Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dantrolene sodium or dantrolene1 is 1([5-(nitrophenyl)furfurylidend] amino) hydantoin sodium hydrate. It is indicated for use in chronic disorders characterised by skeletal muscle spasticity, such as spinal cord injury, stroke, cerebral palsy and multiple sclerosis. Dantrolene is believed to act directly on the contractile mechanism of skeletal muscle to decrease the force of contraction in the absence of any demonstrated effects on neural pathways, on the neuromuscular junction, or on the excitable properties of the muscle fibre membranes. Controlled trials have demonstrated that dantrolene is superior to placebo in adults or children with spasticity from various causes, as evidenced by clinical assessments of disability and daily activities, and by muscle and reflex responses to mechanical and electrical stimulation. It is somewhat less effective in patients with multiple sclerosis than in those with spasticity from other causes. There has been a general clinical impression in controlled trials that dantrolene caused less sedation than would have been expected from therapeutically comparable doses of diazepam. In 2 controlled trials, there was no significant difference between dantrolene and diazepam in terms of reductions in spasticity, clonus, and hyperreflexia, but side-effects such as drowsiness and inco-ordination occurred significantly more frequently on diazepam. Long-term studies have indicated continuing benefit for patients taking dantrolene, though the incidence of side-effects has often been high and there has been a suggestion of exacerbation of seizures in children with cerebral palsy. Dantrolene may be of value in the medical treatment of spasm of the external urethral sphincter due to neurological and non-neurological disease, and animal studies suggest a potential use in the management of malignant hyperpyrexia. Chemical evidence of liver dysfunction may occur in 0.7 to 1% of patients on long-term treatment with dantrolene, with symptomatic hepatitis in 0.35 to 0.5% and fatal hepatitis in 0.1 to 0.2%. The drug commonly causes transient drowsiness, dizziness, weakness, general malaise, fatigue and diarrhoea at the start of therapy. Muscle weakness may be the principal limiting side-effect in ambulant patients, particularly in those with multiple sclerosis, and therapy could be hazardous in patients with pre-existing bulbar or respiratory weakness. The dosage of dantrolene has been fixed in most controlled trials, though long-term studies have indicated the need for individualisation of dosage. The initial dose is usually 25mg once daily, increasing to 25mg two, three or four times daily, and then by increments of 25mg up to as high as 100mg two, three or four times daily. The lowest dose compatible with optimal response is recommended.
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PMID:Dantrolene sodium: a review of its pharmacological properties and therapeutic efficacy in spasticity. 31 89

The University of Kentucky provides neurologic services to rural children by a traveling clinic. In 1978, 438 children (including 231 new patients) made 646 clinic visits. The primary diagnoses were appropriate for a neurology clinic; epilepsy was the most common (74 of 231) among new patients. A community survey of school-age children found the clinic serving 45 percent of "active epileptics." Clinic patients had a higher seizure frequency and came from a more disadvantaged background that nonclinic patients. These data show that an urban-based traveling clinic can identify and care for rural children with neurologic disorders.
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PMID:Extending neurologic services to rural children. 57 10

A 31 month old child developed seizures 30 minutes after the accidental ingestion of toxic quantities of nalidixic acid. The case is unusual because of the age of the patient and the circumstances of the poisoning. It emphasises that this drug is contraindicated in children with previous neurological disease.
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PMID:[Acute nalidixic acid poisoning in children]. 68 50

"Fahr's Disease" is characterized by bilateral and symmetrical calcifications of the Globus Pallidus (systematically extending to the Commisura Anterior and the Capsula Interna, and less commonly to the Putamen, the Centrum Semi-Ovale and the Cerebral Cortex), and of the Cerebellar Nucleus Dentalus (with spreading to the White Matter and the Cortical Lamellae). Lesions or absence of Parathyroids are frequently related, with subsequent metabolic disorders of Phosphorus and Calcium, but idiopathic cases without hypoparathyroid disturbances are also found. A Morgagni-Morel Hyperostosis Frontalis Interna is often associated with "Fahr's Disease", and there could be a relationship between these two affections. We found in three cases the association between "Fahr's Disease" and Morel's Nodular Dysgenesis of the Frontal Cortex. Most of the cases are sporadic, but observations with a clear familial incidence are also found. Clinically, various Neurological Disorders (cerebellar, extrapyramidal, pyramidal, dysarthria, epileptic seizures) are often but not always observed; the Psychiatric Disorders found in some cases could be fortuitious associations (psychoses), connected to hypothyroidism (oligophrenia), and in aged patients, to unrelated cerebral vascular or degenerative lesions; very seldom, a dementing state could be connected to the spreading of calcifications to the Cerebral Cortex.
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PMID:[Pallido-dentate calcifications (apropos of 7 anatomo-clinical case reports)]. 69 68

Seizures in the neonatal period are usually concomitants of serious neurological disease. The convulsive phenomena take certain distinctive and often subtle forms because of the status of the neuroanatomical and neurophysiological development of the neonatal brain. The predominant etiological process is hypoxic-ischemic encephalopathy, but intracranial hemorrhage, intracranial infection, development defects and metabolic disorders are also responsible for a considerable proportion of cases. Prognosis is related primarily to the neurological disease that underlies the seizures. Treatment may be specific for the underlying disorder, e.g., glucose, calcium, magnesium, pyridoxine, but whatever the cause, urgent control of the convulsions is important because they may have deleterious consequences. Phenobarbital is the single, most important anticonvulsant in the management of neonatal seizures.
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PMID:Management of neonatal seizures. 83

