Drug-induced Psychosis Research Articles

Primary psychosis with comorbid drug abuse and drug-induced psychosis: Diagnostic and clinical evolution at follow up.

The study reports a follow-up assessment of 48 patients with concomitant drug abuse at the first admission for psychosis. We focused on the diagnostic distinction between primary psychosis with concomitant drug abuse and drug induced psychosis, to observe whether the diagnoses are stable over time and whether the clinical course significantly differs. The study examined 25 primary psychotic disorder with comorbid drug abuse and 23 drug-induced psychotic disorder patients. Diagnostic and psychopathological assessments were made at baseline and at follow-up. Mean follow-up period was 4.96 years. Patients with comorbid Drug Abuse exhibited higher scores in the item Unusual Content of Thought at baseline than drug-induced psychotic disorder patients: 5.48 vs 4.39 while the two patients groups did not differ in any of the BPRS items evaluated at follow-up. The primary psychosis with comorbid drug abuse and the substance induced psychosis groups were similar regarding diagnostic stability, and a diagnosis of schizophrenia at follow-up occurred similarly. There was no evidence that Drug Induced psychotic patients' symptoms tend to improve more after cessation of drug abuse. An earlier age of onset was found in primary psychotic patients, particularly for patients diagnosed as affected by schizophrenia at follow up. These results might reflect the uncertainty of the distinction between Primary and Drug Induced Psychosis and the difficulties in applying the DSM IV-TR criteria for diagnosing comorbid drug use disorders and psychotic disorders.

Investigating the Role of Serotonin in Methamphetamine Psychosis: Unaltered Behavioral Effects of Chronic Methamphetamine in 5-HT1A Knockout Mice.

Methamphetamine (Meth) is a widely abused stimulant drug, but this abuse is associated with an increased risk of developing psychosis. In addition to its well-known action on brain dopamine, Meth also affects serotonergic (5-HT) neurons. The aim of this study was to investigate this role in mice, which lack one of the main serotonin receptors, the 5-HT1A receptor, which has been implicated in both schizophrenia and Meth-induced psychosis. Male and female wild-type or 5-HT1A knockout (KO) mice received daily treatment with increasing doses of methamphetamine from 6 to 9 weeks of age (1–4 mg/kg/day twice a day). At least 2 weeks after the last injection, the mice underwent a battery of behavioral tests focusing on psychosis-related behaviors, including Meth-induced hyperactivity, prepulse inhibition (PPI), social interaction, elevated plus maze (EPM), and Y-maze. Meth pretreatment resulted in significantly increased hyperlocomotion in response to an acute Meth challenge, but this effect was independent of genotype. Chronic Meth treatment resulted in decreased levels of anxiety in the EPM in both sexes, as well as increased startle responses in female mice only, again independent of genotype. 5-HT1A KO mice showed an increased locomotor response to acute Meth in both sexes, as well as increased PPI and decreased startle responses in female mice only, independent of Meth pretreatment. In conclusion, the effects of chronic Meth appear unaffected by the absence of the 5-HT1A receptor. These results do not support a role of the 5-HT1A receptor in Meth-induced psychosis.

New Repeat Polymorphism in the AKT1 Gene Predicts Striatal Dopamine D2/D3 Receptor Availability and Stimulant-Induced Dopamine Release in the Healthy Human Brain.

