Withdrawal from delirium caused

The abrupt withdrawal from barbiturates may cause tremors, restlessness, anxiety, weakness, nausea and vomiting, seizures, delirium, and cardiac arrest. 

The literature on a withdrawal syndrome (SEDA-10, 17) has been expanded by further reports. One of these (33) involved the development of an acute toxic delirium 3 days after withdrawal of phenelzine, and another (34) concerned patients who became manic after withdrawal of isocarboxazid. A withdrawal state similar to that caused by withdrawal from amphetamines has been described after withdrawal of tranylcypromine (SEDA-16, 8) (SEDA-18,14). 

Acute barbiturate toxicity is characterized by automatism, or a state of drug-induced confusion, in which patients lose track of how much medication they have taken and take more. Death results from respiratory failure. The treatment of poisoning consists of supporting respiration, prevention of hypotension, as well as diuresis, hemodialysis and, in the event of phenobarbital poisoning, the administration of sodium bicarbonate. Tolerance does not develop from lethal doses. The abrupt withdrawal from barbiturates may cause tremors, restlessness, anxiety, weakness, nausea and vomiting, seizures, delirium, and cardiac arrest. 

Alcohol lowers levels of serotonin in the brain, and many alcoholics have dreamless sleep, devoid of rapid eye movement activity. When alcoholics withdraw from alcohol, many experience delirium tremens (DTs), manifest by shaking, sweating profusely, anxiety, and hallucinations. Alcohol depletes the brain of serotonin, the levels of which may rise to higher than normal levels with the withdrawal of alcohol. Excessive production of serotonin is thought to cause the hallucinations, which characterize DTs. 

Knowing the differential pharmacokinetics for a class of drugs allows the clinician to choose specific members to either achieve a faster onset or a delayed offset of action (13, 14, 17, 18). For example, lorazepam is rapidly absorbed from the gastrointestinal tract into the systemic circulation and from there distributed into the brain. In contrast, oxazepam, the most polar BZD, is slowly absorbed from the gastrointestinal tract. Even after oxazepam is in the systemic circulation, it slowly enters tissue compartments, including the brain, during the distribution phase. Unlike lorazepam, oxazepam is not available in either the intramuscular or intravenous formulations. Thus, lorazepam would be preferable to achieve acute control of alcohol withdrawal (e.g., delirium tremens), whereas oxazepam would better stabilize a dependency-prone patient on sedative-hypnotics, because it does not cause the euphoria seen with the more rapidly absorbed members of this class. 

This condition may emerge after a period of relative or absolute abstinence, with the cause being unknown. The duration of drinking and quantity of alcohol required to produce noticeable symptoms vary widely. Abstinence may also result from intercurrent illness, hospitalization for an unrelated illness, or lack of money to buy alcohol. The full spectrum of this syndrome, which ranges from an early, mild withdrawal picture to delirium is frequently seen in large urban hospital emergency room settings. 

Stanilla et al. (1997) described three cases of delirium with psychotic symptoms due to clozapine withdrawal (see also Adams et al., 1991, for an early report of clozapine withdrawal psychosis). They believed that clozapine produces more severe withdrawal symptoms than typical antipsychotic agents. In a 3-year open label study of quetiapine, Margolese et al. (2004) switched 23 male patients from classical antipsychotics and risperidone to quetiapine Six of the seven patients who relapsed after being stabilized on quetiapine for at least three months met the criteria for supersensitivity psychosis. This is a very high rate, again raising questions about whether atypicals may be more prone to cause tardive psychosis. 

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