How does a family history of psychosis influence the risk of methamphetamine-related psychotic symptoms: Evidence from longitudinal panel data.

AIMS: To determine whether the risk of psychotic symptoms during weeks of methamphetamine use was dependent on, increased by, or independent of having a family history of psychosis. DESIGN: Secondary analysis of 13 contiguous 1-week periods of data (1370 weeks). A risk modification framework was used to test each scenario. SETTING: Geelong, Wollongong and Melbourne, Australia. PARTICIPANTS: Participants in a randomized controlled trial of treatment for methamphetamine dependence (n = 148) who did not have a primary psychotic disorder on enrolment. MEASUREMENTS: Psychotic symptoms in the previous week were defined as a score of 3+ on any of the Brief Psychiatric Rating Scale items of hallucinations, unusual thought content or suspiciousness. Any (vs no) methamphetamine use in the previous week was assessed using the Timeline Followback method. Self-reported family history of psychosis was assessed using the Diagnostic Interview for Psychosis. FINDINGS: The risk of psychotic symptoms in the past week was independently associated with methamphetamine use in that week (relative risk [RR] = 2.3, 95% CI = 1.3-4.3) and with having a family history of psychosis (RR = 2.4, 95% CI = 0.9-7.0); the joint risk among participants with a family history of psychosis during weeks when they were using methamphetamine was large (RR = 4.0, 95% CI = 2.0-7.9). There was no significant interaction between a family history of psychosis and methamphetamine use in predicting psychotic symptoms (interaction RR = 0.7 95% CI = 0.3-1.8), but there was a small non-significant excess risk due to the interaction (0.20 95% CI = -1.63 to 2.03). CONCLUSIONS: Among people dependent on methamphetamine, the relative risk of psychotic symptoms during weeks of methamphetamine use does not appear to be dependent on, or increased by, having a family history of psychosis. However, a family history of psychosis does appear to be an independent risk factor that contributes to the absolute risk of psychotic symptoms in this population.

Characteristics of Amphetamine Psychosis with Respect to the Length of Drug Exposure.

BACKGROUND: Over the past decade, the number of individuals requiring medical care for amphetamine-related psychosis has increased. OBJECTIVE: This study aims to examine the psychological characteristics of amphetamine psychosis in drug-addicted patients depending on the length of drug exposure and compared to patients diagnosed with paranoid schizophrenia. METHODS: The study was carried out in psychiatric clinic No. 1 in Kyiv (Ukraine) in 2019, involving 107 patients. Of all the participants, 50 were included in Group 1 (methamphetamine psychosis) and 57 - in Group 2 (paranoid schizophrenia). All patients were treated with medication to relieve exacerbating symptoms. They underwent extensive testing to determine the impairment severity of cognitive function, attention, and task performance during remission. RESULTS: In Group 1, the timing of onset for paranoid symptoms depends on the length of amphetamine exposure (Spearman correlation coefficient = 0.89). The efficacy and dynamics of drug treatment in Group 2 were similar to patients in Group 1. However, the effect of reduction in Group 2 was achieved only in 4 months. Delusions, emotional disturbances, hallucinations in patients of Group 1 occurred 2.3 times more frequently than in Group 2 (p ≤ 0.05). The patients of Group 1 are characterized by the presence of disorders related to the affective and behavioral components. CONCLUSION: All reported exacerbations are related to amphetamine use. Patients in Group 1 learned a smaller number of words compared to those in Group 2. Besides, a large number of errors and difficulties with shifting focus were recorded.

Betaine prevents and reverses the behavioral deficits and synaptic dysfunction induced by repeated ketamine exposure in mice.

