Spinal Cord Syndromes & Myelopathy

Cord Anatomy That Drives the Syndromes

Three tracts. Nearly every cord vignette can be solved by tracking three pathways. Because the spinothalamic tract crosses almost immediately while the other two cross in the medulla, one side of the cord carries same-side strength and position sense but opposite-side pain and temperature.

Blood supply. A single anterior spinal artery supplies the anterior two-thirds of the cord (corticospinal and spinothalamic tracts, anterior horns); paired posterior spinal arteries supply the dorsal columns. The lower thoracic and lumbar cord depends heavily on one radicular feeder, the artery of Adamkiewicz, usually arising on the left, which is why aortic events threaten it.

Where the cord ends. In adults the conus medullaris lies at about the L1–L2 vertebral level; below it the lumbosacral roots form the cauda equina. Lumbar puncture is therefore performed at L3–L4 or L4–L5.

Acute myelopathy is compressive until proven otherwise. A new sensory level, bilateral leg weakness, or sphincter change needs emergent MRI of the spine, with gadolinium, to find a surgical lesion: abscess, hematoma, metastasis, or disc. If nothing compresses the cord, brain MRI and lumbar puncture look for transverse myelitis (multiple sclerosis, neuromyelitis optica spectrum disorder, MOG antibody disease), infection, or vascular causes such as a spinal dural arteriovenous fistula.

Incomplete Cord Syndromes

Central cord syndrome. The classic patient is an older adult with cervical spondylosis who falls forward, strikes the face, and hyperextends the neck, often without a fracture. The arms, and especially the hands, are weaker than the legs, with variable sensory loss below the lesion and urinary retention. Recovery typically begins in the legs, then the bladder, with hand function returning last.

Syringomyelia. A fluid-filled cavity in the central cervical cord, frequently with a Chiari I malformation or after trauma, first interrupts the crossing spinothalamic fibers. The result is bilateral, cape-like loss of pain and temperature over the shoulders and arms with preserved touch and vibration (dissociated sensory loss). As the syrinx expands it destroys anterior horn cells (hand atrophy, arm areflexia), then the corticospinal tracts (spastic legs); Horner syndrome and scoliosis may follow. Painless burns on the hands are the classic clue, and MRI of the cervical spine and brain confirms it.

Anterior cord syndrome. Anterior spinal artery infarction follows thoracoabdominal aortic surgery (cross-clamping), aortic dissection, or profound hypotension. Onset is abrupt: bilateral paralysis, loss of pain and temperature below the lesion, and urinary retention, with vibration and proprioception preserved. Lumbar CSF drainage and blood pressure augmentation are used to protect the cord during thoracoabdominal repair.

Brown-Séquard syndrome. Hemisection, classically from a stab wound but also from tumor, disc, or multiple sclerosis, produces ipsilateral spastic weakness and loss of vibration and proprioception below the lesion, with contralateral loss of pain and temperature beginning 1–2 segments below. A narrow band of complete sensory loss and LMN signs marks the level; a lesion above T1 adds ipsilateral Horner syndrome.

Dorsal Column Disease

Subacute combined degeneration. Vitamin B12 is a cofactor for methionine synthase and methylmalonyl-CoA mutase, and deficiency damages myelin in the dorsal columns and lateral corticospinal tracts, usually alongside a peripheral neuropathy. Symmetric paresthesias of the feet and hands come first, followed by loss of vibration and position sense, sensory ataxia with a positive Romberg sign, spasticity, and Babinski signs; the neuropathy removes the ankle jerks. MRI may show T2 signal along the dorsal columns.

• B12 deficiency: pernicious anemia, gastrectomy or bariatric surgery, metformin, long-term acid suppression, strict vegan diet. Anemia and macrocytosis may be absent.
• Nitrous oxide: oxidizes the cobalt in B12 and inactivates methionine synthase; seen with recreational "whippets" or when anesthesia unmasks marginal B12 stores. Serum B12 can be normal.
• Copper deficiency: bariatric surgery, malabsorption, or excess zinc intake; produces an identical myelopathy, often with anemia and neutropenia; serum copper and ceruloplasmin are low.