The role of the protein kinase Akt1 in dopamine neurotransmission is well recognized and has been implicated in schizophrenia and psychosis. However, the extent to which variants in the AKT1 gene influence dopamine neurotransmission is not well understood. Here we investigated the effect of a newly characterized variant number tandem repeat (VNTR) polymorphism in AKT1 [major alleles: L- (eight repeats) and H- (nine repeats)] on striatal dopamine D2/D3 receptor (DRD2) availability and on dopamine release in healthy volunteers. We used PET and [11C]raclopride to assess baseline DRD2 availability in 91 participants. In 54 of these participants, we also measured intravenous methylphenidate-induced dopamine release to measure dopamine release. Dopamine release was quantified as the difference in specific binding of [11C]raclopride (nondisplaceable binding potential) between baseline values and values following methylphenidate injection. There was an effect of AKT1 genotype on DRD2 availability at baseline for the caudate (F(2,90) = 8.2, p = 0.001) and putamen (F(2,90) = 6.6, p = 0.002), but not the ventral striatum (p = 0.3). For the caudate and putamen, LL showed higher DRD2 availability than HH; HL were in between. There was also a significant effect of AKT1 genotype on dopamine increases in the ventral striatum (F(2,53) = 5.3, p = 0.009), with increases being stronger in HH > HL > LL. However, no dopamine increases were observed in the caudate (p = 0.1) or putamen (p = 0.8) following methylphenidate injection. Our results provide evidence that the AKT1 gene modulates both striatal DRD2 availability and dopamine release in the human brain, which could account for its association with schizophrenia and psychosis. The clinical relevance of the newly characterized AKT1 VNTR merits investigation.SIGNIFICANCE STATEMENT The AKT1 gene has been implicated in schizophrenia and psychosis. This association is likely to reflect modulation of dopamine signaling by Akt1 kinase since striatal dopamine hyperstimulation is associated with psychosis and schizophrenia. Here, using PET with [11C]raclopride, we identified in the AKT1 gene a new variable number tandem repeat (VNTR) marker associated with baseline striatal dopamine D2/D3 receptor availability and with methylphenidate-induced striatal dopamine increases in healthy volunteers. Our results confirm the involvement of the AKT1 gene in modulating striatal dopamine signaling in the human brain. Future studies are needed to assess the association of this new VNTR AKT1 variant in schizophrenia and drug-induced psychoses.

Comparative examination of the differences between cannabis psychosis and methamphetamine psychosis in a psychological state

BackgroundWith the rapid and intensive spread of marihuana abuse among youth, Japanese society is focusing on law enforcement against drug abusers. In 2016, a mass killing allegedly committed by a marihuana abuser was reported in Japan.ObjectivesTo consider that common recognition of the diverse process and potential risks of cannabis psychosis should be shared among psychiatrists.AimsElicit differences between cannabis psychosis and methamphetamine psychosis, and determine whether specific guidelines for treatment of cannabis psychosis are required.MethodIntensive retrospective review of distinctive methamphetamine and cannabis psychosis through case studies in our hospital.ResultMajor symptoms of methamphetamine psychosis include auditory hallucination and paranoia, however recovery is achieved soon after undertaking treatment. In cannabis psychosis, distinctive features are megalomania and by a pseud-enlightenment experience of supernatural existence, abusers stick to an unrealistic self-estimate of omnipotent, which leads them to refuse the fading away of this feeling and repeat abuse.ConclusionPsychological substances have strong suggestibility so abusers’ symptoms are easily modified by their mental state. Involvement of syndicate or perception of illegality reflects abusers’ drastic symptoms, but after dehospitalisation, recurrences are relatively fewer. Cannabis, however, grows wild and is admitted legally in some countries, so abusers lack awareness of guilt by mistaken perception of omnipotence and unrealistic optimism. Due to addiction and depersonalization, they rather enjoy gaining contact with supernatural power and fall into social withdrawal and are implicated to social problems. Considering the difficulty of rehabilitating and returning abusers to the community, we should not disregard the risks of cannabis abuse.Disclosure of interestThe author has not supplied his/her declaration of competing interest.

