Catamenial epilepsy: Definition, prevalence pathophysiology and treatment

Herzog, Andrew G.

doi:10.1016/j.seizure.2007.11.014

Cited by 186 publications

(146 citation statements)

References 57 publications

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“…2,5 Specifically, cyclic progesterone supplement may have greater efficacy where progesterone withdrawal (C1 pattern), rather than estrogen surge (C2-periovulatory pattern) or low midluteal progesterone levels (C3 pattern), are causally implicated. The design also assumed that the mathematically determined cutoff for catamenial designation would match the cutoff for significant progesterone response.…”

Section: Discussionmentioning

confidence: 99%

“…Continuous variables were compared using independent t test for normally distributed data and Wilcoxon rank sum test for otherwise distributed data. Proportions were compared using 2 Patterns and levels of catamenial seizure exacerbation were established using baseline phase data. They were designated as per our previous definitions 5 that compared ADSF during the phase of exacerbation with comparator phases: C1 pattern: ADSF on days Ϫ3 to 3 compared to the midfollicular (days 4 to 9) and midluteal phase (days Ϫ12 to Ϫ4) phases combined; C2 pattern: ADSF on days 10 to Ϫ13 compared to the midfollicular and midluteal phases combined; C3 pattern: ADSF on days 10 to 3 compared to the midfollicular phase.…”

Section: Methodsmentioning

confidence: 99%

“…2 The existence of catamenial epilepsy draws support from findings in some large clinical studies. 4,5 Catamenial epilepsy likely relates to 3 factors: 1) some reproductive steroids have neuroactive properties, 6 -9 2) the serum concentrations of neuroactive reproductive steroids vary across the menstrual cycle, 2 and 3) some brain substrates that are susceptible to epilepsy show sensitive structural and electrophysiologic responses to these steroids.…”

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confidence: 86%

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Progesterone vs placebo therapy for women with epilepsy

Herzog¹,

Fowler²,

Smithson³

et al. 2012

Neurology

154

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Objective: To assess progesterone treatment of intractable seizures in women with partial epilepsy.Methods: This randomized, double-blind, placebo-controlled, phase III, multicenter, clinical trial compared the efficacy and safety of adjunctive cyclic natural progesterone therapy vs placebo treatment of intractable seizures in 294 subjects randomized 2:1 to progesterone or placebo, stratified by catamenial and noncatamenial status. It compared treatments on proportions of Ն50% responders and changes in seizure frequency from 3 baseline to 3 treated menstrual cycles. Results:There was no significant difference in proportions of responders between progesterone and placebo in the catamenial and noncatamenial strata. Prespecified secondary analysis showed that the level of perimenstrual seizure exacerbation (C1 level) was a significant predictor of responders for progesterone but not placebo. With increasing C1 levels, responders increased from 21% to 57% with progesterone vs 19% to 20% with placebo. Reductions in seizure frequency correlated with increasing C1 levels for progesterone but not placebo, progressing from 26% to 71% for progesterone vs 25% to 26% for placebo. A prespecified clinically important separation between progesterone and placebo responders (37.8% vs 11.1%; p ϭ 0.037) was realized among 21.4% of women who had C1 level Ն3. Conclusion:There was no difference in the primary outcome of Ն50% responder rates between progesterone vs placebo for catamenial or noncatamenial groups. Post hoc findings suggest that the level of perimenstrual seizure exacerbation is a significant predictor of responder rate with progesterone and that progesterone may provide clinically important benefit for a subset of women with perimenstrually exacerbated seizures. Classification of evidence:This study provides Class III evidence that cyclic progesterone is ineffective in women with intractable partial epilepsy. Post hoc analysis identified a subset of women with higher levels of perimenstrual seizure exacerbation that were responsive to treatment. There are compelling reasons to investigate the potential role of reproductive steroids in the treatment of intractable seizures in women with epilepsy. Seizures do not occur randomly.

