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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lead encephalopathy was produced in neonatal Long-Evans rats by administering daily doses of lead acetate (600 milligrams of lead acetate/kilogram of body weight) through an esophageal catheter. Experimental rat pups showed behavioral changes, failed to gain weight at the same rate as controls, developed a paraplegia and died by 15 days of age. Lead analysis showed very high blood and tissue lead levels. Sequential histopathologic changes were studied in the cerebellum with observations also made in the choroid plexus, cerebral cortex and corpus striatum. Emphasis was placed on the cerebellum because this region of the brain was most severely altered. Petechial hemorrhages were evident in the cerebellum at three days and two days later the hemorrhagic lesions were almost confluent. The molecular and Purkinje cell layers were most extensively damaged by the hemorrhage. At eight, nine and ten days hemorrhages were fewer and massive amounts of edema fluid accumulated in the internal granular layer. Vascular anomalies of developing lead poisoned rats were examined with electron microscopy and with Golgi preparations. The evidence indicates that growing capillaries are the primary structure of the central nervous system (CNS) damaged by lead intoxication. The endothelial bud (or angioblast) appears to be a structure sensitive to lead poisoning and the encephalopathy probably results from the death of many of these buds.
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PMID:Lead encephalopathy in neonatal Long-Evans rats: morphologic studies. 83 16

The reduction of working ability, because of disease, was considered in 1,053 subjects. 21 groups of maladies were found; the neurological disease and mental retardation (MR) caused various degrees of working inability in 416 subjects, i.e. in the 39.51% of the examined population; orthopaedic changes affected the 15.57% of the patients; psychic disorders determined some inability in 8.93% of the persons. The subjects unable to work receive, by Law, an economic help. This study was limited to neurological patients and to subjects mentally retarded. The working ability was reduced by 5 types of disturbances: neuromotor pathology, mental retardation, mental deterioration and dementia, epilepsy, other neurological diseases. The neuromotor pathology affected 163 subjects; the types of symptomatology: hemiplegia; it was found in 71 patients; 62 times it was the result of cerebrovascular disease; in 4 patients it was caused by a hypoxic-ischaemic pre-perinatal encephalopathy. 43 patients affected by cerebrovascular disease lost their personal autonomy, i.e. they could no longer do the activities of daily living (ADL); 7 patients lost their working ability; 12 subjects kept some ability to work. The hemiplegias which struck after 50 years of age were caused by cerebrovascular disease; paraplegia: 28 paraplegic patients have been seen; the aetiology was: poliomyelitis in 8 subjects; MS in 5 patients; ALS in 2 patients; in 13 patients the aetiology was unknown. 6 patients resulted unable to work; 8 persons kept some working ability; 14 patients lost the ability to do the ADL; tetraplegia, or double/bilateral hemiplegia, was found in 20 patients; the aetiology: poliomyelitis in 4 patients; pre-perinatal hypoxic ischaemic encephalopathy in 4 patients; 3 patients of MS; lesion of the cervical spinal cord because of breech delivery in 2 patients; the aetiology was not known in 7 persons. The ability to do the ADL was lost in 17 patients; 3 subjects kept some working ability. Double or bilateral hemiplegia (Little disease) was the model of neuromotor deficit subsequent natal encephalopathy (Infantile Cerebral Palsy, PCI); brachial plexus paralysis was only found from obstetrical (i.e. natal) origin; poliomyelitis and PKU resulted prevented as of 10 years. Mental Retardation (MR) was considered a borderline pathology between neurology and psychiatry; it included 162 subjects: in patients with severe MR a pre-perinatal hypoxic-ischaemic encephalopathy was found in 40.4% of the cases; in patients affected by moderate or light MR the same encephalopathy was found in the 11.3% of the subjects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Neurologic diseases, mental retardation and reduction in work capacity]. 293 89

