cervical spondylosis

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S1-14 | VOLUME 60 | NUMBER 1 | JANUARY 2007 SUPPLEMENT www.neurosurgery-online.com OVERVIEW James S. Harrop, M.D. Department of Neurosurgery, Jefferson Medical College, Philadelphia, Pennsylvania Amgad Hanna, M.D. Department of Neurosurgery, Jefferson Medical College, Philadelphia, Pennsylvania Marco T. Silva, M.D. Department of Neurosurgery, Jefferson Medical College, Philadelphia, Pennsylvania Ashwini Sharan, M.D. Department of Neurosurgery, Jefferson Medical College, Philadelphia, Pennsyvlania Reprint requests: James S. Harrop, M.D., Department of Neurosurgery, Jefferson Medical College, 909 Walnut Street, Second Floor, Philadelphia, PA 19107. Email: [email protected] M yeloradiculopathy is a clinical syn- drome produced from degenerative changes of the vertebral column resulting in compression of the neural ele- ments, spinal cord (myelopathy), and nerve roots (radiculopathy). The pathophysiology of the radiculopathy and the myelopathy may result from a multimodality process. Factors that may contribute include direct compres- sion of the nerve roots and spinal cord, vascu- lar insufficiency, venous engorgement, and inflammation, along with some degree of a genetic contribution in the ability of neural ele- ments to sustain and respond to injuries. Cervical spondylosis is a common degener- ative condition in industrial populations, in which approximately 50 to 80% of patients have at least one episode of neck pain, with or without associated radicular component, annually (20). The natural history of spondy- lotic cervical myelopathy needs to be further delineated, although its course most likely results in a progressive neurological decline (8, 40). However, occasional reports have sug- gested arresting of the process (4) or subsi- dence of symptoms (27). Through the normal aging process, arthro- pathies or arthritic disorder patients may pres- ent with compressive symptoms with involve- ment of nerve roots or the spinal cord (Figs. 1 and 2). Radicular compression may present as a weakness in the respective myotome, sen- sory losses, or radiating pain in dermatomal distribution. The goals of treatment are to elim- inate symptoms, by methods including pain reduction and strength restoration; this can typically be achieved through conservative treatment algorithms (34). However, occasion- ally, in recalcitrant cases of radicular symptoms or symptomatic spinal cord compression, sur- gery may be warranted (17). Arthropathy, a diffuse disorder, may involve multiple cervical joints and concurrently com- press the spinal cord. Hence, in this setting, multiple nerve root involvement is not uncom- mon. This combination of signs and symptoms are referred to as cervical spondylotic myelo- radiculopathy. The earliest references to cervical disorders as a cause of neurological deterioration are credited to Strumpell (1888), Marie (1898), and von Beckteren (1899), and the disorder was referred to as cervical spondylitis secondary to an assumed infectious or inflammatory condi- tion (4). Horsley first surgically addressed the condition of cervical spondylotic myelopathy in 1892, performing a C6 laminectomy and spinal cord decompression in a patient with a progressive quadriparesis. The patient had a significant improvement and recovery; within 8 months, the patient was able to walk and, at 1 year, was fully recovered (5). In 1952, Brain et al. (4), in his landmark article, redefined the etiology and pathophysiology of this degener- NEUROLOGICAL MANIFESTATIONS OF CERVICAL SPONDYLOSIS: AN OVERVIEW OF SIGNS, SYMPTOMS, AND P ATHOPHYSIOLOGY THE NEUROLOGICAL MANIFESTATIONS of cervical spondylosis include symptomatic compression of the spinal cord (myelopathy), nerve roots (radiculopathy), or a combi- nation of the two (myeloradiculopathy). The term myeloradiculopathy herein defines these often indistinct and inseparable entities. The pathophysiology of myeloradicu- lopathy is multifactorial in nature, and the natural history of untreated myeloradicu- lopathy is not clearly defined. We review the signs, symptoms, and clinical findings of cervical myelopathy, radiculopathy, and myeloradiculopathy. Standard grading tech- niques are also reviewed. KEY WORDS: Cervical spine, Myelopathy, Radiculopathy, Spondylosis, Stenosis Neurosurgery 60:S1-14–S1-20, 2007 DOI: 10.1227/01.NEU.0000215380.71097.EC

