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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

OBJECTIVE: To verify the effects of malnutrition and nutritional rehabilitation regarding seizure threshold, body weight and brain weight in rats. METHODS: Pregnant Wistar rats and their pups were used. Part of the rat pups were submitted to a malnutrition protocol and the rest served as nourished controls. At P15, malnourished and control rats were submitted to status epilepticus induced by flurothyl; and the rehabilitation period started after recovery from seizures. At P30, all rats were submitted to single flurothyl-induced seizures and the threshold was determined. After the seizures, the rats were sacrificed, the brain removed and weighed. Rat pups were weighed daily from age P2 to P30. RESULTS: Significant differences as to body weight between malnourished and nourished rats were observed from P5 onwards. At P30, even after nutritional rehabilitation, there were still differences in terms of body weight. Nourished (mean 1.47 g -/+ 0.17) and male (mean 1.47 g -/+ 0.16) rats had brain weight slightly higher than that presented by malnourished (mean 1.42 g -/+ 0.17) and female (mean 1.38 g -/+ 0.12) rats; however, the difference was not significant. Differences observed in the threshold for the first clonic and tonic seizure at ages P15 and P30 between the groups were not statistically significant. CONCLUSIONS: Our results suggest that malnutrition does not influence seizure threshold in rat pups submitted to flurothyl-induced seizures. Early nutritional rehabilitation seems to have a protective effect on seizure threshold in previously malnourished animals.
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PMID:[Effects of early malnutrition and nutritional rehabilitation in rats] 1464 10

OBJECTIVE: To describe an unusual case with clinical features of the antiphospholipid syndrome. DESCRIPTION: White child, two years and six months old, with renal failure, renal arterial thrombosis, and diagnosis of antiphospholipid syndrome was hospitalized with a history of abdominal pain, pallor, lethargy, and anuria for 36 hours. On physical examination, the patient showed malnutrition, high blood pressure, moderate edema, and hypochondrial pain. Laboratory findings included: urea=112mg/dl, serum creatinine= 4.5 mg/dl, blood pH= 7.47, blood bicarbonate= 12.8 mmol/L, K=7.2 mEq/L. Peritoneal dialysis was started and maintained for 11 days. After 7 weeks, the patient still needed anti-hypertensive drugs and the renal function was still abnormal. Renal biopsy was performed and revealed renal infarction. The result of Doppler ultrasonography revealed absent renal blood flow on the right side. Renal arteriography showed total occlusion of the right renal artery. Results for collagen diseases were negative. A right nephrectomy was performed and the blood pressure was controlled. The child was hospitalized again at 5 years and 8 months old with episodes of absence seizures and abdominal and precordial pain. Anticardiolipin antibody test was positive. The child is now 7 years old, asymptomatic, with negative anticardiolipin antibody, and has been under regular follow-up. COMMENTS: Children with arterial thrombosis should be investigated for a possible association with the antiphospholipid antibody syndrome even in the absence of collagen disease.
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PMID:[Renal arterial thrombosis and the antiphospholipid antibody syndrome: a case report] 1464 33

Numerous studies have shown the pathological influence anti-phospholipid antibodies (APLA) have on the physiology of the single neuron as well as the function of the entire human nervous system. The influence is well demonstrated in the antiphospholipid syndrome (APS). This syndrome is characterized by a triad of arterial or venous thrombotic events, recurrent fetal loss and thrombocytopenic purpura. The syndrome exhibits different neurological pathologies such as: chorea, seizures, transverse myelopathy, migraine, cerebral ataxia, hemiballismus and transient global amnesia, which are not fully explained by the procoagulopathic trait of APLA. A study on mice induced with APS demonstrated hyperactive behavior when compared to the control group. The information gathered from these different studies raised the question whether APLA has any part in the etiology of Attention Deficit/Hyperactive Disorder (ADHD) in children. We compared 41 children diagnosed with ADHD to a control of 28 healthy children. Blood drawn from the two groups was screened using ELISA for the presence of anti-cardiolipin antibodies, anti-beta2GP antibodies, anti-phosphatidyleserine antibodies and anti-ethanolamine antibodies. The results show no significant difference in the level of antiphospholipid antibodies (APLA) measured between the children diagnosed with ADHD and the control group.
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PMID:Lack of association between anti-phospholipid antibodies (APLA) and Attention Deficit/Hyperactivity Disorder (ADHD) in children. 1476 40

