular nerve at the posterior border of
10
the SCM was observed. Contributions of the great auricular nerve to the facial nerve (CNVII)
were found, while the trigeminal nerve (CNV) was found to contribute to the great auricular
nerve promoting the idea of the co-mingling of sensory nerves with the accessory nerve.1 It has
been determined that the SAN is not purely motor since sensory changes following trauma, as
well as through contributions from other sensory nerves have been reported.1 It is proposed that
the spinal accessory nerve should be referred to as the spinal accessory nerve plexus (SANP), in
light of its complex connection to cervical nerve roots.
Clinical Implications
The SAN is typically injured following extreme stretch, blunt trauma, or excision, either
from trauma or RND.2,13 CNXI damage is among the most frequent iatrogenic injuries in RND.
The incidence of SAN-related disability is estimated at approximately 30-40% of patients that
undergo neck dissections.17 Overall, severe functional deficits of the upper extremity have been
reported to be present in 60-80% of those that undergo RND.18 In a retrospective study of 3417
traumatic brain injury (TBI) patients, the accessory nerve was implicated in just 3% of cases.19
However, in patients with low cranial nerve injury (CNIX-CNXII) mortality was as high as
73.3%.20 This suggests poor prognosis for those with CNXI damage following TBI. As a result,
manual muscle testing of the SCM and trapezius following TBI may be effective as a tool in
determining prognosis. In a study of 327 patients assessed for CNXI implication in conjunction
with brachial plexus neuropraxia, 6% of patients were found to have spinal accessory nerve palsy
(SANP); 59% of those with positive SAN involvement exhibited only trapezius palsy, while 32%
had only SCM palsy, and 9% had complete palsy of both the SCM and trapezius.19
CNXI is vulnerable to blunt trauma and extreme stretch trauma in the posterior cervical
triangle when there is significant scapular depression and/or cervical lateral flexion. Excessive
11
stretch of the nerve may result in neuropraxia while forcing a CNXI superficial positioning. In
this position CNXI is also most susceptible to trauma as it becomes subcutaneous. Injury to
CNXI during radical neck dissection commonly occurs at its exit point from the SCM into the
posterior triangle with damage at this location resulting in solely trapezius denervation. The
degree of injury is determined based on the presence and magnitude of symptoms and signs.
Common notable symptoms include decreased scapular active range of motion (AROM)
resulting from trapezius denervation.21 This manifests as scapular dyskinesia, where two degrees
of humeral movement to one degree of scapular movement is not maintained resulting in limited
glenohumeral range of motion (ROM).21 With trapezius denervation, dyskinesia is greatest with
glenohumeral abduction, where scapular depression and upward rotation are necessary to
position the glenoid fossa in the correct position for the humeral head. 21 Rare signs of CNXI
damage resulting in trapezius denervation include trapezius hypertrophy with SCM atrophy
which results from spontaneous motor unit discharge.22 Other suggested clinical indicators
include unilateral trapezius weakness with contralateral SCM weakness which suggests an upper
motor neuron lesion above the oculomotor nerve nucleus.23
Spinal accessory nerve palsy (SANP) is commonly identified by shoulder girdle
depression and protraction with scapular dyskinesia and up to 30% of shoulder strength lost.1
However, assessing the cause of scapular dyskinesia is often unreliable, and manual muscle
testing is controversial, as multiple muscles are responsible for each scapular movement.24 As a
result, the scapular flip sign is proposed as a possible special test to assess middle and lower
trapezius function. (See Figure 6) This test is performed with the patient standing, arms at their
side, and elbow flexed to 90 degrees.24 Glenohumeral external rotation is resisted at the distal
forearm and the vertebral border of the scapula is assessed. Winging of the vertebral border of
12
the scapula from the thoracic wall is a positive test and indicative of middle and lower trapezius
weakness and possible SANP. In a study of 20 subjects with known SANP, all 20 exhibited a
positive scapular flip sign, even though all subjects were found to have clinically functional
rhomboids.24 This test is used as a way to differentiate between the middle and lower trapezius
muscles and the rhomboid muscles. The study found that with horizontal abduction with neutral
arm rotation, there was significant rhomboid and trapezius activation. However, with
glenohumeral external rotation, rhomboid activity did not meet qualifying activation criteria of
palpable contraction.24
The EMG study conducted by Ekstrom, et al25 validates the above mentioned finding as it
was found that glenohumeral external rotation resulted in middle trapezius isolation. It is intuited
that glenohumeral external rotation results in some scapular retraction effectively shortening the
rhomboids past the optimal length-tension relationship. However, since the trapezius attaches to
the spine of the scapula, it is not maximally shortened in this position, allowing it to be isolated.
