Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011206 (delirium)
 5,996 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thallium poisoning is one of the most complex and serious toxicities known to man. The symptomatology of its toxicity is usually nonspecific due to the multi-organ involvement. The initial symptoms of thallium poisoning may include fever, gastrointestinal problems, delirium, convulsions and coma. Symptoms may appear rapidly, but more commonly the acute toxicity subsides to be replaced by a gradual development of mild gastrointestinal disturbances, polyneuritis, encephalopathy, tachycardia, skin eruptions, stomatitis, atrophic changes of the skin, nail changes (Mee's lines), and skin hyperesthesia (mainly in the soles of the feet and the tibia). Degenerative changes of the heart, liver and kidney, subarchanoid hemorrhage, bone marrow depression, and increased radiopacity of the liver may also occur. Development of psychotic behavior with hallucinations and dementia has also been reported. In humans the most characteristic sign of thallium toxicity is alopecia which usually appears in cases when death is delayed for 15-20 days. Other signs and symptoms may develop at any stage of toxicity. The current therapy for thallium poisoning is the use of prussian blue and potassium chloride. Potassium therapy is probably the single most effective agent in the treatment of thallium poisoning. Further research, however, is needed to find an optimal antidote for thallium.
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PMID:Thallium poisoning: a review. 633 55

Among patients with renal failure, there have been impressive modifications of both the duration and quality of life as a result of dialysis, renal transplantation, and improved medical management. However, patients who have renal failure continue to manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. Even after the institution of otherwise adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous system dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. The central nervous system disorders of both untreated renal failure and that persisting despite dialysis are referred to as uremic encephalopathy. The dialytic treatment of end stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system: Dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. This disease also appears to be a complication of the therapy for renal failure.
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PMID:Pathogenesis of dialysis encephalopathy. 636 3

The alkali metals from the Group IA of the periodic table (lithium, sodium, potassium, rubidium, cesium and francium) are reviewed. The neuropsychiatric aspects of alkali metal deficiencies and excesses (intoxications) are described. Emphasis was placed on lithium due to its clinical uses. The signs and symptoms of these conditions are characterized by features of an organic brain syndrome with delirium and encephalopathy prevailing. There are no clinically distinctive features that could be reliably used for diagnoses. Sodium and potassium are two essential alkali metals in man. Lithium is used as therapeutic agent in bipolar affective disorders. Rubidium has been investigated for its antidepressant effect in a group of psychiatric disorders. Cesium is under laboratory investigation for its role in carcinogenesis and in depressive illness. Very little is known of francium due to its great instability for experimental study.
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PMID:Neuropsychiatric manifestations of alkali metal deficiency and excess. 639 36

We reviewed 1,669 patients who survived coronary artery bypass graft surgery between 1969 and 1981. A total of 75 cerebral complications were identified, including (1) altered mental state, (2) stroke, and (3) seizure in 64 patients (3.8%). Altered mental state (delirium, hypoxic-metabolic encephalopathy) occurred in 57 (3.4%). Postoperative arrhythmias were associated with an increased risk of altered mental state. Cerebral infarction occurred in 13 (0.8%). Patients who suffered stroke had a higher occurrence of carotid bruits and history of peripheral vascular disease. Seizures occurred in five patients (0.3%). Mortality in patients with a neurologic complication was 29%.
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PMID:Natural history of cerebral complications of coronary artery bypass graft surgery. 660 94

Pathomorphologic examination of the brain in alcoholic delirium was carried out. Comparison was made between the changes in the brain of patients who died at the height of delirium and those of patients who died suddenly in the postdelirium state. The pathomorphologic picture of the brain in alcoholic delirium may be defined as chronic toxico-dyscirculatory encephalopathy aggravated by acute toxic and dyshemic changes. The latter were largely attributed to the delirium state per se. The characteristic features of the cases studied included considerable depletion of the cortical cells, chronic dystrophic changes in the neurons and gliocytes, and also chronic impairments of vascular wall permeability aggravated by marked acute pathologic phenomena in the microcirculatory vessels.
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PMID:[Pathomorphologic changes in the brain in alcoholic delirium]. 662 24

