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

A multidisciplinary workshop held from September 29 to October 1, 1989, at Airlie House, Warrenton, Virginia, considered the neurologic complications of whooping cough and pertussis vaccine. Pertussis mortality in the U.S. in 2-3/1000 cases. Seizures occur in 1.9% of cases, and encephalopathy in 0.3%. Reviewing all data, it appears likely that a combination of one or more bacterial toxins, asphyxia, CO2 retention and loss of cerebral vascular autoregulation is responsible for neurologic symptoms. The timing of the encephalopathy suggests that it results from increased lysis of bacteria, and release of endotoxin. The encephalopathy is not confined to the paroxysmal phase. In evaluating side-reactions to the vaccine, the following must be kept in mind: 1. Vaccines are not standardized between manufacturers. 2. For a given manufacturer, vaccines are not standard from one batch to the next. 3. Unless the vaccine is properly prepared and refrigerated, its potency and reactivity varies with shelf life. In fact, the whole question of vaccine detoxification has never been systematically investigated. Listed in order of increasing severity, observed adverse reactions include irritability, persistent, unusually high pitched crying, somnolence, seizures, a shock-like "hypotensive, hyporesponsive" state, and an encephalopathy. Since the neurologic picture is not specific for pertussis vaccination, its temporal relationship to the vaccination is the critical variable for determining causation. Although the majority of seizures following pertussis vaccination are associated with fever, it was the consensus of the neurologists attending the workshop, that these do not represent febrile convulsions, but are non-benign convulsions. The incidence of post-vaccine encephalopathy is difficult to ascertain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Workshop on neurologic complications of pertussis and pertussis vaccination. 198 Dec 51

Breathing rate (RR), end-tidal percent CO2, and EEG were obtained in three groups: psychiatric referral subjects presenting with anxiety, panic phobia, depression and migraine; a group of idiopathic seizure sufferers; and a group of asymptomatic controls. Virtually all the noncontrol subjects were found to show moderate to severe hyperventilation and the accompanying EEG dysrhythmia. The seizure group subjects were taught diaphragmatic respiration with end-tidal percent CO2 biofeedback. The training normalized their respiration and altered their EEGs and seizure frequency.
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PMID:Effect of diaphragmatic respiration with end-tidal CO2 biofeedback on respiration, EEG, and seizure frequency in idiopathic epilepsy. 212 89

1. To study the effects of brief periods of hypoxia on cellular functions in the rat hippocampal slice, extracellular and intracellular recordings were made from pyramidal neurons, and interstitial potassium activity ([K+]o) was measured in the pyramidal cell layers. Slices were perfused in an interface chamber at 36-37 degrees C with medium containing 8.5 mM [K+]o. Hypoxia was induced by switching the overflow gas from O2-CO2 to N2-CO2. 2. Brief periods of hypoxia (5-60 s) produced electrographic seizures with typical tonic and clonic components in 53% of 293 slices that generated spontaneous interictal bursts. Hypoxia-induced seizures were usually initiated in and restricted to the Ca1 region; only 2.5% of these slices generated seizures in CA3. In contrast to the CA1 region, the CA3 region could undergo spreading depression during hypoxia. The probability of seizure generation in CA1 was increased with increasing duration of hypoxia and was greatly reduced by lowering the bath temperature a few degrees. 3. [K+]o gradually increased in the CA1 and CA3 cell layers during the 20 s leading up to an hypoxia-induced seizure. [K+]o rose to approximately 9.8 mM (from a base line of 8.5 mM) in CA1 just before a seizure and to 11.4 mM during the seizure. After hypoxia, [K+]o reached a higher level in CA1 than in CA3, regardless of whether 1 microM tetrodotoxin was present to eliminate differences in cell firing in the two regions. CA1 pyramidal cells and glia gradually depolarized by several millivolts during and after hypoxia; no initial hyperpolarizing phase was detected. 4. Burst input from CA3 was necessary for hypoxia-induced seizures. The frequency and intensity of spontaneous burst-firing in CA3 remained steady in the period leading up to a CA1 seizure episode. In contrast, the intensity of synaptically driven bursts in CA1 grew markedly just before seizure onset. N-methyl-D-aspartate (NMDA) receptors participated in the crescendo of increasingly synchronous activity in CA1, because the competitive NMDA receptor antagonist, D-2-amino-5-phosphonovaleric acid (D-APV, 30 microM), stereoselectively reduced seizure intensity. 5. Hypoxia-induced seizures were followed by a depressant phase, which was manifested most prominently by a prolonged (up to several minutes) reduction in the frequency and intensity of burst-firing in the CA3 region, hyperpolarization of CA1 neurons, and undershoot of [K+]o. In normal (3.5 mM) [K+]o, synaptically driven population spikes in CA1 were only reduced in amplitude by hypoxia; hypoxia did not induce seizures in 3.5 mM [K+]o.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Different responses of CA1 and CA3 regions to hypoxia in rat hippocampal slice. 215 21