Four members of a family with an autosomal dominant form of cerebellar degeneration all had slow eye-movements, i.e. slow pursuit with absence of both nystagmus and rapid saccadic movements. Three showed progressive mental deterioration. One patient had nevus of Ota (oculodermal melanocytosis) and a history of grand mal epilepsy. In these four patients the symptoms first occurred between the ages of 10 and 31 years--the onset apparently appearing earlier with successive generations. Current studies implicate a brain-stem lesion of the paramedian pontine reticular formation in the pathogenesis of the oculomotor abnormality. The possibility of a neurocutaneous syndrome, specifically a 'melanophakomatosis', in the patient with seizures and nevus of Ota is discussed; however, absence of these findings in other affected relatives makes a fortuitous association more probable. The literature on nevus of Ota associated with neurological disease is considered.
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PMID:Familial cerebellar degeneration with slow eye-movements, mental deterioration and incidental nevus of ota (oculo-dermal melanocytosis). 93 51

A neurological disease of cattle (maldronksiekte), occurring in a localized area of the Northern Transvaal, was experimentally reproduced by feeding Solanum kwebense plants to cattle. The disease is characterized by temporary loss of balance and transient epileptiform seizures precipitated by a variety of stimuli, such as exercise, handling (dipping, loading, etc) and fright. When not disturbed, most affected animals appear to be completely normal. The most conspicuous histopathological lesion is a neuronopathy manifested by vacuolar degeneration and eventual necrosis of neurones, particularly of the Purkinje cells in the cerebellum. An atrophy of the cerebellar cortex is seen grossly. The history, clinical signs and experimental reproduction of the disease, as well as the pathology of 4 experimental and 18 natural cases, are described.
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PMID:Maldronksiekte in cattle: a neuronopathy caused by Solanum kwebense N.E. Br. 101 91

The case of a child is described who at the age of 2 years showed the first evidence of a developing neurological disease. Within a couple of years, profound mental retardation and severe motor deficit with spastic tetraplegia became established. No seizures and no pigmentation of the retina were observed. The condition remained practically unchanged for some 8 years and the patient died at 12 years of age of terminal bronchopneumonia. At autopsy there was conspicuous diffuse atrophy of the brain. The cerebral cortex was particularly involved. Most of the cortical neurons were destroyed and neuroglia showed abundant proliferation. The few remaining neurons contained inclusion material which was identified as lipofuscin. Noticeable cedifferences from the various types of amaurotic idiocies are noted and similarities to a case of lipidosis recently reported from Finland are suggested.
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PMID:An unusual type of infantile lipofuscinosis. 113 10

A retrospective study of the neurological problems arising in HIV-I seropositive patients in a single defined geographical area was undertaken. Ninety patients were referred for a neurological opinion from a total known HIV-I seropositive population of 436. Minor problems were frequently encountered early in the course of disease (20 at CDC stage II, 12 at CDC stage III), including seizures related to drug abuse in six. The most frequent neurological problem in those patients in CDC group IV (58 patients) were the AIDS dementia complex (14 patients), an axonal sensorimotor neuropathy (12), toxoplasmosis (nine) and cryptococcal meningitis (three). All patients with a structural lesion had appropriate focal signs on examination. The value and role of CT cranial scanning in the diagnosis of toxoplasmosis is discussed and the importance of recognizing potentially treatable causes of both intellectual impairment and cytomegalovirus-related neuropathies is stressed. This is the first report of an unselected series of patients at all stages of HIV-I related neurological disease from a single UK centre.
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PMID:The neurological features of HIV-positive patients in Glasgow--a retrospective study of 90 cases. 132 56

Hemolytic-uremic syndrome is usually a consequence of enteric verotoxigenic Escherichia coli infection, and a prevailing hypothesis contends that systemically absorbed verotoxins are responsible for the multiple organ involvement. In an attempt to determine whether the central nervous system (CNS) manifestations could occur owing to factors that reflect a toxin insult, the authors studied the association of clinical and laboratory variables with the development of neurological disease. Ninety-one patients with hemolytic-uremic syndrome from 1982 through 1990 were included. Twenty-seven (18 female, 9 male) had a CNS disorder; 17 of these had seizures and there were two deaths. Multivariate analyses led to the following observations: female gender (odds ratio [OR] 8.50; 95% confidence interval [CI] 2.08 to 50.0), prolonged use of an antimotility pharmacological agent (OR 8.50; 95% CI 1.69 to 42.81), and an increased hemoglobin level (OR 1.11; 95% CI 1.05 to 1.17) were associated with an increased risk for developing a neurological manifestation. Prior administration of a blood product was associated with a decreased risk (OR 0.12; 95% CI 0.02 to 0.52). The findings suggest that other mechanisms for CNS disease may exist in addition to direct toxin insult.
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PMID:Risk factors for the central nervous system manifestations of gastroenteritis-associated hemolytic-uremic syndrome. 140 19


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