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

Acromegaly was diagnosed in 14 middle-aged to old cats of mixed breeding. Thirteen (93%) of the cats were male and one was female. The earliest clinical signs in the 14 cats included polyuria, polydipsia, polyphagia, all of which were associated with untreated diabetes mellitus. All developed severe insulin resistance within a few months; peak insulin dosages required to control severe hyperglycemia ranged from 20 to 130 U per day. Other clinical findings weeks to months after diagnosis included enlargement of one or more organs (e.g., liver, heart, kidneys, and tongue) (n = 14), cardiomyopathy (n = 13), increase in body size and weight gain (n = 8), nephropathy associated with azotemia and clinical signs of renal failure (n = 7), degenerative arthropathy (n = 6), and central nervous system signs (i.e., circling and seizures) caused by enlargement of the pituitary tumor (n = 2). The diagnosis of acromegaly was confirmed by demonstration of extremely high basal serum growth hormone concentrations (22 to 131 micrograms/l) in all cats. Computerized tomography disclosed a mass in the region of the pituitary gland and hypothalamus in five of the six cats in which it was performed. Two cats were treated by cobalt radiotherapy followed by administration of a somatostatin analogue (octreotide), whereas two cats were treated with octreotide alone. Treatment had little to no effect in decreasing serum GH concentrations in any of the cats. Eleven of the 14 cats were euthanized or died four to 42 months (median survival time, 20.5 months) after the onset of acromegaly because of renal failure (n = 2), congestive heart failure (n = 1), concomitant renal failure and congestive heart failure (n = 3), progressive neurologic signs (n = 2), persistent anorexia and lethargy of unknown cause (n = 1), the owner's unwillingness to treat the diabetes mellitus (n = 1), or unknown causes (n = 1). Results of necropsy examination in ten cats revealed a large pituitary acidophil adenoma (n = 10), marked left ventricular and septal hypertrophy (n = 7), dilated cardiomyopathy (n = 1), arthropathy affecting the shoulder, elbow, or stifle (n = 5), and glomerulopathy characterized by expansion of the mesangial matrix and variable periglomerular fibrosis (n = 10).
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PMID:Acromegaly in 14 cats. 240 66

Movement disorders are well-known presenting signs of metabolic disorders. Focal motor abnormalities may be the chief initial presentation of diabetes mellitus in the nonketotic hyperglycemic state in 6% of patients. Nonketotic hyperglycemia (NKH), in particular, may manifest any of a wide variety of movement disorders. These have been described as focal seizures, epilepsia partialis continua, myoclonus, and opsoclonia. There are descriptions of movement disorders in hyperglycemia that are similar to the coarse flapping tremor of asterixis, the posturing of paroxysmal kinetogenic choreoathetosis, and of "fencing (stance) seizures." Disorders of facial motor function including aphasia, facial muscle twitching and jerking, and disorders of muscular tone have been described. These may include hemiparesis and hemiplegias as well as increased tone, in some cases mimicking the nuchal rigidity of meningitis. The movement disorders in NKH may mimic cerebral vascular accidents, meningitis, or psychiatric disorders, as well as various types of seizures. Clinicians may be able to avoid expensive and time-consuming diagnostic evaluations to rule out NKH in patients with movement disorders. We present two patients with focal motor abnormalities associated with nonketonic hyperglycemia and review the pertinent literature.
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PMID:Movement disorders as a manifestation of nonketotic hyperglycemia. 260 Mar 93

The objective of the present study was to explore metabolic correlates to the appearance of postischemic seizures and the enhancement of brain damage observed in subjects that are made hyperglycemic prior to the induction of ischemia. To that end, transient forebrain ischemia of 10-min duration was induced in normo- and hyperglycemic rats, with subsequent measurements of local CMRglc (LCMRglc) after 3, 6, 12, and 18 h of recirculation. We posed the questions of whether postischemic depression of LCMRglc is exaggerated by preischemic hyperglycemia and whether there are signs of localized increases in LCMRglc in hyperglycemic rats, reflecting subclinical seizure activity. The results confirmed the presence of a long-lasting postischemic depression of LCMRglc in normoglycemic rats. This depression was partially but not tightly related to the degree of reduction of local CBF during ischemia. The depression was most pronounced in neocortical areas and in the hippocampus, but notably it was less pronounced in the densely ischemic caudoputamen. Little or no reduction of LCMRglc was observed in moderately or mildly ischemic structures such as the hypothalamus, red nucleus, and cerebellum. Preischemic hyperglycemia markedly accentuated the postischemic depression of LCMRglc. For example, although the subjects quickly regained wakefulness and motility, they had LCMRglc values in neocortical areas that remained below 50% of control. Corresponding but quantitatively less pronounced reductions in LCMRglc were observed in other areas. Notably, preischemic hyperglycemia reduced postischemic LCMRglc also in areas that showed only moderate to mild reductions in CBF during the ischemia. The results thus demonstrate that preischemic hyperglycemia has pronounced metabolic effects in the postischemic recovery period. The data provide no indication that postischemic seizures, which develop after a recovery period of approximately 24 h, are preceded by the appearance of hypermetabolic "seizure" foci.
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PMID:Preischemic hyperglycemia enhances postischemic depression of cerebral metabolic rate. 273 14

