|SYMPOSIUM - CERVICAL SPONDYLOMYELOPATHY
|Year : 2019 | Volume
| Issue : 1 | Page : 13-19
Clinical spectrum and importance of evaluation systems in degenerative cervical myeloradiculopathy
Ganesh Swaminathan, Vetrivel Muralidharan, Baylis Vivek Joseph
Department of Neurological Sciences, Division of Neurosurgery, Christian Medical College and Hospital, Vellore, Tamil Nadu, India
|Date of Web Publication||11-Jan-2019|
Dr. Baylis Vivek Joseph
Department of Neurological Sciences, Division of Neurosurgery, Christian Medical College and Hospital, Vellore - 632 004, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Degenerative cervical myelopathy includes facet joint arthropathy and/or intervertebral disc prolapse, as well as aberration (hypertrophy, calcification, or ossification) in the ligamentum flavum, and/or posterior longitudinal ligament. Cervical spondylotic myelopathy and ossification of posterior longitudinal ligament are two major conditions under this spectrum. Patients with degenerative changes of the cervical spine can present with wide spectrum of symptoms and signs ranging from axial neck pain, radiculopathy or myelopathy. A combination of history, physical examination, and provocative tests such as Spurling's sign, shoulder abduction test, neck distraction test, Valsalva maneuver, Elvey's upper limb tension/brachial plexus tension test increase the likelihood of diagnosis of cervical radiculopathy. Myelopathy can manifest in the early stage as subtle changes in the upper limb dexterity or mild walking difficulty and in late stage with severe spasticity and flexor spasms. Clinicians are increasingly using quantitative or semi-quantitative scales of neurological impairment. However, there is no gold standard evaluation systems that can reliably assess disease severity.
Keywords: Cervical spondylosis, myelopathy, neck pain, Nurick grade, radiculopathy
|How to cite this article:|
Swaminathan G, Muralidharan V, Joseph BV. Clinical spectrum and importance of evaluation systems in degenerative cervical myeloradiculopathy. Indian Spine J 2019;2:13-9
|How to cite this URL:|
Swaminathan G, Muralidharan V, Joseph BV. Clinical spectrum and importance of evaluation systems in degenerative cervical myeloradiculopathy. Indian Spine J [serial online] 2019 [cited 2023 Mar 28];2:13-9. Available from: https://www.isjonline.com/text.asp?2019/2/1/13/249902
| Introduction|| |
The term degenerative cervical myelopathy (DCM) was proposed in 2015 and was defined as symptomatic cervical myelopathy associated with a broad variety of degenerative changes of the extradural spinal tissues in the cervical spine., This spectrum includes facetal joint arthropathy and/or intervertebral disc prolapse, as well as aberration (hypertrophy, calcification, or ossification) in the ligamentum flavum, and/or posterior longitudinal ligament. Cervical spondylotic myelopathy and ossification of posterior longitudinal ligament are two major conditions under this spectrum.
Boden et al. found that 95% of men and 70% of women in the age group of 60–65 years, have evidence of degenerative changes on a lateral cervical spine radiograph, in a cohort of 200 asymptomatic patients. Asymptomatic spondylotic changes in cervical spine magnetic resonance imaging were noted in up to 20% of patients below 64 years of age, and 57% of patients above 64 years of age, and asymptomatic spinal cord impingement was observed in 16% of patients under 64 years of age, and 26% of patients over 64 years of age. Hence, a thorough clinical evaluation with detailed assessment of functional status of these patients is essential in surgical decision making and predicting outcomes.
| Clinical Spectrum of Cervical Degenerative Conditions|| |
Patients with degenerative changes of the cervical spine can present with wide spectrum of symptoms and signs, ranging from axial neck pain, radiculopathy, myelopathy or a combination of the above.
Neck pain can be an initial manifestation in patients with degenerative spondylosis, and can be associated with neck stiffness. The pain is diffuse dull aching type and is characteristically exacerbated by neck movements. Other common features of neck pain in degenerative spondylosis are referred pain to the occiput, pain between the shoulder blades and pain radiating to the upper limbs. Vague pain and diffuse paresthesias in the limbs, dizziness or vertigo, syncope, migraine or pseudo-angina are rare manifestations.