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Page 1: Cervical Spondylosis

S1-14 | VOLUME 60 | NUMBER 1 | JANUARY 2007 SUPPLEMENT www.neurosurgery-online.com

OVERVIEW

James S. Harrop, M.D. Department of Neurosurgery,Jefferson Medical College,Philadelphia, Pennsylvania

Amgad Hanna, M.D. Department of Neurosurgery,Jefferson Medical College,Philadelphia, Pennsylvania

Marco T. Silva, M.D. Department of Neurosurgery,Jefferson Medical College,Philadelphia, Pennsylvania

Ashwini Sharan, M.D. Department of Neurosurgery,Jefferson Medical College,Philadelphia, Pennsyvlania

Reprint requests: James S. Harrop, M.D.,Department of Neurosurgery,Jefferson Medical College,909 Walnut Street, Second Floor,Philadelphia, PA 19107.Email: [email protected]

Myeloradiculopathy is a clinical syn-drome produced from degenerativechanges of the vertebral column

resulting in compression of the neural ele-ments, spinal cord (myelopathy), and nerveroots (radiculopathy). The pathophysiology ofthe radiculopathy and the myelopathy mayresult from a multimodality process. Factorsthat may contribute include direct compres-sion of the nerve roots and spinal cord, vascu-lar insufficiency, venous engorgement, andinflammation, along with some degree of agenetic contribution in the ability of neural ele-ments to sustain and respond to injuries.

Cervical spondylosis is a common degener-ative condition in industrial populations, inwhich approximately 50 to 80% of patientshave at least one episode of neck pain, with orwithout associated radicular component,annually (20). The natural history of spondy-lotic cervical myelopathy needs to be furtherdelineated, although its course most likelyresults in a progressive neurological decline(8, 40). However, occasional reports have sug-gested arresting of the process (4) or subsi-dence of symptoms (27).

Through the normal aging process, arthro-pathies or arthritic disorder patients may pres-ent with compressive symptoms with involve-ment of nerve roots or the spinal cord (Figs. 1and 2). Radicular compression may present asa weakness in the respective myotome, sen-

sory losses, or radiating pain in dermatomaldistribution. The goals of treatment are to elim-inate symptoms, by methods including painreduction and strength restoration; this cantypically be achieved through conservativetreatment algorithms (34). However, occasion-ally, in recalcitrant cases of radicular symptomsor symptomatic spinal cord compression, sur-gery may be warranted (17).

Arthropathy, a diffuse disorder, may involvemultiple cervical joints and concurrently com-press the spinal cord. Hence, in this setting,multiple nerve root involvement is not uncom-mon. This combination of signs and symptomsare referred to as cervical spondylotic myelo-radiculopathy.

The earliest references to cervical disordersas a cause of neurological deterioration arecredited to Strumpell (1888), Marie (1898), andvon Beckteren (1899), and the disorder wasreferred to as cervical spondylitis secondary toan assumed infectious or inflammatory condi-tion (4). Horsley first surgically addressed thecondition of cervical spondylotic myelopathyin 1892, performing a C6 laminectomy andspinal cord decompression in a patient with aprogressive quadriparesis. The patient had asignificant improvement and recovery; within8 months, the patient was able to walk and, at1 year, was fully recovered (5). In 1952, Brain etal. (4), in his landmark article, redefined theetiology and pathophysiology of this degener-

NEUROLOGICAL MANIFESTATIONS OF CERVICALSPONDYLOSIS: AN OVERVIEW OF SIGNS,SYMPTOMS, AND PATHOPHYSIOLOGY

THE NEUROLOGICAL MANIFESTATIONS of cervical spondylosis include symptomaticcompression of the spinal cord (myelopathy), nerve roots (radiculopathy), or a combi-nation of the two (myeloradiculopathy). The term myeloradiculopathy herein definesthese often indistinct and inseparable entities. The pathophysiology of myeloradicu-lopathy is multifactorial in nature, and the natural history of untreated myeloradicu-lopathy is not clearly defined. We review the signs, symptoms, and clinical findings ofcervical myelopathy, radiculopathy, and myeloradiculopathy. Standard grading tech-niques are also reviewed.

