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Published on: June 25, 2016
Acute symptomatic seizures in cerebral venous thrombosis
Erik Lindgren1, Suzanne M Silvis1, Sini Hiltunen1
1From the Department of Clinical Neuroscience (E.L., J.Z., P.R., A. Ahmed, T.T., K.J.), Institute of Neuroscience and Physiology, Sahlgrenska Academy at University of Gothenburg; Department of Neurology (E.L., J.Z., P.R., A. Ahmed, T.T., K.J.), Sahlgrenska University Hospital, Gothenburg, Sweden; Department of Neurology (S.M.S., S.M.Z., M.S.v.K., J.M.C.), Amsterdam UMC, University of Amsterdam, the Netherlands; Department of Neurology (S.H., T.T., J.P.), Helsinki University Hospital and University of Helsinki, Finland; Department of Neurology (M.R.H., M.A.), Inselspital, Bern University Hospital and University of Bern, Switzerland; National Institute of Neurology and Neurosurgery Manuel Velasco Suarez (F.S., A. Arauz), Mexico City, Mexico; Department of Neurology (M.d.S., T.K.), Royal Adelaide Hospitals and Department of Medicine, University of Adelaide, SA, Australia; Sina Hospital (M.M., M.G.), Hamadan University of Medical Science, Iran; Department of Neurosciences and Mental Health (Neurology) (D.A.d.S., J.M.F.), Hospital de Santa Maria/CHULN; University of Lisbon (D.A.d.S., J.M.F.); Faculdade de Medicina (S.P.), Universidade de Lisboa, Lisbon, Portugal; Manchester Centre for Clinical Neurosciences (S.A.-A., M.N.M.P.), Salford Royal NHS Foundation Trust, UK; Department of Neurology (E.E., N.Y.), Istanbul Faculty of Medicine, Istanbul University, Turkey; Neurosciences Department (M.A.B.), Hospital Dr. R.A. Calderón Guardia, CCSS, San José, Costa Rica; and Department of Biomedicine (V.A., P.A.), Neuroscience and Advanced Diagnostics, University of Palermo, Italy.
Objective:
To identify characteristics, predictors, and outcomes of acute symptomatic seizures (ASS) in cerebral venous thrombosis (CVT), we investigated 1,281 consecutive adult patients with CVT included from 12 hospitals within the International CVT Consortium.
Methods:
We defined ASS as any seizure between symptom onset and 7 days after diagnosis of CVT. We stratified ASS into prediagnosis and solely postdiagnosis ASS. Status epilepticus (SE) was also analyzed separately. We analyzed predictors for ASS and the association between ASS and clinical outcome (modified Rankin Scale) with multivariable logistic regression.
Results:
Of 1,281 eligible patients, 441 (34%) had ASS. Baseline predictors for ASS were intracerebral hemorrhage (ICH; adjusted odds ratio [aOR] 4.1, 95% confidence interval [CI] 3.0-5.5), cerebral edema/infarction without ICH (aOR 2.8, 95% CI 2.0-4.0), cortical vein thrombosis (aOR 2.1, 95% CI 1.5-2.9), superior sagittal sinus thrombosis (aOR 2.0, 95% CI 1.5-2.6), focal neurologic deficit (aOR 1.9, 95% CI 1.4-2.6), sulcal subarachnoid hemorrhage (aOR 1.6, 95% CI 1.1-2.5), and female-specific risk factors (aOR 1.5, 95% CI 1.1-2.1). Ninety-three (7%) patients had solely postdiagnosis ASS, best predicted by cortical vein thrombosis (positive/negative predictive value 22%/92%). Eighty (6%) patients had SE, independently predicted by ICH, focal neurologic deficits, and cerebral edema/infarction. Neither ASS nor SE was independently associated with outcome.
Conclusion:
ASS occurred in one-third of patients with CVT and was associated with brain parenchymal lesions and thrombosis of the superficial system. In the absence of prediagnosis ASS, no subgroup was identified with sufficient risk of postdiagnosis ASS to justify prophylactic antiepileptic drug treatment. We found no association between ASS and outcome.
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