Neck pain associated with “red flag” signs mentioned in [Table 1] should be evaluated for a more serious underlying illness or other systemic etiologies.
|Table 1: Red flags that may suggest malignancy, infection, or inflammation|
Click here to view
Radiculopathy is defined as compression or irritation of a nerve root as it exits the spinal canal by a prolapsed intervertebral disc or an uncovertebral osteophyte. The diagnosis can be made based on history in majority of cases. C7 (C6–C7 herniation) is the most commonly affected root, followed by the C6 (C5–C6 herniation) and C8 (C7–T1 herniation). Impingement of the nerve root by disc material causes local ischemia and triggers a pro-inflammatory cascade mediated by tumor necrosis factor-alpha, interleukin factor-6, and matrix metalloproteinases all of which results in nerve damage.
Disc degeneration leads to a reduction in the disc space height resulting in narrowing of the neural foramen. This further increases the load on the intervertebral joints of Luschka (uncinate joints) and the vertebral body resulting in bony overgrowth. Hypertrophy of the uncinate joint leads to foraminal stenosis and cervical radiculopathy. Hypertrophy of the vertebral endplates can lead to canal stenosis and result in myelopathy due to cord compression.
Clinical localization and characterization
The nature and location of pain and sensory symptoms, motor weakness and diminished deep tendon reflexes (DTR's) help in localizing the level of lesion. Patients with cervical radiculopathy present with neck pain that is usually lateralized to the side of nerve root compression. The pain may radiate to the ipsilateral arm along the affected dermatome, but the absence of arm pain does not rule out cervical radiculopathy. This may be associated with numbness along the affected dermatome, weakness in the corresponding myotome and diminished or absent DTRs. The inter-observer reliability of sensory and motor testing in patients with cervical radiculopathy is only moderate (Kappa statistic 0.4–0.64). An absent deep tendon reflex has good localizing value and correlated with the level of pathology in 82% of cases.
Neurological signs and symptoms for each root is described in detail below.
C1 does not have a dorsal root and hence only results in motor symptoms. Motor deficits manifest as weakness of neck flexion and extension.
The pain is localized to the occiput and neck, with diminished or absent sensations over the scalp posterior to inter-aural line. The motor deficits are in the form of weakness of neck flexion and rotation.
Here, the pain is localized to the occiput and the neck with sensory deficits in the lower occiput and upper neck regions. Motor deficits may be in the form of weakness of neck flexion, rotation and diaphragmatic weakness.
The pain and sensory deficits are localized to the lower neck. There can be weakness of lateral neck flexion, scapular elevation, adduction and also diaphragmatic weakness.
Pain is present in the neck, shoulder, and anterior aspect of the arm, with sensory deficits along the lateral aspect of arm. Motor deficits can manifest as weakness of deltoid, external rotators of arm, and flexors of the elbow. The biceps jerk can be diminished or absent.
Pain radiates along the lateral arm and dorsal forearm. Sensory deficits are located in the lateral forearm, lateral arm, first and second digits. Motor deficits result in weakness of forearm flexion, pronation, finger and wrist extension. Brachioradialis reflexes can be diminished or absent.
Pain is located in the dorsal forearm, with sensory deficits in the third and fourth digits. There can be weakness of arm extension, finger, and wrist flexors and extensors. Triceps jerk can be diminished or absent.
Pain and sensory deficits are localized to the medial forearm, hand, and the 5th digit. Motor deficits are mainly in the form of weakness of intrinsic hand muscles. Finger flexor reflex can be diminished or absent.
Special Clinical Tests
Clinical tests which aid in the diagnosis of cervical radiculopathy and exclude shoulder pathologies have been described below. These include Spurling's sign, shoulder abduction test, neck distraction test, Valsalva maneuver, Elvey's Upper limb/ Brachial plexus tension test (ULTT). The most commonly used provocative test in routine clinical practice is the Spurling's sign.
