Blood Pressure in Seizures and Epilepsy

Abstract

In this narrative review, we summarize the current knowledge of neurally mediated blood pressure (BP) control and discuss how recently described epilepsy- and seizure-related BP alterations may contribute to premature mortality and sudden unexpected death in epilepsy (SUDEP). Although people with epilepsy display disturbed interictal autonomic function with a shift toward predominant sympathetic activity, prevalence of arterial hypertension is similar in people with and without epilepsy. BP is transiently increased in association with most types of epileptic seizures but may also decrease in some, illustrating that seizure activity can cause both a decrease and increase of BP, probably because of stimulation or inhibition of distinct central autonomic function by epileptic activity that propagates into different neuronal networks of the central autonomic nervous system. The principal regulatory neural loop for short-term BP control is termed baroreflex, mainly involving peripheral sensors and brain stem nuclei. The baroreflex sensitivity (BRS, expressed as change of interbeat interval per change in BP) is intact after focal seizures, whereas BRS is markedly impaired in the early postictal period following generalized convulsive seizures (GCS), possibly due to metabolically mediated muscular hyperemia in skeletal muscles, a massive release of catecholamines and compromised brain stem function. Whilst most SUDEP cases are probably caused by a cardiorespiratory failure during the early postictal period following GCS, a profoundly disturbed BRS may allow a life-threatening drop of systemic BP in the aftermath of GCS, as recently reported in a patient as a plausible cause of SUDEP in a few patients.

Keywords: SUDEP; autonomic nervous system; epilepsy; hypertension; hypotension; seizure.

Figure 1

Simplified scheme of central autonomic control of BP homeostasis. Visceral afferents from baro-, volume-, and chemoreceptors reach the NTS, which works as a comparator of information from peripheral visceroaffents and information on behavioral tasks and emotional states signaled by the central autonomic network. These are mediated by indirect and direct connections to the hypothalamus, thalamus, insular cortex, amygdala, cingulate gyrus, and other mPFC areas. These allow adaptations of the neural BP setpoint to given behavioral and emotional states. The NTS asserts control over the NA and DVN, from where parasympathetic efferents mediate a reduction of HR and SV. The NTS regulates sympathetic efferents that originate in the intermediolateral column of the spinal cord by adjusting the caudal and rostral ventrolateral medulla nuclei. The sympathetic system increases total peripheral resistance, HR, and SV. For the sake of clarity, the diagram only shows the indirect “hierarchical” pathways, even though multiple direct pathways from telencephalic and diencephalic visceral control areas to parasympathetic and sympathetic nuclear areas that bypass diencephalic relay centers and the NTS itself exist as well. Arrows indicate predominantly excitatory pathway, dots predominantly inhibitory connections. The figure is adapted from Myers (15), Zanutto et al. (16), and Gianaros and Sheu (19).

Figure 2

BP in FS and FBTCS. Summary graphs of seizure-related SAP (in red) and DAP (in blue) at different time points in 35 FS of 28 patients (A). Summary graphs of seizure-related SAP (in red) and DAP (in blue) at different time points in 10 FBTCS of 9 patients (B). The x-axis represents different peri-ictal time points (e.g., −2 equals two min prior to the seizure-onset, 0 indicates the time of the seizure). The point charts represent mean ± SD. Examples of time-course of SAP and HR during FS in a patient with concomitant increase of SAP and HR (C) and a decrease of SAP and increase of HR in another patient (D). The gray boxes indicate the duration of individual seizures in each figure. Data were previously published in Hampel et al. (70).