Interictal cardiac autonomic dysfunction in temporal lobe epilepsy demonstrated by [123I]metaiodobenzylguanidine-SPECT

Abstract

We studied the post-ganglionic cardiac sympathetic innervation in patients with chronic temporal lobe epilepsy (TLE) by means of [(123)I]metaiodobenzylguanidine-single photon computed tomography (MIBG-SPECT) and evaluated the effects of carbamazepine on cardiac sympathetic innervation. TLE is frequently associated with dysfunction of the autonomic nervous system. Autonomic dysregulation might contribute to unexplained sudden death in epilepsy. Anticonvulsive medication, particularly with carbamazepine, might also influence autonomic cardiovascular modulation. MIBG-SPECT allows the quantification of post-ganglionic cardiac sympathetic innervation, whereas measuring the variability of the heart rate provides only functional parameters of autonomic modulation. Antiepileptic drugs, especially carbamazepine (CBZ), can affect cardiovascular modulation. We determined the index of cardiac MIBG uptake (heart/mediastinum ratio) and heart rate variability (HRV) using time and frequency domain parameters of sympathetic and parasympathetic modulation in 12 women and 10 men (median age 34.5 years) with a history of TLE for 7-41 years (median 20 years). Myocardial perfusion scintigrams were examined to rule out deficiencies of MIBG uptake due to myocardial ischaemia. To assess the possible effects of CBZ on autonomic function, we compared MIBG uptake and HRV in 11 patients who had taken CBZ and 11 patients who had not taken CBZ, and in 16 healthy controls. In order to identify MIBG uptake defects due to myocardial ischaemia, all patients had a perfusion scintigram. Cardiac MIBG uptake was significantly less in the TLE patients (1.75) than in the controls (2.14; P = 0.001), but did not differ between subgroups with and without CBZ treatment. The perfusion scintigram was normal in all patients. Time domain analysis of HRV parameters suggested the predominance of parasympathetic cardiac activity in the TLE patients, but less parasympathetic modulation in the patients treated with CBZ than in those not treated with CBZ (P < 0.05), whereas frequency domain parameters showed no significant difference between the subgroups of patients or between patients and controls. MIBG-SPECT demonstrates altered post-ganglionic cardiac sympathetic innervation. This dysfunction might carry an increased risk of cardiac abnormalities.

Uncommon Clinical Manifestations of Cysticercosis

“…However, the cardiac signs found in our series such as: asystole and bradycardia may also be suggestive of cardiac dysfunction secondary to left insula as has previously been reported in patients with temporal lobe epilepsy [195][196][197][198] and confirmed in 2009 by Koseoglu et al [199] The epileptic activity spreads through the limbic system with the involvement of the amygdala, hypothalamus, and thalamus. These, in turn stimulate the autonomic system at medullar level including the nucleus tractus solitarius and the nucleus ambiguous which generate sympathetic and parasympathetic discharges.…”

Cardiac Asystole in Epilepsy: Clinical and Neurophysiologic Features

“…In a similar manner, other authors reported how ventricular asystole can occur because of vagal activation in the operating room (18). Recently, altered postganglionic cardiac sympathetic innervation with a predominant parasympathetic cardiac activity was demonstrated in patients with TLE by using MIBG-SPECT and domain analysis of heart-rate variability (19,20). Nevertheless, the question whether the underlying mechanism of ictal cardiac arrest is a direct vagally mediated activation of the cardiac conduction system occurring during the seizure, or an uncoordinated autonomic releasing effect (21), remains to be resolved.…”

Current View of Autonomic Findings During Epileptic Seizures

“…The emergence of ictal activity in these structures or spread to these structures can lead to sympathetic and parasympathetic changes that affect the heart rate in patients with epilepsy (7). It was shown that metaiodobenzylguanidine (MIBG) uptake is reduced at myocardial sympathetic nerve terminals in patients with chronic TLE and this reduction has been suggested to be an indicator for reduced post-ganglionic sympathetic innervation (21). Decreased innervation may lead to hypersensitivity of cardiac beta-adrenergic receptors.…”