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

The effects of adding vigabatrin (GVG) to the antiepileptic regimens of 16 children with refractory epilepsy have been studied. One-half of the regimens included sodium valproate (VPA). Parameters studied were seizure reduction, platelet GABA-T activity, and steady-state plasma concentrations (CSS) of GVG and VPA. Add-on GVG reduced the seizure frequency both in patients receiving VPA (from 42.9 to 4.5 seizures/month, p < 0.01) and in those without VPA (from 60.0 to 31.7 seizures/month, p < 0.05). GVG also reduced GABA-T activity in both groups (from 19.4 to 5.4, p < 0.001 and from 8.3 to 4.5 pmol/min/mg of protein, p < 0.05, respectively). Seizure reduction and GABA-T inhibition were greater in patients taking VPA than in those who were not. In patients receiving VPA, no significant changes were observed in VPA CSS values before and after the addition of GVG. On the other hand, no differences were found in GVG CSS values between patients with and without VPA. It is concluded that the coadministration of GVG to valproate reduces the frequency of seizures in refractory epileptic children and does not affect the steady-state plasma concentrations of either drug. Therefore, their association could be useful in clinical practice.
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PMID:Coadministration of vigabatrin and valproate in children with refractory epilepsy. 147 47

Using real-time in vivo umbelliferone fluorescent imaging, cortical intracellular brain pH (pHi) and cortical blood flow (CBF) were measured in New Zealand white rabbits during generalized seizures induced by intravenous metrazole or sodium penicillin. In the former, brain pHi declined from 7.04 +/- 0.07 to 6.78 +/- 0.07 within 15 min of generalized seizures and remained at this level for 1 h. In the penicillin group, pHi fell from 7.05 +/- 0.10 to 6.81 +/- 0.07 and also remained at this level over 60 min. This brain acidosis was uniform across the brain's surface. With the onset of status epilepticus there was a hyperemia which occurred in a heterogeneous pattern with blood flow appearing to be greater adjacent to cortical vasculature and slower in border zones between surface blood vessels. In the metrazole group, there was evidence of vasomotor paralysis with loss of autoregulation involving both cortical surface vasculature and penetrating arterioles with their capillary beds.
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PMID:Panoramic imaging of brain pHi and CBF during penicillin and metrazole induced status epilepticus. 147 98

A retrospective review of pharmacy records during a 7-year period at the Johns Hopkins Oncology Center revealed that 6 patients received greater than 4 g of morphine sulfate per day by continuous infusion (CI). Three patients received high-dose infusions for more than 24 h. Two of these 3 patients developed grand mal seizures, while the third was receiving a neuromuscular blocking agent making detection of seizures difficult. Prolonged administration of high concentrations of the sodium bisulfite preservative contained in the morphine solution is a possible explanation for the development of these seizures. Caution is suggested in using CI, preservative-containing morphine at high doses.
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PMID:Grand mal seizures associated with high-dose intravenous morphine infusions: incidence and possible etiology. 148 21

The effect of human calcitonin and sodium valproate (VPA) on electrically induced seizures in rats was assessed. Intraperitoneal administration of calcitonin (20 and 40 IU/kg) 60 min prior to electroshock significantly reduced the duration of the seizures and their intensity. We also found that combined treatment with calcitonin (20 and 40 IU/kg i.p.) and VPA (100 mg/kg p.o.) did not enhance the anticonvulsant activity. These findings suggest that calcitonin exerts an anticonvulsant influence on rats during electrically induced seizures.
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PMID:Anticonvulsive properties of calcitonin in rats. 149 95

The "transurethral resection of prostate" syndrome (TURPS) is the clinical manifestation of the resorption into the patient's body of a large amount of glycocolle-containing irrigating fluid used for this procedure. The full clinical picture, which is seldom seen, consists of dyspnoea, nausea, arterial hypertension, an increased central venous pressure, cerebral oedema, cardiogenic shock and renal failure. Improved surgical techniques, as well as incomplete and atypical forms of the syndrome could explain this low incidence. Absorption into the blood stream may be rapid, by way of the prostatic venous plexi, or slower, from the spaces around the prostate and under the peritoneum. The present-day pathophysiological theory explains this syndrome by an acute hyponatraemia, sometimes dissociated from the hypoosmolality, the toxicity of glycocolle, and the neurological effects of hyperammonemia. Acute hyponatraemia, with blood sodium concentrations below 115 to 120 mmol.l-1, should be considered as potentially serious. The different mechanisms involved may act alone or together, thus explaining that the minor forms of the syndrome mostly consist of a neurological picture. The emergency treatment depends on the natraemia. It includes diuretics and progressive reloading of the patient with sodium in case of severe hyponatraemia with seizures. The best prevention is a correct surgical indication and technique. The resection should not last for more than 90 to 120 min. The major problem remains the early diagnosis of TURPS. Carrying out this surgery under regional anaesthesia is helpful for this purpose, but, in the near future, the best means might be the monitoring of expired ethanol concentrations.
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PMID:[Prostate transurethral resection syndrome]. 150 91

