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 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although organic solvents are essential components of an industrial economy, they are not used without risk. The relationship between excessive exposure to organic solvents and subsequent development of chronic encephalopathy has been recognized for nearly 100 years. Fifteen industrial painters who underwent evaluation in an occupational health clinic for symptoms that they related to their work were found to have a high prevalence of neurasthenic symptoms, most frequently, memory loss and personality change. Although neurologic and screening laboratory examinations showed no consistent abnormalities, psychological tests documented poor short-term memory and an array of neuropsychologic deficits. Personality profiles revealed depression, anxiety, and preoccupation with somatic concerns. These findings agree well with previous reports of "chronic painter's syndrome." Heightened awareness among industrial physicians and prospective studies to evaluate existing threshold limit values and personal protective equipment requirements are indicated.
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PMID:Organic solvent-induced encephalopathy in industrial painters. 395 Jul 85

A survey of 67 pregnancies in 51 professional women (physicians, psychologists, nurses, administrators, etc.) revealed the occurrence of symptoms of cognitive dysfunction such as forgetfulness, disorientation, confusion and reading difficulties in 28 pregnancies occurring in 21 women. These were unrelated to such factors as age of delivery, percentage weight gain, the baby's sex or birth weight, alcohol consumption, smoking, a history of migraine or allergy or other symptoms occurring during pregnancy such as sleepiness and lack of concentration, irritability, loss of interest in job or nightmares. Nor was there any correlation with hypertension, proteinuria, glycosuria, ketonuria, anemia, or morning sickness. Furthermore, these cognitive disturbances were not related to depression or sleep deprivation. Despite these symptoms, none of the women suffering from them were forced to interrupt their professional activities during pregnancy. The syndrome of benign encephalopathy of pregnancy should be recognized so that simple precautions can be taken to prevent any interference with professional or other activities. The etiology of the syndrome is unknown.
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PMID:Benign encephalopathy of pregnancy. Preliminary clinical observations. 395 58

A 46 year old woman suffered a post-operative cardiac arrest associated with prolonged depression of oxygenation and respiration. She made a good initial recovery but one year later insidiously developed symptoms of widespread central nervous system damage compatible with a delayed post-hypoxic encephalopathy. This case is unusual in the length of time between the hypoxic insult and the later deterioration and also illustrates other atypical features of a delayed post-hypoxic syndrome.
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PMID:Delayed encephalopathy following cardiac arrest. 398 61

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

Portasystemic encephalopathy has been a major deterent to the utilization of total or non-selective shunts. A procedure to determine the maximum rate of urea synthesis (MRUS) has been developed and a depression in the ability to synthesize urea has been shown to correlate closely with the development of encephalopathy. Utilizing this procedure and a modified ammonium tolerance curve, a controlled comparison was instituted between selective and non-selective shunts. Following a non-selective or total shunt, there was a definite deterioration in both the MRUS and the ammonium chloride tolerance curve which was accompanied by a high rate of clinical encephalopathy. In marked contrast, the selective shunt, which maintains portal venous perfusion of the liver, showed little or no change in the MRUS and the ammonium chloride tolerance curve following the selective shunt and there was a very low incidence of encephalopathy. The difference between the non-selective and selective shunt in maintenance of urea synthesis, metabolism of ammonium chloride, and the development of clinical encephalopathy show the selective shunt procedure to be definitively superior in this regard.
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PMID:The metabolic basis of portasystemic encephalopathy and the effect of selective vs nonselective shunts. 441 59