Sleep disorders in childhood are a common phenomenon. A highly differenciated diagnostic effort is required as sleep in children is extremely variable between individuals, undergoes a constant natural development and depends of cultural influences on sleep behavior. The pathogenesis is predominantly due to environmental variables, especially to the child-parent interaction. Besides somatic diseases, as Sleep Related Breathing Disorders, Restless legs syndrome and nocturnal seizures play an etiologic role. Psychological and somatic factors in the development of sleep disorders have in common that they exercise a serious negative impact on cognitive daytime functioning and behavior. In this paper the interdependence of somatic and psychological factors and the relations between disturbed nighttime sleep and impaired daytime functioning will be discussed. Especially in Attention-Deficit Hyperactivity Disorder these relations can be demonstrated. Conclusions are drawn for a specific, stepwise diagnostic approach in children's sleep disorders.
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PMID:[Differential diagnostic correlations of sleep and attention disorders in childhood--comorbid psychological and organic illnesses]. 1500 87

Deficiency of 3-methylcrotonyl-CoA carboxylase (MCC) results in elevated excretion of 3-methylcrotonylglycine (3-MCG) and 3-hydroxyisovaleric acid (3-HIVA). MCC is a heteromeric mitochondrial enzyme comprising biotin-containing alpha subunits and smaller beta subunits, encoded by MCCA and MCCB, respectively. Mutations in these genes cause isolated MCC deficiency, an autosomal recessive disorder with a variable phenotype that ranges from severe neonatal to asymptomatic adult forms. No reported patients have responded to biotin therapy. Here, we describe two patients with a biochemical and, in one case, clinical phenotype of MCC deficiency, both of whom were responsive to biotin. The first patient presented at 3 months with seizures and progressive psychomotor retardation. Metabolic investigation at 2 years revealed elevated excretion of 3-MCG and 3-HIVA, suggesting MCC deficiency. High-dose biotin therapy was associated with a dramatic reduction in seizures, normalization of the electroencephalogram, and correction of the organic aciduria, within 4 weeks. MCC activity in fibroblasts was 25% of normal levels. The second patient, a newborn detected by tandem-mass-spectrometry newborn screening, displayed the same biochemical phenotype and remained asymptomatic with biotin up to the age of 18 months. In both patients, sequence analysis of the complete open reading frames of MCCA and MCCB revealed heterozygosity for MCCA-R385S and for the known polymorphic variant MCCA-P464H but revealed no other coding alterations. MCCA-R385S is unusual, in that it has a normal amount of MCC alpha protein but confers no MCC activity. We show that MCCA-R385S, but not other MCCA missense alleles, reduces the MCC activity of cotransfected MCCA-wild-type allele. Our results suggest that MCCA-R385S is a dominant negative allele and is biotin responsive in vivo.
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PMID:Isolated 3-methylcrotonyl-CoA carboxylase deficiency: evidence for an allele-specific dominant negative effect and responsiveness to biotin therapy. 1535 79

Neuroimaging and management advances require review of indications for excluding cerebral venous sinus (sinovenous) thrombosis (CSVT) in children. Our goals were to examine (i) clinical presentations of CSVT, (ii) prothrombotic risk factors and other predisposing events, (iii) clinical and radiological features of brain lesions in CSVT compared with arterial stroke, and (iv) predictors of outcome. We studied 42 children with CSVT from five European paediatric neurology stroke registries. Patients aged from 3 weeks to 13 (median 5.75) years (27 boys; 64%) presented with lethargy, anorexia, headache, vomiting, seizures, focal signs or coma and with CSVT on neuroimaging. Seventeen had prior chronic conditions; of the 25 previously well patients, 23 had recent infections, eight became dehydrated and six had both. Two children had a history compatible with prior CSVT. Anaemia and/or microcytosis (21 probable iron deficiency, five haemolytic, including two with sickle cell disease and one with beta-thalassaemia) was as common (62%) as prothrombotic disorder (13/21 screened). High factor VIII and homozygosity for the thermolabile methylene tetrahydrofolate reductase polymorphism were the commonest prothrombotic disorders. The superficial venous system was involved in 32 patients, the deep in six, and both in four. Data on the 13 children with bland infarction and the 12 with haemorrhage in the context of CSVT were compared with those from 88 children with ischaemic (AIS) and 24 with haemorrhagic (AHS) arterial stroke. In multiple logistic regression, iron deficiency, parietal infarction and lack of caudate involvement independently predicted CSVT rather than arterial disease. Five patients died, three acutely, one after recurrence and one after 6 months being quadriparetic and blind. Follow-up ranged from 0.5 to 10 (median 1) years. Twenty-six patients (62%) had sequelae: pseudotumour cerebri in 12 and cognitive and/or behavioural disabilities in 14, associated with epilepsy in three, hemiparesis in two and visual problems in two. Eighteen patients, including six with haemorrhage, were anticoagulated. Older age [odds ratio (OR) 1.54, 95% confidence limits (CI) 1.12, 2.13, P = 0.008], lack of parenchymal abnormality (OR 0.17, 95% CI 0.02, 1.56, P = 0.1), anticoagulation (OR 24.2, 95% CI 1.96, 299) and lateral and/or sigmoid sinus involvement (OR 16.2, 95% CI 1.62, 161, P = 0.02) were independent predictors of good cognitive outcome, although the last predicted pseudotumour cerebri. Death was associated with coma at presentation. Of 19 patients with follow-up magnetic resonance (MR) venography, three had persistent occlusion, associated with anaemia and longer prodrome. A low threshold for CT or MR venography in children with acute neurological symptoms is essential. Nutritional deficiencies may be modifiable risk factors. A paediatric anticoagulation trial may be required, after the natural history has been further established from registries of cases with and without treatment.
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PMID:Cerebral venous sinus thrombosis in children: risk factors, presentation, diagnosis and outcome. 1569 61