Inorganic lead produces cerebral dysfunction and clinically definable encephalopathies in man. To date there have been few studies on the biochemical changes in brain following exposure to inorganic lead. Studies correlating toxicity with behavioral and brain neurochemical changes following lead exposure have been hindered because adult laboratory animals are resistant to the central nervous system effects of lead poisoning. Such studies have been impeded by lack of suitable experimental models until Pentschew and Garro showed that brain lesions develop in neonatal rats when a pregnant rat newly delivered of her litter is placed on a 4% lead carbonate containing diet. Lead passes into the developing sucklings via maternal milk. Lead-poisoned new-borns have pronounced retardation of growth and during the fourth week of ilfe develop the severe signs of lead encephalopathy, namely, extensive histological lesions of the cerebellum, brain edema, and paraplegia. There is an approximate 85-fold increase in the lead concentration of both the cerebellum and cerebral cortex relative to controls, but edema and gross vascular changes are confined to the cerebellum. Ingested lead had little effect on RNA, DNA, and protein concentrations of developing rat cerebellum and cerebral cortex. However, there was a reduction of between 10 and 20% in the DNA content of the cerebellum around 3 weeks of age in the lead-exposed sucklings. This suggests a failure of cell multiplication in this part of the brain.A critical evaluation of this experimental approach indicated that under similar dietary conditions experimental lactating rats eat 30% less food than controls resulting in: (a) sustained loss in body weight of nursing mothers and that (b) offsprings who develop paraplegia and cerebellar damage do so after gaining access to lead containing diet. We have studied mothers' food consumption and body weight changes and blood, milk, and brain lead content; and newborns' body and brain weight changes, blood and brain lead content, and brain serotonin (5HT), norepinephrine (NE), dopamine (DA), and gamma-aminobutyric acid (GABA). We have found that a lactating mother rat eating 5% lead acetate (2.73% Pb) produced milk containing 25 ppm lead. When the mothers' diet is changed at day 16 from 5% PbAc to one containing 25 ppm Pb, and neonates allowed free access to the solid diet, the sucklings still have retarded body growth but do not develop paraplegia or grossly apparent vascular damage of the cerebellum. However, during the fourth week these animals exhibit a less severe form of "encephalopathy" consisting of hyperactivity, tremors, and stereotype behavior. Pair-fed controls coetaneous to experimental groups do not display such activities. There was no change in brain 5HT, GABA, or NE, but a 15-20% decrease in brain DA. Change in DA relative to other monoamines suggests a relationship between CNS dysfunction due to lead and DA metabolism in the brain.The experimental design as discribed provides a model of CNS dysfunction due to lead exposure without debilitating histopathologies. It is possible that our findings on increased motor activity and changes in brain dopamine may correspond to early responses to lead exposure before recognized overt signs of toxicity.
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PMID:Animal models of human disease: severe and mild lead encephalopathy in the neonatal rat. 483 Nov 41

Cytostatic long-term treatment for about 36 months was administered to 18 children with acute lymphatic leukaemia who were in long-term remission (43-98 months). Prophylaxis of meningosis involved intrathecal 198Au colloid and methotrexate. Seven recurrences occurred during the long-term remissions: the bone marrow was involved six times, leukaemic meningosis occurred once. Five out of seven recurrences occurred within one year of cessation of treatment. There were no complications induced by intrathecal radio-gold, such as the apathy syndrome or leukoencephalopathy. Intrathecal methotrexate led to side effects before administration of radio-gold: encephalopathy twice, paraplegia once. Symptoms regressed completely in two children, one child with encephalopathy continues to have symptoms. All three children were given 198Au colloid intrathecally thereafter which was tolerated very well. 198Au colloid represents an alternative for prophylaxis of meningosis with 60Co telecobalt irradiation in leukaemias and non-Hodgkin lymphomas in childhood.
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PMID:[Cessation of treatment in childhood acute lymphatic leukemia. Long-term observations after meningosis prevention with intrathecal gold colloid radioisotopes and methotrexate]. 626 99

