Remote Seizures Research Articles

Association of Seizure Control With Cognition in People With Normal Cognition and Mild Cognitive Impairment.

Seizures are common in dementia and associated with accelerated cognitive decline. However, the impact of active vs remote seizures on cognition remains understudied. This study aimed to investigate the impact of active vs remote seizures on cognition in people with normal cognition and mild cognitive impairment (MCI). This longitudinal, multicenter cohort is based on National Alzheimer's Coordinating Center data of participants recruited from 39 Alzheimer's Disease Centers in the United States from September 2005 to December 2021. All participants with normal cognition and MCI and at least 2 visits were included. Primary outcome, that is, cognitive decline, was determined using Clinical Dementia Rating (CDR) from (1) normal-to-impaired (CDR ≥0.5) and (2) MCI-to-dementia (CDR ≥1) groups. The effect of active seizures (over the preceding 12 months), remote seizures (previous seizures but none over the preceding 12 months), and no seizures (controls) on cognition was assessed. Subgroups of chronic seizures at enrollment and new-onset seizures were further analyzed. Cox regression models assessed the risk of all-cause MCI and/or dementia. All models were adjusted for age, sex, education, race, hypertension, and diabetes. Of the 13,726 participants with normal cognition at enrollment (9,002 [66%] female; median age 71 years), 118 had active seizures and 226 had remote seizures. Of the 11,372 participants with MCI at enrollment (5,605 [49%] female; median age 73 years), 197 had active seizures and 226 had remote seizures. Active seizures were associated with 2.1 times higher risk of cognitive impairment (adjusted hazard ratio [aHR] 2.13, 95% CI 1.60-2.84, p < 0.001) in cognitively healthy adults (median years to decline: active seizures = ∼1, remote seizures = ∼3, no seizures = ∼3) and 1.6 times higher risk of dementia (aHR 1.58, 95% CI 1.24-2.01, p < 0.001) in those with MCI (median years to decline: active seizures = ∼1, remote seizures = ∼2, controls = ∼2). This risk was not observed with remote seizures. In this study, active seizures but not remote seizures were associated with earlier cognitive decline in both cognitively normal adults and those with MCI, independent of other dementia risk factors. Therefore, early identification and management of seizures may present a path to mitigation of cognitive decline in the aging epileptic population. A limitation is that causality cannot be confirmed in our observational longitudinal study.

Predictive Model for Estimating the Risk of Epilepsy After Aneurysmal Subarachnoid Hemorrhage: The RISE Score.

The occurrence of seizures after aneurysmal subarachnoid hemorrhage (aSAH) is associated with a poorer functional and cognitive prognosis and less favorable quality of life. It would be of value to promptly identify patients at risk of epilepsy to optimize follow-up protocols and design preventive strategies. Our aim was to develop a predictive score to help stratify epilepsy risk in patients with aSAH. This is a retrospective, longitudinal study of all adults with aSAH admitted to our center (2012-2021). We collected demographic data, clinical and radiologic variables, data on early-onset seizures (EOSs), and data on development of epilepsy. Exclusion criteria were previous structural brain lesion, epilepsy, and ≤7 days' follow-up. Multiple Cox regression was used to evaluate factors independently associated with unprovoked remote seizures (i.e., epilepsy). The best fitting regression model was used to develop a predictive score. Performance was evaluated in an external validation cohort of 308 patients using receiver-operating characteristic curve analysis. From an initial database of 743 patients, 419 met the inclusion criteria and were included in the analysis. The mean age was 60 ± 14 years, 269 patients (64%) were women, and 50 (11.9%) developed epilepsy within a median follow-up of 4.2 years. Premorbid modified Rankin Score (mRS) (hazard ratio [HR] 4.74 [1.8-12.4], p = 0.001), VASOGRADE score (HR 2.45 [1.4-4.2], p = 0.001), surgical treatment (HR 2.77 [1.6-4.9], p = 0.001), and presence of EOSs (HR 1.84 [1.0-3.4], p = 0.05) were independently associated with epilepsy. The proposed scale, designated RISE, scores 1 point for premorbid mRS ≥ 2 (R), VASOGRADE-Yellow (I, Ischemia), surgical intervention (S), and history of EOSs (E) and 2 points for VASOGRADE-Red. RISE stratifies patients into 3 groups: low (0-1), moderate (2-3), and high (4-5) risk (2.9%, 20.8%, and 75.7% developed epilepsy, respectively). On validation in a cohort from a different tertiary care center (N = 308), the new scale yielded a similar risk distribution and good predictive power for epilepsy within 5 years after aSAH (area under the curve [AUC] 0.82; 95% CI 0.74-0.90). The RISE scale is a robust predictor of post-SAH epilepsy with immediate clinical applicability. In addition to facilitating personalized diagnosis and treatment, RISE may be of value for exploring future antiepileptogenesis strategies.

