Agitation is common in γ-hydroxybutyrate toxicity

Zvosec, Deborah L.; Smith, Stephen W.

doi:10.1016/j.ajem.2005.02.003

Cited by 26 publications

(17 citation statements)

References 39 publications

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“…Consequently, there is more extensive literature on adverse psychiatric effects with the nonmedical use of GHB. Zvosec and Smith studied 66 patients presenting to an emergency department with GHB intoxication, and found that 40 of them presented with agitation, including 14 who were described as having ''bizarre'' or selfinjurious behaviors (Zvosec and Smith 2005). Pretty and Hall reported a case of a 28-year-old woman who self-extracted 18 of her teeth while under the influence of GHB (Pretty and Hall 2004).…”

Section: Discussionmentioning

confidence: 98%

“…GHB's pharmacologic mechanism is complex, involving multiple neurotransmitter systems, and GHB receptors have been identified in several structures including the hippocampus, thalamus, and cortex (Mamelak 2009). It is noteworthy that individuals with the hereditary condition gamma-hydroxybutyric aciduria, who have a deficiency in succinic semialdehyde dehydrogenase resulting in high levels of endogenous brain GHB levels, also demonstrate high rates of psychiatric symptoms including aggression, anxiety, and behavioral disturbances (Zvosec and Smith 2005). Psychotic symptoms caused by GHB may be mediated by its effects on dopamine; it is hypothesized that, through its actions at the GABA-B receptor, GHB inhibits the release of dopamine, and likely causes upregulation of dopamine receptors (Tarabar and Nelson 2004).…”

Section: Discussionmentioning

confidence: 98%

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Sodium Oxybate-Induced Psychosis and Suicide Attempt in an 18-Year-Old Girl

Chien

Ostermann

Turkel

2013

Journal of Child and Adolescent Psychopharmacology

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Section: Discussionmentioning

confidence: 98%

Section: Discussionmentioning

confidence: 98%

Sodium Oxybate-Induced Psychosis and Suicide Attempt in an 18-Year-Old Girl

Chien

Ostermann

Turkel

2013

Journal of Child and Adolescent Psychopharmacology

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“…However, the neurobiological background for this is poorly understood. While the ingestion of GHB alone can be problematic (10–13), the co‐ingestion of ethanol, amphetamine, cocaine or other substances altogether increases the toxicity of GHB.…”

Section: Introductionmentioning

confidence: 99%

Gamma-hydroxybutyrate – a drug of abuse

2006

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Gamma-hydroxybutyrate (GHB) is a drug of abuse that causes euphoria, anxiolysis, and hypnosis. The recent rise in the recreational intake of GHB, as well as its association with 'drug rape', has turned the attention to GHB in acute hospital settings. Acutely admitted GHB intoxicated patients may display various levels of sedation or coma, but may also show paradoxical agitation, combativeness, or self-injurious behaviors. The symptoms can be nonspecific and the definite diagnosis therefore normally relies on the detection of GHB in blood or body fluids, which is an analysis that may not be promptly available. As a basis for understanding the clinical features of GHB intoxication and abuse, we here review the pharmacological and neurophysiological knowledge about GHB, which stems from decades of clinical and basic GHB research. In addition, we discuss the latest discoveries in the quest for distinct GHB receptors in the brain, and their possible implications for future therapies of GHB abuse.

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“…Ingested recreationally it exhibits a steep dose–response curve, producing euphoria and hallucinations, agitation and anxiety, severely distorting judgment, and it may result in a prolonged coma‐like state followed by a loss of memory (Tancredi et al. 2003; Zvosec and Smith 2005; Drasbek et al. 2006; Barker et al.…”

mentioning

confidence: 99%

γ‐Hydroxybutyrate and the GABAergic footprint: a metabolomic approach to unpicking the actions of GHB

Nasrallah¹,

Maher²,

Hanrahan³

et al. 2010

Journal of Neurochemistry

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Gamma-hydroxybutyrate is found both naturally in the brain and self-administered as a drug of abuse. It has been reported to act at endogenous γ-hydroxybutyrate (GHB) receptors and GABA(B) receptors [GABA(B)R], and may also be metabolized to GABA. Here, the metabolic fingerprints of a range of concentrations of GHB were measured in brain cortical tissue slices and compared with those of ligands active at GHB and GABA-R using principal components analysis (PCA) to identify sites of GHB activity. Low concentrations of GHB (1.0 μM) produced fingerprints similar to those of ligands active at GHB receptors and α4-containing GABA(A)R. A total of 10 μM GHB clustered proximate to mainstream GABAergic synapse ligands, such as 1.0 μM baclofen, a GABA(B)R agonist. Higher concentrations of GHB (30 μM) clustered with GABA(C)R agonists and the metabolic responses induced by blockade of the GABA transporter-1 (GAT1). The metabolic responses induced by 60 and 100 μM GHB were mimicked by simultaneous blockade of GAT1 and GAT3, addition of low concentrations of GABA(C)R antagonists, or increasing cytoplasmic GABA concentrations by incubation with the GABA transaminase inhibitor vigabatrin. These data suggest that at concentrations > 30 μM, GHB may be active via metabolism to GABA, which is then acting upon an unidentified GABAergic master switch receptor (possibly a high-affinity extrasynaptic receptor), or GHB may itself be acting directly on an extrasynaptic GABA-R, capable of turning off large numbers of cells. These results offer an explanation for the steep dose-response curve of GHB seen in vivo, and suggest potential target receptors for further investigation.

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Agitation is common in γ-hydroxybutyrate toxicity

Cited by 26 publications

References 39 publications

Sodium Oxybate-Induced Psychosis and Suicide Attempt in an 18-Year-Old Girl

Sodium Oxybate-Induced Psychosis and Suicide Attempt in an 18-Year-Old Girl

Gamma-hydroxybutyrate – a drug of abuse

γ‐Hydroxybutyrate and the GABAergic footprint: a metabolomic approach to unpicking the actions of GHB

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