Loss of Vestibular Ocular Reflex in Nonconvulsive Status Epilepticus.

Published

Journal Article

BACKGROUND: Electroencephalogram (EEG) findings of generalized periodic discharges (GPDs) with triphasic morphology were introduced as a metabolic phenomenon, but more recently have been associated with epileptic phenomenon. Resolution of EEG findings along with clinical improvement from treatment is diagnostic. The known causes of reversible, isolated loss of OVR include medication toxicity, lead exposure, and thiamine deficiency, but its association with nonconvulsive status epilepticus (NCSE) has never been published. Medication induced loss of OVR resolves after a 24-hour washout period. We report a case of reversible, isolated loss of vestibular ocular reflex (VOR) associated with epileptic phenomenon. METHODS: This is a case report of a single patient. RESULTS: A 74-year-old male with a history of complex partial seizures admitted for a pneumonectomy had a post-operative course complicated by two instances of coma, the latter associated with an isolated loss of VOR. EEG revealed GPDs with triphasic morphology initially interpreted as a metabolic phenomenon. The patient's mental status, exam and EEG findings improved after low dose infusion of propofol for tracheostomy, and he was eventually discharged at baseline neurological function. Due to this response, his coma, loss of VOR and EEG were later interpreted as a consequence of NCSE. CONCLUSION: The interpretation of GPDs with triphasic wave morphology range from metabolic phenomenon to NCSE. NCSE should be highly considered on the differential for encephalopathy regardless of the circumstances. NCSE may be a potential cause of reversible, isolated loss of the VOR and an AED trial in the appropriate clinical context should be considered. This is the first report of loss of VOR possibly associated with NCSE.

Full Text

Duke Authors

Cited Authors

  • Kang, JH; Husain, AM; Morgenlander, JC

Published Date

  • June 2019

Published In

Volume / Issue

  • 30 / 3

Start / End Page

  • 675 - 680

PubMed ID

  • 29951957

Pubmed Central ID

  • 29951957

Electronic International Standard Serial Number (EISSN)

  • 1556-0961

Digital Object Identifier (DOI)

  • 10.1007/s12028-018-0567-z

Language

  • eng

Conference Location

  • United States