The pull of the rotator cuff on the humerus lifts the vertebral border of the scapula off of the rib
cage and the middle and lower trapezius are unable to resist this pull and hold the scapula on the
rib cage.21 Therefore, the scapular flip sign is proposed as both an evaluative and strengthening
tool. A positive scapular flip sign is proposed as a tool to test the middle and lower trapezius, but
further research is needed to determine specificity and sensitivity.21
Prognosis and Management
In an electromyographic and motor latency study of 8 subjects, 75% of patients with
Wallerian degeneration and axonotmesis of the SAN following iatrogenic injury showed
evidence of spontaneous nerve regeneration over the course of 3-5 months.26 In addition
13
spontaneous nerve regeneration did occur following axonal degeneration from neuralgic
amyotrophy in one case, and nerve regeneration was found to be incomplete following iatrogenic
causes.26
Based on treatment results, it was found that following stretch-induced SAN palsy,
electrical stimulation produces contraction of the upper trapezius, no repair is needed. However,
in proximal injuries the platysma motor branch should be transferred to the accessory nerve, and
in distal injuries the accessory nerve is best repaired with a motor neuron graft.19 However, if
attempted six months post axonal disruption, surgery was found to be ineffective.27 Regardless,
prognosis is poor unless a treatment plan is put in place within six months.
Another surgical intervention for trapezius palsy is the Eden-Lange procedure which
involves transfer of the levator scapulae distal attachment to the spine of the scapula, and transfer
of the rhomboid minor and major attachments to the supraspinatus and infraspinatus fossae,
respectively.28 This procedure effectively creates the actions of scapular upward and downward
rotation with the remaining synergistic musculature. Following this procedure, up to 86% of
patients were capable of greater than 90 degrees of glenohumeral abduction that was not
previously possible.28 In addition, 91% of patients reported a significant decrease in pain postoperatively.28
Therapeutic techniques, both manual and exercise based have been shown to improve
prognosis and facilitate functional improvements if treatment begins within six months of injury.
Scapulo-thoracic manual mobilization has been found to significantly increase scapular and
glenohumeral range of motion. In addition, glenohumeral passive range of motion, as well as
assisted-active range of motion, exercises have been found to improve mobility. 29 The use of
14
passive and active-assisted range of motion exercises was found to significantly improve both
passive range of motion (PROM) and active range of motion (AROM) for all actions of the
scapula and humerus, including greater than 90 degrees of abduction in subjects where the
accessory nerve was damaged superior to cervical plexus contribution. 29 Scapulo-thoracic
strengthening involving retraction, depression and upward rotation, and elevation and downward
rotation used to promote scapulo-humeral rhythm have been found to produce the greatest EMG
results while restoring normal function.29 From EMG analysis, greatest activation of the middle
trapezius was seen during shoulder horizontal abduction with external rotation, while maximal
lower trapezius activation was seen during a prone overhead arm raise. 25 Exercises with the
highest EMG results include sport cord alternating pulls, focusing on retraction, overhead press,
focusing on depression and upward rotation, and shrugs, focusing on elevation and downward
rotation.29
Dissection
An elderly female cadaveric specimen that died as a result of complications related to
Alzheimer’s disease was the subject of this investigation. The dissection was completed from the
posterior aspect with the specimen in the prone position. The skin envelope was methodically
removed using the Grant’s dissector as a guide. Skin flaps were made anterior to posterior and
left to right in order to gain access to the calaveria. During this process, a lipoma was found on
the superior aspect of the frontal bone. The transverse cut was made around the calveria two and
a half inches superior to the base of the occiput. A wedge of the occipital bone was then cut
inferomedially. Musculature was methodically dissected by layers until transverse processes and
the sternocleidomastoid (SCM) muscles were visible. Bilateral pedilectomies and laminectomies
were completed in order to remove spinous and transverse processes at the levels of C1 and C2
15
to gain access to the spinal cord and the brain stem. Structures were dissected and identified
based on bony and soft tissue landmarks.
Figure 3: Connection between Cranial (CAN) and Spinal (SAN) Nerve Roots of the
Accessory Nerve (CNXI)
Figure 4: Posterior path of Accessory Nerve (CNXI)
in relationship to the Internal Jugular Vein
16
The specimen had a clear connection of the cranial and spinal roots of the accessory
nerve inside the jugular foramen, which is described as a variation in the literature (Figure 3).
