1. In this case series of 12 patients with intractable epilepsy, deep brain electrical stimulation of Brodmann area 25 resulted in significant and consistent decreases in systolic blood pressure as compared to no blood pressure changes when stimulating any other structure.
2. During Brodmann area 25 stimulation, diastolic arterial blood pressure was maintained thus indicating that the systolic reduction was likely due to decreased sympathetic drive resulting in decreased cardiac output as opposed to bradycardia or peripheral vasodilation-induced hypotension.
Evidence Rating Level: 3 (Average)
Study Rundown: Sudden unexpected death in epilepsy (SUDEP) is thought to be due to peri-ictal autonomic dysregulation that causes hypotension. Cortical blood pressure control sites that are inhibited during seizures may cause the hypotension. This case series aimed to identify cortical structures in the human brain that are associated with blood pressure control.
Electrical stimulation of Brodmann area 25, the rostral subcallosal neocortex, of the human brain was associated with significant and consistent decreases in systolic blood pressure in patients with intractable epilepsy. Maintenance of normal diastolic arterial pressure suggests that this reduction is due to reduced sympathetic drive as opposed to increased bradycardia or peripheral vasodilation. Deep brain electrical stimulation (DBES) of other identified structures did not induce systolic hypotension. Strengths of this study include direct stimulation and monitoring of blood pressure in cases, however without further study during SUDEP and this study’s small sample size, it is unclear if this may be the sole causative factor.
In-Depth [case series]: This case series took place in the Epilepsy Monitoring Unit at the University Hospitals Cleveland Medical Centre from June 2015 to February 2017. Inclusion criteria were patients older than 18 with intractable epilepsy and intracranial electrodes implanted in one or more regions of interest (orbitofrontal, cingulate, subcallosal, insular, hippocampal, amygdala, temporal, motor, anterior cingulate cortices) and in whom DBES was indicated. The outcome of interest was continuous beat-by-beat blood pressure monitoring, with associated ECG, arterial oxygen saturation, ETCO2, nasal airflow and thoracoabdominal plethysmography monitoring. Stimulation occurred with the above monitoring at the bedside and went from an intensity of 1mA to a maximum of 10 mA. Stimulation was discontinued if seizure was induced. Invasive monitoring was used for blood pressure and the above. Paired-samples t test was used to compare stimulation blood pressure averages with baseline values. Strength of linear association was assessed by Pearson product moment correlation coefficient.
Twelve patients were included in this study, 7 of which were women; the mean (SD) age was 44.25 (12.55) years. 544 electrodes were in each of the areas of interest: 43 amygdala, 87 hippocampal, 16 insular, 31 orbitofrontal, 31 temporopolar, 296 lateral temporal, 4 basal temporal, 13 anterior cingulate, 2 posterior cingulate and 9 subcallosal neocortex (Brodmann area 25). All electrodes stimulated in Brodmann area 25 (of 4 patients) resulted in rapid and consistently reproducible decreases in systolic blood pressure of mean (SEM) drop of 15 (10-42) mm Hg. These decreases occurred within a mean (SEM) of 8.5 (1-14) seconds and began to increase in a mean (SEM) of 12 (1-47) seconds after stimulation was discontinued. No significant drops in diastolic pressure were observed. No significant drops in any blood pressure were observed during DBES of any other areas of interest.
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