LAUSR

We read the interesting position paper by Doehner et al.,1 who reported the impact of central nervous system on control of cardiovascular system, and the relationship between central command in cerebral cortex and activation of autonomic centres located in the medulla. Recent studies have supported the notion that the cardiovascular system is regulated by a central autonomic network (CAN) consisting of insular cortex (Ic), anterior cingulate gyrus and amygdala.2 Because Ic is located in the region of the middle cerebral arteries, its structure tends to be exposed to a higher risk of cerebrovascular disease.3 In addition, Ic damage has been associated with myocardial injury, increased brain natriuretic peptide and incidence of Takotsubo cardiomyopathy.3 Several points should be taken into account when interpreting the scheme of cerebro–cardiac signalling after stroke reported by Doehner et al.1 First, in an earlier study,4 right hemispheric inactivation induced an increase of the high-frequency power of heart rate (HR) and blood pressure (BP), and left hemispheric inactivation induced an increase of the low-frequency power of HR and BP in patients with drug-refractory epilepsy. In addition, Oppenheimer et al.5 identified a site of cardiac representation within the Ic. While tachycardia or pressor effect was observed on the stimulation of the right Ic, bradycardia or depressor effect was significantly more common after stimulation of the left Ic.5 These results suggest that the right hemisphere including the right Ic is predominantly associated with sympathetic autonomic tone, whereas the left hemisphere including the left Ic is associated with parasympathetic autonomic tone. Doehner et al.1 had little descriptions about hemispheric lateralization for the relationship between Ic damage and autonomic deficits in heart failure. Second, the relationship between Ic damage and cardiovascular dysregulation is more complex in patients with stroke, because the stroke subtype such as ischaemia, intracerebral haemorrhage, and subarachnoid haemorrhage (SAH) would affect the impact of Ic damage on the CAN.2 Ic ischaemia might be associated with increased activities on the other Ic as well as increased activities on the subcortical autonomic core system. In contrast, SAH in the sylvian fissure possibly stimulates Ic mechanically and chemically, and induces disruption of CAN activation.2 Doehner et al.1 did not take into account for the relationship of stroke subtype in Ic with autonomic deficits in heart failure. Until now, there have been few reports assessing the central command in heart failure according to hemispheric laterality and stroke subtype of Ic. The data presented in the manuscript by Doehner et al.1 would make much more importance if the exact mechanism underlying that relationship were provided.