As an N-methyl-D-aspartate (NMDA) receptor inhibitor, ketamine has become a popular recreational substance and currently is used to address treatment-resistant depression. Since heavy ketamine use is associated with persisting psychosis, cognitive impairments, and neuronal damage, the safety of ketamine treatment for depression should be concerned. The nutrient supplement betaine has been shown to counteract the acute ketamine-induced psychotomimetic effects and cognitive dysfunction through modulating NMDA receptors. This study aimed to determine whether the adjunctive or subsequent betaine treatment would improve the enduring behavioral disturbances and hippocampal synaptic abnormality induced by repeated ketamine exposure. Mice received ketamine twice daily for 14 days, either combined with betaine co-treatment or subsequent betaine post-treatment for 7 days. Thereafter, three-chamber social approach test, reciprocal social interaction, novel location/object recognition test, forced swimming test, and head-twitch response induced by serotonergic hallucinogen were monitored. Data showed that the enduring behavioral abnormalities after repeated ketamine exposure, including disrupted social behaviors, recognition memory impairments, and increased depression-like and hallucinogen-induced head-twitch responses, were remarkably improved by betaine co-treatment or post-treatment. Consistently, betaine protected and reversed the reduced hippocampal synaptic activity, such as decreases in field excitatory post-synaptic potentiation (fEPSP), long-term potentiation (LTP), and PSD-95 levels, after repeated ketamine treatment. These results demonstrated that both co-treatment and post-treatment with betaine could effectively prevent and reverse the adverse behavioral manifestations and hippocampal synaptic plasticity after repeated ketamine use, suggesting that betaine can be used as a novel adjunct therapy with ketamine for treatment-resistant depression and provide benefits for ketamine use disorders.

Cannabis withdrawal induced brief psychotic disorder: a case study during the national lockdown secondary to the COVID-19 pandemic.

BACKGROUND: Cannabis Withdrawal Syndrome (CWS) is a key feature of Cannabis Use Disorder (CUD). The CWS causes significant distress and disability. While the relationship between CUD and psychosis has been extensively studied, the potential connection between CWS and psychosis has not received as much attention. CASE PRESENTATION: The CARE guideline's methodology is followed in the presentation of this case report. During the national lockdown decreed by the Spanish government for the containment of the CoronaVirus Disease 19 (COVID-19) pandemic, a 29-year-old man suffers a CWS and a subsequent psychotic episode. He is admitted to a psychiatric unit, obtaining a rapid and complete response to treatment. DISCUSSION: Clinical and pathophysiological data that support the hypothesis of CWS-induced psychosis are discussed. Due to the increasing use of cannabis worldwide, we believe that more research is needed on the mental disturbances associated with CUD, including CWS and psychosis. On the other hand, the confinement and social distancing measures adopted in the face of the current COVID-19 pandemic could have restricted the availability and consumption of certain drugs, precipitating the emergence of withdrawal syndromes such as CWS.

Antipsychotic potential of the type 1 cannabinoid receptor positive allosteric modulator GAT211: preclinical in vitro and in vivo studies.

RATIONALE: Antipsychotics help alleviate the positive symptoms associated with schizophrenia; however, their debilitating side effects have spurred the search for better treatment options. Novel compounds can be screened for antipsychotic potential in neuronal cell cultures and following acute N-methyl-D-aspartate (NMDA) receptor blockade with non-competitive antagonists such as MK-801 in rodent behavioral models. Given the known interactions between NMDA receptors and type 1 cannabinoid receptors (CB1R), compounds that modulate CB1Rs may have therapeutic potential for schizophrenia. OBJECTIVES: This study assessed whether the CB1R positive allosteric modulator GAT211, when compared to ∆9-tetrahydrocannabinol (THC), has potential to reduce psychiatric behavioral phenotypes following acute MK-801 treatment in rats, and block hyperdopaminergic signalling associated with those behaviors. METHODS: The effects of GAT211 and THC on cellular signaling were compared in Neuro2a cells, and behavioral effects of GAT211 and THC on altered locomotor activity and prepulse inhibition of the acoustic startle response caused by acute MK-801 treatment were assessed in male, Long Evans rats. RESULTS: GAT211 limited dopamine D2 receptor-mediated extracellular regulated kinase (ERK) phosphorylation in Neuro2a cells, whereas THC did not. As expected, acute MK-801 (0.15 mg/kg) produced a significant increase in locomotor activity and impaired PPI. GAT211 treatment alone (0.3-3.0 mg/kg) dose-dependently reduced locomotor activity and the acoustic startle response. GAT211 (3.0 mg/kg) also prevented hyperlocomotion caused by MK-801 but did not significantly affect PPI impairments. CONCLUSION: Taken together, these findings support continued preclinical research regarding the usefulness of CB1R positive allosteric modulators as antipsychotics.