Though children with febrile convulsions only have seizures in the early stage of a febrile illness and not later, these seizures have been attributed to the fever. We studied the serum electrolyte and metabolite profiles in the later stage to see if there were fuel responses resulting in electrophysiological changes which prevented further seizure activity. On admission there was intracellular glucose starvation, as evidenced by increased ketones and lactate, and the possibility of the failure of some electrolyte pumps, as suggested by hyperuricaemia (energy crisis) and decreased serum Na+, Cl- and Ca2+. However, there was adaptive hyperglycemia and decreased serum K+. It seems likely that the hyperglycemia, induced the uptake of K+ by neurones, enabling their repolarization and hyperpolarization, which prevented further seizure activity, while Cl- influx short-circuited depolarizing currents produced by Na+ influx. Studies during recovery showed a gradual return of the metabolic and electrolyte aberrations to normality, suggesting that the provision of energy through adaptation to the stress, enabled recovery of the aforementioned pumps.
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PMID:Hyperpolarization and short-circuiting as mechanisms of seizure prevention following febrile convulsions. 277 93

The influence of hyperglycemia and moderate hypoglycemia plus electroconvulsive seizure on the permeability of the blood-brain barrier to protein was studied in rats. Evans blue was used as a blood-brain barrier tracer. Following a single electroconvulsive seizure, slight staining of brain tissue was seen. After 10 electroconvulsive stimuli followed by sustained seizure activity, this phenomenon was more pronounced in moderate hypoglycemic animals. In this group, Evans blue albumin extravasation occurred in all regions of the hemispheres, but the most severe protein leakage was seen in the thalamus, hypothalamus, amygdala nuclei, and frontal, parietal, and occipital cortex. Ten repeated electroconvulsive stimuli applied in case of hyperglycemia made no important difference in blood-brain barrier dysfunction according to normoglycemic group. Our results suggest that moderate hypoglycemia provokes the effect of electroconvulsive seizure on the permeability of the blood-brain barrier.
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PMID:Blood-brain barrier permeability after electrically induced seizure in normoglycemic, hypoglycemic, and hyperglycemic rats. 279 94

We present five elderly patients with focal reflex or posture-induced seizures and nonketotic hyperglycemia (NKH). Each patient exhibited interictal focal findings, such as hemiparesis or hemisensory or aphasic deficits. With control of the hyperglycemia, the seizures stopped, and the neurologic deficits resolved. The syndrome of focal reflex epilepsy and neurologic deficits in the elderly is transient and almost invariably related to NKH, thus representing a specific neuroendocrine syndrome.
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PMID:Reflex epilepsy and nonketotic hyperglycemia in the elderly: a specific neuroendocrine syndrome. 292 48

This study addresses the question of whether the cyclooxygenase inhibitors indomethacin and diclofenac and the glucocorticosteroid dexamethasone ameliorate neuronal necrosis following cerebral ischemia. In addition, since these drugs inhibit the production of prostaglandins and depress phospholipase A2 activity, respectively, the importance of free fatty acids (FFAs) on the development of ischemic neuronal damage was assessed. Neuronal damage was determined in the rat brain at 1 week following 10 min of forebrain ischemia. The cyclooxygenase inhibitors, whether given before or after ischemia, failed to alter the brain damage incurred. Animals given dexamethasone were divided into three groups and the drug was administered at a constant dosage of 2 mg/kg: (a) 2 days, 1 day, and 3 h intraperitoneally before (chronic pretreatment), (b) 3 h intraperitoneally before (acute pretreatment), and (c) 5 min intravenously and 6 h and 1 day intraperitoneally after (chronic posttreatment) induction of ischemia. Acute pretreatment did not affect the histopathological outcome. Chronic posttreatment of animals with dexamethasone ameliorated the damage inflicted on the caudate nucleus, but had no effect on other brain areas investigated. Unexpectedly, the chronic pretreatment aggravated the brain damage and caused seizures following ischemia. Histopathological data showed massive neuronal damage in these brains. The accumulation of FFA levels during ischemia was markedly suppressed, and the decrease in the energy charge was curtailed by chronic pretreatment with dexamethasone. However, brain glucose levels in control animals and lactic acid concentrations following 10 min of ischemia were significantly higher both in the cerebral cortex and in the hippocampus of dexamethasone-treated animals. These results suggest that aggravation of neuronal necrosis by chronic dexamethasone pretreatment could be ascribed to lactic acidosis due to hyperglycemia in combination with an action of dexamethasone on glucocorticoid receptors in the brain.
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PMID:Chronic dexamethasone pretreatment aggravates ischemic neuronal necrosis. 309 61

