Patients with cervical radiculopathy (CR) are frequently encountered

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1 Cervical Radiculopathy or Parsonage-Turner Syndrome: Differential Diagnosis of a Patient With Neck and Upper Extremity Symptoms Christopher J. Mamula, MPT, ATC 1 Richard E. Erhard, PT, DC 2 Sara R. Piva, PT, MS, OCS, FAAOMPT 3 Journal of Orthopaedic & Sports Physical Therapy Study Design: Resident s case problem. Background: The signs and symptoms of cervical radiculopathy (CR) warrant the consideration of several other conditions in CR s differential diagnosis. One condition that may mimic CR, which is not well known amongst physical therapists, is Parsonage-Turner syndrome (PTS). PTS is characterized by an onset of intense pain that typically subsides within days to weeks. However, as pain subsides, weakness and/or paralysis may develop in upper extremity muscles. The purpose of this resident s case problem is to describe a patient who presented to our clinic with a diagnosis of CR, but had findings consistent with PTS. Diagnosis: The patient was a 43-year-old male referred to physical therapy with a diagnosis of CR. He had a previous episode of CR 1 year ago that was treated successfully. He had positive magnetic resonance imaging findings of structural abnormalities suggestive of causative factors for CR. The patient was treated for CR with thoracic and cervical spine manipulations and intermittent cervical traction. The initial acute severe pain subsided, but weakness in the upper extremity worsened. Diagnosis of PTS was made upon exclusion of other potential confounding diagnoses and the findings of fibrillation potentials and positive waves in electrodiagnostic studies. Discussion: CR and PTS are characterized by pain in the cervical spine, shoulder, and upper extremity. CR generally has an insidious onset, while PTS has a rapid onset of intense pain. Symptoms of CR are exacerbated with neck movements, while symptoms related to PTS should not be exacerbated with neck movements. In patients that do not respond to conventional therapy and have a progression of upper extremity muscle weakness, regardless of decreased pain, the diagnosis of PTS should be considered. J Orthop Sports Phys Ther 2005;35: Key Words: cervical spine, neck, nerve, upper extremity Patients with cervical radiculopathy (CR) are frequently encountered in outpatient physical therapy practice. 19 The signs and symptoms of CR warrant the consideration of other conditions in CR s differential diagnosis. One uncommon condition that may mimic CR, which is not well known amongst physical therapists, is Parsonage-Turner syndrome (PTS). 1 Staff Physical Therapist/Athletic Trainer, Western PA Sports Medicine and Rehabilitation, Somerset, PA. 2 Assistant Professor, Department of Physical Therapy, School of Health and Rehabilitation Sciences, University of Pittsburgh, PA. 3 Instructor and Doctoral Candidate, Department of Physical Therapy, School of Health and Rehabilitation Sciences, University of Pittsburgh, PA. Address correspondence to Christopher J. Mamula, 346 Linda St, Johnstown, PA chirsmamula@hotmail.com CR is defined as disease of a cervical spine nerve root. 23 The onset of CR is typically insidious and the most common causes are cervical disc herniation or other space-occupying lesion, such as osteophytic encroachment, which may result in nerve root compression and/or inflammation leading to upper extremity symptoms. 1,18,23 Symptoms of CR are generally affected by neck movements and CR s primary manifestations are weakness in a myotomal pattern, decreased deep tendon reflexes, and sensory loss in a dermatomal pattern. Incidence of CR is highest in the fourth to fifth decade of life, when 2.1 cases per 1000 people have been reported. 23 The diagnosis of CR relies primarily on clinical examination. Diagnostic imaging, including magnetic resonance imaging (MRI), helps to identify the underlying structural abnormality possibly leading to CR; however, the imaging diagnostic accuracy for CR is very limited. 5,23 Because many individuals with positive imaging findings may be completely asymptomatic, the presence of cervical disc herniation, spondylosis, or osteophytic spurring of the intervertebral foramen is not RESIDENT S CASE PROBLEM Journal of Orthopaedic & Sports Physical Therapy 659

