Cases reported "Delirium"

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1/35. Occurrence of mirtazapine-induced delirium in organic brain disorder.

    Mirtazapine is the first of a new class of antidepressants, the noradrenergic and specific serotonergic antidepressants. Its antidepressant effect appears to be related to its dual enhancement of both noradrenergic neurotransmission and serotonin 5-HT1 receptor-mediated serotonergic neurotransmission. Mirtazapine has demonstrated superior tolerability to the tricyclic antidepressants, primarily on account of its relative absence of anticholinergic, adrenergic and serotonin-related adverse effects. We observed mirtazapine-induced delirium in one organically depressed and two major depressed patients with subclinical brain disease. The appearance of hallucinations, psychomotoric agitation and cognitive changes after initiation of mirtazapine, and their prompt improvement after drug discontinuation, led to the impression that these were drug-induced phenomena. One possible hypothesis for the observed deliria is a central increase of norepinephrine after acute administration of mirtazapine. Subclinical brain disease might have favoured the occurrence of delirium in the three cases.
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2/35. Paradoxical lithium neurotoxicity: a report of five cases and a hypothesis about risk for neurotoxicity.

    There have been many reports of probable lithium-induced organic brain syndromes occurring when serum lithium levels are within or close to the therapeutic range. The authors report on five patients who developed clinical syndromes suggestive of severe neurotoxicity during lithium treatment. In all cases lithium levels were between .75 and 1.7 mEq/liter. The patients who developed neurotoxicity had markedly higher global ratings of psychotic symptomatology and anxiety in the pretoxic period than did patients who never deveoped neurotoxicity. When the acute manic state is characterized by marked psychotic symptoms and intense anxiety, it may be associated with increased vulnerability to the development of severe lithium neurotoxicity.
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keywords = brain
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3/35. Scleroderma cerebritis, an unusual manifestation of progressive systemic sclerosis.

    A 42-year-old female with scleroderma experienced two exacerbations in which behavioral changes were the main clinical features. On both occasions she presented with paranoid delusions, perceptual aberrations, and disorientation. After treatment with corticosteroids, the patient's mental status returned to normal, and her electroencephalogram showed an increase in alpha wave frequency, which is consistent with a resolving delirium. Unlike systemic lupus erythematosus, scleroderma rarely involves the central nervous system. This case illustrates an unusual manifestation of progressive systemic sclerosis, primary cerebral involvement which presented as an acute organic brain syndrome. connective tissue diseases, notably systemic lupus erythematosus, often present neuropsychiatric symptoms. Despite the fact that there appears to be a clinical and pathological continuum among the connective tissue diseases, an organic psychosis rarely occurs in progressive systemic sclerosis (scleroderma. Described here is a patient with scleroderma in whom behavioral abnormalities were the main features of two exacerbations of the disease.
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4/35. delirium from nicotine withdrawal in neuro-ICU patients.

    Five cases of presumed nicotine withdrawal delirium among brain-injured patients treated in a neurologic intensive care unit are presented. Each patient had a history of heavy tobacco use and experienced dramatic and sustained clinical improvement within hours of transdermal nicotine replacement. These preliminary observations suggest that nicotine withdrawal may be an under-recognized cause of delirium in patients with acute brain injury.
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ranking = 1.3449593661179
keywords = brain injury, brain, injury
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5/35. delirium following a switch from cimetidine to famotidine.

    OBJECTIVE: To describe a patient who developed delirium when switched from cimetidine to famotidine. CASE SUMMARY: An 84-year-old Taiwanese woman was hospitalized for tarry stools. Her past medical history revealed only a decrease in renal function. She tolerated both oral and intravenous cimetidine therapy with a daily dose of 400-900 mg intermittently for 20 years. On hospital days 1-3, cimetidine 300 mg was injected intravenously every eight hours without difficulty. Considering the possible existence of a cimetidine-resistant bleeding ulcer, famotidine 20 mg was given twice daily orally on hospital days 4-7 and then injected intravenously. Six days after being switched from cimetidine to famotidine, the woman's mental status deteriorated. A series of clinical tests revealed no apparent causative factors. famotidine was then suspected as a probable cause of her delirium. Discontinuation of the drug resulted in rapid resolution of the patient's delirious status. DICUSSION: famotidine crosses the blood-brain barrier less easily than cimetidine and was taken for a much shorter period in this patient. Thus, we propose that the occurrence of delirium in this patient was associated with famotidine, but not cimetidine, and was idiosyncratic rather than dose related. Furthermore, this case involved an elderly patient with compromised renal function who developed delirium in response to intravenous, but not oral, administration of famotidine. These factors seem to increase the risk for, famotidine-induced delirium. CONCLUSIONS: Clinicians should be aware of the possible occurrence of delirium following a switch from one histamine2-receptor antagonist to another. In rare instances, patients switched to famotidine from cimetidine may experience delirium, particularly elderly patients with poor renal function who receive intravenous famotidine.
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keywords = brain
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6/35. Acute delirium induced by metoprolol.

