Manic Episode With Psychotic Symptoms Associated With High Dose of Disulfiram

Ceylan, Mehmet Emin; Türkcan, Ahmet; Mutlu, Elif; Önal, Osman

doi:10.1097/01.jcp.0000264974.85205.35

Cited by 16 publications

(6 citation statements)

References 12 publications

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“…Identified and characterized as a developmental morphogen, RA has been primarily studied as a transcriptional regulator during development. However, the link between RA and neuropsychiatric disease also has a surprisingly long history (77)(78)(79)(80)(81)(82)(83)(84), supporting RA's role in cognitive function in adults. Homeostatic plasticity is a form of synaptic plasticity that is distinct from Hebbian plasticity.…”

Section: Discussionmentioning

confidence: 99%

The fragile X mutation impairs homeostatic plasticity in human neurons by blocking synaptic retinoic acid signaling

et al. 2018

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Fragile X syndrome (FXS) is an X chromosome-linked disease leading to severe intellectual disabilities. FXS is caused by inactivation of the fragile X mental retardation 1 () gene, but how inactivation induces FXS remains unclear. Using human neurons generated from control and FXS patient-derived induced pluripotent stem (iPS) cells or from embryonic stem cells carrying conditional mutations, we show here that loss of function specifically abolished homeostatic synaptic plasticity without affecting basal synaptic transmission. We demonstrated that, in human neurons, homeostatic plasticity induced by synaptic silencing was mediated by retinoic acid, which regulated both excitatory and inhibitory synaptic strength. inactivation impaired homeostatic plasticity by blocking retinoic acid-mediated regulation of synaptic strength. Repairing the genetic mutation in the gene in an FXS patient cell line restored fragile X mental retardation protein (FMRP) expression and fully rescued synaptic retinoic acid signaling. Thus, our study reveals a robust functional impairment caused by mutations that might contribute to neuronal dysfunction in FXS. In addition, our results suggest that FXS patient iPS cell-derived neurons might be useful for studying the mechanisms mediating functional abnormalities in FXS.

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Section: Discussionmentioning

confidence: 99%

The fragile X mutation impairs homeostatic plasticity in human neurons by blocking synaptic retinoic acid signaling

et al. 2018

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“…The earliest onset of neuropathy in the patients taking DSF was 10 days. 21,42,43 In the Danish data, 6 reactions (4%) were reported as psychiatric and 13% in World Health Organization reports. 17 Most reports placed the onset of symptoms at several months after commencing treatment and the peak time in the Danish data was 1 year.…”

Section: Discussionmentioning

confidence: 99%

“…[30][31][32][33][34] Four case reports were related to cardiac adverse events (2 ST depression on electrocardiogram (ECG), 1 myocardial infarction, and 1 refractive hypotension). 21,42,43 Three case reports were of neuroimaging findings such as nigral damage and bilateral globus pallidus infarction after DSF intoxication. 21,42,43 Three case reports were of neuroimaging findings such as nigral damage and bilateral globus pallidus infarction after DSF intoxication.…”

Section: Case Reportsmentioning

confidence: 99%

The Relative Safety of Disulfiram

Alharbi

el‐Guebaly

2013

Addictive Disorders &Amp; Their Treatment

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Objectives:Disulfiram (DSF) treatment remains a viable option as a treatment for alcohol dependence. There have been concerns about its safety, which are often used as a reason for withdrawing the treatment or as an argument against starting it. How safe is the current prescription of DSF? This paper aims to provide an update of DSF's safety-related research. Method:A systematic review of the recent literature was drawn from a comprehensive MEDLINE (2000 to 2012) search. Case reports and clinical trials using DSF for the treatment of alcohol and/or cocaine use and/or dependence were reviewed. Result:Within the specified period, there have been 30 case reports and 8 clinical trials regarding DSF's side effects. One was a longer trial of DSF spanning >50 weeks. The case reports were related to neurological, hepatic, cardiac, dermatological, psychiatric adverse events, neuroimaging findings, and drug-drug interaction. Because of exclusion criteria, adverse events in DSF randomized double-blind clinical trials seem to be less serious and less frequent than adverse events reported postmarketing. Conclusions:With the safety recommendations in place, we consider the administration of DSF to be safe practice and within an acceptable risk profile.

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“…One of the side‐effects in patients treated with disulphiram is the emergence of psychotic phenomena which may have an appearance like that of the mood disorders. Dysregulation of biogenic amines signalling may play an important part in such disulphiram‐mediated pathophysiology .…”

Section: Discussionmentioning

confidence: 99%