Is a first acute symptomatic seizure epilepsy? Mortality and risk for recurrent seizure

Purpose:   To compare mortality and subsequent unprovoked seizure risk in a population-based study of acute symptomatic seizure and first unprovoked seizure due to static brain lesions.
Methods:   We ascertained all first episodes of acute symptomatic seizure and unprovoked seizure due to central nervous system (CNS) infection, stroke, and traumatic brain injury (TBI). Subjects were residents of Rochester, Minnesota, identified through the Rochester Epidemiology Project's records-linkage system between 1/1/55 and 12/31/84. Information was collected on age, gender, seizure type, etiology, status epilepticus (SE), 30-day and 10-year mortality, and subsequent episodes of unprovoked seizure.
Results:   Two hundred sixty-two individuals experienced a first acute symptomatic seizure and 148 individuals experienced a first unprovoked seizure, all due to static brain lesions. Individuals with a first acute symptomatic seizure were 8.9 times more likely to die within 30 days compared to those with a first unprovoked seizure [95% confidence intervals (CI) = 3.5–22.5] after adjustment for age, gender, and SE. Among 30-day survivors, the risk of 10-year mortality did not differ. Over the 10-year period, individuals with a first acute symptomatic seizure were 80% less likely to experience a subsequent unprovoked seizure compared with individuals with a first unprovoked seizure [adjusted rate ratio (RR) = 0.2, 95% CI = 0.2–0.4].
Discussion:   The prognosis of first acute symptomatic seizures differs from that of first unprovoked seizure when the etiology is stroke, TBI, and CNS infection. Acute symptomatic seizures have a higher early mortality and a lower risk for subsequent unprovoked seizure. These differences argue against the inclusion of acute symptomatic seizures as epilepsy.     

Quality of life after vagus nerve stimulation for intractable epilepsy: is seizure control the only contributing factor?

We assessed the impact of vagus nerve stimulation on a cohort of patients with intractable epilepsy. A 1-year prospective trial of vagus nerve stimulation for intractable epilepsy was done in 26 patients. Seizure frequency, anti-epileptic drugs, and quality of life were assessed using QOLIE-89, ELDQOL, and a Likert scale of impact of treatment. Seizures were reduced by more than 50% in 19% of the patients, by less than 50% in 46%, and were unchanged in 35% of them. Antiepileptic drugs were reduced in 43% of the patients. There was a significant improvement in the mean overall QOLIE-89 score and other measures of quality of life, but these did not correlate with changes in seizure frequency. Subjective improvement occurred in 84% of the patients. The quality of life improves in some patients following vagus nerve stimulation for intractable epilepsy. The favorable effects of this treatment may be attributable to additional factors besides seizure control which in this study was modest.     

Do the basal ganglia inhibit seizure activity in temporal lobe epilepsy?

There is substantial evidence in the literature that the basal ganglia (BG), namely the striatum and pallidum, are involved in temporal lobe epilepsy (TLE). The BG are probably not involved in elaborating clinical seizures, as they do not produce specific epileptiform activity and there is no evident change in the electrical activity in the BG immediately after seizure onset. The data we obtained by direct ictal recording in the BG [1,2], as well as a large body of experimental and clinical evidence reported by other groups, suggest an inhibitory role of the BG during temporal lobe seizures. The BG may have a remote influence on cortical oscillatory processes related to control of epileptic seizures via their feedback pathways to the cortex.     

Concussive convulsions: seizure or no seizure?

Convulsions following traumatic brain injury (TBI) represent a diagnostic and therapeutic challenge. They can be differentiated into late (> 7 days after TBI), early (1 - 7 days after TBI), immediate (within the first 24 h after TBI), and impact seizures (within seconds after TBI). Some authors suggest that most impact seizures are non-epileptic in origin and hence coined the term "concussive convulsions" for benign impact seizures. Early and late post-traumatic seizures frequently indicate structural brain damage and transition to chronic, post-traumatic epilepsy. The data for impact seizures or concussive convulsions is less clear: only a small percentage of impact seizures is associated with structural brain damage and the development of post-traumatic epilepsy, rather the majority of cases are benign and associated with an excellent prognosis. Here, we present a case report as a starting point for pathophysiological and clinical considerations regarding convulsions that start within seconds after TBI.     

Predictors for long-term seizure outcome in juvenile myoclonic epilepsy: 25-63 years of follow-up

Purpose: The long‐term seizure outcome of juvenile myoclonic epilepsy (JME) is still controversial; the value of factors that are potentially predictive for seizure outcome remains unclear. The aim of this study was both to investigate the long‐term seizure outcome in patients with JME after a follow‐up of at least 25 years and to identify factors that are predictive for the seizure outcome. Methods: Data from 31 patients (19 women) with JME were studied. All of them had a follow‐up of at least 25 years (mean 39.1 years) and were reevaluated with a review of their medical records and direct telephone or face‐to‐face interview. Key Findings: Of 31 patients 21 (67.7%) became seizure‐free; in six of them (28.6%) antiepileptic drug (AED) treatment was discontinued due to seizure freedom. The occurrence of generalized tonic–clonic seizures (GTCS) preceded by bilateral myoclonic seizures (BMS) (p = 0.03), a long duration of epilepsy with unsuccessful treatment (p = 0.022), and AED polytherapy (p = 0.023) were identified as significant predictors for a poor long‐term seizure outcome, whereas complete remission of GTCS under AED significantly increased the chance for complete seizure freedom (p = 0.012). The occurrence of photoparoxysmal responses significantly increases the risk of seizure recurrence after AED discontinuation (p = 0.05). Significance: This study shows conclusively that JME is a heterogeneous epilepsy syndrome. Life‐long AED treatment is not necessarily required to maintain seizure freedom. Several long‐term outcome predictors that can potentially increase the ability of clinicians and their confidence to recommend different treatment options to patients with JME were identified.     