2 sufficient for establishing a diagnosis of CR with certainty. 1,8,23 Reliance on the clinical examination requires the consideration of several other conditions in the differential diagnosis process, such as shoulder pathology, peripheral nerve disorders, thoracic outlet syndrome, brachial plexus pathology, systemic disease, and spinal tumors. 1,23 The authors suggest the addition of PTS when considering the differential diagnosis of CR. PTS, also known as acute brachial neuritis, is an uncommon condition of undetermined etiology. 3,11,15,16 The disorder was first reported in the medical literature in 1897 and has been called Parsonage-Turner Syndrome since At that time, Parsonage and Turner published their findings of 136 servicemen with the disorder during World War II. 11,15 There have been several other published reports of epidemiologic clusters of PTS also. 3,4 The overall incidence has been estimated at 1.64 per individuals in a general population. 4 Incidence of PTS is highest in the third through seventh decades of life, with a peak around 55 years of age. 15 It is more common in males, with the reported ratio of males to females ranging from 2:1 to 11.5:1. 15 While etiology is uncertain, reports of viral infection or immunization preceding the onset of PTS have been published. 3,11,16 PTS has several hallmark features in its presentation. The first is an immediate onset of severe pain without antecedent trauma, often described as waking the patient from sleep. 11 Pain typically originates at the shoulder girdle and often radiates to the neck and upper extremity. Pain usually subsides spontaneously over days to weeks. 16 As pain decreases, weakness and sometimes paralysis and atrophy develop in the involved upper extremity muscles. 16 The lesion corresponds to peripheral nerve impairment rather than central involvement, therefore, weakness, decreased deep tendon reflexes, and mild sensory deficits are expected. 7 Weakness and decreased reflexes may be limited to a single peripheral nerve or be more diffuse, involving any combination of branches of the brachial plexus, peripheral nerves of the upper extremity, or cervical nerve roots. 6 Muscles innervated by the C5 and C6 nerve roots are more commonly involved. 6 The clinical presentation of PTS becomes more apparent over time, as the pain subsides and weakness persists or progressively worsens. 11 The disorder tends to be self-limiting, with good prognosis for full or near full resolution of pain and return of strength over a period of months to years. 3,7,11 The diagnosis of PTS is one that is made by exclusion and can be challenging, especially in a patient presenting soon after onset of symptoms. It may be confused with CR, other shoulder disorders including rotator cuff tear and adhesive capsulitis, amyotrophic lateral sclerosis, or peripheral nerve lesions. 11,15 Because of its presentation, PTS is frequently misdiagnosed. 15 Diagnosis may become clearer as the condition progresses from acute severe pain to persistent or progressive weakness as pain subsides. 15,16 Diagnostic testing can then be useful to rule out other conditions. After excluding other causes of brachial neuritis, electrodiagnostic testing performed approximately 21 days after onset of pain can help confirm the diagnosis of PTS. 15,16 Diagnostic electromyographic (EMG) results may be variable, but typically reveal acute denervation, indicating an axonal neuropathy. 15,16 Positive EMG findings include fibrillation potentials and positive waves, with predilection for upper plexus involvement. 15,16 Nerve conduction velocities often are normal. 15,16 A recent study suggested that the presence of edema in the affected muscles detected during a whole body MRI would be a useful diagnostic tool in PTS. 20 The purpose of this resident s case problem is to describe a patient that presented to our clinic with a diagnosis of CR. The patient had a previous episode of CR approximately 1 year earlier, with positive MRI findings of structural abnormalities consistent with CR, that was treated successfully. As the case progressed, the patient s presentation was consistent with a diagnosis of PTS. History The patient, a 43-year-old male, reported a sudden onset of left-sided neck and upper extremity pain that began 5 days prior to his first visit to our clinic. He stated he awoke with moderate cervical pain that worsened through the morning and radiated to the left upper extremity. He could not identify any movement, posture, or activity that affected the intensity of his symptoms. His past medical history was significant for prior neck pain and radicular symptoms, which were effectively treated by medication approximately 1 year prior to this recent onset of pain. He was unsure of the side of symptom involvement with the previous occurrence. His medical history was otherwise unremarkable and he reported using no medications. The neck disability index (NDI), the numeric pain rating scale, and the body diagram were administered as part of the patient history. The NDI is a reliable and valid tool to assess neck disability and complaints. 21 NDI is graded from 0% to 100%, where high values indicate maximum disability. The initial NDI was 40%, indicating moderate disability. The numeric pain rating scale is a reliable and valid measurement of pain intensity ranging from 0 (none) to 10 (extremely intense). The patient rated his pain at 4/10 for least pain and 660 J Orthop Sports Phys Ther Volume 35 Number 10 October 2005

