Cases reported "Hallucinations"

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1/30. The coincidence of schizophrenia and Parkinsonism: some neurochemical implications.

    The hypothesis has recently been advanced that increased activity of central dopaminergic mechanisms underlies the symptomatology of the schizophrenias. The evidence that dopaminergic transmission in the corpus striatum is impaired in Parkinson's disease suggests that observations on the relationship between Parkinson's disease and schizophrenia may illuminate the patholophysiology of the latter disease. Four cases are reported in which an illness with schizophrenic features developed in the setting of longstanding Parkinson's disease; attention is drawn to earlier reports of schizophrenic illnesses occurring as postencephalitic sequelae in the presence of a parkinsonian syndrome. These observations appear to conflict with the view that increased dopamine release in the striatum is necessary for the expression of schizophrenic psychopathology, but do not exclude the possibility that increased transmission may occur at other dopaminergic sites in the brain, for example the nucleus accumbens, tuberculum olfactorium or cerebral cortex. Similarly the dopamine receptor blockade hypothesis of the therapeutic effects of neuroleptic drugs cannot be maintained with respect to an action in the striatum in view of the differences between the actions of thioridazine and chlorpromazine in this structure, but may be tenable for actions at extra-straital sites.
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2/30. 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 = parkinsonian
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3/30. hallucinations in Parkinson's disease: prevalence, phenomenology and risk factors.

    hallucinations, mainly of a visual nature, are considered to affect about one-quarter of patients with Parkinson's disease. They are commonly viewed as a side-effect of antiparkinsonian treatment, but other factors may be involved. The aim of this study was to determine the phenomenology, prevalence and risk factors of hallucinations in Parkinson's disease. Two-hundred and sixteen consecutive patients fulfilling clinical criteria for Parkinson's disease were studied. Demographic and clinical variables were recorded, including motor and cognitive status, depressive symptoms and sleep-wake disturbances. patients with and without hallucinations were compared using non-parametric tests, and logistic regression was applied to significant data. hallucinations had been present during the previous 3 months in 39.8% of the patients, and fell into three categories: minor forms, consisting of a sensation of a presence (person), a sideways passage (commonly of an animal) or illusions were present in 25.5% of the patients (an isolated occurrence in 14.3%), formed visual hallucinations were present in 22.2% (isolated in 9.3%) and auditory hallucinations were present in 9.7% (isolated in 2.3%). patients with minor hallucinations had a higher depression score than non-hallucinators but did not differ in other respects. Logistic regression analysis identified three factors independently predictive of formed visual hallucinations: severe cognitive disorders, daytime somnolence and a long duration of Parkinson's disease. These findings indicate that, when minor hallucinations are included, the total prevalence is much higher than previously reported. A simple side-effect of dopaminergic treatment is not sufficient to explain the occurrence of all visual hallucinations. The main risk factor in treated patients is cognitive impairment, although sleep-wake cycle disturbances, and possibly other factors related to the duration of the disease, act as cofactors.
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4/30. Central anticholinergic syndrome from orphenadrine in a 3 year old.

    orphenadrine (N,N-dimethyl-2(o-methyl-alpha-phenylbenzyloxy)ethylamine) is an analog of diphenhydramine with central and peripheral anticholinergic properties. It is commonly prescribed both as a muscle relaxant and as an adjunct to antipsychotic medications to prevent parkinsonism. We report a case of orphenadrine poisoning in a 3-year-old boy following ingestion of no more than two 100-mg tablets. Central anticholinergic toxicity was prominent, manifested by hallucinations and severe agitation. orphenadrine can cause profound toxicity in children after ingestion of small doses, and should be considered as a potential cause for acute delirium in childhood.
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ranking = 0.91948836856061
keywords = parkinsonism
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5/30. Leucopenia induced by low dose clozapine in Parkinson's disease recedes shortly after drug withdrawal. Clinical case descriptions with commentary on switch-over to olanzapine.

    Four patients affected by severe Parkinson's disease developed leucopenia (900-1200 WBC) during treatment of psychosis (3) or untreatable insomnia (1) with clozapine (37.5-75 mg/day). clozapine withdrawal was followed by recovery of leucopenia (4000-6000 WBC) in two weeks with no need for the administration of leucokines. After 1-6 months olanzapine was administered (increasing the dose from 2.5 to 10 mg/day) to treat persisting disturbances, but the drug induced severe worsening of parkinsonism and also this drug had to be withdrawn.
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ranking = 0.91948836856061
keywords = parkinsonism
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6/30. Rabbitfish ("aras"): an unusual source of ciguatera poisoning.

