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Neurology · Topical Diagnosis in Neurology

Pyramidal system

Tractus pyramidalis

Pyramidal system (tractus pyramidalis) is a key motor structure that ensures the conduction of voluntary movement impulses from the cerebral cortex to spinal motor neurons and cranial nerve nuclei. It is responsible for performing the most precise and complex isolated motor acts.

Sources of fibers40% from area 4, 60% from the premotor (area 6) and parietal cortex (areas 1, 2, 3)
Betz cellsGiant neurons of layer V form only 3.4–4% of the tract's fibers
Decussation80–85% of the fibers cross to the opposite side in the medulla oblongata
SyndromesLesion of the 1st neuron causes spastic paresis, of the 2nd — flaccid paresis
6 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Course and topography of the corticospinal tract

The descending pathway of voluntary motor activity originates from the motor areas of the cerebral cortex. The axons of the neurons form the corona radiata (corona radiata) and pass compactly through the posterior limb of the internal capsule (capsula interna).

Next, the pathway descends through the brainstem:

  • Midbrain: passes through the central part of the cerebral peduncles;
  • Pons: transits across the pons;
  • Medulla oblongata: forms prominences on the anterior surface — the pyramids (pyramides).

At the border with the spinal cord, the pyramidal decussation (decussatio pyramidum) takes place. About 80–85% of the fibers cross to the opposite side, forming the lateral corticospinal tract in the lateral funiculus. The remaining fibers form the anterior corticospinal tract, crossing later through the anterior white commissure at the level of their respective segment.

Corticobulbar and corticomesencephalic tracts

In addition to the spinal pathway, the pyramidal system includes tracts to the cranial nerves:

  • Corticobulbar (corticonuclear) tract: in the midbrain and pons, it gives off fibers to the motor nuclei of the trigeminal (V), facial (VII), glossopharyngeal (IX), vagus (X), accessory (XI), and hypoglossal (XII) nerves.
  • Corticomesencephalic tract: originates from the frontal eye field (Brodmann area 8). It passes through the internal capsule rostral to the main pathway and heads to the nuclei of the extraocular motor nerves (cranial nerves III, IV, VI), providing conjugate gaze and head turning.

Note: The connection of corticonuclear fibers with the nuclei of cranial nerves III, IV, and VI is not direct, but mediated through a system of interneurons.

Test your knowledge on this topicTasks from the Neurology course bank — immediate answers and explanations.

Somatotopy and cellular composition of the cortex

The primary motor cortex is localized in the precentral gyrus (Brodmann area 4) along the central sulcus. The projection of body parts ("motor homunculus") is inverted:

Precentral gyrus zoneProjected body region
Medial surface and superior marginPelvic sphincters, foot, leg, thigh
Upper and middle lateralTrunk, shoulder, forearm, hand, and fingers
Lower lateralNeck, face, tongue, jaw, larynx, and pharynx

Layer V of the cortex contains large Betz pyramidal cells. Although they give rise to thick, fast-conducting axons, the bulk of the pathway is formed by processes of small pyramidal and spindle-shaped cells from areas 4 and 6, as well as the somatosensory cortex of the parietal lobe.

Clinical syndromes of neuron lesions

The motor pathway consists of two consecutive links, a lesion of which produces opposing symptoms:

  1. Central (first) motor neuron: the cell body lies in the cortex, and the axon descends as part of the pyramidal tract. Damage to it in the brain or spinal cord results in spastic paresis.
  2. Peripheral (second) motor neuron: the cell body is located in the anterior horns of the spinal cord or cranial nerve nuclei, and the axon runs as part of the anterior root and peripheral nerve to the muscle. Damage at this level leads to flaccid paresis.

Feature: The musculature of the trunk and neck receives bilateral cortical innervation thanks to a portion of uncrossed fibers, which is why their function is preserved in unilateral cortical lesions.

Briefly: answers to topical questions

Through which parts of the internal capsule do the corticonuclear and corticospinal tracts pass?

The corticonuclear and corticospinal tracts pass through the genu and the anterior two-thirds of the posterior limb of the internal capsule.

  • Corticonuclear tract (tractus corticonuclearis) — passes through the genu of the internal capsule, where fibers to the face are located.
  • Corticospinal tract (tractus corticospinalis) — passes through the anterior part of the posterior limb of the internal capsule, where fibers to the arm, trunk, and leg are located sequentially from front to back.

What clinical signs and symptoms are characteristic of central spastic paralysis?

Central spastic paralysis is characterized by a combination of muscle weakness with spastic hypertonia and reflex changes.