Delusional hyperthyroidism-A case report

IntroductionDisorders of endocrine function are among the most common etiology of psychiatric illness.The link between psychosis and hyperthyroidism is still poorly understood. We report an unusual presentation of hyperthyroidism as a psychotic state. Careful history, physical examination, and laboratory investigation, including thyroid function tests, should be part of the assessment of patients with any unexplained acute psychosis to detect this potentially curable disease. In this way, this article analyzes the psychiatric, physical and laboratory findings associated with hyperthyroidism and treatment.ObjectivesTo report a case of psychosis in a patient with endocrine disease.MethodsClinical records. Research on PubMed and Medscape using the Mesh Terms “hyperthyroidism”, “psychosis” and “thyroid and psychiatric manifestations”.ResultsWe present the case of a male patient, previously followed on our ambulatory psychiatric service for drug-induced psychosis. He was hospitalized due to psychotic symptoms, without substance abuse. Inpatient evaluation diagnosed hyperthyroidism. The patient did not present any somatic changes, except for psychosis. The patient was effectively treated with antipsychotics. He was referred to further evaluation and started antithyroid therapy.ConclusionsThyroid disease should be considered in the differential diagnosis of a broad spectrum of psychiatric symptoms. Psychosis is a rare complication of hyperthyroidism, ranging between 1–20%. The typical psychosis is reported to simulate manic-depressive psychosis. This association reinforces the need of a careful clinical evaluation in patients presenting with psychosis. Such psychiatric symptoms remit successfully with concomitant administration of antipsychotics and normalization of thyroid levels.Disclosure of interestThe authors have not supplied their declaration of competing interest.

Behavioral sensitization to methamphetamine induces specific interneuronal mRNA pathology across the prelimbic and orbitofrontal cortices

Schizophrenia is associated with significant pathophysiological changes to interneurons within the prefrontal cortex (PFC), with mRNA and protein changes associated with the GABA network localized to specific interneuron subtypes. Methamphetamine is a commonly abused psychostimulant that can induce chronic psychosis and symptoms that are similar to schizophrenia, suggesting that chronic METH induced psychosis may be associated with similar brain pathology to schizophrenia in the PFC. The aim of this study, therefore, was to examine mRNA expression of interneuron markers across two regions of the PFC (prelimbic (PRL) and orbitofrontal cortices (OFC)) following METH sensitization, an animal model of METH psychosis. We also studied the association between GABA mRNA expression and interneuronal mRNA expression to identify whether particular changes to the GABA network could be localized to a specific inhibitory cellular phenotype. METH sensitization increased the transcriptional expression of calbindin, calretinin, somatostatin, cholecyctokinin and vasoactive intestinal peptide in the PRL while parvalbumin, calbindin, cholectokinin and vasoactive intestinal peptide were upregulated in the OFC. Based on our previous findings, we also found significant correlations between GAD67, GAT1 and parvalbumin while GAD67, GAD65 and GAT1 were positively correlated with cholecystokinin in the PRL of METH sensitized rats. Within the OFC, the expression of GABAAα1 was positively correlated with somatostatin while GABAAα5 was negatively associated with somatostatin and calbindin. These findings suggest that METH sensitization differentially changes the expression of mRNAs encoding for multiple peptides and calcium binding proteins across the PRL and the OFC. Furthermore, these findings support that changes to the GABA network may also occur within specific cell types. These results, therefore, provide the first evidence that METH sensitization mediates differential interneuronal pathology across the PRL and OFC and such changes could have profound consequences on behavior and cognitive output.

Current understanding of methamphetamine-associated dopaminergic neurodegeneration and psychotoxic behaviors.

Clinical and preclinical studies have indicated that chronic methamphetamine (MA) use is associated with extensive neurodegeneration, psychosis, and cognitive impairment. Evidence from animal models has suggested a considerable role of excess dopamine or glutamate, oxidative stress, neuroinflammation, and apoptosis in MA-induced neurotoxicity, and that protein kinase Cδ might mediate the interaction among these factors. In addition, the relatively long-lasting and recurrent nature of MA psychosis has been reproduced in animals treated with various dosing regimens of MA, which have shown behavioral sensitization, sociability deficits, and impaired prepulse inhibition. Genetic predisposition as well as dopaminergic and glutamatergic alterations might be important in the development of MA psychosis. Neuroimaging studies have identified functional and morphological changes related to the cognitive dysfunction shown in chronic MA users. Failure in the task-evoked phosphorylation of extracellular signal-related kinase likely underlies MA-induced memory impairment. Recent progress has suggested certain roles of oxidative stress and neuroinflammation in the psychosis and cognitive deficits induced by repeated low doses of MA. This review provides a comprehensive description of pertinent findings from human and animal studies, with an emphasis on the current understanding of the underlying mechanisms of MA neuropsychotoxicity and its relevance to Parkinson's disease or schizophrenia.