    BACKGROUND: ciguatera poisoning is the commonest fish-borne seafood intoxication. It is endemic to warm water tropical areas and is caused by consumption of bottom-dwelling shore reef fish, mostly during spring and summer. The causative agent, ciguatoxin, is a heat-stable ester complex that becomes concentrated in fish feeding on toxic dinoflagellates. The common clinical manifestations are a combination of gastrointestinal and neurologic symptoms. Severe poisoning may be associated with seizures and respiratory paralysis. OBJECTIVE: To describe a series of patients who sustained ciguatera poisoning in an uncommon region and from an unexpected source. patients: Two families complained of a sensation of "electrical currents," tremors, muscle cramps, nightmares, hallucinations, agitation, anxiety and nausea of varying severity several hours after consuming rabbitfish ("aras"). These symptoms lasted between 12 and 30 hours and resolved completely. The temporal relationship to a summer fish meal, the typical clinical manifestations along with the known feeding pattern of the rabbitfish suggested ciguatera poisoning. CONCLUSIONS: The Eastern Mediterranean basin is an unusual region and the rabbitfish an unusual source for ciguatera poisoning. There are no readily available and reliable means for detecting ciguatoxin in humans. A high index of suspicion is needed for diagnosis and a thorough differential diagnosis is essential to eliminate other poisonings, decompression sickness and encephalitis. Supportive therapy is the mainstay of treatment.
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ranking = 0.0023556962393945
keywords = paralysis
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7/30. Successful treatment of behavioural problems in dementia using a cholinesterase inhibitor: the ethical questions.

    OBJECTIVE: To review the effect of cholinesterase inhibitors on the behavioural and neuropsychiatric symptoms of dementia and discuss the current clinical guidelines for the prescription of cholinesterase inhibitors in australia. METHOD: This paper reports the case of a patient with clinical diagnosis of dementia with lewy bodies (DLB) who was referred to an old age psychiatry service for the treatment of severe visual hallucinations and behavioural problems. RESULTS: Pharmacological treatment with olanzapine produced marked parkinsonism, agitation and confusion. A cholinesterase inhibitor, donepezil, was introduced. The introduction of donepezil was associated with cognitive improvement (mini-mental state examination [MMSE] increased from 23 to 27) and complete remission of behavioural symptoms. CONCLUSION: That cholinesterase inhibitors may have a role in the management of behavioural symptoms of dementia and the current Australian PBS guidelines for prescribing cholinesterase inhibitors are clinically restrictive. This has clinical and ethical implications that need to be addressed by consumers, the medical community and regulating authorities.
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ranking = 0.91948836856061
keywords = parkinsonism
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8/30. On the syndrome of the "spare limb": one case.

    We describe a case of a brain-damaged patient who had a peculiar bodily illusion which could not be labelled an hallucination but seemed somatognosically and phenomenologically similar to the phantom limb without amputation. The patient, who showed left hemiplegia, felt a third upper limb (without seeing it) which he himself defined as "spare." The spare limb was not deformed; it could be moved and controlled by the patient, and there was no sensation of pain. The patient did not show psychopathological or cognitive disorders. A possible interpretation of the phenomenon is as a "phantom movement" of the paralysed limb: the mental representation of the movement of the limb was dissociated from the bodily representation of his own limb and so was still present in his consciousness despite the paralysis.
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ranking = 0.0023556962393945
keywords = paralysis
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9/30. Progressive aphasia with lewy bodies.

    dementia with lewy bodies (DLB) may include both Alzheimer and Lewy body pathology, but has never been reported to cause primary progressive aphasia. We report a 69-year-old woman who died 11 years after presenting with the syndrome of progressive aphasia. Six years after aphasia onset she developed visual hallucinations, and subsequently parkinsonism. autopsy examination revealed Alzheimer's disease (AD), cortical lewy bodies, and depigmentation and lewy bodies in the substantia nigra and locus ceruleus. The aphasia most likely reflected the initial onset of AD, and the psychosis and parkinsonism most likely reflected the subsequent onset of Lewy body pathology. This first reported case of progressive aphasia occurring within the context of AD and Lewy body pathology uniquely illustrates the clinical and pathological nosological relationships between these two disease processes, and demonstrates a limitation of the general term, 'DLB'.
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ranking = 1.8389767371212
keywords = parkinsonism
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10/30. Diffuse lewy body disease - a clinical syndrome or a disease entity?

    Most clinicians and researchers still accept diffuse lewy body disease (DLBD) as a clinicopathological entity. dementia with fluctuating cognitive deficits, a parkinsonian syndrome, and visual hallucinations are the core symptoms of this proposed disease entity. From a neuropathological point of view, many examples of patients with progressive dementia showing evidence of extensive Lewy body formation in the cerebral cortex together with the occurrence of lewy bodies in substantia nigra and locus coeruleus have been identified. Confusingly, a large majority of cases showing typical features of DLBD also present with an Alzheimer pathology in the hippocampus and cerebral cortex. It is far from clear that DLBD represents a specific disease entity rather an intermediate variant between alzheimer disease and idiopathic parkinsonian syndromes. Nevertheless, from a clinical point of view it may be of importance to characterize patients with a symptomatology of DLBD because important management issues such as avoidance of severe neuroleptic sensitivity reactions, dopaminergic antiparkinsonian treatment and a beneficial response to cholinesterase inhibitors can be applied.
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keywords = parkinsonian
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