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1/227. dextromethorphan- and pseudoephedrine-induced agitated psychosis and ataxia: case report.

    pseudoephedrine and dextromethorphan are therapeutic constituents of numerous commonly used, over-the-counter cough and cold preparations. Although this drug combination is generally considered quite safe if utilized in recommended doses, overmedication or overdose can result in serious neurologic and cardiovascular abnormalities that occasionally can be life-threatening. We present a case of a 2-year-old child who developed hyperirritability, psychosis, and ataxia after being overmedicated with a pseudoephedrine/dextromethorphan combination cough preparation, and discuss probable mechanisms of toxicity and risk factors for adverse events.
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2/227. meningitis or madness: a delicate balance.

    A child with meningitis who developed a psychosis 2 weeks after commencing treatment with antituberculous therapy is described here. The psychosis resolved with cessation of isoniazid, but the meningitis returned. The meningitis was treated by re-introduction of daily doses of isoniazid, but the psychosis recurred. Successful treatment of the meningitis, with minimal psychotic symptoms, eventually was achieved using isoniazid at 48 h dose intervals. The psychosis resolved completely after completion of therapy for tuberculous meningitis and cessation of isoniazid. This is the first case of isoniazid-associated psychosis reported in a child.
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3/227. schizophrenia - A disturbance of signal interaction between the entorhinal cortex and the dentate gyrus? The contribution of experimental dibenamine psychosis to the pathogenesis of schizophrenia: A hypothesis.

    In addition to the existence of complex memory (similar to the implicit nondeclarative memory of Squire), the existence of a phylogenetically old apparatus of a memory of situations (SMA) is supposed, which is to some extent comparable with the declarative memory of Squire. During actual sensory information the SMA generates a general frame and forms a general 'mark', indicating whether a given information has its origin inside or outside the body, and whether it is new or known. The procedure of this marking process can be explained as the time-depending arrest of a copy of the actual original information-transporting signal 'shower'; this copy must last until the feedback from thalamocortical centers indicates the termination of the processing of the original signal showers. The arrest of the shower copies is the performance of neuronal networks of the entorhinal cortex (EC) and the gyrus dentatus (GD). The psychopathological and biochemical analyses of experimental dibenamine psychosis show a different effect of dibenamine on the noradrenaline (NA) receptors of the EC and GD, respectively: these effects are responsible for the repeated perception cycles of a single situation. N,N-Dibencylamine blocks the postsynaptic alpha(1)-receptors of the EC without influencing the beta-receptors of the GD. Thus the interaction between EC and GD is changed: instead of new scenes, perceptions that have just been experienced get repeated presence and the quality of familiarity. The prolonged arrest of shower copies simultaneously blocks the entrance of new signal showers from the EC to the GD. No information-transporting signal showers can come in as long as the arrest lasts. In case of a disturbance in NA-dependent actions within the EC and the GD, the duration of arrest of information-transporting signal showers is shortened. Thus the formal frame of experience receives the quality of novelty instead of familiarity, and in addition the qualities of uncertainty, vagueness, and alienity. These very changes in perception and experience represent the basic disturbance of schizophrenia. All the symptoms of schizophrenia may be explained by this basic disturbance. The analysis of biochemical aspects turns attention to the energetic situation of NA and N-methyl-D-aspartate systems. These considerations suggest a genetic background of the basic disturbance of schizophrenia: transmitter effects on membranes of neurons and possibly also on glial cells, and energy supply of these effects may be predetermined genetically. It may be assumed that the compensation of such membrane-dependent disturbances will be possible within wide areas of the neural network, except for the 'bottleneck' of the overlapping region of the iso- and allocortex.
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4/227. Acute psychotic symptoms induced by topiramate.

