MSK · EP 15 · SPINE
Before You Listen
Episode Setup
- Topic in one line: the degenerative cascade that produces lumbar spinal stenosis (with its position-dependent neurogenic claudication) and cervical myelopathy (with upper motor neuron signs below the lesion), the spondylolysis-to-spondylolisthesis pipeline at L5-S1 in young athletes versus L4-L5 facet arthropathy in older adults, and the facet-mediated pain syndrome diagnosed by the dual comparative medial branch block and treated with radiofrequency ablation.
- Prerequisites: vertebral column anatomy and the upper motor neuron versus lower motor neuron distinction.
- Runtime: 1 hour 18 minutes.
Vignette. A 68-year-old retired teacher has bilateral leg pain, numbness, and a sense of heaviness in the thighs and calves that begins after walking about half a block. She can walk for an hour pushing a shopping cart at the grocery store but cannot walk to the mailbox without stopping. She rides a stationary bicycle without difficulty. Her dorsalis pedis and posterior tibial pulses are normal bilaterally; the ankle-brachial index is 1.05 on each side. A magnetic resonance imaging study of the lumbar spine shows multilevel facet hypertrophy, ligamentum flavum thickening, and central canal narrowing maximal at L4-L5.
What is the diagnosis, why does pushing a shopping cart relieve symptoms, why does she tolerate the stationary bicycle but not walking, what would the contrasting vascular condition look like, and what is the rehabilitation prescription?
(Answer at the end of this chapter)
Section 1: Cervical Stenosis and Cervical Myelopathy
Bottom line: cervical stenosis is the narrowing of the cervical canal to where the spinal cord itself is compressed; absolute stenosis is less than 10 mm anteroposterior diameter; cervical myelopathy is the resulting clinical syndrome with upper motor neuron signs below the level of compression and lower motor neuron signs at the level of compression; magnetic resonance imaging is the imaging of choice with T2 hyperintensity in the cord predicting clinical severity; surgical decompression is the definitive treatment because cervical myelopathy does not respond reliably to conservative care.
Cervical stenosis is narrowing of the cervical spinal canal to a degree that compresses the spinal cord. A normal cervical canal measures approximately 17 mm in anteroposterior diameter, and the cord occupies about 10 mm. Relative stenosis begins below 12 mm; absolute stenosis exists below 10 mm. At absolute stenosis there is no room for cerebrospinal fluid around the cord and the neural tissue is being directly compressed.
The distinction between radiculopathy and myelopathy is one of the most critical differentiations in spine medicine. Radiculopathy involves compression of an individual nerve root and produces lower motor neuron signs at a single dermatomal and myotomal level. Myelopathy involves compression of the spinal cord itself, an upper motor neuron structure, and produces a different clinical picture. The hallmark pattern is upper motor neuron signs below the level of compression combined with lower motor neuron signs at the level of compression. At the compressed segment the exiting nerve root is damaged directly, producing lower motor neuron findings (weakness, diminished reflexes) in the muscles innervated by that root. Below the level of compression the descending corticospinal and other long tracts are disrupted, releasing the segmental reflexes from their normal inhibition and producing exaggerated reflexes, spasticity, and pathologic reflexes.
The clinical presentation is insidious and progressive. Patients have gait disturbance described as stiff, clumsy, or unsteady; the gait is spastic because the corticospinal tracts controlling the lower extremities are impaired. Balance deteriorates and falls become more frequent. A hallmark early finding is hand clumsiness (“myelopathy hand”): difficulty with fine motor tasks such as buttoning shirts, handling coins, or writing, with frequent dropping of objects. This hand dysfunction results from compression of the corticospinal fibers controlling the intrinsic hand muscles.
