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Background and Objective: Bupropion is generally considered safe and is widely used both as a monotherapy and as an augmentation agent for the treatment of major depression. Concerns have been raised about bupropion's propensity to precipitate new psychosis and worsen existing psychotic symptoms, although the mechanism is poorly understood. Three cases are reported in which bupropion use was associated with psychosis. The aim of the study was to explore the risk factors and possible mechanisms of psychosis in each case., Case Reports: Case 1 describes the interaction of cocaine abuse sensitization in a patient who developed psychosis with a lower dosage of bupropion. Cases 2 and 3 discuss the role of traumatic brain injury and structural brain lesions in increasing the risk of psychosis when using bupropion., Conclusions: Cocaine abuse, traumatic brain injury, and preexisting brain lesions appear to be risk factors for developing psychosis in persons taking bupropion. In such cases, clinicians should carefully assess the risks and benefits and closely monitor patients for symptoms of psychosis.

Ketamine can induce a transient psychosis via its influence on ionotropic N-methyl-d-aspartate receptors. Unlike dopamine agonists, which specifically mimic the positive symptoms seen in psychotic illnesses such as schizophrenia, ketamine may provide a better model because it is able to induce not only positive symptoms but also schizophrenia-like cognitive and negative symptoms. To test the veracity of the ketamine model further, research is attempting to replicate a range of cognitive deficits associated with schizophrenia in healthy controls under the influence of ketamine. Facial processing is one area that is impaired in schizophrenia. More specifically, research suggests that schizophrenia is associated with a reduced facial inversion effect reflecting abnormalities in configural face processing. The purpose of the current study was to determine whether ketamine would also reduce the facial inversion effect. This study was a double-blind, placebo-controlled repeated-measures design in which data are presented for 14 participants who received ketamine on one occasion and saline on another. The results supported the ketamine model, with the participants demonstrating an intact inversion effect in the placebo condition but no inversion effect under the influence of ketamine. Further, participants' self-reported deficits in visual processing correlated with their inversion score and errors on the faces task. Future studies should examine a wider range of facial processing tasks with a larger sample to confirm the current results and to determine the specificity of ketamine's ability to mimic schizophrenia facial processing deficits. The current study is supportive of the role of glutamate system in the processing of configural face information.

There have been a number of case reports of antibiotic-associated psychosis in the literature that have not been systematically reviewed. Urinary tract infections (UTIs) are among the most common bacterial infections and have also been associated with acute psychosis. We performed a systematic review of cases of antibiotic-associated acute psychosis during treatment of a UTI and evaluated the strength of the association for each case. We identified reports by searching PubMed, PsychINFO, and Web of Knowledge, and the reference lists of identified reports. We systematically evaluated the quality of the causal relationship between antibiotic treatment of UTI and psychosis. Fourteen articles (describing 15 different cases) met the inclusion criteria. The primary findings were as follows: (1) a majority (60%) of reported cases were "highly suggestive" of a potential causal relationship between antibiotic treatment and psychosis, including 3 cases with a recurrence of psychosis after rechallenge with the same antibiotic; (2) 3 different classes of antibiotics were implicated in this association, including fluoroquinolones, penicillins, and trimethoprim-sulfamethoxazole; (3) for most of the reported cases, both the onset and resolution of psychosis occurred within 1 week of initiation and discontinuation of the antibiotic, respectively; (4) approximately half of the cases did not require treatment with antipsychotics; and (5) affected men were significantly more likely to have a psychiatric history. Our findings suggest that acute psychosis is a potential adverse effect of antibiotic treatment of UTI, although the mechanism(s) underlying this association remains unclear.

