The CNS depressants include barbiturates, nonbarbitu-rate sedatives, and the benzodiazepines. As the medical use of barbiturates decreased, primarily because of their high addiction liability and the danger of acute lethality, the use of the benzodiazepine anxiolytics in-creased. The most commonly abused barbiturates are secobarbital, pentobarbital, and amobarbital. Pheno-barbital is not generally abused, because of its slow on-set of action. The most commonly abused anxiolytics include diazepam, chlordiazepoxide, midazolam, lo-razepam, and flurazepam. These drugs are readily at-tainable from illicit sources.
Abused nonbarbiturate sedatives include glutethi-mide and meprobamate.
CNS depressants, including barbiturate, benzodiazepine, and ethanol, produce a similar intoxication. These drugs are abused for their euphoric effects and as a means to reduce anxiety and limit insomnia. As the dose of de-pressant increases, along with the degree of intoxication, the effects progress from anxiety reduction and muscle relaxation to motor impairment and unconsciousness. The difference between the classes of drugs is primarily dose responsiveness. Intoxication progresses from mild to severe over a relatively narrow dose range in the case of the barbiturates. The benzodiazepine dose–response curve is such that great increases in dose are necessary to make such a transition. Thus, the benzodiazepines are a safer class of depressant drugs.
The acute effects of depressants can include eupho-ria, anxiety reduction, anticonvulsant activity, sedation, ataxia, motor incoordination, impaired judgment, anes-thesia, coma, and respiratory depression resulting in death. The benzodiazepines are rarely involved in lethal-ity, but all CNS depressants enhance the effects of other depressant drugs. The physiological effects of high-dose depressants include miosis, shallow respiration, and re-duction in reflex responses.
Tolerance to many of the effects of the depressants de-velops. Unlike opioids, barbiturate and benzodiazepine tolerance develops slowly. Also, tolerance is incomplete in some instances or does not influence some pharma-cological effects. One such exception is the lack of tol-erance to barbiturate lethality. The lethal dose in a tol-erant individual is not much different from that of the general population. Cross-tolerance develops to some degree between the depressant classes of drugs.
Dependence on benzodiazepines, as evidenced by a withdrawal syndrome, can develop to large doses of drugs. Mild dependence is produced at therapeutic doses.
Individuals report some craving for drug during withdrawal from benzodiazepines, but the level is not as great as among those who abuse alcohol. Once the withdrawal syndrome has dissipated, the abusers of benzodiazepines are not as likely to resume drug con-sumption as are alcoholics. Withdrawal signs appear to be more likely following chronic exposure to short-acting benzodiazepines, such as alprazolam (half-life of less than 15 hours) or lorazepam than long-acting drugs. Despite gradual dose reduction, individuals may have anxiety attacks, confusion, agitation, restlessness, sweat-ing, clouded sensorium, heightened sensory perception, perceptual disturbances, sleep disruption, muscle cramps, muscle twitches, and tremors; 2% of addicts may have a seizure during withdrawal. Withdrawal signs peak the second day after abrupt withdrawal and last for at least 5 to 7 days. Withdrawal symptoms following long-acting benzodiazepines (diazepam, clorazepate) peak during the second week of abstinence. In contrast to alcohol and the barbiturate sedatives, withdrawal from benzodiazepines is not life threatening.
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