New-Onset Prolonged Psychosis Following Synthetic Cannabinoid Use in an Older Patient: A Case Report.

Synthetic cannabinoids (SCs), a class of new psychoactive substances (NPS) commonly known as "spice," has rapidly gained popularity and become the most ubiquitous NPS on the illegitimate drug market. SCs, unlike natural cannabis (NC), are not controlled by international drug conventions, posing a significant risk to public health. These substances are easily accessible, relatively inexpensive, and challenging to detect in routine drug screenings. The existing literature provides strong evidence of an association between NC use and psychosis, but there is significantly less data on SC psychosis. We present a clinical case report of a 51-year-old African American female with no known psychiatric history who was admitted to the inpatient psychiatric unit after reported paranoia and altered mental status for the preceding six days. During hospitalization, she exhibited disorganization, persecutory delusions, extreme agitation, and bizarre behaviors that included the concealment of a set of stolen keys in her vagina, necessitating an ethics consult. After consideration of differentials, the patient was diagnosed with substance-induced psychotic disorder secondary to SC. The patient was stabilized on 3 mg Risperidone at bedtime. After 16-day hospitalization, she reached her baseline and later revealed that she had recently smoked SC for the first time. The primary goal of this case is to highlight the sequelae of SC-associated psychosis. A SC-associated psychosis could drastically vary from NC and is often undetectable on a typical UDS, which may result in a lifelong primary psychotic disorder misdiagnosis.

A systematic review and meta-analysis of synthetic cathinone use and psychosis.

RATIONALE: Synthetic cathinones (SC), commonly referred to as "bath salts", are stimulants resembling the natural alkaloid cathinone found in the khat plant. These substances have the potential to induce serious health risks such as hallucinations, delusions, paranoia and agitation which can lead to substance-induced psychotic disorders. Despite growing concerns, there is a limited understanding of the association between SC consumption and the devolvement of such psychopathologies. METHODS: We conducted a systematic review to investigate the frequency of substance-induced psychotic disorder (SIPD) and associated conditions in humans following synthetic cathinone consumption. We qualitatively and quantitatively analyzed SC exposure cases. RESULTS: A total of 32 studies were included, with a diverse range of demographics, synthetic cathinone types, and consumption patterns. The proportion of individuals developing psychotic symptoms was reported at 0.380 (Random-effects model, 95% CI 0.289 - 0.475). Additionally, the significant heterogeneity in diagnostic approaches limited our ability to provide a precise estimate of prevalence. CONCLUSIONS: Synthetic cathinone consumption is associated with the risk of developing psychotic symptoms as indicated by the prevalence of hallucinations and/or delusions. Due to the lack of information on classifying factors, particularly duration of symptoms, we are unable to conclude synthetic cathinone-induced psychosis. Further research is warranted to elucidate the underlying mechanism linking synthetic cathinone consumption and psychosis. This review underscores the urgency of addressing the growing health risks posed by synthetic cathinone use. Additionally, it highlights the necessity of proper quantification of psychotic symptoms through scales and reporting of classification criteria to accurately diagnose SIPD.

Psychopathology and Pattern of Remission of Cannabis-Induced Psychotic Disorder.

Objective: To analyze the psychopathology and pattern of remission in cannabis-induced psychotic disorder with treatment.Methods: This was a prospective cohort study of a group of patients admitted with new-onset psychosis, cannabis use, and no evidence of other drug abuse from January 1 to June 31, 2019, to the psychiatry inpatient department of a multispecialty tertiary care hospital in Kerala, India. Patients were evaluated at admission and after 1 week in the hospital and 1 month after discharge using the Structured Clinical Interview for the Positive and Negative Syndrome Scale and the Clinical Global Impressions-Severity of illness scale.Results: Fifty-six male subjects were recruited for the study. The mean age of the subjects was 22.2 years, and the majority were active smokers of nicotine and cannabis. Total duration of abuse and family history of substance use in first-degree relatives correlated with severity of psychosis. Hostility, excitement, and grandiosity were the predominant positive symptoms, and these symptoms showed a steady reduction toward the end of the study. The most frequent negative symptoms were emotional withdrawal, passive or apathetic social withdrawal, and difficulty in abstract thinking, and these symptoms also showed significant improvement (P < .001 for all). For symptoms such as somatic concern and guilt feelings, significant treatment response was noted only in the initial week (P < .001).Conclusions: Cannabis-induced psychosis in the Indian setting presents with predominant positive symptoms and minimal affective symptoms. The steady improvement noted with complete cessation of cannabis indicates a possible contributory role for cannabis in precipitating psychosis.