Drug Abuse and Psychosis: New Insights into Drug-induced Psychosis.

Addictive drug use or prescribed medicine abuse can cause psychosis. Some representative symptoms frequently elicited by patients with psychosis are hallucination, anhedonia, and disrupted executive functions. These psychoses are categorized into three classifications of symptoms: positive, negative, and cognitive. The symptoms of DIP are not different from the symptoms of schizophrenia, and it is difficult to distinguish between them. Due to this ambiguity of distinction between the DIP and schizophrenia, the DIP animal model has been frequently used as the schizophrenia animal model. However, although the symptoms may be the same, its causes are clearly different in that DIP is acquired and schizophrenia is heritable. Therefore, in this review, we cover several DIP models such as of amphetamine, PCP/ketamine, scopolamine, and LSD, and then we also address three schizophrenia models through a genetic approach with a new perspective that distinguishes DIP from schizophrenia.

Association of polymorphisms in GAD1 and GAD2 genes with methamphetamine dependence.

Association between polymorphisms in GAD genes and methamphetamine (METH) dependence was investigated in the Thai population. Genotypes of rs769404 and rs701492 in GAD1 and rs2236418 in GAD2 polymorphisms were determined in 100 METH-dependent male subjects and 102 matched controls. The genotype and allele frequencies of rs2236418 (GAD2) were associated with METH dependence and METH with psychosis, in which the G allele was related to increased risk. The presence of the rs769404-rs701492 (GAD1) C-C haplotype was associated with METH psychosis. This study indicates that genetic variability in GAD1 and GAD2 contributes to risk of METH dependence and METH psychosis in the Thai population and indicates the role of the GABAergic system in these disorders.

First-Rank Symptoms in Methamphetamine Psychosis and Schizophrenia

Background: Methamphetamine psychosis (MAP) symptomatology has been described as indistinguishable from that of schizophrenia (SZ), yet research comparing these two disorders on specific psychotic symptoms such as schneiderian first-rank symptoms (FRS) is lacking. We aimed to determine and compare the occurrence and associations of FRS in patients diagnosed with MAP and with SZ. Sampling and Method: Data from SCID-I interviews performed on patients with either a diagnosis of SZ or MAP were compared. We calculated the prevalence of different FRS between MAP and SZ patients and used logistic regression to assess the association between FRS and diagnosis. Results: 102 patients were included in the study (MAP = 33, SZ = 69). Thought broadcasting occurred significantly more often in SZ (42%) than in MAP (24.2%) patients (adjusted OR = 3.02; 95% CI: 1.12-8.15; p = 0.028), while auditory hallucinations (voices conversing) were significantly higher in MAP (48.5%) than in SZ (20.3%) patients (adjusted OR = 0.27; 95% CI: 0.10-0.66; p = 0.004). However, there was no significant difference in the occurrence of one or more FRS in MAP and SZ, with most FRS showing overlap. Conclusions: We found that first-rank auditory hallucinations were more prevalent in MAP, whereas first-rank delusions of thought broadcasting were more prevalent in SZ. However, there was a substantial overlap in MAP and SZ for most FRS. This is consistent with the finding that FRS may have limited diagnostic specificity and that there is significant overlap in the symptoms of MAP and SZ. Future research into the neurobiology of delusions and hallucinations needs to take FRS into account.