The authors studied the brain and heart of 40 patients (30 males and 10 females) who were hospitalized with the clinical diagnosis of alcoholic delirium, Gaye-Wernike's encephalopathy, and acute alcoholic intoxication due to chronic alcoholism. The morphological alterations in the brain and heart were as follows: compromised vascular permeability, dystrophic changes in the neurons and cardiomyocytes, proliferative reaction of microgliocytes and the development of small cardiosclerosis. Such disorders can be defined as an exacerbation of chronic alcoholic encephalopathy and cardiomyodystrophy. Alcoholic damage to the heart seems to be one of the additional factors that disrupt cerebral hemodynamics which results in hypoxia of the cerebral tissue and is accompanied by impairment of the central regulation of cardiac activity and progression of cerebral changes, i. e. the pathological process develops according to the vicious circle principle.
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PMID:[Morphology of the brain and heart in alcoholic psychoses]. 662 25

Patients with renal failure may manifest a variety of neurologic disorders. Patients with chronic renal failure who have not yet received dialytic therapy may develop a symptom complex progressing from mild sensorial clouding to delirium and coma, with tremor, asterixis, multifocal myoclonus, and seizures. After the institution of adequate maintenance dialysis therapy, patients may continue to be afflicted with more subtle nervous dysfunction, including impaired mentation, generalized weakness, and peripheral neuropathy. These central nervous system disorders are referred to as uremic encephalopathy. The dialytic treatment of end-stage renal disease has itself been associated with the emergence of two distinct, new disorders of the central nervous system; dialysis dysequilibrium and dialysis dementia. The dialysis disequilibrium syndrome consists of headache, nausea, muscle cramps, obtundation, and seizures, and is a consequence of the initiation of dialysis therapy in some patients. Dialysis dementia is a progressive, generally fatal encephalopathy which affects patients on chronic hemodialysis. There are at least three different forms of dialysis encephalopathy: sporadic, epidemic; and that associated with renal disease in children. In addition to the foregoing neurologic diseases which are specifically related to uremia and/or dialysis, a number of other neurologic disorders occur with increased frequency in patients with end-stage renal disease on chronic hemodialysis. These include subdural hematoma, electrolyte disorders, vitamin deficiencies, drug intoxication, hypertensive encephalopathy, and acute trace element intoxication. Renal transplantation is associated with a variety of central nervous system infections, reticulum cell sarcoma, and central pontine myelinosis. The present manuscript will review the clinical, structural, and biochemical components of those neurologic disorders which are peculiar to the uremic state and its treatment with dialysis.
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PMID:Uremic encephalopathies: clinical, biochemical, and experimental features. 675 30

The diagnosis in patients who have psychiatric or neurologic manifestations as the result of toxins of great variety is not particularly difficult and usually can be achieved with a discerning history and physical examination. The EEG is a useful but not a necessary adjunct. The most difficult of these patients to sort out etiologically are those brought into the hospital, without history, in a flaccid coma or wild delirium or with mild or subtle delirium. The dementias are the main differential diagnosis. The hallmarks of metabolic encephalopathy are reduced awareness and fluctuating attention with defects in orientatioN, interpretation, memory, retention, and recall and with hesitant and clumsy motor performance. Prompt treatment is necessary to preserve the integrity of the master organ, the brain. Delay in treatment may convert metabolic encephalopathy into permanent dementia.
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PMID:Metabolic encephalopathy: neurologic and psychiatric considerations. 692 51

Typical clinical signs and symptoms of bismuth intoxication are illustrated in a cases of a 45-year-old woman. Initially psychasthenia appears followed by acute delirium with ataxia, myoclonic jerks and occasionally coma. If patients survive the acute phase they recover only gradually following discontinuation of bismuth medication. In cases of extreme intoxication, permanent memory deficits may occur. Etiology, pathogenesis, laboratory findings, differential diagnosis and therapy of this rare iatrogenic encephalopathy are discussed.
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PMID:[Acute delirium in bismuth poisoning]. 713 55

A 55-year-old chemical laboratory technician developed mydriasis and ocular hypertension, which lasted for 6 weeks, after synthesizing several kilograms of a scopolamine-related test agent with anticholinergic action and then decanting a powdery intermediary substance, the dust of which he may have inhaled. Six weeks later he suddenly had symptoms of an acute intoxication while synthesizing a scopolamine-related substance. The anticholinergic delirium regressed completely within one day requiring no treatment. But subsequently he developed symptoms of a toxic encephalopathy. This only partially regressed over the following 3 years. Its probable cause is thought to have been either the manifestation of an already existing organic cerebral psychiatric syndrome or an as yet unknown effect of the test substance.
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PMID:[Encephalopathy following poisoning with an anticholinergic agent]. 773 40


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