Five observations of infants with transcutaneous intoxication by 6,3 p. 100 hexachlorophene contaminated talcum powder are reported. The diaper dermatitis is particular because of its topography (red pants shape), of its sudden occurring, of its papyraceous aspect evoking caustic origin, and of its association with severe encephalopathy. The neurological signs start with epileptic fits leading rapidly to coma. Prognosis is serious leading either to death or to paraplegia. Enquiry on that epidemic shows that mortality raised up to 18 p. 100. The neurological signs with oedematous degeneration of myelin are characteristic of hexachlorophene toxicity. Plasma levels of toxics range up to 15,94 mg/ml i.e. 30 times more than the rates observed by Curley in a premature washed with a commercial solution containing 3 p. 100 hexachlorophene. During a toxic neurological syndrome, the existence of diaper dermatitis with red plants shape must lead to an aetiological diagnosis of the possibility of transcutaneous intoxication even if the product seems as harmless as talcum powder.
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PMID:[Caustic diaper dermatitis and encephalitis secondary to the application of talcum contaminated with hexachlorophene]. 651 46

The course of typical dialysis encephalopathy (D.E.) in 12 patients is described. Five patients are still alive from 31 to 57 months after the onset of the disease. Their mental state has improved, but 3 have severe, residual paraplegia. Improvement was associated with the presence of a well functioning renal transplant or dialysis with deionized water. Only one case has developed since deionization of water containing more than 50/micrograms/l of aluminium has been routine. The patients' histories suggest that immobilization, surgery, administration of corticosteroids and hypophosphatemia, all of which induce a negative calcium balance, may release aluminium or another toxic substance from bone and precipitate the onset of D.E.
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PMID:Dialysis encephalopathy: precipitating factors and improvement in prognosis. 724 21

Encephalopathy is widely known as one of the neurological complications of chronic hepatic disease. Recently, the occurrence of progressive myelopathy in patients with advanced hepatic disease has been well documented and differentiated from encephalopathy. We describe a 76-year-old man with decompensatory liver cirrhosis due to hepatitis C virus infection who suffered from progressive paraplegia. Postmortem examination revealed demyelination of the lateral column of the spinal cord, especially of the thoracic segment. No evidence of spontaneous portosystemic shunts was found. These findings suggest that the patient had been affected with hepatic myelopathy, which is a rare complication of liver cirrhosis.
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PMID:Hepatic myelopathy: an unusual neurological complication of advanced hepatic disease. 784 90

To evaluate the topographical neurological distribution, patterns of abnormal tone and related functional neuromotor impairment after grade 3 and grade 4 intraventricular/periventricular haemorrhage (IPVH), 33 children with previous grade 3 or 4 IPVH of mean gestational age 30.9 weeks (range 25-40 weeks) and mean birth weight 1743 g (range 866-3600 g) were examined neurologically at 4.7 years (range 0.75-10.8 years). Neurological signs were absent in 10/33 cases which were equally distributed between the grade 3 and grade 4 IPVH groups. The largest single topographical neurological distribution was hemiparesis in 8/23, followed jointly by diplegia (cerebral paraplegia) in 6/23 and triplegia in 6/23 cases and finally quadriplegia in 3/23 cases. Grade 4 IPVH tended to result in asymmetrical syndromes, accounting for 7/8 cases of hemiparesis and 5/6 cases of triplegia, whereas all 3/3 cases of quadriplegia followed grade 3 IPVH. The 6/23 cases of diplegia were shared between the grade 3 and grade 4 IPVH groups. Tone was normal in 7/8 of the hemiparetic subjects. Dystonia was the commonest tone abnormality, affecting 8/23 children with neurological disturbance, followed by ataxia/hypotonia in 4/23 and mixed dystonia/hypotonia in 3/23. Only 1/23 cases had signs of spasticity. Spasticity is rare following severe IPVH. Diplegic children had a better functional neuromotor grade than hemiparetic children, who in turn did better than triplegic children. Ataxia hypotonia resulted in better functional outcome than dystronia, which in turn was more favourable than mixed tone patterns. Cranial imaging by ultrasound (US) or computed tomographic (CT) scanning proved an unreliable prognostic indicator except in the case of hemiparesis, for which US scans correctly predicted the affected side in 5/7 cases. The neurological syndromes following severe IPVH differ from the classical encephalopathy of prematurity, and this should lead to a re-appraisal of the trends in the prevalence of cerebral palsy. Caution should be exercised in the interpretation of cranial imaging with regard to pessimistic prognoses in the presence of changes or undue optimism in their absence.
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PMID:Heterogeneity of neurological syndromes in survivors of grade 3 and 4 periventricular haemorrhage. 840 2

