Rev Neurol France
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T cell apoptosis has been studied in animal models for human autoimmune disorders of the nervous system and in other tissues devoid of specialized immune-defense mechanisms. Our data suggest that the central nervous system has a high potential to eliminate T cell inflammation, whereas this mechanism is less effective in the peripheral nervous system, and even more in muscle and skin. In-vitro experiments indicate different scenarios how specific cellular and humoral elements in the nervous system may synergize and sensitize T cells for apoptosis in-vivo. ⋯ This is further substantiated since neutralization of TNF-alpha in MS patients increased cellular inflammation and relapses. Therapeutically several conventional and novel approaches like glucocorticosteroids and high-dose antigen therapy induce T cell apoptosis in-situ. We also discuss regulatory, proapoptotic mechanisms such as the Fas/FasL system and counterregulatory mechanisms that have been utilized to limit tissue damage.
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Case Reports
[Transient high-intensity T2 signal in the splenium of the corpus callosum in a non-epileptic patient].
Transient splenial lesions of the corpus callosum have been mainly reported in epileptic patients. We report the case of a non-epileptic woman with bipolar affective disorder treated by oxcarbazepine which was withdrawn because of a mild hyponatremia (128 mmol/l). A confusional state followed withdrawal and the electroencephalogram was free of spike or sharp waves. ⋯ Different mechanisms of this brain MRI abnormality are discussed including the sudden withdraw of oxcarbazepine. Prognosis of transient splenial lesions of the corpus callosum is good. Clinicians should search for recent metabolic disorders and therapeutic modifications.