Workup and treatment. Elevated methylmalonic acid and homocysteine confirm tissue B12 deficiency; methylmalonic acid stays normal in folate deficiency. Neurologic disease is treated with parenteral B12 (and cessation of nitrous oxide), and copper deficiency with copper replacement and removal of excess zinc.

Giving folate alone to a B12-deficient patient can correct the anemia while the cord damage progresses.

Romberg sign: a patient steady with eyes open who sways or falls with eyes closed has proprioceptive (sensory) ataxia from dorsal column or large-fiber disease, not cerebellar ataxia.

Tabes dorsalis. Tertiary neurosyphilis, appearing years to decades after untreated infection, damages the dorsal roots and dorsal columns. Features are sensory ataxia with a stamping, wide-based gait worse in the dark, positive Romberg sign, lancinating "lightning" pains, areflexia, urinary retention, Charcot (neuropathic) joints, and Argyll Robertson pupils that constrict to accommodation but not to light. There are no corticospinal signs. Diagnosis rests on a reactive serum treponemal test and CSF studies (the CSF VDRL is specific); treatment is IV aqueous penicillin G for 10–14 days, because benzathine penicillin does not reach adequate CSF levels.

Spinal Emergencies

Spinal epidural abscess. Risk factors are IV drug use, diabetes, bacteremia, hemodialysis, alcohol use disorder, and recent spinal procedures or catheters. Staphylococcus aureus, including MRSA, causes most cases. Focal back pain and tenderness come first, then radicular pain, weakness, and sphincter loss. The full triad of fever, back pain, and neurologic deficit is present in only a minority at presentation, so a febrile or high-risk patient with focal spinal pain needs imaging; ESR and CRP are usually elevated.

Spinal epidural hematoma. Risks include anticoagulants, antiplatelet drugs, coagulopathy, trauma, and lumbar puncture or epidural anesthesia, including catheter removal. Sudden severe back or radicular pain is followed within hours by weakness, sensory loss, and retention. Management is emergent MRI, reversal of anticoagulation, and surgical decompression; outcome depends on time to surgery.

Before neuraxial puncture or catheter removal, hold prophylactic-dose LMWH for at least 12 hours and therapeutic-dose LMWH for at least 24 hours; give the next LMWH dose at least 4 hours after catheter removal.

Metastatic cord compression. New back pain in a patient with cancer (prostate, breast, lung, myeloma) warrants dexamethasone and emergent MRI of the whole spine, followed by radiation or surgery.

Conus Medullaris vs Cauda Equina

Management. Red flags in a patient with back pain (saddle numbness, new retention or incontinence, bilateral leg deficits, reduced anal tone) demand emergent lumbosacral MRI. A bladder scan showing a large post-void residual supports the diagnosis. Decompress as soon as possible; outcomes are better when surgery occurs within 48 hours.

Cervical Spondylotic Myelopathy

Presentation. The most common myelopathy in older adults develops insidiously as disc-osteophyte bars, ligamentum flavum hypertrophy, or ossification of the posterior longitudinal ligament narrow the canal. Patients report numb, clumsy hands (buttons, handwriting, dropping objects) and gait imbalance; neck pain may be absent. Examination shows LMN signs at the compressed level and UMN signs below it: Hoffmann sign, hyperreflexia, Babinski signs, and sometimes a Lhermitte sign.

Differential. UMN signs separate myelopathy from bilateral carpal tunnel syndrome, whose Tinel sign, thenar wasting, and nocturnal paresthesias stay below the wrist. ALS lacks sensory symptoms, and B12 deficiency adds absent ankle jerks.

Management. MRI of the cervical spine shows cord compression, often with T2 signal change. Moderate, severe, or progressive myelopathy warrants surgical decompression; mild cases need close follow-up. Neck manipulation should be avoided, and minor hyperextension trauma in these patients can precipitate central cord syndrome.