Glutamate transporter-1 link astrocytes with heightened aggressive behavior induced by steroid abuse in male CF1 mice.

The astrocytic glutamate transporter GLT-1 performs glutamate uptake thereby mediating NMDAr responses in neurons. Ceftriaxone (CEF) upregulates astrocytic GLT-1 expression/activity, which could counteract excessive glutamate levels and aggressive behavior induced by anabolic synthetic steroids such as nandrolone decanoate (ND). Here, adult male CF-1 mice were allocated to oil (VEH), ND, CEF, and ND/CEF groups. Mice were subcutaneously (s.c.) injected with ND (15 mg/kg) or VEH for 19 days, and received intraperitoneal (i.p.) injections of CEF (200 mg/kg) or saline for 5 days. The ND/CEF group received ND for 19 days plus coadministration of CEF in the last 5 days. On the 19th day, the aggressive phenotypes were evaluated through the resident-intruder test. After 24 h, cerebrospinal fluid was collected to measure glutamate levels, and the pre-frontal cortex was used to assess GLT-1, pGluN2BTyr1472, and pGluN2ATyr1246 by Western blot. Synaptosomes from the left brain hemisphere was used to evaluate mitochondrial function including complex II-succinate dehydrogenase (SDH), Ca2+ handling, membrane potential (ΔÑ°m), and H2O2 production. ND decreased the latency for the first attack and increased the number of attacks by the resident mice against the intruder, mechanistically associated with an increase in glutamate levels and pGluN2BTyr1472 but not pGluN2ATyr1244, and GLT-1 downregulation. The abnormalities in mitochondrial Ca2+ influx, SDH, ΔÑ°m, and H2O2 implies in deficient energy support to the synaptic machinery. The ND/CEF group displayed a decreased aggressive behavior, normalization of glutamate and pGluN2BTyr1472levels, and mitochondrial function at synaptic terminals. In conclusion, the pharmacological modulation of GLT-1 highlights its relevance as an astrocytic target against highly impulsive and aggressive phenotypes.

Differential effects of cannabis exposure during early versus later adolescence on the expression of psychosis in homeless and precariously housed adults.

Longitudinal studies of cannabis exposure during early adolescence in the general population frequently report an increased risk of subsequently developing psychotic symptoms or a psychotic illness. However, there is a dearth of knowledge about the effects of early cannabis exposure on psychosis in homeless and precariously housed adults, who represent a population afflicted with high rates of psychosis. The aim of the present study was to examine how early cannabis exposure (by age 15) compared to later first use (after age 15) affected the expression of adult psychosis in this population. Secondary measures of psychopathology, drug use, cognition and brain structure were also collected. 437 subjects were recruited from single room occupancy hotels in the urban setting of the Downtown Eastside of Vancouver, Canada. Psychiatric diagnoses were determined, and psychotic symptom severity was measured with the 5-factor PANSS. Participants completed a battery of neurocognitive tests, and brain structure was assessed using structural and diffusion tensor imaging MRI scans. Results indicated that early cannabis exposure was associated with an increased risk (OR = 1.09, p < .05) of developing substance induced psychosis, whereas later first use increased risk (OR = 2.19, p < .01) of developing schizophrenia or schizoaffective disorder. There was no group difference in neurocognitive function, although differences were observed in the lateral orbitofrontal cortex and white matter tract diffusivity. These findings indicate that early cannabis exposure in this population may increase the risk of developing drug associated psychoses, which could potentially be mediated in part through altered neurodevelopmental brain changes.