We report a case of a permanent flaccid paraplegia, with a sensory loss at T12 level, not associated with cerebral damage, subsequent to a cardiac arrest of 15 minutes duration, in a 67-year-old patient, undergoing haemorragic surgery for gangrenous purulent cholecystitis. Besides cardiovascular collapse and subsequent circulatory arrest, possible favouring factors include anatomical anomalies in the territory of anterior spinal artery, surgical posture with hyperlordosis generating venous stasis, emergency haemostatic maneuvers with compression of the arterial territory providing spinal blood supply. Spinal cord lesions are probably more frequent than expected, as the often associated cerebral anoxic encephalopathy impedes their recognition. Only a systematic anatomopathological examination of the spinal cord, in patients who died after a cardiac arrest, would provide the accurate incidence of spinal complications.
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PMID:[Paraplegia after cardiac arrest]. 873 42

Renal failure is relatively common, but except in association with spina bifida or paraplegia it is unlikely to occur as a result of disease of the CNS. Renal failure, however, commonly affects the nervous system. The effects of kidney failure on the nervous system are more pronounced when failure is acute. In addition to the important problems related to renal failure there are both acquired and genetically determined diseases which may affect the kidney and the brain. Those acquired diseases include the vasculitides, the paraproteinaemias, and various granulomatous conditions (considered in other chapters of Neurology and Medicine). In two of the most commonly encountered genetically determined diseases, Von Hippel-Lindau disease and polycystic kidney disease, location of pathogenic mutations will provide improved screening programmes and, possibly, allow therapeutic intervention. Uraemia may affect both the central and peripheral nervous systems. Whereas the clinical features of uraemia are well documented, the pathophysiology is less well understood and probably multifactorial. Uraemic encephalopathy, which classically fluctuates, is associated with problems in cognition and memory and may progress to delirium, convulsions, and coma. The encephalopathy may initially worsen with periods of dialysis and almost certainly relates to altered metabolic states in association with ionic changes and possibly impaired synaptic function. Renal failure may affect the peripheral nervous system, resulting in a neuropathy which shows a predilection for large diameter axons. This may be reversed by dialysis and transplantation. The myopathy seen in renal failure, often associated with bone pain and tenderness, is similar to that encountered in primary hyperparathyroidism and osteomalacia. Dialysis itself is associated with neurological syndromes including the dysequilibrium syndrome, subdural haematoma, and Wernicke's encephalopathy. Dialysis dementia, which was prevalent during the 1970s, has reduced in frequency with the use of aluminium free dialysate. With the introduction of transplantation and the concomitant use of powerful immunosuppressive drugs, the pattern of neurological problems encountered in renal replacement therapy has shifted. Five per cent of patients develop nerve injuries during renal transplantation, and up to 40% of patients experience neurological side effects from cyclosporine. Furthermore, CNS infections, often fungal in type, have been reported in up to 45% of transplant patients coming to postmortem. The nature of the involvement of neurologists with their nephrology colleagues is therefore evolving.
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PMID:Neurology and the kidney. 985 55


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