The test is performed by turning the patients head to the affected side and simultaneously applying axial loading force, and extending the neck. The test is considered positive when the patient experiences pain in the neck and the ipsilateral upper limb along the dermatome that corresponds to the affected root. Additional maneuvers, such as neck rotation or rotation with neck extension which result in narrowing of the neural foramen, can be used to reproduce patients symptoms.
Rubinstein et al. in their systematic review concluded that Spurling's test demonstrated low-to-moderate sensitivity and high specificity, as did traction/neck distraction, and Valsalva's maneuver in degenerative spondylotic myelopathy.
Shah and Rajshekhar have reported that Spurling's test has a sensitivity of 92% and specificity of 95% with positive predictive value of 96.4% and negative predictive value of 90.9% in predicting a diagnosis of a soft lateral cervical disc prolapse.
Shoulder abduction test
This test is performed by asking the seated patient to place their hand over the vertex of their head. The asymptomatic arm is used first to help establish a baseline finding for the side assumed to be normal and then repeated on the side with symptoms. The patient should hold the hand in the testing position for 5–10 seconds. Patients with shoulder pathology will have worsening of pain during the test, and those with radicular pain due to root compression will have pain relief.
Upper Limb Tension Test (ULTT)
The shoulder, elbow, forearm, wrist, and fingers are kept in specific position to put stress on particular nerves (nerve roots proximally and peripheral nerve distally). Further, modification of each joint is done as “sensitizer.” The ULTT's are the upper limb equivalent to the straight leg raise for the lumbar spine roots. Each test is done on the normal/asymptomatic side first. The order of joint positioning is as follows: shoulder followed by forearm (pronation/supination), wrist, fingers, and finally elbow (flexion/extension). Each joint positioning component is added until the pain is provoked or symptoms are reproduced. To further sensitize the upper limb tests, lateral flexion of cervical spine can be added. If pain is provoked in the very initial position, there is no need to add further sensitizers.
The upper limb tension test (ULTT) demonstrated high sensitivity and low specificity, while the shoulder abduction test demonstrated low-to-moderate sensitivity and moderate-to-high specificity. Common methodological flaws included lack of an optimal reference standard, disease progression bias, spectrum bias, and review bias.
Neck distraction test
The patient lies supine and the neck is comfortably positioned. The examiner securely grasps the patient's neck, either by placing each hand around the patient's mastoid processes, while standing at the head end of the table placing one hand on the patient's forehead and the other on the occiput. Slight flexion of the patient's neck along with pulling the head toward the examiner is done to apply a distraction force. A positive test is the reduction or elimination of symptoms with traction as the maneuver relieves compression of the root.
Thoomes et al. concluded that there is limited evidence for accuracy of physical examination tests for the diagnosis of cervical radiculopathy. When consistent with patient history, clinicians may use a combination of Spurling's and axial traction to increase the likelihood of a cervical radiculopathy. The sensitivity and specificity of each test is tabulated in [Table 2].
Radhakrishnan et al. showed that at 4-year follow-up, nearly 90% of patients with cervical radiculopathy were either asymptomatic or only mildly symptomatic, without any surgical intervention. A recent systematic review of literature seeking to evaluate the course of untreated cervical radiculopathy concluded that the majority of patients see substantial improvements within 4–6 months which is generally maintained over 2–3 years. This systematic review also showed that there was no progression to myelopathy in patients with cervical radiculopathy.
| Myelopathy|| |
The cervical myelopathy syndrome was first described in 1952, by Brain and colleagues. The primary pathophysiological change that leads to cervical myelopathy is a reduction in the sagittal diameter of the spinal canal. Static and dynamic factors are responsible for spinal cord damage, in the setting of a narrowed canal. Vascular factors also contribute to additional spinal cord injury. Myelopathy manifests with symptoms and signs involving upper and lower limbs. Recognition of severe cervical myelopathy is straightforward because the clinical manifestations are so dramatic. There is weakness of all four extremities together with a sensory level, below which there is reduced or absent appreciation of pain, touch, vibration, or position sense. Reflexes are exaggerated and may be self-sustaining as with ankle clonus. Muscular tone is increased, and some degree of spasticity of the extremities is present. This increased muscle tone is also present in the bladder wall, producing frequency and nocturia.
