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

Primary varicella-zoster virus (VZV) infections in adults generally follow a more severe course than in children and are more often associated with life-threatening complications. In the years 1992 to 1995 we observed 7 immunocompetent adults with a severe course of primary VZV infection. All 7 patients presented initially with a characteristic rash. In 6 patients the diagnosis of VZV was confirmed by ELISA on material taken from the lesions, and in all of them it was confirmed by serology. The following complications were observed: pneumonia (5x), elevated liver enzymes (4x), myocarditis (1x), encephalitis (1x) and myelitis (1x). Pulmonary lesions were characterized by bilateral interstitial infiltrates on chest-x-ray and required mechanical ventilation in 2 patients. The liver enzymes were only slightly elevated and clinically not significant. Myocarditis in one case was postulated in view of elevated creatine kinase levels, ECG-repolarization changes and AV-block III which required the insertion of a transitory pacemaker. Encephalitis presented as abnormal behaviour at work followed by seizures. Myelitis was suspected due to ascending sensory motor tetraparesis and confirmed by MRI. All patients were treated with high doses of parenteral acyclovir (3 x 10 mg/kg body weight i.v. per day) for 5-12 days. 6 patients recovered completely and only the patient with myelitis has residual neurological deficits 3 months after discharge. Although we cannot exclude the possibility that supportive therapy without acyclovir would have had the same outcome, we recommend high-dose parenteral acyclovir for treatment of visceral and neurological complications in primary VZV infections in adults.
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PMID:[Visceral and neurological complications in Varicella infections of adults]. 864 43

Loss of consciousness and falling are the key features of syncope. Common accompaniments include tonic and myoclonic muscle activity, eye deviations, automatisms, vocalizations and hallucinations which may render the distinction from epileptic seizures difficult. Differential diagnosis is based on the specific features and not the mere presence of these phenomena. Recognition of syncope depends also on accurate information about precipitants, premonitory symptoms and postictal events: the absence of postictal confusion has been identified as the single most powerful factor discriminating syncope from epileptic seizures whereas incontinence and head injury are common in both conditions. Investigations such as electroencephalogram, tilt testing and postictal prolactin or creatine kinase levels may be helpful but are never diagnostic in isolation. Exceptionally, hypoxic and epileptic mechanisms interact within a single attack.
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PMID:Recognizing syncope: pitfalls and surprises. 877 33

The present experiments were undertaken to study how preischemic hyperglycemia, which is known to exaggerate ischemic damage and to trigger delayed postischemic seizures affects the bioenergetic state and the intracellular pH (pHi) of brain tissue at early (6 h) and late (18 h) recirculation times. To that end, normo- and hyperglycemic rats were subjected to 10 min of forebrain ischemia, and neocortical tissue was frozen in situ for analyses of labile energy metabolites. Animals with preischemic hyperglycemia failed to show a postischemic reduction of the phosphorylation state of the adenine nucleotide pool, or a rise in tissue lactate content, nor did they show a change in tissue redox state. However, the hyperglycemia led to a rise in phosphocreatine (PCr) content after 6 h of recirculation. Calculations of intracellular pH (pHi) from the creatine kinase (CK) equilibrium showed a rise in pHi above normal, a finding which was supported by a limited number of 5,5-dimethyl[2-14C]oxazolidine-2,4-dione (DMO) measurements. The preischemic hyperglycemia also blunted the postischemic rise in tissue glycogen content, which is usually observed in normoglycemic rats. The results thus fail to reveal that the hyperglycemia-triggered, massive exaggeration of ischemic brain damage, which is heralded by generalized seizures after 18-24 h of recirculation, is preceded by mitochondrial dysfunction of a degree which affects the bioenergetic state or the redox potential of the tissue. However, the results suggest that the hyperglycemia enhances and/or prolongs the postischemic alkalosis. It is discussed whether the rise in pH contributes to the mitochondrial dysfunction which subsequently develops.
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PMID:Changes in labile energy metabolites, redox state and intracellular pH in postischemic brain of normo- and hyperglycemic rats. 883 45

A three-year-old, male Yorkshire terrier was presented with blindness, circling, hind limb weakness, and convulsive seizure for the past 3 months. Characteristic clinical findings were chronic, progressive neurological signs involving cerebrum and brain stem, an elevation of brain-type isoenzyme of serum creatine kinase, appearance of high voltage slow activity in electroencephalogram, and multifocal lesions in the cerebral hemispheres on magnetic resonance imaging. Necrotizing encephalitis of Yorkshire terrier was diagnosed after postmortem pathological examination. This is the first case report of the disease in Japan.
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PMID:Clinical and pathological findings of a Yorkshire terrier affected with necrotizing encephalitis. 884 3

Thirty-one patients (26 males, 5 females) with mean age 35 +/- 19 years (range 8 to 85 years) were diagnosed as non-traumatic rhabdomyolysis by clinical findings and elevation of serum creatine kinase (CK) between January 1989 and December 1993. Causes, laboratory measures, clinical courses, and outcome were reviewed retrospectively. Drug abuse, seizure, and excessive activity are the most common etiologies for non-traumatic rhabdomyolysis. Twelve patients presented with muscular pain and seven patients with muscle weakness. Twenty eight patients had urinalysis and five of them (18%) had negative orthotolidine dipstick test. Only seven patients (25%) were detected positive orthotolidine test without microscopic hematuria. Patients with acute renal failure had higher levels of potassium and uric acid. The patients who developed acute renal failure after admission had significantly higher levels of uric acid. The peak levels of CK did not correlate with development of acute renal failure. There was no episode of hyercalcemia. Seventeen patients (55%) had acute renal failure. Hemodialysis was required in nine cases. All survivors recovered with normal renal function except one who needed maintenance hemodialysis after two months follow-up. Two patients died of multi-organ failure and sepsis.
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PMID:Non-traumatic rhabdomyolysis and acute renal failure. 893 69

