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 21,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fourteen patients with AIDS were treated for 23 neurologic complications: four episodes of acute meningoencephalitis; eight episodes of subacute encephalopathy; two cases of progressive multifocal leukoencephalopathy; and nine cases of polyneuropathy. Nine patients were treated with 9-(1,3-dihydroxy-2-propoxymethyl)guanine (DHPG), one with 3'-azido-3'-deoxythymidine (AZT), and four initially with DHPG directed against cytomegalovirus (CMV) retinitis or encephalitis and subsequently with AZT against human immunodeficiency virus (HIV) encephalopathy. CMV retinitis was a helpful clinical observation indicating neurologic involvement. DHPG produced improvement in two of three cases of acute meningoencephalitis but was ineffective in cases of subacute encephalopathy or neuropathy. AZT therapy resulted in resolution in both of the two treated cases of acute confusional state and in two of the four treated cases of polyradiculoneuropathy with paraparesis but was ineffective in the late stage of subacute encephalopathy. These results suggest that CMV is important in some cases of acute meningoencephalitis, whereas HIV is a dominant pathogen in subacute dementia and polyneuropathy in patients with AIDS. DHPG may be beneficial in the former, whereas AZT appears to be effective in the latter complications.
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PMID:Responses of neurologic complications of AIDS to 3'-azido-3'-deoxythymidine and 9-(1,3-dihydroxy-2-propoxymethyl) guanine. I. Clinical features. 316 17

Blunt trauma to the head results in acceleration of the brain within the skull. This takes 2 forms: linear or translational acceleration which produces focal lesions, and rotational acceleration which results in 'sheering stresses' with stretching of nerves and bridging veins. Deceleration of the brain within the skull occurs when the head strikes a stationary object (e.g. floor, ring post). Cerebrovascular events are not infrequently encountered. The most common vascular sequalae is the subdural haematoma, which is also the most frequent cause of death in boxers. Epidural bleeds rare, and are generally due to deceleration of the brain. Subarachnoid bleeds have been rarely reported, but, like intraparenchymal haemorrhages, they do occur. Sudden flexion/extension of the neck is suggested as the mechanism of the occasional brainstem haemorrhage reported in boxing. Thrombosis of the internal carotid artery can occur secondary to direct blows to the neck or stretching of the contralateral carotid artery. The best known sequalae of boxing is traumatic encephalopathy--the 'punch drunk' syndrome. This is most common in second-rate and slugging type fighters. Severity correlates with the length of a boxer's career and total number of bouts, with an incidence of approximately 18%. Three stages of clinical deterioration are seen, the encephalopathy may be progressive or may remain clinically stable at any level. The first stage consists of affective disturbances with psychiatric symptoms being most marked. During the second stage an accentuation of the psychiatric symptoms occurs and signs/symptoms of Parkinsonism develop. The final stage consists of a decrease in general cognitive function together with pyramidal tract disease. Generally 2 to 3 years elapse between the first and final stages. Neuropathological studies reveal abnormalities of the septum pellucidum, scarring of the cerebellar and cerebral cortices, and loss of pyramidal neurons in the substantia nigra with neurofibrillary tangles in the absence of senile plaques. A 'groggy state' can occur in some fighters with confusion, impaired active attention and alteration of consciousness. During this period the boxer is at greater risk to suffer brain injury as defensive reflexes are frequently lost. Other neurological syndromes have been reported in addition to the 'groggy state'. These include a midbrain syndrome, headaches and cervical spinal injuries. Additionally, boxing appears to be a significant risk factor for the development of meningiomas.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Neurological sequelae of boxing. 329 90

We describe severe central nervous system (CNS) toxicity, manifested by confusion, cortical blindness, quadriplegia, seizures, and coma, associated with cyclosporine treatment in three patients undergoing liver transplantation. CT and magnetic resonance studies disclosed a severe, diffuse disorder of the white matter. All side effects and radiographic findings were reversed with discontinuation or a reduction in the dose of cyclosporine. We also observed an inverse association between CNS side effects and total serum cholesterol levels after transplantation. A retrospective analysis of 54 liver transplantations performed in 48 patients revealed that 13 patients had symptoms of CNS toxicity associated with the use of cyclosporine. These patients' total serum cholesterol levels in the first week after transplantation were reduced as compared with those in patients without symptoms (mean +/- SE, 94 +/- 4 mg per deciliter vs. 132 +/- 6, or 2.44 +/- 0.10 mmol per liter vs. 3.43 +/- 0.16). We conclude that cyclosporine therapy for immunosuppression in liver transplantation may cause a syndrome of encephalopathy, seizures, and white-matter changes and that this is most likely to occur in patients with low total serum cholesterol levels after transplantation.
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PMID:Central nervous system toxicity after liver transplantation. The role of cyclosporine and cholesterol. 330 86

