S82. Paroxysmal sympathetic hyperactivity evident as cyclical pattern on quantitative EEG analysis

Abstract

Introduction Episodic fluctuations in sympathetic activity following traumatic brain injury (TBI) have been described for decades, with paroxysmal sympathetic hyperactivity (PSH) being the currently accepted term for this entity. While early reports postulated an epileptic mechanism, our understanding of the pathophysiology of PSH has evolved. Current hypotheses center around deregulation of central descending inhibitory inputs from the insula and cingulate cortex, resulting in increased sympathetic output from the hypothalamus, diencephalon and brainstem. We present a case of PSH with evidence of disrupted sympathetic arousal networks. Methods A 41-year-old woman suffered a TBI with multifocal supratentorial hemorrhages and intraparenchymal contusions. Eight days post-MVA she developed episodes of tachycardia, hypertension, diaphoresis, back-arching and extensor posturing of the upper extremities upon stimulus. These events were assumed to be epileptic and treated with lorazepam (up to 16 mg/24 h) and phenobarbital (up to 345 mg/24 h) to no avail. Episodes improved with dexmedetomidine and clonidine. Continuous video-EEG was ordered for event characterization. Results EEG background was characterized by reactive generalized theta activity without interictal discharges. Multiple stimulus-induced stereotypical events were captured on the first EEG, prior to initiation of anti-epileptic drugs and dexmedetomidine. These were time-locked with static generalized rhythmic delta activity, often sharply contoured (GRDA + S). Quantitative EEG cycled between GRDA+S and polymorphic theta; transitions were often associated with stimulation or arousal. Thus, the events were shown to be stimulus/arousal-induced PSH time-locked with GRDA+S. The second EEG on lorazepam (2 mg q6h) and dexmedetomidine (26 mcg/kg/h) demonstrated less GRDA and no PSH. The third EEG on phenobarbital (130 mg qhs) and less dexmedetomidine (1.5 mcg/kg/h) demonstrated polymorphic delta slowing during episodes of PSH. Therefore, PSH was seen prior to initiation of dexmedetomidine and while on a low dose, but not while on a higher dose. Phenobarbital did not improve PSH. Conclusion Episodes of PSH were non-epileptic and concordant with cyclical stimulus or arousal-induced GRDA. This pattern is thought to represent cortical-subcortical dysfunction rather than hyperexcitability, as shown in a recent retrospective analysis of critical care continuous EEG in which no association was found between GRDA and seizures. The cyclical pattern on scalp and quantitative EEG reflected increased generalized rhythmicity with arousal and episodes of PSH; akin to stimulus/arousal-induced rhythmic or periodic or ictal discharges (SIRPIDs) seen in critically ill patients. The pattern seen on the cEEG reflects network disruption during PSH rather than a hyperirritable cortex; we believe that treatment of PSH should target sympathetic arousal networks rather than cortical hyperexcitability.