Involuntary intoxication

It may be argued that some individuals will not lose ethical restraint regardless of the nature or intensity of an involuntary intoxication. However, even if some individuals are relatively immune to behaving badly under the influence of drugs, while others seem especially susceptible, this merely reflects human variation, a factor that complicates most research in medicine and behavioral science. The reality of human variation does not undermine the validity of the association between certain drugs and... 

The regular pattern of. involuntary intoxications is a good indicator for the large scope of expansion of Inocybe aeruginascens into new habitats during the 1980s. For example, at the time of the initial intoxications - when the species was still restricted to a few easily quantifiable collections - the mushrooms had spread from Potsdam to the location known in 1982, and from there moved on to several other locations in the vicinity, where more than 150 mushrooms were found (see Figure 34). 

Of course, there is the question whether this substance contributes to the psychoactive effects of Inocybe aeruginascem. It is remarkable that all cases of involuntary intoxication... 

These species, however, are not significant contributors in terms of involuntary intoxications, because, for the most part, these Inocybe species are extremely rare and grow almost exclusively in forests. Also, their psilocybin levels were lower than those found in Inocybe aeruginascens. 

Nicotinic signs of intoxication include muscle weakness, tremor and fasciculations, and involuntary twitching. Muscle weakness that affects the respiratory muscles may contribute to dyspnea and cyanosis. Tachycardia may result from stimulation of sympathetic ganglia in cardiac tissue and may mask the bradycardia due to the muscarinic action on the heart. Nicotinic action at the sympathetic ganglion may also result in pallor, high blood pressure, and hyperglycemia. 

With severe intoxication by all routes, an excess of acetylcholine at the neuromuscular junctions of skeletal muscle causes weakness aggravated by exertion, involuntary twitchings, fasciculations, and eventually paralysis. The most serious consequence is paralysis of the respiratory muscles. Effects on the central nervous system include giddiness, confusion, ataxia, slurred speech, Cheyne-Stokes respiration, convulsions, coma, and loss of reflexes. The blood pressure may fall to low levels, and cardiac irregularities, including complete heart block, may occur. ... 

With severe intoxication by all routes, an excess of acetylcholine at the neuromuscular junctions of skeletal muscle causes weakness aggravated by exertion, involuntary twitchings. 

With liquid nerve agent exposure, moderate intoxication will yield Gl symptoms of nausea, vomiting, abdominal pain and cramps from increased peristalsis, increased Gl secretions and involuntary defecation, etc. If the only sign of Gl symptoms is nausea, one should consider the possibility that this effect could also be due to vapor nerve agent exposure precipitating miosis in the eyes. It is well documented that the development of miosis can cause nausea. 

B. Bromocriptine intoxication may present with hallucinations, paranoid behavior, hypertension, and tachycardia. Involuntary movements, hallucinations, and hypotension are reported with pergolide. 

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