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A decrease in frontal lobe NAA levels is associated with impaired executive functioning and processing speed in neuro-performance tests. [6] The volume of the corpus callosum, a large white matter tract that connects the two cerebral hemispheres, is shown to decrease with alcohol abuse due to a loss of myelination. This integration between the ...
the frontal lobe. In addition to the damage seen in these areas there have been reports of damage to cortex, although it was noted that this may be due to the direct toxic effects of alcohol as opposed to thiamine deficiency that has been attributed as the underlying cause of Wernicke-Korsakoff Syndrome. [26]
There are hospital protocols for prevention, supplementing with thiamine in the presence of: history of alcohol misuse or related seizures, requirement for IV glucose, signs of malnutrition, poor diet, recent diarrhea or vomiting, peripheral neuropathy, intercurrent illness, delirium tremens or treatment for DTs, and others.
Alcohol-related dementia can produce a variety of psychiatric problems including psychosis (disconnection from reality), depression, anxiety, and personality changes. Patients with alcoholic dementia often develop apathy, related to frontal lobe damage, that may mimic depression. [3]
The long-term impact of alcohol on the brain has become a growing area of research focus. While researchers have found that moderate alcohol consumption in older adults is associated with better cognition and well-being than abstinence, [1] excessive alcohol consumption is associated with widespread and significant brain lesions.
Alcohol affects brain development quite significantly especially during adolescence when the brain is still developing. The main lobes that are involved in decision making and complex thought processes are undergoing their final development phase during adolescence and binge drinking can negatively stunt the growth of these frontal lobes. [37]
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]
Neuroimaging studies also show that cortical shrinkage in "uncomplicated alcoholism" is most severe in the frontal lobe in comparison to the other divisions of the cerebral cortex. [15] In addition, neurological diseases that co-occur with excessive alcohol consumption—such as Wernicke–Korsakoff syndrome (WKS)—are characterized by ...