Abstract
Hilz MJ, Devinsky O, Doyle W, Mauerer A, Dutsch M.
Brain 2002;125(Pt 5):985–995
In temporal lobe epilepsy (TLE), there is evidence of ictal and interictal autonomic dysregulation, predominantly with sympathetic overactivity. The effects of TLE surgery on autonomic cardiovascular control and on baroreflex sensitivity (BRS) have not been studied. To evaluate such effects, we monitored heart rate (HR), systolic blood pressure [BP(sys)], and respiration in 18 TLE patients 3–4 months before and after TLE surgery. We used Blackman-Tukey spectral analysis to assess sympathetic and parasympathetic modulation as powers of HR and BP(sys) oscillations in the low-frequency (LF, 0.04–0.15 Hz) and high-frequency (HF, 0.15–0.5 Hz) bands. BRS was determined as the LF transfer function gain between BP and HR. After surgery, HR, BP(sys), respiration, and HF powers remained unchanged, whereas LF powers of HR [1.57 ± 1.54 beats/min(2)] and BP(sys) [2.19 ± 1.34 mm Hg(2)] and BRS (0.68 ± 0.31 beats/min/mm Hg) were smaller than presurgical LF powers of HR [3.87 ± 3.26 beats/min(2)] and BP(sys) [4.80 ± 3.84 mm Hg(2)] and BRS (1.12 ± 0.39 beasts/min/mm Hg; P < 0.05). After TLE surgery, there is a reduction of sympathetic cardiovascular modulation and BRS that might result from decreased influences of interictal epileptogenic discharges on brain areas involved in cardiovascular autonomic control. TLE surgery seems to stabilize the cardiovascular control in epilepsy patients by reducing the risk of sympathetically mediated tachyarrhythmias and excessive brady-cardiac counterregulation, both of which might be relevant for the pathophysiology of sudden unexpected death in epilepsy patients (SUDEP). Thus TLE surgery might contribute to reducing the risk of SUDEP.
Commentary
In this study, Hilz et al. demonstrate a reduction of sympathetic cardiovascular modulation and baroreflex sensitivity after anterotemporal lobectomies in 18 patients with pharma-coresistant temporal lobe epilepsy (TLE). Such changes in sympathetic autonomic function are thought to minimize the risk of sympathetic-mediated cardiac arrhythmias as well as extreme bradycardic counterregulations, two pathogenic mechanisms thought to be operant in SUDEP. Most of these cardiac arrhythmias have been directly attributed to ictal activity (more often during generalized tonic–clonic seizures). Hilz et al., however, citing data from experimental studies done in animals, also suggest a pathogenic role of interictal epileptic discharges through an enhancement of the sympathetic tone. Other authors have suggested that intense sympathetic stimulation after recurrent seizures can cause a nidus of myocardial irritability during periods of prolonged cardiac repolarization (evidenced by long QT intervals) (7). Such processes eventually result in “cardiac electrical instability” that can be reversed after surgical treatment. For example, in a study of 15 patients with refractory TLE who underwent an anterotemporal lobectomy, Frysinger et al. (8) found wider variations in heart rate (measured with spectral plots of the RR interval) among patients with persistent seizures after surgery than in seizure-free patients and controls. Eventually, pathologic evidence of these disturbances can be identified in the myocardium of victims of SUDEP. Falconer and Rajs (9) described minor areas of fibrosis and scarring in the myocardium of nine victims of “epilepsy deaths.” It is clear, therefore, that the impact of epilepsy surgery reaches beyond seizure remission. It reduces the risk of SUDEP in a patient population where its prevalence is not insignificant.