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There have been descriptions throughout history of symptoms and signs that would now be recognized as belonging to an alcohol withdrawal syndrome. The Edinburgh physician Thomas Sutton is credited with describing delirium tremens in 1813 and attributing the condition to alcohol withdrawal. Con rmation of the connection between drinking, stopping drinking and the experience of withdrawal is, however, relatively recent. In the classic study by Isbell et al. (1955), 10 ex-morphine addicts received daily dosing with alcohol for periods of up to 12 weeks. On abrupt withdrawal of alcohol, the subjects experienced signi cant symptoms, including tremor, sweating, vomiting, diarrhoea, hyper-re exia, fever, raised blood pressure and insomnia; two subjects experienced convulsions and four subjects experienced hallucinations or delirium. The work of Isbell and colleagues left questions unanswered but was a suf cient basis for proceeding with further elucidation of the nature of withdrawal by the use of laboratory-style experimentation in human beings. In a selective review of this research, Gross (1977) concluded that the severity of the alcohol withdrawal syndrome would relate to alcohol intake modi ed by the contribution of residual effects of previous drinking and the abruptness of withdrawal. He went on to describe a factor structure of withdrawal: Factor 1 hallucinogenic consists of nausea, tinitus, visual disturbance, pruritis, parasthesiae, muscle pain, agitation, sleep disturbance, tactile hallucinations, and hallucinations which are auditory or visual or both: Factor 2 affective and physiological consists of anxiety, depression, tremor and sweats: Factor 3 delirium consists

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-/M/l-FCFS-HOL node After we have introduced multiple classesand considered the reverse order of priorities, we derive the following formulae from Eqs. (6.106) and (6.107):

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A variant on this theme contains mixed acyl groups. In the absence of a specific reference it may be speculated that the synthesis starts with the diacetyl derivative (15). Controlled hydrolysis would probably give the monoacetate U 6 ) since the ester para to the ketone should be activated by that carbonyl function. Acylation with anisoyl chloride followed by reduction would then afford nisobuterol (18).