Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glutamic acid decarboxylase (GAD) activity in cerebrospinal fluid (CSF) was determined in 53 patients with neurological diseases as follows: Epilepsy (n:17), febrile convulsions (n:3), meningoencephalitis (n:17), encephalopathies (n:10), CNS leukemia (n:3), congenital hydrocephalus (n:2) and pseudoileus neonatorum (n:1). Compared with the mean normal value (5.2 +/- 2.5 pmol CO2 formed/hr/ml) reported in Part I, a significant increase of GAD activity in CSF was demonstrated in patients with uncontrolled epileptic seizures (11.4 +/- 3.9 pmol CO2 formed/hr/ml), febrile convulsions (13.5 +/- 8.7), viral meningitis with or without encephalitis (20.3 +/- 13.6), encephalopathies (30.0 +/- 25.9), CNS leukemia (11.1 +/- 5.0), congenital hydrocephalus (20.5 +/- 7.3) and pseudoileus neonatorum (28.6). Markedly high GAD activity was found in patients with CNS leukemia several days after intrathecal injection of methotrexate (39.8 +/- 18.0). On the other hand, significantly low GAD activity was shown in patients with bacterial meningitis or brain abscess (1.3 +/- 1.2). This suggests that some bacterial factors may be inhibitory toward GAD activity in CSF. High GAD activity in CSF may be useful as an indicator of aseptic brain dysfunction, although it was not always correlated with the severity of symptoms.
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PMID:Glutamic acid decarboxylase in cerebrospinal fluid in infancy and childhood Part II. Glutamic acid decarboxylase activity in cerebrospinal fluid of children with neurological diseases. 666 Apr 21

Interictal positron computed tomography (PCT) with 18F-fluorodeoxyglucose was performed on 50 patients with partial seizures disorders. Electroencephalographic (EEG) monitoring was carried out during the metabolic studies using scalp and sphenoidal electrodes in 33 patients and stereotaxically implanted depth electrodes in 17. Four patients in this series had focal abnormalities on x-ray computed tomographic scans, but these were at the site of the presumed epileptogenic lesion in only 2. One or more discrete zones of hypometabolism were identified in 35 patients, and only 1 patient appeared to show focal interictal hypermetabolism. No quantitative relationship could be demonstrated between the degree of focal hypometabolism and either the frequency of interictal EEG spikes of the presence of focal nonepileptiform EEG changes. It was concluded that metabolic and electrophysiological techniques measure different aspects of cerebral dysfunction in seizure disorders. Although interictal PCT in patients with partial epilepsy usually demonstrates zones of hypometabolism this finding, per se, does not reveal the epileptic nature of the abnormality.
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PMID:Interictal cerebral glucose metabolism in partial epilepsy and its relation to EEG changes. 681 96

The clinical and laboratory features of 24 patients with proven mitral valve prolapse (MVP) and brain dysfunction are reported. The age range of affected patients was between 20 and 63 years (average of 43) and 70 percent were women. MVP was documented prior to the brain illness in only 4 patients. The majority of patients experienced bland cerebral infarction. Disorders also included transient ischemic attacks, cerebellar infarctions, parencymatous and subarachnoid hemorrhage, seizures and retinal artery occlusion. Significant risk factors for stroke other than MVP were lacking in the patient group. Cerebral angiograms occasionally showed distal occlusions of small arteries suggesting embolic brain lesions. Our study suggests that MVP is a risk factor for stroke. We recommend echocardiography in patients with cerebral ischemia who lack clear, recognized risk factors for stroke. We believe the basis for this brain disorder to be emboli from damaged mitral valve leaflets.
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PMID:Brain events associated with mitral valve prolapse. 742 82

To clarify the changes occurring in EEG and ECG from seizure induction to sudden death, 25 weanling male Sprague-Dawley rats were fed a severely Mg-deficient diet for 18 days. In nine of 25 Mg-deficient rats, both EEG and ECG were recorded from the beginning of seizures induction until sudden death. When flattening of EEG became after seizure occurrence, all nine Mg-deficient rats did not recover and death occurred within a few minutes. These results may support the idea that sudden death in Mg-deficient rats resulted from brain dysfunction after repetitive episodes of noise-induced seizures and not from simple apnoea due to tonic contraction of respiratory muscle.
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PMID:Sudden sound-induced death in magnesium-deficient rats after repetitive episodes of seizures result from brain dysfunction. 766 7

Investigators disagree on the significance of and the best treatment for neonatal seizures. Each year more data are revealed and the controversy continues. A foundation must be laid for discussing this controversy by reviewing neonatal seizure classification and etiology. Neonatal seizures may occur with and without electroencephalogram (EEG) correlation. Although some seizures may not correlate with an abnormal EEG, they may still be a sign of significant brain dysfunction. The nurse's understanding of these principles and the ability to recognize and report these events will enable the neonate to receive the proper care and treatment in the most expedient manner.
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PMID:Neonatal seizures: the debate continues. 770 40