Differences between substance-induced psychotic disorders and non-substance-induced psychotic disorders and diagnostic stability. / Diferencias y estabilidad diagnóstica entre trastornos psicóticos inducidos por sustancias y trastornos psicóticos no inducidos.

Several hypotheses have been proposed to explain the comorbidity between psychotic disorders and substance use, one of them being the capacity of some to induce psychotic symptoms, although the transition from psychotic episodes induced by substances to schizophrenia has been less studied. In this study, differential variables between patients with induced and non-induced psychosis are determined, and the evolution and change of diagnosis of those induced to schizophrenia in the follow-up is analyzed. This is an observational case-control study with 238 patients admitted to the acute care unit for psychotic episodes between December 2003 and September 2011. The group of non-substance-induced psychotic disorders (NSIPD) included 127 patients, with 111 in the substance-induced (SIPD) group, according to the International Classification of Diseases. Sociodemographic and clinical characteristics, personal and family history, substance use, diagnostic stability and progression were compared. The NSIPD group showed higher scores in severity and in negative symptoms and more family history of psychosis. The SIPD group presented more personal history of personality disorder and family history of addictions and more positive symptoms At 6 years of follow-up, 40.9% of ISDP changed to a diagnosis of schizophrenia, presenting more family history of psychotic disorders and worse progression with more visits to the emergency department and readmissions, than subjects who maintained diagnostic stability. Therefore, special attention should be paid to this group of patients because of the potential severity and the increased risk of developing a chronic psychotic disorder.

Se han propuesto distintas hipótesis para explicar la comorbilidad entre trastornos psicóticos y por consumo de sustancias, siendo una de ellas la capacidad de algunas de inducir cuadros psicóticos, aunque la transición de episodios psicóticos inducidos por sustancias a esquizofrenia ha sido menos estudiada. En este trabajo se determinan variables diferenciales entre individuos con psicosis inducidas y no inducidas, y se analiza la evolución y el cambio de diagnóstico de las inducidas a esquizofrenia en el seguimiento. Es un estudio observacional de casos y controles con 238 pacientes ingresados en la unidad de agudos de un Hospital General de Madrid (España) por episodios psicóticos entre diciembre de 2003 y septiembre de 2011. Se incluyeron 127 en el grupo de trastornos psicóticos no inducidos por sustancias (TPNIS) y 111 en el de inducidos por sustancias (TPIS), según la Clasificación Internacional de Enfermedades. Se compararon características sociodemográficas, clínicas, antecedentes personales y familiares, de consumo de sustancias, estabilidad diagnóstica y evolución. El grupo de TPNIS presentó mayores puntuaciones en gravedad y sintomatología negativa mientras que el de TPIS tuvo más antecedentes personales de trastorno de personalidad y familiares de adicciones, y más sintomatología positiva. A los seis años un 40,9% de TPIS cambió a diagnóstico de esquizofrenia, presentando más antecedentes familiares de trastornos psicóticos y de adicciones, y una peor evolución con más visitas a urgencias y reingresos que los sujetos con estabilidad diagnóstica. Por tanto, habrá que prestar especial atención a este grupo de sujetos por su potencial gravedad y por el mayor riesgo de desarrollar un trastorno psicótico crónico.

Methamphetamine use and psychotic symptoms: findings from a New Zealand longitudinal birth cohort.

BACKGROUND: This study examined the association between methamphetamine use and psychotic symptoms in a New Zealand general population birth cohort (n = 1265 at birth). METHODS: At age 18, 21, 25, 30, and 35, participants reported on their methamphetamine use and psychotic symptoms in the period since the previous interview. Generalized estimating equations modelled the association between methamphetamine use and psychotic symptoms (percentage reporting any symptom, and number of symptoms per participant). Confounding factors included childhood individual characteristics, family socioeconomic circumstances and family functioning. Long term effects of methamphetamine use on psychotic symptoms were assessed by comparing the incidence of psychotic symptoms at age 30-35 for those with and without a history of methamphetamine use prior to age 30. RESULTS: After adjusting for confounding factors and time-varying covariate factors including concurrent cannabis use, methamphetamine use was associated with a modest increase in psychosis risk over five waves of data (adjusted odds ratio (OR) 1.33, 95% confidence interval (CI) 1.03-1.72 for the percentage measure; and IRR 1.24, 95% CI 1.02-1.50 for the symptom count measure). The increased risk of psychotic symptoms was concentrated among participants who had used at least weekly at any point (adjusted OR 2.85, 95% CI 1.21-6.69). Use of methamphetamine less than weekly was not associated with increased psychosis risk. We found no evidence for a persistent vulnerability to psychosis in the absence of continuing methamphetamine use. CONCLUSION: Methamphetamine use is associated with increased risk of psychotic symptoms in the general population. Increased risk is chiefly confined to people who ever used regularly (at least weekly), and recently.

