Spinal Cord Syndromes

Few regions of the nervous system reward anatomical reasoning as richly as the spinal cord. Within a structure barely the width of a finger run three great longitudinal tracts, each carrying a distinct function and — decisively — each crossing the midline at a different point along the neuraxis. Because of this, a single, well-placed cord lesion does not produce diffuse, undifferentiated dysfunction; it produces a pattern. Learn the three pathways and where they decussate, and the classic cord syndromes stop being a list to memorize and become predictions you can derive at the bedside. This page walks the major syndromes in that spirit, beginning with the anatomy that generates all of them.

The Three Tracts — and the Rule of Decussation

Three pathways dominate spinal cord localization. What matters most is not merely what each carries, but where each one crosses to the opposite side, because that single fact determines whether a deficit appears on the same side as the lesion or the opposite side.

• Lateral corticospinal tract (motor). Runs in the lateral column. These fibers have already crossed in the pyramidal decussation of the lower medulla, well above the cord. A lesion of this tract therefore causes ipsilateral upper-motor-neuron weakness below the level of the lesion (weakness, spasticity, hyperreflexia, extensor plantar response).
• Dorsal columns (vibration, proprioception, fine touch). Run in the posterior columns and ascend uncrossed, on the same side, all the way to the lower medulla, where they synapse and only then decussate as the internal arcuate fibers. A cord lesion of the dorsal columns therefore causes ipsilateral loss of vibration and joint position sense below the level.
• Spinothalamic tract (pain and temperature). Runs in the anterolateral column. Its fibers cross within the cord, in the anterior (ventral) white commissure, within about one to two segments of entry, then ascend on the opposite side. A cord lesion of this tract therefore causes contralateral loss of pain and temperature, beginning a segment or two below the lesion.

The unifying idea: within the cord, pain/temperature has already crossed, while motor and vibration/proprioception have not. That is the entire engine behind dissociated sensory loss and behind Brown-Séquard's striking split between the two sides of the body. One more cardinal sign ties the cord together: the sensory level — a horizontal cutoff across the trunk, normal above and abnormal below — which is the unmistakable signature that the lesion is in the cord rather than in a nerve, root, or brain.

Complete Cord Transection

When the cord is interrupted across its full width — by trauma, transverse myelitis, compression, or infarction — everything below the level is lost. Expect:

• Bilateral weakness below the level — paraplegia for thoracic or upper-lumbar/conus cord lesions, quadriplegia for a cervical lesion. The adult cord ends near L1–L2 (the conus), so lesions below the conus affect the cauda equina roots rather than the cord itself.
• Loss of all sensory modalities below the level, with a clear sensory level on the trunk.
• Sphincter (bladder and bowel) dysfunction and autonomic disturbance below the lesion.
• An evolving motor picture: acutely there is spinal shock — flaccid, areflexic paralysis with absent plantar responses — which over days to weeks gives way to the expected upper-motor-neuron pattern of spasticity, hyperreflexia, and extensor plantar responses.

Brown-Séquard Syndrome (Cord Hemisection)

A lesion confined to one half of the cord — the classic teaching lesion, more often approximated than seen in pure form (trauma, compression, demyelination) — produces a signature crossed picture below the level:

• Ipsilateral upper-motor-neuron weakness (lateral corticospinal tract, not yet crossed).
• Ipsilateral loss of vibration and proprioception (dorsal columns, not yet crossed).
• Contralateral loss of pain and temperature, beginning a few segments below the lesion (spinothalamic tract, already crossed within the cord).

Pearl: the patient's body diagrams the decussation chart for you — weakness and position-sense loss on one side, pinprick loss on the other. A narrow band of segmental signs (sometimes a strip of ipsilateral sensory loss or lower-motor-neuron weakness) may mark the exact level where the lesion sits.