The mechanisms that give rise to ischemic brain damage have not been definitively determined, but considerable evidence exists that three major factors are involved: increases in the intercellular cytosolic calcium concentration (Ca++i), acidosis, and production of free radicals. A nonphysiological rise in Ca++i due to a disturbed pump/leak relationship for calcium is believed to cause cell damage by overactivation of lipases and proteases and possibly also of endonucleases, and by alterations of protein phosphorylation, which secondarily affects protein synthesis and genome expression. The severity of this disturbance depends on the density of ischemia. In complete or near-complete ischemia of the cardiac arrest type, pump activity has ceased and the calcium leak is enhanced by the massive release of excitatory amino acids. As a result, multiple calcium channels are opened. This is probably the scenario in the focus of an ischemic lesion due to middle cerebral artery occlusion. Such ischemic tissues can be salvaged only by recirculation, and any brain damage incurred is delayed, suggesting that the calcium transient gives rise to sustained changes in membrane function and metabolism. If the ischemia is less dense, as in the penumbral zone of a focal ischemic lesion, pump failure may be moderate and the leak may be only slightly or intermittently enhanced. These differences in the pump/leak relationship for calcium explain why calcium and glutamate antagonists may lack effect on the cardiac arrest type of ischemia, while decreasing infarct size in focal ischemia. The adverse effects of acidosis may be exerted by several mechanisms. When the ischemia is sustained, acidosis may promote edema formation by inducing Na+ and Cl- accumulation via coupled Na+/H+ and Cl-/HCO3- exchange; however, it may also prevent recovery of mitochondrial metabolism and resumption of H+ extrusion. If the ischemia is transient, pronounced intraischemic acidosis triggers delayed damage characterized by gross edema and seizures. Possibly, this is a result of free-radical formation. If the ischemia is moderate, as in the penumbral zone of a focal ischemic lesion, the effect of acidosis is controversial. In fact, enhanced glucolysis may then be beneficial. Although free radicals have long been assumed to be mediators of ischemic cell death, it is only recently that more substantial evidence of their participation has been produced. It now seems likely that one major target of free radicals is the microvasculature, and that free radicals and other mediators of inflammatory reactions (such as platelet-activating factor) aggravate the ischemic lesion by causing microvascular dysfunction and blood-brain barrier disruption.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pathophysiology and treatment of focal cerebral ischemia. Part II: Mechanisms of damage and treatment. 150 80

Classification, management and prevention of seizures in children are summarized for clinicians in Papua New Guinea. Seizures are classified as febrile with or without underlying brain pathology, and afebrile, including neonatal fits, infantile spasms, myoclonic jerks, akinetic seizures, tonic clonic fits, petit mal, benign focal, and psychomotor seizures. In all cases the first step is to secure the airway, then do a fingerstick and treat hypoglycemia, and finally stop the fit if it is prolonged with paraldehyde, diazepam, phenobarbitone or phenytoin. A cause for the seizure should be sought: physical exam, especially tympanic membranes and throat, blood slide for malaria, lumbar puncture for signs of meningitis, blood culture, serum calcium, and other chemistries. Some empirical treatments to use for negative findings include: dextrose, calcium gluconate, magnesium SO4, pyridoxine, quinine and Fansidar. Hyperthermia in a febrile child can be reversed with cool sponging. The author recommends prescribing phenobarbitone to prevent subsequent simple febrile seizures if the child has 3 or more, then slowly withdrawing the drug if the child is seizure free for a year. Drug therapy for the various other types of seizures available in Papua New Guinea include sodium valproate by special order, and phenobarbitone, phenytoin, carbamazepine, nitrazepam, ethosuximide, and prednisolone. A table is provided to help select the drug for each seizure type, e.g. ethosuximide for petit mal, prednisolone for infantile spasms, and carbamazepine for various types of focal and psychomotor seizures.
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PMID:Convulsions in children. 150 14