Remote seizures and drug-resistant epilepsy after a first status epilepticus in adults.

Long-term consequences after status epilepticus (SE) represent an unsettled issue. We investigated the incidence of remote unprovoked seizures (RS) and drug-resistant epilepsy (DRE) in a cohort of first-ever SE survivors. A retrospective, observational, and monocentric study was conducted on adult patients (age ≥ 14 years) with first SE who were consecutively admitted to the Modena Academic Hospital, Italy (September 2013-March 2022). Kaplan-Meier survival analyses were used to calculate the probability of seizure freedom following the index event, whereas Cox proportional hazard regression models were used to identify outcome predictors. A total of 279 patients were included, 57 of whom (20.4%) developed RS (mean follow-up = 32.4 months). Cumulative probability of seizure freedom was 85%, 78%, and 68% respectively at 12 months, 2 years, and 5 years. In 45 of 57 patients (81%), the first relapse occurred within 2 years after SE. The risk of RS was higher in the case of structural brain damage (hazard ratio [HR] = 2.1, 95% confidence interval [CI] = 1.06-4.01), progressive symptomatic etiology (HR = 2.7, 95% CI = 1.44-5.16), and occurrence of nonconvulsive evolution in the semiological sequence of SE (HR = 2.9, 95% CI = 1.37-6.37). Eighteen of 57 patients (32%) developed DRE; the risk was higher in the case of super-refractory (p = 0.006) and non-convulsive SE evolution (p = 0.008). The overall risk of RS was moderate, temporally confined within 2 years after the index event, and driven by specific etiologies and SE semiology. Treatment super-refractoriness and non-convulsive SE evolution were associated with DRE development.

Incident Breakthrough Seizures, Serum Matrix Metalloproteinase-9 and Perfusion Magnetic Resonance Imaging Parameters in a Cohort of Children and Adolescents With Neurocysticercosis: A Longitudinal Observational Study

BackgroundThe current study estimated incident breakthrough seizures, serum matrix metalloproteinase-9 (MMP-9), and perfusion magnetic resonance imaging (MRI) parameters in five- to 18-year-olds with neurocysticercosis (NCC) from colloidal or vesicular through calcified stages over at least 24 months’ follow-up. MethodsSingle, colloidal, or vesicular parenchymal NCC cases were treated with albendazole and steroids and followed at a tertiary care north Indian hospital. Serum MMP-9 was estimated in colloidal or vesicular treatment-naive state and in a subset of calcified cases at six-month follow-up. The same subset of calcified cases also underwent perfusion MRI of the brain at six-month follow-up. ResultsAmong 70 cases, 70% calcified at six-month follow-up. Over a median follow-up of 30 months, the incidence of breakthrough seizures was 48.6% (61.2% in calcified and 19.2% in resolved, P = 0.001; 32.9% early [within six months] and 15.7% late [beyond six months], P = 0.02).Serum MMP-9 levels were higher in colloidal and vesicular compared with calcified stage (242.5 vs 159.8 ng/mL, P = 0.007); however, there was no significant association with breakthrough seizures and/or calcification in follow-up. In a subgroup of calcified cases (n = 31), the median relative cerebral blood volume on perfusion MRI in and around the lesion was lower in those with seizures (n = 12) than in those without (n = 19) (10.7 vs 25.2 mL/100 g, P = 0.05). ConclusionsIn post-treatment colloidal or vesicular NCC, incident breakthrough seizures decrease beyond six months. In calcified NCC with remote breakthrough seizures, significant perilesional hypoperfusion is seen compared with those without seizures.

Prediction of long-term unprovoked seizures after status epilepticus.

