Cases reported "Hallucinations"

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1/117. Asymptomatic pancreatitis associated with clozapine.

    Besides the well-known adverse effects of clozapine, such as granulocytopenia, tiredness and hypersalivation, acute pancreatitis is known to be a very rare complication of the drug. In the literature a total of five case reports have been published so far. We report a case of asymptomatic pancreatitis subsequent to clozapine treatment at therapeutic doses in a 38-year-old male patient with chronic paranoid-hallucinatory schizophrenia. The patient was rehospitalized after an acute exacerbation of the psychosis subsequent to an attempt to change medication on an outpatient basis. Treatment with clozapine was initiated again. During phases of progressively increasing the clozapine dose, serum levels of amylase and lipase were increased; after maintaining daily doses of clozapine of 300 mg and/or 600 mg the pancreatic enzymes normalized quickly within a few days. The patient did not report any pancreas-related complaints, nor did specific diagnostic studies produce any indicative result, only a minor thickening of the head and body of the pancreas in the ultrasound. It is assumed that the phenomenon of subclinical, asymptomatic pancreatitis during increasing dosage of clozapine occurs more often than previously supposed. The monitoring of serum amylase levels during slow increase in clozapine is recommended; if leukocytosis or eosinophilia is present, the possibility of even a subclinical and asymptomatic pancreatitis should be considered.
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ranking = 1
keywords = paranoid, psychosis
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2/117. Olanzapine in dementia with lewy bodies: a clinical study.

    OBJECTIVES: dementia with lewy bodies (DLB) is now a well-recognized form of dementia in which psychosis and behavioural disturbance are common. Treatment with conventional neuroleptics is often very poorly tolerated. Olanzapine, a newly introduced atypical neuroleptic which binds to multiple receptor types with relatively low affinity for D2 receptors, may be a useful treatment option in DLB. MAIN OUTCOME MEASURES: The Behavioural pathology in Alzheimer's disease Rating Scale, The Neuropsychiatric Inventory, Unified Parkinson's disease Rating Scale and The Webster Disability Scale. DESIGN: We present the results of eight DLB patients with associated psychotic and behavioural difficulties. All patients were given olanzapine 2.5-7.5 mg. Their psychotic phenomena and behavioural and extrapyramidal symptoms were monitored at 2-weekly intervals. RESULTS: Three out of the eight patients could not tolerate olanzapine even at the lowest available dose. Two patients had clear improvement in psychotic and behavioural symptoms. Three patients were able to tolerate olanzapine but gained only minimal benefit. CONCLUSIONS: Olanzapine at the doses used conferred little advantage over conventional neuroleptics and should only be given with great caution to patients with DLB. The utility of smaller doses deserves further evaluation.
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ranking = 0.33821513951435
keywords = psychosis
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3/117. 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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ranking = 1.6910756975717
keywords = psychosis
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4/117. 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 = 2.014645418543
keywords = paranoid, psychosis
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5/117. Deterioration of parkinsonian symptoms following treatment of dopaminergic hallucinosis with olanzapine.

    The atypical antipsychotic drug olanzapine has been proposed for treatment of dopaminergic psychosis in Parkinson's disease (PD). We report on a 68-year-old patient who developed a severe akinetic-rigid extrapyramidal syndrome, accompanied by additional paranoid symptoms, following olanzapine treatment of optic hallucinosis in PD. Olanzapine may also induce clinically relevant extrapyramidal side effects in PD patients.
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keywords = paranoid, psychosis
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6/117. hallucinations, REM sleep, and Parkinson's disease: a medical hypothesis.