The disparity between the seizure sensitivity of the dorsal and ventral hippocampus to opioid peptides was studied by an in vitro electrophysiological method. Slices taken from the ventral (temporal) and dorsal (septal) regions of rat hippocampi were perfused in artificial cerebrospinal fluid bubbled continuously with 95% O2-5% CO2 at 34 degrees C. A stimulating electrode was placed in the stratum radiatum of CA3 region and electrical activity was recorded from the pyramidal cell body layer of the CA3b region. Paired dorsal and ventral hippocampal slices were perfused with [N-Me-Phe3-D-Pro4]morphiceptin (PL017), a specific mu opioid receptor agonist. Application of 0.05 microM PL017 produced triggered and spontaneous bursting in 20% of ventral hippocampal slices, but no such effect was observed in dorsal hippocampal slices. At 0.5 microM PL017, 80% of ventral hippocampal slices developed spontaneous bursting, whereas only 10% of dorsal hippocampal slices had spontaneous bursting. Slices from the ventral hippocampus consistently produced greater degrees of bursting at lower doses relative to the dorsal hippocampus. The addition of 0.1 microM naloxone before or after PL017 inhibited the triggered response but could not block the spontaneous bursting. Perfusion of ACSF for 1 hr also eliminated the triggered response but could only reduce the frequency of the spontaneous bursting. These results suggest that the ventral hippocampus has a higher susceptibility to PL017-induced epileptiform bursting, and this effect is mediated, at least in part, through mu opioid receptors.
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PMID:Opioid-induced epileptiform bursting in hippocampal slices: higher susceptibility in ventral than dorsal hippocampus. 215 97

Sudden incapacitations can affect a pilot and even a whole crew during a flight, preventing them from performing their task in complete safety. In some cases, they could even cause an accident. Our study examines the causes of sudden in-flight incapacitation in Air France pilots and flight engineers from 1968-88. Ten cases were reported out of a population of 1,800 cockpit crew, each flying an average of 600 h/year. These incapacitations were due to cardiac disorders (1 atrial fibrillation, 1 sinus tachycardia), epileptic attacks (2 generalized seizures), duodenal hemorrhages (2 cases), infection (1 case of severe vertigo due to viral labyrinthitis), metabolic disorders (1 case of hypoglycemia), and sometimes disorders affecting the whole crew (1 case of hypoxia due to a pressurization deficiency, 1 case of CO2 intoxication caused by the inadequate packaging of a container refrigerated in dry ice). Seven times out of ten, incapacitations occurred during cruising, twice during approach, and once on the ground before starting up, with closed doors (CO2 intoxication). Two of these incapacitations led to flight diversions. None of them caused an accident. In this series, incapacitations of a cardiac nature were rarer and less serious than those caused by gastrointestinal or neurological disorders. Prevention is based on detection during systematic medical check-ups, and on crews being trained to recognize subtle incapacitations early and to ensure that the flight continues safely when such a case occurs.
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PMID:Clinical aspects of inflight incapacitations in commercial aviation. 231 81

