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

Magnesium sulfate is used for seizure prophylaxis in patients with preeclampsia. It also has significant effects on calcium metabolism and could, therefore, alter the pressor response to calcium-dependent vasoconstrictors. The present in vivo rat study examined the effect of magnesium sulfate to alter the pressor response to norepinephrine (NE) and angiotensin II (A II). Magnesium doses were chosen to approximate those used in treating preeclampsia. NE resulted in a significant rise in mean arterial pressure (delta MAP, 46 +/- 3.7 mmHg; p < 0.001). A II also resulted in a significant rise in MAP (delta MAP, 23 +/- 3.6 mmHg, p < 0.02). Magnesium sulfate alone had no significant effect on MAP but attenuated the pressor response to both NE (delta MAP, 16 +/- 1.5 mmHg) and A II (delta MAP, 12 +/- 2.5 mmHg). After discontinuation of the magnesium sulfate infusion, the control pressor responses to NE and A II were again seen (delta MAP, 39 +/- 3.5 mmHg and delta MAP, 28 +/- 4.2 mmHg, respectively). Although magnesium sulfate is not a primary antihypertensive agent, it may have effects on blood pressure by attenuating the actions of circulating vasoconstrictors.
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PMID:Effect of magnesium sulfate on the vascular actions of norepinephrine and angiotensin II. 141 60

L-Cycloserine dose-dependently inhibited the activity of gamma-aminobutyric acid (GABA)-transaminase (GABA-T) and elevated the level of GABA in whole mouse brain with a peak effect 3-4 hr after a single intraperitoneal injection. At a dose (30 mg/kg) which elevated the level of GABA almost 4-fold, L-cycloserine moderately increased the content of alanine and slightly reduced that of aspartate, glutamate and glycine in the brain. L-Cycloserine (10-30 mg/kg, p.o. or i.p.) prevented tonic seizures induced by 3-mercaptopropionic acid (3-MPA) and audiogenic seizures in DBA/2 mice, without affecting those evoked by pentylenetetrazol, bicuculline and electroshock. Similarly small doses of L-cycloserine reduced the level of cGMP in the cerebellum of rats, prevented its elevation by 3-MPA and attenuated the hypothalamically-elicited rage reaction in cats. Larger doses of L-cycloserine (greater than 30-100 mg/kg) impaired the performance of mice in the rotarod, chimney and horizontal wire tests, and reduced spontaneous locomotor activity of rats. Upon repeated administration the inhibitory effect of L-cycloserine on the activity of GABA-T and on seizures elicited by 3-MPA in mice increased. In contrast, the depressant action of L-cycloserine on motor performance and locomotion declined in subchronically-treated mice and rats. The levels of amino acids in brain after repeated administration did not differ markedly from those in acutely-treated mice. It is suggested that small doses of L-cycloserine, probably by increasing GABAergic inhibition, reduce hyperexcitability in the brain in acute- and subchronically-treated animals. Larger doses of L-cycloserine, possibly by inducing multiple neurochemical changes, evoke central depressant effects which diminish during subchronic treatment.
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PMID:L-cycloserine: behavioural and biochemical effects after single and repeated administration to mice, rats and cats. 301 1

In experiments on male mice, we studied the effects of gamma-aminobutyric acid (GABA), angiotensin II (AT II), administered intracerebroventricularly, diazepam, injected intraperitoneally, and combinations of GABA + AT II and diazepam + AT II on convulsive seizures induced by pentylenetetrazol (PTZ) (80 mg/kg subcutaneously) and 3-mercaptopropionic acid (3-MPA) (40 mg/kg intraperitoneally). The anticonvulsant effects of GABA and diazepam on PTZ-induced seizures were increased by AT II in doses which did not significantly influence seizures. AT II applied together with GABA or diazepam in ineffective doses provoked a strong anticonvulsant effect on both PTZ- and 3-MPA-induced seizures. These results indicate that the anticonvulsant effects of GABA and diazepam on PTZ- and 3-MPA-induced seizures might effectively be potentiated by the octapeptide AT II. It is suggested that AT II operates as an endocoid acting on GABA, respectively benzodiazepine recognition sites in the CNS.
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PMID:Interactions between angiotensin II, GABA and diazepam in convulsive seizures. 373 89