In Indian scenario, early symptoms such as loss of dexterity and subtle paresthesia may be overlooked till profound disability limits the activities of daily living. Hence, it is important to have a high index of clinical suspicion for DCM and should look for possible signs.
This includes neck pain, neck stiffness, loss of dexterity (writing, typing, drawing and other learned skills using hands), slippage of objects from hand, thinning of muscles of hand, tingling sensation in hands and toes, decrease in pace of walking and not able to keep up with peers due to stiffness of the lower limbs.
Inability to mix food/tear chapatti, buttoning/unbuttoning shirts, loss of hand grip, inability to lift hand overhead, inability to walk, difficulty in rolling over side to side in bed, flexor spasms and being bedridden. Autonomic symptoms include increased urinary frequency, incomplete evacuation, constipation and erectile dysfunction.
Upper limb manifestations
Upper limb involvement is invariably present in almost all cases of cervical spondylotic myelopathy. The patient presents with difficulty in performing fine motor tasks such as buttoning or unbuttoning of shirt, eating with hand/spoon, typing on a computer keyboard, using mobile phones, or a recent change in handwriting., They may complain of pain, paresthesias, and numbness in the upper limbs which is usually diffuse, but at times can have a dermatomal pattern, with exaggerated upper limb reflexes and clumsiness of the hands. Examination findings are usually asymmetrical and include wasting of the upper limb and parascapular muscles with associated weakness.
The sensory examination can be variable depending on the level of compression, characterized by loss of touch and pinprick sensation. In cases with profound posterior column dysfunction, it is not uncommon to find involuntary, slow, writhing stereotyped piano playing movements which worsen with eye closure called pseudoathetosis, resulting from loss of proprioception and dystonia during writing secondary to deafferentation.
High versus low cervical cord compression localization
All the upper limb DTR's may be exaggerated in high cervical cord compression (C2 and above). In patients with compression at lower cervical levels (below C2) an absent deep tendon reflex corresponds to the level of compression and has a good localizing value.
The inverted supinator reflex, introduced by Babinski in 1910 is characterized by reactive flexion of the ipsilateral fingers while eliciting the brachioradialis reflex. Although not a true inverted reflex, it is widely accepted as pathognomonic for spinal cord compression at C5–C6 level. A true inverted triceps reflex characterized by paradoxical elbow flexion, can be caused by a compressive lesion at C7, due to activation of the antagonist muscles. Hyperactive pectoralis reflex and scapulothoracic reflex may indicate upper cervical cord compression, but are of uncertain clinical significance. The presence of ipsilateral Horner's syndrome maybe seen in lower cervical cord compression due to involvement of the cervical sympathetic chain. The jaw jerk is contraction of the masseter and temporalis muscles when the patient's lower jaw is tapped. The afferent limb is through the mandibular division of the trigeminal nerve to the mesencephalic nucleus of the trigeminal nerve and the efferent limb also travels through mandibular fibers that originate in the motor nucleus of the trigeminal nerve. Lesions anywhere along this reflex arc result in the depression of the ipsilateral jaw reflex, whereas bilateral supranuclear lesions result in an accentuated response.
Hoffman and Tromner sign
Hoffman sign is elicited by flicking downward on the nail of the middle finger, causing forced flexion, resulting in an involuntary flexion of a varied combination in the neighboring fingers. It was found to be a highly sensitive marker for occult cervical cord compression when present bilaterally.
Tromner sign is elicited by flicking the palmar surface of the distal phalanx of the middle finger, held partially flexed between the examiner's finger and thumb, while grasping the subject's hand, with the wrist in a relaxed dorsiflexed position. A positive response is described as involuntary flexion of the subject's distal phalanxes of both index finger and thumb. It was found to have high sensitivity (94%) and relatively high negative predictive value (85%) and was found to be useful in ruling out DCM.
Additional signs of cervical myelopathy in the upper limbs include deficient adduction and/or extension of the ulnar two or three fingers which is described as the finger escape sign. This is further divided into five grades (0–4) based on the severity of involvement and reduction in the ability to grip and release rapidly with fingers (normal individuals can grip and release 20 times in 10 s).
