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Since axonal damage in DAI is largely a result of secondary biochemical cascades, it has a delayed onset, so a person with DAI who initially appears well may deteriorate later. Thus injury is frequently more severe than is realized, and medical professionals should suspect DAI in any patients whose CT scans appear normal but who have symptoms ...
Vascular thalamic amnesia occurs when the thalamus is affected by Korsakoff's syndrome or damaged by lacunar infarcts or hemorrhages. [1] Another common cause for damage to the thalamus that may contribute to the development of amnesia is a stroke. [ 2 ]
The CBGTC loop has been implicated in many diseases. For example, in Parkinson's disease, degeneration of dopaminergic neurons leading to decreased activity of the excitatory pathway is thought to result in hypokinesia, [15] and in Huntington's disease, degeneration of GABAergic neurons driving the inhibitory pathway is thought to result in the jerky body movements. [2]
Hypothalamic disease is a disorder presenting primarily in the hypothalamus, which may be caused by damage resulting from malnutrition, including anorexia and bulimia eating disorders, [1] [2] genetic disorders, radiation, surgery, head trauma, [3] lesion, [1] tumour or other physical injury to the hypothalamus. The hypothalamus is the control ...
For example, if this type of injury effects the hand region in the primary somatosensory cortex for one cerebral hemisphere, a patient with closed eyes cannot perceive the position of the fingers on the contralateral hand and will not be able to identify objects such as keys or a cell phone if they are placed into that hand.
Korsakoff syndrome stems from damage to the mammillary body, the mammillothalamic fasciculus or the thalamus. [ 68 ] [ 69 ] Fatal familial insomnia is a hereditary prion disease in which degeneration of the thalamus occurs, causing the patient to gradually lose their ability to sleep and progressing to a state of total insomnia , which ...
This process is still in the early stages but early results are promising. An example of this therapy might involve implanting cells genetically modified to express tyrosine hydroxylase which, in the body, could be converted to dopamine. Increasing dopamine levels in the basal ganglia could possibly offset the effects of the Parkinson's Disease ...
Before activation of the direct pathway, these two nuclei were actively sending inhibitory signals to the ventrolateral nucleus of the thalamus, which prevented the development of significant activity in the motor cerebral cortices. This behavior ceases on activation of the direct pathway.