corticospinal tract

**Origin:** ~30% from primary motor cortex (area 4, precentral gyrus), ~30% from premotor cortex and supplementary motor area (area 6), ~40% from somatosensory cortex (parietal lobe). Axons are from layer V pyramidal cells (including Betz cells).

**Course (mnemonic: "Come Inside, Make Pyramids, Cross, Step down"):** 1. Corona radiata 2. Posterior limb of the internal capsule (a common site for lacunar stroke; pure motor hemiparesis) 3. Midbrain: middle 3/5 of the cerebral peduncle (crus cerebri) 4. Pons: basilar pons, scattered among the pontine nuclei 5. Medulla: forms the pyramids 6. Caudal medulla: ~85-90% of fibers decussate at the pyramidal decussation, forming the **lateral corticospinal tract** (controls limb/distal musculature). The remaining ~10-15% stay uncrossed as the **anterior (ventral) corticospinal tract**, which controls axial/proximal muscles and decussates at the segmental level in the spinal cord (cervical and upper thoracic). 7. Synapse in the anterior horn (lamina IX) on lower motor neurons (alpha motor neurons) → exits via the ventral root → neuromuscular junction.

**Somatotopy:** In the lateral corticospinal tract, cervical (arm) fibers lie medial and sacral (leg) fibers lie lateral. In the internal capsule and cortex, the motor homunculus applies (leg medial near the interhemispheric fissure, supplied by the ACA; face/hand lateral, supplied by the MCA).

**Function:** Voluntary, skilled, fine motor movement, especially of the distal extremities (fingers and hands). Works with the corticobulbar tract (cranial nerve motor nuclei).

**Lesion localization (high-yield):** - **Upper motor neuron (UMN) signs:** spastic paralysis (clasp-knife spasticity), hyperreflexia, clonus, **Babinski sign (extensor plantar reflex)**, weakness, little muscle atrophy (only disuse atrophy), and loss of superficial abdominal and cremasteric reflexes. Initially, acute lesions may cause flaccid paralysis and hyporeflexia (spinal shock or cerebral diaschisis) before spasticity develops. - **Above the pyramidal decussation (cortex, internal capsule, midbrain, pons, upper medulla):** **contralateral** weakness. - **Below the decussation (spinal cord):** **ipsilateral** weakness. - **Internal capsule infarct (lenticulostriate branches of the MCA):** pure motor stroke, contralateral hemiparesis involving the face, arm, and leg. - **Medial medullary syndrome (anterior spinal artery):** contralateral hemiparesis (pyramid), contralateral loss of proprioception/vibration (medial lemniscus), and ipsilateral tongue deviation (CN XII). Remember: "tongue points toward the lesion." - **Brown-Séquard syndrome (spinal cord hemisection):** ipsilateral spastic paralysis below the lesion (corticospinal), ipsilateral loss of proprioception/vibration/fine touch (dorsal column), contralateral loss of pain and temperature 1-2 levels below the lesion (spinothalamic), and ipsilateral LMN signs at the level of the lesion. - **ALS (amyotrophic lateral sclerosis):** combined UMN (corticospinal degeneration, lateral sclerosis) and LMN (anterior horn cell loss) findings, with spared sensation and no sphincter dysfunction. Riluzole (glutamate antagonist) and edaravone are used. - **Subacute combined degeneration (vitamin B12 deficiency):** degeneration of the dorsal columns and lateral corticospinal tracts (and spinocerebellar tracts) → spastic weakness, ataxia, and loss of vibration/proprioception. - **Poliomyelitis / Werdnig-Hoffmann disease (SMA type 1):** LMN lesions only (anterior horn), not corticospinal tract. - **Cerebral palsy (spastic type):** UMN involvement. - **Anterior spinal artery syndrome:** bilateral loss of corticospinal and spinothalamic function below the lesion, with dorsal columns spared. - **Hereditary spastic paraplegia:** progressive degeneration of corticospinal tract axons causing spasticity of the legs.

**UMN vs LMN comparison:** - UMN: ↑ tone, ↑ reflexes, + Babinski, no fasciculations, minimal atrophy. - LMN: ↓ tone, ↓ reflexes, − Babinski, fasciculations, marked atrophy.

**Clinical pearls:** Corticospinal tract fibers are myelinated and heavily involved in the Babinski reflex. This reflex is normal in infants under ~1 year because of incomplete myelination of the tract. Pathologic in adults.