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

Perinatal factors associated with death or disability at 2 years were identified in an inborn cohort of 196 live births with a birth weight of 500-999 g. Antepartum haemorrhage, multiple pregnancy, breech presentation, perinatal asphyxia, hypothermia on admission, hyaline membrane disease, persistent pulmonary hypertension, severe respiratory failure, and intraventricular haemorrhage were associated with increased mortality. Factors associated with increased survival included maternal hypertension, caesarean birth, increasing maturity or size at birth, female sex, and fetal growth retardation. Stepwise multiple discriminant function analysis showed that six factors correctly classified the outcome in 83% of infants: intraventricular haemorrhage was the most important factor followed by the presence of acidosis and hypoxia in the early neonatal period, birth weight, pre-eclamptic toxaemia, and caesarean birth. This study also showed that intraventricular haemorrhage, seizures, antepartum haemorrhage and delay in regaining birth weight were associated with increased disability among survivors.
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PMID:Perinatal factors and adverse outcome in extremely low birthweight infants. 372 24

Gastric lavage has been used to manage toxic ingestions since the early 1800s. The entire realm of gastrointestinal decontamination has been extensively studied for the past 30 years. Recommendations are still evolving and remain controversial. The current indications for lavage are obtundation, unprotected airway, seizures, the need for urgent removal, and the tendency to form concretions. Hydrocarbon management depends on specific toxicity and viscosity. Contraindications for this procedure are insignificant ingestions, prolonged time since ingestion, and caustic poisoning. Proper technique minimizes complications and maximizes toxin removal. Activated charcoal and a cathartic are given after lavage. Complications include nasal trauma, esophageal perforation, tracheal intubation, aspiration, electrolyte imbalance, and hypothermia.
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PMID:Gastric lavage. 373 88

Mice genetically susceptible (withdrawal seizure prone; WSP) and resistant (withdrawal seizure resistant; WSR) to ethanol (EtOH) withdrawal convulsions have been developed by selective breeding. WSP mice show much more severe EtOH withdrawal than WSR mice after equal intensities of exposure to EtOH. The present experiments report a systematic comparison between WSP and WSR mice with respect to their neurosensitivity to two effects of EtOH, EtOH-induced hypothermia (HT) and loss of righting reflex (RR). The degree of tolerance developed to these effects was also compared between the lines. WSP and WSR mice did not differ in sensitivity to EtOH-induced HT. When EtOH was administered daily for 3 days, both lines developed tolerance as evidenced by attenuated HT, but there was no line difference. Because blood EtOH concentrations did not change, the tolerance was functional rather than pharmacokinetic. When twice-daily injections were given for 4 days before testing on the 5th day in an effort to increase the degree of tolerance achieved, functional tolerance was slightly greater in the WSR line than in the WSP line 90 to 120 min, but not 30 to 60 min, after EtOH. In similar experiments, WSP and WSR mice were found to have the same ED50 to EtOH-induced loss of RR. The brain EtOH concentrations of WSP and WSR mice were the same at the time RR was lost and at the time RR was regained. Thus, neither line developed acute functional tolerance to this effect of EtOH. WSR mice lost RR more quickly than WSP mice.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sensitivity and tolerance to ethanol in mice bred to be genetically prone or resistant to ethanol withdrawal seizures. 377 97

Sulfolane dosages that alter seizure susceptibility were determined using audiogenic (AG), pentylenetetrazol (PTZ) and hippocampal afterdischarge (AD) seizure models. The presence of AG seizures and potentiation of PTZ seizures were investigated in rats injected IP with 0, 200, 400 or 800 mg/kg; AD activity was assessed only at the highest and lowest dosages. The dose-dependent hypothermia associated with sulfolane treatment was controlled in Experiment I and a replication study (Experiment II) by testing under isothermic conditions. The effect of body temperature was measured directly in Experiment III by comparing AG seizure incidence and characteristics exhibited by hypothermic and normothermic animals. Audiogenic seizures were elicited in nearly half of the 800 mg/kg animals in both Experiments I and II. Sulfolane-induced hypothermia, maximal at 3 hours, partially protected against AG seizure characteristics. Potentiation of PTZ seizure severity (800 mg/kg) and duration (800 and 400 mg/kg) also were observed. None of the hippocampal AD parameters was affected significantly by sulfolane treatment. The similarity of the convulsants sulfolane and PTZ is discussed.
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PMID:Sulfolane effects on audiogenic, pentylenetetrazol and afterdischarge seizure activity. 380 77

The formation of tolerance to the hypothermic effect of ethanol was inhibited in rats after intraperitoneal injection of the neurotoxin DSP-4 50 mg/kg. The neurotoxin also significantly suppressed the ethanol withdrawal syndrome; hyperlocomotion, audiogenic seizures and spasticity. These behavioural changes were accompanied by a 52% decrease of the brain norepinephrine (NE) content, with no alterations in the dopamine or serotonin levels. The results indicate that intact NE neurons are necessary for the development of tolerance to ethanol-induced hypothermia and are involved in the expression of the ethanol withdrawal syndrome.
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PMID:Suppression of ethanol tolerance and dependence in rats treated with DSP-4, a noradrenergic neurotoxin. 381 31

Neonates are susceptible to infection since several elements of the immune system are deficient. At present, the most common pathogens are Group B streptococci and Escherichia coli. Prolonged rupture of membranes with amnionitis is a high-risk setting. Clinical signs suggesting neonatal sepsis include respiratory distress, poor feeding, hypothermia, seizures and hypotonia. After the sepsis work-up is completed, the initial choice of antibiotics is based on the prevailing organisms and antibiotic sensitivities within the community.
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PMID:Neonatal sepsis. 389 74