The incidence of creatine phosphokinase (CPK) elevation was evaluated in patients presenting to an urban emergency department with any complaint related to cocaine use within the preceeding 24 hours. Patients with obvious causes of CPK elevation (ie, seizure) were excluded. Forty patients were enrolled. CPK values were elevated in 21 patients (53%). The mean CPK value for patients with an elevated CPK was 1,071 IU/L. There was no statistically significant difference between the patient's initial complaint (muculoskeletal, psychiatric, or cardiovascular) and the incidence of CPK elevation (P = .35). Thirty of the 40 patients admitted to using some other drug(s) in addition to cocaine in the preceding 24 hours. Some degree of skeletal muscle injury and CPK elevation appears to be common in patients using cocaine.
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PMID:Creatine phosphokinase elevation in patients presenting to the emergency department with cocaine-related complaints. 914 72

Coenzyme Q10 (CoQ10) transfers electrons from complexes I and II of the mitochondrial respiratory chain to complex III. There is one published report of human CoQ10 deficiency describing two sisters with encephalopathy, proximal weakness, myoglobinuria, and lactic acidosis. We report a patient who had delayed motor milestones, proximal weakness, premature exertional fatigue, and episodes of exercise-induced pigmenturia. She also developed partial-complex seizures. Serum creatine kinase was approximately four times the upper limit of normal and venous lactate was mildly elevated. Skeletal muscle biopsy revealed many ragged-red fibers, cytochrome c oxidase-deficient fibers, and excess lipid. In isolated muscle mitochondria, impaired oxygen consumption was corrected by the addition of decylubiquinone. During standardized exercise, ventilatory and circulatory responses were compatible with a defect of oxidation-phosphorylation, which was confirmed by near-infrared spectroscopy analysis. Biochemical analysis of muscle extracts revealed decreased activities of complexes I+II and I+III, while CoQ10 concentration was less than 25% of normal. With a brief course of CoQ10 (150 mg daily), the patient reported subjective improvement. The triad of CNS involvement, recurrent myoglobinuria, and ragged-red fibers should alert clinicians to the possibility of CoQ10 deficiency.
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PMID:Mitochondrial encephalomyopathy with coenzyme Q10 deficiency. 915 50

Brain creatine kinase (CK) catalyzed phosphorus fluxes between phosphocreatine (PCr) and ATP and changes in reactant concentrations were measured using [31P] nuclear magnetic resonance spectroscopy ([31P]NMR) before and during pentylenetetrazole-induced seizures in 7 and 21 day old rats. The CK rate constants measured before seizures were three times higher in the older than in the younger rats. The rate constants increased 60% during seizures in the older rats but did not change or decreased in the younger. Small decreases in PCr were seen during seizures at both ages. A small decrease in ATP was seen at 7 days but not at 21 days.
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PMID:Brain creatine kinase reaction rates and reactant concentrations during seizures in developing rats. 916 86

Mitochondrial and cytosolic creatine kinase (CK) isozymes are active in cells with high and variable ATP metabolic rates. beta-Guanidinopropionic acid (GPA), a competitive inhibitor of creatine transport, was used to study the hypothesis that the creatine-CK-phosphocreatine (PCr) system is important in regulating brain ATP metabolism. The CK-catalyzed reaction rate and reactant concentrations were measured in vivo with 31P nuclear magnetic resonance spectroscopy during energy deficit (hypoxia) or high-energy turnover (seizures) states in urethane-anesthetized mice fed GPA, creatine, or standard chow (controls). Brain phosphagen (i.e., cellular energy reserves) or PCr plus phosphorylated GPA (GPAP) concentrations were equal. The phosphagen-to-NTP ratio was lower than in controls. In vivo CK reaction rate decreased fourfold, whereas ex vivo CK activity that was biochemically measured was doubled. During seizures, CK-catalyzed fluxes increased only in GPA-fed mice. Phosphagen increased in GPA-fed mice, whereas PCr decreased in controls. Survival was higher and brain phosphagen and ATP losses were less for hypoxic GPA-fed mice than for controls. In contrast to mice fed GPA, hypoxic survival and CK reactant concentrations during hypoxia and seizures were the same in creatine-fed mice and controls. Thus GPA, GPAP, or adaptive changes in ATP metabolism stabilize brain ATP and enhance survival during hypoxia in mice.
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PMID:In vivo brain phosphocreatine and ATP regulation in mice fed a creatine analog. 917 48

Confusion between syncope and epileptic seizures is a common problem in clinical practice. Recently, new insights into the phenomenology of transient cerebral hypoxia have been gained from video analysis of experimentally induced syncope. Common elements of syncope include multifocal and generalized myoclonus, tonic body extension, automatisms, vocalizations, eye deviations and hallucinations. Thus, it is not the presence or absence of these features but their specific character that distinguishes syncope from epileptic seizures. Other clues for differential diagnosis include precipitating factors, premonitory symptoms and postictal events, such as tongue bites and postictal confusion, which has been identified as the single most powerful factor discriminating syncope from epileptic seizures. In contrast, incontinence and head injury are common in both conditions. Investigations such as electroencephalogram, tilt testing and postictal prolactin or creatine kinase levels may aid diagnosis but are never diagnostic in isolation. In rare cases, hypoxic and epileptic mechanisms may interact within one attack.
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PMID:[Syncope. Phenomenology and differentiation from epileptic seizures]. 938 Feb 6


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