HP09: Cardiac reactivity to electric brain stimulations: A SEEG study

Abstract

Although it is now widely accepted that the brain contributes to the autonomic regulation, the cortical autonomic network is not clearly identified. Here, we provide a functional mapping of cardiac responses to brain stimulations. Methods: The cardiac effects of 1504 intracortical stimulations were divided into tachycardia, bradycardia, and no cardiac response according to the magnitude of RR interval reactivity in 44 patients with epilepsy (32.8±8.6 years, 19 women). Bipolar stimulations were performed with an intensity between 0.2–3.5 mA. Generalized Estimating Equation and odd ratio (OR) were used to explore the relationship between cardiac responses and brain regions, independently of sex, age and type, intensity, lateralization of stimulations and number of stimulations per patient. Results: Cardiac responses were induced by 320 stimulations (21.3%), including in 10.7% bradycardia (n=161) and in 10.6% tachycardia (n=159). Bradycardia was frequently and significantly evoked in posterior insula (OR=18.3), frontal motor (OR=7.5) and premotor (OR=8.3) cortex, temporal internal pole (OR=12.1), less frequently in amygdala (OR=5.2), parahippocampus (OR=5.2), anterior insula (OR=4.6), superior temporal cortex (OR=3.5), and hippocampus (OR=2.1). Tachycardia was frequently induced in posterior insula (OR= 26.8), anterior cingulate (OR= 19.5), parietal superior lobule (OR= 12.3), orbitofrontal cortex (OR= 9.0), and temporal internal pole (OR=8.3) and temporal fusiform inferior gyrus (OR=8.0); and less frequently in parahippocampus (OR=5.6), frontal motor cortex (OR=4.9), amygdala (OR=4.0), hippocampus (OR=2.4), anterior insula (OR=2.0), and temporal external pole (OR=2.0). Conclusions: These results illustrate i) brain networks underpinning tachycardia or bradycardia with ii) more extensive brain networks which may also contribute to cardiac autonomic control.