In Connecticut, physicians followed 19 women with tractable epilepsy for 3-5 months to determine baseline seizure frequency. 14 women agreed to enter a clinical trial evaluating synthetic medroxyprogesterone acetate's (MPA) ability to reduce seizure frequency by adding MPA to the usual antiepileptic drug regimen. They all received 10 mg MPA pills 2-4 times each day. 6 women who did experience amenorrhea later received 120-150 mg intramuscular MPA injections (Depo-Provera) every 6-12 weeks instead of oral MPA. The physicians followed the women for 12 months. 11 women eventually experienced amenorrhea and always had low levels of serum progesterone ( or = ng/ml). Seizure frequency fell significantly from a mean of 8.3 seizures/month before MPA administration to 5.1 seizures/month after MPA administration, equaling 39% fewer seizures (p = .02). 7 women who experienced obvious improvement had 52% fewer seizures on average (25-71%) reduction. All women who had fewer seizures did experience partial seizures, however. MPA did not affect the steady state levels of antiepileptic drugs. MPA levels were higher in women receiving oral MPA than they were in those receiving MPA injections (5.2 ng/ml vs. 2.6 ng/ml). Most women had some spotting, particularly during the first few months of the study. Some of these women discontinued treatment because of this side effect, especially women who did not appear to benefit from the treatment. Menstruation returned in 6-12 months in women receiving MPA injections. Further research on MPA's effect on catamenial seizures is needed.
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PMID:Treatment of seizures with medroxyprogesterone acetate: preliminary report. 654 Apr 15

Injection of kainic acid into rat induced a limbic seizure and increased the activities of two protein kinases with Mrs of 42 kDa and 44 kDa in the hippocampus. These two protein kinases were identified as MAP kinases by an anti-MAP kinase antibody. These MAP kinases were phosphorylated at least at a tyrosine residue. The time course of the MAP kinase activation was roughly parallel with that of the seizure. These results indicate that the kainic acid-induced seizure induces MAP kinase activation in rat hippocampus.
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PMID:Phosphorylation and activation of mitogen-activated protein kinase by kainic acid-induced seizure in rat hippocampus. 751 21

Glutamate decarboxylase (EC 4.1.1.15, GAD) activity was studied in the brain of 12-day-old and adult rats treated with 3-mercaptopropionic acid (3-MPA), an inhibitor of GAD competitive with glutamate. Control GAD activity in the brains of immature animals (91.8 +/- 18.2 nmol/h/mg of protein) was lower than that of the adult rats (228 +/- 37.5 nmol/h/mg of protein). Brain GAD inhibition in adult rats was 58% at the onset of seizures (9 min on the average after administration of 70 mg 3-MPA/kg). At the same time, 3-MPA-treated young rats exhibited 76% inhibition of GAD despite the fact that at 9 min these animals were not yet having seizures. At the onset of seizures (19 min after 3-MPA on the average) their GAD activity remained at the same level. The difference between the groups was not related to the presence of the coenzyme pyridoxal-5'-phosphate in the enzyme assay. The inhibition of GAD by 3-MPA in vitro in the immature and adult brains was similar (Ki at 5.1 microM and 4.8 microM concentrations of 3-MPA, respectively). Identical values were found for Km of GAD (at 4.5 mM concentration of L-glutamate). Calculations based on the results suggest that 3-MPA enters the immature brain more easily than the brain of the adult animals. While GAD inhibition by 3-MPA is the primary cause of seizures, their onset is influenced by other factors, in which the immature brain differs from the adult one and which may include less sensitivity to GABA decrease due to relative overactivity of the GABA system.
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PMID:Differences between immature and adult rats in brain glutamate decarboxylase inhibition by 3-mercaptopropionic acid. 779 89

The convulsant action of 3-mercaptopropionic acid (3-MPA), a known inhibitor of glutamate decarboxylase activity, was studied in 7-, 12-, 18- and 25-day-old rats and in adult animals. 3-MPA elicited predominantly clonic, minimal seizures as well as generalized tonic-clonic (major) seizures at all developmental stages studied. The CD50 for major seizures did not change during development; CD50 for minimal seizures was significantly lower in 18-day-old rats than in older animals. Latency to the onset of seizures was shortest in 18-day-old rats and extremely long in 12- and, especially, in 7-day-old rats. This long latency might signify either changing molecular properties of glutamate decarboxylase during development or slow turnover of GABA at early postnatal stages. Electrocorticographic recordings demonstrated sharp EEG components in the frontal region as a first sign of 3-MPA action, and seizure patterns exhibited similar developmental changes as found with other seizure models (a decrease in duration of individual graphoelements and an increase in synchronization among various cortical regions). This indicates the primary importance of brain maturation in the expression of epileptic EEG phenomena. The correlation between EEG and motor phenomena was poor in the youngest animals and it ameliorated with age, but it never became perfectly coincidental.
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PMID:Motor and electrocorticographic epileptic activity induced by 3-mercaptopropionic acid in immature rats. 824 36

