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Introduction: MRI is negative in a large percentage of autoimmune encephalitis cases or lacks findings specific to an antibody. Even rarer is literature correlating the evolution of imaging findings with treatment timepoints. We aim to characterize imaging findings in autoimmune encephalitis at presentation and on follow up correlated with treatment timepoints for this rare disease. Methods: A full-text radiological information system search was performed for "autoimmune encephalitis" between January 2012 and June 2022. Patients with laboratory-identified autoantibodies were included. MRI findings were assessed in correlation to treatment timepoints by two readers in consensus. For statistical analysis, cell-surface vs intracellular antibody groups were assessed for the presence of early limbic, early extralimbic, late limbic, and late extralimbic findings using the χ2 test. Results: Thirty-seven patients (female n = 18, median age 58.8 years; range 25.7 to 82.7 years) with 15 different autoantibodies were included in the study. Twenty-three (62%) patients were MRI-negative at time of presentation; 5 of these developed MRI findings on short-term follow up. Of the 19 patients with early MRI findings, 9 (47%) demonstrated improvement upon treatment initiation (7/9 cell-surface group). There was a significant difference (p = 0.046) between the MRI spectrum of cell-surface vs intracellular antibody syndromes as cell-surface antibody syndromes demonstrated more early classic findings of limbic encephalitis and intracellular antibody syndromes demonstrated more late extralimbic abnormalities. Conclusion: MRI can be used to help narrow the differential diagnosis in autoimmune encephalitis and can be used as a monitoring tool for certain subtypes of this rare disease.
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Importance: Acute 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. Objective: To compare mortality and risk of epilepsy following different types of acute symptomatic seizures. Design, Setting, and Participants: This 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. Exposures: Type of acute symptomatic seizure. Main Outcomes and Measures: All-cause mortality and epilepsy (at least 1 unprovoked seizure presenting >7 days after stroke). Results: A 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 Relevance: In 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.
Assuntos
Epilepsia , AVC Isquêmico , Estado Epiléptico , Acidente Vascular Cerebral , Adulto , Humanos , Masculino , Feminino , Idoso , Estudos de Coortes , Prognóstico , AVC Isquêmico/complicações , Epilepsia/tratamento farmacológico , Acidente Vascular Cerebral/complicações , Estado Epiléptico/tratamento farmacológicoRESUMO
Purpose: To quantitatively assess lateral geniculate nucleus (LGN) volume loss in the presence of lesions in the postgeniculate pathway and its correlation with optical coherence tomography retinal parameters. Methods: This was a case control study of patients recruited at the University Hospital Zurich, Switzerland. Nine patients who were suffering from lesions in the postgeniculate pathway acquired at least 3 months earlier participated. Retinal parameters were analyzed using spectral domain optical coherence tomography and a newly developed magnetic resonance imaging protocol with improved contrast to noise ratio was applied to measure LGN volume. Results: The affected LGN volume in the patients (mean volume 73.89 ± 39.08 mm3) was significantly smaller compared with the contralateral unaffected LGN (mean volume 131.43 ± 12.75 mm3), as well as compared with healthy controls (mean volume 107 ± 24.4 mm3). Additionally, the ganglion cell layer thickness corresponding with the affected versus unaffected side within the patient group differed significantly (mean thickness 40.5 ± 4.11 µm vs 45.7 ± 4.79 µm) compared with other retinal parameters. A significant linear correlation could also be shown between relative LGN volume loss and ganglion cell layer thickness decrease. Conclusions: Corresponding LGN volume reduction could be shown in patients with postgeniculate lesions using a newly developed magnetic resonance imaging protocol. LGN volume decrease correlated with ganglion cell layer thickness reduction as a sign of trans-synaptic retrograde neuronal degeneration.