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Wernicke encephalopathy (WE), also Wernicke's encephalopathy, [1] or wet brain is the presence of neurological symptoms caused by biochemical lesions of the central nervous system after exhaustion of B-vitamin reserves, in particular thiamine (vitamin B 1). [2]
It was originally thought [5] that raised CSF protein without pleocytosis ('albuminocytological dissociation') was a characteristic feature, as it is in Guillain–Barré syndrome, but this has not been supported in more recent work. [7] In only 30% of cases is an MRI brain scan abnormal. Nerve conduction studies may show an axonal ...
Leukodystrophy is characterized by specific symptoms, including decreased motor function, muscle rigidity, and eventual degeneration of sight and hearing. While the disease is fatal, the age of onset is a key factor, as infants have a typical life expectancy of 2–8 years, while adults typically live more than a decade after onset.
The mortality rate of early infantile Krabbe disease is 90% before the age of two. Later onset of symptoms is associated with longer life expectancy, with older children generally surviving two to seven years after the initial diagnosis. [22] Krabbe disease occurs in about one in 100,000 births. [23]
The brain and nervous system are not affected pathologically, [3] but lung and, rarely, kidney impairment may occur. Patients in this group usually bruise easily (due to low levels of platelets) and experience fatigue due to low numbers of red blood cells. Depending on disease onset and severity, type I patients may live well into adulthood.
Symptoms of the most common (and most serious) form of Canavan disease typically appear in early infancy usually between the first three to six months of age. [4] Canavan disease then progresses rapidly from that stage, with typical cases involving intellectual disability, loss of previously acquired motor skills, feeding difficulties, abnormal muscle tone (i.e., initial floppiness ...
Korsakoff syndrome (KS) [1] is a disorder of the central nervous system characterized by amnesia, deficits in explicit memory, and confabulation.This neurological disorder is caused by a deficiency of thiamine (vitamin B 1) in the brain, and it is typically associated with and exacerbated by the prolonged, excessive ingestion of alcohol. [2]
[4] [9] Exposure to brain or spinal tissue from an infected person may also result in spread. [4] There is no evidence that sporadic CJD can spread among people via normal contact or blood transfusions, [4] although this is possible in variant Creutzfeldt–Jakob disease. [10] [11] Diagnosis involves ruling out other potential causes. [4]