Possible long-term consequences of status epilepticus (SE) include cognitive and behavioral impairment and the development of chronic epilepsy. However, these aspects have not been systematically studied in clinical practice. We aimed to evaluate long-term seizure recurrence after SE and the potential risk factors for their development. Data were obtained from a prospective registry of all SE episodes occurring in adult patients who attended our center from February 2011 to April 2022. Clinical data, electroencephalographic findings, treatment, and long-term data were prospectively recorded. We performed a cross-sectional study of consecutive SE patients without previous epilepsy diagnosis, and analyzed the development of unprovoked remote seizures. A total of 849 patients were registered in the database. After excluding in-hospital mortality (198/849, 23.3%) and patients with prior epilepsy history (291/849, 44.7%), 360 patients (42.4%) with a first SE episode were included. The median age was 68 years (interquartile range [IQR] = 56-79), and 176 patients (48.9%) were women. The median time to first-line treatment initiation was 2 h (IQR = .7-7.4), and it was correlated with SE duration (R = .375, p < .001). One hundred nine patients (30.3%) presented unprovoked seizures during a median follow-up of 1.8 years (IQR = .5-4.3). After adjusting for identifiable confounders in a multivariable Cox regression analysis, progressive symptomatic etiology (hazard ratio [HR] = 1.97, 95% confidence interval [CI] = 1.17-3.33, p = .011), time to first-line treatment initiation > 1.5 h (HR = 1.89, 95% CI = 1.25-2.87, p = .003), and superrefractory SE (HR = 2.34, 95% CI = 1.26-4.33, p = .007) were independently associated with a greater risk of unprovoked seizure recurrence. In contrast, older patients (HR = .99, 95% CI = .97-.99, p = .021) and an acute symptomatic etiology (HR = .44, 95% CI .28-.68, p < .001) were at lower risk of unprovoked seizure recurrence. The etiology of SE, the delay in initiating SE treatment, and the presence of superrefractoriness have been identified as potentials factors associated with unprovoked remote seizures following a new onset SE. Therefore, prompt and appropriate management should be applied to avoid seizure recurrence.

Pediatric Cerebral Sinovenous Thrombosis and Risk for Epilepsy

BackgroundCerebral sinovenous thrombosis (CSVT) is a rare form of pediatric stroke with significant morbidity. We determined cumulative incidence and predictors of acute seizures, remote seizures, and epilepsy after pediatric CSVT. MethodsRetrospective analysis of 131 neonates and children with neuroimaging-confirmed CSVT enrolled between 2008 and 2020 from a single-center prospective consecutive cohort. Acute seizures occurred within 7 days of CSVT. Remote seizures occurred >7 days after CSVT. Epilepsy was defined as 2 or more remote seizures at least 24 hours apart. Survival methods determined the incidence of and risk factors for remote seizures and epilepsy. ResultsAcute seizures occurred in 14/33 neonates (42%) and 19/98 children (19%). Among children, hemorrhage predicted acute seizures (OR 6.6, 95% CI 1.9 to 22.4, P = 0.003). Remote seizures occurred in six neonates; five developed epilepsy. Remote seizures occurred in 14 children; 10 developed epilepsy. In neonates, 1- and 3-year epilepsy-free survival were 86% (95% CI 62% to 95%) and 66% (95% CI 32% to 87%). One- and 3-year epilepsy-free survival in children were 88% (95% CI 76% to 92%) and 84% (95% CI 59% to 86%). In multivariable analysis for children, acute seizures predicted epilepsy (HR 3.8, 95% CI 1.1-13.3, P = 0.039). In both cohorts, Pediatric Stroke Outcome Measure scores at last follow-up were worse in those with epilepsy compared to those without. ConclusionsAcute seizures occurred in approximately one quarter of our cohort and are an epilepsy risk factor in children with CSVT. Neonates and children with epilepsy had worse outcomes than those without.

Beware of nonconvulsive seizures in prolonged disorders of consciousness: Long-term EEG monitoring is the key

ObjectiveEvaluate the prevalence of epileptic seizures (ES) and epileptiform discharges (EDs) in patients with prolonged disorders of consciousness (DOC), and potential influence of amantadine on epilepsy. MethodsWe conducted a retrospective study in 34 patients hospitalized in a DOC care unit for prolonged DOC between 2012 and 2018, who received a long-term EEG monitoring (LTM). We reviewed the prevalence of ES, EDs and nonconvulsive seizures (NCSz), the type of DOC recovery treatment administered, and neurological outcome. ResultsLTM was more effective than standard EEGs in detecting EDs (32% vs 21% respectively). Moreover, 12% of the LTM showed NCSz. Among patients with EDs in LTM, 73% showed no EDs in standard EEG recordings, even when performed more than once. The presence of EDs and/or NCSz in LTM was significantly associated with the occurrence of remote clinical epileptic seizures (p = 0.017) but did not influence neurological outcome (p = 1). Amantadine was not associated with higher occurrence of EDs/NCSz or clinical seizures. ConclusionIn our prolonged DOC population, LTM showed more pathological results (EDs and NCSz) than standard EEGs, which was significantly associated with remote clinical seizures. SignificanceThe use of LTM might be advised to rule out NCSz in patients with prolonged DOC.