Thiamine-deficient encephalopathy is characterized by morphologic lesions in the brainstem and less extensively in the cerebellum, but the early neurologic signs reverse rapidly and fully with thiamine, indicating a metabolic disorder. The suggested causal mechanisms of the encephalopathy involve two thiamine-dependent enzymes: (a) impairment of pyruvate decarboxylase activity with decreased cerebral energy (ATP) synthesis, and (b) reduction of transketolase activity with possible impairment of the hexose monophosphate shunt and subsequent decrease in NADPH formation. The latter may be important in maintaining glutathione in a reduced form (GSH), which apparently functions by keeping enzymes in a reduced (active) conformation. To examine some of these postulated mechanisms, in this study we measured pyruvate decarboxylase and transketolase activity, lactate, ATP and GSH levels in the cerebral cortex, cerebellum, and brainstem, and thiamine concentration in whole brain of rats with diet-induced low thiamine encephalopathy. Pair-fed and normally fed asymptomatic control animals were similarly investigated. To assess the functional importance of some of our results, we repeated the studies in rats, immediately (16-36 hr) after reversal of the neurological signs with thiamine administration. THE DATA OBTAINED LED TO THE FOLLOWING CONCLUSIONS: (a) Brain contains a substantial reserve of thiamine in that thiamine level has to fall to below 20% of normal before the onset of overt encephalopathy and an increase in brain thiamine to only 26% of normal results in rapid reversal of neurologic signs. (b) Both cerebral transketolase and pyruvate decarboxylase activities are impaired in low thiamine encephalopathy and the abnormality in the pyruvate decarboxylase is reflected in a rise in brain lactate. These biochemical abnormalities occur primarily in the brainstem and cerebellum, the sites of the morphologic changes. (c) Although the fall in cerebral transketolase is about twofold greater than that of pyruvate decarboxylase activity during encephalopathy, both enzymes rise on reversal of neurologic signs and the degree of the transketolase rise is slight. Accordingly, this study cannot ascertain the relative functional importance of these two pathways in the induction of the encephalopathy. The data suggest, however, that the depression of transketolase is not functionally important per se, but may only be an index of some other critical aspect of the hexose monophosphate shunt. (d) The normal cerebral ATP concentration and small GSH fall during encephalopathy, with little GSH rise on reversal of neurologic signs, suggest that a depletion of neither substance is instrumental in inducing thiamine-deficient encephalopathy.
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PMID:Encephalopathy of thiamine deficieny: studies of intracerebral mechanisms. 567 22

Twenty-five patients with various forms of dyskinesia were given tiapride for three months. Maximal dosage was 900 mg per day. A double-blind trial of tiapride versus placebo showed significantly better results in the group given tiapride. The forms of dyskinesia which responded best to tiapride were the following: iatrogenic dyskinesia, tics (Gilles de la Tourette syndrome), and chronic chorea (Huntington disease). Patients with complex dyskinesia resulting from neonatal encephalopathy or vascular disease were not improved. The protocol used in l-dopa-induced dyskinesia is described. Changes in dyskinesia and "on-off" effect following variations in tiapride and l-dopa dosage are detailed. An unequivocal, although minor, tiapride-induced parkinson syndrome was recorded in a few patients. No instances of tiapride-induced dyskinesia or akathisia were seen. The other side-effects were either psychic (depression, drowsiness, agitation) or endocrinologic (menstrual disorders, overeating, galactorrhea).
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PMID:[Clinical trial of tiapride in patients with dyskinesia (author's transl)]. 628 45

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

Nine children treated for acute leukemia or lymphosarcoma developed subacute encephalopathy starting with listlessness, depression and impairment of speech. Walking difficulties, ataxia, spasticity and sphincter disorders developed later. Transient intracranial hypertension and abnormal movements respectively developed in two patients. EEG frontal slow waves, raised CSF protein, abnormal white matter radioisotope uptake and CT scan hypodensity with patchy contrast enhancement were evident at the onset. Later, dilated ventricles and calcification appeared in the younger patients. Post-mortem neuropathological studies of three patients disclosed predominantly perivascular myelin loss in areas of white matter necrosis, abnormalities of small vessels and numerous axonal swellings. The spinal cord showed secondary degeneration of the corticospinal tracts. Analysis of the aetiological factors in this series points to the prevailing danger of cranial radiotherapy, probably increased by the young age of patients and by associated drug administration.
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PMID:Necrotising leukoencephalopathy complicating treatment of childhood leukaemia. 669 15

Reanimatology is a science aimed at preventing central nervous system (CNS) destruction and completely restoring function after terminal states and clinical death. The most important present trends in reanimatology are the study of the limits of ischemic tolerance by cerebral cortical neurons and investigations into the basic mechanisms of pathology and viability during and after hypoxia. After terminal states there are changes in the content, electrophoretic patterns and physico-chemical properties of brain proteins, and in lysosomal and cytoplasmic hydrolase activities. Cell membrane permeability is increased and brain ATP content is decreased. At 14 to 21 days after resuscitation, brain RNA and later DNA levels are reduced, reflecting posthypoxic cerebral dysfunction. Guidelines for the prevention and therapy of postresuscitation encephalopathy are presented. There seem to be specific indications and contraindications for brain stimulation versus depression during recovery. There are advanced methods for treating clinical death. Treatments of postresuscitation pulmonary, cardiovascular, and renal complications using hemodialysis and blood detoxification appear promising.
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PMID:Reanimatology and its urgent problems. 674 8


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