KEY WORDS: Cervical spine, Myelopathy, Radiculopathy, Spondylosis, Stenosis

Neurosurgery 60:S1-14–S1-20, 2007 DOI: 10.1227/01.NEU.0000215380.71097.EC

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ative condition in relation to neurological injury and deteriora-tion and referred to the process as cervical spondylosis.

Definitions of Spinal Disorders (30)

Spondylosis: any or various degenerative diseases of the spineMyelopathy: any disease or disorder of the spinal cord or bone

marrowRadicular: of, relating to, or involving a nerve root Radiculopathy: any pathological condition at the nerve roots.

EXAMINATION

In the evaluation of a patient with cervical spondyloticmyelopathy with or without a concurrent radiculopathy, partic-ular attention must be placed on the assessment of motor func-tion, the different modalities of sensation, and the signs ofspinal cord compression (long-tract signs).

Individual muscle groups supplied by specific nerves shouldbe isolated and tested for weakness. The grading of key mus-cle groups is performed bilaterally, using a six-point scale(1, 25). Additionally, attention to the muscle tone, flaccid orspastic, is helpful.

Sensory modalities consist of light touch, pin prick, andvibratory or proprioception, which are all transmitted throughthe spinal cord via different neuronal tracts. The sensorymodalities should be recorded and scored on a three-point scale(0 � none; 1 � impaired partial or altered appreciation, includ-ing hyperesthesia; and 2 � normal) (1).

Deep tendon reflexes are generally a simple monosynapticreflex consisting of an afferent input with a synapse in thespinal cord and an efferent output. Upper motor neuronsinhibit the efferent signal. Thus, if the reflex is increased, adecrease in upper motor influence is inferred. Reflexes aregraded between 0 and 4� where, a Grade 3� or 4� (Table 1)reflex suggests an upper motor nerve dysfunction. Hyper-activity of the muscle stretch reflexes is characterized by adecrease in the reflex threshold, an increase in the speed ofresponse, exaggeration in the vigor and range of movement,prolongation of muscle contraction, repeated contractions andrelaxations, extension of the reflexogenous zone (zone of provo-cation), and propagation of the reflex response (Table 2) (16).

FIGURE 1. A, sagittal T2-weighted magnetic resonance imaging (MRI)scan of the cervical spine in an asymptomatic patient with degenerativechanges or cervical spondylosis. Note the normal caliber of the spinal cordwith some effacement of the anterior thecal sac caused by disc and osteophytecomplexes (arrow), but no spinal cord compression. B, axial T2-weightedMRI scan of the cervical spine on the same patient with tomogram markerseen in (A) at the C5–C6 interspace. Note the encroachment on the nerveroots as they exit the canal through the foramen (arrow) caused by uncal ver-tebral joint hypertrophy.

A B

FIGURE 2. Cervical flexion (A) and extension (B) plain x-rays of a 55-year-old man who presented with an acute C5 radiculopathy. Plain x-rays illustratesevere degenerative changes with loss of disc height and osteophyte formation,particularly at C5–C6 (arrow). Note the increased motion at C4–C5 and sub-luxation.

A B

TABLE 1. Deep tendon reflex gradesa

Grade Definition

0 Absent1 Palpable contraction2 Full ROM with gravity eliminated3 Full ROM with gravity present4 Active movement with resistance5 Normal strength

NT Not tested

a ROM, range of motion; NT, not tested (from, Medical Research Council:Aids to the Investigation of the Peripheral Nervous System. Condon, HMSO,1943 [25].

TABLE 2. Reflex grading

0 Complete absence� Diminished�� Normal reflex��� Hyperactive reflex���� Markedly hyperactive, often with clonus

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Clonus: Rhythmic involuntary muscle movement with stimu-lation

Tone of the muscle: The degree of tension of the muscle at restSpasticity: Increased muscle tone or a resistance to motionFlaccidity: Yielding to pressure for want of firmness, lack of

tone

SIGNS AND SYMPTOMS:RADICULOPATHY

Primary compression of the nerve root without impingementof the spinal cord can result in a radicular pain pattern, loss ofstrength and/or sensation, or diminished-to-absent reflexes.This is contrary to lesions of the spinal cord, which typicallyproduce hyperreflexia and/or nondermatomal or nonmy-otomal sensory or motor disturbances.