The presence of these signs indicate the involvement of upper cervical spinal cord, and its absence in patients with marked spastic paraplegia, indicates a lesion at or below the cervicodorsal junction.
Cervical spondylotic amyotrophy (CSA)
DCM can present with a clinical syndrome characterized by extensive muscular atrophy in the upper extremities, with less prominent sensory deficits and lower extremity symptoms. The proximal-type patients have atrophy of the C5 and C6 myotomes and the distal-type amyotrophy have atrophy of C7, C8 and T1 myotomes. The examination findings are usually unilateral and include weakness of shoulder abduction, positive arm-drop sign, or positive wrist-drop sign. Severe atrophy of the neck muscles can be present with dropped head syndrome. Distal-type CSA is a rare form of CSM that should be differentiated from motor neuron disease on the basis of subtle sensory symptoms or signs in the upper limbs, and the presence of significant cord compression on the MR imaging as these patients have been reported to have good outcome with central corpectomy. In addition, characteristic EMG findings will be present in the lower limb and bulbar muscles in motor neuron disease, but not in distal-type CSA.
Finally, patients with cervical myelopathy have decreased range of shoulder movements often due to periarthritis of the shoulder. This should be considered when the patient has restricted shoulder movements and complains of pain, during passive movements of the shoulder and this should not be interpreted as weakness.
Lower limb manifestations
Lower limb involvement in DCM is often asymmetrical and has a distal to proximal progression. Patients typically complain of walking difficulty which is characterized by tightness of the lower limbs, an unstable gait with tendency to fall forward on walking fast and on uneven ground. Indian patients can complain of loss of ability to grip footwear, buckling of knees, and inability to stand up from squatting position due to proximal muscle weakness.
Examination findings include spasticity of lower limbs with or without ankle and/or patellar clonus. Flexor spasms characterized by involuntary muscle contractions resulting in dorsiflexion at the ankle, with flexion at the knee and hip, can occur as a result of nociceptive spinal release reflex and indicates spinal cord compression. Reliable examination of motor power may not be feasible in a background of severe spasticity. Sensory findings include loss of touch and pinprick sensation. Posterior column involvement is characterized by loss of joint position and vibration sense, often coupled with a positive Romberg sign due to loss of postural control in the absence of visual input.
The knee and ankle jerks will be exaggerated and the plantar response is extensor. A positive Babinski's sign has a high specificity (99%, 95% confidence interval: 97.7–100) in identifying involvement of the corticospinal tracts.
Urinary disturbance usually occurs later in the disease process and may lead to progressive renal damage if neglected. The presence of neurogenic bladder is considered to be an indication for surgery. Feeling of urinary urgency, sense of difficulty in passing urine, incomplete evacuation of bladder, and nocturia are common presentations.
More objective methods are maintaining a voiding diary in which the details of frequency, timing, and voided volumes are recorded. More detailed evaluation includes urodynamic studies and abdominal ultrasound to estimate the postvoid urinary residue, and look for hydroureteronephrosis. Urodynamic studies are useful to classify the bladder dysfunction as underactive bladder (bladder that is not overactive in filling phase and underactive or acontractile in voiding phase) or as overactive bladder (bladder that is overactive in filling phase). Both overactive and underactive bladder can be seen in patients with DCM. Neurogenic bladder is generally believed to have a strong correlation with severe motor paresis. The patients with urinary complaints had significantly longer durations of myelopathy and delayed motor evoked potential latencies than those without urinary complaints.
The presence of subclinical respiratory dysfunction in DCM has been well-established across studies. Bed side tools for assessment such as the single breath count, chest expansion, and tidal percussion may offer clues to the presence of poor pulmonary reserve. In cases with poor performance on bedside testing a formal pulmonary function testing is mandatory for assessment of respiratory dysfunction.
| Clinical Syndromes|| |
Various attempts have been made in the past to classify syndromes associated with DCM. Crandall and Batzdorf divided DCM into transverse lesion syndrome, motor system syndrome, central cord syndrome, Brown-Sequard syndrome, and brachialgia cord syndrome. Ferguson and Caplan described lateral or radicular syndrome, medial, or spinal (myelopathic) syndrome, combined medial and lateral syndrome with both long tract and radicular signs and symptoms (the most common in their experience), and a vascular syndrome with painless acute or subacute onset of myelopathy. Various described clinical syndromes are tabulated in [Table 3].
