Addiction to nonbarbiturate sedative and tranquilizing drugs

Essig, Carl F.

doi:10.1002/cpt196453334

Cited by 77 publications

(20 citation statements)

References 22 publications

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“…38]. It is well-recognized that tolerance with continued use of large doses of nonbenzodiazepinc sedative-hypnotics for prolonged periods of time leads to depen dence [10]. For benzodiazepines there have been fewer reports of withdrawal reactions [65][66][67][68][69], and their dependence liability has generally been considered far lower in com parison to that of nonbenzodiazepinc seda tive-hypnotics.…”

Section: Clinical Implications Of Rebound Insomniamentioning

confidence: 99%

“…Development of a clinical sy ndrome fol lowing withdrawal from chronically adminis tered large doses of sedative-hypnotics and tranquilizers has been recognized for many years [1][2][3][4][5][6][7][8][9][10]. Clinical observations docu mented withdrawal sy ndromes characterized by symptoms opposite to those for which drug treatment was intended (agitation, tre mulousness.…”

Section: Introductionmentioning

confidence: 99%

“…Clinical observations docu mented withdrawal sy ndromes characterized by symptoms opposite to those for which drug treatment was intended (agitation, tre mulousness. insomnia, hyperpyrexia, and even convulsive seizures) [1][2][3][4][5][6][7][8][9][10].…”

Section: Introductionmentioning

confidence: 99%

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Rebound Insomnia and Rebound Anxiety: A Review

et al. 1983

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Rebound insomnia and rebound anxiety are clinical conditions related to withdrawal of certain benzodiazepine drugs. Numerous studies of benzodiazepine and nonbenzodiazepine hypnotics conducted in our sleep laboratory demonstrated that rebound insomnia developed following withdrawal from benzodiazepines with a rapid or intermediate elimination rate. Several studies conducted by other investigators also indicated the development of rebound insomnia under similar conditions. Rebound insomnia and rebound anxiety are discussed in terms of their interrelationship, clinical implications, and receptor mechanisms. Evidence suggests that drugs producing rebound insomnia and rebound anxiety also show a more rapid development of tolerance and greater potential for drug dependence than benzodiazepines where the parent compound or its metabolites have a long elimination half-life.

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Section: Clinical Implications Of Rebound Insomniamentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Rebound Insomnia and Rebound Anxiety: A Review

et al. 1983

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“…It has long been recognized that continued use of large doses of nonbenzodiazepine seda tive hypnotics for prolonged periods of time leads to dependence and a fully developed withdrawal syndrome [67][68][69][70][71][72][73][74], Also, there have been numerous reports on withdrawal reactions with benzodiazepine anxiolytics and hypnotics as well [75][76][77][78][79][80][81][82][83][84][85]. In most cases, fully developed withdrawal reactions with benzodiazepines have also followed their pro longed use in high doses.…”

Section: Withdrawal Phenomena (Rebound Insomnia and Anxiety)mentioning

confidence: 99%

Benzodiazepine Side Effects: Role of Pharmacokinetics and Pharmacodynamics

Vgontzas

Kales

Bixler³

1995

Pharmacology

103

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Benzodiazepines have a wide variety of indications. However, CNS and psychiatric adverse reactions, tolerance, and withdrawal effects of benzodiazepines are becoming increasingly recognized and must be better understood for proper drug use. Certain benzodiazepines are associated with memory impairment and other cognitive defects and hyperexcitability phenomena during treatment (early-morning insomnia, daytime anxiety) and following withdrawal (rebound insomnia and anxiety, seizures). Elimination half-life, receptor-binding affinity, effects on the locus coeruleus-norepinephrine (LC-NE) and hypothalamic-pituitary-adrenal (HPA) axes, and the interaction of these factors appear to be major determinants of frequency and severity of these untoward effects. Rapid drug elimination and high receptor-binding affinity were initially suggested as primary underlying factors which determine frequency, severity, and type of the side effects of benzodiazepines during administration and withdrawal. Newer data and information on triazolobenzodiazepines indicate that these psychiatric adverse reactions also relate to whether the benzodiazepine has strong direct effects on the LC-NE and HPA systems. Initial suppression of the LC-NE and HPA systems is followed, on an interdose basis, by a significant rebound and activation. This repetitive pattern of suppression followed by rebound results in a neurophysiologic and behavioral sensitization (kindling) of the limbic system and consequently contributes to central nervous system and psychiatric adverse reactions. The tendency of certain of these side effects to worsen over time supports empirically this neurophysiologic and biochemical model.

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“…When we tient's daily dose was immedi-4 days attempting to complete last contacted this patient, he had ately reduced to a 10 mg. tablet detoxification before returning to been paying weekly visits to the twice a day, and again he did not the same pharmacist in an at-outpatient clinic for approxi-experience withdrawal symptoms. (41)(42)(43)(44)(45)(46)(47).…”

Section: Abusers Of Pentazocine Onlymentioning

confidence: 99%