Burton, H., Dixit, S., Litkowski, P., & Wingert, J. R. (2009). Functional connectivity for somatosensory and motor cortex in spastic diplegia. Somatosensory & Motor Research, 26(4), 90-104. doi:10.3109/08990220903335742
Chapter 11 in the textbook briefly discusses cerebral palsy and how it is a disorder of motor function resulting from brain damage that occurs prenatally. Cerebral palsy results in loss of axons and neurons in the cerebral white and gray matter. This study focuses on a subtype of cerebral palsy, spastic diplegia, which is distinguished by a non-progressive periventricular white matter injury that causes extremely high muscle tone in the legs, hips, and pelvis. The disorder reduces a child’s cortical inhibitory function. The researchers in this study hypothesized that the cortical networks that are linked to somatosensory and motor cortex areas would be disordered and possibly smaller in spastic diplegia than in the normal controls. Cortical networks were measured by functional connectivity analyses (fcMRI). There were twenty-three participants in this study, twelve had spastic diplegia and eleven had no neurological disabilities. Seed regions (sROI) were centered on foci that were activated by stimulation on the second fingertip in both the somatosensory region and the motor region. Those participants with spastic diplegia were found to have had expanded functional connectivity in the somatosensory area but not the motor area compared to the participants with no neurological disorders in the somatosensory areas of the parietal cortex. Also, a relationship was found between the networks of the parietal cortex somatosensory regions and the precentral motor cortex. A possible explanation for these results is that those individuals with spastic diplegia have damage to their upper motor subplate neurons from white matter injury, which more than likely occurred prenatally in the third trimester. Because these neurons are not properly developed, they significantly impact the functions of brain regions such as the motor cortex and basal ganglia, which ultimately cause abnormalities in movement.
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