Sleep Deprivation & Amphetamine Induced Psychosis.

Objectives: To explore the relationship between sleep deprivation and amphetamine-induced psychosis. Methods: The patient group included 78 patients with a diagnosis of amphetamine (Captagon)-induced psychosis. The control group included 49 patients with no current or past history of amphetamine (Captagon)-induced psychosis. All study subjects underwent the following: a demographic sheet, a structured clinical interview for SM-IV (SCID 1), a drug use questionnaire, a questionnaire to explore any relationship between sleep deprivation and Captagon-induced psychosis, routine medical investigation, and urine screening for detection of drugs. Results: The patient group showed significantly higher both regular and maximum daily doses of Captagon. Patients showed more periods of sleep deprivation with the use of Captagon in comparison to controls, especially with the increase of the Captagon dose. Patients believed that the occurrence and termination of sleep deprivation were the cause of the start and end of psychotic experiences (more so than the increase and decrease or stoppage of Captagon doses). Conclusion: sleep deprivation plays an essential role in the development of psychotic symptoms in patients who are using Captagon.

Cannabis - miracle medicine or psychosis-inducing drug? / Cannabis ­ mirakelmedisin eller psykosefremkallende rusmiddel?

Throughout history, cannabis has been suggested as a treatment for numerous diseases. Despite being in use for over 5000 years, cannabis is still a hot topic of debate and the subject of discussion among politicians and the medical community.

Psychosis beas a rare side effect of sildenafil: a case report.

BACKGROUND: Sildenafil citrate is a commonly used medication for the management of erectile dysfunction. Previous studies have described some neuropsychiatric side effects of this medication. So far, however, there has been little discussion about sildenafil-induced psychosis. CASE PRESENTATION: We here present the case of a 32-year-old Iranian male, without a known psychiatric history, who developed psychotic symptoms following initiation of sildenafil. We also postulate a mechanism by which this may occur. CONCLUSIONS: This report highlights the importance of watchful observation for the occurrence of this rare but serious side effect. Further studies are needed to clarify the precise mechanism that causes sildenafil-induced psychosis.

Reassessment of amphetamine- and phencyclidine-induced locomotor hyperactivity as a model of psychosis-like behavior in rats.

Locomotor hyperactivity induced by psychotomimetic drugs, such as amphetamine and phencyclidine, is widely used as an animal model of psychosis-like behaviour and is commonly attributed to an interaction with dopamine release and N-methyl-D-aspartate (NMDA) receptors, respectively. However, what is often not sufficiently taken into account is that the pharmacological profile of these drugs is complex and may involve other neurotransmitter/receptor systems. Therefore, this study aimed to assess the effect of three antagonists targeting different monoamine pathways on amphetamine- and phencyclidine-induced locomotor hyperactivity. A total of 32 rats were pre-treated with antagonists affecting dopaminergic, noradrenergic and serotonergic transmission: haloperidol (0.05 mg/kg), prazosin (2 mg/kg) and ritanserin (1 mg/kg), respectively. After 30 min of spontaneous activity, rats were injected with amphetamine (0.5 mg/kg) or phencyclidine (2.5 mg/kg) and distance travelled, stereotypy and rearing recorded in photocell cages over 90 min. Pre-treatment with haloperidol or prazosin both reduced amphetamine-induced hyperactivity although pre-treatment with ritanserin had only a partial effect. None of the pre-treatments significantly altered the hyperlocomotion effects of phencyclidine. These findings suggest that noradrenergic as well as dopaminergic neurotransmission is critical for amphetamine-induced locomotor hyperactivity. Hyperlocomotion effects of phencyclidine are dependent on other factors, most likely NMDA receptor antagonism. These results help to interpret psychotomimetic drug-induced locomotor hyperactivity as an experimental model of psychosis.

Application Prospect of Integrative Omics in Forensic Identification of Methamphetamine-Associated Psychosis.