Synthetic Cathione and Cannabinoid Toxicity and Treatment

Submit Manuscript | http://medcraveonline.com [4] and 4-methylcathinone (mephedrone). MDPV is a dopamine and norepinephrine reuptake inhibitor that acts as a stimulant. Mephedrone is thought to be a monoamine reuptake inhibitor. The mechanism of action includes an increase in serotonin, norepinephrine, and dopamine levels. Mephedrone [5] is a derivative of phenethylamine, which is the active ingredient in the African plant khat. Khat is similar to amphetamine and is associated with a history of abuse. Federal legislation was passed in September of 2011 to restrict the possession or distribution of any substance containing MDPV, methadone, or methylone. However, synthetic stimulants are difficult to regulate. These substances are easily manipulated into other compounds as soon as legislation banning a specific compound is passed. The drug class of phenethylamines, which these compounds belong to, is unable to be banned outright because this class also contains FDA-approved medications, such as bupropion, dopamine, and epinephrine. The Federal Analog Act (21 USC 813) was passed in an effort to avoid the need for legislation to be passed on each individual analog. However, the Analog Act only applies to products meant for human consumption. Bath salts are labeled “not for human consumption” as a way around this law. The American Association of Poison Control Centers [6] report the number of calls related to bath salts increasing from 304 in 2010 to 2,655 in 2012. The patients’ ages ranged from 1 day to 61 years, with a median age of 29.2 years. The clinical effects were primarily neurological or cardiovascular. In a recent retrospective review of hospital visits reported to poison control centers, 1,633 patients with reported bath salt toxicity were examined. Death resulted in 0.6% of patients. The reported reasons for death include suicide, serotonin syndrome, fever, and seizures. Major outcomes, defined as life threatening or resulting in significant disability or disfigurement, occurred in 15.5% of patients. The route of administration and age of the patient have been shown as factors influencing the occurrence of major outcomes or death. The injection of bath salts was predicted to have more serious effects than snorting bath salts. There was no difference in major outcomes or death between oral ingestion and injection. Patients aged 47 years or greater also had a higher risk of major outcomes than the younger populations. This older population also was shown to have higher rates of injection and co-ingestions, as well. Co-ingestions of other substances presenting with bath salt toxicities have a relatively low occurrence as compared to other substances of abuse, around 26%. The most common co-ingestion was with opioids in 6.2% of the reported cases from November 2011 to November 2012, followed by marijuana in 5.4% of reported case. This data suggests that the majority of bath salt abusers are seeking “legal highs” [7]. The treatment of the sympathomimetic toxidrome associated with bath salts should start with the administration of benzodiazepines. It is reported that benzodiazepines are used in about 60% of patients. Amphetamine-induced seizures typically result from an imbalance of excitatory and inhibitory neurotransmitters that do not originate in a specific location of the brain. Amphetamine-induced seizures respond to benzodiazepines, which also act to sedate the patient for the safety of the healthcare team. Phenytoin and Fosphenytoin should not be used as they work by isolating the focal point of a seizure and can induce arrhythmias. Lorazepam and Diazepam are the preferred agents via the intravenous route. Sedation is also a common treatment strategy used in this patient population. Sedative agents commonly used include propofol, barbiturates, and antipsychotics. Almost 10% of patients presenting with bath salt intoxication require ventilation. Psychotic symptoms typically resolve within 12 hours to 3 days of admission, although one patient remained symptomatic for 11 days. Caution must be used when administering anti-psychotic medications for drug-induced psychoses, as they may lower the seizure threshold.

Methamphetamine-induced psychosis is associated with DNA hypomethylation and increased expression of AKT1 and key dopaminergic genes.

Methamphetamine, one of the most frequently used illicit drugs worldwide, can induce psychosis in a large fraction of abusers and it is becoming a major problem for the health care institutions. There is some evidence that genetic and epigenetic factors may play roles in methamphetamine psychosis. In this study, we examined methamphetamine-induced epigenetic and expression changes of several key genes involved in psychosis. RNA and DNA extracted from the saliva samples of patients with methamphetamine dependency with and without psychosis as well as control subjects (each group 25) were analyzed for expression and promoter DNA methylation status of DRD1, DRD2, DRD3, DRD4, MB-COMT, GAD1, and AKT1 using qRT-PCR and q-MSP, respectively. We found statistically significant DNA hypomethylation of the promoter regions of DRD3 (P = 0.032), DRD4 (P = 0.05), MB-COMT (P = 0.009), and AKT1 (P = 0.0008) associated with increased expression of the corresponding genes in patients with methamphetamine psychosis (P = 0.022, P = 0.034, P = 0.035, P = 0.038, respectively), and to a lesser degree in some of the candidate genes in non-psychotic patients versus the control subjects. In general, methamphetamine dependency is associated with reduced DNA methylation and corresponding increase in expression of several key genes involved in the pathogenesis of psychotic disorders. While these epigenetic changes can be useful diagnostic biomarkers for psychosis in methamphetamine abusers, it is also consistent with the use of methyl rich diet for prevention or suppression of psychosis in these patients. However, this needs to be confirmed in future studies. © 2016 Wiley Periodicals, Inc.

