1: Cervical Spondylotic Myelopathy

Published on 22/05/2015 by admin

Filed under Physical Medicine and Rehabilitation

Last modified 22/05/2015

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 3 (1 votes)

This article have been viewed 1842 times


Cervical Spondylotic Myelopathy

Avital Fast, MD

Israel Dudkiewicz, MD


Cervical radiculitis

Degeneration of cervical intervertebral disc

Cervical spondylosis without myelopathy

Cervical pain

ICD-9 Codes

721.0  Cervical spondylosis without myelopathy

722.4  Degeneration of cervical intervertebral disc

723.3  Cervical pain

723.4  Cervical radiculitis

ICD-10 Codes

M47.812  Cervical spondylosis without myelopathy or radiculopathy

M48.02   Spinal stenosis in cervical region

M48.03   Spinal stenosis in cervicothoracic region

M50.30   Degeneration of cervical disc

M50.32   Degeneration of mid-cervical region

M50.33   Degeneration of cervicothoracic region

M54.2 Cervical pain

M54.12   Cervical radiculitis

M54.13   Cervicothoracic radiculitis


Cervical spondylotic myelopathy (CSM) is a frequently encountered entity in middle-aged and elderly patients. The condition affects both men and women. Progressive degeneration of the cervical spine involves the discs, facet joints, joints of Luschka, ligamenta flava, and laminae, leading to gradual encroachment on the spinal canal and spinal cord compromise. CSM has a fairly typical clinical presentation and, frequently, a progressive and disabling course.

As a consequence of aging, the spinal column goes through a cascade of degenerative changes that tend to affect selective regions of the spine. The cervical spine is affected in most adults, most frequently at the C4-C7 region [1,2]. Degeneration of the intervertebral discs triggers a cascade of biochemical and biomechanical changes, leading to decreased disc height, among other changes. As a result, abnormal load distribution in the motion segments causes cervical spondylosis (i.e., facet arthropathy) and neural foraminal narrowing. Disc degeneration also leads to the development of herniations (soft discs), disc calcification, posteriorly directed bone ridges (hard discs), hypertrophy of the facets and the uncinate joints, and ligamenta flava thickening. On occasion, more frequently in Asians but not infrequently in white individuals, the posterior longitudinal ligament and the ligamenta flava ossify [3]. These degenerative changes narrow the dimensions and change the shape of the cervical spinal canal. In normal adults, the anteroposterior diameter of the subaxial cervical spinal canal measures 17 to 18 mm, whereas the spinal cord diameter in the same dimension is about 10 mm. Severe CSM gradually decreases the space available for the cord and brings about cord compression in the anterior-posterior axis. Cord compression usually occurs at the discal levels [46].

The encroaching structures may also compress the anterior spinal artery, resulting in spinal cord ischemia that usually involves several cord segments beyond the actual compression site. Spinal cord changes in the form of demyelination, gliosis, myelomalacia, and eventually severe atrophy may develop [4,79]. Dynamic instability, which can be diagnosed in flexion or extension lateral x-ray views, further complicates matters. Disc degeneration leads to laxity of the supporting ligaments, bringing about anterolisthesis or retrolisthesis in flexion and extension, respectively. This may further compromise the spinal cord and intensify the presenting symptoms [2,4].


CSM develops gradually during a lengthy period of months to years. Not infrequently, the patient is unaware of any functional compromise, and the first person to notice that something is amiss may be a close family member. Whereas pain appears rather early in cervical radiculopathy and alerts the patient to the presence of a problem, this is usually not the case in CSM. A long history of neck discomfort and intermittent pain may frequently be obtained, but these are not prominent at the time of CSM presentation.

Most patients have a combination of upper motor neuron symptoms in the lower extremities and lower motor neuron symptoms in the upper extremities [4]. Patients frequently present with gait dysfunction resulting from a combination of factors, including ataxia due to impaired joint proprioception, hypertonicity, weakness, and muscle control deficiencies.

Studies have demonstrated that severely myelopathic patients display abnormalities of deep sensation, including vibration and joint position sense, which is attributed to compression of the posterior columns [10,11]. Paresthesias and numbness may be frequently mentioned. Compression of the pyramidal and extrapyramidal tracts can lead to spasticity, weakness, and abnormal muscle contractions. These sensory and motor deficits result in an unstable gait. Patients may complain of stiffness in the lower extremities or plain weakness manifesting as foot dragging and tripping [5]. Symptoms related to the upper extremities are mostly the result of fine motor coordination deficits. At times, the symptoms in the upper extremities are much more severe than those related to the lower extremities, attesting to central cord compromise [4]. Most patients do not have urinary symptoms. However, urinary symptoms (i.e., incontinence) may occasionally develop in patients with long-standing myelopathy [12]. As CSM develops in middle-aged and elderly patients, the urinary symptoms may be attributed to aging, comorbidities, and cord compression. Bowel incontinence is rare.

Physical Examination

Because of sensory ataxia, the patient may be observed walking with a wide-based gait. Some resort to a cane to increase the base of support and to enhance safety during ambulation. Patients with severe gait dysfunction frequently require a walker and cannot ambulate without one. Many patients lose the ability to tandem walk. The Romberg test result may become positive. Examination of the lower extremities may reveal muscle atrophy, increased muscle tone, abnormal reflexes—clonus or upgoing toes (Babinski sign), and abnormalities of position and vibration sense. Muscle fasciculations may be observed. The foot tapping test (number of sole tappings while the heel maintains contact with the floor in 10 seconds) is an easy and useful quantitative tool for lower extremity function in these patients [13].

In the upper extremities, weakness and atrophy of the small muscles of the hands may be noted. The patient may have difficulties in fine motor coordination (e.g., unbuttoning the shirt or picking a coin off the table). The patient frequently displays difficulty in performing repetitive opening and closing of the fist. In normal individuals, 20 to 30 repetitions can be performed in 10 seconds.

Buy Membership for Physical Medicine and Rehabilitation Category to continue reading. Learn more here