Psicosis inducida por cannabis: características clínicas y su diferenciación con la esquizofrenia con y sin consumo de cannabis asociado / Cannabis-induced psychosis: clinical characteristics and its differentiation from schizophrenia with and without cannabis use

El consumo de cannabis se considera un factor de riesgo establecido para el desarrollo de psicosis. Diferenciar los trastornos inducidos por cannabis de la esquizofrenia resulta útil desde el punto de vista pronóstico y terapéutico. Se diferenciaron tres grupos de pacientes hospitalizados: psicosis inducida por cannabis (PIC) (n = 69; Media de edad = 27,4, DE = 6,5; 82,6 % varones), esquizofrenia con abuso o dependencia de cannabis (EZ + CB) (n = 57; Media de edad = 31,9, DE = 10,1; 94,7% varones) y esquizofrenia sin abuso o dependencia de cannabis (EZ) (n = 181; Media de edad = 41,8, DE = 13,3; 54,1% varones). Se utilizó la escala Psychiatric Research Interview for Substance and Mental Disorders (PRISM-IV) para la diferenciación de cuadros inducidos. El grupo PIC presentó puntaciones inferiores en la subescala PANSS negativa (M = 12,9, DE = 5,9; F = 32,24; p < 0,001), menos alucinaciones auditivas (60,3%; ÷² = 6,60; p = 0,037) y mayor presencia de manía (26,1% vs. 12,3%; ÷² = 32,58; p < 0,001) en comparación con el grupo EZ + CB. Hubo pocas diferencias clínicas entre los pacientes con esquizofrenia, independientemente del consumo de cannabis. La edad del primer ingreso por psicosis fue menor en ambos grupos de psicóticos consumidores (M = 26,1, DE = 6,4 en PIC y M = 25,3, DE = 6,2 en EZ + CB; ÷² = 20,02; p < 0,001). No se observó un patrón clínico característico de las psicosis inducidas por cannabis, aunque sí se demostró el papel precipitante del cannabis en la aparición de psicosis, dada la menor edad de ingreso en los consumidores

Cannabis use is considered an established risk factor for psychosis development. Differentiating between cannabis-induced disorders and schizophrenia is useful for prognostic and therapeutic purposes. Three inpatients groups were differentiated: cannabis-induced psychosis (CIP) (n = 69; mean age = 27.4, SD = 6.5; 82.6% males), schizophrenia with cannabis abuse or dependence (SZ + CB) (n = 57; mean age = 31.9, SD = 10.1; 94.7% males) and schizophrenia without cannabis abuse or dependence (SZ) (n = 181; mean age = 41.8, SD = 13.3; 54.1% males). The Psychiatric Research Interview for Substance and Mental Disorders (PRISM-IV) scale was used to differentiate induced psychosis. The CIP group presented lower mean scores on the negative PANSS subscale (M = 12.9, SD = 5.9; F = 32.24, p < 0.001), fewer auditory hallucinations (60.3%; χ² = 6.60, p = 0.037) and greater presence of mania (26.1% vs. 12.3%; χ² = 32.58, p < 0.001) than the SZ + CB group. There were few clinical differences between patients with schizophrenia, regardless of previous cannabis use. The age of first admission due to psychosis was lower in both psychotic inpatients groups with cannabis use (M = 26.1, SD = 6.4 in CIP and M = 25.3, SD = 6.2 in SZ + CB; χ² = 20.02, p < 0,001). A clinical pattern characteristic of cannabis-induced psychosis was not observed, but the precipitating role of cannabis in the appearance of psychotic symptoms was demonstrated, given the lower age of first admission due to psychosis in cannabis user groups

Thought Suppression in Primary Psychotic Disorders and Substance/Medication Induced Psychotic Disorder.