The abduction relief sign and Spurling’s sign are two confir-matory examination maneuvers that implicate compression ofa nerve root at the level of the foramen. Abduction relief sign:the patient abducts the shoulder by placing the hand of affectedside onto the top of his or her head. A positive sign is relief ofthe radicular symptoms (10). This may worsen a patient’ssymptoms if thoracic outlet syndrome was the etiology of thepain. Spurling’s sign: the examiner places axial pressure on thecranium, with the patient holding their neck in extension, witha concurrent lateral bend of their neck towards the affectedside. A positive test provokes the radicular pain.

Identifying the process as radicular in nature is extremelyimportant in localizing the concordant pathology on x-rayfilms. However, the distribution of the nerves may vary consid-erably because of the variability of the brachial plexus anatomyand extradural anastomosis of nerves (36). Cervical disc protru-sion or foraminal stenosis that results in compression of thenerve roots C1–C4 does not manifest as weakness or atrophyunless there is concurrent compression of the spinal cord.

C3 Nerve Root The C3 nerve root exits the spinal canal through the C2–C3

neural foramina. It is unusual to have a patient present withsigns or symptoms of a C3 radiculopathy. This is thought to becaused by the paucity of movement at the C2–C3 segment (31).Concurrently, the C2–C3 has the largest foramen and is tra-versed by the smallest cervical nerve root (29). Clinical symp-toms include radicular pain, often referred to by the patient asa headache, caused by the sensory distribution of the nerveover the upper neck and occiput or sensory loss. There is nodistinct motor distribution for this nerve.

C4 Nerve Root The C4 nerve root exits the spinal canal through the C3–C4

neural foramina. The increased mobility and smaller foramina-to-nerve ratio predisposes this nerve to an increased risk forcompression. However, it is also uncommon for patients topresent with a pure C4 radiculopathy (17). Pain may radiateto the posterior neck and trapezius region and to the anterior

chest (21), but does not typically radiate into the upperextremity. Jenis and An (21) presented a series of 12 patientswith neck pain from C4 radiculopathy and all had normalneurological examinations.

C5 Nerve Root A C5 radiculopathy typically radiates from the neck over the

posterior shoulder girdle and into the proximal lateral arm. AC5 lesion can demonstrate weakness in the deltoid musclesand, to a lesser extent, in the biceps muscles and the supra-spinatus and infraspinatus muscles. Clinically, patients withC5 motor weakness are typically unable to abduct or raise theirarm over their head, and this manifests during dressing or hairbrushing. Signs of nerve dysfunction may be visualized as adiminished pectoralis, biceps, or brachioradialis reflex.Numbness can be isolated to the lateral aspect of the arm in thedeltoid region (26). A C5 nerve root lesion can be difficult todistinguish from a primary shoulder disorder, although a care-ful physical exam of the nerves and dermatomes along withmanipulation and rotation of the shoulder joint may help dif-ferentiate the two.

C6 Nerve Root C6 compression is the most common radiculopathy, largely

because the greatest amount of degenerative change (spondy-losis) is usually seen at the C5–C6 level (8, 31). C6 nerve rootweakness will typically present through the biceps musclealong with the extensor carpi radialis (longus and brevis).The extensor carpi radialis muscle is unique because it isinnervated solely by the C6 nerve and functionally performsextension at the wrist. The C6 nerve may manifest as weakbiceps and/or brachioradialis reflexes. The C6 nerve also sup-plies the sensation to the thumb and the lateral portion of theindex fingers. Numbness can be isolated over this region, butit is not unusual for numbness to be absent (26). Radicularsymptoms typically consist of pain referred from the neck,down the shoulder and medial border of the scapula and intothe lateral arm and radial forearm down to the thumb andindex fingers (36).

