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

We describe a 29-year-old man with mitochondrial encephalomyopathy. The patient's disorder was characterized by lactic acidosis, hemiparesis, seizures, aphasia, and hemianopia. CT revealed low-density areas that corresponded to the symptoms. His 56-year-old mother is also involved subclinically, demonstrating that muscle biopsy is an important requisite in the final determination of a familial inheritance pattern in mitochondrial myopathy. Neuronal mitochondrial disorders are suggested as the pathogenesis of his neurologic symptoms.
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PMID:Mitochondrial encephalomyopathy: fluctuating symptoms and CT. 649 93

The concept that a challenge to a system may overcome compensatory mechanisms and thereby reveal otherwise hidden neurotoxicant-induced damage is reviewed from a neurophysiological perspective. Two broad classes of neuronal challenges, poststimulation neuronal recovery processes and epileptogenesis, are discussed in terms of their potential value for detection and characterization of neurotoxicity. Neuronal recovery studies have typically involved presentation of pairs or trains of stimuli with various interstimulus intervals. Studies involving simple (e.g., monosynaptic) systems may allow mechanistic interpretation of alterations. Paired-pulse studies involving more complex (e.g., polysynaptic sensory) systems have detected alterations more readily than other electrophysiological methods, but interpretation may not be as straightforward as the monosynaptic case. The properties of elicited seizures, as well as the threshold for production of seizures, have been used with some success for detection of neurotoxicity. Several seizure models are discussed. It is concluded that both classes of neuronal challenge hold promise for future studies of neurotoxicity.
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PMID:Use of neurophysiological challenges for the detection of toxicity. 664 53

Neuronal lesions in the brain occur in conditions associated with a reduced supply of oxygen (hypoxia and ischemia) and glucose (hypoglycemia) as well as in those associated with a pathologically enhanced neuronal activity (status epilepticus). In only two of these conditions (hypoxia and ischemia) are the lesions correlated to cellular oxygen lack, and gross energy failure is absent in one condition (status epilepticus). Although anaerobic mechanisms seem responsible for the cell injury in hypoxia and ischemia, oxidative mechanisms could operate in hypoglycemia and status epilepticus. Since the supply of oxygen has not ceased altogether in hypoxia and incomplete ischemia, and since reoxygenation/recirculation leads to a transient increase in tissue oxygen tensions, one cannot exclude the possibility that oxidative mechanisms contribute to the final damage following all types of cellular oxygen lack. We have failed to obtain evidence that peroxidative degradation of cellular constituents occurs in hypoglycemia and status epilepticus. Thus, there is neither a perturbation of the redox state of the glutathione pool of the tissue nor a measurable degradation of polyenoic phospholipid-bound fatty acids. It is emphasized that the cascade of events triggered by an accumulation of free polyenoic fatty acids, mainly arachidonic acid, may contribute to cell lesions by leading to cell edema and/or microcirculatory changes. During seizures, such an accumulation occurs even though energy failure is moderate and it may conceivably contribute to cell damage. In general, though, mechanisms of cell damage in the brain remain partly elusive.
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PMID:Neuronal cell damage in the brain: possible involvement of oxidative mechanisms. 693 2

Neuronal migration disorders may manifest as epilepsy alone and this is usually the case in nodular subependymal heterotopia, of which we present 5 cases. We consider this entity to be a well-defined epileptic syndrome because it is found nearly exclusively in women and is characterized by nearly constant seizures which start in the second or third decade of life, familial aggregation of cases, a clinical and EEG profile that suggests a temporal focus and the absence of associated cognitive or motor deficits. Seizures are usually controllable with medication.
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PMID:[Nodular subependymal heterotopia and epilepsy]. 871 78

