Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0494475 (tonic-clonic seizure)
 1,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported serial changes of MRIs in a case of acute disseminated encephalomyelitis (ADEM). On November 1, 1990, a previously healthy 73-year-old man had a grand mal seizure following myoclonic jerks of the right arm for six days. On admission, he was drowsy and presented with right facial palsy and incomplete tetraparesis. He became coma on the next day of admission. There was moderate leukocytosis. A spinal tap showed a normal opening pressure, 2 white blood cells/mm3, a total protein of 84 mg/dl, glucose of 89 mg/dl. CSF IgG (6.2 mg/dl) and myelin basic protein (6.7 ng/dl) were slightly increased. Serological examinations for virus titer were all negative. A CT scan on the 2nd day showed no abnormal findings, but MRI revealed small high intensity areas in the left thalamus, left prefrontal gyrus and right corona radiata, internal capsule on both the T2-weighted and proton density sequences. An MRI on the 14th day showed high intensity signals in the white matter of the bilateral frontal lobes, left operculum and right corona radiata. In contrast, the left thalamic lesion became smaller and less conspicuous than on the initial scans, but was enhanced with Gd on the T1-weighted sequences. Our findings indicate that MRIs are valuable in detecting pathophysiological changes of ADEM from the acute to chronic phases.
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PMID:[Serial changes of magnetic resonance imagings in acute disseminated encephalomyelitis]. 161 77

After her first grand mal seizure a 30-year-old woman was given a fructose infusion by an emergency doctor. On admission to hospital she complained of severe nausea. Ultrasonography revealed hepatosplenomegaly and the gamma-GT concentration was raised to 25 U/l. As hyperinsulinism was suspected an oral glucose tolerance test was suggested, but refused by the patient. She reported marked aversion to all sweet foods. Examination of an endoscopically obtained liver biopsy revealed clear reduction in fructoaldolase activity in liver tissue, i.e. the diagnosis of hereditary fructose intolerance. Three of the patient's siblings were also affected. The widespread use of infusion solutions containing sorbitol and fructose has twice proved acutely hazardous in this patient and is generally life-threatening for persons with an inborn error of metabolism whose pathologic status often remains undiagnosed to an adult age.
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PMID:[Adults with hereditary fructose intolerance: risks of fructose infusion]. 196 93

Hypoglycemia associated with nonislet cell tumor was found in 13 dogs. In each dog, clinical signs were related directly to adrenergic and neuroglucopenic effects of hypoglycemia and included collapsing episodes, tremors, restlessness, weakness, and grand mal seizures that were responsive to glucose administration. Eight of the dogs had hepatocellular carcinoma; surgical resection of the tumor achieved remission of clinical signs in 3 of these dogs. Other hepatic tumors associated with hypoglycemia included leiomyosarcoma and hemangiosarcoma involving solitary lobes of the liver. Nonhepatic tumors included splenic hemangiosarcoma, diffuse metastatic melanoma, and salivary gland adenocarcinoma.
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PMID:Hypoglycemia associated with nonislet cell tumor in 13 dogs. 298 Dec

The intrinsic processes involved in the initiation and arrest of seizures are not completely understood. Cortical and cerebellar inhibitory mechanisms, accumulation of metabolic products, and glial uptake of extracellular potassium (K+o), anions, and released neurotransmitters are all important processes that limit focal firing and terminate a seizure once it has been initiated. Of these, the intrinsic cortical inhibitory mechanisms--i.e., recurrent and surround inhibition--appear to be the most important. Active cation and anion transport processes are two metabolic events that have yet to be elucidated but clearly could be involved in terminating a seizure discharge. For example, without an active mechanism to transport chloride, opening of the chloride channel by the inhibitory transmitter GABA would not result in increased chloride permeability. The transient hypoxia and hypercapnia and lactic acidosis that follows a severe tonic-clonic seizure produces a mixed systemic metabolic and respiratory acidosis. In experimental animals, the hypercapnia that results is sufficient to block seizure discharges. Increasing the CO2 concentration significantly reduces the extension to flexion (E/F) ratio of mice given maximal electroshock seizures (MES) and increases the time required for 50% of the animals to recover sufficiently from a first MES to be able to have another MES. The decreased E/F ratio and the increased recovery time (RT50) are both indicative of a decrease in seizure activity. Since the extent to which CO2 is allowed to accumulate in the brain is regulated by the glial specific enzyme carbonic anhydrase (CA), it follows that the glial cell has an integral role in the mechanisms involved in arresting seizure activity. In contrast, hypoxia increased the E/F ratio and decreased the RT50, evidence that seizure activity was enhanced. Another metabolic factor affecting duration of seizure activity, susceptibility to seizures, and recovery from seizures is glucose. Recovery from seizures depends in part on an adequate supply of this energy source. An inverse correlation (R = 0.95) between RT50 and blood sugar was found when the blood sugar was altered experimentally by treatments that altered the endocrine status (pancreatectomy, treatment with alloxan, cortisol, insulin, glucagon, and dextrose). Since glial cells contain (as glycogen) the small amount of glucose present in the brain, they probably hasten the ability of the brain to recover normal function following a seizure.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Role of glial cation and anion transport mechanisms in etiology and arrest of seizures. 370 23

