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    seroquel + cocaine? 
    #1
    I just found out that some people like to mix the two. This seems totally ridiculous to me based on my meager understanding of pharmacology. As far as I know, quetiapine is an antagonist at dopamine and adrenergic receptors. Does anyone know why a person would do this? The only people I have heard about who abuse seroquel are desperate inmates.

    There has to be a pharmacological explanation for this, people wouldn't do it if it didn't do something.
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    #2
    --> od
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    #3
    why?
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    #4
    bdd. simple combo question.
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    #5
    I don't know, but at least one researcher at Brown has suggested that quetiapine may become a controlled substance soon.

    I have a related question: How much Seroquel do I need to plug before I'm full of shit?
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    #6
    wouldnt take long considering its also an acetylcholine antagonist.

    muscarinic, that is.
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    #7
    ^Good one.
    Find the full text of this article. I haven't been able to.
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    #8
    Bluelighter Sweet P's Avatar
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    Quote Originally Posted by seep View Post
    I don't know, but at least one researcher at Brown has suggested that quetiapine may become a controlled substance soon.
    Why on earth would quetiapine become a controlled substance? It's non-addictive with minimal (if any) abuse potential.
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    #9
    Quote Originally Posted by Sweet P View Post
    Why on earth would quetiapine become a controlled substance? It's non-addictive with minimal (if any) abuse potential.
    Cuz for every 10000 people who agree with us, there's one guy who swears that seroquel fucks him the fuck up an feels exactly like ____ (where ____ is anything from methamphetamine to sodium pentothal).
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    #10
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    Quote Originally Posted by seep View Post

    I have a related question: How much Seroquel do I need to plug before I'm full of shit?
    lol! treséLOL
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    #11
    If you are psychotic don't use cocaine buddy.
    We always see patients who are paranoiac with cocaine so schizoid troubles and paranoia .... brrr

    But Seroquel doesn't act on the same receptors than C so.... I guess there are no effects with this combo but I'm VERY not sure.
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    #12
    Quote Originally Posted by seep View Post
    I have a related question: How much Seroquel do I need to plug before I'm full of shit?
    hahahahahahahahaha!!!!!!!!!!!
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    #13
    Bluelighter Sweet P's Avatar
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    Quote Originally Posted by Pierrot the clown View Post
    But Seroquel doesn't act on the same receptors than C so.... I guess there are no effects with this combo but I'm VERY not sure.
    I'm no medical expert, but from what I've read, cocaine and seroquel do act on some of the same receptors - but in opposing ways. Cocaine is a D1, 5-HT2 and 5-HT3 agonist, whereas seroquel is (among other things) a D1 and 5-HT2 antagonist.

    Back to the original topic, I've just found something interesting from Wikipedia: "If dopamine antagonists are infused directly into the nucleus accumbens, well-trained rats self-administering cocaine will undergo extinction (i.e. initially increase responding only to stop completely) thereby indicating that cocaine is no longer reinforcing (i.e. rewarding) the drug-seeking behavior."
    Last edited by Sweet P; 26-01-2010 at 00:06. Reason: Grammar
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    #14
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    all seroquel really seems to do is make you tired...it's hard for me to tell, as I take it regularly, as well as sneaking doses and snorting it...and I have yet to try it mid-day...but I know I snuck my cousin 50 milligrams, and it knocked him out in about 20-30 mins...that stuff is powerful shit...
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    #15
    NSFW:
    Review
    The role of antihistaminic effects in the misuse of quetiapine: A case report and review of the literature

    Bernard A. Fischera, b, Corresponding Author Contact Information, E-mail The Corresponding Author and Douglas L. Boggsa

    aMaryland Psychiatric Research Center, University of Maryland School of Medicine, Baltimore, USA

    bVeterans Affairs Capital Network (VISN 5) Mental Illness Research, Education, and Clinical Center (MIRECC), Baltimore, USA
    Received 22 July 2009;
    revised 28 October 2009;
    accepted 2 November 2009.
    Available online 6 November 2009.

