The spinal cord transmits information up to the brain and down from it through a small number of named tracts running in defined columns of white matter. Each tract carries a specific kind of information, decussates at a specific level, and produces a specific clinical pattern when injured. The patterns of dissociated sensory loss that occur in spinal cord disease — pain and temperature gone but vibration preserved, or vice versa, or one side and not the other — are explained entirely by which tracts have been damaged. Memorizing the cord tracts and where they cross is the foundation of spinal cord localization.

This page covers the major ascending and descending tracts of the spinal cord, where they decussate, and the clinical syndromes they produce. The functional system pages cover the corresponding pathways at the brainstem and cortical levels.

The Cord in Cross Section

White matter columns and their contents (cervical cord, where all tracts are present):

The Two Major Ascending Sensory Systems

The cord has two principal ascending sensory pathways. They differ in modality, fiber type, and — crucially — the level at which they cross the midline.

Dorsal Column-Medial Lemniscus System

Carries fine touch, vibration, joint position sense, and the discriminative sensations.

• Primary sensory neuron: cell body in dorsal root ganglion.
• Central process enters cord and ascends ipsilaterally in the dorsal columns. From below T6, fibers run in the gracile fasciculus (medial). From above T6, additional fibers from upper extremities and trunk run in the cuneate fasciculus (lateral).
• First synapse: in the nucleus gracilis and nucleus cuneatus of the lower medulla.
• Second-order neurons cross the midline as internal arcuate fibers, forming the contralateral medial lemniscus.
• The medial lemniscus ascends through the brainstem to the VPL of the thalamus.
• Third-order neurons project to the primary somatosensory cortex.

Key clinical point: the decussation is in the medulla. Below the medulla, dorsal column information is on the same side as the body it reports from. Above the medulla, it is on the opposite side.

Spinothalamic (Anterolateral) System

Carries pain, temperature, and crude touch.

• Primary sensory neuron: cell body in dorsal root ganglion. Small fibers (Aδ and C).
• Central process enters the cord and ascends 1-3 segments in Lissauer’s tract.
• First synapse: in the dorsal horn (especially substantia gelatinosa, lamina II).
• Second-order neurons cross the midline through the anterior white commissure at or near the segmental level of entry and ascend in the contralateral lateral spinothalamic tract.
• The spinothalamic tract ascends through the brainstem to the VPL of the thalamus.
• Third-order neurons project to primary somatosensory cortex.

Key clinical point: the decussation is in the cord, at or one to three segments above the level of entry. Above the cord level of entry, spinothalamic information reflects the contralateral body.

Trigeminal Sensory System

The face’s sensory pathways follow similar principles. Pain and temperature from the face are carried by CN V to the spinal trigeminal tract and nucleus, which extends from the lower pons down through the medulla and into the upper cervical cord. Second-order neurons cross and ascend in the trigeminothalamic tract to VPM of the thalamus. Touch and proprioception from the face use the principal sensory nucleus in the mid-pons.

The Two Major Descending Motor Systems

Corticospinal (Pyramidal) Tract

The principal voluntary motor pathway from cerebral cortex to spinal cord.

• Cell bodies of origin: primary motor cortex (about 30% of fibers), premotor and supplementary motor cortex (about 30%), primary somatosensory cortex (about 30%), and other cortical regions.
• Axons descend through the corona radiata, internal capsule, cerebral peduncle, basis pontis, and medullary pyramid.
• At the pyramidal decussation at the cervicomedullary junction, about 85% of fibers cross to the opposite side and descend as the lateral corticospinal tract.
• About 10-15% descend uncrossed as the anterior corticospinal tract, eventually crossing at the segmental level.
• Most fibers synapse on interneurons; a minority synapse directly on alpha motor neurons in the ventral horn.

Key clinical point: a cord lesion below the pyramidal decussation produces motor deficits on the same side as the cord lesion (the corticospinal fibers have already crossed in the medulla). A brain or upper brainstem lesion produces motor deficits on the opposite side.