Neurophysiologic and local cerebral metabolic mapping techniques indicate that seizures associated with lidocaine toxicity originate in subcortical brain structures. Normally local cerebral blood flow (l-CBF) is quantitatively coupled to local cerebral metabolic rate for glucose (l-CMRg). In the present study the response of l-CBF to a lidocaine-induced preconvulsive state (localized seizure activity in the absence of a grand mal seizure) was evaluated in rats anesthetized with 60% nitrous oxide. Lidocaine administered as a bolus (20 mg/kg) followed by an infusion (4 mg/kg) over 5.5 min resulted in progressive alteration in the electroencephalogram (EEG). L-CBF was studied with the 14C-iodoantipyrine autographic method when the preconvulsive EEG pattern consisted of a repetitive spike and wave complex at a frequency of 14 +/- 1 X min-1 complexes, superimposed on practically isoelectric background activity. Under these conditions high doses of lidocaine significantly (P less than 0.05) decreased (range -30% to -68%) l-CBF in 71% of the 34 brain regions studied. The greatest exception to this trend for l-CBF to decrease was observed in the limbic system wherein l-CBF remained within control ranges in eight of the 11 structures evaluated. Qualitative comparison of lidocaine l-CBF changes with l-CMRg changes obtained under similar conditions indicated a general trend for local flow and metabolism to decrease in parallel. Exceptions to this were confined to certain limbic areas (amygdala and hippocampus) in which increases in l-CMRg were more than 100% greater than slight (P greater than 0.05) increases in l-CBF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Local cerebral blood flow during lidocaine-induced seizures in rats. 371 40

The mechanisms involved in the production of hypoglycemic coma were studied in rabbits. Measurements were made in brain, cerebrospinal fluid (CSF), and plasma of osmolality, Na(+), K(+), Cl(-), water content, exogenous insulin, glucose, lactate, and glutamate, while pH, Pco(2), Po(2), and bicarbonate were evaluated in arterial blood, 35 min after i.v. injection of insulin (50 U/kg), plasma glucose did not change, but brain K(+) content increased significantly. Grand mal seizures were observed in unanesthetized animals (+/-SD) 133+/-37 min after administration of insulin, at a time when brain glucose was normal, but brain tissue content of Na(+), K(+), osmoles, and water was significantly greater than normal. Coma supervened 212+/-54 min after insulin injection, at which time brain glucose, lactate, and glutamate were significantly decreased. At both 35 and 146 min after insulin administration, exogenous insulin was present in brain, but not in the CSF. After 208 min of insulin administration, animals were given i.v. glucose and sacrificed 35 min later. Most changes in the brain produced by hypoglycemia were reversed by the administration of glucose. Hypoxia (Po(2) = 23 mm Hg) was produced and maintained for 35 min in another group of animals. Hypoxia caused brain edema but did not affect brain electrolyte content. However, brain lactate concentration was significantly greater than normal. The data indicate that the seizures noted early in the course of insulin-induced hypoglycemia are temporally related to a rise in brain osmolality secondary to an increased net transport into brain of Na(+) and K(+), probably caused by insulin, per se. As hypoglycemia persists, there is also depletion of energy-supplying substrates (glucose, lactate, glutamate) in the brain, an event which coincides with the onset of coma. The brain edema observed during hypoxia is largely due to an increase in brain osmolality secondary to accumulation of lactate.
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PMID:Mechanisms of seizures and coma in hypoglycemia. Evidence for a direct effect of insulin on electrolyte transport in brain. 485 37

A 4 10/12 yr-old white male presented with a history of occasional grand mal seizures and hypoglycemic episodes after overnight fasting. Upon evaluation, he became hypoglycemic after 1 g/kg oral glycerol challenge (plasma glucose: 31 mg/dl in 45 min), but had normal glucose, alanine and fructose tolerance tests. He responded well to a glucagon challenge after 11 hr fast but he became hypoglycemic and could not normalize his blood glucose after a 2nd glucagon stimulation test after 17 hr of fasting. Studies conducted on a percutaneous liver biopsy, and compared with 3 non-hypoglycemic controls, showed reduced activities (20%-30% of normal) of alpha-glycerophosphate dehydrogenase, alpha-glycerophosphate oxidase and fructose-1,6-diphosphatase. Alpha glycerophosphate in the patient's liver was elevated. Two types of electrophoresis showed absence of one enzymatically active zone and overall decrease of staining intensity for alpha-glycerophosphate dehydrogenase. Other liver enzymes tested were normal. The 50% inhibition of the patient's liver fructose-1,6-diphosphatase by alpha-glycerophosphate occurred, in vitro, or lower concentration than in controls (11 versus 22-40 mM). Electron microscopy revealed hepatocytes with moderately swollen mitochondria that very occasionally contained dense inclusions in the inner mitochondrial matrix. After discharge from the hospital, the patient followed a normal course, with a regimen of multiple snacks and avoidance of high-fat food in the morning.
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PMID:Glycerol-induced hypoglycemia: a syndrome associated with multiple liver enzyme deficiencies. Clinical and in vitro studies. 713 31