| Evaluation Systems|| |
Clinicians are increasingly using quantitative or semi-quantitative guidelines, including grading of neurological impairment using the Ranawat scoring system, and rating of functional disability using Japanese Orthopedic Association (JOA) scale, Nurick grade or the 30 m walking test. Many of these objective assessments also allow for the quantification of the severity of myelopathy. Sing et al. in their systematic review stated that an ideal scale should be one that is quantifiable, valid, sensitive, responsive, easy to perform, having high inter/intra-observer reliability, internal consistency and a suitable distribution, and is one-dimensional and relevant. Nurick grade and modified JOA scale are tabulated in [Table 4] and [Table 5], respectively.
|Table 5: Modified Japanese Orthopedic Association (mJOA) score for cervical myelopathy|
Click here to view
| Objective Tests of Upper Limb Function|| |
- Rapid hand opening test is a simple and reliable bedside method of assessing improvement in hand function in the early postoperative period. In this test, the subject is seated on a chair with the elbow and forearm resting on a bed and is asked to open and close the hand as fast as possible with complete flexion and extension of the fingers. The time taken to perform 20, 40, and 60 repetitions is noted.
- The nine hole peg test is a useful measure of hand function in postoperative follow up. In this test the patient is seated in front of a table that has a peg board with nine slots on it and nine pegs. On being given a verbal cue, the patient takes the pegs one by one and places them in the slots provided. The test is terminated at the instant the last peg is placed. The time taken from the patient touching the first peg to the time when the last peg was placed is recorded in seconds and is more sensitive than other tests in detecting postoperative improvement at three months.
| Objective Tests of Lower Limb Function|| |
- 30 m walking test (30MWT) is the most common timed walk test used. The patient is asked to walk a distance of 30 m as quickly as possible using any assistive device he or she would normally use while walking (e.g., cane, walker). The test correlated moderately with other validated scales (mJOA and Nurick score).
- 10 s step test is done by counting the number of steps taken by a patient in 10 s. This is a bed side quantitative test and can also be used during follow-up to assess improvement.
- Foot tapping test counts the number of foot taps in a 10 s interval while keeping the heel in contact with floor. This test was found to correlate with the lower extremity motor function of mJOA score.
- The triangle step test counts the number of times the patient places his foot on the stepping points in the corners of a triangular board, measuring 30 cm in a 10 s interval. This test also correlated with the lower extremity motor function of mJOA score.
In the context of degenerative spondylotic myelopathy, it is essential that the scale also addresses the pathophysiology, its key signs and symptoms as well as its natural history. Tetreault et al. in their systematic review of predictors of outcome, identified that results may differ depending on what scale was used to evaluate the outcome. Using the Nurick grade, its association with various predictors was less conclusive. They also identified that relationship between preoperative condition and Nurick grade was unclear, as the duration of symptoms correlated with a worse outcome. Given that CSM typically affects the lateral corticospinal and the spinocerebellar tracts, a scale that assesses voluntary movement, balance and coordinated activity is likely be more sensitive and relevant than one that does not. In addition, a scale that can detect mild symptoms will address the insidious and slowly progressive nature of the disease. Singh et al. stated that mJOA and Nurick grade should be used in combination with more sensitive and quantitative measures including various walking tests or the grip and release test. There still remains a lack of a gold standard outcome measure that can assess disease severity over time and objectively determine a patient's improvement following intervention. This prevents the establishment of standard quantitative guidelines used to direct and implement appropriate treatment programs and makes it more challenging to accurately predict surgical outcome.
| Conclusion|| |
In summary, it is essential for a clinician to approach a patient with degenerative spondylotic myelopathy with an accurate history, assess the nature of disease progression and be able to exactly localize the level of cord compression based on a thorough neurological examination as the degenerative process is usually diffuse and radiology may often show multilevel canal stenosis. In addition, it may be beneficial to use a combination of grading systems to assess disease progression and patient response to therapy. Also, it is necessary that the grading system should suit the ethnic practices of the local population.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Nouri A, Tetreault L, Singh A, Karadimas SK, Fehlings MG. Degenerative cervical myelopathy: Epidemiology, genetics, and pathogenesis. Spine (Phila Pa 1976) 2015;40:E675-93.
