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

Both naturally occurring disease processes and experimental models of human disease in the Mongolian gerbil were reviewed. The gerbil was highly susceptible to cerebral infarction following unilateral ligation of one common carotid artery and was useful in studies of the pathogenesis of stroke. Spontaneous epileptiform seizures mimicked those of human idiopathic epilepsy, and both seizure-sensitive and resistant strains have been bred. Perhaps because of its more efficient nephron, the gerbil accumulated four to six times as much renal lead as the rat, and the gerbil has been proposed as an experimental model of lead nephropathy. On standard diets, about 10% of the animals became obese, and some showed decreased glucose tolerance, elevated serum immunoreactive insulin and diabetic changes in the pancreas and other organs. Some breeders exhibited hyperactivity of the adrenal cortex associated with hyperglycemia, hyperlipidemia and degenerative vascular disease. Although dietary supplements of cholesterol were toxic and did not induce atherosclerosis, the gerbil was useful in other studies of cholesterol absorption and metabolism. Spontaneous, insidious periodontal disease became evident after about 6 months on standard diets, and dental caries were induced by cariogenic diets or by pathodontic streptococci. Spontaneous neoplasia occurred in 8.4--24% of gerbils, usually after 2 years of life. Adrenal cortical, ovarian and cutaneous tumors were the most consistently reported neoplasms.
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PMID:The pathology of the Mongolian Gerbil (Meriones unguiculatus): a review. 9 95

Nonketotic hyperglycemia has a definite convulsive effect, which may manifest itself in generalized or focal seizures. This report deals specifically with focal convulsive phenomena. Two patients with nonketotic hyperglycemia focal seizures are described. Focal seizures are of motor Jackson, aphasic, adversive or of the 'epilepsia partialis continua' type. Different types of focal seizures may appear in one and the same patient. Focal epilepsy can be the first manifestation of a diabetic disorder. Focal epileptic seizures are linked with moderate nonketotic hyperglycemia with values of 360 mg% sugar and 310 osm. Higher values lead to generalized seizures and coma. The mechanisms are discussed and pertinent literature is reviewed.
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PMID:Moderate nonketotic hyperglycemia--a cause of focal epilepsy. Report of two cases and review of literature. 9 31

A 57-year-old diabetic woman presented with focal right-sided seizures and hyperglycemia. She later showed periodic lateralized epileptiform discharges (PLEDs), originating in the left hemisphere, which were temporally associated with nystagmus retractorius. It appears that the left hemisphere epileptiform activity diffusely excited brainstem structures via polysynaptic pathways to produce the nystagmus.
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PMID:Periodic lateralized epileptiform discharges (PLED's) and nystagmus retractorius. 40 37

A 12-year-old juvenile diabetic was inadvertently given 500 ml of hypertonic saline intravenously. He developed hypernatremia, hyperosmolality, metabolic acidosis, and hyperglycemia. Seizures and stupor ensued, followed by coma and death. Computerized cranial tomography revealed numerous small subcortical hemorrhages that were verified postmortem.
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PMID:Hypernatremic hemorrhagic encephalopathy. 47 54

Hyperglycemia is known to worsen the outcome of transient global or forebrain ischemia. The aggravating effect is believed to be mediated by the additional formation of lactate- and of H+. Recent evidence suggests that reactive oxygen species contribute to the damage after brain ischemia. Since acidosis accelerates free radical damage in vitro, we decided to explore if ischemic damage in hyperglycemic subjects is ameliorated by dimethylthiourea (DMTU), an established free radical scavenger. In one series of hyperglycemic rats, we studied whether preischemic administration of DMTU alters the clinical outcome, notably the incidence and frequency of seizures. In two different series, the effect of DMTU on tissue damage was assessed by light microscopy after 15 h of recovery. Longer periods could not be studied since seizures developed. In the first of these series the animals were anesthetized with isoflurane, and in the second with halothane. The latter anesthesia largely suppressed the "early" postischemic seizures, i.e. those occurring after 1-4 h. Dimethylthiourea treatment altered the clinical outcome after ischemia. Thus, the "late" postischemic seizures appeared milder and occurred significantly later than in untreated animals. The fatal outcome was also delayed since treated animals died after 35.5 +/- 8.2 h (mean +/- SD) of recirculation, as compared to 19.8 +/- 3.6 h of recirculation in control animals. However, all DMTU-treated (and control) animals died. In the first morphological series (isoflurane anesthesia) the histopathological analysis was complicated by the occurrence of prefixation seizures; such seizures were recognized in 4/16 animals. When these 4 animals were excluded from the analysis (2 treated and 2 control animals), DMTU pretreatment did not ameliorate the damage, except in the substantia nigra pars reticulata (P < 0.05). In the second series, comprising animals anesthetized with halothane, only one animal out of 16 had "early" seizures, and none showed "late" seizures before death. Among these animals DMTU treatment significantly ameliorated damage to caudoputamen and cingulate cortex (P < 0.01). We conclude that treatment with the free radical scavenger DMTU partly ameliorates ischemic brain damage associated with excessive acidosis, and marginally delays the development of post-ischemic seizures. However, the effects were moderate and could, at least in part, have been caused by nonspecific effects of DMTU. Furthermore, all DMTU-treated animals died. The results thus give little support to the notion that the aggravating effects of acidosis is due to enhancement of free radical production.
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PMID:Effects of dimethylthiourea on ischemic brain damage in hyperglycemic rats. 148 54

Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na+)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na+] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II. 153 29

Preischemic hyperglycemia worsens brain damage after ischemia, and characteristically leads to post-ischemic seizures and a pan-necrotic lesion in substantia nigra pars reticulata (SNPR). The excitatory input to SNPR could contribute to the damage observed. By performing a unilateral frontal cortex lesion 6-19 days prior to the ischemia, we wanted to explore whether a decrease in excitatory input to the ipsilateral SNPR ameliorate the seizures or alter the light microscopical damage in SNPR. Our results demonstrate that unilateral frontal cortex lesion did not alter the development of fatal post-ischemic seizures after 10 min of ischemia in hyperglycemic subjects. Thus, 7/8 animals developed seizures and died within 20 h of recovery. This study also failed to show any difference between the left and right side in post-ischemic SNPR damage after 15 h of recovery in animals with preischemic unilateral frontal cortex lesion. Furthermore, no side difference was observed in any other brain region evaluated. The results thus suggest that the pan-necrotic lesion in SNPR after hyperglycemic ischemia is not caused by excessive excitatory input from frontal cortex. A decrease in the GABA-ergic inhibitory input from caudoputamen to SNPR may be a more important mechanism for the ensuing excitotoxic post-ischemic SNPR damage, and for seizure development.
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PMID:Frontal cortex lesion prior to hyperglycemic ischemia: no decrease in ensuing substantia nigra pars reticulata damage or fatal post-ischemic seizures. 157 9

The case of a non diabetic 6-year-old boy affected by Down's syndrome, who developed hyperosmolar hyperglycemic non-ketotic coma following the infusion of hypertonic dextrose solution during general anesthesia for a surgical procedure for cryptorchidism is reported. Following surgery, the patient remained deeply comatose and generalized seizures occurred. Hyperosmolarity due to hyperglycemia and acidosis were reduced by administration of insulin at low rate, hypotonic saline and sodium-bicarbonate solutions. The patient's clinical conditions promptly improved following normalization of blood glucose levels. An oral glucose tolerance test performed three months later was normal. The authors emphasize the potential risk of hyperosmolar hyperglycemic non-ketotic coma also in non diabetic patients treated with hypertonic dextrose solutions, during surgery events.
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PMID:A case of hyperglycemic hyperosmolar non-ketotic coma during anesthesia: a possible cause of failed re-awakening. 168 69

Three elderly patients with partial motor seizures triggered by movement of posture of an extremity are presented. They had a history of diabetes mellitus. Two of them had nonketotic hyperglycemia. Hemiparesis was present in the three patients, which resolved in two. In the other patient, hemiparesis resulted from a previous stroke. All patients had transitory parietal syndrome. During seizures, EEG showed discharges in the parieto-occipital area in two cases and in the mid-temporal area in one. Seizures were resistant to conventional anticonvulsant therapy, and ceased only after treatment of metabolic disturbances. A search for reflex seizures and hyperglycemia should be carried out routinely in the elderly with repeated spontaneous focal motor seizures. This may be important for treatment and prognosis.
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PMID:[Partial motor seizures induced by movement in diabetic patients]. 184 94

The cases of three patients with focal seizure associated to non-cetotic hyperglycemia are reported. Two patients presented motor epilepsy partialis continua (EPC). One case showed EPC as the first clinical manifestation of diabetes mellitus. Neurological exam was normal in all patients. CT and CSF were normal in the cases they were evaluated. Scalp EEG registered during a focal seizure revealed a bilateral temporal spiky activity. Glycemia levels were 455, 660 and 439 mg/dl. Two patients presented hyponatremia simultaneously. No patients had benefit with phenytoin or diazepam, and one patient got worse after them. Seizure control occurred after insulin and electrolytic treatment. It is important to diagnose this type of condition to avoid changes of non-cetotic hyperglycemia syndrome in a hyperosmolarity and coma state, disturbance which brings a higher mortality.
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PMID:[Focal seizures in nonketotic hyperglycemia]. 184 95


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