Extrapyramidal Descending Tracts

Several non-pyramidal descending tracts modulate motor activity:

• Vestibulospinal tracts: from the vestibular nuclei. Lateral vestibulospinal tract drives extensor tone for postural support; medial vestibulospinal tract coordinates head and neck movements with vestibular input.
• Reticulospinal tracts: from the reticular formation of the pons and medulla. Modulate posture, locomotion, autonomic function.
• Tectospinal tract: from the superior colliculus. Coordinates head movements with visual orienting reflexes. Small in humans.
• Rubrospinal tract: from the red nucleus. Small in humans (vestigial compared to other primates).

These tracts together support the postural and reflexive components of motor control that operate beneath voluntary movement.

The Spinocerebellar Tracts

Carry unconscious proprioceptive and somatosensory information from the body to the cerebellum:

• Dorsal spinocerebellar tract: from the cells of Clarke’s nucleus (in the dorsal horn at T1-L2). Carries proprioception from the lower body. Travels uncrossed to the cerebellum via the inferior cerebellar peduncle.
• Ventral spinocerebellar tract: from cells in the lumbar cord. Crosses at the cord level, ascends in the contralateral ventral column, and crosses back in the brainstem to enter the cerebellum via the superior cerebellar peduncle. Net result: ipsilateral to the body it reports from.
• Cuneocerebellar tract: the upper extremity equivalent of the dorsal spinocerebellar tract. From cells in the lateral cuneate nucleus of the medulla.
• Rostral spinocerebellar tract: the upper extremity equivalent of the ventral spinocerebellar tract.

Spinocerebellar information is the substrate for cerebellar coordination of movement and gait. Damage produces sensory ataxia indistinguishable from cerebellar ataxia in some respects (loss of unconscious proprioception), though the dorsal column system provides much of the conscious proprioception that supports voluntary movement.

Patterns of Dissociated Sensory Loss

The geometric arrangement of cord tracts and their decussation patterns produces characteristic dissociated patterns of sensory loss that are diagnostic of specific cord lesions.

Brown-Séquard Syndrome (Hemisection)

Cord hemisection produces:

• Ipsilateral motor weakness below the level (corticospinal tract, already decussated in medulla).
• Ipsilateral loss of vibration and joint position sense below the level (dorsal columns; ipsilateral until decussation in medulla).
• Contralateral loss of pain and temperature beginning a few segments below the level (spinothalamic tract; fibers crossed at the segmental level of entry, 1-3 segments above the lesion).

The crossed pattern — ipsilateral dorsal column loss with contralateral pain/temperature loss — is the bedside hallmark and is one of the most useful localizing findings in clinical neurology.

Anterior Cord Syndrome

Anterior spinal artery infarction. Damage to the anterior two-thirds of the cord:

• Loss of motor function (corticospinal tract) below the level.
• Loss of pain and temperature (spinothalamic tract) bilaterally below the level.
• Preserved vibration and joint position sense (dorsal columns are in the posterior cord, spared).

Posterior Cord Syndrome

Damage to the dorsal columns:

• Loss of vibration, joint position sense.
• Sensory ataxia and positive Romberg.
• Preserved pain, temperature, and motor function.

Causes: tabes dorsalis (now rare), B12 deficiency (subacute combined degeneration), posterior column infarction, demyelination.

Central Cord Syndrome (Syringomyelia)

Expanding central cavity disrupts the spinothalamic fibers crossing through the anterior commissure. Result:

• Bilateral loss of pain and temperature in a “cape” or “shawl” distribution over shoulders, arms, and upper trunk.
• Preserved sensation in the lower body (the laterally placed spinothalamic fibers from the lower body are spared until late).
• Preserved dorsal column function.
• As syrinx expands: anterior horn cell loss (arm weakness and atrophy) and lateral corticospinal involvement (leg spasticity).

Subacute Combined Degeneration

B12 deficiency. Selective damage to dorsal columns and lateral corticospinal tracts, with relative sparing of spinothalamic tract and lower motor neurons. Combined picture:

• Loss of vibration and joint position sense, sensory ataxia, Romberg.
• Spastic paresis with upgoing toes.
• Mixed reflex pattern (some areas hyperreflexic, some hyporeflexic from concurrent neuropathy).
• Often cognitive changes and macrocytic anemia, but not required.

