The heart side of brain neuromodulation

Abstract

Neuromodulation refers to invasive, minimally invasive or non-invasive techniques to stimulate discrete cortical or subcortical brain regions with therapeutic purposes in otherwise intractable patients: for example, thousands of advanced Parkinsonian patients, as well as patients with tremor or dystonia, benefited by deep brain stimulation (DBS) procedures (neural targets: basal ganglia nuclei). A new era for DBS is currently opening for patients with drug-resistant depression, obsessive-compulsive disorders, severe epilepsy, migraine and chronic pain (neural targets: basal ganglia and other subcortical nuclei or associative fibres). Vagal nerve stimulation (VNS) has shown clinical benefits in patients with pharmacoresistant epilepsy and depression. Non-invasive brain stimulation neuromodulatory techniques such as repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) are also being increasingly investigated for their therapeutic potential in several neurological and psychiatric disorders. In this review, we first address the most common neural targets of each of the mentioned brain stimulation techniques, and the known mechanisms of their neuromodulatory action on stimulated brain networks. Then, we discuss how DBS, VNS, rTMS and tDCS could impact on the function of brainstem centres controlling vital functions, critically reviewing their acute and long-term effects on brain sympathetic outflow controlling heart function and blood pressure. Finally, as there is clear experimental evidence in animals that brain stimulation can affect autonomic and heart functions, we will try to give a critical perspective on how it may enhance our understanding of the cortical/subcortical mechanisms of autonomic cardiovascular regulation, and also if it might find a place among therapeutic opportunities in patients with otherwise intractable autonomic dysfunctions.

Cardiac autonomic dynamics during sleep are lost in patients with TIA and stroke

“…In physiological conditions, cardiac autonomic control fluctuates during sleep stages, with a predominant vagal modulation during NREM sleep and a sympathetic overactivity during REM (Benarroch, ; Busek et al., ; Ferri et al., ; Rossi et al., ; Tobaldini, Nobili et al., ; de Zambotti et al., ). However, data on autonomic control during sleep after acute ischaemic stroke are lacking.…”

“…Central control of the autonomic nervous system implicates a widespread cortical and subcortical network, including the bilateral insular cortex, anterior cingulate gyrus, amygdala and hypothalamus (Beissner, Meissner, Bär, & Napadow, ; Benarroch, ; Hilz et al., ; Ozdemir & Hachinski, ; Rossi, Santarnecchi, Valenza, Ulivelli, & Rossi, ; Verberne & Owens, ; de Zambotti, Trinder, Silvani, Colrain, & Baker, ). The insula has a prominent role and stroke affecting the insula (especially on the right side) is associated with elevated cardiac troponin, electrocardiogram (ECG) changes (altered repolarization phase and prolonged QTc) and cardiac arrhythmias (Abboud, Berroir, Labreuche, Orjuela, & Amarenco, ; Christensen, ; Colivicchi, Bassi, Santini, & Caltagirone, ; De Raedt et al., ).…”

Low intensity transcranial electric stimulation: Safety, ethical, legal regulatory and application guidelines

“…Since tDCS may affect sympathetic tone (Rossi et al, 2016) and cardiovascular stability is crucial, particularly in the acute post-stroke period (Al-Qudah et al, 2015; Beeli et al, 2008; Makovac et al, 2016; Santarnecchi et al, 2014; Vandermeeren et al, 2010; Vernieri et al, 2010) there might be a theoretical risk of arrhythmias or hypertensive crisis in stroke patients. However, prolonged monitoring during and after tDCS in healthy subjects failed to show an influence on vital functions.…”

The Reason Why rTMS and tDCS Are Efficient in Treatments of Depression

“…It should be noted that antidepressant application of both rTMS and tDCS is based on previous findings that these two methods help in the case of hypoactivity of the left dorsolateral prefrontal cortex (DLPFC) (Grimm et al, 2006). Those structural and functional differences probably introduce abnormal physiological complexity demonstrated in electroencephalographic (EEG) (Ahmadlou et al, 2012;Bachmann et al, 2013;Hosseinifard et al, 2014;De la Torre-Luque and Bornas, 2017;Jaworska et al, 2018;Lebiecka et al, 2018) as well as in electrocardiographic (ECG) signals in depression (Migliorinni et al, 2012;Rossi et al, 2016;Iseger et al, 2019).…”