    The incidence of psychosis during clinical trials of topiramate was 0.8%, not significantly different from the rate for placebo or reported rates of psychosis in patients with refractory epilepsy. We observed psychotic symptoms in five patients soon after initiation of topiramate therapy. We performed a retrospective chart review of the first 80 patients who began on topiramate after approval for clinical use, between January and April 1997. Symptoms suggestive of psychosis, including hallucinations and delusions, were sought for analysis. Cognitive effects such as psychomotor slowing, confusion, and somnolence were not included. Five patients developed definite psychotic symptoms 2 to 46 days after beginning topiramate. Dosages at symptom onset were 50-400 mg/day. Symptoms included paranoid delusions in four patients and auditory hallucinations in three. Symptoms of psychosis and other psychiatric symptoms resolved quickly with discontinuation of topiramate in three patients, dose reduction from 300 to 200 mg/day in one and with inpatient treatment and neuroleptics in another. One patient had a history of auditory hallucinations, one of aggressive and suicidal thoughts, but three had no significant psychiatric history. physicians should be aware of the possibility of psychotic symptoms, even in patients without a previous psychiatric history, when prescribing topiramate. Symptoms resolve quickly with discontinuation.
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ranking = 0.81428310618625
keywords = psychosis, paranoid
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5/227. A case of interferon alpha-induced manic psychosis in chronic hepatitis c.

    It is well known that mood disorder such as depression occasionally develops during interferon (IFN) therapy for chronic viral hepatitis. So far, however, IFN-induced manic disorder has been rarely reported. We present a case of manic psychosis which developed during IFN treatment for chronic hepatitis c. A 35-year-old man with chronic hepatitis positive for hepatitis c virus rna in serum was treated with natural IFN alpha with a daily dosage of 5 million units. Six weeks later he complained of insomnia, and then became exhilarated, talkative, restless and aggressive. Since the mental state was compatible with manic disorder, IFN therapy was immediately ceased. Simultaneously, psychotropic drugs were administered. One week later, the psychiatric disturbances disappeared. He has been keeping his usual social interactions without the psychotropic drugs after that. It is suggested that manic psychosis happened secondary to IFN alpha treatment.
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keywords = psychosis
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6/227. Non-steroidal anti-inflammatory drugs with adverse psychiatric reactions: five case reports.

    Adverse drug reactions of non-steroidal anti-inflammatory drugs (NSAIDs) are quite prevalent, but there are few reports about possible adverse psychiatric reactions, which may be ignored or underestimated. We describe here five psychiatric outpatients, two with major depressive disorders, one bipolar disorder, one schizophrenic disorder and one anxiety disorder, who were treated with NSAIDs for pain due to rheumatoid arthritis, osteoarthritis or other painful neuromuscular conditions. All five patients developed a moderate to severe depressive state, three patients became obviously paranoid, and four had either thoughts of suicide or an attempt while undergoing co-administration of NSAIDs. The psychiatric symptoms remitted when the NSAIDs were stopped. The depressive and paranoid symptoms returned on seven occasions of re-use or re-challenge with the same or a different type of NSAID in all five patients. When the NSAIDs were stopped again, the patients had another remission of the adverse psychiatric reactions, and eventually recovered to their baseline mental states in clear temporal relationships. The cases presented suggest that NSAIDs can induce or exacerbate idiosyncratic reproducible adverse psychiatric symptoms in certain vulnerable patients, including those with a variety of psychotic or neurotic disorders, and also in elderly persons, but these undesirable side-effects were generally transient and disappeared on withdrawal of the NSAIDs.
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ranking = 0.028566212372495
keywords = paranoid
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7/227. procainamide-induced psychosis: a case report and review of the literature.

    OBJECTIVE: To describe a case of procainamide-induced psychosis in an adult treated for atrial fibrillation. CASE SUMMARY: A 45-year-old Native American woman developed acute psychosis within 72 hours of initiating procainamide for atrial fibrillation. Symptoms abated within 24 hours of discontinuing procainamide. serum procainamide/N-acetylprocainamide concentrations were therapeutic throughout treatment. sotalol was started without recurrence of symptoms. DISCUSSION: Psychosis is a rare complication of treatment with procainamide, but the exact mechanism for this adverse event is not fully understood. Seven cases implicating procainamide as the cause of acute psychosis are reported in the literature. Cases of psychosis involving other antiarrhythmic agents have also been reported. CONCLUSIONS: Healthcare personnel should be aware of this adverse event related to procainamide and other antiarrhythmic agents.
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keywords = psychosis
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8/227. ethambutol-induced psychosis: a case report.