P.3.b.039 - First-episode primary psychosis with comorbid drug abuse and drug-induced psychosis: diagnostic stability and clinical evolution at long-term follow up

To assess the mechanism by which a collaborative care (CC) intervention improves self-reported abstinence among primary care patients with opioid and alcohol use disorders (OAUD) compared to treatment as usual.Secondary data analysis of SUMMIT, a randomized controlled trial of CC for OAUD. Participants were 258 patients with OAUD receiving primary care at a multi-site Federally Qualified Health Center. Using a mediation analysis decomposition of a total effect into a mediated and a direct effect, we examined the effect of CC on abstinence at six months, attributable to the HEDIS treatment initiation and engagement measures for the total sample, for individuals with alcohol use disorders alone, and for those with a co-morbid opioid use disorder.Although the CC intervention led to an increase in both initiation and engagement, among the full sample, only initiation mediated the effect of the intervention on abstinence (3.8%, CI=[0.4%, 8.3%]; 32% proportion of the total effect). In subgroup analyses, among individuals with comorbid alcohol and opioid use disorders, almost 100% of the total effect was mediated by engagement, but the effect was not significant. This was not observed among the alcohol use disorder only group.Among primary care patients with OAUDs, treatment initiation partially mediated the effect of CC on abstinence at 6-months. The current study emphasizes the importance of primary care patients returning for a second substance-use related visit after identification. CC may work differently for people with co-morbid opioid use disorders vs. alcohol use disorders alone.

Differenzialdiagnose psychotischer Symptome

Many patients with psychiatric and organic disorders may present primary or secondary psychotic symptoms. Based on the ICD 10 classification, this article describes the possible underlying diseases and their subdivision. The main focus will be differential-diagnostic evaluations of psychotic syndromes. In the clinical setting, the differential diagnosis of the paranoid schizophrenia and other psychotic disorders into three main disease groups is important: 1. other psychiatric diseases, 2. primary and secondary organic diseases and 3. autoimmune diseases. The first group contains, for example, drug-induced psychoses, affective disorders, personality disorders. The second group includes forms of dementia, forms of deliria or metabolic diseases. Recently, another focus is set on autoimmune diseases, especially encephalitides. A detailed medical history, a physical examination and organic diagnostic can lead to the correct diagnosis and therapy. The differential-diagnostic classification and the detection of organic causes is an important part of psychiatric care, but often a good cooperation with organic specialties is needed.

Psychosis induced by amphetamines.

The study reviews publications on the use of methamphetamine and amphetamine in relation to psychotic symptoms, substance-induced psychosis, and primary psychosis published between July 2014 and December 2015. The databases MEDLINE, Embase, and PsycINFO were searched using the terms 'amphetamine psychosis' and 'methamphetamine psychosis' for the time period 1 July 2014 to 31 December 2015. There were 37 studies published on the subject during this time period. Risk factors for psychotic symptoms, substance-induced psychosis, and primary psychosis included patterns of drug use, but results also pointed to the importance of nondrug-related vulnerability. Cognitive impairment is associated with both amphetamine use and psychosis, and the impairment among those with amphetamine-induced psychosis resembles that of schizophrenia. At the neuronal level, GABAergic mechanisms may offer some understanding about the association between stimulant use and psychosis. Several different types of antipsychotic medication are effective for treating agitation and psychosis, but drugs with high DRD2 blockade should be used with caution. Some novel treatments are described, but are not sufficiently repeated to be recommended. During the past 18 months, studies have been published that cover risk factors, neuronal mechanisms, and treatment. These recent results do not differ from previous understandings, but the role of cognition and GABAergic dysfunction should be further investigated, and knowledge about resilience factors is still scarce. Also, a clearer evidence base for medical treatment of psychosis with concurrent amphetamine use is warranted. VIDEO ABSTRACT.

