Acute confusional state after designer tryptamine abuse

Itokawa, Masanari; Iwata, Ken; Takahashi, Misako; Sugihara, Gen‐Ichi; Sasaki, Takeshi; Abe, Yuichiro; Uno, Minari; Hobo, Mizue; Jitoku, Daisuke; Inoue, Kikue; Arai, Makoto; Yasuda, Ichiro; Shintani, Masahiro

doi:10.1111/j.1440-1819.2007.01638.x

Cited by 57 publications

(6 citation statements)

References 5 publications

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“…Similar to other psychedelics, tryptamine psychedelics alter perception and can induce psychological disturbances in users, including acute psychosis (Meatherall and Sharma 2003;Nichols 2004Nichols , 2016Shulgin and Shulgin 1997;Taljemark and Johansson 2012). Adverse effects of tryptamine designer drugs include restlessness, disorientation, clouding of consciousness, confusion, hallucinations, amnesia, catalepsy, mydriasis, tachypnea, hypertension, and tachycardia (Alatrash et al 2006;Itokawa et al 2007;Jovel et al 2014;Muller 2004;Smolinske et al 2005). 5-Methoxy-N,N-diisopropyltryptamine (5-MeO-DiPT) use has been associated with hallucinogen-persisting perception disorder and was proposed to play a role in the development of prolonged delusions (Fuse-Nagase and Nishikawa 2013; Ikeda et al 2005).…”

Section: Adverse Effects Of Tryptaminesmentioning

confidence: 99%

Designer drugs: mechanism of action and adverse effects

2020

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Psychoactive substances with chemical structures or pharmacological profiles that are similar to traditional drugs of abuse continue to emerge on the recreational drug market. Internet vendors may at least temporarily sell these so-called designer drugs without adhering to legal statutes or facing legal consequences. Overall, the mechanism of action and adverse effects of designer drugs are similar to traditional drugs of abuse. Stimulants, such as amphetamines and cathinones, primarily interact with monoamine transporters and mostly induce sympathomimetic adverse effects. Agonism at l-opioid receptors and c-aminobutyric acid-A (GABA A) or GABA B receptors mediates the pharmacological effects of sedatives, which may induce cardiorespiratory depression. Dissociative designer drugs primarily act as N-methyl-D-aspartate receptor antagonists and pose similar health risks as the medically approved dissociative anesthetic ketamine. The cannabinoid type 1 (CB 1) receptor is thought to drive the psychoactive effects of synthetic cannabinoids, which are associated with a less desirable effect profile and more severe adverse effects compared with cannabis. Serotonergic 5-hydroxytryptamine-2A (5-HT 2A) receptors mediate alterations of perception and cognition that are induced by serotonergic psychedelics. Because of their novelty, designer drugs may remain undetected by routine drug screening, thus hampering evaluations of adverse effects. Intoxication reports suggest that several designer drugs are used concurrently, posing a high risk for severe adverse effects and even death.

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Section: Adverse Effects Of Tryptaminesmentioning

confidence: 99%

Designer drugs: mechanism of action and adverse effects

2020

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“…Infections (eg, cerebral malaria 125 ) and autoimmune disorders such as N-methyl-D-aspartate (NMDA)-receptor encephalitis, 126 systemic lupus erythematosus, 127 and others 128,129 may also present with echolalia. Drug-induced echolalia was noted with isoniazid, 130 topiramate, 131 ofloxacin, 132 the NMDAreceptor antagonist methoxphenidine, 133 cocaine, 134 designer tryptamine, 135 and phencyclidine ("angel dust," "crystal"). 136 Other underlying causes of echolalia are encephalitis lethargica, 94 catatonia, 137 functional neurological disorders (Video 1M 101 ), and endemic startle syndromes such as the Jumping Frenchmen of Maine, 138 Latah, 97 and the Ragin' Cajuns of Louisiana.…”

Section: Palilaliamentioning

confidence: 99%

The spectrum of involuntary vocalizations in humans: A video atlas

et al. 2019

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In clinical practice, involuntary vocalizing behaviors are typically associated with Tourette syndrome and other tic disorders. However, they may also be encountered throughout the entire tenor of neuropsychiatry, movement disorders, and neurodevelopmental syndromes. Importantly, involuntary vocalizing behaviors may often constitute a predominant clinical sign, and, therefore, their early recognition and appropriate classification are necessary to guide diagnosis and treatment. Clinical literature and video‐documented cases on the topic are surprisingly scarce. Here, we pooled data from 5 expert centers of movement disorders, with instructive video material to cover the entire range of involuntary vocalizations in humans. Medical literature was also reviewed to document the range of possible etiologies associated with the different types of vocalizing behaviors and to explore treatment options. We propose a phenomenological classification of involuntary vocalizations within different categorical domains, including (1) tics and tic‐like vocalizations, (2) vocalizations as part of stereotypies, (3) vocalizations as part of dystonia or chorea, (4) continuous vocalizing behaviors such as groaning or grunting, (5) pathological laughter and crying, (6) vocalizations resembling physiological reflexes, and (7) other vocalizations, for example, those associated with exaggerated startle responses, as part of epilepsy and sleep‐related phenomena. We provide comprehensive lists of their associated etiologies, including neurodevelopmental, neurodegenerative, neuroimmunological, and structural causes and clinical clues. We then expand on the pathophysiology of the different vocalizing behaviors and comment on available treatment options. Finally, we present an algorithmic approach that covers the wide range of involuntary vocalizations in humans, with the ultimate goal of improving diagnostic accuracy and guiding appropriate treatment. © 2019 The Authors. Movement Disorders published by Wiley Periodicals, Inc. on behalf of International Parkinson and Movement Disorder Society.

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“…Indeed the hallucinogenic alkaloids 1 and 3 have not yet been reported to be present in plants used in ayahuasca preparations (McKenna, 2004;Callaway, 2005;Callaway et al, 2005). The presence of compound 2 is also interesting because this has been found in bodily fluids in cases of tryptamine intoxication (Itokawa et al, 2007). The isolation of the β-carboline derivative 4 is noteworthy because it is known that this class of compound enhances the hallucinogenic effects of tryptamine alkaloids by inhibiting monoamine oxidase (Shen et al, 2010a).…”

Section: Introductionmentioning

confidence: 99%