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

The inborn seizure response of Papio papio to intermittent light stimulation has been reviewed as a model of human epilepsy. The electrographic and clinical features have been described and useful methodology has been outlined. A diurnal cyclicity in seizure responsiveness has been described with greatest seizure severity at 8 AM in parallel with a rise in urinary output of cortisol. Hormonal influences on the seizure response have been described for ethinyl estradiol, thyroxin, and triiodothyronine. Evidence regarding neurotransmitter involvement has been reviewed. Data regarding use of the animal for anticonvulsant testing in single and chronic doses has been discussed. Particular advantages of the model for study of age-related drug effects and the assessment of the effects of chronically administered anticonvulsant agents on learning and memory have been described.
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PMID:Photomyoclonic seizures in the baboon, Papio papio. 3 8

Hormones influence brain function from gestation throughout life and may affect the seizure threshold by altering neuronal excitability. Estrogen enhances and progesterone diminishes neuronal excitability experimentally, whereas testosterone and corticosteroids have less consistent effects. Hormonal effects in the CNS also depend on the region of brain in which the hormone acts. Sites of action for most steroid hormones include the hypothalamus and limbic cortex, providing a mechanism for modulating behavior and endocrine function. Seizure patterns may change at certain life stages, perhaps as a result of alterations in hormones. At puberty, epilepsy and benign rolandic epilepsy often remit, while juvenile myoclonic and photosensitive epilepsy may arise. Other types of epilepsy do not respond predictably to events in the reproductive life or to advancing age. In some women, fluctuations in hormones over the menstrual cycle appear to increase seizure vulnerability, probably reflecting changes in relative amounts of estrogen and progesterone. Seizure patterns can be altered, for better or worse, during pregnancy. Whether this reflects the effects of hormones or changes in levels of antiepileptic drugs is not resolved. More information is needed about changes in established epilepsy at menopause and in the elderly. Better understanding of endocrine effects on seizures over a lifetime should lead to more effective epilepsy therapies.
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PMID:Hormones and epilepsy through the lifetime. 142 94

5 cases of ischemic strokes in young women who used oral contraceptives and smoked cigarettes are described in clinical and angiographic detail, the risk factors for moyamoya disease are discussed in a review or strokes in pill users, and the notion that oral contraceptive and smoking may cause a moyamoya pattern of stroke is proposed. The women were aged 20-32, used the pill from 2 weeks-8 years, had smoked approximately 10-20 pack-years. 2 women had headaches and 4 had transient ischemic attacks before their multifocal symptoms in visual, somatosensory and motor function, language, speech and cognition. 2 had seizures. Angiographic patterns of either supraclinoid stenosis (4) or proximal carotid artery stenosis (1) with the collateral circulation characteristic of moyamoya disease were evident in all, but there was no evidence of hemorrhagic infarction. There were no signs of atherosclerosis. Subtle signs of an immunologic process included antinuclear antibody titer of 1:160 in 1 woman, elevated sedimentation rate and elevated circulating immune complexes in another patient, and elevated cerebrospinal protein and IgG in a third woman. 4 of the patients remained stable after stopping oral contraceptives and stopping or reducing smoking. The 5th, who continued smoking, had progressive symptoms for 10 years. It was suggested that antibodies to ethinyl estradiol, a possible cause of this disorder, be further investigated.
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PMID:Accelerated intracranial occlusive disease, oral contraceptives, and cigarette use. 841 56

Reported is the case of a 24-year-old Finnish woman who developed malignant hypertension while taking an oral contraceptive (OC) that contained 30 mcg of ethinyl estradiol. She presented with blurred vision, but reported no other remarkable signs or symptoms during the 5 months in which she had been using OCs. Laboratory tests at admission revealed incomplete systemic lupus erythematosus (SLE) with DNA antibodies and high levels of antiphospholipid antibodies. Her blood pressure was 220-140 mmHg. OC use was discontinued and antihypertensive treatment initiated, with good results. 2 years later, however, the patient developed epileptic seizures and an area of local atrophy in the cerebellum was identified through computerized tomography. In the 4-6th years after initial presentation, the patient experienced 3 miscarriages, all at 7-8 weeks of gestation. 1 year after presentation, the patient satisfied 4 of the criteria for SLE (positive DNA and antiphospholipid antibodies, thrombocytopenia, leukopenia, and proteinuria). At present, the patient's symptoms are being controlled with carbamazepine and metroprolol. The patient's older sister, who had never used OCs, had SLE. It appears that high levels of antiphospholipid antibodies are an additional risk factor for the development of vascular complications in OC users but are not induced by OCs. Similarly, while OCs are not believed to cause SLE, they can exacerbate the disease or unmask a lupus diathesis.
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PMID:Malignant hypertension and antiphospholipid antibodies as presenting features of SLE in a young woman using oral contraceptives. 174 6

