Autonome Modulation des Herzens bei prodromalem und manifestem idiopathischem Parkinson-Syndrom, Multisystematrophie und Progressiver Supranukleärer Blickparese

Autonomic disturbances as part of the spectrum of non-motor-symptoms are common in Parkinson’s disease. They are brought into focus as they can develop prior to the characteristic motor-symptoms to potentially predict the future development of Parkinson’s disease and support the accuracy of the diagnosis. They occur also in patients with REM sleep behaviour disorder (RBD), thereof more than 80% convert into an alpha-synucleinopathy (Schenck et al. 2013). Alpha-synucleinopathies include i.a. Parkinson’s disease (IPS) and multiple system atrophy (MSA). However progressive supranuclear palsy (PSP), an atypical parkinsonian syndrome just as MSA, is identified as tauopathy. The appearance and intensity of autonomic disturbances varies in different parkinsonian syndromes. While autonomic failure is not a characteristic feature of PSP, it is in MSA. Szintigraphic proof of myocardial postganglionic sympathetic denervation can be seen in early stage IPS (Postuma et al. 2015; Orimo et al. 1999), whereas preganglionic structures are affected in MSA (Orimo et al. 2001). Assessment of heart rate variability (HRV) is a non-invasive, cost-effective method to quantify autonomic modulation of heart frequency, and hence disturbances of cardiac innervation. The deceleration capacity (DC) is a relatively new parameter of high sensitivity referring to the vagal modulation of heart frequency (Bauer et al. 2006a). In this study we compared HRV in different parkinsonian syndromes to gain further insight of cardiac autonomic changes. Therefore patients with IPS (n=10), RBD (n=10), MSA (n=10) and PSP (n=9) and healthy controls (n=10) underwent 30 minutes of Holter monitoring at rest. Time-based (MHR, SDNN, RMSSD), geometrical (HRVI) and frequency based (LF, LFn, HF, HFn, LF/HF Ratio) parameters were evaluated as well as the DC through phase-rectified signal averaging. DC was significantly lower in patients with MSA and PSP compared to healthy controls. Significant reduction of the DC was also seen in patients with PSP compared to patients with IPS. HRVI was reduced in patients with PSP. There were no significantly different HRV data in patients with IPS and RBD compared to controls. Interpretations of HRV measurements are sometimes contradictory in literature and the corresponding pathophysiology is poorly understood. Our study shows limited capability of the modulation of heart frequency in patients with MSA compatible to their clinical characteristics. Our data as well show a strongly limited capacity to modulate heart frequency in patients with PSP indicating cardiovascular autonomic dysfunction. Therefore testing for cardiac autonomic disturbances should be part of clinical diagnostics in different parkinsonian syndromes.