"Seizure and neurodegeneration": Understanding the nature of seizure in patients with cognitive disorder, A chicken and egg situation

AbstractBackgroundThe prevalence of epileptic seizures in dementia is higher than healthy individuals and seizures occur in 10‐22% of individuals with Alzheimer's Disease (AD). This exploratory study investigated the clinicopathological biomarkers and risk factors of individuals with/without active seizures following post‐mortem evaluation.MethodThe study included 1047 subjects with remote and 572 with active seizures. The data was obtained from National Alzheimer’s Coordinating Center(NACC) Dataset. The Chi‐square analysis was performed by using SPSS 26 Package Program with seven variables which consist of 1) major pathological changes (Yes/No/Unknown), 2) Thal phase for amyloid plaques (Phase‐0 to Phase‐5/Unknown), 3) Density of neurocortical plaques (No plaque/Sparse/Moderate/Frequent/Unknown), 4) NIA‐AA AD neuropathological change (No AD/Low‐ADNC/ADNC/Intermediate‐ADNC/High‐ADNC,Unknown), 5)Cerebral amyloid angiopathy (None/Mild/Moderate/Severe/Unknown), 6) AD‐Related genes (Yes/No/Unknown), and 7) Braak stage for neurofibrillary degeneration (Stage‐0 to Stage‐6/Unknown/The presence of tauopathy precludes Braak staging). Post‐hoc comparisons were done by using adjusted residuals.ResultThe chi‐square analysis showed that major pathological changes (χ2=18.107) are more common in patients with active seizures (27.5%) than remote seizures (19.9%). Thal phase for amyloid plaques (χ2=38.771) was significantly different in Stage‐0 and Stage‐1 the percentage of patients with active seizures was higher (5.7%, 4.8%) than remote seizures (1.8%, 1.7%). Braak stage for neurofibrillary degeneration (χ2=81.632) significantly differs among groups. Post‐hoc analysis showed that patients with active seizures (4.4%) had a higher percentage than remote seizures (1.1%) in Stage‐5. Density of neurofibrillary plaques (χ2=36.345) differs in groups showing that frequent plaques are more common in patients with active seizures (11.2%) than remote (6.9%). Cerebral amyloid angiopathy (χ2=51.946) showed a difference indicating mild angiopathy is more common in patients with active seizures (9.6%) than remote (3.9%). (All p&lt;0.001)ConclusionThese results may indicate that seizures are the result of widespread and severe degeneration in the brain or the degeneration is due to these seizures.

Vascular Epilepsy

Seizures can be a presenting feature of acute stroke. They may complicate its early clinical course or be a late complication or sequel. The incidence of combined “early” and “late” seizures after stroke has been reported to be approximately 10% and the prevalence is of 2-4%. Mechanisms leading to post stroke seizures and chronic epilepsy, in both ischemic and hemorrhagic strokes, are diverse. Focal slowing or diffuse slowing activities, rhythmic slow waves are associated with a low risk of early onset seizures whereas focal spikes, sharp waves, periodic lateralized, or periodic bilateral discharges are associated with a higher risk. There are no randomised controlled trials performed in stroke patients evaluating management strategies for poststroke seizures and epilepsy. Treatment options should be extrapolated from those of epilepsy in general, taking into consideration hepatic and renal function, tolerability, costs, interactions between antiepileptic drugs (AED), interactions with antithrombotic and other treatments. However, randomised controlled trials of AED prophylaxis for acute and remote seizures are essential to improve the evidence level of current guidelines and recommendations for the management of post-stroke seizures

Risk Factors of Post-Stroke Epilepsy in Children; Experience from a Tertiary Center and a Brief Review of the Literature

ObjectivesAcute seizures and post-stroke epilepsy have been reported more frequently in patients with pediatric stroke than adults. Acute seizures in the first days of a stroke may deteriorate stroke and ischemia-related neurodegeneration and contribute to the development of post-stroke epilepsy. In this study, we aimed to investigate risk factors for the development of post-stroke epilepsy in children with arterial ischemic stroke. Materials and MethodsWe recruited 86 children with arterial ischemic stroke. We analyzed variables, including age at admission, gender, complaints at presentation, focal or diffuse neurologic signs, neurologic examination findings, laboratory investigations that were conducted at admission with stroke (complete blood cell count, biochemical-infectious-metabolic-immunological investigations, vitamin B12 levels, vitamin D levels), neuroimaging results, etiologies, time of the first seizure, time of remote seizures, and development of neurologic deficit retrospectively. Seizures during the first six hours after stroke onset were defined as ‘very early seizures’. ‘Early seizures’ were referred to seizures during the first 48 h. Patients who experienced two or more seizures that occurred after the acute phase of seizures were classified as ‘epileptic.’ A binary logistic regression analysis was used to estimate risk factors. ResultsAn acute seizure was detected in 59% and post-stroke epilepsy developed in 41% of our cohort. Binary logistic regression analysis demonstrated that ‘very early seizures’ increased epilepsy risk six-fold. Epilepsy was 16 times higher in patients with ‘early seizures’. Low vitamin D levels were defined as a risk factor for post-stroke epilepsy. ConclusionSeizures in the very early period (within the first six hours) are the most significant risk factors for the development of post-stroke epilepsy Further studies regarding seizure prevention and neuroprotective therapies are needed because post-stroke epilepsy will affect long term prognosis in patients with pediatric stroke.