Altered brain GABA, phosphocreatine and adenosine triphosphate have been documented in paroxysmal (px) chicks in earlier studies, suggesting perturbations in energy metabolism as a causative factor in this syndrome that is characterized by spontaneous neural degeneration of several central sensory systems, grand mal seizures, and progressive anorexia. In this study, brain sections from 5-, 7-, and 10-day-old px and normal White Leghorn-cross chicks were stained by immunocytochemistry to localize and quantify GABA. Serum glucose was measured to assess adequacy of circulating energy substrate. Differences between px and normal brains were found in GABA staining intensity in nuclei and tracts associated with auditory, vestibular and oculomotor function, and in several septal areas. Staining appeared to be confined primarily to terminals, and increasingly larger numbers of stained terminals were found in older px brains. This progressive increase appears to parallel the degenerative changes that occur over time in px brain and progressive manifestation of clinical signs. Px chicks appear to have adequate circulating glucose, suggesting that alterations in brain energy substrates are not a function of inadequate supply.
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PMID:Elevated brain GABA correlates with systemic dysfunctions in paroxysmal chick. 789 2

Tumor-associated hypoglycemia has been reported in dogs with pancreatic beta-cell tumors, hepatic tumors, and, rarely, with other neoplasms. This article describes 4 dogs with marked hypoglycemia associated with smooth muscle tumors (jejunal leiomyoma, gastric leiomyoma and leiomyosarcoma, and splenic leiomyosarcoma). Presenting clinical signs included grand mal seizures, lethargy, weakness, ataxia, and, in 1 dog, polyuria/polydipsia. The serum insulin concentration was low in 1 dog and normal in the other dog evaluated. Immunohistochemical staining for insulin was negative in the 4 tumors; the 3 tumors arising from the stomach and jejunum stained diffusely positive for glucagon. Blood glucose concentrations rapidly returned to normal after complete surgical resection of the tumors, and clinical signs associated with hypoglycemia resolved. Long-term follow-up available in 3 of the 4 dogs found no recurrence of clinical signs related to hypoglycemia at 15, 31, and 38 months after surgery, respectively.
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PMID:Hypoglycemia in four dogs with smooth muscle tumors. 855 89

We reported a case of non-herpetic acute encephalitis with unilateral temporal cortex lesion revealed by MR imaging and SPECT study. The patient was an eighteen years old woman who developed tonic-clonic seizure after common cold symptom. She was healthy before this episode. Neurological abnormality was only a single convulsion at onset and there was no other abnormal physical and neurological signs except for low grade fever. Electroencephalogram showed spike and slow wave complex of 2 Hz focused on a right posteriotemporal point (T 6) and an MR FLAIR (fluid-attenuated inversion recovery) image revealed a high signal intensity area at right temporal cortex. There was a decrease of cerebral blood flow in the same portion on SPECT study. This lesion was obscure on T1 and T2 MR images. Cerebrospinal fluid showed pleocytosis with normal glucose level and protein concentration. Bacterial and fungal cultures of CSF were negative and a detection of tubercule bacillus by PCR hybridization method was also negative. Although CSF findings suggested viral infection of CNS, virological study could not demonstrate infections of herpes simplex virus type 1, type 2, varicella-zoster virus, cytomegalovirus, measles virus, mumps virus, Japanese encephalitis virus, and influenza virus type A and B. After infusion of acyclovir and antibiotics, the patient was discharged from our hospital without sequelae of encephalitis. EEG was normal at this point and a high intensity area of MR FLAIR image disappeared two months later. SPECT findings were normalized six months later. The encephalitis presenting unilateral temporal cortex lesion without the infection of herpes simplex virus is thought to be very rare. Our case was distinguished from non-herpetic acute limbic encephalitis by an extent of the lesion and clinical manifestations. MR FLAIR image was useful for the detection of the lesion in this case.
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PMID:[A case of non-herpetic acute encephalitis presenting high intensity lesion at unilateral temparal cortex on MR FLAIR image]. 1054 15


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