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)

The responsibility of the folate deficiency in some neuropsychiatric disorders is recent knowledge. The role of the folate on the nervous system is not yet well definite, but the action on the metabolism of the amino-acids, on the purine and the pyrimidine synthesis and on the metabolism of the catecholamins are certainly essential. The neuropsychiatric diseases secondary to the folate deficiency are numerous: dementia, schizophrenia like syndromes, insomnia, irritability, forgetfulness, endogenous depression, organic psychosis, pueperal psychosis, peripheral neuropathy, myelopathy (spinal cord syndrome and/or pyramidal tract damage), restless legs syndrome. Clinically the diagnosis may be difficult with sub acute combined degenration secondary to the pernicious anaemia, and the dosage of the folate (in serum, in red-cells and in cerebrospinal fluid) is necessary. The congenital defects in the uptake or utilization of the folate are associated with neuropsychiatric disturbances. The treatment is easy and safe if the vitamin B12 deficiency is eliminated and if employed with caution in epileptic patients because folate can induced seizures.
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PMID:[Folate and the nervous system (author's transl)]. 22 16

CNS involvement is a rare manifestation of collagen disease. But in three patients with lupus erythematosus (L.E.) the disease was from its onset characterized by CNS signs: epileptic seizures, cerebellar ataxia, and organic psychosis. The combination of epilepsy or organic psychosis with inflammatory joint disease should make one consider L.E. in the differential diagnosis, even if there is no close time relationship between the occurrence of these signs. Muscle biopsy, EEG recordings and CSF examinations may be of diagnostic value in addition to serological and immunological studies.
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PMID:[Early CNS manifestations in lupus erythematosus (author's transl)]. 118 35

Observation of neurosarcoidosis in a thirty-year-old black female characterised predominantly by bilateral facial nerve paralysis gave rise to a review of literature since 1978 and also to a comparison with an early study in 1963. As described 1963 the clinical picture is characterized by increased protein content of the CSF (33.8%), facial nerve paresis (25.5%), pleocytosis (23%), diabetes insipidus (21%), hemiparesis (17.2%), organic psychosis (16.9%), papilloedema (15.5%), ataxia (13%), convulsive seizures (12.5%), optic atrophy (12.5%), loss of hearing (12.2%), nystagmus (8.6%) and numerous other symptoms more rarely found. This corresponds to the symptoms of chronic basal meningitis with an infiltration in the neighbouring structures of brain and less frequently the spinal cord. In only 58.7% of the cases (presumably at the onset of sarcoidosis) was the bronchial tract (or the lungs) affected, in 11.5% the skin or the eyes. Although the clinical picture is clear enough the etiology has yet to be determined. Evidence of a pathogen or a pathogenic agent (analogous to berylliosis) has never been established to date. On the other hand there are some indications of a disturbance in the immune system, perhaps of a particular genetic foundation since sarcoidosis strikes black patients with conspicuous frequency. There exist more cases in one family. Exceeding expected random distribution, many patients have the HLA-Factor B 8 (on the chromosome 6) and DR 3. The Kveim-Test was in 71 cases positive, in 12 cases negative. The possibilities of carrying out studies of CSF - analogous to the studies of bronchial lavage - in the most cases of neurosarcoidosis have not been exhausted as to determine the activity of the T-lymphocytes, the interleucines, the angiotensin-converting enzyme while the Gallium 67 scintigraphy and other methods to determine the non-specific activity of the inflammation. The efficiency of the treatment with corticosteroids (Prednison or Triamcinolonacetonid) depends of the phase of the inflammatory process. 12% of the registered cases died.
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PMID:[Neurosarcoidosis. Comparative analysis of the clinical profile based on 537 cases from the world literature up to 1963 and from 1976-1988]. 240 26

Metrizamide, a nonionic, water-soluble contrast medium, has been increasingly used for myelography. We saw a patient with cortical blindness, seizure, organic psychosis, and asterixis after undergoing attempted metrizamide myelography via C1-2 puncture. Computed tomography demonstrated early penetrance of metrizamide into the brain parenchyma, most prominently in the occipital lobes. A mechanism of direct metrizamide neurotoxicity was proposed.
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PMID:Cortical blindness after metrizamide myelography. Report of a case and proposed pathophysiologic mechanism. 669 31

Water-soluble contrast media, which have been employed in the examination of the lumbar spinal canal for 30 years, can sometimes result in severe complications, such as arachnoiditis, epileptic seizures, and myoclonic spasm. These complications have been seen less frequently since the advent of metrizamide, a new non-ionic water-soluble contrast medium. However, a further neurological complication has now arisen--mental disorder, varying in kind and degree; for example, organic psychosis and perceptual disturbance. Some characteristic cases are described. A series of 75 patients, all of whom received varying amounts of metrizamide for the purpose of cervical, thoracic and lumbar myelography, has been studied. Seven patients were found to have a pronounced organic psychosis and three patients had visual illusions or hallucinations. It is suggested that there is some degree of correlation between the total amount of iodine received and patient age. By careful enquiry and examination, similar disturbances were also found some 4-8 h after myelography with other water-soluble contrast media.
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PMID:Mental disorders after myelography with metrizamide and other water-soluble contrast media. 738 36