We present here magnetic resonance imaging (MRI) and single photon emission computed tomography with 123I-N-isopropyl-p-iodoamphetamine (123I-IMP-SPECT) of a patient suffering from Klinefelter's syndrome with various neuropsychiatric symptoms. He was a 30-year-old male, who showed impaired consciousness seizures, auditory hallucination, delusion of reference, delusion of grandeur, psychomotor excitement and intellectual impairment. Although no focal lesion was detected by computed tomography or T1-weighted MRI, T2-weighted MRI provided a heterogeneous high-signal-intensity lesion of the inferior part of the left temporal lobe, which was not enhanced with Gd-DTPA. In addition 123I-IMP-SPECT exhibited focal hypoperfusion in the left temporal lobe on the early images. We suggest that the neuropsychiatric symptoms of this case are associated with the focal organic brain dysfunction which was revealed by MRI and 123I-IMP-SPECT.
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PMID:MRI and SPECT of Klinefelter's syndrome with various neuropsychiatric symptoms: a case report. 791 Nov 67

Chronic alcoholism is associated with hypercortisolemia and low serum zinc (Zn). Hypercortisolemia could be responsible for alcoholic cerebral atrophy and is also associated with enhanced NMDA neurotoxicity. It is hypothesized that low brain Zn, noted in chronic alcoholics, enhances NMDA excitotoxicity and ethanol withdrawal seizure susceptibility. Also, Zn deficiency can produce neuronal damage through increased free radical formation. Clinically, Zn replacement therapy may be a rational approach to the treatment of alcohol withdrawal seizures and alcohol-related brain dysfunction.
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PMID:Zinc deficiency and corticosteroids in the pathogenesis of alcoholic brain dysfunction--a review. 797 2

Paralysis induced by neuromuscular blocking agents facilitates ventilation of seriously ill patients but may preclude clinical recognition of seizures. We describe the occurrence of severe cognitive impairment in a 14-year-old girl in whom status epilepticus was recognized only when pancuronium was withdrawn after 14 hours of paralysis. This patient emphasizes a potential danger of paralysis from drugs in patients with acute cerebral dysfunction.
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PMID:Failure to recognize status epilepticus in a paralysed patient. 822 90

A thiopental test 2 weeks after insertion of intracranial electrodes may be used to evaluate patients with refractory epilepsy for surgical therapy. Barbiturates normally produce beta activity on the electroencephalogram. The absence of this response in a monitored brain region implies focal cerebral dysfunction. We describe a technique used to perform this test and the resultant morbidity. The thiopental test consists of intravenous injection of thiopental, 25 mg, every 30 s until either corneal reflexes are abolished, 1,000 mg of thiopental has been administered, or adverse events occur. In children, the dose is adjusted to approximately 0.3 mg/kg of thiopental every 20 s. A retrospective chart review was performed on 104 patients who underwent thiopental tests at the University of Pittsburgh Epilepsy Center. Records were systematically reviewed for thiopental dose, mean arterial blood pressure, heart rate, oxygen saturation in arterial blood, time to responsivity, need for airway intervention, and occurrence of nausea or vomiting. Thirty-six patients developed upper airway obstruction which required jaw lift maneuver, six patients were given 1,000 mg of thiopental without loss of corneal reflexes, and one patient briefly sustained an arterial saturation of 67%. Five patients exhibited electrographic seizures with clinical seizures evident in two patients. No permanent effects were evident in any patient as a consequence of the test. We conclude, with appropriate monitoring and personnel, that the thiopental test, as described, can be performed safely with acceptable morbidity.
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PMID:Anesthetic care during thiopental tests to evaluate epileptic patients for surgical therapy. 840 Jul 55

A 7 year old girl with epilepsy and spastic quadriplegia secondary to an episode of status epilepticus at 4 months of age is reported. At the age of 6 years, she began to experience increased generalized myoclonic and tonic seizures during treatment with carbamazepine (CBZ) 200 mg/day and clonazepam 1.5 mg/day. When the CBZ was increased to 400 mg/day, the seizures increased dramatically in frequency. Following discontinuation of CBZ, the seizure frequency decreased to a level less than that prior to starting CBZ. Serial electroencephalograms displayed multifocal independent epileptiform discharges (MIED) characterized by shifting localization, which could be one of the risk factors for exacerbation by CBZ. In this case MIED may indicate widespread rather than localized cerebral dysfunction.
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PMID:Carbamazepine-exacerbated epilepsy with multifocal shifting independent epileptiform discharges on electroencephalogram: a case report. 860 37


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