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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]
Rarer mimics of encephalopathy are meningitis, encephalitis, Wernicke's encephalopathy and Wilson's disease; these may be suspected on clinical grounds and confirmed with investigations. [9] [16] The diagnosis of hepatic encephalopathy is a clinical one, once other causes for confusion or coma have been excluded; no test fully diagnoses or ...
Wernicke-Korsakoff syndrome (WKS) is the combined presence of Wernicke encephalopathy (WE) and alcoholic Korsakoff syndrome (AKS [clarification needed]). Due to the close relationship between these two disorders, people with either are usually diagnosed with WKS as a single syndrome.
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]
Symptoms are assessed on a case-by-case basis. [5] Some cysts in the CNS can be asymptomatic (producing or showing no symptoms), depending on their location in the brain or spinal cord. If the cysts develop in critical areas of the central nervous system, they can present one or more of the following symptoms: [6]
Wernicke syndrome is an ambiguous term. It may refer to: Wernicke aphasia: the eponymous term for receptive or sensory aphasia.; Wernicke encephalopathy: an acute neurological syndrome of ophthalmoparesis, ataxia, and encephalopathy brought on by thiamine deficiency.
Symptomatic features of paraneoplastic syndrome cultivate in four ways: endocrine, neurological, mucocutaneous, and hematological.The most common presentation is a fever (release of endogenous pyrogens often related to lymphokines or tissue pyrogens), but the overall picture will often include several clinical cases observed which may specifically simulate more common benign conditions.
The exact definition of "rapid" is somewhat debatable, and different sub-divisions exist, which are based on the time from onset of first hepatic symptoms to onset of encephalopathy. One scheme defines "acute hepatic failure" as the development of encephalopathy within 26 weeks of the onset of any hepatic symptoms.