A 3-year open-label study was conducted to determine the long-term safety and efficacy of quetiapine monotherapy in schizophrenia and schizoaffective disorder.Twenty-three male outpatients previously stable but with inter-episode residual symptoms on classical antipsychotics and/or risperidone and who had complained of side effects were selected. To initiate quetiapine, patients were hospitalized for 13 days and then treated as outpatients. Quetiapine dosage was adjusted according to therapeutic effects. Only five patients (21.7%) completed 77 to 96 weeks of the study. Initial dose was 261 +/- 65.6 mg/day (mean +/- S.D.) administered in divided doses, with an ending dose of 487 +/- 209.6 mg/day, corresponding with an 86.6% dose increase over the course of the study. For those completing 12 weeks or less (n = 11), mean ending dose was 362 +/- 184.8 mg/day a 38.7% dose increase over baseline. For those completing 25 weeks or more (n = 12), mean ending dose was 592 +/- 178.2 mg/day, a 126.8% dose increase over baseline. Six of the seven patients who relapsed after being stabilized on quetiapine for at least three months met criteria for supersensitivity psychosis (SSP).Therapeutic tolerance and rebound psychosis were found to develop with quetiapine in male patients with a history of chronic treatment with classical antipsychotics. Seeman and Tallerico3 have proposed pharmacologic explanations for quetiapine and clozapine drug-induced rebound phenomena.

The significance of increased sensitivity to stress associated with noradrenergic hyperactivity involving dopaminergic change in spontaneous recurrences of methamphetamine (MAP) psychosis (flashbacks) was examined. Plasma monoamine metabolite levels were assayed in 18 subjects with flashbacks who had been exposed to stressful events plus MAP-induced frightening psychotic symptoms (N = 11) or frightening psychotic symptoms alone (N = 7) during previous MAP use, in 15 nonflashbackers with a history of MAP psychosis, in 8 subjects with persistent MAP psychosis, and in 27 control subjects. Monoaminergic values were subjected to a square-root transformation, rendering the distribution normal. The numbers of stressful events (mostly threatening events) and frightening psychotic symptoms were significantly higher in the flashbackers than in the nonflashbackers. Factors triggering flashbacks were mild psychosocial stressors (mostly a mild fear of other people). During flashbacks, plasma norepinephrine levels increased, and the flashbackers, 11 of whom had experienced stressful events plus frightening psychotic symptoms, had an additional small increase in plasma levels of 3-methoxytyramine, which is indicative of dopamine release. Thus, threatening stressful events, together with MAP use, may induce noradrenergic hyperreactivity to subsequent mild stressors. Threatening, stressful events plus frightening psychotic symptoms may further induce increased dopamine release in response to mild stressors. Increased sensitivity to stress associated with noradrenergic hyperactivity involving increased dopamine release may have elicited memories of MAP psychosis related to frightening, stressful experiences. The increased sensitivity may be critical for the development of flashbacks.

Haloperidol levels in blood were measured monthly in 43 refractory chronic schizophrenic patients referred to a locked skilled nursing facility for long-term treatment. Gross toxic side effects (seizures, catatonia, confusion) and Neuroleptic Induced Deficit Syndrome in conjunction with blood levels over 30 ng/ml were identified in 13 of our 43 patients. Blood level reductions contributed to a reduction of side effects and clinical improvement and led to the expedited discharge of 6 of these 13 patients of the toxic subgroup. Considerable blood level variation was evident in single samples, and four levels appeared necessary to develop confidence for accuracy. Significant dose to blood level interindividual variability was identified, thereby bringing into question fixed-dose approaches to patients. The results strongly suggest the utility of haloperidol blood levels in the clinical setting.

Two persons are described who demonstrated prolonged neuropsychiatric syndromes after the ingestion of large doses of (+-)-3,4-methylenedioxymethamphetamine (MDMA), a recreationally used amphetamine analog. These cases suggest that MDMA, known to be neurotoxic to serotonin neurons in several experimental animals, may also produce untoward effects in humans. In addition, they provide evidence that ingestion of large doses of MDMA can produce lasting adverse functional consequences in vulnerable persons.

In a prospective study of all geriatric patients treated with tricyclic antidepressants over an 18-month period, a lower incidence of adverse psychiatric reactions than literature based on chart reviews has suggested was found. In only three of the 43 patients studied (7%) did a picture consistent with toxic delirium develop. None of the seven patients with senile dementia of the Alzheimer type suffered an adverse psychiatric reaction despite having achieved therapeutic blood levels of medication. Difficulties in determining the type and pathogenesis of untoward reactions that do occur as a source of error in establishing frequency are emphasized. The relationship of such reactions to the neurobiology of aging, the central anticholinergic syndrome, and the putative role of acetylcholine in contributing to the clinical picture of senile dementia of the Alzheimer type is discussed.