Epileptic seizures and outcome in different subtypes of subarachnoid haemorrhage – Results of a single-center retrospective analysis

BackgroundSymptomatic epileptic seizures are an important complication in subarachnoid haemorrhage (SAH) with a frequency of 0.9–25% with importance for patient outcome. The majority of previous studies investigated the incidence of symptomatic epileptic seizures after aneurysmatic SAH. Here we compared the seizure incidence and its impact on the outcome between non-aneurysmatic and aneurysmatic SAH. MethodsWe analysed retrospectively 109 consecutive patients with spontaneous, non-traumatic SAH. Patients were divided in three groups (perimesencephalic, non-aneurysmatic and aneurysmatic SAH). All patients received standard-of-care treatment. The occurrence of acute (0–7 days after SAH) and remote symptomatic epileptic seizures (7 days or more after SAH), severity of SAH as well as clinical outcome parameters (modified Rankin scale [mRS]) at discharge and the frequency of in-house complications were assessed. mRS scores were dichotomized in 0–3 vs. 4–6 to stratify for good versus bad outcome. ResultsPerimesencephalic SAH patients did not experience acute seizures whereas non-aneurysmatic and aneurysmatic SAH patients showed acute seizures with similar frequency (9% and 11%, p = 0.23). The frequency of remote symptomatic seizures was similar in all subgroups (12% vs. 9% vs. 7%, p = 0.72). Seizure occurrence was not predictive for a poor outcome (mRS >4; acute seizures: OR 0.35 [95%CI: 0.02–6.96], p = 0.49; remote seizures: OR 1.72 [95%CI: 0.14–20.1], p = 0.67). ConclusionsSeizures are important neurologic complications of SAH of all etiologies. Nevertheless, acute as well as remote symptomatic seizures are unrelated to the short-term outcome. These results should be treated as hypothesis generating and require confirmation.

Etiology, seizure type, and prognosis of epileptic seizures in the emergency department

Epileptic seizures are a common reason for emergency department (ED) admittance. We aimed to describe the etiological distribution of epileptic seizures and the relationships between etiology and semiology in patients admitted to the emergency room, and to identify early prognostic factors for recurrence and mortality. MethodsA retrospective observational study was conducted in adult patients consecutively attended in the emergency room with epileptic seizures over a 2-year period. We recorded data on the etiological and syndromic classification of the seizure, and on recurrence and mortality at 1 year of follow-up. ResultsIn total, 289 patients were included. Mean age was 55.9 (±21.9 years). There were 38.6% with a previous diagnosis of epilepsy and 49.8% with new-onset seizures. Among structural epilepsies, a vascular etiology was the most common overall (28.3%) but particularly in elderly (>65 years) patients (50.9%), followed by brain tumors (15.5%). In both etiologies, most patients presented with nonconvulsive seizures.Seizure recurrence during follow-up was reported in 37.1% and was most common in patients with symptomatic remote seizures (50 patients, 41%). Brain tumors (odds ratio (OR): 5.1, confidence interval (CI): 1.7–11.8; p < 0.01), younger age (OR: 0.9, CI: 0.97–0.99; p < 0.05), and a previous diagnosis of epilepsy (OR: 3.5, CI: 1.9–6.3; p < 0.01) were independent predictors of recurrence. Overall mortality was 8.6%. Symptomatic epilepsy was an independent predictor of mortality (hazard ratio (HR): 6.3, CI 1.4–23.4; p < 0.05). ConclusionsThe most common etiologies of seizures in patients admitted to the ED are seizures of unknown cause and vascular disorder-related seizures. Seizures are more likely to recur in younger patients with a tumor whereas symptomatic epilepsy is associated with a higher risk of death at a 1-year follow-up.

European Stroke Organization guideline for the diagnosis and treatment of cerebral venous thrombosis - endorsed by the European Academy of Neurology.