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 retrospective clinical study of 22 heavy alcohol drinkers is reported in which postmortem study showed diffuse chromatolysis of neurons identical to that found in neurological pellagra, associated in 13 cases with Marchiafava-Bignami disease and/or Wernicke-Korsakoff disease. The clinical features included confusion and/or clouding of consciousness, marked oppositional hypertonus ('gegenhalten') and myoclonus. Because of the frequent coexistence of other alcoholic encephalopathies in the same patient, alcoholic pellagra was often unrecognized. Fifteen patients received thiamine and pyridoxine therapy without niacin. It appeared to aggravate the neurological state or to trigger the development of alcoholic pellagra encephalopathy in 9 cases. The relationship between pellagra occurring during thiamine and pyridoxine therapy and 'nicotinic acid deficiency' is discussed. Multiple vitamin therapy should be given in the treatment of undiagnosed encephalopathies in alcoholic patients.
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PMID:The clinical spectrum of alcoholic pellagra encephalopathy. A retrospective analysis of 22 cases studied pathologically. 340 85

Recognized risk factors for metrizamide myelography are seizure disorder, seizure-threshold-lowering drugs, dehydration, and possibly age. After observing serious neurologic complications in diabetic patients after routine metrizamide myelography, a retrospective study was conducted to determine if diabetes should be considered another independent and important risk factor. Forty-one diabetic patients who had lumbar metrizamide myelograms were compared with a control group of 110 nondiabetic patients. A significantly higher incidence was found of severe vomiting (15% vs. 3%, p less than 0.01) and neurologic complications (20% vs. 2%, p less than 0.001) in the diabetic population. Neurologic complications included one case each of seizure, severe encephalopathy, auditory and visual hallucinations, and prolonged somnolence and four cases of confusion-anxiety. Four of the diabetic patients had major transient elevations of blood pressure. These findings suggest that diabetics are a high-risk population for metrizamide myelography. The dose of metrizamide should be minimized, whenever possible. The new nonionic myelographic agents may prove to be safer in this population, but caution and careful follow-up should be exercised in the initial trials with these patients.
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PMID:Neurologic complications in diabetics after metrizamide lumbar myelography. 348

Two cases of phenytoin toxicity in patients with chronic liver disease who were taking 300 mg phenytoin daily are described. Each patient developed encephalopathy, characterized by confusion, disturbed conscious state, asterixis, and nystagmus, which was resistant to treatment with protein restriction, lactulose, and neomycin, but responsive to withdrawal of phenytoin. We suggest that the phenytoin did not precipitate hepatic encephalopathy, but caused an encephalopathy that mimicked it. We recommend that phenytoin be used cautiously in patients with liver disease, and that the drug's unbound serum level be measured if encephalopathy occurs.
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PMID:Phenytoin toxicity and hepatic encephalopathy: simulation or stimulation? 361 89

In a prospective study from 1972 to 1982, 38 patients with bleeding oesophageal varices and relatively good liver function were treated by semi-elective or emergent shunt 2-4 weeks after admission. There were no deaths within 3 months of surgery. This constituted 30% of the total 125 patients admitted with bleeding varices during that period. No referred case for treatment of portal hypertension was included in this study. The procedures performed were end-to-side portacaval shunt in 30 cases, lieno renal shunt in seven cases and interposition mesenterico-caval shunt in one case. All patients were admitted to a special unit with a two stage policy of management. Immediate endoscopic diagnosis and balloon tamponade in those with continued bleeding was followed by shunt in selected cases. Follow-up of the 38 patients showed a cumulative survival at 1 year of 89%, at 3 years of 75% and 5 years of 65%. In four cases (13%) a clinical diagnosis of portal systemic encephalopathy was made, all were controlled by medical management. In four of ten follow-up deaths, liver failure was the cause, in none of these cases was encephalopathy a problem. It is concluded that with a policy of early diagnosis and control of haemorrhage, 30% of a typical series of prospectively studied patients admitted with bleeding varices can be treated without mortality by definitive surgery. There was low incidence of encephalopathy and no cases of incapacitating mental confusion. Centralization of treatment and prospective study is essential for the implementation of such a policy of management.
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PMID:A ten year prospective experience with semi-elective shunt in selected patients for bleeding oesophageal varices. 387 23

In summary, then, it can be said that hepatic encephalopathy is a process caused by the underlying inability of the certain products to be metabolized in a damaged liver. These products lead to altered neurotransmission with the resulting neurologic finding of altered affect, confusion, somnolence, or coma. Augmentation of the neurologic deficit occurs when the patient suffers additional metabolic insults. Treatment of the patient with hepatic encephalopathy requires careful monitoring and aggressive therapy for those factors known to precipitate encephalopathy, as well as treatment of the underlying hepatic process and encephalopathy.
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PMID:Hepatic encephalopathy. 391 82

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


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