C7 Nerve Root The C7 nerve root supplies motor innervation to the triceps

muscle and performs extension of the arm at the elbow joint.Signs of a compressive lesion may also manifest as a dimin-ished or absent triceps reflex as well as weakness in this mus-cle. Sympathetic dysfunction from impairment of the auto-nomic system may present as Horner’s syndrome, althoughthis is a variable finding (17, 26). Numbness may be isolated tothe middle and index finger (26). Pain is usually in the inter-scapular area and radiates through the mid-arm and mid-forearm, down to the middle three fingers.

C8 Nerve Root The C8 nerve root controls the hand intrinsic and finger

flexor muscles and can present as Benediction sign (the inabil-

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ity to extend the fourth and fifth digits). Sympathetic dysfunc-tion from impairment of the autonomic system may present asHorner’s syndrome, although this is also variable (17, 26). Painradiates through the medial aspect of the arm, the medialaspect of the forearm, and the medial two fingers. Motor loss orweakness can be isolated to all of the wrist extensor muscles(except the extensor carpi radialis) as well as the flexors (exceptcarpi radialis) and the hand intrinsic muscles.

T1 Nerve Root T1 radiculopathies are extremely rare, and Murphey et al.

(26) reported their occurrence to be less than 1% in their seriesof 648 patients. These lesions tend to be acute disc hernia-tions and not related to spondylotic degenerative changes.Harrop et al. (17), in their series of cervicothoracic radicu-lopathies, reported on three patients; two of the patients hadcervicothoracic radiculopathies resulting from disc hernia-tions and the third had a cervicothoracic radiculopathies froma foraminal stenosis. These patients can be differentiated fromC8 radiculopathy patients by the significant hand intrinsicweakness, typically with minimal pain. Patients also can haveatrophy of the first dorsal interosseous muscles and aFroment’s sign. Sympathetic dysfunction from impairment ofthe autonomic system may present as Horner’s syndrome,although this is variable (17, 26). Numbness occasionally ispresent and usually is located over the ulnar side of the fore-arm (26).

SIGNS AND SYMPTOMS: MYELOPATHY

The clinical definition of a myelopathy is the presence oflong-tract signs, which are the results of inhibition of the spinalafferent or efferent (pyramidal) nerve tracts. Some myelopathicsigns include hyperreflexia of the deep tendon reflexes of theupper and lower extremities, increased muscle tone or clonus,and the presence of pathological reflexes, including Babinski’ssign (plantar reflex) and/or Hoffman’s sign. The plantar reflex(Babinski’s sign) is elicited using a blunt object to stimulate thelateral aspect of the plantar surface of the foot, from the heel tothe ball of the foot, and curving medially across the ball. Thenormal response is a plantar flexion of the toes. Babinski’s signconsists of slow tonic dorsiflexion of the big toe accompaniedby fanning of the other toes (3, 11). There are numerous varia-tions of Babinski’s sign, such as Oppenheim’s, Gordon’s,Schaefer’s, Bing’s, Chaddock’s, Gonda’s, and Allen’s signs.Oppenheim’s sign is elicited by applying heavy pressure withthe thumb and index over the tibial bone and stroking downfrom the infrapatellar region to the ankle. Gordon’s sign isobtained by squeezing or applying deep pressure to the calfmuscles. Schaefer’s sign is produced by deep pressure on theAchilles tendon. Chaddock’s sign is elicited by stimulating thelateral aspect of the foot with a blunt point. Gonda and Allenhave independently described a sign that is elicited by forcefuldownward stretching or snapping of the distal phalanx ofeither the second or the fourth toe (11). Bing’s sign describes astimulus that is nociceptive to the great toe with a pin prick. All

of these variations of Babinski’s sign are considered a positiveresponse with dorsiflexion of the great toe.

The upper extremities may be affected with compression ofthe cervical spinal cord. Hoffman’s sign is referred to as the“upper extremity Babinski’s sign.” Hoffman’s sign is elicitedby stimulating the extensor tendon to the third digit byforcible flexion of the distal phalanx, followed by a suddenrelease, resulting in a flexion and adduction of the thumb andconcurrent flexion of the index finger (12, 42). Sometimesthere is flexion of the other fingers as well. The sign is incom-plete if only the thumb or only the index finger responds (11).Hoffman’s sign has a significant false positive rate, particu-larly in younger women, and care must be taken with inter-preting this sign (12, 42).

