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Central nervous system depressants
Published in Ilana B. Crome, Richard Williams, Roger Bloor, Xenofon Sgouros, Substance Misuse and Young People, 2019
GHB (γ-hydroxybutyric or 4-hydroxybutanoic acid) is a CNS depressant that it is naturally present at trace amounts in mammalian tissues, including the brain (Nasrallah et al., 2010; Busardo and Jones, 2015). Although its exact role remains unclear, it exhibits many of the functions of a neurotransmitter or neuromodulator (Nasrallah et al., 2010). It is also found in small quantities in some wines and other alcoholic beverages, as a result of fermentation (Elliott and Burgess, 2005). GHB is odourless and colourless, difficult to detect and may be disguised in water bottles as users top up their levels during the day.
Sedative/Hypnotics
Published in Frank A. Barile, Barile’s Clinical Toxicology, 2019
Frank A. Barile, Anirudh J. Chintalapati
Since its synthesis in 1960, GHB has been promoted and abused for sleep disorders (narcolepsy), as an anesthetic agent, as treatment for alcohol and controlled substance withdrawal, and currently, as an inducer of growth hormone (bodybuilding) and aphrodisiac. The tasteless, odorless, liquid or gel form makes it convenient for use as a “date-rape” drug.
NPS
Published in Ornella Corazza, Andres Roman-Urrestarazu, Handbook of Novel Psychoactive Substances, 2018
Máté Kapitány-Fövény, Aviv M. Weinstein, Zsolt Demetrovics
Palamar and Halkitis (2006) described how the short effect duration of GHB, its capability of producing an energy boost, its role as sleep assistance, the increase in libido, and its limited and tolerable after-effects make this substance a preferable choice for its users.
Gamma-Hydroxybutyrate (GHB) Withdrawal in a Patient with Polysubstance Use
Published in Journal of Psychoactive Drugs, 2021
Gamma-hydroxybutyrate (GHB) was first introduced in the 1960s as an anesthetic (Dyer, Roth, and Hyma 2001). Over the decades, its uses varied from an operating room sedative to a facilitator of sexual assault (Weir 2001) to a recreational substance (Andresen et al. 2011). These uses of GHB arise from the fact that its backbone is an endogenous neurotransmitter with similarities to GABA and glycine (Carter, Koek, and France 2009). GHB and its chemical derivatives are now easily found and sold online leading to more widespread use (Andresen et al. 2011; Brennan and Van Hout 2014). People who chronically use GHB or use GHB at high doses may experience a reduced effect from GHB alone and may attempt to use GHB in combination with other substances to re-create their initial euphoria (Barker, Harris, and Dyer 2007) as tolerance develops. Although there is a “lack of familiarity” regarding the treatment of GHB intoxication and withdrawal (Brennan and Van Hout 2014), physicians must be more aware of its course, treatments, and adjuncts due to its more extensive use. Furthermore, as GHB is commonly combined with other substances such as alcohol (Brennan and Van Hout 2014), methylene dioxymethamphetamine (ecstasy), marijuana, and benzodiazepines (Anderson et al. 2008), treatment becomes complicated making recovery more uncertain. The author reports a case that highlights the difficult in correctly diagnosing GHB intoxication and withdrawal. Additionally, the author presents a timeline of ultimately successful interventions which may be potentially duplicated in cases of severe GHB withdrawal with co-morbid polysubstance use.
Successful treatment of severe, treatment resistant GHB withdrawal through thiopental-coma
Published in Substance Abuse, 2021
Cornelis F. Vos, Monica Pop-Purceleanu, Maarten J. W. van den Berg, Arnt F. A. Schellekens
It is poorly understood how barbiturates can be effective when pharmaceutical GHB, benzodiazepines, and baclofen fail to counteract GHB withdrawal. Barbiturates also act on GABA-A and -B receptors, but in addition antagonize glutamatergic AMPA and kainate receptors.30 It has been suggested that antagonizing glutamatergic receptors might explain the effectiveness of barbiturates in the treatment of resistant GHB withdrawal, particularly in case of manifest glutamatergic overactivity.14 Indeed, GHB has dose-dependent effects on glutamate and dopamine release,4,9 and GHB withdrawal has been associated with glutamatergic hyperactivation, resulting in agitation and motor restlessness.8,14 Similar effectiveness of barbiturates in case of treatment-resistant alcohol withdrawal further supports the idea that barbiturate-induced coma might be a last resort option if withdrawal symptoms are treatment-resistant.31,32
Characteristics and circumstances of death related to gamma hydroxybutyrate (GHB)
Published in Clinical Toxicology, 2020
Shane Darke, Amy Peacock, Johan Duflou, Michael Farrell, Julia Lappin
Gamma hydroxybutyrate (GHB) is a central nervous system depressant, an agonist for the GHB and GABAB receptors, with a half-life of approximately 30 min [1]. First synthesised in 1960 for anaesthesia, it was found to have poor analgesic properties and is now prescribed in some countries for the treatment of narcolepsy [2]. GHB is also an endogenous metabolite, present in human tissue at low concentrations with levels potentially rising substantially after death [1]. Since the 1990s, GHB has gained popularity as an illicit recreational drug [3]. Positive effects include euphoria, disinhibition, increased libido and increased sociality. Effects are felt within 10–15 min, and persist for approximately three hours [1]. The closely related metabolic precursors that are also sold illicitly, gamma-butyrolactone (GBL) and 1,4-butanediol, rapidly convert to GHB in vivo, and have the same spectrum of effects [1,4–6]. GHB is generally taken orally, dissolved in water to form a clear solution, but may be insufflated or injected.