Background: Stroke is one of the leading causes of acquired epilepsy in adults. An

The purpose of this study was to identify risk factors for acute symptomatic seizures and post-stroke epilepsy after acute ischemic stroke and evaluate the effects of reperfusion treatment. Methods: We assessed the risk factors for post-stroke seizures using logistic or Cox regression in a multicenter study, including adults from 8 European referral centers with neuroimaging-confirmed ischemic stroke. We compared the risk of post-stroke seizures between participants with or without reperfusion treatment following propensity score matching to reduce confounding due to treatment selection. Results: In the overall cohort of 4,229 participants (mean age 71 years, 57% men), a higher risk of acute symptomatic seizures was observed in those with more severe strokes, infarcts located in the posterior cerebral artery territory, and

Objective: To describe the neuropathological features of N-methyl-D-aspartate receptor (NMDAR)-encephalitis in an archival autopsy cohort. Methods: We examined four autopsies from patients with NMDAR-encephalitis; two patients were untreated, three had comorbidities: small cell lung cancer, brain post-transplant lymphoproliferative disease (PTLD), and overlapping demyelination. Results: The two untreated patients had inflammatory infiltrates predominantly composed of perivascular and parenchymal CD3 + /CD8 À T cells and CD79a + B cells/plasma cells in basal ganglia, amygdala, and hippocampus with surrounding white matter. The hippocampi showed a significant decrease of NMDAR-immunoreactivity that correlated with disease severity. The patient with NMDAR-encephalitis and immunosuppression for kidney transplantation developed a brain monomorphic PTLD. Inflammatory changes were compatible with NMDAR-encephalitis. Additionally, plasma cells accumulated in the vicinity of the necrotic tumor along with macrophages and activated microglia that strongly expressed pro-inflammatory activation markers HLA-DR, CD68, and IL18. The fourth patient developed demyelinating lesions in the setting of a relapse 4 years after NMDAR-encephalitis. These lesions exhibited the hallmarks of classic multiple sclerosis with radially expanding lesions and remyelinated shadow plaques without complement or immunoglobulin deposition, compatible with a pattern I demyelination. Interpretation: The topographic distribution of inflammation in patients with NMDAR-encephalitis reflects the clinical symptoms of movement disorders, abnormal behavior, and memory dysfunction with inflammation dominantly observed in basal ganglia, amygdala, and hippocampus, and loss of NMDAR-immunoreactivity correlates with disease severity. Co-occurring pathologies influence the spatial distribution, composition, and intensity of inflammation, which may modify patients' clinical presentation and outcome.

ImportanceAcute symptomatic seizures occurring within 7 days after ischemic stroke may be associated with an increased mortality and risk of epilepsy. It is unknown whether the type of acute symptomatic seizure influences this risk.ObjectiveTo compare mortality and risk of epilepsy following different types of acute symptomatic seizures.Design, Setting, and ParticipantsThis cohort study analyzed data acquired from 2002 to 2019 from 9 tertiary referral centers. The derivation cohort included adults from 7 cohorts and 2 case-control studies with neuroimaging-confirmed ischemic stroke and without a history of seizures. Replication in 3 separate cohorts included adults with acute symptomatic status epilepticus after neuroimaging-confirmed ischemic stroke. The final data analysis was performed in July 2022.ExposuresType of acute symptomatic seizure.Main Outcomes and MeasuresAll-cause mortality and epilepsy (at least 1 unprovoked seizure presenting >7 days after stroke).ResultsA total of 4552 adults were included in the derivation cohort (2547 male participants [56%]; 2005 female [44%]; median age, 73 years [IQR, 62-81]). Acute symptomatic seizures occurred in 226 individuals (5%), of whom 8 (0.2%) presented with status epilepticus. In patients with acute symptomatic status epilepticus, 10-year mortality was 79% compared with 30% in those with short acute symptomatic seizures and 11% in those without seizures. The 10-year risk of epilepsy in stroke survivors with acute symptomatic status epilepticus was 81%, compared with 40% in survivors with short acute symptomatic seizures and 13% in survivors without seizures. In a replication cohort of 39 individuals with acute symptomatic status epilepticus after ischemic stroke (24 female; median age, 78 years), the 10-year risk of mortality and epilepsy was 76% and 88%, respectively. We updated a previously described prognostic model (SeLECT 2.0) with the type of acute symptomatic seizures as a covariate. SeLECT 2.0 successfully captured cases at high risk of poststroke epilepsy.Conclusions and RelevanceIn this study, individuals with stroke and acute symptomatic seizures presenting as status epilepticus had a higher mortality and risk of epilepsy compared with those with short acute symptomatic seizures or no seizures. The SeLECT 2.0 prognostic model adequately reflected the risk of epilepsy in high-risk cases and may inform decisions on the continuation of antiseizure medication treatment and the methods and frequency of follow-up.

Patients with nodal/paranodal antibodies represent a specific subgroup of inflammatory peripheral neuropathies, whose clinical presentation with a prolonged subacute phase, additional symptoms such as ataxia and tremor, and poor treatment response to IV immunoglobulin (IVIG) often differs from classic Guillain-Barré syndrome (GBS) or chronic inflammatory demyelinating polyneuropathy (CIDP). 1 Previous studies on nodo/paranodopathies mainly focused on adult patients, whereas the clinical spectrum of pediatric patients is less well established. We reviewed the clinical presentation of 54 children with GBS (n = 42) and CIDP (n = 12) and retrospectively screened for antibodies against neurofascin155 (NF155), NF186, NF140, contactin-1 (CNTN1), contactinassociated protein1 (CASPR1), and glycine-receptor (GlyR) using cell-based assays 2,3 ; 1 patient was additionally tested with CNTN1-ELISA. 4 All cases with sufficient serum were tested for ganglioside-IgG-, IgA-, and IgM-antibodies against GM1 (n = 42), GD1a (n = 18), GD1b (n = 23), and GQ1b (n = 21). 5 Clinical and paraclinical information of all patients is summarized in the table. The study was approved by the ethics committee (EK1773/2016). Children with classic GBSOf 42 children with GBS, 26 were classified as acute inflammatory demyelinating polyneuropathy (AIDP), 7 as acute motor/motor-sensory axonal neuropathy (AMAN/AMSAN) by nerve conduction velocity according to Hadden criteria, 6 4 as Miller-Fisher syndrome (MFS), and 2 as MFS/GBS overlap. Three patients with GBS could not be classified because of lack of nerve-conduction studies. In 25 of 35 patients (71.4%), an infection was reported within 4 weeks before symptom onset (13 gastrointestinal, 4 respiratory, and 8 unspecified). Eight patients had IgG-ganglioside antibodies (19.0%), 6 IgM (14.2%), and 1 IgA (2.4%). Nodal/ paranodal antibodies were not detected. Patients with AMAN/AMSAN (5/7 with reported infection: 1 campylobacter jejuni, 1 varicella-zoster virus, and 3 unspecified) were more often ganglioside antibody positive (6/7) than patients with AIDP (4/26; likelihood ratio 12.419) or MFS (2/4).