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Case Report, Oct./16: "Eszopiclone-induced Parasomnia with Suicide Attempt"


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This case report looks at an extreme example of a risk associated with Z-drugs and benzodiazepines. In the discussion section, there's an interesting explanation of the neurotransmitters involved, and I will post that here. It mentions not only GABAa, but also serotonin and dopamine. I know the focus around here is usually GABAa, but it's important to note the effects on the other neurotransmitters. In this particular case, there's also a drug-drug interaction, which appears to have played an important role.


I should warn you that the "Case Report" section describes what happened to a particular gentleman, and it's a bit graphic. He had an adverse response to the medication on the second night he took it. So, if you don't want to read the details, just skip that part.




Eszopiclone is a potentiator of three major alpha subunits of gama-aminobutyric acid (anion) receptors (GABAA), the neuropsychiatric roles of which have been generally defined in various studies over the years. Potentiation at alpha-1 is believed to primarily mediate sedation, but is also involved in fear-reduction and anxiolysis; alpha-2 is the main subunit involved in anxiolysis; and alpha-3 is predominantly involved in fear-reduction.11,12 One major pharmacologic difference between eszopiclone and other popular “Z-drugs,” such as zaleplon and zolpidem, is that eszopiclone is not selective for the alpha-1-GABAA subtype (Figure 3), and thus produces broader effects that are more similar to those produced by benzodiazepines.8, 12


Benzodiazepines are notorious for adverse side-effects, such as parasomnias and amnesia.13, 14 Benzodiazepines have also been known to cause “paradoxical reactions” (e.g., behavioral disinhibition, impulsivity, agitation) in which patients may engage in uncharacteristic behaviors, such as suicidality, assaults, theft, or sexual indiscretions, without any history of similar behaviors before use or after discontinuation. 15 Benzodiazepines and alcohol are believed to exert depressogenic effects by two mechanisms: 1) by decreasing serum serotonin levels and inhibiting serotonergic function both acutely and chronically16 and 2) via dopamine depletion (acute) or a “recalibration” (chronic) of baseline dopamine levels in the nucleus accumbens, which is known as the “pleasure center” of the brain.17 Benzodiazepine-like medications exerting a similar depressogenic effect may explain the acute suicidality in our patient.



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It also underscores how little they really know about Lunesta -- f**king mad about this.  So scary.  One bloody horror case is not enough.  They need large test populations.  Thank you Lap for this info -- thank you!  WBB
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Hey abcd and wannabe,

This one is going to stick with me for a long while. The lack of similar case reports points to the fact that most of these cases are missed or put down to some other cause. This is likely one of many strange and horrible things that have taken place as a result of bad combinations of medications and interactions with individual genetic makeups. I'm so glad this man was NOT put into the psych ward, and that someone was intelligent and perceptive enough to understand that this was a terrible, terrible adverse reaction to a medication.


So, at least there was a bit of good news.


I was also really pleased to see the explanation of how many neurotransmitters are affected by benzodiazepines. Of course, around here, we're all aware that there's an effect on the GABAa receptors, but as well, this report talks about the effect on serotonin and dopamine, both of which are major neurotransmitters too. There's a domino effect. It's not as if each neurotransmitter acts alone.


Okay, I appreciate the feedback, so thanks for chiming in on this case report. I was thinking..... If they wrote a case report on each one of us, then there would be a massive amount of medical literature on benzodiazepine withdrawal that could be reviewed by the medical community.


Wishful thinking.



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