Atonic seizures in children with surgically remediable epilepsy: a motor system seizure phenotype?

Aim. Atonic seizures are common in some epileptic syndromes beginning in infancy or early childhood but they are rarely described in epilepsy with focal seizures of structural aetiology. We aimed to characterize the electroclinical features of atonic seizures in surgically remediable paediatric patients and to study the spatiotemporal organization of the underlying epileptogenic networks. Methods. We retrospectively analysed two consecutive, longitudinally evaluated and surgically treated paediatric patients presenting with atonic seizures as a manifestation of pharmacoresistant epilepsy of structural aetiology, evidenced by scalp‐ and stereotactic intracerebral video‐EEG‐recordings. A quantitative analysis of the epileptogenic zone organization was performed using the “epileptogenicity index”. Results. Long‐lasting generalized ictal atonia, occurring in infancy, was a predominant clinical feature in both patients, with some hints of focal origin present in one case. The seizure phenotype evolved at later age into subtle segmental atonia, associated with prominent positive motor signs. The epileptogenic zone was localized within the dorsolateral or mesiolateral premotor region. Its spatial organization was focal, matching the lesional cortex in one and distributed involving several lesional and non‐lesional structures in the other case. The emergence of atonic semiology temporally correlated with involvement of both lateral and mesial premotor, as well as primary motor areas. Conclusion. We hypothesize that atonic seizures may be considered as a motor system seizure phenotype in the setting of structural epilepsy. Complete removal of the epileptogenic area provided excellent seizure control.     

Acute symptomatic seizures and hippocampal sclerosis: the major contributor for post-stroke epilepsy?

Journal of Neurology - Hippocampal sclerosis (HS) is a prominent biomarker of epilepsy. If acquired later in life, it usually occurs in the context of degenerative or acute inflammatory-infectious...     

Failed epilepsy surgery: is this the end?

Resective epilepsy surgery can lead to sustained seizure control in 70–80% of patients evaluated for epilepsy surgery, indicating that up to 30% of patients still have recurrent seizures after surgery. Definitions of failed epilepsy surgery vary amongst studies. This review focuses on seizure outcome predictors after reoperation, possible mechanisms of failure and best management for this difficult patient population.     

Oxidative injury in epilepsy: potential for antioxidant therapy?

Biological ill effects of oxidative injury from excess free radical production are implicated in many human conditions. Epilepsy is a chronic, dynamic neurological disorder associated with ongoing neuronal damage, particularly when uncontrolled. Oxidative injury may play a role in the initiation and progression of epilepsy, and therapies aimed at reducing oxidative stress may ameliorate tissue damage and favorably alter the clinical course. There is abundant in vivo evidence of oxidative injury in animal models of epilepsy and for efficacy of antioxidant therapy in reducing this injury in animal models of epileptogenesis. However, there is sparse direct clinical data on the use of antioxidants in human epilepsy. This review examines the evidence for the role of oxidative injury in epilepsy, the rationale for use of antioxidant therapy in epilepsy and appraises the current clinical performance of the studies of antioxidant therapies.     

Does epilepsy surgery lower the mortality of drug-resistant epilepsy?

Drug-resistant epilepsy has proved to be associated with an increased standardized mortality ratio (SMR), primarily due to seizure-related fatalities including sudden unexpected death (SUDEP). Recent studies have suggested that the surgical cure of temporal lobe epilepsy (TLE) was likely to normalize the SMR of patients suffering from refractory TLE. However, these studies raise a number of methodological issues, which have not always been fully addressed. Some conclusions have relied on previously reported data, indicating a SMR of approximately 5, and a SUDEP incidence of 9/1000 patient-years in drug-resistant epilepsy. In fact, as shown in this review, SMR varied considerably, from 2 to 16, in the various series of patients with refractory epilepsy, whereas the average SUDEP incidence in the same populations was calculated at 3.7/1000 patient-years. Other conclusions were based on the comparison of either surgically and medically treated patients, or cured and non-cured operated patients. In both situations, the two groups included a different proportion of excellent and poor surgical candidates. The biological differences that distinguish these two populations might explain part of the differences observed in their mortality rate, regardless of the effect of surgery. In particular, temporal-plus epilepsies involving the insula, the frontal orbital, or the frontal operculum region, might favour ictal arrhythmias, central apnoea and secondary generalization, which in turn would increase the risk of SUDEP. Future studies are thus warranted to specifically address these issues.