    BACKGROUND: patients with PD can have disabling visual hallucinations associated with dopaminergic therapy. sleep disorders, including vivid dreams and REM sleep with motor behaviors (RBD), are frequent in these patients. methods: The association of hallucinations and REM sleep both at night and during the day was examined in 10 consecutive nondemented patients with long-standing levodopa-responsive PD and hallucinations. Seven patients presented with paranoia and paranoid delusions. Overnight sleep recordings and standard multiple daytime sleep latency test were performed. The results were compared to those of 10 similar patients with PD not experiencing hallucinations. RESULTS: RBD was detected in all 10 patients with hallucinations and in six without. Although nighttime sleep conditions were similar in both groups, hallucinators tended to be sleepier during the day. delusions following nighttime REM period and daytime REM onsets were observed in three and eight of the hallucinators, and zero and two of the others. Daytime hallucinations, coincident with REM sleep intrusions during periods of wakefulness, were reported only by hallucinators. Postmortem examination of the brain of one patient showed numerous lewy bodies in neurons of the subcoeruleus nucleus, a region that is involved in REM sleep control. CONCLUSION: The visual hallucinations that coincide with daytime episodes of REM sleep in patients who also experience post-REM delusions at night may be dream imagery. Psychosis in patients with PD may therefore reflect a narcolepsy-like REM sleep disorder.
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ranking = 0.86292450193598
keywords = paranoid, paranoia
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7/117. Dimethylacetamide, ethylenediamine, and diphenylmethane diisocyanate poisoning manifest as acute psychosis and pulmonary edema: treatment with hemoperfusion.

    CASE REPORT: A 27-year-old man, employed by a synthetic fiber company, had been exposed to dimethylacetamide, ethylenediamine, and diphenylmethane diisocyanate in a confined space continuously for 4-6 hours per day for 3 days before admission. hallucinations and delusions were noted at admission; pulmonary edema developed subsequently. The electroencephalogram showed diffuse moderate cortical dysfunction and slow waves at 4-7 Hz, 20-80 microV. seizures, liver injury, and rhabdomyolysis were noted on the 4th hospital day. The patient was treated by hemoperfusion with a decrease in urine dimethylacetamide from 3,265 mg/g to 4 mg/g creatinine over 4 days. Serial urinary dimethylacetamide and electroencephalogram correlated with the clinical condition.
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ranking = 1.3528605580574
keywords = psychosis
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8/117. Antiepileptic drug-induced visual hallucinations in a child.

    The neurologic signs and symptoms of carbamazepine and phenytoin toxicity, such as ataxia, dysarthria, and nystagmus, are well known. The psychiatric manifestations of toxicity, such as psychosis and hallucinations, however, are less widely recognized. This study reports the case of a 9-year-old male with seizures who developed intermittent complex visual hallucinations after therapy with antiepileptic drugs was begun. This study considered seizures, migraine, underlying psychiatric diathesis, and drug toxicity as possible etiologies but after extensive investigation concluded that his symptoms were most likely a drug side effect.
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ranking = 0.33821513951435
keywords = psychosis
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9/117. Valproate-induced tinnitus misinterpreted as psychotic symptoms.

    Valproate sodium is an anticonvulsant medication, which has also been shown to be effective in the treatment of bipolar disorder. We report a case of valproate-induced tinnitus that was initially misinterpreted as increasing psychotic symptoms, which began approximately 2 days after initiation of valproate therapy. tinnitus worsened during the next 6 days of treatment until it was recognized that this symptom was related to valproate. After discontinuance of the medication, the tinnitus gradually resolved over a period of 10 days with no residual effects. Although it is a rare adverse effect, valproate-induced tinnitus should be included in the differential diagnosis for tinnitus in patients receiving this medication. tinnitus may be difficult to recognize in patients with active psychosis or mania.
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ranking = 0.33821513951435
keywords = psychosis
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10/117. The emergency treatment of depression complicated by psychosis or agitation.

    With the availability of newer, safer antidepressants in the past decade, initiation of definitive treatment for depression in the emergency setting has become an accepted practice. However, the use of newer antidepressants and atypical antipsychotics in depression complicated by psychosis or agitation has not yet been well studied. This article will review relevant data and make recommendations for the emergency management of psychotic and agitated depressive syndromes.
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ranking = 1.6910756975717
keywords = psychosis
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