Focal Onset Epilepsy Research Articles

Heart rate variability during interictal epileptiform discharges

Rationale: Seizures may produce a variety of autonomic alterations. These alterations may occur due to evoked autonomic reflexes or as a direct cortical effect on autonomic control. In animal studies, lock step phenomena of interictal discharges to autonomic output have been repeatedly documented. However, the association of interictal discharges and autonomic output is not as well established in humans. Methods: RR intervals timely locked to interictal epileptiform discharge (RR n ) were compared to RR intervals immediately following (RR n+1 ) interictal discharges in 40 patients with focal onset epilepsy and low baseline heart beat variability. Results: In 20 patients with 200 left sided interictal epileptiform discharges, RR n shortened in 100 and prolonged in 31 when compared to RR n+1 intervals. While in 20 patients with 200 right sided interictal epileptiform discharges RR n intervals shortened in 17 and prolonged in 116 (Chi square P<0.001). No consistent differences in RR n intervals variability between frontal versus temporal localization of the interictal discharges from the same side was found. Conclusions: Interictal discharges, may influence autonomic control over the cardiac cycle and agree with animal studies. Further study of the relationship of interictal discharges to autonomic output is needed to delineate the potential lateralized influences over autonomic nervous system.

The significance of stress in the development of fibromyalgia syndrome

To extend our knowledge and practical application of the concept of catamenial epilepsy.The review focuses on the impact of the NIH Progesterone Trial on our understanding of the pathophysiology and treatment of catamenial epilepsy.Catamenial epilepsy refers to the cyclic exacerbation of seizures in relation to the menstrual cycle. An interaction between seizures and the menstrual cycle is suggested by variations in seizure frequency according to the day, phase and ovulatory status of the menstrual cycle. There are three commonly recognized patterns: perimenstrual (C1: Day −3 to +3), peri-ovulatory (C2: Day 10 to 3) and entire luteal phase in anovulatory cycles (C3: Day 10 to 3). Pathophysiological determinants include 1) the neuroactive properties of reproductive steroids, 2) the variation of neuroactive steroid levels across the menstrual cycle and 3) the differential susceptibility of epileptic substrates to neuroactive steroid effects. Perimenstrual seizure exacerbation may result from the premenstrual withdrawal of progesterone which is accompanied by withdrawal of allopregnanolone, a potent positive allosteric modulator of the GABAA receptor, and changes in the subunit composition of the GABAA receptor to the α4 subtype which is insensitive to benzodiazepine and GABA. Bioidentical progesterone supplement is no better than placebo in the treatment of women with focal onset epilepsy overall but shows superior efficacy in women whose seizures show robust perimenstrual exacerbation.There is sound evidence for the existence of catamenial epilepsy and class 3 evidence for adjunctive progesterone treatment of the perimenstrually exacerbated subtype.

Does the Cause of Localisation‐Related Epilepsy Influence the Response to Antiepileptic Drug Treatment?

We investigated the response to antiepileptic drug (AED) therapy in patients with localisation-related epilepsy associated with different underlying causes. Five hundred and fifty adolescent and adult patients who had partial epilepsy treated with AEDs and who had undergone magnetic resonance imaging of brain were followed up prospectively from 1984 at a single centre. More than 70% were newly diagnosed. None had had epilepsy surgery. Three hundred and twelve (57%) patients had been seizure free at their last clinic visit for at least a year. Patients with mesial temporal sclerosis (MTS; n = 73, 42% seizure free) were less likely to be controlled (p < 0.01) than were those with arteriovenous malformation (AVM; n = 14, 78%), cerebral infarction (n = 46, 67%), primary tumour (n = 35, 63%), cortical gliosis (n = 81, 57%), cerebral atrophy (n = 49, 55%), and cortical dysplasia (CD; n = 63, 54%). Among the seizure-free patients, those with MTS were more likely to require more than one AED compared with those with other aetiologies (48 vs. 35%; p < 0.05). There was no difference in outcome between patients with symptomatic and cryptogenic epilepsy (n = 361, 58% vs. n = 189, 56% seizure free, respectively). Patients with MTS, CD, and cryptogenic epilepsy were more likely (p = 0.02) to have a family history of epilepsy than were the other groups. MTS patients also had a higher incidence of febrile convulsions (p < 0.001). The majority of patients with focal-onset epilepsy became seizure free on AED treatment. MTS-related seizures had the worst prognosis. Although many patients with this pathology may benefit from epilepsy surgery, a considerable number will be controlled with AED therapy.

Seizures in neurofibromatosis 1

Neurofibromatosis 1 is a common, genetically transmitted neurodevelopmental disorder with a high potential to cause subcortical focal brain lesions. Although seizures occasionally complicate neurofibromatosis 1, they have not been characterized adequately in the disease. Other phacomatoses with attendant subcortical focal brain lesions have been associated with an evolution from generalized to focal-onset epilepsy. This evolution may be related to the cortical dysplasias that also appear in such disorders. Cortical dysplasias, although occasionally found in neurofibromatosis 1 epileptic patients, are not as frequent as in other phacomatoses. The authors retrospectively screened 499 neurofibromatosis 1 patients for the prevalence and etiology of seizures, their response to therapy, and the evolution of seizure type over time. The prevalence of epileptic seizures (4.2%) was about twice the prevalence in the general population. There were no significant cortical dysplasias identified radiographically nor was there a relationship among the presence of subcortical focal brain lesions and seizure type, response to treatment, or evolution of epilepsy in the neurofibromatosis 1 population. The authors’ data do not suggest an ontogeny of epilepsy in neurofibromatosis 1 that is different from the general epileptic population.