Abstracts

Pontine Ischemic Infarct Mimicking Seizure with Non-reactive Beta Coma

Abstract number : 2.016
Submission category : 3. Neurophysiology / 3B. ICU EEG
Year : 2019
Submission ID : 2421467
Source : www.aesnet.org
Presentation date : 12/8/2019 4:04:48 PM
Published date : Nov 25, 2019, 12:14 PM

Authors :
Hyeyoung Seol, SUNY Downstate College of Medicine; Julien J. Cavanagh, SUNY Downstate College of Medicine; Katherine A. Mortati, SUNY Downstate College of Medicine; Susan W. Law, SUNY Downstate College of Medicine; Helen A. Valsamis, SUNY Downstate Colleg

Rationale: Beta coma is usually seen in sedative intoxication with substances such as barbiturates or benzodiazepines. Few case reports mention beta waves in comatose patients from anoxic brain injury or brainstem lesions. We present the case of a comatose patient with a pontine ischemic infarct whose EEG showed beta activity without reactivity. Methods: Case report and review of literature Results: A 67-year-old woman, with history of hypertension and hyperlipidemia, had a sudden episode of straightening of arms and trembling of hands at home. Upon arrival in the ER, the patient was unresponsive with right-gaze deviation. A 24-hour continuous EEG was obtained out of concern for seizure and nonconvulsive status epilepticus. The EEG showed generalized beta activity without reactivity even 72 hours after last benzodiazepine administration. MRI revealed a massive pontine ischemic infarct. The patient remains comatose. Conclusions: Various EEG patterns can be expected among comatose patients; some have a prognostic value. Alpha coma shows rhythmic alpha waves, most prominently in the frontal area, without reactivity. It can be seen in anoxic brain injury, toxic metabolic encephalopathy, or deefferented state (locked-in syndrome). Apart from intoxication with barbiturates or benzodiazepines, beta coma is not well understood. Compared to alpha invariability, beta unreactivity is very rarely associated with brainstem lesions or clinical prolonged coma. There have been only a few case reports of beta coma resulting from anoxic brain injury or brainstem lesions. This case was a rare presentation of brainstem ischemic stroke with decerebrating posturing on initial presentation. Because this mimicked seizure, we promptly obtained an EEG, which revealed beta waves. As brainstem lesions rarely present with seizure-like activity, it is not common to obtain EEG so early in the course of the disease. This could explain why it is not described in the literature. In our case, EEG showed a predominance of beta activity suggestive of an activated alert state, but there was no EEG reactivity (lack of changes of background upon stimulation). With a clinical exam compatible with coma, we made the diagnosis of beta coma. This case demonstrates the existence of beta coma in brainstem lesions and calls for larger electrophysiological studies among brainstem-injured patients. Funding: No funding
Neurophysiology