3 movement. 16 There was limitation of movement and left side tenderness at the C5/C6 level during right side glide. Treatment and Outcomes Journal of Orthopaedic & Sports Physical Therapy FIGURE. Body diagram with the symptoms drawing of the patient at the first visit. 7/10 for worst pain in the previous 24 hours. 11,12 The patient drew his symptoms on the body diagram, which can be seen in the Figure. DIAGNOSIS Physical Examination Physical examination revealed limited active range of motion of the cervical spine in forward flexion to 25, extension to 55, left and right lateral flexion to 26 and 58, respectively, as measured with a gravity goniometer. The technique used to measure neck range of motion has been described in details elsewhere and demonstrated good reliability. 16,21 Using visual assessment, left cervical rotation was estimated to be limited by 40% compared to right rotation. Thoracic movements were visually assessed during patient active trunk rotation while seated with the hands on the opposite shoulders. Left thoracic rotation was minimally limited compared to right thoracic rotation. All cervical motions increased the left upper extremity symptoms. Brachioradialis deep tendon reflex (C6) was diminished (1+) on the left side as compared to the right side (2+). All the other deep tendon reflexes were deemed normal. Upper extremity manual muscle testing 13 revealed 5/5 grades bilaterally, with 2 exceptions: biceps brachii and wrist extensors on the left side were graded 4/5. A study that determined intrarater reliability of muscle strength grades reported Kappa values ranging from 0.65 to Passive intervertebral accessory movement of the cervical spine was tested with the patient in supine. The clinician passively glided each vertebral segment to both sides while assessing pain and limitation of Interventions at the first visit consisted of highvelocity, small-amplitude traction manipulation of the thoracic spine and then manipulation with traction and minimal rotation of the cervical spine. These 2 techniques have been described elsewhere. 17 Indications for thoracic dysfunction were limited forward flexion, with increased in distal symptoms and decreased left thoracic rotation. High-velocity, smallamplitude cervical manipulation was done with the goal of increasing the opening of the left intervertebral foramen between C5 and C6 in an attempt to release compression of the C6 spinal nerve on the left. Cervical spine active range of motion was immediately reassessed after the manipulation techniques and was increased to 36 for flexion, 65 for extension, 55 for left lateral flexion, and near full left cervical rotation. Right lateral flexion and rotation were unchanged. Thoracic rotation was symmetrical. Although not quantified, the patient reported decreased pain during the movements. Reassessment was followed with intermittent mechanical cervical traction. In our experience, patients with arm symptoms increased by neck movements and with myotomal weakness respond well to intermittent cervical traction. Traction was applied with the patient supine and the neck in approximately 25 of flexion (from the horizontal plane). Maximum pull was 11 kg (25 lb) of force for 25 seconds and minimum pull was 3 kg (7 lb) for 5 seconds. The patient tolerated the treatment without alteration of arm symptoms and reported decreased cervical spine pain. MRI for the cervical spine ordered by the referring physician was performed between the first 2 visits. The report indicated C5-6 herniated disc, with an associated osteophyte causing moderate right neural foramina stenosis and left mild neural foramina, and central canal stenosis at that level. Although all symptoms were on the left side, the imaging suggested anatomical abnormalities that were worse on the right. The patient reported some improvement in symptoms at the second visit 3 days later. He reported that he no longer had sharp pain below the elbow. Numeric pain rating scale rating was 3/10 for least pain and 7/10 for worst pain in the previous 24 hours. NDI score was 48% at this visit, representing increased self-perceived disability compared to the first visit. He also reported aching pain and numbness of the hand that was not reported at the first visit. Cervical active range of motion was improved from 25 to 45 of flexion, extension was unchanged RESIDENT S CASE PROBLEM J Orthop Sports Phys Ther Volume 35 Number 10 October

4 at 55, lateral flexion was symmetrical, and left rotation improved from 40% to approximately 25% deficit compared to right rotation. Left arm symptoms were increased with cervical spine flexion and right side flexion. Reflexes were noted to be equal bilaterally (2+). Manual muscle testing was not performed. After examination, thoracic and cervical manipulation and intermittent cervical traction were used, as performed during the first visit. No exercises were given to the patient but improving postural awareness while seated was discussed. On the third visit, 1 week after the second visit, cervical active range of motion was 35 for lateral flexion bilaterally, 35 for flexion, 58 for extension, and left rotation was still limited by approximately 25% as compared to right rotation. Pain was rated at 3/10 at best and 