Anatomy Atlas

Corticospinal tract

Tractus corticospinalis
Also: Pyramidal tract · Upper motor neuron · UMN · Lateral corticospinal tract · Babinski sign
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Main voluntary motor pathway from the motor cortex to the spinal cord. It crosses in the lower medulla; damage causes upper motor neuron signs — weakness, spasticity, hyperreflexia and an extensor plantar response.

Core anatomy

Origin

Upper motor neurons in the primary motor cortex (precentral gyrus, including the giant Betz cells of layer V), premotor and supplementary motor areas, and parietal cortex.

Course

Corona radiata → posterior limb of the internal capsule → middle of the cerebral peduncle (midbrain) → scattered bundles in the basilar pons → pyramids of the medulla oblongata → 85–90% cross in the pyramidal decussation and descend in the lateral corticospinal tract of the contralateral cord → synapse on lower motor neurons in the ventral horn (directly or via interneurons). The uncrossed 10–15% descend in the anterior corticospinal tract (axial muscles) and mostly cross at segmental levels.

Motor

Voluntary skilled movement, especially of the distal limbs (fine finger movements); lower motor neurons carry the signal to muscle via the spinal nerves.

Relations

Corticobulbar fibers accompany it to cranial nerve motor nuclei (most receive bilateral input, except the lower face and — partly — CN XII, which are mainly contralateral).

Notes

A lesion above the decussation (cortex, capsule, brainstem) causes contralateral weakness; a spinal cord lesion causes ipsilateral weakness below it.

Mentioned in

Generated automatically from links in other entries.

Spinal cord cross-section: major tractsCross-section of the cervical cord with the dorsal side at the top. The dorsal columns (fasciculus gracilis medially, cuneatus laterally) lie between the dorsal horns and carry vibration, fine touch and proprioception on the same side. The lateral corticospinal tract lies in the lateral funiculus and carries motor commands to the same side of the body below. The spinothalamic tract lies in the anterolateral funiculus and carries pain and temperature from the opposite side; its fibers cross in the anterior white commissure in front of the central canal. The anterior corticospinal tract lies beside the anterior median fissure.Fasciculus gracilis (legs)Fasciculus cuneatus (arms)Dorsal horn (sensory)Lateral corticospinal tract(ipsilateral motor)Anterior white commissure(crossing pain fibers — syrinx)Spinothalamic tract(contralateral pain, temp)Ventral horn (LMN)Anterior corticospinal tractDorsal ↑ · cervical levelBlue: dorsal columns — cross in the medullaGreen: spinothalamic — crosses within 1–2 segmentsRed: corticospinal — crossed in the medulla, descends on the same side it acts onHemisection → ipsilateral weakness and vibration loss, contralateral pain/temperature loss

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Spinal cord tracts (cross-section). Cervical cord, dorsal at the top. Dorsal columns and lateral corticospinal tract serve the same side of the body; the spinothalamic tract serves the opposite side because its fibers cross in the anterior white commissure (dashed green) within 1–2 segments.
Original schematic, created for this atlas.
Corticospinal fibers descending from the motor cortex through the internal capsule, cerebral peduncle, pons and pyramids, crossing at the decussation of the pyramids into the lateral corticospinal tract
The motor tract from the cortex through the internal capsule, brainstem and pyramidal decussation.
Henry Vandyke Carter, Gray's Anatomy of the Human Body, 20th ed. (1918), Fig. 764. Source · Public domain (Public domain in the US: published before January 1, 1931 (per Wikimedia Commons))
Cross-section of the spinal cord showing the ascending tracts (fasciculus gracilis and cuneatus, spinocerebellar and spinothalamic) and descending tracts (lateral and anterior corticospinal, rubrospinal, vestibulospinal)
Lateral and anterior corticospinal tracts in the cord.
Henry Vandyke Carter, Gray's Anatomy of the Human Body, 20th ed. (1918), Fig. 672. Source · Public domain (Public domain in the US: published before January 1, 1931 (per Wikimedia Commons))

Clinical correlations

Upper vs lower motor neuron lesions PANCE

Mechanism / lesion

UMN — damage anywhere along the corticospinal tract (stroke, MS, cord compression, B12 deficiency). LMN — ventral horn cell, root, plexus or peripheral nerve.