The effects of pregnancy on acute metabolic complications of diabetes may have important consequences for both mother and fetus. The consequences of pregnancy for chronic complications of diabetes, including retinopathy, nephropathy, neuropathy, and hypertension, are not clear. Recent data are reviewed so that health care providers will be able to provide reasonable advice to insulin-dependent diabetic women contemplating pregnancy both for problems that may potentially arise during gestation and those that may affect long-term health and survival. Diabetic ketoacidosis is an uncommon problem that arises during gestation. Acute alterations in pH and electrolyte concentrations as well as hyperglycemia, however, may have important consequences for mother and fetus, including perinatal asphyxia and reduced fetal oxygen delivery. Hypoglycemia, on the other hand, may result in maternal coma or seizures and, when frequent, has been associated with infant respiratory distress syndrome. Background retinopathy often worsens during gestation, with regression common postpartum. Data suggest that progression of background disease is related to both glycemic control and the acute institution of intensive insulin therapy with those patients with poor control requiring more aggressive therapeutic intervention most adversely affected. The course of proliferative retinopathy is more variable, with both progression and regression reported. Preconception photocoagulation may prevent progression. Preconceptional ophthalmologic evaluation with frequent assessments during pregnancy is advised. Increases in 24-hour protein excretion are common during gestation in patients with preexisting renal disease and resolve in many patients postpartum. Serum creatinine and creatinine clearance increase during the first trimester and generally do not change during the remainder of pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of pregnancy on complications of insulin-dependent diabetes mellitus. 313 6

This study explores how hyperglycemia and enhanced tissue lactic acidosis influence the density and distribution of ischemic brain damage. Ischemia of 10-min duration was produced in glucose-infused rats by bilateral carotid clamping combined with hypotension, and the brains were perfusion-fixed with formaldehyde following recirculation of 3, 6, 12 and 18 h. After about 24 h the hyperglycemic animals developed seizures, and at that time two groups were added, one fixed prior to, and one after the onset of seizures. Similar experiments were made on normoglycemic animals with recirculation times of 1.5 to 96 h. After fixation the brains were embedded in paraffin, subserially sectioned and stained with celestine blue/acid fuchsin. In both normo- and hyperglycemic animals, neurons in the dentate hilus of the hippocampal formation and in the thalamic lateral reticular nucleus showed early and dense neuronal necrosis. In neocortex, hippocampal CA1 sector and caudoputamen, hyperglycemia shortened the delay before damage occurred and markedly enhanced the damage. Specific for the hyperglycemic animals was damage of the substantia nigra, pars reticulata (SNPR), manifest already at the earliest recovery periods studied; this finding is discussed in relationship to the role SNPR is assumed to play in preventing spread of seizure discharge.
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PMID:Morphological lesions in the brain preceding the development of postischemic seizures. 321 28

Preischemic hyperglycemia induced by feeding or glucose infusion worsens the brain damage and the clinical outcome following ischemia of a given duration and density, and characteristically causes postischemic seizure activity. Light microscopy has previously showed that, in the rat, transient hyperglycemia ischemia induced by bilateral carotid occlusion in combination with arterial hypotension causes a uni- or bilateral lesion in the pars reticulata of the substantia nigra. Since this region has a central role in preventing seizure discharges the present study was carried out to determine the ultrastructural characteristics of this lesion. In rats with 10 min of transient hyperglycemic ischemia followed by recirculation for 1 to 18 h, the pars reticulata of the substantia nigra showed signs of status spongiosus, as well as extensive nerve cell alterations. These changes were observed after all recovery periods studied. The spongiotic appearance was mainly caused by swelling of dendrites and, to a lesser degree, by astrocytic swelling. The dendrites were expanded at all recovery times but the severity increased during the later periods of recirculation. These swollen dendrites contained severely expanded mitochondrias and endoplasmic reticulum. The cytoskeletal elements showed disordered lining of microtubules. Two major types of nerve cell alterations were present: a "pale" and a "dark" variety. The pale type was the most frequent cell alteration. It occurred in all experimental groups and at all time points. Redistribution of the nuclear chromatin and of cytoplasmic organelles as well as swelling of the same type as in the dendrites were the essential changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Substantia nigra damage induced by ischemia in hyperglycemic rats. A light and electron microscopic study. 332 23


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