Cervical Myelopathy

Populations and Risk Factors

• Most common in adults over age 55, with prevalence increasing with age as degenerative cervical spondylosis progresses
• Men are affected approximately twice as frequently as women
• Pre-existing cervical spondylosis (degenerative disc disease, osteophyte formation, facet hypertrophy) — the most common underlying cause, present to some degree in the majority of adults over 60
• Congenital cervical stenosis — individuals born with a narrower cervical canal (anteroposterior diameter <13 mm) have less reserve space for the spinal cord and become symptomatic with less degenerative change
• Occupations or activities requiring sustained cervical extension or repetitive cervical loading (overhead work, heavy manual labor)
• Ossification of the posterior longitudinal ligament (OPLL) — more common in East Asian populations (prevalence 2–4% in Japanese populations vs. <1% in Western populations)
• History of significant cervical trauma — post-traumatic disc herniation, fracture, or instability can produce acute myelopathy
• Rheumatoid arthritis — atlantoaxial subluxation can compress the upper cervical cord
• Down syndrome — atlantoaxial instability predisposes to cervical cord compression

Causes and Pathophysiology

How the Spinal Cord Gets Compressed

The cervical spinal canal normally provides adequate space for the spinal cord, with a margin of cerebrospinal fluid (CSF) surrounding it. Myelopathy develops when this space is reduced to the point where the cord is physically compressed:

• Degenerative spondylosis (most common): Progressive disc desiccation and height loss → posterior disc bulging into the canal + osteophyte formation at the vertebral body margins and uncovertebral joints + hypertrophy of the ligamentum flavum from behind. These three changes collectively narrow the canal from both front and back, creating a pincer effect on the cord. C5–C6 and C6–C7 are the most commonly affected levels because they have the greatest range of motion and therefore the most degenerative wear.
• Disc herniation: A large central or paracentral disc herniation can compress the cord directly. Unlike the lateral herniations that produce radiculopathy (nerve root compression), myelopathic herniations are central — they compress the cord rather than a single root.
• OPLL: The posterior longitudinal ligament, which runs along the posterior surface of the vertebral bodies inside the canal, gradually calcifies and thickens. This rigid bar of bone progressively narrows the canal from the front.
• Ligamentum flavum hypertrophy: The ligamentum flavum thickens with age and degenerative change, and it buckles into the canal during extension. This narrows the canal from behind, compounding the anterior compression from discs and osteophytes.

What Happens to the Compressed Spinal Cord

When the spinal cord is compressed, the pathological sequence progresses through identifiable stages:

• Demyelination phase: Sustained compression disrupts the myelin sheath surrounding the long ascending and descending tracts (corticospinal, spinothalamic, posterior columns). Demyelination impairs signal conduction along these tracts, producing the early clinical findings — hand clumsiness and gait unsteadiness.
• Ischemic injury: The compression also occludes the small blood vessels that supply the cord's gray and white matter, particularly the anterior spinal artery territory. Ischemia compounds the demyelination injury and accelerates cell death.
• Gliosis and irreversible damage: Prolonged compression produces gliosis (scarring within the cord) and neuronal death. At this stage, the damage is irreversible — surgical decompression can prevent further deterioration but cannot restore lost function. This is why early recognition matters.

The Upper Motor Neuron Pattern

Because the spinal cord contains the descending corticospinal tracts (which carry motor commands from the brain to the lower motor neurons), compression produces upper motor neuron (UMN) signs below the level of compression:

• Spasticity — velocity-dependent increase in muscle tone (the faster you stretch the muscle, the more it resists)
• Hyperreflexia — exaggerated deep tendon reflexes below the compression level
• Positive Babinski sign — great toe extension with fanning of the other toes on plantar stimulation
• Positive Hoffmann sign — flexion of the thumb and index finger when the middle finger's distal phalanx is flicked
• Clonus — rhythmic involuntary oscillation at the ankle with sustained dorsiflexion

At the level of compression, the cord damage may also produce lower motor neuron signs in the upper extremities (weakness, atrophy, fasciculations in the hands) because the compression directly damages the anterior horn cells at that segmental level.

Why Gait Is Affected Early

The corticospinal tracts that control the lower extremities are located in the lateral columns of the spinal cord. These lateral columns are the most vulnerable to external compression because they are positioned closest to the canal walls. Even mild compression can disrupt these tracts before the more centrally located upper extremity tracts are affected. This explains the characteristic early finding of gait disturbance (spastic gait, wide-based, unsteady) appearing before hand symptoms in many patients.

Signs and Symptoms

Early Presentation

• Gait disturbance: Wide-based, unsteady gait; feeling of "legs giving way" or "walking on cotton"; difficulty with balance, especially in the dark (loss of proprioceptive input from the posterior columns); the patient may describe difficulty walking on uneven surfaces or feeling drunk
• Hand clumsiness: Difficulty with fine motor tasks — buttoning shirts, handling coins, writing, turning keys; the patient may describe "dropping things more often" or "my hands don't work like they used to"
• Neck stiffness: Progressive reduction in cervical ROM, particularly extension; neck pain may be present but is often surprisingly mild relative to the severity of the neurological findings

