Nervous system alcoholism

Eckardt MJ, File SE, Gessa GL et al. Effects of moderate alcohol consumption on the central nervous system. Alcohol Clin Exp Res 1998 22 998-1040. 

Meyerhoff, D.J., Effects of alcohol and HIV infection on the central nervous system, Alcohol Res. Health, 25, 288, 2001. 

Depressants Drugs that reduce the activity of the nervous system Alcohol, downers, and narcotics arc all depressants. 

Alcohols Alcohols contain a single-OH group. Methanol (200 ppm) slowly produces toxic metabolites and has been associated with fatalities and injuries, vision impairment, and optic nerve injury. Ethanol (1,000 ppm) is quickly metabolized and converted to CO2 it is the least toxic of the alcohols. Propanol (200 ppm), metabolized to toxic by-products, is more toxic than ethanol, but less toxic than other alcohols. Alcohol has a depressant, not a stimulant effect on the central nervous system. Alcohols reduce brain and spinal cord activity. Exposures to extremely high doses can result in death by involuntary ceasing of the respiratory system. The Ever can also be a vulnerable target organ for alcohols. 

Overexposure to tetrachloroethylene by inhalation affects the central nervous system and the Hver. Dizziness, headache, confusion, nausea, and eye and mucous tissue irritation occur during prolonged exposure to vapor concentrations of 200 ppm (15). These effects are intensified and include incoordination and dmnkenness at concentrations in excess of 600 ppm. At concentrations in excess of 1000 ppm the anesthetic and respiratory depression effects can cause unconsciousness and death. A single, brief exposure to concentrations above 6000 ppm can be immediately dangerous to life. Reversible changes to the Hver have been reported foUowing prolonged exposures to concentrations in excess of 200 ppm (16—22). Alcohol consumed before or after exposure may increase adverse effects. 

Solvents acetone, methyl ethyl ketone (MEK), toluene, xylene, glycol, ethers, alcohol defats and dries skin some may be absorbed may carry other components through skin high volatility, exposure possible irritation central nervous system depression (e.g. dizziness, loss of coordination) low to high toxicity, longterm effects... 

Ethanol is classified for medical purposes as a central nervous system (CNS) depressant. Its effects—that is, being drunk—resemble the human response to anesthetics. There is an initial excitability and increase in sociable behavior, but this results from depression of inhibition rather than from stimulation. At a blood alcohol concentration of 0.1% to 0.3%, motor coordination is affected, accompanied by loss of balance, slurred speech, and amnesia. When blood alcohol concentration rises to 0.3% to 0.4%, nausea and loss of consciousness occur. Above 0.6%, spontaneous respiration and cardiovascular regulation are affected, ultimately leading to death. The LD50 of ethanol is 10.6 g/kg (Chapter 1 Focus On). 

Neuropathic pain is initiated or caused by a primary lesion in the peripheral or central nervous system. The causative agent may be trauma, nerve-invading cancer, herpes zoster, HIV, stroke, diabetes, alcohol or other toxic substances. Neuropathic pain is refractory to most analgesic drugs. Altered sodium channel activity is characteristics of neuropathic pain states. 

There is an increased central nervous system (CNS) depressant effect when the skeletal muscle relaxants are administered with other CNS depressants, such as alcohol, antihistamines, opiates, and sedatives. There is an additive anticholinergic effect when cyclobenzaprine is administered with other drugs with anticholinergic effects (eg, antihistamines, antidepressants, atropine, haloperidol). See Chapter 30 for information on diazepam. 

There is an increase in anticholinergic effects when antihistamines are administered with the monamine oxidase inhibitors (MAOIs) and additive sedative effects if administered with central nervous system depressants (eg, narcotic analgesics or alcohol). When cimetidine and loratadine are administered together there is a risk for increased loratadine levels. 

Other central nervous system (CNS) depressants and alcohol may cause additive depressant effects when administered with antitussives containing codeine. 

There is an increased risk for bone marrow suppression when levamisole or hydroxyurea are administered witii other antineoplastic dni. Use of levamisole witii phenytoin increases die risk of phenytoin toxicity. Pegaspargase may alter drug response of the anticoagulants. When procarbazine is administered with other central nervous system (CNS) depressants, such as alcohol, antidepressants, antihistamines, opiates, or the sedatives, an additive CNS effect may be seen. Procarbazine may potentiate hypoglycemia when administered witii insulin or oral antidiabetic dru . ... 

Alcohol can affect the metabolism of trichloroethylene. This is noted in both toxicity and pharmacokinetic studies. In toxicity studies, simultaneous exposure to ethanol and trichloroethylene increased the concentration of trichloroethylene in the blood and breath of male volunteers (Stewart et al. 1974c). These people also showed "degreaser s flush"—a transient vasodilation of superficial skin vessels. In rats, depressant effects in the central nervous system are exacerbated by coadministration of ethanol and trichloroethylene (Utesch et al. 1981). 

Azcona, O., Barbanoj, M. J., Torrent, J., and Jane, F., Evaluation of the effects of alcohol-caffeine interaction on the central nervous system. Journal of Psychopharmacology 6, 136, 1992. 

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