Tonic Eye-Opening Associated with the «Burst-Suppression» Pattern in Patients with Acute Anoxic Brain Injury (Case Series)

Abstract

Massive anoxic brain injury caused by cardiac arrest leads to wakefulness suppression up to coma. The prediction of outcome is based on the analysis of the clinical features and the results of instrumental tests. One of the well-known signs of an unfavorable prognosis is involuntary motor activity, which is most commonly represented by myoclonus. In case of their cortical origin, they are accompanied by epileptiform activity in the electroencephalogram (EEG).Material and methods. We present a case series and literature review concerning a very rare fatal sign, non-rhythmic spontaneous eye opening accompanied by a «burst-suppression» pattern (BS) in the EEG. All patients suffered from transient acute hypotension or arrhythmia that required cardiopulmonary resuscitation (CPR) in three cases. A literature search found only 11 publications describing post-anoxic tonic eye-opening (PATEO).Results. The PATEO with BS was observed for less than a day followed by cessation of brain bioelectric activity in all patients. Only two patients exhibited isolated eye-opening and closing, while the rest had axial and limbs myoclonus just after CPR. In one case, eyelid opening was followed by a clonic movement of the head to the right, the EEG bursts were prolonged and had spike-like morphology. Three patients received antiepileptic and sedative therapy. All patients died in 3-43 days after the fatal cardiovascular event.Visual superposition of bursts in EEG and myogram of m. orbicularis oculi demonstrating identical morphology for EEG and myographic bursts was described for the first time. Our cases and literature review confirm that, regardless of the intensive treatment, patients with PATEO have fatal outcomes.Conclusion. The clinical and electrographic PATEO with BS phenomenon always indicates a lethal prognosis. The origin of PATEO is still under discussion. We suggest that it could be caused by disinhibition of subcortical and stem structures during extensive death of cerebral cortical neurons.