This connection is similar to the one reported by Ryan et al3 as the connection is made at an
oblique angle distal to the jugular foramen. Upon exit from the jugular foramen, this specimen
exhibited a posterolateral path of the accessory nerve (Figure 4). This is considered a variation
based on various intra-operative and cadaveric studies reported in the literature.
Figure 5. Innervation of SCM and Trapezius
Figure 6. Ascending spinal root of
Muscles by the Accessory Nerve (CNXI)
Accessory Nerve (CNXI)
17
Figure 7. Accessory Nerve (CNXI)
Figure 8. Cervical plexus providing peripheral
spatial relationship to spinal cord
sensory contribution to the trapezius
Along this path, a contribution from the level of the C3 nerve root is visible which is
consistent with the literature, and has been reported in EMG studies to supply partial innervation
to the SCM muscle. The nerve then bifurcated into two portions upon the entry of the superior
third of the SCM muscle, with one portion creating a webbing innervation of the muscle, and the
other piercing through and travelling to the trapezius muscle (Figure 5).
On the contralateral side, the posterior cervical region was dissected in order to
investigate the ascending spinal accessory nerve as well as cervical plexus contribution. Spinal
nerve rootlets were identified from anterior rami and from its ascending path next to the spinal
cord, and pictured at the level of C3 (Figure 6). In addition, the cervical plexus was seen to
contribute innervations directly to the trapezius at the levels of C3 and C4 (Figure 8). Overall,
this serves to show the complexities of SCM and trapezius innervations.
18
Conclusion
This research was intended to broaden the understanding of the structure and function of
the accessory nerve in order to improve differential diagnosis during evaluation, knowledge of
prognosis, and treatment of accessory nerve damage. From literature review, it was determined
that in the majority of the population, a distinct connection between the cranial and spinal roots
of the accessory nerve is not present. However, a dissection case report was presented where
these neural elements co-mingled. As a result, in some cases manual muscle testing may be
successful in determining damage. In addition, it is critical in TBI assessment, as CNXI nerve
damage following TBI is indicative of a high mortality rate. However, as a result of the evidence
for the lack of a consistent connection, as well as a complex relationship to the cervical plexus,
manual muscle testing is not conclusive nor an absolute determinant in differential diagnosis.
In the literature, there is the suggestion that the accessory nerve may be predominant in
the posterior triangle and follow purely superior to inferior path reflecting possible increased risk
to both direct trauma as well as stretch-based pathologies such as neuropraxia with lateral flexion
to the opposite side and scapular depression on the same side as the injury. The combination of
these etiologies may present the greatest risk to the nerve as lateral flexion to the opposite side
puts the nerve on stretch, bringing it most superficial. It is clear that the greatest risk for the
accessory nerve outside of the vertebral column is iatrogenic injury from radial neck dissection.
The frequency of cervical contributions, whether directly to the target tissue or through
connection to the accessory nerve influences the level of functionality of the innervated muscle.
Complete excision of the accessory nerve more often results in loss of the upper trapezius than
any other portion of the muscle. As a result, scapular dyskinesia, especially during scapular
depression and upward rotation that are necessary for glenohumeral abduction may be an
19
indicator of possible injury. In addition, the scapular flip sign is proposed as a possible tool to
differentiate between scapular winging from trapezius denervation and serratus anterior
denervation.
Once accessory nerve damage is diagnosed, treatment within six months of original
injury results in greater outcomes. In non-iatrogenic injuries, physical therapy techniques as well
as motor neuron grafts could result in full recovery from axonotmesis if treated within six
months. However, prognosis was poor following iatrogenic excision regardless of the timetable.
Overall, the main predictor of prognosis was the length of time that was taken for diagnosis.
Therapeutic exercise has also been found to be effective especially with range of motion
exercises and integrated, resisted exercises that improve scapulo-humeral rhythm. Most effective
exercises include scapular elevation for the upper trapezius, horizontal abduction with
glenohumeral external rotation for the middle trapezius, and the prone overhead arm raise for the
lower trapezius. However, exercise interventions are only effective if implemented within six
months of initial injury.
Improved anatomical knowledge is critical in differential diagnosis, in order to expedite
the time between injury and treatment resulting in better patient outcomes. In addition, increased
knowledge in rehabilitation settings allows for the creation of an optimal, evidence-based plan of
care.
20
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