Barbiturates withdrawal

Because alcohol and barbiturates also act, in part, via the GABA receptor-mediated chloride ion channel, benzodiazepines show cross-tolerance with these substances. Thus, benzodiazepines are used frequently for treating alcohol or barbiturate withdrawal and detoxification. Alcohol and barbiturates are more dangerous than benzodiazepines because they can act directly at the chloride ion channel at higher doses. In contrast, benzodiazepines have no direct effect on the ion channel the effects of benzodiazepines are limited by the amount of endogenous GABA. 

Buspirone is a partial agonist at serotonin type 1A (5-HTj ) receptors. Unlike benzodiazepines, barbiturates, and alcohol, buspirone does not interact with the GABA receptor or chloride ion channels. Thus, it does not produce sedation, interact with alcohol, impair psychomotor performance, or pose a risk of abuse. There is no cross-tolerance between benzodiazepines and buspirone, so benzodiazepines cannot be abruptly replaced with buspirone. Likewise, buspirone cannot be used to treat alcohol or barbiturate withdrawal and detoxification. Like the antidepressants, buspirone has a relatively slow onset of action. 

Barbiturates, which preceded benzodiazepines as the most commonly abused sedative hypnotics (after ethanol), are now rarely prescribed to outpatients and therefore constitute a less common prescription drug problem than they did in the past. Street sales of barbiturates, however, continue. Management of barbiturate withdrawal and addiction is similar to that of benzodiazepines. 

Barbiturate withdrawal time is related to whether the drug is short or long-lasting. Symptoms accompanying withdrawal include apprehension, weakness, tremors, anorexia, muscle twitches, and possible delirium. However, barbiturate withdrawal is seldom symptom-free and can be more difficult than heroin withdrawal. 

Most addicts realize that they will suffer a great amount of pain and discomfort from barbiturate withdrawal if they stop taking the drug. The withdrawal of barbiturates for an addict can be... 

Delirium Delirium due to barbiturate withdrawal is, again, similar to that seen with abrupt alcohol withdrawal. The chief sign is one of impaired memory, of both recent and past memories. Delirium is also associated with confusion and disorientation (not knowing person, place or time). The hallucinations associated with delirium are more visual in nature and are described as terrifying. Often, patients develop a high fever. These symptoms stop by the third or fourth day, and rarely last longer than a week. 

Romero, C. E. et al. Barbiturate Withdrawal Following Internet Purchase of Fioricet. Archives of Neurology 61 (2004) 1111-1112. 

Heroin withdrawal is much less dangerous than alcohol and barbiturate withdrawal. Withdrawal symptoms are craving for opioid, restlessness, irritability, increased sensitivity to pain, nausea, cramps, muscle and bone aches, insomnia, anxiety, cold flashes with goose bumps (cold turkey), and movements (kicking the habit).5... 

One major reason for the movement away from the medical use of barbiturates involves tolerance and dependence. Tolerance develops fairly rapidly to many effects of the barbiturates. Whereas a given dose may be effective at inducing sleep for a while, if the drug is used regularly the patient soon may require a higher dose in order to sleep. If doses escalate too much and regular use persists, the patient will experience an abstinence syndrome when he or she attempts to withdraw from barbiturates. The symptoms of the barbiturate withdrawal syndrome are similar to those of alcohol— shakes, perspiration, confusion, and in some cases full-blown delirium tremens (DTs) (see Chapter 9)—but convulsions and seizures are more likely to occur in barbiturate... 

Many people became dependent on barbiturates even though the drugs were used only under medical supervision. Suppose someone is in crisis—say, after the death of a spouse or other loved one. A physician may prescribe a sleeping pill to help the person rest during the crisis. After a tew weeks the patient may feel emotionally ready to sleep without the drug—and indeed may be. But the first night he or she attempts to sleep without the barbiturate, the person may have a great deal of trouble because one of the features of barbiturate withdrawal is rebound insomnia (Mendelson, 1980). That is, after the chronic use of barbiturates, abstinence produces insomnia even in someone who was untroubled with insomnia previously. 

So even if the tired patient is able to get to sleep without drugs during barbiturate withdrawal, he or she may awaken early in the morning and not be able to get back to sleep. Other factors may be involved, but it is clear that once dependence on sleeping pills has developed, considerable time must pass before normal sleep patterns return (Mendelson, 1980). All of these factors make it ea.sy to understand why dependence on drugs such as barbiturates for sleeping so often develops. Dependence certainly limits the usefulness of these and other depressants as a treatment of sleep disorders. 

It has been su ested, but not confirmed, that because increased levels of carbon dioxide in the tissues can increase the sensitivity to oxygen-induced convulsions, carbonic anhydrase inhibitors, such as acetazolamide, are contraindicated in those given hyperbaric oxygen, because they cause carbon dioxide to persist in the tissues. Nor should hyperbaric oxygen be given during opioid or barbiturate withdrawal because the convulsive threshold of such patients is already low. ... 

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