    Abstract

    Recent case reports and case series suggest that the atypical antipsychotic quetiapine has the potential for misuse. This includes drug-seeking behaviors motivated by quetiapine as well as inappropriate (intranasal or intravenous) administration. We present an additional case of quetiapine misuse and review other published cases. In general, quetiapine misuse is associated with prior CNS depressant use and is more common in forensic settings. The mechanism of reinforcement for this misuse is unknown, but we hypothesize that it is related to quetiapine's pharmacological profile as an antihistamine with a relative low affinity for dopamine receptors. The risks to individuals and society of exaggerating/simulating symptoms to obtain high-dose quetiapine in the absence of a clinical indication are discussed. This includes the unwelcome possibility of restricting access to this effective medication.

    Keywords: Quetiapine; Antipsychotic; Substance misuse; Substance abuse; Antihistamine
    Article Outline

    1. Introduction
    2. Case report
    3. Review of the literature
    4. Possible mechanism
    5. Risks of quetiapine misuse
    6. Conclusion
    References

    1. Introduction
    Prescription medications are misused if they are taken in a way other than as prescribed or if symptoms are invented or exaggerated in order to acquire a prescription. No medication is completely harmless and patients can be put at significant risk by misuse of medications. This article presents the case of a patient embellishing symptoms in an attempt to obtain increased doses of the atypical antipsychotic quetiapine. Following the case, we review the literature on quetiapine misuse and discuss possible mechanisms underlying the phenomenon. We conclude with a consideration of the risks of unrecognized quetiapine misuse to individuals and to society at large.

    2. Case report

    Mr. A was a married, employed, white 53-year-old male. He presented with several weeks of depressed mood following a third arrest for driving while intoxicated (DWI). At intake, he denied any discrete periods of elevated, expansive, or irritable mood, sleeplessness, grandiosity, pressured speech (observed by family or friends), racing thoughts or increased goal-directed behavior. Despite the 3 arrests, Mr. A denied regular alcohol use and his laboratory results (including liver function tests and complete blood count) were within normal limits. Mr. A did report a history of compulsive gambling, which had left him in significant debt. He had never been seen by a psychiatrist or counselor and had never been prescribed any psychotropics. He was started on duloxetine and his mood improved.

    Mr. A was extremely intelligent and began investigating a not-criminally responsible defense. As his hearing approached, he began reporting recollections of symptoms consistent with previous manic episodes. In contrast to his evaluation visits, he now reported his gambling had come in discrete periods coupled with euphoric mood. He also began reporting the events of the DWI differently making a point of saying he was “manic” when he was stopped that night. Because there was some clinical doubt as to Mr. A's true diagnosis, and duloxetine monotherapy put him at theoretical risk for mood instability, he was started on quetiapine.

    Mr. A was allowed to serve his DWI sentence part-time several days/week. He continued to attend the clinic. During his sessions he began pressing for higher and higher doses of quetiapine. Rather than experiencing relief after dose increases, he reported worsening irritability and insomnia. He was finally presented the option of switching to a different mood-stabilizing agent. He then acknowledged quetiapine made him feel “dreamy” and reported he was trying to get the dose high enough that he could “sleep through” his incarceration.
    3. Review of the literature

    A search of PubMed using the string “quetiapine AND (abuse OR dependence OR misuse OR addiction)” yielded eight published case reports/case series of quetiapine misuse in English ([Chen et al., 2009], [Hussain et al., 2005], [Morin, 2007], [Murphy et al., 2008], [Paparrigopoulos et al., 2008], [Pinta and Taylor, 2007], [Reeves and Brister, 2007] and [Waters and Joshi, 2007]) as well as a letter describing a general misuse phenomenon in Los Angeles County Jail (Pierre et al., 2004); see Table 1.
    Table 1.