Kato S, Fehlings M. Degenerative cervical myelopathy. Curr Rev Musculoskelet Med 2016;9:263-71.
Boden SD, McCowin PR, Davis DO, Dina TS, Mark AS, Wiesel S, et al.
Abnormal magnetic-resonance scans of the cervical spine in asymptomatic subjects. A prospective investigation. J Bone Joint Surg Am 1990;72:1178-84.
Teresi LM, Lufkin RB, Reicher MA, Moffit BJ, Vinuela FV, Wilson GM, et al.
Asymptomatic degenerative disk disease and spondylosis of the cervical spine: MR imaging. Radiology 1987;164:83-8.
Rhee JM, Yoon T, Riew KD. Cervical radiculopathy. J Am Acad Orthop Surg 2007;15:486-94.
Radhakrishnan K, Litchy WJ, O'Fallon WM, Kurland LT. Epidemiology of cervical radiculopathy. A population-based study from Rochester, Minnesota, 1976 through 1990. Brain 1994;117(Pt 2):325-35.
Iyer S, Kim HJ. Cervical radiculopathy. Curr Rev Musculoskelet Med 2016;9:272-80.
Viikari-Juntura E, Porras M, Laasonen EM. Validity of clinical tests in the diagnosis of root compression in cervical disc disease. Spine (Phila Pa 1976) 1989;14:253-7.
Yoss RE, Corbin KB, Maccarty CS, Love JG. Significance of symptoms and signs in localization of involved root in cervical disk protrusion. Neurology 1957;7:673-83.
Wainner RS, Gill H. Diagnosis and nonoperative management of cervical radiculopathy. J Orthop Sports Phys Ther 2000;30:728-44.
Samuels MA. Localization in clinical neurology, ed 2. By Paul W. Brazis, Joseph C. Masdeu, and Jose Biller, Boston, Little, Brown, 1990 509 pp, illustrated, $65.0. Ann Neurol 2018;31:453.
Rubinstein SM, Pool JJ, van Tulder MW, Riphagen II, de Vet HC. A systematic review of the diagnostic accuracy of provocative tests of the neck for diagnosing cervical radiculopathy. Eur Spine J 2007;16:307-19.
Shah KC, Rajshekhar V. Reliability of diagnosis of soft cervical disc prolapse using spurling's test. Br J Neurosurg 2004;18:480-3.
Thoomes EJ, van Geest S, van der Windt DA, Falla D, Verhagen AP, Koes BW, et al.
Value of physical tests in diagnosing cervical radiculopathy: A systematic review. Spine J 2018;18:179-89.
Wong JJ, Côté P, Quesnele JJ, Stern PJ, Mior SA. The course and prognostic factors of symptomatic cervical disc herniation with radiculopathy: A systematic review of the literature. Spine J 2014;14:1781-9.
McCormick WE, Steinmetz MP, Benzel EC. Cervical spondylotic myelopathy: Make the difficult diagnosis, then refer for surgery. Cleve Clin J Med 2003;70:899-904.
Williams AN. Mobile phone sign of degenerative cervical myelopathy. BMJ 2018;361:k1713.
Tracy JA, Bartleson JD. Cervical spondylotic myelopathy. Neurologist 2010;16:176-87.
Watson JC, Broaddus WC, Smith MM, Kubal WS. Hyperactive pectoralis reflex as an indicator of upper cervical spinal cord compression. Report of 15 cases. J Neurosurg 1997;86:159-61.
Sharp FR, Rando TA, Greenberg SA, Brown L, Sagar SM. Pseudochoreoathetosis. Movements associated with loss of proprioception. Arch Neurol 1994;51:1103-9.
Lance JW, Degail P. Spread of phasic muscle reflexes in normal and spastic subjects. J Neurol Neurosurg Psychiatry 1965;28:328-34.