7/10 at worst over the previous 24 hours. NDI had decreased to 36%. Manual muscle testing revealed increased weakness of biceps brachii, shoulder external rotators, and wrist extensors, all graded as 4/5. At that time, the referring physician was contacted with the suggestion of performing electrodiagnostic testing. The test was deferred until 3 weeks after onset of symptoms. In the meantime, the patient was followed for 3 additional visits. Over this time the intensity of his pain slowly but consistently decreased and centralized. At the sixth visit, pain in the neck was rated 2/10 at worst over the previous 24 hours and the patient did not complain of upper extremity pain. Conversely, weakness progressively worsened and, by the sixth visit, shoulder external rotation strength on the left side was graded 1/5 by manual muscle testing, with only trace muscle activity noted by palpation. Otherwise, strength was noted to be normal throughout the left upper extremity, including the biceps brachii and wrist extensors, which had previously been weak. Brachioradialis reflex (C6) on the left was diminished (1+) compared to the right. At this time, nerve conduction velocity testing was performed for the median and ulnar nerves (sensory and motor), musculocutaneous and medial brachial cutaneous nerves (sensory), and axillary nerve (motor). Nerve conduction velocities were all normal. EMG was performed for the deltoid, biceps, triceps, pronator teres, flexor digitorum superficialis, abductor pollicis brevis, infraspinatus, serratus anterior, and latissimus dorsi. The results showed evidence of left infraspinatus P waves and fibrillations, suggesting mononeuropathy characterized as severe, with axonal loss. There were no other significant findings in the left upper extremity. The EMG report suggested this could be due to nerve entrapment or from brachial neuritis. After receiving the results the patient was followed for 2 more visits for a total of 8 visits over 4 weeks. At the time of the final visit the patient demonstrated full cervical active range of motion without local or referred pain on movement. He reported no pain, although he did report some residual numbness and sensation of heaviness of his left upper extremity. Left shoulder external rotation strength was not improved. Reflexes were deemed as normal (2+). His NDI was 36%. The limitations in the NDI appeared attributable mainly to the questions relating to lifting, work, driving, and recreational activities, all of which, according to the patient, were limited due to his continued weakness. The patient was discharged and was instructed in home exercises to maintain shoulder range of motion. The patient was followed up by phone at approximately 1 year after discharge. He denied receiving any further medical intervention. He reported that he continued to be relatively pain free, but had some mild persistent weakness and occasional soreness of the left shoulder with vigorous activity. DISCUSSION This patient was referred to our clinic with a diagnosis of CR. He had reported similar symptoms and diagnosis in the past, which were successfully treated with anti-inflammatory medications. Thus the patient and referring physician assumed a recurrence of the prior condition. CR and PTS both do have features that can cause them to be easily confused, particularly at the time of onset. Both conditions are characterized by pain in the cervical spine, shoulder, and upper extremity, and have higher incidence around the fifth decade of life. Both CR and PTS typically occur spontaneously and without trauma. 4,23 CR generally has an insidious onset, with presentation varying from patient to patient, 1,23 while PTS is more consistently described as having a rapid onset of intense pain, frequently described as waking the patient from sleep. 11,14,15 However, because in some instances CR may have a rapid onset, the original clinical presentation of this patient was not considered unusual. Furthermore, the patient did not have any recent illness or vaccination that has been associated with PTS. 3,11,15 Symptoms of CR are typically exacerbated with neck movements, as seen in this patient, while symptoms of PTS are not. The patient presented with some limitation in cervical range of motion and had reproduction of symptoms with cervical movement that confounded initial diagnosis. During the initial visit we concluded that the pain and limitation in neck movements were indications of a mechanical neck dysfunction in the lower cervical spine, which was probably causing a compression/inflammation of a nerve root resulting in CR. The decreased brachioradialis reflex (1+) and weakness of the biceps brachii and wrist extensors (4/5) was an indication of a CR likely affecting the C6 nerve root. The treatment administered during the initial visits did seem to offer some improvement with pain, movement, and the strength of the biceps 662 J Orthop Sports Phys Ther Volume 35 Number 10 October 2005

