Stroke can lead to cardiac complications such as arrhythmia, myocardial injury, and cardiac dysfunction, collectively termed stroke-heart syndrome (SHS). These cardiac alterations typically peak within 72 h of stroke onset and can have long-term effects on cardiac function. Post-stroke cardiac complications seriously affect prognosis and are the second most frequent cause of death in patients with stroke. Although traditional vascular risk factors contribute to SHS, other potential mechanisms indirectly induced by stroke have also been recognized. Accumulating clinical and experimental evidence has emphasized the role of central autonomic network disorders and inflammation as key pathophysiological mechanisms of SHS. Therefore, an assessment of post-stroke cardiac dysautonomia is necessary. Currently, the development of treatment strategies for SHS is a vital but challenging task. Identifying potential key mediators and signaling pathways of SHS is essential for developing therapeutic targets. Therapies targeting pathophysiological mechanisms may be promising. Remote ischemic conditioning exerts protective effects through humoral, nerve, and immune-inflammatory regulatory mechanisms, potentially preventing the development of SHS. In the future, well-designed trials are required to verify its clinical efficacy. This comprehensive review provides valuable insights for future research.

Tachycardia-bradycardia syndrome (TBS) is a variant of sick sinus syndrome (SSS) characterized by alternating tachycardia and bradycardia. A few cases of SSS secondary to structural lesions in the medulla have been reported, but there has never been a reported case of the rare sign akin to TBS following acute non-medullary brainstem infarction. Furthermore, new-onset cardiac arrhythmias in stroke often presented in one continuous pattern - either as bradycardia or tachycardia, but instances of an alternating fashion have been rarely reported. We present the case of a 46-year-old female who developed severe dizziness with vomiting, diplopia, and slurred speech, which gradually worsened to quadriplegia, severe hypophonia, and dysphagia. Brain magnetic resonance imaging (MRI) demonstrated acute midbrain and pontine infarction. Except for neurological symptoms, the patient experienced unexpected TBS with the symptoms of excessive sweating, palpitations, and irritability without any other predisposing factors. The frequency of the episodes gradually declined until it spontaneously disappeared the 5th day after admission. Given the unpredictable nature of the tachycardia and bradycardia, it was challenging to manage the arrythmias with medications. A pacemaker was recommended, but financial reasons led the patient to reject this option. Two weeks after antithrombotic therapy and rehabilitation, she was discharged with residual symptoms of diplopia, moderate dysarthria, mild quadriplegia, and no cardiac symptoms. Our case highlighted the occurrence of TBS as a new-onset arrhythmia that can manifest during the acute phase of non-medullary brainstem infarcts. Further research into brainstem lesions contributing to TBS is warranted us to elucidate the underlying mechanisms.

The central autonomic network (CAN) plays a critical role in the body\'s sympathetic and parasympathetic control. However, functional connectivity (FC) changes of the CAN in patients with multiple system atrophy (MSA) remain unknown.
To investigate FC alterations of CAN in MSA patients.
Prospective.
Eighty-two subjects (47 patients with MSA [44.7% female, 60.5 ± 6.9 years], 35 age- and sex-matched healthy controls [HC] [57.1% female, 62.5 ± 6.6 years]).
3-T, resting-state functional magnetic resonance imaging (rs-fMRI) using gradient echo-planar imaging (EPI), T1-weighted three-dimensional magnetization-prepared rapid gradient echo (3D MPRAGE) structural MRI.
FC alterations were explored by using core modulatory regions of CAN as seeds, including midcingulate cortex, insula, amygdala, and ventromedial prefrontal cortex. Bartlett factor score (BFS) derived from a factor analysis of clinical assessments on disease severity was used as a grouping factor for moderate MSA (mMSA: BFS < 0) and severe MSA (sMSA: BFS > 0).
For FC analysis, the one-way ANCOVA with cluster-level family-wise error correction (statistical significance level of P < 0.025), and post hoc t-testing with Bonferroni correction or Tamhane\'s T2 correction (statistical significance level of adjusted-P < 0.05) were adopted. Correlation was assessed using Pearson correlation or Spearman correlation (statistical significance level of P < 0.05).
Compared with HC, patients with MSA exhibited significant FC aberrances between the CAN and brain areas of sensorimotor control, limbic network, putamen, and cerebellum. For MSA patients, most FC alterations of CAN, especially concerning FC between the right anterior insula and right primary sensorimotor cortices, were found to be significantly correlated with disease severity. FC changes were found to be more significant in sMSA group than in mMSA group when compared with HCs.
MSA shows widespread FC changes of CAN, suggesting that abnormal functional integration of CAN may be involved in disease pathogenesis of MSA.
2 TECHNICAL EFFICACY: Stage 3.

There is solid evidence for the prominent involvement of the central autonomic and default mode systems in shaping personality. However, whether functional connectivity of these systems can represent neural correlates and predictors of individual variation in personality traits is largely unknown. Resting-state functional magnetic resonance imaging data of 215 healthy young adults were used to construct the sympathetic (SN), parasympathetic (PN), and default mode (DMN) networks, with intra- and internetwork functional connectivity measured. Personality factors were assessed using the five-factor model. We examined the associations between personality factors and functional network connectivity, followed by performance of personality prediction based on functional connectivity using connectome-based predictive modeling (CPM), a recently developed machine learning approach. All personality factors (neuroticism, extraversion, conscientiousness, and agreeableness) other than openness were significantly correlated with intra- and internetwork functional connectivity of the SN, PN, and DMN. Moreover, the CPM models successfully predicted conscientiousness and agreeableness at the individual level using functional network connectivity. Our findings may expand existing knowledge regarding the neural substrates underlying personality.

