Abstract
Cardiovascular autonomic dysfunction is common in multiple sclerosis (MS) and contributes significantly to disability. We hypothesized that cerebral MS‐lesions in specific areas of the central autonomic network might account for imbalance of the sympathetic and parasympathetic cardiovascular modulation. Therefore, we used voxel‐based lesion symptom mapping (VLSM) to determine associations between cardiovascular autonomic dysfunction and cerebral MS‐related lesion sites. In 74 MS‐patients (mean age 37.0 ± 10.5 years), we recorded electrocardiographic RR‐intervals and systolic and diastolic blood pressure. Using trigonometric regressive spectral analysis, we assessed low (0.04–0.15 Hz) and high (0.15–0.5 Hz) frequency RR‐interval‐and blood pressure‐oscillations and determined parasympathetically mediated RR‐interval–high‐frequency modulation, mainly sympathetically mediated RR‐interval–low‐frequency modulation, sympathetically mediated blood pressure‐low‐frequency modulation, and the ratios of sympathetic and parasympathetic RR‐interval‐modulation as an index of sympathetic‐parasympathetic balance. Cerebral MS‐lesions were analyzed on imaging scans. We performed a VLSM‐analysis correlating parameters of autonomic dysfunction with cerebral MS‐lesion sites. The VLSM‐analysis showed associations between increased RR‐interval low‐frequency/high‐frequency ratios and lesions most prominently in the left insular, hippocampal, and right frontal inferior opercular region, and a smaller lesion cluster in the right middle cerebellar peduncle. Increased blood pressure‐low‐frequency powers were associated with lesions primarily in the right posterior parietal white matter and again left insular region. Our data indicate associations between a shift of cardiovascular sympathetic‐parasympathetic balance toward increased sympathetic modulation and left insular and hippocampal lesions, areas of the central autonomic network. The VLSM‐analysis further distinguished between right inferior fronto‐opercular lesions disinhibiting cardiac sympathetic activation and right posterior parietal lesions increasing sympathetic blood pressure modulation.
Highlights
Region of interest-based studies (Acevedo, Nava, Arriada, Violante, & Corona, 2000; Saari et al, 2004; Vita et al, 1993) associated cardiovascular autonomic dysregulation in Multiple sclerosis (MS)-patients either with their total lesion load and lesions in the midbrain and parietal white matter (Saari et al, 2004) or with pontine lesions (Acevedo et al, 2000; Vita et al, 1993), we hypothesize that neuroinflammatory lesions close to or within specific supratentorial master controllers of the autonomic nervous system account for an imbalance of the sympathetic and parasympathetic cardiovascular modulation
To identify neuro-inflammatory lesion sites associated with cardiovascular autonomic dysregulation, we assessed the lesion load throughout the whole brain using magnetic resonance imaging (MRI) and applied voxel-based lesion symptom mapping (VLSM) to correlate the location of lesions with changes in the sympathetic and parasympathetic balance of cardiovascular modulation in MS-patients (Bates et al, 2003; Rorden, Karnath, & Bonilha, 2007; Winder et al, 2015, 2016)
Among outpatients seen between November 2012 and October 2014 at the Multiple Sclerosis Clinic at the University Hospital Erlangen of the Friedrich-Alexander Universität ErlangenNürnberg, we screened 90 patients (62 females; mean age 37.2 ± 10.3 years) who had been diagnosed with relapsing remitting MS according to the 2010 revised McDonald criteria (Polman et al, 2011)
Summary
Multiple sclerosis (MS) is frequently associated with autonomic dysfunction which afflicts up to 84% of MS-patients and may comprise cardiovascular dysregulation, bowel, bladder, and sexual dysfunction, or sudomotor abnormalities (Hilz, 2016; Kaplan, Berkowitz, & Samuels, 2015; Merkelbach et al, 2006; Racosta, Kimpinski, Morrow, & Kremenchutzky, 2015; Winder et al, 2016). MS-associated lesions in the periventricular white matter, juxtacortical U-fibers, the brainstem, the cerebellum or spinal cord areas (Ge, 2006; Vigeveno, Wiebenga, Wattjes, Geurts, & Barkhof, 2012; Winder et al, 2016) might compromise the centrally mediated sympathetic and parasympathetic cardiovascular modulation (Hilz, 2016; Racosta et al, 2015). Region of interest-based studies (Acevedo, Nava, Arriada, Violante, & Corona, 2000; Saari et al, 2004; Vita et al, 1993) associated cardiovascular autonomic dysregulation in MS-patients either with their total lesion load and lesions in the midbrain and parietal white matter (Saari et al, 2004) or with pontine lesions (Acevedo et al, 2000; Vita et al, 1993), we hypothesize that neuroinflammatory lesions close to or within specific supratentorial master controllers of the autonomic nervous system account for an imbalance of the sympathetic and parasympathetic cardiovascular modulation. To identify neuro-inflammatory lesion sites associated with cardiovascular autonomic dysregulation, we assessed the lesion load throughout the whole brain using magnetic resonance imaging (MRI) and applied voxel-based lesion symptom mapping (VLSM) to correlate the location of lesions with changes in the sympathetic and parasympathetic balance of cardiovascular modulation in MS-patients (Bates et al, 2003; Rorden, Karnath, & Bonilha, 2007; Winder et al, 2015, 2016)
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