Pimavanserin: An Inverse Agonist Antipsychotic Drug.

Approximately all clinically useful antipsychotic drugs have known activity as dopamine receptor antagonists, but many of these drugs also are inverse agonists at the serotonin-2A (5HT2A) receptor. Pimavanserin is an inverse agonist at the 5HT2A receptor, with a lower binding affinity at the serotonin-2C receptor and sigma 1 receptor, but no significant binding to dopamine or other receptors. Because of its unique pharmacology, pimavanserin was approved for the treatment of psychosis associated with Parkinson's disease, and it has a low risk for exacerbating motor symptoms compared to standard antipsychotic medications. Whether pimavanserin can treat psychotic symptoms in schizophrenia, psychotic depression, psychotic mania, delirium, or drug-induced psychosis, is not known. Based on its inverse agonist effect at 5HT2A receptors, pimavanserin may have potential for treating symptoms associated with the use of hallucinogen drugs and for treating akathisia associated with antipsychotic medications. [Journal of Psychosocial Nursing and Mental Health Services, 54 (6), 21-24.].

PM293. Efficacy and Safety of Aripiprazole for Maintenance Treatment of Methamphetamine Dependence Following Methamphetamine Psychosis: A Naturalistic Retrospective Study

PM293. Efficacy and Safety of Aripiprazole for Maintenance Treatment of Methamphetamine Dependence Following Methamphetamine Psychosis: A Naturalistic Retrospective Study

Use of novel psychoactive substances by inpatients on general adult psychiatric wards

ObjectivesNon-illicit alternatives to controlled drugs, known as novel psychoactive substances (NPS), have recently risen to prominence. They are readily available, with uncertain pharmacology and no widely available assay. Given that...

Moxifloxacin-Induced Visual Hallucinations: A Case Report and Review of the Literature

Fluoroquinolones are extensively used to treat a variety of common bacterial infections. Due to their extensive use in clinical practice, increases in neuropsychiatric events have been reported. We discuss the case of a young female who developed visual hallucinations after 2 doses of moxifloxacin. After discontinuation of the moxifloxacin, the patient’s symptoms completely resolved. While one other case report exists with moxifloxacin, this case is unique in comparison. Our patient was a young female with no kidney dysfunction, no drug abuse history, absence of polypharmacy, and no previous psychological history that would have put her at an increased risk of drug-induced psychosis. Due to the prevalence of medication-induced hallucinations, it is imperative that clinicians are able to recognize offending medications in an effort to prevent misdiagnosis of a psychiatric illness.

Altered social cognition in male BDNF heterozygous mice and following chronic methamphetamine exposure

Growing clinical evidence suggests that persistent psychosis which occurs in methamphetamine users is closely related to schizophrenia. However, preclinical studies in animal models have focussed on psychosis-related behaviours following methamphetamine, and less work has been done to assess endophenotypes relevant to other deficits observed in schizophrenia. Altered social behaviour is a feature of both the negative symptoms and cognitive deficits in schizophrenia, and significantly impacts patient functioning. We recently found that brain-derived neurotrophic factor (BDNF) heterozygous mice show disrupted sensitization to methamphetamine, supporting other work suggesting an important role of this neurotrophin in the pathophysiology of psychosis and the neuronal response to stimulant drugs. In the current study, we assessed social and cognitive behaviours in methamphetamine-treated BDNF heterozygous mice and wildtype littermate controls. Following chronic methamphetamine exposure male wildtype mice showed a 50% reduction in social novelty preference. Vehicle-treated male BDNF heterozygous mice showed a similar impairment in social novelty preference, with a trend for no further disruption by methamphetamine exposure. Female mice were unaffected in this task, and no groups showed any changes in sociability or short-term spatial memory. These findings suggest that chronic methamphetamine alters behaviour relevant to disruption of social cognition in schizophrenia, supporting other studies which demonstrate a close resemblance between persistent methamphetamine psychosis and schizophrenia. Together these findings suggest that dynamic regulation of BDNF signalling is necessary to mediate the effects of methamphetamine on behaviours relevant to schizophrenia.