The clinical symptoms and signs of methamphetamine-associated psychosis (MAP) and schizophrenia are highly similar, but the situation is completely different when MAP and schizophrenia patients need to be assessed for criminal responsibility after they comitted a harmful behavior. Therefore, the distinction between the two psychoses is very important in forensic psychiatry. At present, the identification of these two psychoses is mainly dependent on the corresponding criteria such as the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the Chinese Classification of Mental Disorders Version 3 (CCMD-3). It's challenging to diagnose and distinguish between the two in practical cases due to their similar clinical symptoms and the lack of effective objective indexes. Different from the limitations of single omics, integrative omics intergrates data from multiple dimensions and has been extensively studied in the field of schizophrenia and has achieved some preliminary results. In view of the correlation between MAP and schizophrenia and the potential application value of integrative omics, this paper proposes an integrative omics strategy for MAP pathogenesis and forensic identification, aiming to improve the further understanding of the relationship between the two psychoses and the corresponding pathogenesis. It also provides references for the future exploration of integrative omics in forensic precise identification and effective monitoring and early warning methods.

Remission of persistent methamphetamine-induced psychosis after cariprazine therapy: presentation of a case report.

In this case report, we described a patient admitted with persistent methamphetamine-induced psychotic symptoms, accompanied by negative symptoms, who appeared to respond to cariprazine treatment regarding his psychotic and craving symptoms. To our knowledge, no cariprazine-related data has been published about these type of patients. Our case suggests that cariprazine may improve both psychotic and addictive symptoms in subjects with persistent substance-induced psychotic disorders. Notably, our patient reported an abrupt decrease in substance craving and use, and an improvement in positive and negative psychotic symptoms. Although it is not possible to generalize the observations and findings gathered with this single case, it detected a potential effect of cariprazine on a drug naïve patient with persistent psychotic symptoms induced by methamphetamine for the first time.

Application Prospect of Integrative Omics in Forensic Identification of Methamphetamine-Associated Psychosis / 法医学杂志

The clinical symptoms and signs of methamphetamine-associated psychosis (MAP) and schizophrenia are highly similar, but the situation is completely different when MAP and schizophrenia patients need to be assessed for criminal responsibility after they comitted a harmful behavior. Therefore, the distinction between the two psychoses is very important in forensic psychiatry. At present, the identification of these two psychoses is mainly dependent on the corresponding criteria such as the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) and the Chinese Classification of Mental Disorders Version 3 (CCMD-3). It's challenging to diagnose and distinguish between the two in practical cases due to their similar clinical symptoms and the lack of effective objective indexes. Different from the limitations of single omics, integrative omics intergrates data from multiple dimensions and has been extensively studied in the field of schizophrenia and has achieved some preliminary results. In view of the correlation between MAP and schizophrenia and the potential application value of integrative omics, this paper proposes an integrative omics strategy for MAP pathogenesis and forensic identification, aiming to improve the further understanding of the relationship between the two psychoses and the corresponding pathogenesis. It also provides references for the future exploration of integrative omics in forensic precise identification and effective monitoring and early warning methods.

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.

Forced normalization of Lennox-Gastaut syndrome using lacosamide: A case report.

PURPOSE: Forced normalization (FN) indicates psychotic episodes associated with seizure remission and disappearance of epileptiform activity on EEG. FN is likely to occur when frequent seizures are abruptly terminated by anti-epileptic drugs (AEDs) or epilepsy surgery. METHODS: We describe an atypical case of a patient with FN induced by lacosamide (LCM). RESULTS: A 23-year-old female patient with Lennox-Gastaut syndrome (LGS) was administered AEDs for LGS and hospitalised with weight loss and abnormal behaviour. Her condition fulfilled the FN criteria, which was considered to be induced by LCM. After a reduction in LCM dose, her abnormal behaviour and appetite improved. During LCM use, the patient developed no seizures, and the high amplitude diffuse sharp and slow wave complexes that were frequently observed before LCM disappeared on EEG. The LCM dose was tapered to 150 mg per day, and she became calmer with socially appropriate behaviours, although a few mild focal seizures relapsed. CONCLUSION: LCM was effective for treating LGS in this patient and induced FN. Initially, it was difficult to recognise FN in cases of psychiatric disorders, especially in patients with intellectual disability. Patients with FN induced by LCM are rare, and only four patients have been previously reported who were treated by antipsychotic drug for psychosis.

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.