Presented is the case of a normal two-month-old girl who developed seizures secondary to water intoxication. The infant had been fed 20 to 30 oz of water daily for three days, while her usual formula was withheld because of vomiting and diarrhea. On the day of admission, the infant exhibited signs of water intoxication in the form of lethargy, vomiting, and seizures. Hyponatremia, hypothermia, and hyperglycemia were noted on admission, and are common features of the syndrome. The patient responded well to fluid restriction and salt replacement. Previous reports have attributed water intoxication to feeding mismanagement, vigorous hydration, dilute formulas, and swimming lessons.
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PMID:Water intoxication with seizures. 396 5

The acute effects of diisopropylfluorophosphate (DFP) were assessed in DBA/2Ibg, C57BL/6Ibg and C3H/2Ibg mice. The DFP was administered by intraperitoneal injection in saline. Brain acetylcholinesterase (AChE) activity was maximally inhibited within 5 min after injection. All mice showed signs of organophosphate intoxication including salivation, lacrimation, diarrhea, respiratory distress, tremor and, at high doses, seizures. The C57BL mice were most susceptible to these effects of DFP. The LD50 values for DFP were 8.0, 7.6, and 6.8 mg/kg for male DBA, C3H, and C57BL mice, respectively. The LD50 values for females were nearly the same. Body temperature and brain AChE activity decreased in a dose-dependent manner following injections of DFP of 3.17, 4.22, 5.28, and 6.33 mg/kg. Maximum temperature depression occurred 2 hours after DFP administration; by 24 hours temperatures had returned to normal except for C57BL mice treated with the highest dose of DFP. The C57BL strain was most susceptible to the DFP-induced hypothermia, the C3H strain was the most resistant, and the DBA strain was intermediate. Maximum temperature depression and residual AChE activity, as measured 24 hours after injection, were linearly related. These strain differences do not seem to be explained easily by a differential inhibition of AChE activity.
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PMID:Genetically determined differences in acute responses to diisopropylfluorophosphate. 399 71

DBA mice were fed lab chow containing phenobarbital for seven or eight days. Upon withdrawal of the phenobarbital diet, dependence was evidenced by appearance of hypothermia, handling-induced convulsions and lethal seizures. Functional tolerance was determined by injecting phenobarbital into mice treated with the phenobarbital diet or a pair-fed control diet and measuring the brain concentration of phenobarbital at the time of loss of righting reflex and the time of regaining righting reflex. Both measures demonstrated that chronic consumption of phenobarbital resulted in functional tolerance. When the diet was withdrawn for two days, tolerance was no longer present, indicating a rapid reversal of the adaptive changes. The veratridine-stimulated uptake of 24Na by isolated brain synaptosomes was used as a measure of membrane function. Sodium uptake was inhibited in vitro by pentobarbital and ethanol, and the inhibitory effects of these drugs were attenuated by chronic in vivo phenobarbital treatment. The fluidity of brain synaptic plasma membranes was estimated by the fluorescence polarization of the fluorescent probe molecules 1-(4-trimethylammonium phenyl)-6-phenyl-1,3,5-hexatriene and 1,6-diphenyl-1,3,5-hexatriene. Synaptic membranes from mice treated chronically with phenobarbital did not differ from those of control mice with regard to either the baseline fluorescence polarization of the probes or the decrease in fluorescence polarization produced by in vitro exposure to phenobarbital or ethanol. Taken together, these results indicate that although chronic phenobarbital ingestion resulted in tolerance and dependence (studied in vivo), and adaptation of sodium channels (studied in vitro), there was no evidence that these changes were due to alterations in the membrane physical properties.
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PMID:Barbiturate tolerance and dependence: effects on synaptosomal sodium transport and membrane fluidity. 404 Jun 39

Cyclopiazonic acid (CPA) was found to have many pharmacological properties in common with the antipsychotic drugs chlorpromazine and reserpine. Thus, in mice CPA at ip doses of 5-14 mg/kg body weight produced hypokinesia, hypothermia, catalepsy, ptosis, sedation without loss of righting reflex, tremor, gait disturbance, dyspnoea, opisthotonus, atypical convulsion and prolonged barbiturate-induced sleep. The ip LD50 of CPA was found to be 13 +/- 0.05 mg/kg. The tremors induced by near-lethal doses of CPA were associated with voluntary or forced movements (action tremors); they worsened during the days following treatment, but they were weak compared with the exhausting and continuous tremors of the whole body caused by 20 mg tremorine/kg (used for comparison). When death occurred only 24-259 min after administration of CPA (11-14 mg/kg), it was preceded by dypsnoea, cyanosis, opisthotonus and clonic leg movements and tonic extension of hind legs (convulsions). When death was delayed (2-6 days after CPA administration), it was preceded by prostration, ptosis, hypothermia, tremor and cessation of food and water intake resulting in cachexia; convulsions were not seen in this group of mice. CPA did not affect the rate of convulsion or death caused by either maximal electroshock or metrazol administration but it did delay the onset of metrazol-induced seizures. In rabbits, 10 mg CPA/kg body weight initially produced tachycardia, tachypnoea and sedation with an activated electroencephalogram. Of three rabbits given 10 mg CPA/kg one died, and in this rabbit slow delta waves were seen just before and during a brief period with clonic leg movements. In this animal death was accompanied by tonic extension of the hind legs, respiratory arrest and cardiac fibrillation; and epileptiform EEG was not seen at any time. The unexpected EEG activation with sedation in rabbits treated with CPA was similar to the effect of reserpine on EEG.
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PMID:Toxicity and neuropharmacology of cyclopiazonic acid. 404 83


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