Abstracts

Electroencephalography in West Nile Virus Neuroinvasive Disease

Abstract number : 2.104
Submission category : 3. Neurophysiology / 3C. Other Clinical EEG
Year : 2017
Submission ID : 348726
Source : www.aesnet.org
Presentation date : 12/3/2017 3:07:12 PM
Published date : Nov 20, 2017, 11:02 AM

Authors :
Angela M. Parsons, Mayo Clinic; Anteneh M. Feyissa, Mayo Clinic; Jeffrey W. Britton, Mayo Clinic; Sara E. Hocker, Mayo Clinic; Marie F. Grill, Mayo Clinic; and Amy Crepeau, Mayo Clinic Arizona

Rationale: West Nile virus (WNV) is a flaviviridae virus transmitted by mosquitoes. Neuroinvasive disease occurs in less than 1% of those infected, and may manifest as meningitis, encephalitis, and/or acute flaccid paralysis. Since 1999, there have been over 17,000 cases of neuroinvasive disease with 1700 deaths. Electroencephalography (EEG) provides a means to identify nonconvulsive seizures and status epilepticus in those patients at risk, and may enhance understanding of this disease process. Our aim is to determine the frequency of seizures as well as to describe specific EEG patterns in WNV neuroinvasive disease. Methods: A retrospective chart review was conducted searching for patients 18-99 years of age, admitted to Mayo Clinic (Arizona, Jacksonville, and Rochester), from January 2000 to May 2017, with a diagnosis of WNV neuroinvasive disease. Inclusion criteria consisted of 1) presence of WNV IgM antibodies in both cerebrospinal fluid (CSF) and serum, 2) presence of WNV IgM antibodies in serum only and CSF consistent with meningitis, or 3) presence of serum or CSF WNV PCR and CSF consistent with meningitis. Patients with a prior history of abnormal EEG were excluded. EEG reports were classified in categories based on the presence of epileptiform activity, focal slowing, triphasic waves, and frontal intermittent rhythmic delta activity (FIRDA). EEG findings were allowed to meet criteria for multiple categories. Results: Thirty-five patients were identified. EEG results were categorized as follows: generalized slowing (n=31), epileptiform discharges 17.1% (n=6), focal slowing 17.1% (n=6), FIRDA 11.4% (n=4) and triphasic waves in 20% (n=7). Pure generalized slowing was seen in 37% of patients (n=13). Of the patients with epileptiform activity, 5 were noted to have clinical or subclinical seizures. Of the patients with triphasic waves, one had hyponatremia (Na=123), one had hyperammonemia (ammonia=94), one had elevated creatinine (Cr=5.2) and one had sedative effect from intermittent propofol use. An anterior predominance of EEG abnormalities was observed in 54.5% (n=6) of the 11 patients with epileptiform discharges and/or focal slowing. None of these 6 patients had imaging findings to correlate with the respective EEG abnormality. Conclusions: Patients with WNV neuroinvasive disease can present with a multitude of EEG abnormalities ranging from non-specific slowing, epileptiform activity, focal slowing, triphasic waves and FIRDA. A previous study of 13 patients by Gandelman-Marton et al. in 2003 reported an anterior predominance of EEG changes in 62% of patients. A prior Mayo Rochester study in 2008 by Rodriguez identified non-specific EEG changes in 5 patients with WNV neuroinvasive disease. In our study, an anterior predominance of EEG changes was observed in more than half of those with epileptiform discharges and/or focal slowing. In patients with meningoencephalitis of undetermined etiology, a corresponding EEG demonstrating an anterior predominance of abnormalities should prompt testing for West Nile virus.
Neurophysiology