Elimination Kinetics and Symptomatology of Diazepam Withdrawal in Abusers

Rhodes, Pamela J.; Rhodes, Richard S.; McCurdy, H. Horton

doi:10.3109/15563658408992568

Cited by 4 publications

(2 citation statements)

References 8 publications

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“…Half-lives vary according to the formulation and duration of abuse. Midazolam is short acting with a half-life of 2-5 h, and that for diazepam is between 20 and 50 hours (Rhodes and Rhodes, 1984). Benzodiazepines are thought to act by enhancing GABA (␥-aminobutyric acid)-mediated inhibition to cause anxiolysis, hypnosis and muscle relaxation.…”

Section: Benzodiazepinesmentioning

confidence: 99%

The role of recreational drugs in trauma

Vidhani

Parr

2001

Trauma

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The association of trauma with illicit/recreational drugs is being increasingly recognized but is difficult to quantify. Significant amounts of these substances are readily available and may be taken alone, in combination with other drugs or with alcohol. The acute and chronic effects of these drugs result in numerous difficulties in management. Health-care workers involved in the treatment of trauma must have a high index of suspicion for the presence of drugs and a detailed knowledge of their effects. In this article we will review the scale of the problem, the common drugs abused and their effects, and we will discuss guidelines for management.

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Section: Benzodiazepinesmentioning

confidence: 99%

The role of recreational drugs in trauma

Vidhani

Parr

2001

Trauma

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“…A study with high-dose users also suggests that an important factor is the rate of disappearance of drug from the brain. The severity of withdrawal was related to the disappearance of diazepam, and desmethyldiazepam both modified and prolonged the withdrawal syndrome (Rhodes et al 1984). Following abrupt termination of treatment, Tyrer et al (1981) compared the rate of decrease of plasma diazepam and desmethyldiazepam in patients with and without a withdrawal syndrome.…”

Section: Withdrawal Syndromesmentioning

confidence: 99%

The biological basis of benzodiazepine dependence

Lader¹,

File²

1987

Psychol. Med.

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EDITORIALThe biological basis of benzodiazepine dependence 1Benzodiazepines are the most widely prescribed psychotropic drugs and while the specific neural pathways mediating their several therapeutic effects remain largely unknown, at least their initial site of action has been identified. For the last decade we have known that the central nervous system contains high affinity, stereospecific binding-sites for the benzodiazepines. These sites are found on a supramolecular complex with y-aminobutyric acid (GABA) receptors and with a chloride ionophore (channel across the cell membrane), which also has binding-sites for drugs such as the barbiturates (Olsen, 1982).Recently there has been a growing appreciation that benzodiazepines induce dependence and that tolerance can occur to their behavioural effects. Although initially these phenomena were linked with long-term use, more recent evidence suggests that similar changes can be observed after short-term or even a single administration.This review covers both the clinical evidence and relevant experimental studies and attempts to explore the possible underlying mechanism(s). Although the precise mechanism is still unknown, we conclude that both rebound and withdrawal symptoms are reflections of a common dependence mechanism and also that tolerance is simply another manifestation of this same mechanism. We further conclude that the same underlying mechanism mediates the rebound phenomena and tolerance seen after short-term or acute benzodiazepine administration. DEPENDENCEDependence is a hypothetical construct for the state induced by the compensatory change that occurs, for example, in the central nervous system as a result of drug administration. The nature of the compensatory change induced by the benzodiazepines remains unknown, but evidence for physical dependence comes from rebound and withdrawal symptoms. To date rebound and withdrawal have been separated in the literature because the former follows acute or short-term, and the latter chronic, drug treatment. We shall follow the literature and describe each separately, but we shall then argue that the two phenomena cannot be distinguished and therefore that each reflects the same common mechanism of dependence, albeit to a different degree. REBOUND SYNDROMERebound can be defined as the increase in severity of the original symptoms, beyond pre-treatment levels, after short or long-term drug administration. Rebound effects have been described after sleep-laboratory studies involving 1-2 weeks of benzodiazepine administration (Kales et al. 1983 a), as well as after longer-term administration (Adam et al. 1976;Oswald et al. 1982). Rebound insomnia after the use of benzodiazepines as hypnotics is now well-documented (for review, see Lader & Lawson, 1987). It is more severe than the original insomnia, and is characterized by a delayed onset of sleep and by frequent awakenings. The elimination half-life of the benzodiazepine is important in determining the timing and the severity of rebound. Short-acting drugs (e....

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Anaesthetic implications of drug abuse in trauma patients

Parr¹,

Hadfield²

1999

Trauma Operative Procedures

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Elimination Kinetics and Symptomatology of Diazepam Withdrawal in Abusers

Cited by 4 publications

References 8 publications

The role of recreational drugs in trauma

The role of recreational drugs in trauma

The biological basis of benzodiazepine dependence

Anaesthetic implications of drug abuse in trauma patients

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