Neuronal degeneration in the hippocampus, a region of the brain important for acquisition of memory in humans, occurs in various pathological conditions, including Alzheimer's disease, brain ischaemia and epilepsy. When neuronal activity is stimulated in the adult rat and mouse hippocampus, tissue plasminogen activator (tPA), a serine protease that converts inactive plasminogen to the active protease plasmin, is transcriptionally induced. The activity of tPA in neural tissue is correlated with neurite outgrowth, regeneration and migration, suggesting that it might be involved in neuronal plasticity. Here we show that tPA is produced primarily by microglia in the hippocampus. Using excitotoxins to induce neuronal cell loss, we demonstrate that tPA-deficient mice are resistant to neuronal degeneration. These mice are also less susceptible to pharmacologically induced seizures than wild-type mice. These findings identify a role for tPA in neuronal degeneration and seizure.
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PMID:Excitotoxin-induced neuronal degeneration and seizure are mediated by tissue plasminogen activator. 756 88

The effect of repeated episodes of asphyxia on the fetal cardiovascular system and CNS was examined. The umbilical cord was occluded for 5 min, four times, at 30-min intervals in 11 chronically instrumented fetal sheep (118-126 d). Fetal electrocorticogram (ECoG), cortical impedance, ECG, heart rate, and blood pressure were continuously recorded for 3 d, after which neuronal loss was determined histologically. Each occlusion resulted in fetal hypoxemia and bradycardia accompanied by increased T/QRS ratio. Progressively severe hypotension and lactic acidosis developed during successive occlusions. The ECoG was depressed and cortical impedance increased with each occlusion. During the final occlusion, blood pressure fell to 3.5 +/- 1 kPa and heart rate to 93 +/- 9 bpm, T/QRS ratio increased to 0.44 +/- 0.3, and lactate rose to 7.2 +/- 1.2 mM/L. Three animals died from cardiac fibrillation during recirculation after the third or fourth occlusion. After the asphyxial episodes, blood pressure and heart rate returned to normal, and the T wave was inverted for 310 +/- 155 min. Lactate returned to baseline within 24 h. The ECoG remained depressed for 90 +/- 35 min, and intermittent seizures developed at 3.3 +/- 1.4 h after the last occlusion. Neuronal loss was primarily found in the striatum. The extent of neuronal loss correlated with the degree of hypotension, increase in T/QRS ratio, duration of postasphyxial ECoG depression, and number of seizures. These results indicate that transient asphyxial episodes compromise the ability of the heart to tolerate additional insults and further suggest that neuronal loss is a consequence of cardiovascular compromise secondary to asphyxia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Repeated episodes of umbilical cord occlusion in fetal sheep lead to preferential damage to the striatum and sensitize the heart to further insults. 765 53

Two children with severe neurodevelopmental retardation and elevated liver function tests developed intractable seizures during the first year of life. Detectable neurometabolic conditions have been ruled out. At the time of seizures evidence for systemic selenium deficiency could be documented. The youngest patient, who manifested intractable fits from the fourth day of life, died at the age of ten months. Neuropathologic examination was consistent with Progressive Neuronal Degeneration of Childhood (PNDC) with liver disease or formerly known as Alpers disease. In the oldest child, whose diet was normally balanced, fits started from the age of 11 months and features of long-standing selenium deficiency became apparent from the age of 1 1/2 years and consisted of liver function disturbances, depigmented hair and osteoarthropathy. Oral substitution with selenium supplements in both children (3-5 micrograms/kg body weight) resulted in reduction of seizures and improvement of the EEG recordings after two weeks while liver function became normal. Two of the seleno-dependent enzymes Glutathione Peroxidase (GPX) and Phospholipid Hydroperoxide Glutathione Peroxidase (PHGPX) are speculated to play a key-role in the defence of neuronal cells against oxygen radical formation and peroxidative processes. Our findings support the hypothesis that the presence of selenium depletion in the brain amongst patients with epilepsy constitutes an important triggering factor for the origin of intractable seizures and subsequent neuronal damage.
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PMID:Selenium deficiency triggering intractable seizures. 782 95

