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At least 289 records · Page 16Linked to original sources
PubMed1985

The corticomotoneuronal component of the pyramidal tract: corticomotoneuronal connections and functions in primates.

Corticomotoneuronal fibers make up a functional component of the pyramidal tract-corticospinal system which is characteristic of primates. The corticomotoneuronal fibers include large, rapidly conducting axons. They arise from somatotopically arranged areas of precentral cortex and the largest concentration of pyramidal cells of origin in the deep part of lamina V is in area 4. Their influence is exerted contralaterally on the spinal cord, where monosynaptic excitation of spinal motoneurons occurs. Motoneurons innervating distally acting muscles are preferentially excited and marked convergence of corticomotoneuronal influences occurs on these. The excitatory post-synaptic potentials in these motoneurons are characterized by the property of temporal facilitation. Intraspinal divergence of the terminal arborizations of individual corticomotoneuronal fibers could permit the engagement of large populations of motoneurons and also the activation of excitatory and inhibitory interneurons and propriospinal neurons for that region of the spinal cord. Corticomotoneuronal synapses may be located more distally on the dendrites of motoneurons than are the monosynaptic connections from group Ia afferents. The corticomotoneuronal excitation has been demonstrated to be effective in natural functional states when the conscious animal is performing learned movement tasks. Abolition of corticomotoneuronal influences causes a permanent deficit in the fractionation of use of distal muscles and an inability to carry out independent movements of the fingers.

Animals↗
PubMedDate not supplied

Cranial MR in Wilson disease: abnormal white matter in extrapyramidal and pyramidal tracts.

PURPOSE: To describe abnormal white matter in the brain on MR in Wilson disease and to compare with anatomic location of white matter tracts. METHODS: Forty-six patients with Wilson disease were examined. Axial T1-weighted inversion-recovery, axial T2-weighted spin-echo, and coronal T2*-weighted gradient-echo MR images were performed. Imaging studies were compared with clinical data. RESULTS: Seventeen patients showed abnormalities in the region coinciding with the following white matter tracts: corticospinal tract (24%, n = 11), dentatorubrothalamic tract (24%, n = 11), and pontocerebellar tract (17%, n = 8). CONCLUSION: Abnormal extrapyramidal and pyramidal white matter tracts are part of the neuroimaging spectrum of Wilson disease. No significant correlation was found with neurologic groups and individual white matter tracts affected.

Basal Ganglia Diseases↗
PubMed2000

Compensatory sprouting and impulse rerouting after unilateral pyramidal tract lesion in neonatal rats.

After lesions of the developing mammalian CNS, structural plasticity and functional recovery are much more pronounced than in the mature CNS. We investigated the anatomical reorganization of the corticofugal projections rostral to a unilateral lesion of the corticospinal tract at the level of the medullary pyramid (pyramidotomy) and the contribution of this reorganization and other descending systems to functional recovery. Two-day-old (P2) and adult rats underwent a unilateral pyramidotomy. Three months later the corticofugal projections to the red nucleus and the pons were analyzed; a relatively large number of corticorubral and corticopontine fibers from the lesioned side had crossed the midline and established an additional contralateral innervation of the red nucleus and the pons. Such anatomical changes were not seen after adult lesions. Intracortical microstimulation of the primary motor cortex with EMG recordings of the elbow flexor muscles were used to investigate possible new functional connections from the motor cortex of the pyramidotomy side to the periphery. In rats lesioned as adults, stimulation of the motor cortex ipsilateral to the pyramidotomy never elicited EMG activity. In contrast, in P2 lesioned rats bilateral forelimb EMGs were found. EMG latencies were comparable for the ipsilateral and contralateral responses but were significantly longer than in unlesioned animals. Transient inactivation of both red nuclei with the GABA receptor agonist muscimol led to a complete loss of these bilateral movements. Movements and EMGs reappeared after wash-out of the drug. These results suggest an important role of the red nucleus in the reconnection of the cortex to the periphery after pyramidotomy.

Afferent Pathways↗