The direct motor component of the pyramidal tract runs from the precentral gyrus through the posterior limb of the internal capsule and into the midbrain, where it gives slips to the oculomotor, trochlear, and abducens nuclei. It then enters the pons, where it gives off fibers to the trigeminal motor and facial nuclei, which control the muscles of the face. From the pons, the tract continues through the medullary pyramids, giving off fibers to the nuclei of the ninth, tenth, eleventh, and twelfth cranial nerves. The major part of the tract then crosses to the opposite side of the brainstem at the pyramidal decussation, and the crossed fibers continue to all levels of the spinal cord as the lateral corticospinal tract. A smaller group of uncrossed fibers continues to the cervical spinal cord as the anterior (direct) corticospinal tract. The fibers end by synapsing with motor neurons in the anterior horn of the spinal cord (see Plate 2-13).
The pyramidal tract exhibits a somatotopic organization throughout its course. The homunculus at the top of the illustration indicates the orderly topographic arrangement of areas within the precentral gyrus, from which muscles in various parts of the body can be activated. The area controlling the face lies most laterally, with the areas related to the hand, arm, trunk, and hip following, in order, toward the midline. The areas representing the leg continue downward along the medial aspect of the cortex. Within each area, movements involving distal muscles are represented posteriorly, and proximal muscles, anteriorly. The initial somatotopic organization at the cortex persists in the arrangement of fibers along the course of the tract (see Plate 2-14). The control of voluntary movements probably relates, however, to distributed networks that are capable of modification rather than to discrete representations. There appears to be considerable plasticity of representations and cell properties in the primary motor cortex, probably related to the horizontal neuronal connections in the cortex. The primary motor cortex is not a simple static motor control structure but contains a dynamic substrate that participates in motor learning.
Lesions of the motor cortex may produce discrete pareses, depending upon the type and size of the lesion and its somatotopic location. Irritative lesions of the cortex can lead to abnormal movements and ultimately to jacksonian seizures as the irritative focus spreads. Damage to the internal capsule produces contralateral paralysis, along with cranial nerve involvement.
In general, pyramidal tract disturbances produce an initial flaccid paralysis and areflexia, followed by spastic paralysis and hyperactive reflexes. Brainstem lesions cause paralysis contralateral to the lesion, accompanied by ipsilateral or contralateral cranial nerve deficits, depending on the level of the lesion. Spinal cord damage to the tract is usually accompanied by alterations in the autonomic and sensory systems.

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