Computerized electroencephalography and thalamic ventro-posterior lateral (VPL) unit activities were recorded from pyridoxine-deficient and pair-fed pyridoxine-supplemented adult male rats. Pyridoxine-deficient animals exhibited slow electroencephalograms (EEG) represented by the dominance of delta activity and reduced seizure thresholds to local (VPL) application of either picrotoxin or pentylene tetrazole. Frequency and amplitude of thalamic VPL unit activity were significantly reduced in pyridoxine-deficient rats as compared to pyridoxine-supplemented controls. Pyridoxine-deficient rats exhibited irregular unit activity with frequent bursts and electrosilent periods in response to local (VPL) picrotoxin or pentylene tetrazole microinjections. They also exhibited severe seizure discharge activity of prolonged duration at any given dose of either picrotoxin or pentylene tetrazole. This was represented by significantly increased burst frequency, burst duration and reduced seizure latencies. Unit activity was transformed into burst discharge activity with intermittent electrosilent zones during picrotoxin or pentylene tetrazole epileptogenesis. Cerebral gamma aminobutyric acid (GABA) level was reduced and glutamate concentration increased in pyridoxine-deficient rats when compared with pyridoxine-supplemented controls. Local (VPL) microinjection of GABA or pyridoxine induced neuronal recovery in both convulsant-treated normal and pyridoxine-deficient rats. Neuronal recovery was however delayed in pyridoxine-deficient rats. Neuronal recovery was associated with a significant increase in EEG background frequency and reduction in delta frequencies in the EEG records of both normal and pyridoxine-deficient rats. Reduced seizure threshold and delayed neuronal recovery are related to the significantly reduced brain regional GABA and elevated glutamate levels in pyridoxine-deficient rats.
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PMID:Picrotoxin and pentylene tetrazole induced seizure activity in pyridoxine-deficient rats. 790 54

We studied the efficacy of the competitive NMDA receptor antagonist CGP 40116 in protecting against seizure-induced neuronal necrosis from lithium-pilocarpine-induced status epilepticus (SE). Rats were given CGP 40116 either before SE (12 mg/kg i.p.) or 15 min after the onset of SE (4, 12 and 24 mg/kg); controls received normal saline 15 min after SE began. Diazepam and phenobarbital were given i.p. after 3 h of SE to stop the seizures. Rats were killed 24 h later, and their brains were processed for light microscopic examination. Neuronal damage occurred in 24 of 25 brain regions examined in saline-injected animals. Protection was maximal in rats given 12 and 24 mg/kg CGP 40116 after SE onset: 19 and 21 of the 24 damaged regions were protected respectively, but the 24 mg/kg group had a mortality rate comparable to saline-injected controls. No necrotic neurons were found in posterior cingulate and retrosplenial neurons at the two highest CGP 40116 doses, suggesting that the transient cytoplasmic vacuolization induced by NMDA receptor antagonists does not progress to frank necrosis. In rats given CGP 40116 seizure discharges were not eliminated, but their amplitudes were significantly reduced 2 h after SE began. The periodic epileptiform discharge (PED) EEG pattern, probably a sign of widespread neuronal damage, developed in saline-injected controls after 2-2.5 h of SE but not in rats given 12 and 24 mg/kg of CGP 40116. CGP 40116 provided widespread protection against seizure-induced neuronal necrosis, suggesting that an essential step in its production is NMDA receptor activation by endogenous glutamate. The neuroprotection provided was not simply an antiepileptic effect, since electrographic seizures persisted despite NMDA receptor blockade. CGP 40116 and NMDA receptor antagonists in general could be useful as adjunctive neuroprotectants in patients with refractory SE.
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PMID:The competitive NMDA receptor antagonist CGP 40116 protects against status epilepticus-induced neuronal damage. 791 91

Neuronal migration disorders are rare malformations which can be associated with epileptic seizures. We report about a 14-year-old female patient suffering from epilepsy with infantile spasms, myoclonic-astatic seizures and absences. The EEG showed generalized 2.5-3/sec spike-wave paroxysms. As the possible cause of the disease the MRI scan exhibited a bilateral band heterotopia.
Seizure 1994 Jun
PMID:Band heterotopia: a rare cause of generalized epileptic seizures. 808 43


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