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

More effective anti-epileptic drugs, therapeutic plasma monitoring of drug effects, and better understanding of the risk factors for pregnancy have made it possible for women with epilepsy to have healthy, normal children. Nonetheless, women with epilepsy face special problems with regard to contraception, pregnancy, and lactation. Since enzyme-inducing anti-epileptic drugs lower estrogen concentrations by 40-50%, thereby compromising contraceptive effectiveness, hormonal contraceptives prescribed to women with epilepsy should contain at least 50 mcg of ethinyl estradiol. During pregnancy, up to one-third of women with epilepsy experience an increase in seizure frequency as drug plasma concentrations decline. Epileptic women are also at greater risk of obstetric complications during pregnancy and delivery, including anemia, vaginal bleeding, pre-eclampsia, abruptio placentae, premature labor, and stillbirth. The research literature suggests that the risk of congenital abnormalities, most notably neural tube defects, is 4-8% for infants exposed in utero to anti-epileptic drugs compared to 2-3% for the general population. To date, six clinical anti-epileptic-drug-related fetal syndromes have been identified. Since anticonvulsant drugs are secreted in breast milk, infants may become sleepy and stop feeding prior to satiation. Despite these potential complications, the likelihood of a positive pregnancy outcome can be enhanced by preconceptional use of folic acid supplements, monthly monitoring of treatment drug levels to prevent seizures, and ultrasound or amniocentesis at 16-18 weeks of gestation to detect neural tube defects.
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PMID:Contraception, pregnancy and lactation in women with epilepsy. 906 87

Cyclic AMP response element-binding protein (CREB) is a transcription factor that has been implicated in the activation of a number of genes. We reported that CREB levels decline following a severe hypoglycemic episode in the hippocampus and cortex in the male rat brain. The present experiment was undertaken to investigate whether 17beta-estradiol prevents the decline in CREB-immunoreactive cells following seizure in female rats. Rats were divided into four groups: ovariectomized (OVX), ovariectomized and insulin-treated (OVX-I), estrogen-replaced (E2), and estrogen-replaced and insulin-treated (E2-I). Generalized seizures were induced by injections with insulin (12.5 IU/kg, intraperitoneally) and animals were recovered by administration of glucose within 5 min of the occurrence of seizure. Control animals were injected with saline instead of insulin. All animals were perfused 90 min after recovery and the brains were processed for CREB immunoreactivity. CREB-positive neurons were counted using a computer-assisted program. Insulin treatment of OVX rats caused a significant decline in CREB-positive neurons in the CA1, CA3, and dentate gyrus compared to OVX rats. Estrogen treatment of OVX rats significantly increased CREB-positive neurons in the CA1 and dentate gyrus and attenuated the insulin-induced decline of CREB-positive neurons in all three regions compared to OVX rats. In conclusion, estrogens appear to induce CREB expression and attenuate its decline in the hippocampus following a severe hypoglycemic episode.
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PMID:17beta-estradiol attenuates CREB decline in the rat hippocampus following seizure. 940 16