5 and wrist extensors. However, the new finding of weakness of the shoulder external rotators raised concerns. CR affecting C6 nerve root could have caused the external rotation weakness. However, the fact that the shoulder external rotation weakness was progressive and not showing improvement, along with decreased pain and increased strength of the biceps and wrist extensors, were key findings that suggested further investigation with electrodiagnostic testing. During the third visit electrodiagnostic testing was suggested to try to clarify the source of weakness. Nerve conduction velocity results were all normal as would be expected with PTS. 15 EMG is the electrodiagnostic testing recommended to help confirm the diagnosis of PTS. 8,15,16 In this case, EMG findings indicated that there was an isolated suprascapular nerve lesion. Other causes of this type of isolated nerve lesion are trauma, radical neck dissection, and ganglion cysts. 2 The first 2 causes were able to be ruled out by patient history. Shoulder MRI could further investigate the possibility of a ganglion cyst and could also have ruled out primary shoulder pathology, such as rotator cuff tear. After having the EMG results, we did not elect to request shoulder MRI. PTS typically affects the upper trunk of the brachial plexus, which is formed by the C5 and C6 nerve roots. The suprascapular nerve exits the upper trunk of the brachial plexus and is also formed by the C5 and C6 nerve roots. We believe the initial neuritis caused by the PTS affected not only the suprascapular nerve, but also the surrounding upper trunk of the brachial plexus. Perhaps the EMG only showed damage at the suprascapular nerve because it may have been the focal point of the inflammation. A neuritis affecting the upper trunk of the brachial plexus and the proximal suprascapular nerve would likely cause diminished reflexes and weakness of the muscles innervated by the C5 and C6 nerve roots, and pain in the lateral arm and forearm. Our patient had diminished brachioradialis reflex, lateral arm and forearm pain, and weakness in the biceps (C5/C6), wrist extensors (C6/C8), and shoulder external rotators (C5/C6), which may all be explained by PTS. As it has been reported that PTS causes neck pain, 16 our patient s complaint of neck pain could also be explained by PTS. The limitation in neck range of motion could have been caused by muscle guarding due to the pain. It could also have suggested the presence of a concomitant mechanical neck dysfunction. In this case, the patient s initial severe pain subsided and weakness progressed, which is a trademark of PTS. This was clearly observed during the patient s sixth visit, as he was demonstrating pain resolution and normal cervical range of motion, but had severe weakness with external rotation of the shoulder. Shoulder external rotation weakness was not a finding during his initial examination. The patient s presentation should remind physical therapists that the resolution of pain is not always a sign of patient s progress. Given the patient s presentation of acute pain followed by weakness, and EMG findings of brachial neuritis consistent with a diagnosis of PTS, we felt quite confident in the diagnosis of PTS. This diagnosis is supported by the patient s continued improvement of strength and lack of pain at 1 year, despite no additional intervention. Because there is no reference standard to diagnose PTS, we cannot completely discard the possibility that the patient s signs and symptoms were caused by a mechanical neck dysfunction that caused a CR; but we do believe, in retrospect, that CR was very unlikely given the progression of symptoms and signs, as well as EMG findings, all of which were consistent with PTS. This patient was seen before we had access to the evidence that the presence of muscle edema during whole body MRI helps the diagnosis of PTS, 9 so we did not order such imaging. We suggest that future research further investigate a reference standard for this disorder. The treatment administered seems to have helped any potential concomitant neck problem, but likely had minimal effect on the overall outcome of PTS for this patient. We initially were providing treatment under the assumption of a mechanical cervical dysfunction due to the unremarkable initial presentation. There is no evidence of any intervention being particularly useful in the treatment of PTS. The signs and symptoms of PTS are generally described as self-limiting, with good prognosis for full or near full recovery of pain and strength without treatment. 15,16 We suggest that the importance of being aware of PTS is to recognize this disorder, which will assist in the process of obtaining a proper diagnosis, and reassuring the patient about the potential recovery. It has been reported that the frequent misdiagnosis of PTS had lead to unnecessary interventions, including surgical procedures. 3,11,16 Following the initial physical therapy session, the patient had an MRI of the cervical spine. The diagnostic value of the MRI in this particular patient was to rule out other potential pathologies. The MRI results indicated anatomical alterations that could cause CR. 1,23 However, it has been suggested that treatment should proceed based upon patient s presenting symptoms and physical findings, as imaging findings are not always clearly correlated to patient presentation. 18 In this case, anatomic alterations were significantly worse on the uninvolved side where the patient was symptom free. CONCLUSION PTS is an uncommon disorder that should be considered in the differential diagnosis of patients presenting with neck, shoulder, and upper extremity RESIDENT S CASE PROBLEM J Orthop Sports Phys Ther Volume 35 Number 10 October