Spinal Reflexes

The cord mediates several reflexes essential to motor function:

Monosynaptic Stretch Reflex (Deep Tendon Reflex)

Muscle stretch activates Ia afferents from muscle spindles, which directly excite alpha motor neurons innervating the same muscle (and antagonist muscles via inhibitory interneurons). The result: contraction of the stretched muscle. This circuit underlies the patellar reflex (L3-L4), the Achilles reflex (S1), the biceps reflex (C5-C6), the triceps reflex (C7-C8), and others.

Withdrawal (Flexor) Reflex

Painful stimulus activates nociceptive afferents, which (through polysynaptic circuits) excite ipsilateral flexor motor neurons and inhibit extensors, producing withdrawal. The Babinski sign is part of this flexor synergy, with the great toe extension being a vestigial component.

Crossed Extensor Reflex

Accompanies the withdrawal reflex. Contralateral extensor activation supports posture while the affected limb withdraws.

Renshaw Cell Inhibition

Alpha motor neurons send collateral axons to Renshaw cells (inhibitory interneurons), which feed back to inhibit the alpha motor neurons. Provides feedback regulation of motor neuron firing. Strychnine blocks glycine receptors on Renshaw cells, removing this inhibition and producing the dramatic hyperexcitability of strychnine poisoning.

Autonomic Outflow

The cord has autonomic outflow that varies by level:

• Sympathetic (thoracolumbar) outflow: from the intermediolateral cell column at T1-L2. Preganglionic sympathetic fibers exit with ventral roots, synapse in the sympathetic chain or in prevertebral ganglia.
• Parasympathetic (sacral) outflow: from the intermediolateral cell column at S2-S4. Innervates pelvic viscera (bladder, sigmoid colon, rectum, reproductive organs).

Cord lesions above T1 disrupt sympathetic outflow to the entire body, producing the autonomic instability of cervical cord injury. Cord lesions at the sacral level disrupt parasympathetic control of bladder, bowel, and sexual function.

Spinal Shock

Acute severe cord injury produces immediate flaccid paralysis below the level, with loss of all reflexes and sensation. This “spinal shock” lasts days to weeks. Over time, spinal reflexes return below the level, often with increased excitability — producing the spastic, hyperreflexic state characteristic of chronic cord transection. The pathophysiology of spinal shock involves loss of descending facilitation of spinal motor neurons.

🔍 Did You Know?

The classical “onion-skin pattern” of facial sensory loss reflects a specific anatomical organization in the spinal trigeminal nucleus. The rostral portion of the nucleus represents the perioral region; the caudal portion represents the peripheral face (forehead, temple, preauricular area). A lesion at the upper end of the spinal trigeminal nucleus (in the medulla) therefore produces sensory loss in a concentric pattern centered on the mouth, expanding outward — not respecting the trigeminal divisions at all. A patient with circumoral pain or numbness without involvement of the peripheral face has a brainstem lesion until proven otherwise. The onion-skin pattern is one of the more striking demonstrations that neuroanatomical organization can predict clinical findings in non-intuitive ways.

Pitfalls and Pearls

• Dorsal columns decussate in the medulla; spinothalamic tract decussates at the cord level of entry. This single fact underlies every pattern of dissociated sensory loss in cord disease.
• The Brown-Séquard pattern is the most useful single localizer for cord hemisection: ipsilateral motor and dorsal column loss with contralateral pain/temperature loss.
• Anterior cord syndrome spares vibration and joint position sense. Look for this dissociation when motor and pain/temperature are gone.
• Central cord lesions (syringomyelia) produce suspended pain/temperature loss in a cape distribution, sparing the lower body.
• Subacute combined degeneration from B12 deficiency affects both dorsal columns and corticospinal tracts. Mixed reflex pattern is characteristic.
• The lateral corticospinal tract carries 85% of corticospinal fibers after the pyramidal decussation. Cord lesions below the decussation produce ipsilateral motor deficits.
• Spinal shock produces initial flaccid paralysis; spasticity develops over weeks. Reflexes return below the level eventually.
• The sensory level on the trunk often lies one to three segments below the cord lesion, because spinothalamic fibers ascend in Lissauer’s tract before crossing.
• The spinal trigeminal nucleus has somatotopic organization that produces the onion-skin pattern of facial sensory loss in brainstem lesions.
• Always image one or two segments above the bedside sensory level when looking for cord pathology — the lesion is often higher than the sensory level suggests.

References

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