Additional signs of cervical myelopathy are the invertedradial reflex and the finger escape sign. The inverted radialreflex is tested by stimulating the distal brachioradialis ten-don through gentle percussion, producing hyperactive fin-ger flexion (14). The finger escape sign is provoked by plac-ing the patient’s arms forward with the elbow pronated. Apositive sign is noted if the patient is unable to maintaintheir hands in an extended position and the third throughfifth digits abducted. Inability to grip and release rapidlywith these fingers is an additional sign of a myelopathichand (28). Occasionally, patients describe an electrical shock-like sensation shooting down the spine, with flexion of theneck, known as Lhermitte’s sign. Originally described withmultiple sclerosis and thought to be the result of posteriorcolumn dysfunction, this phenomenon may be seen inpatients with severe cervical cord compression from stenosisor a disc herniation.

Myelopathy may also manifest as a loss of proprioception,and, more commonly, gait or fine motor dysfunction, such asdifficulty in buttoning one’s shirt or changes in the handwrit-ing. Spillane et al. (40) noted that the early phase of cervicalspondylotic myelopathy is also characterized by clumsinessand unsteadiness with gait. Severe muscle atrophy caudal tothe level of stenosis is uncommon with a spondylotic myelopa-thy, unless it is detected in much latter stages. Therefore, ifatrophy is present, physicians must evaluate for fasciculations,particularly proximal to the level of stenosis (i.e., tongue), andexclude amyotrophic lateral sclerosis.

A patient with cervical spondylotic myelopathy can pres-ent acutely after a trauma. The central cord syndrome,described originally by Schneider et al. (38) in 1954, is char-acterized by greater motor impairment in the upper extrem-ities than the lower extremities, bladder dysfunction, fre-quent urinary retention, and various degrees of sensory lossbelow the level of the lesion. Burning hands, with paresthe-sias and dysesthesias in the hands, was later described as amild variant of central cord injury. Central cord syndromeoccurs in patients with cervical spondylosis if they sufferneck trauma, especially in hyperextension (24). Various func-tional classifications (Appendix 1) are used to evaluatepatients with cervical spondylosis. They are all based on pureclinical testing to evaluate the patient’s progress during the

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course of the disease and to document response to differenttreatment schemes.

SIGNS AND SYMPTOMS: MYELOPATHYWITH RADICULOPATHY

Cervical radiculopathy occurs in a subset of the myelopathicpatients. In this process, the spinal cord is stenotic along withconcurrent focal compression on one or more particular nerveroot(s). These radicular symptoms, mainly including pain, typ-ically motivate patients to seek medical attention. The physi-cian must carefully evaluate the patient with a myeloradicu-lopathy with a thorough history and physical exam. Importantelements in the history are to elucidate the timing and progres-sion of symptoms, function and integrity of muscle groups,loss of dexterity, gait function, bowel and bladder function,and fine motor control.

The majority of the patients who present with myelopathicfeatures have concurrent axial neck pain. However, approxi-mately 20% may not have neck discomfort at all (15). Crandalland Batzdorf reported that neck and shoulder pain was pres-ent in less than half of the 62 patients in their series, andapproximately one-quarter of patients had a cervical radicu-lopathy that could be reproduced with a Spurling test (8).Interestingly, the most frequent clinical finding or myelopathicsign that patients presented with was spasticity (61 out of 62),followed by weakness (40 out of 62) (8). This spasticity wasoften noted in the hands, manifesting as a slowness and stiff-ening when opening and closing the fist, particularly in theflexor forearm muscles (8). Crandall and Batzdorf (8) illus-trated that this is a diffuse disorder with a two-level diseaseaffecting C4–C5 and C5–C6 more than C5–C6 and C6–C7, andmore than C3–C4 and C4–C5; and three-level involvementaffecting C4–C7 more than C3–C6 (Figs. 2 and 3).