INTRODUCTION: First episode-psychosis (FEP) represents a stressful/traumatic event for patients. To our knowledge, no study to date has investigated thought suppression involved in FEP in a Romanian population. Our objective was to investigate thought suppression occurring during FEP within primary psychotic disorders (PPD) and substance/medication induced psychotic disorders (SMIPD). Further, we examined the relationship between thought suppression and negative automatic thoughts within PPD and SMIPD. METHODS: The study included 30 participants (17 females) with PPD and 25 participants (10 females) with SMIPD. Psychological scales were administered to assess psychotic symptoms and negative automatic thoughts, along a psychiatric clinical interview and a biochemical drug test. RESULTS: Participants in the PPD group reported higher thought suppression compared to SMIPD group. For the PPD group, results showed a positive correlation between thought suppression and automatic thoughts. For the SMIPD group, results also showed a positive correlation between thought suppression and automatic thoughts. CONCLUSIONS: Patients with PPD rely more on thought suppression, as opposed to SMIPD patients. Thought suppression may be viewed as an unhealthy reaction to FEP, which is associated with the experience of negative automatic thoughts and might be especially problematic in patients with PPD. Cognitive behavioral therapy is recommended to decrease thought suppression and improve patients' functioning.

[Risk of psychosis with treatment for ADHD]. / Kans op psychose bij behandeling van ADHD.

The study by Moran et al. on the risk of psychosis among adolescents in the US who are treated with a stimulant for ADHD is important. This is because ADHD is a common disorder (3-5%), because psychosis often emerges in adolescence, because ADHD and psychosis share increased comorbidity and because ADHD is treated with stimulant medication that may increase the risk of psychosis. This means there is a multifactorial relationship between ADHD and psychosis.The outcome of the study is that stimulants increase the risk of psychosis to a limited extent, i.e. 0.10% for methylphenidate and 0.21% for dexamphetamine. It is recommended to opt for methylphenidate in adolescents with ADHD. This is confirmed by a Swedish registry study that controlled for a history of psychosis and showed that methylphenidate did not increase the incidence of psychosis after one year, regardless of a history of psychosis.

Monoamine oxidase A inhibition with moclobemide enhances the anti-parkinsonian effect of L-DOPA in the MPTP-lesioned marmoset.

Whereas monoamine oxidase (MAO) type B inhibitors are used as adjunct to L-3,4-dihydroxyphenylalanine (L-DOPA) in the treatment of Parkinson's disease (PD), the enzyme MAO type A (MAO-A) also participates in the metabolism of dopamine in the human and primate striatum. Here, we sought to assess the effect of the selective reversible MAO-A inhibitor moclobemide on L-DOPA anti-parkinsonian in the gold standard animal model of PD, the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned primate. We also assessed the effect of moclobemide on L-DOPA-induced dyskinesia and psychosis-like behaviours (PLBs). Experiments were performed in six MPTP-lesioned marmosets chronically treated with L-DOPA and exhibiting stable dyskinesia and PLBs upon each administration. In a randomised within-subject design, animals were administered a therapeutic dose of L-DOPA in combination with moclobemide (0.1, 1 and 10 mg/kg) or its vehicle, after which the severity of parkinsonism, dyskinesia, and PLBs was rated by an experienced blinded rater. Moclobemide significantly reduced the global parkinsonian disability (- 36% with 0.1 mg/kg, P < 0.05; - 38% with 1 mg/kg, P < 0.01; - 47% with 10 mg/kg, P < 0.01), when compared with its vehicle. This reduction of parkinsonism was not accompanied by an exacerbation of dyskinesia or PLBs. Reversible MAO-A inhibition with moclobemide appears as an effective way to increase the anti-parkinsonian action of L-DOPA, without negatively affecting dyskinesia or dopaminergic psychosis.

Selective metabotropic glutamate receptor 2 positive allosteric modulation alleviates L-DOPA-induced psychosis-like behaviours and dyskinesia in the MPTP-lesioned marmoset.