    OBJECTIVE: To describe a case of delirium associated with use of metoprolol and to analyse 24 such cases including 22 cases reported to Australian Adverse Drug Reaction Advisory Committee and one case previously published (S. Ahmad, Am Fam Physician, 1991;44:1142, 1144). CASE SUMMARY: An 89 year old caucasian man with an acute coronary syndrome who had no psychiatric history and no infections, brain injury, stroke, metabolic nor neoplastic disease developed delirium after two small doses of metoprolol (25 mg). The delirium disappeared within 20 hours after metoprolol was ceased, despite continuing all other medications. THE COMBINED SERIES: Of 24 patients (12 women, mean age 71.8 years), 83% were older than 60 years. The duration of therapy before onset of delirium in 14 (58%) subjects was within one week; 23 of 24 patients were receiving therapeutic amounts of the drug (25-200 mg/day). Clinical features included confusion/disorientation in all subjects, agitation in 13, aggression in 6, visual hallucinations in 7, auditory hallucinations in 1, paranoid delusions in 3, vivid dreams in 2 and language disturbances in 3 persons. bradycardia was reported in 4 cases, hypotension in 2, fatigue/tiredness in 3, Raynaud's phenomenon in 1 and skin rash in 1 patient. DISCUSSION: The mechanism of metoprolol-induced delirium is unclear. It could be due to impairment of hepatic metabolism (especially in the ageing liver) and complex neurotransmitter-related effects on brain beta-adrenoceptors and serotonin (5-HT) receptors. CONCLUSIONS: physicians should be aware that metoprolol, a widely used beta-blocker, may rarely cause delirium, especially in the elderly population.
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ranking = 1.3449593661179
keywords = brain injury, brain, injury
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7/35. Use of atypical anti-psychotics in the management of post-traumatic confusional states in traumatic brain injury.

    The use of atypical anti-psychotics (AAP) in the treatment of organic neuropsychiatric syndromes is little reported. We present a case of post-traumatic delirium with delusions treated with risperidone and discuss the use of AAP's in this situation.
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ranking = 9.1738809443089
keywords = brain injury, traumatic brain injury, traumatic brain, brain, injury
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8/35. loxapine versus olanzapine in the treatment of delirium following traumatic brain injury.

    The use of typical neuroleptics has always been the mainstay of treatment for delirium following traumatic brain injury (TBI). Given the recent application of atypical neuroleptics to various psychiatric conditions formerly treated with typical neuroleptics, one questions whether this new class of drugs is superior to its predecessor in treating delirium post-TBI. We present a case of one patient with TBI-induced delirium where in fact the use of the typical mid-potency neuroleptic, loxapine, appeared to have a better clinical effect over the atypical neuroleptic, olanzapine.
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ranking = 11.467351180386
keywords = brain injury, traumatic brain injury, traumatic brain, brain, injury
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9/35. Acute postpartum mental status change and coma caused by previously undiagnosed ornithine transcarbamylase deficiency.

    BACKGROUND: Acute postpartum mental status change usually represents postpartum blues or depression. Psychosis and coma are rare. This is a case report of a patient with previously undiagnosed ornithine transcarbamylase deficiency presenting as postpartum acute mental status change and coma. CASE: A 28-year-old multipara developed acute mental status change and coma 3 days after cesarean delivery. A metabolic profile and neurologic workup were unrevealing. An electroencephalogram revealed diffusely slow brain activity. She developed hyperammonemia and hyperglutaminemia and was diagnosed with ornithine transcarbamylase deficiency. Her newborn son was diagnosed with ornithine transcarbamylase deficiency on the previous day. Treatment with oral lactulose resulted in normalization of her ammonia level and resolution of her coma within 48 hours. She suffers no long-term sequelae. Dietary avoidance of protein was advised; outpatient treatment with sodium benzoate, sodium phenylacetate, and lactulose was initiated. A pedigree analysis is ongoing. CONCLUSION: ornithine transcarbamylase deficiency should be included in the differential diagnosis of acute postpartum coma. hyperammonemia, hyperglutaminemia, and orotic aciduria are diagnostic, facilitate early treatment, and mitigate the risk of permanent neurologic impairment or death.
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keywords = brain
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10/35. Successful treatment of wernicke encephalopathy in terminally ill cancer patients: report of 3 cases and review of the literature.

    Although wernicke encephalopathy has been reported in the oncological literature, only one terminally ill cancer patient with wernicke encephalopathy has been reported. wernicke encephalopathy, a potentially reversible condition, may be unrecognized in terminally ill cancer patients. In this communication, we report three terminally ill cancer patients who developed wernicke encephalopathy. Early recognition and subsequent treatment resulted in successful palliation of delirium. Two of the three patients did not show the classical triad of Wernicke encephalopathy. Common clinical symptoms were delirium and poor nutritional status. Intravenous thiamine administration dramatically improved the symptoms of delirium in all three patients. In terminally ill cancer patients, clinicians must remain aware of the possibility of wernicke encephalopathy when patients with a poor nutritional status present with unexplained delirium. Early intervention may correct the symptoms and prevent irreversible brain damage and the quality of life for the patient may improve.
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