CONCLUSION

The diagnosis of cervical spondylotic myelopathy, with orwithout a concurrent radiculopathy, is determined through athorough clinical evaluation and physical examination.Radicular symptoms can be diagnosed and isolated to a spe-cific spinal level by a careful evaluation of motor and sensorydistributions. Concurrent spinal cord compression must beevaluated for the presence of long-tract dysfunction. The clin-ical evaluation must be correlated with radiographic analysis todirect the appropriate surgical intervention.

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FIGURE 3. Sagittal computed tomographic scan reformatted image (A) andT2-weighted MRI scan (B) of a myelopathic patient. Note the loss of the canaldiameter on the computed tomography images measured at 6.3 mm, along withthe loss of the cerebrospinal fluid on the corresponding MRI scan.

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APPENDIX

Grading Systems

1. The American College of Rheumatology (Steinbrocker’s)grading system (1949) (41) is a general disability gradingsystem, not specifically designed for spondylotic myelopa-thy

I: Complete ability to carry out all the usual duties with-out disability

II: Adequate for normal activities despite discomfort orlimited motion for one of the joints

III: Limited or none of the duties of usual occupation orself-care

IV: Incapacitated, largely or wholly bedridden or confinedto a wheelchair with little or no self-care

2. Nurick grading (1972) (27) includes six grades of disabilityGrade 0: Signs or symptoms of root involvement but with

out evidence of spinal cord diseaseGrade 1: Signs of spinal cord disease but no difficulty in

walkingGrade 2: Slight difficulty in walking that did not prevent

full-time employmentGrade 3: Difficulty in walking that prevented full-time

employment or the ability to do all housework,but which was not so severe as to require someone else’s help to walk

Grade 4: Able to walk only with someone else’s help orwith the aid of a frame

Grade 5: Chair-bound or bedridden3. Ranawat classification (1979) (33) was originally designed

for patients with cervical myelopathy caused by rheuma-toid arthritis

Class I: No neural deficit Class II: Subjective weakness with hyperreflexia and

dysesthesiaClass III: Objective findings of weakness and long-tract signs

III A: Could walkIII B: Quadriparetic, nonambulatory

4. The modified Japanese Orthopedic Association (2) incorpo-rated a grading scale assessing upper extremity, lowerextremity, and bladder function as well as sensation

Modified Japanese Orthopedic Association Cervical SpineMyelopathy Functional Assessment Scale

Motor dysfunction score of the upper extremities 0: Inability to move hands 1: Inability to eat with a spoon, but able to move hands 2: Inability to button shirt, but able to eat with spoon 3: Able to button shirt with great difficulty 4: Able to button shirt with slight difficulty 5: No dysfunction

Motor dysfunction score of the upper extremities 0: Complete loss of motor and sensory function 1: Sensory preservation without ability to move legs 2: Able to move legs, but unable to walk 3: Able to walk on flat floor with aid (cane/crutch) 4: Able to walk up and/or down stairs with hand rail 5: Moderate to significant lack of stability, but able to walk

up and/or down stair without handrail6: Mild lack of stability but walks with smooth reciproca-

tion unaided7: No dysfunction

Sensory dysfunction score of the upper extremities0: Complete loss of hand sensation 1: Severe sensory loss or pain

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HARROP ET AL.

2: Mild sensory loss 3: No sensory loss

Sphincter dysfunction score0: Inability to micturate voluntary1: Marked difficulty with micturition3: Normal micturition5. Casey et al. (1996) (7) developed a functional scoring

system for rheumatoid arthritis patients with cervical

myelopathy. A questionnaire filled out by the patientsincluded six questions related to usual daily activities,and was graded from 0 to 3 with a score of zero whenperformed with no difficulty and 3 when unable to per-form. The system had a total possible score of 30 points.

6. Singh and Crockard (39) developed a 30-m walking testas a quantifiable measure of severity of cervical spondy-lotic myelopathy.

Wilhelm Braune. 1831-1892. Topographisch-anatomischer Atlas, nach Durchschnitten an gefrornen Cadavern. Leipzig:Verlag von Veit & Comp., 1867-1872. (Courtesy of the U.S. National Library of Medicine, National Institutes ofHealth, Bethesda, Maryland).