    Summary of case reports of quetiapine misusea.
    Reference Sex Race Age Diagnosis (non-substance related) Prior addictive behavior Route of administration Comments
    Fischer and Boggs (present report) M W 53 Mood disorder not otherwise specified Yes (alcohol abuse, gambling) Oral Related to incarceration
    Hussain et al. (2005) F – 34 Borderline personality disorder, depressive episodes Yes (polysubstance dependence) Intranasal; IV Related to incarceration
    Morin (2007) F W 28 Schizoaffective disorder (bipolar type) Yes (polysubstance abuse) Intranasal Court-ordered hospitalization
    Waters and Joshi (2007) M W 33 – Yes (polysubstance dependence) IV with cocaine Combination reported as “hallucinogenic”
    Pinta and Taylor (2007) M – 39 Generalized anxiety disorder Yes (opiate abuse) Unreported (oral assumed) Related to incarceration
    Reeves and Brister (2007) M – 49 None Yes (alcohol dependence, benzodiazepine abuse) Unreported (oral assumed) Urine being monitored after multiple DUIs
    Reeves and Brister (2007) M – 23 None Yes (benzodiazepine dependence) Unreported (oral assumed) Stole quetiapine from girlfriend with schizophrenia
    Reeves and Brister (2007) M – 39 Bipolar disorder – Unreported (oral assumed) Outpatient misuse
    Paparrigopoulos et al. (200 M – 48 Generalized anxiety disorder; “depressive reaction” Yes (alcohol dependence, benzodiazepine dependence) Oral with benzodiazepines Reported to augment benzodiazepine feeling; preferred to alcohol
    Murphy et al. (200 M W 29 Probable malingering None known (negative urine toxicology) Oral Outpatient misuse
    Chen et al. (2009) F – 59 Bipolar disorder Yes (concurrent benzodiazepine dependence) Unreported (oral assumed) Outpatient misuse
    Pierre et al. (2004) – – – – Yes Oral; intranasal Report of widespread misuse in Los Angeles County Jail
    Full-size table
    a M: male, F: female; W: White, Caucasian; DO: disorder; IV: intravenous; DUI: driving while under the influence; “–” indicates information not reported or not applicable.

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    Reports of quetiapine misuse include taking the medication intravenously ([Hussain et al., 2005] and [Waters and Joshi, 2007]) or intranasally ([Hussain et al., 2005], [Morin, 2007] and [Pierre et al., 2004]), taking excessive amounts ([Chen et al., 2009], [Murphy et al., 2008], [Paparrigopoulos et al., 2008] and [Reeves and Brister, 2007]), malingering symptoms to obtain the drug ([Murphy et al., 2008] and [Reeves and Brister, 2007]), and acquiring/selling quetiapine “on the street”([Murphy et al., 2008], [Pierre et al., 2004], [Pinta and Taylor, 2007] and [Reeves and Brister, 2007]). When the effect of quetiapine is described, it is often similar to the effect described by Mr. A, i.e. “dreamy”, calming, or soporific ([Chen et al., 2009], [Hussain et al., 2005], [Morin, 2007], [Paparrigopoulos et al., 2008], [Pierre et al., 2004], [Pinta and Taylor, 2007] and [Reeves and Brister, 2007]). Only one report describes a “hallucinogenic” effect, but this was in response to an intravenous quetiapine and cocaine combination (Waters and Joshi, 2007). Street slang for quetiapine includes “Susie-Q”(Pinta and Taylor, 2007), “baby-heroin”(Waters and Joshi, 2007), and “quell” (Pierre et al., 2004). The intravenous combination of quetiapine and cocaine is referred to as “Q-Ball” in one report (although it is unclear if this is street slang or a label from the authors (Waters and Joshi, 2007)).

