Current Neurobiology Open Access

Development and Plasticity of the Corticospinal Tract in Children with Neurological Disorders

Karen Perez^* Department of Neurological Surgery, The Miami Project to Cure Paralysis, UNIVERSITY OF MIAMI, Miami, FL, USA
^*Correspondence: Karen Perez, Department of Neurological Surgery, The Miami Project to Cure Paralysis, UNIVERSITY OF MIAMI, USA, Email:

Received: 20-Oct-2021 Published: 10-Nov-2021

Introduction

Because the young human brain is highly plastic, brain lesions that occur during development interfere with the innate development of architecture, connectivity, and function mapping and cause changes in structure, wiring, and representations. The motor cortex and/or the corticospinal tract are common sites of brain damage in childhood, and the most common time for brain damage to occur is during the prenatal or immediately perinatal period. It is now widely recognised that the corticospinal system is capable of significant reorganisation following lesions, and that this reorganisation is likely to underpin the partial recovery of function [1-3].

For skilled movements, the corticospinal tract (CST) is the primary motor control pathway. It has a long postnatal development period, making it vulnerable to perinatal brain and spinal cord injury. According to research, the motor signs of cerebral palsy (CP) reflect the loss of CST connections as well as the development of abnormal motor system connections, particularly between the developing CST and spinal motor circuits. We discuss a feline model of CP that we developed in this paper. The animals develop an abnormal pattern of CST connections that is strikingly similar to that seen in hemiplegic CP and visuomotor impairments. We developed neural activity-based therapeutic approaches based on this model to repair the abnormal CST connections and restore normal skilled movement control [4]. According to our findings, more active CST connections can maintain strong synaptic connections with spinal motor circuits.

The corticospinal tract originates in several areas of the brain, including the motor areas as well as the primary somatosensory cortex and premotor areas. The majority of neurons originate in the primary motor cortex or the premotor frontal areas. About 30% of corticospinal neurons originate in the primary motor cortex, 30% in the premotor cortex and supplementary motor areas, and the remaining 40% in the somatosensory cortex, parietal lobe, and cingulate gyrus. These upper motor neurons begin in the neocortex's layer V pyramidal cells and travel through the forebrain's posterior limb of the internal capsule to enter the cerebral crus at the base of the midbrain. Both tracts then travel through the brain stem, from the pons to the medulla [5].

The corticospinal and corticobulbar tracts form two pyramids on either side of the brainstem's medulla, giving rise to the term pyramidal tracts. Corticospinal neurons synapse directly onto alpha motor neurons to control muscles directly.

Betz cells are very large, easily visible under a microscope cells that, despite accounting for only about 5% of cells projecting to the spinal cord, are widely regarded as the most important for motor signal communication.These cells are notable for their fast conduction rate, which exceeds 70m/sec, making them the fastest signal conduction from the brain to the spinal cord [6].

The corticospinal and corticobulbar tracts form two pyramids on either side of the brainstem's medulla, giving rise to the term pyramidal tracts. Corticospinal neurons synapse directly onto alpha motor neurons to control muscles.Betz cells are large, easily visible under a microscope cells that, despite accounting for only about 5% of cells projecting to the spinal cord, are widely considered to be the most important for motor signal communication.These cells are notable for their fast conduction rate, which exceeds 70m/sec, making them the fastest signal conduction from the brain to the spinal cord.

REFERENCES

1. Amassian VE, Eberle L, Maccabee PJ, Cracco RQ (1992) Modelling magnetic coil excitation of human cerebral cortex with a peripheral nerve immersed in a brain-shaped volume conductor: the significance of fiber bending in excitation. Electroencephalogr Clin Neurophysiol 85: 291-301.
2. Angeli CA, Edgerton VR, Gerasimenko YP, Harkema SJ (2014) Altering spinal cord excitability enables voluntary movements after chronic complete paralysis in humans. Brain 137: 1394-1409.
3. Bi Gq, Poo Mm (1998) Synaptic modifications in cultured hippocampal neurons: dependence on spike timing, synaptic strength, and postsynaptic cell type. J Neurosci 18: 10464-10472.
4. Brouwer P, Bugaresti J, Ashby P (1992) Changes in corticospinal facilitation of lower limb spinal motor neurons after spinal cord lesions. J Neurol Neurosurg Psychiatry 55: 20-24.
5. Bunday KL, Perez MA (2012) Motor recovery after spinal cord injury enhanced by strengthening corticospinal synaptic transmission. Curr Biol 22: 2355-2361.
6. Bunday KL, Urbin MA, Perez MA (2018) Potentiating paired corticospinal-motoneuronal plasticity after spinal cord injury. Brain Stimul 11: 1083-1092.