The physical examination reveals a constellation of upper motor neuron signs. Brisk reflexes are found in the lower extremities and often in the upper extremities below the level of the lesion. Clonus may be elicited at the ankles by rapidly dorsiflexing the foot and sustaining the dorsiflexion pressure. The Hoffmann sign is elicited by flicking the nail of the patient’s relaxed middle finger downward; a positive response is involuntary flexion of the thumb and index finger. The Babinski sign is tested by stroking the lateral sole from heel to ball; a positive response is extension of the great toe with fanning of the remaining toes, pathognomonic for upper motor neuron dysfunction. An inverted brachioradialis reflex (tapping the tendon produces finger flexion instead of elbow flexion) suggests cord compression at the C5-C6 level. The Lhermitte sign (electric shock sensation down the spine with neck flexion) may also be present.
Magnetic resonance imaging is the imaging modality of choice. The critical finding is increased signal intensity within the spinal cord on T2-weighted sequences. T2 hyperintensity represents edema, demyelination, or gliosis within the compressed cord and correlates with clinical severity. T1 hypointensity in severe cases suggests irreversible myelomalacia and carries a worse prognosis.
Two grading systems classify the severity of cervical myelopathy. The Nurick grading system is a six-level scale (Grade 0 through Grade 5) based on ambulatory function and employment status. Grade 0 indicates root signs only; Grade 1 indicates signs of cord involvement without difficulty walking; Grade 2 is slight ambulation difficulty without preventing employment; Grade 3 is severe ambulation difficulty preventing employment; Grade 4 is ambulation only with assistance; Grade 5 is chairbound or bedridden. The modified Japanese Orthopaedic Association (mJOA) score evaluates upper extremity motor, lower extremity motor, sensory, and sphincter function on an 18-point scale. Mild myelopathy is mJOA 15 or higher; moderate is 12 to 14; severe is less than 12.
The causes of cervical myelopathy extend beyond simple disc herniation. Degenerative spondylosis with osteophyte formation is the most common mechanical cause. The differential includes tumor, arteriovenous malformation, spinal cord infarction, multiple sclerosis, syringomyelia, amyotrophic lateral sclerosis, and tabes dorsalis. A particularly important cause is atlantoaxial instability from rheumatoid arthritis: pannus erodes the transverse ligament, allowing C1 to sublux anteriorly on C2 and compress the upper cervical cord. Any patient with rheumatoid arthritis undergoing general anesthesia requires cervical spine imaging to rule out atlantoaxial instability before intubation.
Surgical decompression is the definitive treatment for cervical myelopathy with progressive neurological deficits or moderate to severe functional impairment. The key teaching point is that cervical myelopathy does not respond reliably to conservative management. Once cord compression produces clinical myelopathy, the natural history is progressive deterioration, and early surgical intervention produces better outcomes than watchful waiting.
High Yield — Cervical stenosis and myelopathy
- Normal cervical canal ~17 mm; relative stenosis less than 12 mm; absolute stenosis less than 10 mm.
- Myelopathy = upper motor neuron signs below the lesion + lower motor neuron signs at the lesion.
- Hallmarks: spastic gait, myelopathy hand (fine motor loss, dropping objects), hyperreflexia, Hoffmann sign, Babinski, clonus, Lhermitte sign, inverted brachioradialis reflex.
- MRI with T2 cord hyperintensity correlates with clinical severity.
- Grading: Nurick 0-5 (gait); mJOA 18 max (≥15 mild, 12-14 moderate, less than 12 severe).
- Rheumatoid pannus eroding the transverse ligament → atlantoaxial instability → check before intubation.
- Surgical decompression is the definitive treatment; cervical myelopathy does not reliably respond to conservative care.
Those long descending cables, specifically the corticospinal tracts, normally provide this constant stream of inhibitory signals down to your local reflexes. Your brain is constantly telling your leg reflexes to just calm down and not overreact. But when those tracts are choked off up in the neck, that calming inhibition is lost entirely, and that is exactly why you see exaggerated hyperactive reflexes and severe muscle spasticity in the lower limbs when a patient has a severe compression way up in their neck.
— MSK-15 podcast, ~9:19