The corticospinal tract

Motor control signals from M1 and the NPMAs travel to the spinal cord via several descending tracts (Fig. 2.4). The corticospinal tract is the most

Figure 2.4. Pathway of the corticospinal tract (green, thick line), reticulospinal tract (blue, thinner line), and the rubrospinal tract (red, dashed line).

direct pathway from the cerebral cortex to the spinal motoneurons. The corticospinal tract originates from multiple areas in the frontal and parietal lobes. In the frontal lobe of primates, the greatest proportion of axons originates from M1 (approximately 30% of the total corticospinal tract), with the remaining frontal lobe axons (another 30% of the total corti-cospinal tract) originating from the SMA, the pre-motor areas, and the cingulate motor areas (Dum and Strick, 1991). In the parietal lobe, corticospinal axons originate from Brodmann's areas 1, 2, 3, 5, and 7 (approximately 40% of the total corticospinal tract) and project to the dorsal horn of the spinal cord to regulate sensory inflow.

Corticospinal axons arise from the large pyramid-shaped cell bodies in cortical layer V The axons leave the cortex, pass through the corona radiata, and enter the internal capsule, along with many other corti-cofugal projections. In the internal capsule, the cor-ticospinal axons are found in the posterior limb, where axons from the NPMAs pass through the genu and anterior third of the posterior limb, axons from M1 pass through the middle third of the posterior limb, and axons from parietal areas pass through just posterior to the primary motor axons (Fries et al., 1993; Axer and Keyserlingk, 2000; Morecraft et al., 2002). As the axons descend through the internal capsule, they shift posteriorly (Axer and Keyserlingk, 2000) and pass below the thalamus. The corticospinal tract then descends through the cerebral peduncle of the midbrain, concentrating in its middle third. In the pons, the corticospinal axons pass around the nuclei in the base of the pons (basis pontis). In the medulla, the corticospinal tract forms the medullary pyramid. At the spinomedullary junction, the majority of corticospinal axons cross the midline and form the lateral corticospinal tract on the opposite side of the spinal cord. The remaining corticospinal axons descend uncrossed as the ventral corticospinal tract near the ventral midline of the spinal cord. In the spinal cord, the corticospinal axons branch and enter the spinal gray matter, synapsing on interneurons in the intermediate zone and synapsing directly on motoneurons in the ventral horn. Axons traveling in the crossed lateral corticospinal tract tend to synapse on motoneurons and interneurons involved in the control of more distal musculature, whereas axons traveling in the uncrossed ventral corticospinal tract tend to synapse on motoneurons and interneurons involved in the control of axial and more proximal limb muscles. A small number of corticospinal axons recross the midline in the spinal cord and terminate in the ventral horn ipsilateral to their origin.

In humans, strokes affecting the white matter in the territory of the middle cerebral artery frequently damage the corticospinal tract, as well as other structures, resulting in hemiparesis. Relatively isolated lesions of the corticospinal tract can occur in humans when a small ischemic lesion is located in the posterior limb of the internal capsule or in the basis pon-tis, resulting in the clinical syndrome of pure motor hemiparesis (Fisher and Curry, 1964; Fisher, 1979). After damage to the corticospinal tract, axons carried in the uncrossed ventral corticospinal tract from the opposite hemisphere may be able to exert compensatory control over muscles on the affected side of the body (Fisher, 1992; Cao et al., 1998). These uncrossed axons terminate in the ventromedial portion of the ventral horn and are likely to exert more control over proximal and axial rather than distal musculature (Kuypers and Brinkman, 1970). This spared ventromedial input to spinal motoneurons controlling the affected side of the body may therefore account for the relative preservation of axial and proximal motor control seen after stroke (Colebatch and Gandevia, 1989).

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