Central Cord Syndrome

Pathology that begins in the center of the cord and expands outward — a syrinx, or a hyperextension injury in an older adult with pre-existing cervical spondylosis — strikes the crossing spinothalamic fibers in the anterior white commissure first, before the deficit reaches the long tracts at the periphery. The result:

• Dissociated, "suspended" loss of pain and temperature in a cape-like or shawl distribution over the shoulders and arms at the level of the lesion, with vibration and proprioception preserved (dorsal columns spared).
• Arms weaker than legs. In the cervical cord, the corticospinal fibers serving the arms lie more medially than those serving the legs, so a central lesion affects the upper limbs disproportionately — the hands often bear the brunt.
• With syringomyelia, the deficit is chronic and slowly progressive; with traumatic central cord syndrome, it is acute and follows a hyperextension mechanism.

Anterior Cord Syndrome (Anterior Spinal Artery Territory)

Infarction in the territory of the single anterior spinal artery damages the anterior two-thirds of the cord — the corticospinal and spinothalamic tracts — while sparing the dorsal columns, which draw their supply from the paired posterior spinal arteries. The picture below the lesion is therefore:

• Bilateral upper-motor-neuron weakness.
• Bilateral loss of pain and temperature.
• Preserved vibration and proprioception — the dorsal columns are spared because their blood supply is separate.

This is the dissociated picture of vascular myelopathy and is most often seen with aortic disease or surgery, hypotension, or atherosclerosis.

Posterior Cord Syndrome

Selective involvement of the dorsal columns — far less common in isolation — strips away vibration and joint position sense while leaving pain, temperature, and strength relatively intact. The clinical hallmark is sensory ataxia: an unsteady, broad-based gait that worsens markedly when visual compensation is removed, producing a positive Romberg sign. A positive Romberg reflects proprioceptive and/or vestibular inadequacy unmasked by eye closure (it is not a test of cerebellar function); in this setting the deficit is the loss of dorsal-column proprioceptive input.

Subacute Combined Degeneration (Vitamin B12 Deficiency)

Cobalamin deficiency injures the cord in a characteristically combined distribution, picking off two tracts at once: the dorsal columns and the lateral corticospinal tracts, frequently with a coexisting peripheral neuropathy. The result is a blend of signs:

• Loss of vibration and position sense, often the earliest finding, with sensory ataxia and a positive Romberg.
• Spastic weakness with extensor plantar responses from corticospinal involvement.
• A paradoxical reflex picture: when a superimposed peripheral neuropathy is present, the ankle jerks may be absent even though the plantar responses are extensor — a clue that lower-motor-neuron and upper-motor-neuron pathology coexist.

Pearl: the combination of brisk knees, absent ankles, and upgoing toes should always prompt a B12 level (and consideration of copper deficiency and HIV-associated myelopathy, which can mimic it). Treat early — neurologic recovery falls off the longer the deficiency persists.

Conus Medullaris versus Cauda Equina

At the caudal end of the cord, two syndromes sit anatomically adjacent and are perpetually confused. The conus medullaris is the tapered terminal cord (roughly L1–L2 in the adult); below it, the lumbosacral roots descend as the cauda equina. Distinguishing them turns on symmetry, pain, the motor pattern, and the timing of sphincter loss.

• Conus medullaris — early and symmetric saddle anesthesia, early and prominent sphincter (bladder/bowel) dysfunction, relatively less pain, and a mixed picture that can show both upper- and lower-motor-neuron signs.
• Cauda equina — asymmetric deficits, prominent radicular pain, a pure lower-motor-neuron pattern (flaccid, areflexic weakness), saddle anesthesia, with sphincter involvement appearing later.

Either one with acute, progressive deficits — particularly urinary retention and saddle numbness — is a surgical emergency warranting urgent imaging.

Summary Table

Bedside Pearls

• Find the sensory level. A horizontal trunk cutoff is the cord's calling card. Always examine the back and pin down the level — it directs imaging and frames the differential.
• Dissociation localizes. Loss of pain/temperature with spared vibration/proprioception (or the reverse) is the fingerprint of a cord lesion; let the split tell you which tract is involved and on which side.
• "Arms worse than legs" points to the central cervical cord. In an older patient after a fall on the face or forehead, think traumatic central cord syndrome on a spondylotic background.
• Acute weakness with a sensory level is a time-critical compression until proven otherwise — urgent MRI of the relevant cord segment.
• Brisk knees, absent ankles, upgoing toes → check B12 (and copper, and consider HIV myelopathy).