  • Muscle weakness — decreased strength and difficulty in performing fine movements.
  • Muscle hypertonia — spastic increase in muscle tone.
  • Hyperreflexia — pathological increase in deep (tendon and periosteal) reflexes; clonus may appear.
  • Pathological reflexes — appearance of extensor and flexor pyramidal signs (Babinski, Rossolimo, etc.).
  • Reduction of superficial reflexes — weakening or loss of cutaneous (abdominal, cremasteric) reflexes.
  • Syncinesias — involuntary associated movements.
  • Absence of early atrophy — mild disuse hypotrophy develops only in later stages.

What clinical signs are characteristic of peripheral flaccid paralysis?

Peripheral flaccid paralysis is characterized by a triad of main clinical symptoms caused by damage to the peripheral motor neuron.

  • Atonia or hypotonia — a sharp decrease or complete absence of muscle tone.
  • Areflexia or hyporeflexia — reduction or complete loss of deep (tendon and periosteal) reflexes.
  • Muscle atrophy — early-onset and pronounced thinning of muscle tissue.

Additionally, fascicular and fibrillary twitches may be observed (with lesions of the anterior horns), and when nerve plexuses or peripheral nerves are involved, paralysis is accompanied by sensory and autonomic disorders.

Which cranial nerve nuclei receive only unilateral cortical innervation?

Only contralateral cortical innervation is received by:

  • Hypoglossal nerve nucleus (cranial nerve XII).
  • Lower part of the facial nerve motor nucleus (cranial nerve VII), which innervates the lower half of the face.

The upper part of the facial nerve nucleus receives bilateral cortical innervation.

What pathological pyramidal reflexes occur in lesions of the pyramidal pathway?

Lesions of the pyramidal pathway result in pathological reflexes, which are subdivided into extensor and flexor reflexes.

  • Babinski reflex (Babinski reflex) — extension of the great toe upon stroking the lateral aspect of the sole.
  • Oppenheim sign — extension of the great toe when stroking down the anteromedial surface of the tibia.
  • Gordon sign — extension of the great toe upon squeezing the gastrocnemius muscle.
  • Rossolimo reflex (Rossolimo reflex) — plantar flexion of the toes when tapping their distal phalanges.
  • Trömner reflex (Trömner reflex) — flexion of the fingers when tapping the palmar surface of the distal phalanx of the middle finger.
  • Hoffmann sign — pathological finger flexor reflex.

What are alternating syndromes, and at what level of the pyramidal system lesion do they develop?

Alternating syndromes are crossed syndromes characterized by a combination of cranial nerve dysfunction on the side of the lesion (ipsilaterally) and limb muscle paralysis (hemiparesis) on the opposite side of the body (contralaterally).

They develop when the pyramidal system is damaged at the brainstem level. Due to the high density of cranial nerve nuclei and the adjacent descending motor pathways, even a small lesion in the brainstem (midbrain, pons, or medulla oblongata) causes combined damage to these structures. An example is Weber syndrome caused by a midbrain peduncle lesion.

How to memorize

Sequence of anatomical levels of the pyramidal tract from top to bottom: Corona $\rightarrow$ Capsule $ ightarrow$ Peduncles $ ightarrow$ Pons $ ightarrow$ Pyramids ("All Capsules Penetrate Pontine Pyramids").

Class and exam questions

Which cytoarchitectonic areas form the pyramidal tract?

Approximately 40% of the fibers originate from the primary motor cortex (Brodmann area 4). The remaining 60% originate from the premotor area (area 6), the eye-field area 8, and the somatosensory cortex of the parietal lobe (areas 1, 2, 3).

What is the difference between the lateral and anterior corticospinal tracts?

The lateral tract consists of 80–85% of fibers that have crossed in the medulla oblongata and descends in the lateral funiculus. The anterior tract consists of uncrossed fibers and runs in the anterior funiculus, crossing segment by segment at their respective levels.

How does upper motor neuron lesion differ from lower motor neuron lesion?

Damage to the upper motor neuron leads to spastic paresis with increased tone and reflexes. Lesion of the lower motor neuron causes flaccid paresis with hypotonia, areflexia, and muscle atrophy.

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What else to study on this topic

  • Topography of pathways in the posterior limb of the internal capsule
  • Cytoarchitectonic layers of the precentral gyrus cortex according to Golgi
  • Features of cortical innervation of the facial (VII) and hypoglossal (XII) cranial nerve nuclei
  • The role of spinal cord anterior horn interneurons in transmitting impulses to alpha and gamma motor neurons
  • Interaction of the pyramidal system with the basal ganglia and cerebellum

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