Cerebrale Blutflussregulation bei orthostatischer Hypotension im Rahmen des Morbus Parkinson

As recent publications indicate, the orthostatic hypotension in patients with Parkinson's disease has a high prevalence of up to 50.3%. While this phenomenon in the past was attributed to a side effect of Parkinson's medication, studies now have shown that a disease-associated disruption of Baroreflexes and a loss of postganglionic sympathetic innervation are present. The literature reports a significant number of asymptomatic patients with orthostatic hypotension. However, little is known so far about the cerebral autonomous regulation. We have observed that Parkinson's patients, even with a drastic loss of blood pressure up to > 40 mm Hg only showed comparatively small changes of cerebral blood flow. With these patients, we looked closer at the cerebral autoregulation abilities. In this study, 33 patients with idiopathic Parkinson's syndrome were compared with 30 healthy control volunteers. These were examined with transcranial Doppler ultrasonography of the middle cerebral artery and posterior cerebral artery and non-invasive blood pressure measurement on the tilt table. The analysis focused on changes in cerebral blood flow velocity and systemic blood pressure depending on the position. Through spectral analysis of spontaneous oscillations in both signals, the dynamic autoregulation was investigated with the test persons both lying down and standing. The spontaneous oscillations were examined for Gain, the coefficient of variation, and the phase shift angles, from which you can draw conclusions on the compensation mechanisms. 18 of the 33 patients formally met the criteria for definition of a hypo-sympathetic orthostatic dysregulation. None of these patients suffered from a syncope. The blood pressure in the whole group was significantly lower than in the control group (syst 135.27 ± 22.65 mmHg vs. 145.21 ± 15.43 mmHg in the supine, p <0.05 / 121.81 ± 20.30 mmHg vs. 137.23 ± 16.41 mmHg in 3 minutes, p <0005), and by changing the position of the patient the flow velocity dropped significantly. (MCA: 53.13 ± 11.89 cm/s to 43.94 ± 11.08 cm/s, p <0.01 / PCA: 37.13 ± 9.10 cm/s to 31.58 ± 10, 63 cm/s, p <0.05) However, the threshold of 28% difference in the flow behavior during the tilt table examination was not exceeded. Therefore, the cerebrovascular compensation for all participants in the study was considered to be sufficient. With the dynamic testing of autoregulation modified compensation mechanisms appeared through increased dampening effects, which could adjust the high blood pressure instability. The Gain significantly decreased under orthostatism (M-Waves: MCA 2.66 ± 1.26 to 1.51 ± 0.45, p <0.0001 / PCA 3.83 ± 1.67 to 2.92 ± 1 58, p <0.05), the coefficient of variation in blood pressure increased significantly (M-Wave: MCA 1.07 ± 0.66% to 2.35 ± 1.76%, p <0.0005, PCA 1.13 ± 0.65% to 2.43 ± 2.02%, p = 0001) as a sign of increased orthostatic blood pressure instability. The fact that in contrast to this the coefficients of variation in the flow velocity were not significantly increased (M-Wave: MCA 2.38 ± 0.92% to 2.75 ± 1.02%, PCA 3.90 ± 1.46% to 4 , 34 ± 1.06%), could be interpreted as a result of greater damping of blood pressure in the transfer to the blood flow. Our results show that even in advanced stages of Parkinson's disease with and without orthostatic intolerance, a sufficient cerebral compensation exists. These results confirm the findings of other research groups, which also described a cerebral compensation of orthostatic hypotension in autonomous dysfunction, as for example in the context of diabetes mellitus. For the first time, we have selectively shown this for patients with idiopathic Parkinson's disease. However, a final explanation remains to be given. The compensation seems to be related to an increased damping of spontaneous blood pressure oscillations, mainly represented by the significant drop in Gain. Our results therefore are consistent with the recent studies indicating that the orthostatic hypotension is based on a purely peripheral lesion, but not a central autonomous abnormality. The question remains whether the cerebrovascular compensation mechanism applies only for a longer duration of Parkinson's disease. Through repeated measurements in the course of the disease, the cerebral autoregulation has to be systematically investigated. The main objective for this is to identify patients which could benefit from preventive measures, such as selective ß1 blockade to prevent blood pressure instabilities.

Grantor dc:publisher

Publikationsserver der RWTH Aachen University

Year dc:date

2008

Author dc:creator

• Pies, Katrin Barbara

Contributors dc:contributor

• Klötzsch, Christof

• info:eu-repo/classification/ddc/610
• Parkinson-Krankheit
• Hypotension
• Medizin
• Orthostase
• Cerebrale Autoregulation
• Parkinson s disease
• orthostatism
• cerebral autoregulation

Statement dc:rights

• info:eu-repo/semantics/openAccess

Language dc:language

ger

Identifier

https://publications.rwth-aachen.de/search?p=id:%22RWTH-CONV-112805%22

OAI record oai:identifier

https://publications.rwth-aachen.de/oai2d?verb=GetRecord&metadataPrefix=oai_dc&identifier=oai%3Apublications.rwth-aachen.de%3A50254