ObjectiveWe conducted a retrospective, case–control study of neurocysticercosis patients to ascertain early markers that identify subjects likely to develop treatment‐resistant seizures.MethodsClinical histories and imaging studies from 38 neurocysticercosis patients who had been followed for 18 months after treatment were evaluated. Both pairwise and multifactorial analyses were conducted to identify factors associated with continued seizures.ResultsEleven of 38 patients continued to have seizures during the follow‐up period. On univariate analysis, the number of neurocysticercosis lesions, number of bands on the baseline neurocysticercosis western blot, edema volumes on follow‐up MRI scans, edema volume changes between baseline and follow‐up images, and proportion of calcified lesions with perilesional edema were all significantly increased in subjects who had persistent seizures during the 18‐month follow‐up period. On multivariate analyses using recursive partition and random forest algorithms, variables associated with persistent seizures included: the number of total and calcified lesions, presence of perilesional edema, the rate of change in the lesion and edema volumes from baseline to follow‐up, and the number of bands on the neurocysticercosis western blot.InterpretationMeasures of both inflammation and disease burden are key risk factors for persistent seizures despite anticonvulsant treatments in patients with neurocysticercosis. Inflammation is therefore a potentially modifiable risk factor for the frequently seen severe seizure disorders in patients with neurocysticercosis.
A 60-year-old woman with history of multiple myeloma was in remission after stem cell transplant 6 years prior. She was undergoing work-up for headaches that were thought to be secondary to a right mastoiditis seen on magnetic resonance imaging (MRI). On routine eye exam, papilloedema was noted. A lumbar puncture was performed, with elevated opening pressure with normal constituents. She was an atypical age for idiopathic intracranial hypertension, and her mastoiditis raised concern for secondary cerebral venous sinus thrombosis. Magnetic resonance venography (MRV) was performed showing poor flow in the right sigmoid sinus, and computed tomography venography (CTV) showed lack of contrast enhancement distal to the right sigmoid sinus, consistent with occlusion. There was also an enhancing mass inferior to the right occipital bone. Biopsy confirmed recurrent plasma cell myeloma. She was treated with chemotherapy, radiation, and warfarin for presumed cerebral venous sinus thrombosis. ARTICLE HISTORY
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