This study was designed to investigate the hemodynamic characteristics of cavernous angiomas of the brain. Five adult patients with a cavernous angioma underwent local cortical blood flow studies and vascular pressure measurements during surgery for the excision of the cavernous angioma. Clinical presentation included headache in four patients, seizures in four patients, and recurring diplopia in one patient. Magnetic resonance imaging demonstrated the cavernous angiomas in all patients and revealed an associated small hematoma in two. Four patients with a cerebral cavernous angioma were operated on in the supine position and the remaining patient, whose lesion involved the brain stem, was operated on in the sitting position. Mean local cortical blood flow (+/- standard error of the mean) in the cerebral cortex adjacent to the lesion was 60.5 +/- 8.3 ml/100 gm/min at a mean PaCO2 of 35.0 +/- 0.6 torr. Mean CO2 reactivity was 1.1 +/- 0.2 ml/100 gm/min/torr. The local cortical blood flow results were similar to established normal control findings. Mean pressure within the lesion in the patients undergoing surgery while supine was 38.2 +/- 0.5 mm Hg; a slight decline in cavernous angioma pressure occurred with a drop in mean systemic arterial blood pressure and PaCO2. Mean pressure in the cavernous angioma in the patient operated on in the sitting position was 7 mm Hg. Jugular compression resulted in a 9-mm Hg rise in cavernous angioma pressure in one supine patient but no change in the patient in the sitting position. Direct microscopic observation revealed slow circulation within the lesions. The hemodynamic features demonstrated in this study indicate that cavernous angiomas are relatively passive vascular anomalies that are unlikely to produce ischemia in adjacent brain. Frank hemorrhage would be expected to be self-limiting because of relatively low driving pressures.
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PMID:Vascular pressures and cortical blood flow in cavernous angioma of the brain. 239 87

The effect of maturation and motor activity on recovery from hypoxic apnea by gasping (autoresuscitation) was investigated in Swiss Webster mice and a SW-related strain. Apnea was induced with 97% N2-3% CO2 and air given at its onset. In 69 Swiss Webster-related strain mice that gasped for at least 5s, the survival rates were 100% in 1- to 16-day-old mice, 19% in 17- to 23-day-old mice, and 90% in adults. The rates in 81 Swiss Webster mice were 100, 70, and 95%, respectively. The decrease in survival in 17- to 23-day-old mice was statistically significant for both strains, as was the difference in survival in 17- to 23-day-old mice between the two strains. Gasping was absent or of brief (less than 5s) duration in 15 Swiss Webster mice that failed to recover. Seizure-like activity was observed during hypoxic apnea and gasping but was not seen significantly more often in mice that died. Simultaneous recordings of limb movement (electromyogram) and breathing pattern indicated that movement did not interfere with the occurrence of gasping. We conclude that in adults and very young mice autoresuscitation is a powerful mechanism for recovery from hypoxia, but at an intermediate age, it is frequently unsuccessful.
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PMID:Effect of maturation on spontaneous recovery from hypoxic apnea by gasping. 274 3

Cerebral blood flow was measured and compared in 10 symmetrical brain regions following unilateral trigeminal ganglionectomy (n = 13), sham operation (n = 6), or trigeminal root section (rhizotomy) (n = 8) in cats. Multiple determinations were obtained in anesthetized and paralyzed animals using radiolabeled microspheres during (i) normocapnia-normotension, (ii) hypercapnia (5% CO2/95% room air), (iii) angiotensin-induced acute severe hypertension (190 greater than mean arterial blood pressure less than 210 mmHg), or (iv) bicuculline-induced seizures. Flow was symmetrical in all brain regions at rest and during increases induced by hypercapnia in the three groups. During severe hypertension or seizures, marked elevations developed bilaterally (approximately 93% and approximately 130%, respectively). In ganglionectomized animals, increases due to hypertension or seizures were attenuated by 28-32% on the denervated side within cortical gray matter regions corresponding to the anterior, middle, and posterior cerebral arteries. Flow was symmetrical within all brain regions in sham-operated animals and in the rhizotomy group, despite comparable increases in regional cerebral blood flow induced by angiotensin. Hence, the trigeminal nerve mediates blood flow adaptations during severe hypertension and seizures. Furthermore, since trigeminal cell bodies and peripheral axons are destroyed or degenerate following ganglionectomy but not following rhizotomy, local "axon reflex-like" mechanisms mediate these increases in cerebral blood flow.
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PMID:Trigeminovascular fibers increase blood flow in cortical gray matter by axon reflex-like mechanisms during acute severe hypertension or seizures. 291 86

