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Query: UMLS:C0011206 (delirium)
 5,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Four cases on a combination of lithium and thioridazine developed severe neurotoxic symptoms, e.g., delirium, seizures, encephalopathy and grossly abnormal EEG's. All patients had been on lithium without thioridazine prior to and after the neurotoxic episode with no complications or EEG changes. The possible risk of combining lithium and neuroleptics (thioridazine) is discussed and repeated EEGs are recommended as a preventive measure.
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PMID:Neurotoxicity with combined use of lithium and thioridazine. 10 47

The authors studied the traits of psychotic attacks in 40 patients with terminal stages of chronic renal insufficiency. They were expressed in atypical delirious, delirio-amentive and amentive conditions. 8 cases were studied morphologically. The pathological process in the brain was characterized as toxico-dyshomeostatic encephalopathy. The pathogenesis of such disorders is discussed.
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PMID:[Features of episodes of mental disorders in chronic renal insufficiency (clinico-morphologic study)]. 96 Dec 87

The EEG is a useful and, at times, an essential test in the evaluation of delirium. In most patients with delirium, the EEG will show diffuse slowing and thus is helpful in differentiating organic etiologies from functional, psychiatric disorders. The degree of the EEG changes correlates with the severity of the encephalopathy so that the EEG may be used to help monitor therapy. In some delirious patients, the EEG may indicate whether the patient is suffering from focal, rather than global, impairment. Furthermore, the EEG is the only test that can identify an ongoing epileptic state (e.g., nonconvulsive status epilepticus) as being responsible for the clinical picture of confusion. Other electrophysiological tests that may prove helpful in the evaluation of delirium, such as computerized EEG spectral analysis, topographic brain mapping, and sleep studies, are briefly reviewed.
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PMID:Utility of EEG in delirium: past views and current practice. 181 75

A case of sporadic shigellosis is reported. A 30 year old woman, presented neurologic dysfunction, mild watery diarrhea and fever which had started one week before her admission. Abdominal tenderness, confusion, delirium, impairment of orientation and of recent memory were found. Abnormal motor activity with rigidity, tremors, myoclonus around the mouth also existed. There were neither focal signs nor signs of meningeal irritation. Computed tomography and nuclear magnetic resonance of the brain were normal. Laboratory analyses did not explain the anomalies. Several deep ulcers were disclosed by colonoscopy and a S. flexneri was isolated from the material extracted by endoscopy. Nonspecific colitis was informed by pathology. The patient was treated with 400 mg ciprofloxacin for 14 days, with improvement of the clinical picture. The most prominent aspect in this case was the clinical presentation with predominant neurologic symptoms creating the impression of a primary nervous system disease. Admission diagnosis was viral encephalitis. We believe that all of the anomalies present in our patient, the diarrhea and encephalopathy, were produced by the same etiologic agent, S. flexneri and by its toxins.
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PMID:[Encephalopathy in an adult with Shigella]. 192 94

Delayed neurological deterioration following anoxia is known to result from carbon monoxide exposure. However, it may also occur with anoxia of other types as well. The present report describes a case of delayed postanoxic encephalopathy with bilateral striatal lesions demonstrated by magnetic resonance imaging. A 27-year-old man exhibited anoxic anoxia caused by upper airway obstruction following general anesthesia for shoulder fracture surgery. Initially he was delirious and markedly excited for one day and became apparently normal for the following three days. Then he relapsed into delayed neurological deterioration with speech and gait disturbance, clumsiness of hand, pyramidal signs and metamorphopsia. Thereafter, he became bed-ridden and fell into semicomatose state with marked motor restlessness, involuntary movement of the tongue and decorticate posture. Twenty-five days later he had a second recovery period after hyperbaric oxygenation that lead to the sequelae with speech and motor disturbances and mild mental changes. I examined the present case as an expert witness in a civil suit eleven years after initial anoxia. The patient showed slight intellectual impairment and personality change. Impairment in figure-ground differentiation and disorders of spatial thought were also observed. Neurological examination revealed anisocoria, dysarthria with acquired stuttering, disturbances of fractionated movement of fingers, writer's cramp and Babinski's sign bilaterally. Postural dystonia of both hands and fingers, rigidity and spasticity of all extremities were also present. Magnetic resonance imaging (MRI) showed bilateral lesions of the corpus striatum, especially of the putamen. Some portion of the caudate nucleus was also involved. Cerebral cortices and white matter were slightly atrophic. From the above clinical course and neurological findings, we diagnosed the present case as delayed postanoxic encephalopathy. Ginsberg (1979) noted that in cases of anoxia not related to carbon monoxide, diffuse demyelinative changes of cerebral hemispheral white matter tended to be associated with relapsing clinical course, and gray matter injury was only seen in a few cases. MRI findings in the present case suggest that main site of the lesion to be in gray matter of the corpus striatum. In this respect, the present case is considered to be noteworthy.
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PMID:[A case of delayed postanoxic encephalopathy with bilateral lesions of the corpus striatum]. 281 6