The tragic life of Vincent van Gogh is summarized, emphasizing his early departure from formal education, failure as a successful salesman in the art world, attempt at religious studies, difficulty with female and family relationships, return to the art world, and tendencies toward extremes of poor nutrition or near self-starvation and excessive drinking and smoking. In Paris he joined the Impressionists, but drank very heavily both absinthe and cognac. Southward he went to Arles and was joined by Paul Gauguin, with whom he had major personality problems, causing van Gogh to cut off part of his left ear. He experienced paranoid ideation and confinement in mental institutions in Arles, and then returned to Paris and onto Auvers-sur-Oise, where he committed suicide at age 37. Possible physical diagnoses include glaucoma, Meniere's disease, acute intermittent porphyria, and chronic lead poisoning, but these diagnoses seem unlikely. Possible psychiatric diagnoses include borderline personality disorder, anxiety-depressive disorder with episodes of depression and hypomania, and also paranoid schizophrenia. Van Gogh did not have spontaneous seizures and, therefore, did not have epilepsy. Before he began to drink heavily, when he was near starvation, he had "fainting fits," and after drinking, especially absinthe, a convulsant drug, he continued to have similar attacks. His episodes of unconsciousness can be well explained by chronic malnutrition and alcohol abuse, only possibly exacerbated by drinking large quantities of absinthe. Although van Gogh is an excellent example of the Geschwind syndrome, at times associated with temporal lobe epilepsy, this fact does not establish such an epilepsy. Thus, the syndrome is an orphan without the parent condition.
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PMID:A reappraisal of the possible seizures of Vincent van Gogh. 1590 45

Clinically, we most often associate Wernicke's encephalopathy (WE) with an alcohol abusing population. However, it is important to consider other causes of malnutrition and vitamin deficiency as risk factors for the development of this disorder. We present a case of a 51-year-old man with schizophrenia and malnutrition who presented with delirium, ophthalmoplegia, and seizures. He responded rapidly to the administration of IV thiamine. Because of the high rate of mortality and morbidity, WE should be high on the differential of any patient at risk for malnutrition or with ophthalmoplegia, regardless of alcohol history. This is particularly important in psychiatric patients where the syndrome may be masked and thus treatment delayed.
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PMID:Wernicke's encephalopathy in a patient with schizophrenia. 1692 99

Alexander disease is a rare, sporadic leukoencephalopathy characterized by white-matter abnormalities with frontal predominance and, as a rule, clinically associated with megalencephaly, seizures, spasticity, and psychomotor deterioration. We describe a boy who was diagnosed as affected by anorexia nervosa because of his refusal to eat, progressive weight loss, and psychologic disturbances. The observation of a hyperintense lesion on T(2)-weighed magnetic resonance images (MRIs) was initially explained as a pontine and extrapontine myelinolysis related to malnutrition. Following MRI and DNA analysis, we diagnosed a juvenile type of Alexander disease. Therefore, we can affirm the importance of the history and clinical examination to look for brainstem dysfunction in patients presenting with atypical anorexia nervosa.
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PMID:Unusual diagnosis in a child suffering from juvenile Alexander disease: clinical and imaging report. 1715 3

There have been several reports in the literature about hypernatraemic dehydration and severe malnutrition in exclusively breastfed infants. The authors report a series of four such cases admitted to the Newborn Special Care Unit of the University Hospital of the West Indies over a seven-year period. All four were term infants who had weight loss of greater than 20% of their birthweight, serum sodium levels greater than 175 mmol/L, metabolic acidosis and pre-renal failure at presentation. Three of the infants had seizures shortly after presentation. One of the infants died soon after admission to hospital, the three others had normal neurological development clinically at the time of last review.
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PMID:Hypernatraemic dehydration in exclusively breastfed infants: a potentially fatal complication. 1724 18


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