Current guidelines on cerebral venous thrombosis (CVT) diagnosis and management were issued by the European Federation of Neurological Societies in 2010. We aimed to update the previous European Federation of Neurological Societies guidelines using a clearer and evidence-based methodology. We followed the Grading of Recommendations, Assessment, Development and Evaluation system, formulating relevant diagnostic and treatment questions, performing systematic reviews and writing recommendations based on the quality of available scientific evidence. We suggest using magnetic resonance or computed tomographic angiography for confirming the diagnosis of CVT and not routinely screening patients with CVT for thrombophilia or cancer. We recommend parenteral anticoagulation in acute CVT and decompressive surgery to prevent death due to brain herniation. We suggest preferentially using low-molecular-weight heparin in the acute phase and not direct oral anticoagulants. We suggest not using steroids and acetazolamide to reduce death or dependency. We suggest using antiepileptics in patients with an early seizure and supratentorial lesions to prevent further early seizures. We could not make recommendations concerning duration of anticoagulation after the acute phase, thrombolysis and/or thrombectomy, therapeutic lumbar puncture, and prevention of remote seizures with antiepileptic drugs. We suggest that, in women who have suffered a previous CVT, contraceptives containing oestrogens should be avoided. We suggest that subsequent pregnancies are safe, but use of prophylactic low-molecular-weight heparin should be considered throughout pregnancy and puerperium. Multicentre observational and experimental studies are needed to increase the level of evidence supporting recommendations on the diagnosis and management of CVT.

European Stroke Organization guideline for the diagnosis and treatment of cerebral venous thrombosis – Endorsed by the European Academy of Neurology

The current proposal for cerebral venous thrombosis guideline followed the Grading of Recommendations, Assessment, Development, and Evaluation system, formulating relevant diagnostic and treatment questions, performing systematic reviews of all available evidence and writing recommendations and deciding on their strength on an explicit and transparent manner, based on the quality of available scientific evidence. The guideline addresses both diagnostic and therapeutic topics. We suggest using magnetic resonance or computed tomography angiography for confirming the diagnosis of cerebral venous thrombosis and not screening patients with cerebral venous thrombosis routinely for thrombophilia or cancer. We recommend parenteral anticoagulation in acute cerebral venous thrombosis and decompressive surgery to prevent death due to brain herniation. We suggest to use preferentially low-molecular weight heparin in the acute phase and not using direct oral anticoagulants. We suggest not using steroids and acetazolamide to reduce death or dependency. We suggest using antiepileptics in patients with an early seizure and supratentorial lesions to prevent further early seizures. We could not make recommendations due to very poor quality of evidence concerning duration of anticoagulation after the acute phase, thrombolysis and/or thrombectomy, therapeutic lumbar puncture, and prevention of remote seizures with antiepileptic drugs. We suggest that in women who suffered a previous cerebral venous thrombosis, contraceptives containing oestrogens should be avoided. We suggest that subsequent pregnancies are safe, but use of prophylactic low-molecular weight heparin should be considered throughout pregnancy and puerperium. Multicentre observational and experimental studies are needed to increase the level of evidence supporting recommendations on the diagnosis and management of cerebral venous thrombosis.

Remote preoperative tonic-clonic seizures do not influence outcome after surgery for temporal lobe epilepsy

ObjectivesTonic-clonic seizures are associated with greater chance of seizure relapse after anterior temporal lobectomy. We investigated whether the interval between the last preoperative tonic-clonic seizure and surgery relates to seizure outcome in patients with drug-resistant mesial temporal lobe epilepsy (MTLE). MethodsIn this retrospective study, patients were prospectively registered in a database from 1986 through 2014. Postsurgical outcome was categorized as seizure freedom or relapse. The relationship between surgical outcome and the interval between the last preoperative tonic-clonic seizure and surgery was investigated. ResultsOne-hundred seventy-one patients were studied. Seventy nine (46.2%) patients experienced tonic-clonic seizures before surgery. Receiver operating characteristic curve of timing of the last preoperative tonic-clonic seizure was a moderate indicator to anticipate surgery failure (area under the curve: 0.657, significance; 0.016). The best cutoff that maximizes sensitivity and specificity was 27months; with a sensitivity of 0.76 and specificity of 0.60. Cox-Mantel analysis confirmed that the chance of becoming free of seizures after surgery in patients with no or remote history of preoperative tonic-clonic seizures was significantly higher compared with patients with a recent history (i.e., in 27months before surgery) (p=0.0001). ConclusionsThe more remote the occurrence of preoperative tonic-clonic seizures, the better the postsurgical seizure outcome, with at least a two year gap being more favorable. A recent history of tonic-clonic seizures in a patient with MTLE may reflect more widespread epileptogenicity extending beyond the borders of mesial temporal structures.

Long-term outcome of patients with disorders of consciousness with and without epileptiform activity and seizures: a prospective single centre cohort study.

