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Abstract Details

Status Epilepticus per se Did Not Lead to CSF Pleocytosis within the First 24 Hours
Epilepsy/Clinical Neurophysiology (EEG)
P3 - Poster Session 3 (12:00 PM-1:00 PM)
12-011
To assess whether status epilepticus (SE) per se is associated with cerebrospinal fluid (CSF) pleocytosis within the first 24 hours after onset. The SE-induced neuroinflammation leading to pleocytosis significantly increases at 18-24 hours. Therefore, we hypothesize that any CSF pleocytosis in the first 24 hours of SE onset could be due to other causes.

It was previously claimed that SE causes CSF pleocytosis. However, attributing the CSF pleocytosis solely to SE, while not considering alternate underlying causes, might lead to devastating outcomes. Compared to prior studies, we are using more advanced diagnostic imaging and laboratory technologies to better elucidate alternate causes of CSF pleocytosis. 

We completed a historical cohort study of patients with SE admitted to the intensive care unit (ICU) of Vancouver General Hospital between March 2010-May 2019. Patients were identified in ICU database and excluded if no CSF sample obtained within 24-hour, SE unconfirmed, had any subarachnoid-hemorrhage or traumatic-tap.

Of 441 patients with SE, 72 met the criteria. Of these, 12 (17%) demonstrated CSF pleocytosis, in all of which a cause was identified. Interestingly, even in patients without CSF pleocytosis, 53% (31/58) showed elevated protein, however, CSF protein in pleocytosis group was significantly higher (2758 vs 693 mg/L, p<0.01).

Within the first 24 hours of onset, SE per se was not seen to cause CSF pleocytosis. Therefore, we suggest any CSF pleocytosis in the first 24 hours should be empirically treated and fully investigated for an etiology. In addition, CSF protein elevation may occur as a result of SE per se, and therefore, is not a reliable marker for empirical treatment. These results are different from prior studies as we have exclusively assessed CSF pleocytosis in the first 24 hours to exclude the effect of SE-related neuroinflammation and we have ruled out other causes using more advanced technology. 
Authors/Disclosures
Sargun Bajaj
PRESENTER
No disclosure on file
No disclosure on file
No disclosure on file
Farzad Moien Afshari, MD (University of British Columbia) No disclosure on file