While the clinical toxicity of tricyclic antidepressants, particularly the development of seizures and arrhythmias, has been strongly correlated with a QRS interval of greater than or equal to 100 msec on electrocardiography, the resolution pattern of QRS abnormalities remains poorly defined. We prospectively monitored 22 consecutive patients who were referred to a regional poison center after a tricyclic antidepressant ingestion associated with a QRS interval of greater than 100 msec. An ECG was obtained every 6-8 h in all patients until the QRS interval was less than 100 msec. Among enrolled patients the mean maximal QRS interval was 145 msec. Ten patients (45.5%) developed seizures while 6 (27%) developed cardiac arrhythmias. The time from ingestion to the last ECG demonstrating a widened QRS interval was a median 12.3 h (range 1-70 h); the time from ingestion to the first ECG with a QRS less than 100 msec was a median 19.3 h (range 3-78 h). No patients developed seizures or life-threatening cardiac arrhythmias after the QRS interval was less than 100 msec. Ten patients received sodium bicarbonate while 12 did not. There were no significant differences in the duration of QRS widening between the two groups. These data suggest that the typical period of QRS prolongation after severe tricyclic antidepressant ingestion is 12-18 h but may be as long 3 d. The factors which determine the duration of QRS widening are unclear. Sodium bicarbonate may not reduce the total duration of QRS disturbances.
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PMID:Duration of QRS disturbances after severe tricyclic antidepressant intoxication. 151 11

Intrathecal (IT) administration of vasopressin produces antinociception, scratching behavior, and motor suppression. The present experiments characterized these effects with regards to the following: 1) VP receptor specificity, 2) possible involvement of endogenous opiates, 3) possible involvement of seizure activity, and 4) whether the antinociception is due to direct actions of VP at the spinal cord. These studies showed that IT administration of a V1-specific vasopressin antagonist completely blocked the antinociception, scratching behavior, and motor suppression produced by 25 ng IT vasopressin. Furthermore, IT administration of the vasopressin metabolite, [pGlu4,Cyt6]AVP(4-9), produced none of the effects produced by vasopressin. Systemic administration of the opiate antagonists naloxone (1 mg/kg IP) and naltrexone (10 mg/kg IP) had no significant effect on the antinociception produced by IT vasopressin, whereas naltrexone potentiated the scratching behavior. Neither the IT vasopressin-induced antinociception nor scratching behavior was affected by pretreatment with the anticonvulsant sodium valproate. In addition, IT vasopressin inhibited the tail flick reflex in rats with transected spinal cords, demonstrating direct spinal effects of vasopressin. In conclusion, IT administration of vasopressin produces antinociception, scratching behavior, and motor suppression via activation of VP-specific receptors in the spinal cord.
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PMID:Characterization of intrathecal vasopressin-induced antinociception, scratching behavior, and motor suppression. 153 7

Cerebral cell volume regulatory mechanisms are activated by sustained disturbances in plasma osmolality. Acute hypernatremia causes a predictable shrinkage of brain cells due to the sudden imposition of a plasma-to-cell osmolal gradient. However, during chronic hypernatremia cerebral cell volume is maintained close to the normal range as a result of the accumulation of electrolytes and organic osmolytes including myo-inositol, taurine, glutamine, glycerophosphorylcholine, and betaine. The increased cytosolic level of these molecules is generally accomplished via increased activity of sodium (Na+)-dependent cotransport systems. The slow dissipation of these additional osmotically active solutes from the cell during treatment of hypernatremia necessitates gradual correction of this electrolyte abnormality. Acute hyponatremia leads to cerebral cell swelling and severe neurological dysfunction. However, prolonged hyponatremia is associated with significant reductions in brain cell electrolyte and organic osmolyte content so that cerebral cell volume is restored to normal. While acute hyponatremia can be treated with the administration of moderate doses of hypertonic saline in order to control seizure activity, chronic hyponatremia should be corrected slowly in order to prevent subsequent neurological deterioration. If the rate of correction exceeds 0.5 mmol/l per hour, or if the total increment in serum [Na+] exceeds 25 mmol/l in the first 48 h of therapy, then there is an increased risk of the development of cerebral demyelinating lesions. Chronic hyperglycemia activates the brain cell volume regulatory adaptations in the same manner as hypernatremia. Therefore, during the treatment of diabetic ketoacidosis, it is imperative to restore normoglycemia gradually in order to prevent the occurrence of cerebral edema.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Cell volume regulation: a review of cerebral adaptive mechanisms and implications for clinical treatment of osmolal disturbances: II. 153 29


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