Evidence suggests peripheral autonomic structures may contribute to autonomic dysfunction in idiopathic rapid eye movement sleep behaviour disorder (iRBD). However, whether the central autonomic network (CAN) is affected in iRBD remains unclear. Magnetic resonance imaging data were acquired from 65 participants (32 patients with iRBD and 33 matched healthy controls). We investigated the CAN in patients with iRBD using a combined voxel-based morphometry and resting-state functional connectivity analysis and characterised the relationships between alterations of the CAN and autonomic symptoms. Patients with iRBD had significantly reduced grey matter volume in the brainstem, anterior cingulate and insula compared with healthy controls. Functional connectivity analysis revealed reduced functional connectivity between the brainstem and the cerebellum posterior lobe, temporal lobe and anterior cingulate in patients with iRBD. In patients with iRBD, both reduced grey matter volume and decreased functional connectivity of the CAN were negatively correlated with the Scales for Outcomes in Parkinson\'s Disease-Autonomic scores. The present study demonstrated that both the structure and the functional connectivity of the CAN were abnormal in patients with iRBD. In addition, correlation analysis suggested that CAN abnormalities may also play a role in the development of autonomic symptoms in iRBD.

The neurovisceral integration model has shown a key role of the amygdala in neural circuits underlying heart rate variability (HRV) modulation, and suggested that reciprocal connections from amygdala to brain regions centered on the central autonomic network (CAN) are associated with HRV. To provide neuroanatomical evidence for these theoretical perspectives, the current study used covariance analysis of MRI-based gray matter volume (GMV) to map structural covariance network of the amygdala, and then determined whether the interregional structural correlations related to individual differences in HRV. The results showed that covariance patterns of the amygdala encompassed large portions of cortical (e.g., prefrontal, cingulate, and insula) and subcortical (e.g., striatum, hippocampus, and midbrain) regions, lending evidence from structural covariance analysis to the notion that the amygdala was a pivotal node in neural pathways for HRV modulation. Importantly, participants with higher resting HRV showed increased covariance of amygdala to dorsal medial prefrontal cortex and anterior cingulate cortex (dmPFC/dACC) extending into adjacent medial motor regions [i.e., pre-supplementary motor area (pre-SMA)/SMA], demonstrating structural covariance of the prefrontal-amygdala pathways implicated in HRV, and also implying that resting HRV may reflect the function of neural circuits underlying cognitive regulation of emotion as well as facilitation of adaptive behaviors to emotion. Our results, thus, provide anatomical substrates for the neurovisceral integration model that resting HRV may index an integrative neural network which effectively organizes emotional, cognitive, physiological and behavioral responses in the service of goal-directed behavior and adaptability.

Previous neuroimaging studies have highlighted the functional neural correlates of cardiac vagal activity, providing convergent evidence that the cardiac vagal function is controlled by a number of brain regions in the central autonomic network (CAN). However, it remains largely unknown whether the underlying anatomical basis of those identified regions are associated with individual difference in vagal function. To address the above issue, this study used a large sample of healthy subjects (n = 185) and voxel-based morphometry (VBM) analysis to verify brain morphometry associated with vagal control and the associations varied as a function of gender and age. Our results showed that high frequency component of heart rate variability (HF-HRV) was negatively correlated with grey matter volumes in the right putamen, caudate, amygdala, insula, superior temporal gyrus, temporal pole, and parahippocampal gyrus, demonstrating brain morphological variation in the right-sided striatal and limbic structures of the CAN associated with individual difference in cardiac vagal function. Additionally, gender and age effects on the relationship between cardiac vagal control and brain morphometry were not significant in the current dataset. These findings underscore the importance of striatal and limbic structures in parasympathetic control, and shed light on the underlying anatomical substrates of cardiac vagal activity.

OBJECTIVE: Symptomatic internal carotid artery occlusion (ICAO) is an important cause of cerebral ischemia with poor long-term outcome. Reductions in baroreflex function is reported in carotid atherosclerosis and implicated in increased risk of recurrent cardiovascular events. A distributed network of forebrain regions can exert modulatory influences over the cardio-vagal and baroreflex functions. The successful clinical translation of these approaches offers insights into underlying modulatory mechanisms and to possible therapeutic strategy.
METHODS: This study enrolled 20 symptomatic ICAO survivors, 20 patients with small vessel disease (SVD) as risk control, and 20 healthy controls. All underwent a standardized evaluation of cardiovascular autonomic function testing that included baroreflex sensitivity (BRS), Valsalva ratio (VR), and heart rate response to deep breathing (HR_DB). The regional cerebral blood flow (rCBF) of the central autonomic network (CAN) was obtained from arterial spin-labeling magnetic resonance imaging. Parameters of autonomic function between symptomatic ICAO survivors with and those without recurrent cardiovascular events were compared.
RESULTS: Valsalva ratio and HR_DB levels were significantly higher in the control group, followed by the SVD and ICAO groups (p=0.009 and p=0.007, respectively). Spontaneous BRS and BRS during the early phase II of Valsalva maneuver levels were both significantly higher in the control group, followed by the SVD and ICAO groups (p<0.001 and p=0.042, respectively). The rCBF of CAN inversely correlated with spontaneous BRS.
CONCLUSIONS: Autonomic dysregulation, including reduced BRS and impaired cardio-vagal function in the convalescent stage ICAO, can persist for a long time. Reduced BRS is inversely correlated with CAN activity.