Cerebral cortex alcoholism

Benzodiazepines, especially lorazepam, are used to prevent and treat CINV.5,10 Lorazepam is thought to prevent input from the cerebral cortex and limbic system from reaching the central vomiting center in the brain stem.10 Sedation and amnesia are common side effects. Respiratory depression can occur with high doses or when other central depressants such as alcohol are combined with benzodiazepines. 

CNS neurodegenerative disorders often accompany the impairment of memory and other cognitive functions. This impairment is probably due to selective neuronal death in the cerebral cortex and hippocampus, brain regions that are crucially involved in learning and memory. It has recently been found that the alcohol extract of pistils of C. sativus L. (CSE) affects learning and memory in mice. Oral administration of CSE (125 to 500 mg/kg) alone had no effect on learning behavior of mice in passive avoidance tests, but significantly improved ethanol-induced impairment of memory acquisition. 

As a CNS depressant, ethyl alcohol (ethanol) obeys the law of descending depression, in that it first inhibits the cerebral cortex, then the cerebellum, spinal cord, and medullary center. 

GABA (gamma- aminobutyric acid) Inhibitory. Secreted by neurons in the cerebral cortex, subcortical area, and spinal cord. Anxiety states, also involved in chemical dependency. Diffusely affected by many medications. Many antianxiety medications work on GABA receptor sites, especially in the frontal lobe of the brain. Alcohol, benzodiazepines, and barbiturates all affect GABA receptors, as do other drugs. 

Rajgopal, Y., Chetty, C.S., and Vemuri, M.C. (2003). Differential modulation of apoptosis-assodated proteins by ethanol in rat cerebral cortex and cerebellum. Eur. J. Pharmacol. 470 117-124. Ramachandran, V., Perez, A., Chen, J., Senthd, D., Schenker, S., and Henderson, G.I. (2001). In utero ethanol exposure causes mitochondrial dysfunction which can result in apoptotic cell death in fetal brain A potential role for 4-hydroxynonenal. Alcoholism Clin. Exp. Res. 25 862-871. 

Quisling RG, Mickle JP, Ballinger WB, et al. (1984) Histopathologic analysis of intraarterial polyvinyl alcohol microemboli in rat cerebral cortex. AJNR Am J Neurora-diol 5 101-104... 

Compared with controls, recent cocaine abusers had significantly reduced cerebral blood flow in 11 of 14 brain regions, with the largest reductions in the frontal cortex and parietal cortex and greater cerebral blood flow in the brain stem. These perfusion defects appeared to be primarily due to combined abuse of alcohol and cocaine. Frontal but not parietal defects appeared to resolve partially during 21 days of abstinence. 

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