A case is reported in which tocainide, a relatively new cardiac antiarrhythmic for oral use, is believed to have caused a delirium. The patient had been admitted to a coronary intensive care unit for the treatment of ventricular arrhythmia and had developed confusion, impairment in concentration and severe anxiety. Her EEG was compatible with metabolic encephalopathy. The clinical picture varied with the use of tocainide so closely that it appeared to be the most likely cause of the delirium. Other factors were taken into consideration but did not seem to adequately disprove this impression. Tocainide has been known to cause minor, transient and treatable side effects in the form of gastrointestinal and central nervous symptoms--mainly nausea, tremor and dizziness. There have also been three case reports of paranoid psychoses. It is suggested that psychiatrists be aware of the above complications as they may have occasion to see patients taking tocainide, especially in consultation-liaison work. A table with the more common side effects and their frequencies is included.
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PMID:Mental changes associated with tocainide, a new antiarrhythmic. 310 61

Three cases of leucoencephalopathy induced by carmofur (1-hexylcarbamoyl-5-fluorouracil), an antineoplastic derivative of 5-fluorouracil are reported and the literature is reviewed. Initial symptoms were unsteady gait and dementia developing several weeks or months after carmofur had been started. Symptoms increased gradually even after stopping the drug. Severe encephalopathy with confusion, delirium or coma appeared frequently. Symptoms were usually reversible but death occasionally occurred. The EEG showed marked slowing. Computed tomography of the brains of severely intoxicated patients showed marked hypodensity of the entire cerebral white matter. Carmofur must be discontinued immediately if any psychomotor symptoms develop.
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PMID:Subacute leucoencephalopathy induced by carmofur, a 5-fluorouracil derivative. 330 92

A 50-year-old chemical engineer, routinely screened for occupational arsenic exposure, was admitted with a delirium for which no known etiology was found. Elevated levels of arsenic were found in the urine and hair. The patient received chelation treatment with British anti-Lewisite; substantial amounts of arsenic were excreted and the toxic encephalopathy improved gradually over the 8-month follow-up period. The patient was tested at 6 weeks, 4 months, and 8 months postdelirium with a battery of neuropsychological tasks. The pattern of results showed verbal learning and memory to be severely impaired while tests of general intellectual abilities and language remained unaffected. Follow-up examinations with no subsequent reexposure revealed improvements on specific cognitive tasks. It is unclear whether recovery of cortical functions occurred or if compensatory strategies were developed. It is proposed that a subacute exposure to arsenic may have contributed to the neuropsychological deficits.
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PMID:Neuropsychological impairment following inorganic arsenic exposure. 361 24

Irrespective of the etiology, a water and electrolyte imbalance provoking a hypo- or hyperosmolar state causes metabolic encephalopathy, as may occur with any metabolic disturbance. The pathophysiology of metabolic encephalopathy relies on a diffuse neuronal dysfunction which occasionally shows a focal maximum. To the clinician it presents in the form of nonspecific symptoms or signs, such as altered level of alertness or awareness of the environment, or impaired attention, cognition or orientation. When the onset of hypo- or hyperosmolality is rapid, delirium may develop or the level of consciousness can decrease to the point of coma. Myoclonic jerks, gait disturbance and focal or generalized fits are additional nonspecific signs. When the water and electrolyte imbalance coincides with or is caused by brain disease, the signs of the two conditions are added. On the other hand, complicating hemorrhages, sinus thrombosis, or brainstem herniation or compression may be taken for a primary structural brain lesion, and the water and electrolyte imbalance may easily be overlooked. Pathophysiology, symptoms and signs, and therapy of hypo- and hyperosmolar states are discussed. Central pontine myelinolysis is considered separately.
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PMID:[Neurologic manifestations of osmolality disorders]. 389 13

The acquired immunodeficiency syndrome (AIDS) and its related conditions are a public health problem of unprecedented proportions due to the debilitating and fatal nature of the disease, the sociocultural implications related to contagion, and its initial appearance in certain socially stigmatized groups. The ability of patients to tolerate the consequences of the disease depends on their psychological ability to cope based on emotional strength and the availability of social support. The psychological and social impact of AIDS may result in psychiatric symptoms similar to those seen in other life-threatening diseases, including anxiety, depression, and delirium. Neurologic complications are frequent, the commonest being an encephalopathy and dementia that is poorly understood. It is difficult in the early stages of AIDS to separate reactive depression and psychomotor retardation from symptoms associated with central nervous system complications. Guidelines are needed to manage the psychological problems posed by AIDS and its related conditions.
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PMID:The psychosocial and neuropsychiatric sequelae of the acquired immunodeficiency syndrome and related disorders. 405 51


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