Spinal cord tracts

Dorsal column fibres ascend uncrossed to the medulla, so a cord hemisection removes ipsilateral vibration and joint position sense. Spinothalamic fibres cross in the anterior white commissure within one to two segments of entry, so the same lesion cuts fibres that came from the opposite side, and the contralateral pain and temperature level sits one to two segments below the lesion. The lateral corticospinal tract has already crossed at the pyramids, so the UMN weakness is ipsilateral, with a band of LMN weakness and complete sensory loss at the level itself.

The cavity expands from the central canal and first destroys the spinothalamic fibres crossing in the anterior white commissure at the affected segments, usually cervical, producing a bilateral cape-like loss of pain and temperature. The dorsal columns lie posteriorly and are untouched until late, so the loss is dissociated. As the syrinx enlarges it reaches the anterior horns (hand wasting) and the lateral corticospinal tracts (spastic legs).

Vitamin B12 deficiency demyelinates the dorsal columns (loss of vibration and joint position sense, sensory ataxia, positive Romberg) and the lateral corticospinal tracts (spasticity, brisk knee jerks, Babinski sign), but it also causes a peripheral neuropathy that interrupts the reflex arc, so ankle jerks are lost. Nitrous oxide misuse and copper deficiency produce the same picture; giving folate before B12 can precipitate it.

Dorsal column-medial lemniscus: after the first synapse in the nucleus gracilis and cuneatus, the internal arcuate fibres cross in the caudal medulla. Spinothalamic: after the first synapse in the dorsal horn (laminae I and V), the second-order axons cross in the anterior white commissure of the cord one to two segments above entry. Lateral corticospinal: 85 to 90 per cent of pyramidal fibres cross at the pyramidal decussation at the cervicomedullary junction; the remaining 10 to 15 per cent run uncrossed as the anterior corticospinal tract and cross segmentally in the anterior white commissure.

In both the spinothalamic and lateral corticospinal tracts the sacral fibres lie outermost and the cervical fibres innermost. An extramedullary compressive lesion damages sacral fibres first, so the sensory level climbs from below and the perineum is not spared. An intramedullary lesion such as a syrinx or ependymoma damages the inner fibres first and gives sacral sparing, usually with dissociated sensory loss and early LMN signs at the level.

UMN lesions (cortex to lateral corticospinal tract) give spasticity, hyperreflexia, clonus, an extensor plantar response and pyramidal pattern weakness with little wasting. LMN lesions (anterior horn cell to muscle) give flaccidity, hyporeflexia, wasting, fasciculations and a flexor or absent plantar. The side follows the pyramidal decussation: a lesion above it causes contralateral weakness, a lesion below it (in the cord) causes ipsilateral weakness.