Shimizu T, Shimada H, Shirakura K. Scapulohumeral reflex (Shimizu). Its clinical significance and testing maneuver. Spine (Phila Pa 1976) 1993;18:2182-90.
Houten JK, Noce LA. Clinical correlations of cervical myelopathy and the hoffmann sign. J Neurosurg Spine 2008;9:237-42.
Chaiyamongkol W, Laohawiriyakamol T, Tangtrakulwanich B, Tanutit P, Bintachitt P, Siribumrungwong K, et al.
The significance of the trömner sign in cervical spondylotic myelopathy patient. Clin Spine Surg 2017;30:E1315-20.
Ono K, Ebara S, Fuji T, Yonenobu K, Fujiwara K, Yamashita K, et al.
Myelopathy hand. New clinical signs of cervical cord damage. J Bone Joint Surg Br 1987;69:215-9.
Jiang SD, Jiang LS, Dai LY. Cervical spondylotic amyotrophy. Eur Spine J 2011;20:351-7.
Srinivasa Rao NV, Rajshekhar V. Distal-type cervical spondylotic amyotrophy: Incidence and outcome after central corpectomy. J Neurosurg Spine 2009;10:374-9.
Trompetto C, Marinelli L, Mori L, Pelosin E, Currà A, Molfetta L, et al.
Pathophysiology of spasticity: Implications for neurorehabilitation. Biomed Res Int 2014;2014:354906.
Lanska DJ, Goetz CG. Romberg's sign: Development, adoption, and adaptation in the 19th
century. Neurology 2000;55:1201-6.
Isaza Jaramillo SP, Uribe Uribe CS, García Jimenez FA, Cornejo-Ochoa W, Alvarez Restrepo JF, Román GC, et al.
Accuracy of the babinski sign in the identification of pyramidal tract dysfunction. J Neurol Sci 2014;343:66-8.
Gregorius FK, Estrin T, Crandall PH. Cervical spondylotic radiculopathy and myelopathy. A long-term follow-up study. Arch Neurol 1976;33:618-25.
Diokno AC, Wells TJ, Brink CA. Comparison of self-reported voided volume with cystometric bladder capacity. J Urol 1987;137:698-700.
Fukuda K, Ozaki T, Tsumura N, Sengoku A, Nomi M, Yanagiuchi A, et al.
Neurogenic bladder associated with pure cervical spondylotic myelopathy: Clinical characteristics and recovery after surgery. Spine (Phila Pa 1976) 2013;38:104-11.
Menon N, Gupta A, Taly AB, Khanna M, Kumar SN. Neurogenic bladder following myelopathies: Has it any correlation with neurological and functional recovery? J Neurosci Rural Pract 2014;5:S13-6.
Misawa T, Kamimura M, Kinoshita T, Itoh H, Yuzawa Y, Kitahara J, et al.
Neurogenic bladder in patients with cervical compressive myelopathy. J Spinal Disord Tech 2005;18:315-20.
Crandall PH, Batzdorf U. Cervical spondylotic myelopathy. J Neurosurg 1966;25:57-66.
Singh A, Tetreault L, Casey A, Laing R, Statham P, Fehlings MG, et al.
Asummary of assessment tools for patients suffering from cervical spondylotic myelopathy: A systematic review on validity, reliability and responsiveness. Eur Spine J 2015;24 Suppl 2:209-28.
Prabhu K, Babu KS, Samuel S, Chacko AG. Rapid opening and closing of the hand as a measure of early neurologic recovery in the upper extremity after surgery for cervical spondylotic myelopathy. Arch Phys Med Rehabil 2005;86:105-8.
John S, Moorthy RK, Sebastian T, Rajshekhar V. Evaluation of hand function in healthy individuals and patients undergoing uninstrumented central corpectomy for cervical spondylotic myelopathy using nine-hole peg test. Neurol India 2017;65:1025-30.
] [Full text]
Tetreault LA, Karpova A, Fehlings MG. Predictors of outcome in patients with degenerative cervical spondylotic myelopathy undergoing surgical treatment: Results of a systematic review. Eur Spine J 2015;24 Suppl 2:236-51.
[Table 1], [Table 2], [Table 3], [Table 4], [Table 5]