Although animal models consistently indicate that gamma-amino-butyric acid (GABA) synaptic function (GABA levels, synthesis, uptake and/or receptors) is decreased in seizure states, there is little evidence to date in support of such a hypothesis for human epilepsy. This chapter presents the results of an in-depth study of the activity of the GABA-synthesizing enzyme L-glutamic acid decarboxylase (GAD) in brain tissue removed during neurosurgical resection for intractable epilepsy. The tissue studied is unique in that identified (by stereo EEG) foci were excised (rather than large blocks of tissue containing mixtures of foci and nonepileptic material) and compared with nonepileptic (stereo EEG and morphological definitions) tissue from the same patients. In patients in which there was no indication of a tumor, GAD activity in the foci was low in more than 50% of the patients examined. Furthermore, when the population distribution of GAD was compared in epileptic versus nonepileptic tissue fragments from all patients, the peak distribution of epileptic tissue fragments occurred at much lower GAD activities than for the nonepileptic fragments (0-20 versus 41-80 nmol CO2/mg protein X hr, respectively). A small subgroup of epileptic fragments occurred with a normal GAD distribution, indicating that the presence of an epileptic focus was not invariably associated with low GAD activity. When the low levels of GABA "A" binding sites in these epileptic tissue fragments are taken into consideration in combination with the low GAD levels, then it can be estimated that 60 to 70% of the present patient population had deficient GABAergic transmission in epileptic foci as compared to nonepileptic brain tissue from the same patients. It follows that the GABA hypothesis of human epilepsy is not an exclusive or unitary hypothesis, and some patients appear to have normally functioning GABA synapses (as assessed biochemically) in epileptogenic areas. Thus, other neurotransmitter and neurohumoral systems certainly play a role in the epileptic process.
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PMID:Alterations of GABA-mediated synaptic transmission in human epilepsy. 301 Jun 75

The relationships between inhibition of carbonic anhydrase (CA) activity in cytoplasmic, microsomal, and myelin subcellular fractions obtained from cerebral cortex, subcortex, and cerebellum and electroshock seizure threshold (EST) and modification of the extension/flexion (E/F) ratio following maximal electroshock seizures (MES) were ascertained in Swiss-Webster mice given 40 and 200 mg/kg acetazolamide. The parameters were determined at 1, 4, and 24 h after administration of acetazolamide. The results showed that changes in the E/F ratio induced by acetazolamide correlated linearly (r = 0.90) with changes in CA activity in the cytoplasm of the subcortex. However, there was an inverse power function correlation (r = 0.92) between EST and CA activity in the myelin fraction of the cerebral cortex. The time course of acetazolamide inhibition of CA activity in these two fractions also paralleled the time course of its effects on EST and E/F ratio. Thus, acetazolamide decreases susceptibility to seizures (raises EST) by inhibiting myelin CA and prevents spread of seizure activity by inhibiting CA in the cytoplasm of glial cells. The CO2 that accumulates as a result of CA inhibition in these two fractions causes profound changes in brain function.
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PMID:Correlation between effects of acute acetazolamide administration to mice on electroshock seizure threshold and maximal electroshock seizure pattern, and on carbonic anhydrase activity in subcellular fractions of brain. 309 9


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