A leading patient complaint is headaches which tend to occur more often in women than men. Nonvascular headache is the most common and is caused by tension or muscle contraction. Oral contraceptives (OCs) do not affect nonvascular headaches. They can also be safely used in women who experience common migraines whose symptoms do not become more severe or frequent during OC use. On the other hand, women who have classic migraine (headache accompanied by focal neurologic symptoms) or common migraine with symptoms becoming more severe or frequent during OC use should discontinue OC use. Instead, they should use a barrier method or the IUD. Estradiol treatment appears to be effective in treating menstrual migraine. Since the data are inconclusive about the effect of OCs on young women who have experienced a stroke or transient ischemic attacks, it would be best for them to use a barrier method. Most antiepileptic drugs (phenobarbital, phenytoin, paramethadione, and carbamazepine) cause enzyme induction which may be linked to decreased levels of estrogen and increases in irregular bleeding, thereby increasing the likelihood of an epileptic OC user becoming pregnant. Possible contraceptive failure exposes a developing fetus to the teratogenic properties of the antiepileptic drugs. Thus, physicians should prescribe OCs with 50 mcg of ethinyl estradiol rather than 35 mcg ethinyl estradiol. Epileptic women can also use Depo-Provera, because it is not only effective in preventing pregnancy but reduces seizure frequency. It is important for any contraceptive method chosen for epileptic women to be effective because pregnancy intensifies seizures which in turn can damage the mother and/or fetus and cause neonatal distress.
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PMID:Contraceptive methods for women with neurologic disorders. 851 48

The immediate early gene-encoded enzyme, MAP kinase phosphatase 1 (MKP-1), is thought to be a key element in controlling cellular signalling pathways activated by MAP kinases. Since MAP kinase have been demonstrated to participate in neuronal stimulus-transcription coupling following seizure activity, the present study investigated the induction of MKP-1 in the rat brain after limbic epilepsy. MKP-1 expression was studied with a polyclonal antiserum by Western blots, immunocytochemistry and immuno-electron microscopy at different time periods between 1 and 24 h after kainic acid-induced limbic seizures. MKP-1 induction was identified in dentate granule cells of the hippocampus but not in pyramidal neurons, furthermore in neurons of the outer layers of the neocortex, as well as in neurons of the lateral nucleus of the bed of the stria terminalis. Immuno-electron microscopy demonstrated that MKP-1 was localized in the neuronal nucleus, where the substrate of MKP-1, activated MAP kinases, are also found. In view of the restricted areas of MKP-1 expression and the widespread areas of altered MAP kinases activity it can be concluded that in the majority of CNS populations other mechanisms than MKP-1 induction are responsible for the shut-off of MAP kinases following seizure activity. MKP-1 may contribute in the specific subpopulations where it is induced to the post-translational control of inducible transcription factors of the fos, jun and myc family.
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PMID:Transient expression of the mitogen-activated protein kinase phosphatase MKP-1 (3CH134/ERP1) in the rat brain after limbic epilepsy. 888 36

US teenagers have had access to the injectable contraceptive depot medroxyprogesterone acetate (DMPA; Depo-Provera) since the US Food and Drug Administration approved it in 1992. DMPA suppresses follicle stimulating hormone and luteinizing hormone (LH) levels, which in turn prevents the LH surge and thus inhibits ovulation. It also causes a thick cervical mucus (reducing sperm penetration). Since DMPA also changes tubal mobility and creates shallow and atrophic endometrium, implantation is prevented. DMPA must be administered every 3 months to be effective. Its first-year failure rate is 0.3%, which is lower than that of oral contraceptives (3%). Advantages of DMPA are that it: allows for privacy; improves compliance (since action is required every 3 months rather than every day); has no estrogen-related complications (e.g., thrombophlebitis); is effective; is safe for breast feeding teenagers; reduces seizure frequency in teenagers with epilepsy; has a favorable effect on sickle cell disease or coagulopathy; reduces menstrual flow, thus preventing iron-deficiency anemia; reduces menstrual pain and pre-menstrual symptoms; and decreases risk of pelvic inflammatory disease. The leading disadvantages are menstrual irregularities and spotting. Some other possible disadvantages include weight gain (most common reason for discontinuation), delayed return of fertility, headaches, acne, and nervousness. Health providers must perform a complete history of teenagers requesting DMPA. They should determine the presence or absence of absolute and relative contraindications to DMPA. Absolute contraindications are known or suspected pregnancy, undiagnosed or abnormal vaginal bleeding, known or suspected history of breast cancer, acute liver disease or jaundice, thromboembolism, and sensitivity to DMPA. DMPA is administered intramuscularly at a concentration of 150 mg/ml. Health providers need to use a frank, nonjudgmental, empathic, and unhurried approach to facilitate a trusting relationship and rapport with teenagers. Advanced counseling on the pros and cons of DMPA, how DMPA works, and DMPA's inability to protect against sexually transmitted diseases is essential.
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PMID:Use of depo-provera in teens. 892 Mar 51


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