    Clinically, ethambutol (EMB)-induced psychosis is rare. In our review of the literature, most cases of antituberculosis agent-associated psychoses were caused by isoniazid (INH). We report the case of a 51-year-old man with suspected tuberculosis (TB) pleurisy. An anti-TB trial with INH, rifampicin and EMB was given initially. dizziness, disorientation, and auditory and visual hallucinations developed after seven days of therapy. Laboratory examinations, including routine biochemistry tests, serum titer of antinuclear antibodies, cerebrospinal fluid analysis and computerized tomography of the head showed no abnormal findings. Following discontinuation of anti-TB agents, the psychiatric symptoms subsided. When the patient was challenged with EMB, the same psychiatric symptoms recurred, but resolved again after discontinuation of EMB. It is important to be aware that EMB can induce psychosis when anti-TB medications are prescribed.
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keywords = psychosis
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9/227. Efficacy of quetiapine in Parkinson's patients with psychosis.

    Eleven patients with Parkinson's disease (PD) and acute psychosis received flexible doses of quetiapine between 25 and 300 mg/day based on clinical response and tolerance. Ten patients were receiving dopaminergic agents at baseline. Serial efficacy ratings (brief psychiatric rating scale, Clinical Global Impressions Scale), neuromuscular symptom assessments (Abnormal Involuntary movement Scale, Simpson-Angus Scale, Unified Parkinson's disease Rating Scale [UPDRS]), and adverse events monitoring were performed for up to 52 weeks. The patients had moderate hallucinations and/or delusions at baseline before the initiation of quetiapine. Nine of the 11 patients completed at least 12 weeks of treatment. Quetiapine was well tolerated in all but one patient, who became dizzy within the first week and withdrew from the study. Ten patients presented with moderate visual hallucinations. Quetiapine was markedly effective in controlling visual hallucinations in six of these patients. Symptoms of paranoia or delusions were less responsive to quetiapine. Four patients withdrew because of adverse events or comorbid medical problems, two withdrew because of a lack of efficacy, and five completed 52 weeks of treatment. The introduction of quetiapine did not exacerbate parkinsonian symptoms. Motor dysfunction, as measured by the UPDRS, revealed a slow, gradual worsening consistent with the progression of PD. Atypical antipsychotic medications such as quetiapine have a reduced likelihood of causing adverse drug-induced parkinsonism and therefore a possible role in treating psychotic symptoms in patients with PD.
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ranking = 1.0025620596216
keywords = psychosis, paranoia
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10/227. Psychotic episodes during zonisamide treatment.

    Several articles have appeared over the last years devoted to mental side effects during zonisamide (ZNS) treatment. In this study, we were particularly interested in psychotic episodes. Seventy-four epileptic patients with a history of ZNS treatment were surveyed retrospectively over the period spanning 1 March 1984 to 30 June 1994. They were divided into two groups according to the presence or absence of psychotic episodes during ZNS treatment. We analysed various factors pertaining to psychotic episodes during ZNS treatment. Of the 74 patients 14 had psychotic episodes. We found that the incidence of psychotic episodes during ZNS treatment was several times higher than the previously reported prevalence of epileptic psychosis, and that the risk of psychotic episodes was higher in young patients. In 13 patients, psychotic episodes occurred within a few years of commencement of ZNS. In children, obsessive-compulsive symptoms appeared to be related to psychotic episodes. It is important to terminate ZNS as soon as possible if psychotic episodes develop and never restart, even if seizures become worse. It cannot definitely be proved that ZNS causes psychotic episodes, as information on mental side effects during ZNS monotherapy is scant, but it does appear likely that ZNS contributes to psychotic episodes during polytherapy.
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ranking = 0.2
keywords = psychosis
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