Psychosis and dyskinesia significantly diminish the quality of life of patients with advanced Parkinson's disease (PD). Available treatment options are unfortunately few and their use is limited by adverse effects. We have recently shown that activation of metabotropic glutamate 2 and 3 (mGlu2/3) receptors produced significant relief of L-3,4-dihydroxyphenylalanine (L-DOPA)-induced psychosis-like behaviours (PLBs) and dyskinesia in experimental models of PD. Here, using the highly-selective mGlu2 positive allosteric modulator (PAM) LY-487,379, we seek to determine the contribution of selective mGlu2 activation on both L-DOPA-induced PLBs and dyskinesia, in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-lesioned primate. We first determined the pharmacokinetic (PK) profile of LY-487,379 in the common marmoset, following which we administered it (0.1, 1 and 10 mg/kg) or its vehicle to 6 MPTP-lesioned marmosets previously exposed to L-DOPA to elicit stable PLBs and dyskinesia. We found that LY-487,379 provided a ≈45% reduction of the global PLBs observed and reduced global dyskinesia score by ≈ 55%. Moreover, LY-487,379 enhanced the anti-parkinsonian effect of L-DOPA, by reducing global parkinsonian score by ≈ 15%. Our data suggest that selective mGlu2 positive allosteric modulation with LY-487,379 may represent a potential therapeutic approach to alleviate both L-DOPA-induced PLBs and dyskinesia in PD.

Respiratory and hemodynamic effects of three different sedative regimens for drug induced sleep endoscopy in sleep apnea patients. A prospective randomized study.

BACKGROUND: Drug induced sleep endoscopy (DISE) has emerged as a promising tool for customizing the adequate surgical approach to relieve airway obstruction in sleep apnea patients. We aimed to compare propofol, dexmedetomidine or ketofol with regards their efficacy and safety for sedation in patients with obstructive sleep apnea (OSA) undergoing DISE procedure. METHODS: Sixty adult OSA patients scheduled for DISE procedure were randomly allocated into three equal groups to receive either propofol (group P), dexmedetomidine (group D), or ketofol (group K). Incidence of oxygen desaturation <90%, hemodynamic variables, time to achieve sufficient sedation level, recovery time, patients' and endoscopists' satisfaction, and incidence of adverse effects were recorded. RESULTS: Higher incidence of oxygen desaturation <90% was observed in group P as compared to groups D and K (70%, 35%, and 30% respectively, P=0.021*). Group D showed a significantly longer time to reach target sedation level, prolonged recovery time with more consumption of rescue propofol as compared to group P and group K (P=0.000*, 0.000*, 0.000* respectively). Heart rate values were lower in group D after the loading dose till 30 min postoperative as compared to the other two groups, while blood pressure was lower in both P and D groups at five, 10, 15 min, and on reaching recovery room compared to K group. Two patients in the K group had psychomimetic symptoms with no difference between groups as regards other adverse events or patients' and endoscopist's satisfactions. CONCLUSIONS: Dexmedetomidine and ketofol provided a safe respiratory profile compared to propofol during DISE without significant hemodynamic adverse events.

Structural, functional, and neurochemical neuroimaging of methamphetamine-associated psychosis: A systematic review.

Methamphetamine is a highly addictive psychostimulant. A subset of methamphetamine users develops methamphetamine-associated psychosis (MAP), which causes poorer prognoses and cognitive function than those with no psychosis (MNP). Comprehensive and integrative summaries of studies utilizing various neuroimaging modalities (structural, functional, and neurochemical) are limited. We conducted a systematic review of literature regarding clinical neuroimaging research published between January 1988 and July 2018 using the PubMed, Web of Science, Scopus, and ScienceDirect databases. Studies comparing the neuroimaging of patients with MAP with healthy controls or patients with MNP or schizophrenia were included to understand the distinct profiles associated with MAP. A total of six structural, three functional, and three neurochemical studies were reviewed. A general trend was identified that showed MAP-related brain alterations were mainly in the frontal lobe (especially the orbitofrontal cortex), striatum, and limbic systems (amygdala and hippocampus). Furthermore, some clinical manifestations, such as the severity of psychotic symptoms and cognitive performance, were correlated with neuroimaging abnormalities. In summary, distinct structural, functional, and neurochemical changes, especially in the frontostriatal circuit and network dynamic systems, play critical roles in the pathophysiology of MAP. Future studies using longitudinal study designs and including individuals with MNP and schizophrenia as controls are warranted.