Brain-injured patients can experience epileptic seizures beyond 1week from injury (unprovoked remote symptomatic epileptic seizures). In our longitudinal observational study, we analysed occurrence of unprovoked remote epileptic seizures and interictal epileptiform activity in 130 traumatic, vascular or anoxic inpatientswith disorders of consciousness (DOC), with a clinical diagnosis of vegetative state (n=97) or minimally conscious state (n=33). We also investigated impact of epileptic seizures and epileptiform activity on clinical outcome (30months post-onset). Epileptic seizures occurred in 35/130 patients (26.9%), epileptiform activity in 61/130 (46.9%) patients, without significant differences related to clinical diagnosis or aetiology. Among patients with epileptiform activity, only 26/61 (42.6%) developed clinically evident seizures. Mortality at 30months was not significantly influenced by the presence of seizures or epileptiform activity. The proportion of patients who recovered at long-term follow-up was higher in patients without than in patients with epileptic seizures, but was similar in patients with or without epileptiform activity. The presence of epileptic seizures but not of epileptiform activity, significantly affected the level of responsiveness at final outcome. In conclusion, seizures were detected in about one third of the whole sample, and in about a half of patients with epileptiform activity, regardless of clinical diagnosis or aetiology. Although epileptic seizures or epileptiform activity did not significantly affect mortality rate, we demonstrated that epileptic seizures could hamper recovery of consciousness. Epileptic seizures thus qualify as one of the factors largely undetermined at the moment which can influence prognosis in DOC patients.

Neonatal seizures triple the risk of a remote seizure after perinatal ischemic stroke.

To determine incidence rates and risk factors of remote seizure after perinatal arterial ischemic stroke. We retrospectively identified a population-based cohort of children with perinatal arterial ischemic stroke (presenting acutely or in a delayed fashion) from a large Northern Californian integrated health care system. We determined incidence and predictors of a remote seizure (unprovoked seizure after neonatal period, defined as 28 days of life) by survival analyses, and measured epilepsy severity in those with active epilepsy (≥1 remote seizure and maintenance anticonvulsant treatment) at last follow-up. Among 87 children with perinatal stroke, 40 (46%) had a seizure in the neonatal period. During a median follow-up of 7.1 years (interquartile range 3.2-10.5), 37 children had ≥1 remote seizure. Remote seizure risk was highest during the first year of life, with a 20% (95% confidence interval [CI] 13%-30%) cumulative incidence by 1 year of age, 46% (CI 35%-58%) by 5 years, and 54% (CI 41%-67%) by 10 years. Neonatal seizures increased the risk of a remote seizure (hazard ratio 2.8, CI 1.3-5.8). Children with neonatal seizures had a 69% (CI 48%-87%) cumulative incidence of remote seizure by age 10 years. Among the 24 children with active epilepsy at last follow-up, 8 (33%) were having monthly seizures despite an anticonvulsant and 7 (29%) were on more than one anticonvulsant. Remote seizures and epilepsy, including medically refractory epilepsy, are common after perinatal stroke. Neonatal seizures are associated with nearly 3-fold increased remote seizure risk.

Abstract WMP103: Epilepsy is Associated With Poorer Neurologic Outcome After Pediatric Arterial Ischemic Stroke

Introduction: Post-stroke epilepsy is common in children, but the relationship of childhood epilepsy with stroke outcome is poorly understood. Hypothesis: Children with epilepsy after arterial ischemic stroke have worse outcomes than those without epilepsy. Methods: We prospectively enrolled children (birth-18 years) with arterial ischemic stroke and identified remote seizures (occurring ≥ 7 days post-stroke). At one-year, patients with active epilepsy (≥ 1 remote seizure + maintenance anti-convulsant) were identified and Pediatric Stroke Outcome Measure (PSOM) was scored. Total PSOM scores range from 0-10; higher values reflect more severe neurologic deficits. Ordinal logistic regression was used to evaluate the relationship between clinical factors and PSOM scores. PSOM scores were categorized 0-1, 1.5-3, 3.5-6, 6.5-10 to depict stratified distribution. Results: Among 94 children (54% male; 20% Hispanic; 25% neonatal strokes; median age for childhood strokes 6.1 years, IQR 1.3-12), 12 had ≥ 1 remote seizure during the first year post-stroke. At one-year follow-up, 19 children were taking a maintenance anti-convulsant and 10 children had active epilepsy. Median PSOM score at one-year for the overall cohort was 0.5 (IQR 0-1.5). Median PSOM score among children with active epilepsy was 3.3 (IQR 0.5-6). Figure demonstrates distribution of categorized PSOM scores stratified by the presence of active epilepsy. On univariable regression analyses, older age (OR 1.1, 95% CI 1.0-1.1, P=0.02), maintenance anti-convulsant at one-year (OR 2.7, 95% CI 1.0-7.0, P=0.04) and active epilepsy (OR 6.3, 95% CI 1.7-25, P=0.007) were associated with higher total PSOM scores. After multivariable adjustment for age and maintenance anti-convulsant, active epilepsy remained associated with higher total PSOM score (OR 7.8, 95% CI 1.3-46, P=0.02). Conclusions: Active epilepsy one-year after pediatric arterial ischemic stroke is associated with poorer neurologic outcome.