6 symptoms. PTS is a diagnosis of exclusion that often becomes more apparent as the case progresses. PTS symptoms should not be exacerbated by cervical movement or provocation tests, as would be expected of symptoms associated with CR. MRI or other imaging techniques may help to rule out discogenic or shoulder pathology. 15 However, as demonstrated with this patient, MRI results must be interpreted carefully and correlated with findings of the physical examination. In addition to CR, other pathologies, including lesions of the shoulder, brachial plexus, and peripheral nerves, must be ruled out to arrive at a diagnosis of PTS. The diagnosis of PTS will become more obvious through the patient s history as the case progresses from the initial onset of severe pain to increasing upper extremity weakness. As this pattern of pain followed by weakness is noted, diagnosis may be confirmed through electrodiagnostic testing. Once a diagnosis of PTS has been established, treatment is largely supportive, consisting of analgesics as needed and exercise to maintain range of motion and assist in restoring upper extremity strength. In most cases prognosis is excellent for full resolution of pain and full to near full return of strength. REFERENCES 1. Ahlgren BD, Garfin SR. Cervical Radiculopathy. Orthop Clin North Am. 1996;27: Anto C, Aradhya P. Clinical diagnosis of peripheral nerve compression in the upper extremity. Orthop Clin North Am. 1996;27: Auge WK, 2nd, Velazquez PA. Parsonage-Turner syndrome in the Native American Indian. J Shoulder Elbow Surg. 2000;9: Beghi E, Kurland LT, Mulder DW, Nicolosi A. Brachial plexus neuropathy in the population of Rochester, Minnesota, Ann Neurol. 1985;18: Bredella MA, Tirman PF, Fritz RC, Wischer TK, Stork A, Genant HK. Denervation syndromes of the shoulder girdle: MR imaging with electrophysiologic correlation. Skeletal Radiol. 1999;28: Claussen GD, Tseng A, Mussel H, Kwon KH, Oh SJ. Cervical root involvement in neuralgic amyotrophy. Muscle Nerve. 1997;20: Darby MJ, Wass AR, Fodden DI. Neuralgic amyotrophy presenting to an accident and emergency department. J Accid Emerg Med. 1997;14: de Araujo MP. Electrodiagnosis in compression neuropathies of the upper extremities. Orthop Clin North Am. 1996;27: Erhard RE. Manual Therapy in the Cervical Spine. Home Study Course. Alexandria, VA: American Physical Therapy Association, Orthopedic Section; Florence JM, Pandya S, King WM, et al. Intrarater reliability of manual muscle test (Medical Research Council scale) grades in Duchenne s muscular dystrophy. Phys Ther. 1992;72: ; discussion Helms CA, Martinez S, Speer KP. Acute brachial neuritis (Parsonage-Turner syndrome): MR imaging appearance report of three cases. Radiology. 1998;207: Jensen MP, Miller L, Fisher LD. Assessment of pain during medical procedures: a comparison of three scales. Clin J Pain. 1998;14: Katz J, Melzack R. Measurement of pain. Surg Clin North Am. 1999;79: Kendall FP, McCreary EK, Provance RG. Muscles Testing and Function. 4th ed. Baltimore, MD: Williams & Wilkins; McCarty EC, Tsairis P, Warren RF. Brachial neuritis. Clin Orthop Relat Res. 1999; Misamore GW, Lehman DE. Parsonage-Turner syndrome (acute brachial neuritis). J Bone Joint Surg Am. 1996;78: Piva SR, Childs JD, Erhard RE, Browder DA. Intertester reliability of passive intervertebral and active movements of the cervical spine. Man Ther. In press. 18. Piva SR, Erhard RE, Al-Hugail M. Cervical radiculopathy: a case problem using a decision-making algorithm. J Orthop Sports Phys Ther. 2000;30: Radhakrishnan K, Litchy WJ, O Fallon WM, Kurland LT. Epidemiology of cervical radiculopathy. A populationbased study from Rochester, Minnesota, 1976 through Brain. 1994;117 ( Pt 2): Ryan M, Twair A, Nelson E, Brennan D, Eustace S. Whole body magnetic resonance imaging in the diagnosis of Parsonage Turner syndrome. Acta Radiol. 2004;45: Vernon H, Mior S. The Neck Disability Index: a study of reliability and validity. J Manipulative Physiol Ther. 1991;14: Wainner RS, Fritz JM, Irrgang JJ, Boninger ML, Delitto A, Allison S. Reliability and diagnostic accuracy of the clinical examination and patient self-report measures for cervical radiculopathy. Spine. 2003;28: Wainner RS, Gill H. Diagnosis and nonoperative management of cervical radiculopathy. J Orthop Sports Phys Ther. 2000;30: J Orthop Sports Phys Ther Volume 35 Number 10 October 2005