    In most cases, misuse of quetiapine was connected to a forensic setting such as incarceration (including the present report ([Hussain et al., 2005], [Pierre et al., 2004] and [Pinta and Taylor, 2007])), court-ordered hospitalization (Morin, 2007), or other oversight by the legal system (e.g. monitoring urines (Reeves and Brister, 2007)). In almost every report, the person misusing quetiapine is described as having a prior drug or alcohol problem. Prior drug misuse was mainly polysubstance abuse/dependence or problems with opiates, alcohol, or benzodiazepines ([Hussain et al., 2005], [Morin, 2007], [Paparrigopoulos et al., 2008], [Pinta and Taylor, 2007], [Reeves and Brister, 2007] and [Waters and Joshi, 2007]). Quetiapine does not seem to be substitute for more activating drugs such as cocaine or amphetamines.
    4. Possible mechanism

    The reinforcing properties of quetiapine have not been examined in human or non-human behavioral research, but its pharmacology suggests two plausible explanations for its misuse. Although it was initially believed quetiapine had minimal anticholinergic activity (Goldstein and Brecher, 2000 J.M. Goldstein and M. Brecher, Clarification of anticholinergic effects of quetiapine, J. Clin. Psychiatry61 (2000), p. 680. View Record in Scopus | Cited By in Scopus (1)Goldstein and Brecher, 2000), trials of high-dose quetiapine have demonstrated anticholinergic effects in humans ([Boggs et al., 2008] and [Pierre et al., 2005]) and there are multiple case reports of anticholinergic drug abuse/misuse in the literature ([Buhrich et al., 2000], [Hidalgo and Mowers, 1990], [Land et al., 1991] and [Pullen et al., 1984]). However, these reports have almost uniformly described anticholinergic intoxication as euphoric and stimulatory. This does not fit the clinical description of quetiapine's effects, which more closely resemble central nervous system depressants (Tcheremissine, 200. Quetiapine has a high antagonistic affinity for the histamine H1 receptor; especially in relationship to its antagonistic affinity for the D2 receptor (Kroeze et al., 2003). These antihistaminic effects offer a more likely explanation for the misuse/abuse potential of quetiapine.

    Several reports have shown antihistamines are misused in humans ([Bailey and Davies, 2008], [Halpert et al., 2002] and [Thomas et al., 2009]), but the exact mechanism behind their reinforcing properties has not been clearly explained. In rodent studies, peripheral administration of antihistamines increases dopamine release in the ventral striatum (Dringenberg et al., 199 and substances with an abuse potential, no matter what their mechanism of action, enhance excitatory neurons of midbrain dopaminergic neurons (Saal et al., 2003). Also, lesions of the rostroventral tuberomammillary nucleus, the histamine-producing area of the brain, increase rewarding self-stimulatory behavior in rats (Wagner et al., 1993). This suggests histamine has an inhibitory effect on the reward system. The reinforcing effects of antihistamines could be a result of disinhibition of a primed reward system. This may explain why misuse of quetiapine and other antihistamines have largely been reported in people with a previous history of substance abuse. Substance abuse increases long-term potentiation of the reward system (Saal et al., 2003) and a hyperactive reward system may be necessary for antihistaminic medications to have a reinforcing effect.

    People with a history of sedative abuse have ranked antihistamines significantly higher on “liking” versus placebo (Preston et al., 1992) and not significantly different from the benzodiazepine lorazepam (Mumford et al., 1996). Whether the reinforcing properties for antihistamines would be similar among people with a history of stimulant abuse is not known, but the majority of antihistamine and quetiapine misuse cases are among people who report previous use of CNS depressants.

    Behavioral studies in non-human primates have found antihistamines can maintain responses in cocaine-conditioned animals ([Bergman and Spealman, 1986] and [Sannerud et al., 1995]) and lead to motor excitation (Evans and Johanson, 1989). In contrast, the effect of antihistamines in humans is calming or sedating. The difference of effect between non-human primates and humans may indicate divergent reinforcing mechanisms and perhaps a limited relevance of animal models.

