In itself, the presence of prions causes reduced glucose use by the thalamus and a mild hypo-metabolism of the cingulate cortex. The extent of this symptom varies between two variations of the disease, these being those presenting methionine homozygotes at codon 129 and methionine/valine heterozygotes being the most severe in the latter one. Given the relationship between the involvement of the thalamus in regulating sleep and alertness, a causal relationship can be drawn, and is often mentioned as the cause.
types of Transmissible spongiform encephalopathy
symptom of Transmissible spongiform encephalopathy
medical cause of Japanese encephalitis
medical cause of Metachromatic leukodystrophy
symptoms of Rabies
Marburg acute multiple sclerosis
medical cause of Hepatic encephalopathy
complications of West Nile fever