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Section: Discussionmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 86%

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Progesterone vs placebo therapy for women with epilepsy

Herzog¹,

Fowler²,

Smithson³

et al. 2012

Neurology

154

View full text Add to dashboard Cite

show abstract

“…This increased severity of symptoms is followed by a sudden remission with an elevation of E 2 levels during postmenstrual period in majority of these neurological diseases. In contrast to other disorders, a higher frequency of seizures is associated with hyperestrogenic state during periovulatory period in women with catamenial epilepsy, a pattern of epilepsy seen in more than 30% of women epilepsy patients [Herzog, 2008]. We could not trace any study attempting to correlate AD propensity with menstrual cycle which might be attributed to relatively late onset of symptoms, after the cessation of menstrual cycle in majority of patients.…”

Section: Menstrual Cyclementioning

confidence: 70%

Genetic variability in estrogen disposition: Potential clinical implications for neuropsychiatric disorders

Grover

Talwar

Baghel

et al. 2010

American J of Med Genetics Pt B

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Variability in the physiological levels of neuroactive estrogens is widely believed to play a role in predisposition to several disorders of the central nervous system. Local biosynthesis of estrogens in the brain as well as their circulating serum levels are known to contribute to this pool of neuroactive steroids. It has been well accepted that estrogens modulate neuronal functions by affecting genesis, differentiation, excitability, and degeneration of nerve cells. These actions of estrogens appear to be more prominent in females with higher concentrations and marked variability of circulating serum levels occurring over a woman's lifetime. However, our knowledge regarding the variability of neuroactive steroid levels is very limited. Furthermore, several studies have recently reported differences in the synchronization of circulating and neuronal levels of estradiol. In the absence of reliable circulating steroid levels, knowledge of genetic variability in estrogen disposition may play a determining factor in predicting altered susceptibility or severity of neuropsychiatric disorders in women. Over the past decade, several genetic variants have been linked to both differential serum estrogen levels and predisposition to diverse types of neuropsychiatric disorders in women. Polymorphisms in genes encoding estrogen-metabolizing enzymes as well as estrogen receptors may account for this phenotypic variability. In this review, we attempt to show the contribution of genetics in determining estrogenicity in females with a particular emphasis on the central nervous system. This knowledge will further provide a driving force for unearthing the novel field of "Estrogen Pharmacogenomics." © 2010 Wiley-Liss, Inc.

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“…In total, incidence and prevalence of epilepsy in different countries range from 3 to 5 and 5 to 10 per 1000 people, respectively (7,8). Lifetime risk of epilepsy has been estimated as 3% and its incidence rate is higher in developing countries (9).…”

Section: Introductionmentioning

confidence: 99%

The Causes of Secondary Epilepsy in Epileptic Patients Referred to Neurology Clinics of Mashhad Hospitals

et al. 2015

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Background: Epilepsy is a group of disorders characterized by recurrent unprovoked seizures. It is recognized as one of the most common neurological diseases affecting different age groups. Objectives: This study aimed to determine the causes of secondary epilepsy in patients with epilepsy at Mashhad hospitals in 2011 -2012. Patients and Methods:In this cross-sectional, descriptive study, 300 participants were selected via available sampling from patients with epilepsy referred to hospitals affiliated to Islamic Azad University of Mashhad. Diagnosis of epilepsy was based on the criteria of the International League Against Epilepsy. Patients' demographic and medical profile questionnaires were completed, using clinical examinations, electroencephalography (EEG) and brain imaging. Results: In this study, 54% and 46% of participants were male and female, respectively (mean age = 31.5 ± 15.3 years). Head trauma was the most common cause of secondary epilepsy, observed in 26% of patients. Brain tumor (9.7%), stroke (9.3%), brain infection (8.3%), metabolic disease (3.3%) and birth trauma or congenital anomalies (2.3%) were other causes. Findings of the last performed EEG were normal and abnormal in 49% and 51% of participants, respectively. Moreover, results of brain imaging were normal in 85.3% and abnormal in 14.7% of subjects. Conclusions: This study evaluated the causes of secondary epilepsy. Our findings showed that 45.3% of the subjects had secondary epilepsy. Some patients presented with multiple conditions and there was more than one cause of secondary epilepsy in these cases. This study showed that the average age of patients with previous history of stroke was higher than that of other participants. However, previous history of stroke and head trauma mostly observed in males.

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Catamenial epilepsy: Definition, prevalence pathophysiology and treatment

Cited by 186 publications

References 57 publications

Progesterone vs placebo therapy for women with epilepsy

Progesterone vs placebo therapy for women with epilepsy

Genetic variability in estrogen disposition: Potential clinical implications for neuropsychiatric disorders

The Causes of Secondary Epilepsy in Epileptic Patients Referred to Neurology Clinics of Mashhad Hospitals

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