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Published in Philip Winn, Dictionary of Biological Psychology, 2003
Complete paralysis of one side of the body, consequent to CONTRALATERAL brain damage (often a consequence of infarct of the middle cerebral artery). However this term is also often as a synonym for HEMIPARESIS. Hemiplegia is a consequence of a LESION in one of the PYRAMIDAL TRACTS. Typically large lesions in the CEREBRAL CORTEX are necessary, although the tract becomes quite narrow in the INTERNAL CAPSULE where a small infarct can produce a dense hemiplegia. Hemiplegia can be less severe in the contralateral leg than the contralateral face and arm.
A review of magnetoencephalography use in pediatric epilepsy: an update on best practice
Published in Expert Review of Neurotherapeutics, 2021
Hiroshi Otsubo, Hiroshi Ogawa, Elizabeth Pang, Simeon M Wong, George M Ibrahim, Elysa Widjaja
Auditory evoked fields (AEF) are typically stimulated using pure tones presented to one ear while the other ear received a masking stimulus to prevent bilateral activation of auditory pathways. Activation from stimuli presented to one ear travels into the lower brainstem, where the majority of fibers cross and ascend the contralateral pathways through the brainstem up to the cortex, while a minority of fibers continue ipsilateral, resulting in bilateral activation of auditory cortices. Masking stimulation in the opposite ear reduces ipsilateral activation of the stimulated ear, thus producing a clearer contralateral brain response. Activation localizes to the contralateral superior temporal gyrus in primary auditory cortex (Brodmann areas 41 and 42) [111]. Pure tones are required as the auditory cortex is organized tonotopically, and simultaneous activation of more than one frequency would result in a smearing of the location and increased error [112,113].
Effects of constraint-induced movement therapy on brain glucose metabolism in a rat model of cerebral ischemia: a micro PET/CT study
Published in International Journal of Neuroscience, 2018
Ying-Ying Li, Bei Zhang, Ke-Wei Yu, Ce Li, Hong-Yu Xie, Wei-Qi Bao, Yan-Yan Kong, Fang-Yang Jiao, Yi-Hui Guan, Yu-Long Bai
We detected increased FDG uptake in subregions of the midbrain, such as the superior and inferior colliculus, the VTA, as well as the entorhinal cortex, posterior hippocampus, pons, and medulla of the contralesional hemisphere at d7 (P <0.05). These results imply that these areas participate in the natural short-term recovery process seven days post-MCAO surgery. Following CIMT treatment, we observed increased glucose uptake in the acbcore shell and cortex insular in the contralesional hemisphere. This leads us to speculate that improvements in the neurological outcomes may be associated with enhanced neuronal activity in the contralesional hemisphere (Figure 7). In addition, we also observed lower SUVs in the cingulate cortex, motor cortex, somatosensory cortex, and anterodorsal hippocampus in the lesional left hemisphere of the CIMT group compared to the Control group. We believe that the decreased glucose uptake in the lesional left hemisphere plays a role in protecting the brain in order to enable the compensatory role of the contralateral brain areas.
Neuroanatomical and electrophysiological recovery in the contralateral intact cortex following transient focal cerebral ischemia in rats
Published in Neurological Research, 2018
Sheng-Yang Huang, Chih-Han Chang, Hsin-Yi Hung, Yu-Wen Lin, E-Jian Lee
Optimal sensorimotor function requires both anatomical integrity and functional linkage between gray and white matter [4,7]. These structures and their axonal synapto-dendritic connections, as well as the functional, metabolic, and electrophysiological linkage, are involved in the processing and integration of sensorimotor information [12,25]. Remote dendritic spine changes may cause the development of transhemispheric electrophysiological diaschisis after stroke. Consistent with previous work, our data indicated that electrophysiological diaschisis occurs in the remote area quickly, but improves slowly over time both in the ipsilateral and contralateral hemispheres [4,16]. Dendritic spine density and electrophysiological outcomes returned to normal simultaneously in the contralateral hemisphere by 28 days after stroke. One of the most reasonable explanations for diaschisis in the contralateral brain is transhemispheric/transcallosal deafferentation [12]. Moreover, these remote neuronal activity changes have also been linked with decreased γ-aminobutyric acid receptor expressions [26] and are observed in models of both transient and permanent arterial occlusions [12,27] or intracerebral hemorrhage models [26,28].