Progressive Presentation

• Lower extremity spasticity: Legs feel stiff and heavy; difficulty with stairs; increased falls; the stiffness is velocity-dependent (UMN pattern) — not the protective guarding seen in musculoskeletal conditions
• Upper extremity weakness: Grip weakness, intrinsic hand muscle wasting, difficulty with power grip and fine pinch; may be bilateral or asymmetric depending on the pattern of cord compression
• Sensory changes: Numbness or paresthesia in the hands and feet; Lhermitte sign (electric shock sensation down the spine or into the limbs with cervical flexion); loss of position sense (proprioception) contributing to gait instability
• Bladder dysfunction: Urinary urgency, frequency, or hesitancy in advanced cases — this is a late finding and indicates significant cord compromise; medical referral is urgent

Key Clinical Distinction: Myelopathy vs. Radiculopathy

Assessment Profile

Subjective Presentation

• Chief complaint: "My hands are clumsy" or "I keep dropping things" or "I feel unsteady when I walk" or "my legs feel stiff and heavy"; neck pain may be present but is often not the primary complaint — the patient is more concerned about the functional decline
• Pain quality: Neck stiffness more than sharp pain; diffuse, poorly localized numbness or "heaviness" in the hands and feet; may describe an electric shock sensation radiating down the spine with neck flexion (Lhermitte sign)
• Onset: Insidious and slowly progressive — symptoms develop over months to years; the patient often cannot identify a specific onset date; occasional stepwise deterioration (a period of stability followed by a sudden worsening, which may coincide with a minor trauma)
• Aggravating factors: Cervical extension (narrows the canal further); prolonged walking or standing (fatigue reveals gait instability); activities requiring fine motor control (writing, buttoning)
• Easing factors: Cervical flexion (opens the canal slightly); rest; using assistive devices (railings, wide-grip tools)
• Red flags: Bilateral hand clumsiness with gait disturbance → refer for neurological evaluation; do not attribute to cervical spondylosis alone; Lhermitte sign → refer for MRI; any bowel or bladder dysfunction → urgent referral; progressive weakness in any distribution → refer

Observation

• Local inspection: No visible swelling or deformity at the cervical spine in most cases; in advanced cases, visible intrinsic hand muscle wasting (interossei, thenar, hypothenar) may be present bilaterally; may see muscle fasciculations in the upper extremities
• Posture: Cervical kyphosis or loss of lordosis is common in the setting of cervical spondylosis; the patient may hold the head in slight flexion (which opens the canal and reduces symptoms); rounded shoulders and forward head posture may be present as comorbid findings
• Gait: Wide-based, spastic gait — legs appear stiff with reduced knee flexion during swing phase; shuffling pattern; may demonstrate circumduction gait (swinging the stiff leg outward in an arc); difficulty with tandem walking (heel-to-toe); balance impairment visible when turning

Palpation

• Tone: Bilateral upper trapezius and cervical paraspinal hypertonicity from chronic cervical spondylosis; the distinctive myelopathic finding is in the extremities — UMN spasticity in the lower extremities (velocity-dependent resistance to passive stretch, particularly in the hip adductors, quadriceps, and ankle plantarflexors) and possible LMN flaccidity or atrophy in the hands at the level of compression
• Tenderness: Cervical paravertebral tenderness at the involved levels (most commonly C5–C6, C6–C7); spinous process tenderness with posterior-anterior pressure may be present but is nonspecific; unlike radiculopathy, there is no dermatomal referred path tenderness because the cord compression produces diffuse rather than segmental symptoms
• Temperature: Normal in most cases; no vascular or inflammatory temperature changes are expected
• Tissue quality: Cervical paraspinal muscles may be fibrotic from chronic spondylotic changes; intrinsic hand muscles may feel atrophied and wasted on palpation in advanced cases; lower extremity muscles may feel spastic (increased resting tone with a velocity-dependent quality distinct from musculoskeletal guarding)

Motion Assessment

• AROM: Cervical ROM is typically globally restricted, with extension most limited and most provocative (extension narrows the canal and compresses the cord). Flexion may actually improve symptoms (opens the canal). Lateral flexion and rotation are restricted by spondylotic changes. The pattern is one of global restriction from degenerative stiffness rather than the specific directional limitation seen in acute disc herniation.
• PROM / end-feel: Cervical PROM reveals a hard or bony end-feel in the directions limited by osteophytic changes — this is distinctly different from the muscular/guarded end-feel of acute cervical conditions. Extension PROM should be performed cautiously and may be contraindicated if myelopathic signs are significant, as extension further narrows the canal.
• Resisted testing: The pattern depends on the level of cord compression. At the compression level: LMN weakness in the upper extremity myotomes (grip weakness, finger abduction weakness). Below the compression level: UMN pattern — muscles may test strong or may show a "give-way" pattern from spasticity rather than true weakness. The key finding is that the weakness pattern does not follow a single nerve root — it is broader and often bilateral.

Special Test Cluster

The test cluster for cervical myelopathy is oriented toward confirming UMN involvement and differentiating cord compression from root compression. These are red flag screening tests rather than condition-specific provocation tests.

Cluster interpretation: The Grip and Release Test is the most sensitive initial screening test — if a patient cannot achieve 20 grip-and-release cycles in 10 seconds, myelopathy should be suspected. Hoffmann Sign and Babinski Sign are UMN confirmatory tests — either one positive in a patient with gait disturbance and hand clumsiness constitutes a strong indication for urgent neurological referral. Lhermitte Sign specifically implicates the posterior columns of the cervical cord. The Inverted Radial Reflex is the most specific sign for cervical myelopathy at C5–C6 but requires practice to elicit reliably.

Differential Diagnoses