The temporolimbic structures of the brain that subserve emotional representation are highly epileptogenic and play an important role in the modulation of hormonal secretion and mediation of hormonal feedback. Estrogen is highly epileptogenic and exerts energizing and antidepressant effects. Excessive estrogen influence produces anxiety, agitation, irritability, and lability. It can promote the development of anxiety manifestations (e.g., panic, phobias, and obsessive-compulsive disorder). Progesterone and its metabolites inhibit kindling and seizure activity. They have potent anxiolytic effects, possibly by virtue of their GABAergic activity. Excessive progesterone influence produces sedation and depression. Testosterone has two major metabolites: estradiol, which can exacerbate seizures, and dihydrotestosterone, which blocks NMDA-type glutamate transmission and may be responsible for antiseizure effects. Testosterone has energizing effects and increases sexual desire in both men and women. In excess, however, it may promote aggressive, impulsive, and hypersexual behavior. Hormonal effects tend to be exaggerated or idiosyncratic in the setting of an abnormal or anomalous temporolimbic substrate, especially temporolimbic epilepsy. This may reflect altered neuronal responsivity to hormonal exposure perhaps by virtue of changes in the number of dendritic spines and receptors.
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PMID:Psychoneuroendocrine aspects of temporolimbic epilepsy. Part I. Brain, reproductive steroids, and emotions. 1010 Apr 30

Epilepsy is a common neurological disorder that may be affected by reproductive hormones and may complicate reproductive health. Many women with epilepsy experience changes in seizure frequency and severity with changes in reproductive cycles, including at puberty, over the menstrual cycle, with pregnancy and at menopause. Ovarian steroids alter neuronal excitability at the membrane and in the genome. Altered protein synthesis as a consequence of changes in RNA mediated gene transcription is one mechanism for steroid mediated effects on excitability. These genomic effects are delayed and sustained. In contrast, membrane effects are immediate and short duration. These effects are mediated at both the GABA-A and NMDA receptors. Estrogen also dynamically alters synaptic connectivity. Estrogen enhances excitability and lowers the seizure threshold, whereas progesterone enhances inhibition and increases the seizure threshold. In experimental models of epilepsy, estrogen is proconvulsant and progesterone is anticonvulsant. The net effect of these steroid actions is to alter neuronal excitability over physiological cycles. Some epilepsy syndromes are expressed or worsened at puberty. One third to one half of women with epilepsy have catamenial seizure patterns, with seizures most likely to occur in the perimenstrual period and at ovulation. More research is needed to understand the effects of menopause on epilepsy. Antiepileptic drugs may exacerbate the risk of reproductive endocrine disorders in women with epilepsy. Fertility rates are lower for women with epilepsy. Women with epilepsy are more likely to have anovulatory menstrual cycles, abnormal pituitary LH release and altered ovarian steroid concentrations. Polycystic ovaries are detected more often in women with epilepsy, particularly those on valproate. Treatment of hormone sensitive seizures relies on standard AEDs. Small trials suggest that adjunctive progesterone therapy is sometimes helpful. The newer AEDs, gabapentin and lamotrigine may have some advantages for women with epilepsy. These drugs do not alter levels of steroid hormones and do not interfere with effectiveness of hormonal contraception. Experience in pregnancy is limited. The dynamic effects of hormones on seizure expression and of seizures on reproductive health complicate the management of epilepsy in women. Newer AEDs may offer advantages for women with epilepsy in the reproductive years.
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PMID:Epilepsy in women: the science of why it is special. 1048 15

Recent evidence suggests that reproductive steroids are important players in shaping stroke outcome and cerebrovascular pathophysiologic features. Although women are at lower risk for stroke than men, this native protection is lost in the postmenopausal years. Therefore, aging women sustain a large burden for stroke, contrary to a popular misconception that cancer is the main killer of women. Further, the value of hormone replacement therapy in stroke prevention or in improving outcome remains controversial. Estrogen has been the best studied of the sex steroids in both laboratory and clinical settings and is considered increasingly to be an endogenous neuroprotective agent. A growing number of studies demonstrate that exogenous estradiol reduces tissue damage resulting from experimental ischemic stroke in both sexes. This new concept suggests that dissecting interactions between estrogen and cerebral ischemia will yield novel insights into generalized cellular mechanisms of injury. Less is known about estrogen's undesirable effects in brain, for example, the potential for increasing seizure susceptibility and migraine. This review summarizes gender-specific aspects of clinical and experimental stroke and results of estrogen treatment on outcome in animal models of cerebral ischemia, and briefly discusses potential vascular and parenchymal mechanisms by which estrogen salvages brain.
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PMID:Estrogen as a neuroprotectant in stroke. 1077 8


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