Epilepsy in patients with malignant middle cerebral artery infarcts and decompressive craniectomies

Patients with malignant middle cerebral artery (MCA) infarctions who have undergone craniectomy are susceptible to the development of vascular epilepsy. Our objective was to study the factors that might influence the occurrence of seizures in this group of patients. All patients who developed malignant MCA infarction and had undergone decompressive craniectomy in our center between November 2002 and January 2014 were evaluated. In the subsequent follow-up, we evaluated the clinical outcomes and attempted to identify the factors that were related to the occurrence of seizures. We evaluated a total of 80 patients. The median time at which the craniectomy was performed was 40.5h after the stroke. Seizures occurred in 47.5% of all patients. The mortality rate within the first week was 16%, and of those who survived 53.7% developed seizures; 9% of these seizures were acute symptomatic, and 44.8% were remote. The median onset of remote seizures was seven months, and the majority of these were motor seizures with generalization. Notably, the patients with seizures exhibited longer delays from stroke to craniectomy, greater involvements of the temporal lobe and a higher rate of post-craniectomy recanalization of the occluded artery. Regarding the timing of the surgeries, a significantly greater proportion of those who underwent surgery more than 42h after the stroke developed epilepsy (p=0.004). Logistic regression revealed that only prolonged delay (>42h) independently predicted the development of epilepsy (OR 5.166; IC 95% 1.451-18.389; p=0.011). More than half of patients with malignant MCA infarcts who underwent decompressive craniectomy developed epilepsy. The occurrence of seizures in these patients was related to the delay to the performance of the craniectomy.

Epileptic seizure propagation from the second somatic sensory area to the fronto-medial region, by insular redistribution. A case report and a connectome description

SUMMARY Introduction. The seizure propagation phenomenon by inducing remote symptoms brings several difficulties in finding the seizure onset and delineating the epileptic network which should be taken into consideration in epilepsy surgery. By demonstrating a difficult (MRI negative) epilepsy surgery case explored with invasive presurgical evaluation we highlight the importance to recognise the secondary sensory area and to explore the the parieto-opercular-insular-medial frontal network in certain cases. A further conclusion is the consideration of the redistributory role of the insula as a special structure in the cerebral connectome, having a role in epileptic network organisation. Aims. To support the role of the insula in the organisation of an opercular – medial frontal epileptic network and to confirm Penfield’s the “second somatic sensory leg area” by way of a case report. We try to give an up to date exploration of our patient’s remote epileptic seizures by way of a connectome. Methods. The epileptic disorder was studied with intensive video EEG monitoring and two times 3T MRI. Interictal FDG (fluorodeoxyglucose) PET was also undertaken. Beside the scalp EEG and computerized frequency analysis, the evaluation was performed by invasive EEG with 2 grids and 2 strips and an insular deep electrode in addition. Electrical cortical stimulation and cortical mapping were also undertaken. Results. The video-EEG study revealed the complex seizure semiology. The left sided global somatosesensory aura in the leg, followed supplementary motor area manifestations represented a remote seizure. The seizure onset zone and the symptomatogenic zone were localised by the invasive electrophysiology. With the insular deep electrode we succeeded to explore the propagation of ictal activity to the insula and later to frontal medial surface. The PET, the negative 3T MRI results and the postprocessing morphometry confirmed the lesional origin and localised the epileptogenic area to the second somato-sensory field where a dysgenesis was located. Conclusions. By preoperative invasive video-EEG evaluation, the second somato-sensory leg area was delineated as the seizure onset zone. The resection of this area by IIb type cortical dysgenesis, resulted in a complete relief of the seizures. The invasive video-EEG revealed the peculiar role of the insula in the propagation of the epileptic seizure from the second sensory leg area to the ipsilateral fronto-medial supplemetary motor area. Our results, confirm, that the insula has a relay or node function on the parietal opercular-fronto-medial epileptic network. The connectome of the insula is a further additive of the scale-free features of the remote epileptic networks.