Classic presentation

UMN: weakness in a pyramidal pattern (arm extensors, leg flexors), spasticity (velocity-dependent, "clasp-knife"), hyperreflexia, clonus, Babinski sign (extensor plantar), Hoffmann sign, little atrophy. Acutely (spinal shock) tone and reflexes may be reduced. LMN: weakness, atrophy, fasciculations, hypotonia, hyporeflexia, flexor plantar.

Amyotrophic lateral sclerosis (ALS) PANCE

Mechanism / lesion

Degeneration of both upper and lower motor neurons (corticospinal tracts and ventral horn/brainstem motor nuclei); sensation spared.

Classic presentation

Mixed UMN and LMN signs in the same limb — weakness, atrophy, fasciculations with hyperreflexia and Babinski; bulbar dysarthria and dysphagia; no sensory loss. EMG; riluzole; respiratory failure is the usual cause of death.

Cervical spondylotic myelopathy PANCE

Mechanism / lesion

Degenerative narrowing of the cervical canal compressing the cord (older adults).

Classic presentation

Clumsy hands, gait imbalance, UMN signs in the legs (and arms below the level), positive Hoffmann sign, bladder urgency; neck pain may be minimal. MRI cervical spine; surgical decompression if progressive.

High-yield PANCE pearls

  • UMN: spasticity, hyperreflexia, clonus, Babinski; LMN: atrophy, fasciculations, hyporeflexia.
  • UMN + LMN signs, no sensory loss → ALS.
  • Crosses at the pyramidal decussation (lower medulla) → brain lesions give contralateral weakness, cord lesions ipsilateral.
  • Older adult with clumsy hands, unsteady gait, Hoffmann sign → cervical myelopathy → MRI.

Imaging anatomy

CT

Noncontrast CT head in acute weakness (stroke protocol).

MRI

MRI brain or spine at the suspected level — stroke (DWI), demyelination, cord compression; EMG/nerve conduction studies to confirm LMN disease (ALS).

Physical exam

Strength / function testing

Pronator drift (arms outstretched, palms up, eyes closed — the weak arm pronates and drifts down); strength grading (0–5); tone (spasticity); reflexes; plantar response; clonus at the ankle; Hoffmann sign; gait (circumduction).

Babinski sign (plantar response)

Technique

Stroke the lateral sole firmly from the heel toward the little toe and across the ball of the foot.

Positive test

Extension (dorsiflexion) of the great toe, with fanning of the other toes.

Significance

Upper motor neuron lesion (corticospinal tract). Normal in infants under about 1–2 years.

Hoffmann sign

Technique

Flick the nail of the relaxed middle finger downward.

Positive test

Flexion of the thumb and index finger.

Significance

Suggests an upper motor neuron lesion affecting the arms, e.g. cervical myelopathy (can occur in some normal people).

Self-quiz

Q1.

A 58-year-old has progressive weakness of the right hand with wasting and fasciculations, brisk reflexes in all limbs, and bilateral Babinski signs. Sensation is normal. What is the most likely diagnosis?

Show answer

B

Combined UMN (hyperreflexia, Babinski) and LMN (atrophy, fasciculations) signs without sensory loss are the hallmark of ALS.

Q2.

Which finding indicates an upper motor neuron lesion?

Show answer

C

An extensor plantar response (Babinski sign) indicates corticospinal tract (UMN) dysfunction. The other findings suggest a lower motor neuron lesion.

Q3.

Where do most corticospinal fibers cross the midline?

Show answer

B

About 85–90% of corticospinal fibers cross in the pyramidal decussation at the medulla–cord junction. Lesions above it cause contralateral weakness; cord lesions cause ipsilateral weakness.

Q4.

Immediately after an acute complete spinal cord injury, what are tone and reflexes like below the lesion?

Show answer

D

In spinal shock, tone and reflexes are initially reduced or absent below the lesion. Upper motor neuron signs (spasticity, hyperreflexia, Babinski) develop later.

Q5.

A cortical stroke causes weakness of the opposite lower face but spares the forehead. Why?

Show answer

C

Most cranial motor nuclei receive bilateral corticobulbar input, but the part of the facial nucleus for the lower face receives mainly contralateral input, so an upper motor neuron lesion weakens only the opposite lower face.

Flashcards

See also