Overview

Axons per pyramid≈1 million

Fibres crossing at pyramids≈85–90%

Fibres from Betz cells≈3–5%

Myelination complete≈2 years of age

About 1 million axons form each pyramid. Roughly one-third arise from the primary motor cortex (area 4, precentral gyrus), including the giant pyramidal Betz cells of layer V, which account for only ≈3–5% of fibres. About another third come from the premotor and supplementary motor areas (area 6), and the rest from the parietal lobe (areas 3, 1, 2, 5 and 7), where they modulate sensory transmission.

The fibres descend through the corona radiata and the posterior limb of the internal capsule (face → arm → leg from anterior to posterior), the middle three-fifths of the cerebral peduncle (crus cerebri), and the basilar pons, where they are broken into bundles. They regroup as the medullary pyramid. At the cervicomedullary junction, ≈85–90% decussate (the pyramidal decussation) to form the lateral corticospinal tract in the lateral funiculus. These fibres end, directly or through interneurons, on anterior horn motor neurons, mainly those controlling distal limb muscles; the direct cortico-motoneuronal connections are essential for fractionated finger movements. The uncrossed ≈10–15% descend as the anterior corticospinal tract, most crossing at segmental level in the anterior white commissure. They supply axial and proximal muscles and end in the cervical and upper thoracic cord.

The parallel corticobulbar tract leaves at brainstem levels to supply the motor nuclei of the cranial nerves. Most of these nuclei receive bilateral cortical input. Important exceptions are the part of the facial nucleus supplying the lower face (contralateral only) and, largely, the hypoglossal nucleus (mostly contralateral). This explains why an UMN facial palsy spares the forehead.

Parts & subdivisions

Lateral corticospinal tract
The crossed tract (85–90%) in the lateral funiculus. It is laminated with cervical fibres medial and sacral fibres lateral, controls distal limb muscles and skilled movement, and runs the full length of the cord.
Anterior corticospinal tract
The uncrossed tract (10–15%) in the anterior funiculus. It crosses at segmental level, controls axial and proximal muscles, and ends by about the mid-thoracic cord.
Corticobulbar (corticonuclear) tract
Cortical fibres to the cranial nerve motor nuclei (V, VII, IX, X, XI, XII) via the genu of the internal capsule. Input is bilateral except to the lower facial nucleus and mostly the hypoglossal nucleus. Bilateral lesions cause pseudobulbar palsy.
Medullary pyramid and decussation
The pyramids are the only place where the tract is "pure". The decussation lies at the cervicomedullary junction, so a lesion above it gives contralateral weakness and a lesion below it gives ipsilateral weakness.

Anatomy

Course: Motor cortex (UMN) → corona radiata → posterior limb of internal capsule → cerebral peduncle (crus) → basilar pons → medullary pyramid → pyramidal decussation (85–90%) → lateral corticospinal tract → anterior horn LMN. The uncrossed fibres form the anterior corticospinal tract and cross segmentally.
Development: Myelination is completed by about 2 years of age. Before then an extensor plantar (Babinski) response is normal.

Function

Voluntary, skilled, fractionated movement, especially of the hand and fingers.
Facilitates flexor motor neurons and modulates spinal reflexes and interneurons.
Modulates ascending sensory transmission through its fibres from the parietal cortex.

Clinical significance

Upper versus lower motor neuron signs

UMN lesion (corticospinal anywhere from cortex to cord): weakness in a pyramidal pattern (upper-limb extensors and lower-limb flexors weakest), spasticity (velocity-dependent, clasp-knife), hyperreflexia, clonus, extensor plantar response (Babinski sign), pronator drift, no fasciculations and little wasting. LMN lesion (anterior horn, root, nerve): flaccidity, hypo- or areflexia, marked wasting, fasciculations, and flexor or absent plantars. In the acute phase (cerebral or spinal shock) a UMN lesion may briefly look flaccid.

Internal capsule lacunar stroke

A small infarct of the posterior limb (lenticulostriate branches of the MCA) where the fibres are tightly packed. It produces pure motor hemiparesis affecting face, arm and leg equally on the contralateral side.

Amyotrophic lateral sclerosis

Degeneration of the corticospinal tracts (sclerosis of the lateral columns) and anterior horn cells produces mixed UMN and LMN signs.

Compiled from standard anatomy and physiology references — see the Nervous System sources. For education only; not medical advice.