    Other antipsychotics (e.g. clozapine, olanzapine, and chlorpromazine) also have antihistaminic effects, but have not been linked to have high abuse potential. Why would quetiapine have a higher abuse potential than other antihistaminic antipsychotics? One answer is the superior safety profile of quetiapine for side effects, especially movement disorders (Farah, 2005). The rarity of dystonia and extrapyramidal side effects may make quetiapine a more attractive option for misuse compared to other antipsychotics. Quetiapine has a low affinity for and quickly dissociates from dopamine receptors ([Kapur and Seeman, 2000] and [Tauscher et al., 2004]). Dopamine is another important molecule in reward circuitry. High dopamine D2 receptor antagonism in humans is correlated with antipsychotic-induced dysphoria (Mizrahi et al., 2007) and rodent data shows dopamine D1 antagonism abolishes the antihistaminic potentiation of other substances of abuse ([Suzuki et al., 1990] and [Suzuki et al., 1991]). Quetiapine, due to its low affinity and fast disassociation from both D1 and D2 receptors ([Kapur and Seeman, 2000] and [Tauscher et al., 2004]), may have less potential to disrupt any reinforcing antihistaminic effects.
    5. Risks of quetiapine misuse

    Side effects of atypical antipsychotics such as quetiapine are not benign and can include metabolic disturbances such as weight gain and glucose intolerance (ADA, 2004). Although quetiapine-induced movement disorders are extremely rare, there has been at least one reported case of resulting tardive dyskinesia (Rizos et al., 2007). Individuals without a primary psychotic disorder may be at increased risk for antipsychotic-induced movement disorders including tardive dyskinesia (Kane, 1999). Exposure to antipsychotics, as with any medication, should be limited to those individuals with a clinical indication.

    In addition to personal risks, quetiapine misuse has harmful implications for society. Atypical antipsychotics are expensive drugs. Providing quetiapine to malingering individuals in forensic settings effects mental health budgets in these institutions, which ultimately rely on public resources. Murphy et al. (200 also point out that injudicious prescription of quetiapine may cause tighter federal regulations over the drug including possible schedule as a controlled substance. This, in turn, would present obstacles in getting the medication to people who truly need it.
    6. Conclusion

    Quetiapine occupies a distinct place in the pharmacopoeia and needs to be available to treat the individualized needs of people with psychiatric disorders. However, some individuals will embellish or simulate symptoms in order to get the medication inappropriately. The misuse potential of quetiapine is likely related to its histaminic blockade coupled with its comparatively mild action at dopamine receptors. Accordingly, quetiapine substitutes for sedating agents and individuals with a history of alcohol, benzodiazepine, or opiate abuse are particularly at risk. Misuse is increased in forensic settings, although the phenomenon is not restricted to this situation. Given individual and societal dangers, the potential for quetiapine misuse should be recognized and should factor into clinical decision-making.
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    Wagner et al., 1993 U. Wagner, P. Segura-Torres, T. Weiler and J.P. Huston, The tuberomammillary nucleus region as a reinforcement inhibiting substrate: facilitation of ipsihypothalamic self-stimulation by unilateral ibotenic acid lesions, Brain Res. 613 (1993), pp. 269–274. Abstract | PDF (550 K) | View Record in Scopus | Cited By in Scopus (37)

    Waters and Joshi, 2007 B.M. Waters and K.G. Joshi, Intravenous quetiapine-cocaine use (“Q-ball”), Am. J. Psychiatry 164 (2007), pp. 173–174. Full Text via CrossRef | View Record in Scopus | Cited By in Scopus (10)


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    #16
    "Quetiapine, due to its low affinity and fast disassociation from both D1 and D2 receptors ([Kapur and Seeman, 2000] and [Tauscher et al., 2004]), may have less potential to disrupt any reinforcing antihistaminic effects."

    Interesting. So maybe there is some abuse potential for people that like antihistamines. I hate them personally.

    Low affinity and fast disassociation just might allow one to feel some of the dopamine flood that happen with cocaine. Still sounds like a shitty drug though.


    oh this makes some sense:

    "Also, lesions of the rostroventral tuberomammillary nucleus, the histamine-producing area of the brain, increase rewarding self-stimulatory behavior in rats (Wagner et al., 1993). This suggests histamine has an inhibitory effect on the reward system. The reinforcing effects of antihistamines could be a result of disinhibition of a primed reward system."

    now that is quite interesting.
    Last edited by onmyway; 26-01-2010 at 03:11.
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