Trend level gene-gender interaction effect for the BDNF rs6265 variant on age of onset of psychosis.

A BDNF rs6265 [A/A] by gender by cannabis use interaction has been associated with age of onset of psychosis (AoP). We examined the gender and cannabis use-adjusted association between BDNF rs6265 [G>A] and AKT1 rs2494732 [T>C] and AoP. Data from 167 Caucasians on AoP and age at first regular cannabis use were collected. Kaplan-Meier and Cox regression analyses were conducted. A trend level gene-gender interaction effect was observed for the BDNF rs6265 A/A genotype, controlling for age at first regular cannabis use. Larger collaborative research projects are required to further investigate this effect.

Methamphetamine use in an early psychosis service: a cross-sectional retrospective cohort study.

OBJECTIVE: Methamphetamine-associated psychotic symptoms are common among regular users, and can overlap with the emergence of a primary psychotic disorder. In contrast to previous research, this retrospective observational study aims to describe the characteristics of young people experiencing early psychosis who use methamphetamine regularly. We also aimed to investigate associations between regular methamphetamine use and markers of psychosocial functioning, psychosis outcomes and substance use. METHOD: This study involved 116 young people (19 using methamphetamine regularly) referred to the Camperdown Early Intervention in Psychosis Service from January 2015 to January 2016. Variables including demographic information, psychosocial functioning and psychosis outcomes were collected on referral to the service, updated throughout treatment and at discharge. RESULTS: There were significant associations found between regular methamphetamine use and a criminal history (p<0.001), regular cannabis use (p=0.002) and regular nicotine use (p<0.001). CONCLUSION: This study suggests that in early psychosis, regular methamphetamine use could signify a subgroup of young people who use multiple substances and may engage in criminal activity. Addressing substance use in early psychosis may be an important treatment target for this vulnerable group of young people.

The Relevance of Sex in the Association of Synthetic Cannabinoid Use With Psychosis and Agitation in an Inpatient Population.

BACKGROUND: Current evidence suggests that women are more sensitive to the effects of cannabinoids. The aim of this study was to investigate the relevance of sex in the association of synthetic cannabinoid (SC) use with psychosis and agitation. METHODS: A retrospective chart review was conducted for patients admitted to a psychiatric unit (2014-2016) to extract information on demographic factors, use of substances, clinical symptoms, and pharmacologic treatments. Study groups were defined as SC users (anyone who reported use of SCs over the past 3 months), cannabis users (positive toxicology screen for Δ9-tetrahydrocannabinol [THC]), and controls (those who denied use of SCs over the past 3 months and had negative toxicology for THC). RESULTS: Digital charts of 983 patients were reviewed. A total of 162 subjects reported use of SCs over the past 3 months (76% male), and 292 subjects had positive toxicology screen for THC (67% male). A total of 38.9% of SC users (n = 63) had positive urine toxicology screen for THC. SC users had higher risks of psychotic presentations (adjusted odds ratio [AOR] = 3.390; 95% CI, 1.390-8.267) and agitation (AOR = 4.643; 95% CI, 1.974-10.918) compared to the controls. While women had lower rates of psychosis than men in the cannabis and control groups, the rates were markedly potentiated with SC use to high levels (79%) approximately equal to that seen in men (80%). There was also a significant interaction between SC use and sex for agitation (AOR = 0.308; 95% CI, 0.117-0.808). Female SC users were significantly more agitated than male SC users (73.7% vs 47.6%, respectively, P = .005). CONCLUSIONS: SC users are more likely than nonusers to be psychotic or agitated in an inpatient setting. The potentiated rates of psychosis and agitation with SC use in women suggest that they may have a greater sensitivity to these synthetic compounds.​.