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International Journal of Clinical Research & Trials Volume 3 (2018), Article ID 3:IJCRT, 03 pages
https://doi.org/10.15344/2456-8007/2018/122
Research Article
Cerebral Vasoreactivity in Parkinson's Disease: A Pilot Study

Giuliano Sette1, Elisabetta Indelicato1,2, Alessandra Fanciulli2, Jacob Shofany3 and Francesco E. Pontieri1,3*

1Department of Neuroscience, Mental Health and Sensory Organs (NESMOS), “Sapienza” University of Rome, Italy
2Department of Neurology, Medical University of Innsbruck, Austria
3Department of Clinical and Behavioral Neurology, IRCCS “Santa Lucia Foundation”, Rome, Italy
Dr. Francesco E. Pontieri, Department of Clinical and Behavioral Neurology, IRCCS Santa Lucia Foundation, Rome, Italy; E-mail: fe.pontieri@gmail.com
14 November 2017; 11 January 2018; 13 January 2018
Sette G, Indelicato E, Fanciulli A, Shofany J, Pontieri FE, et al. (2018) Cerebral Vasoreactivity in Parkinson's Disease: A Pilot Study. Int J Clin Res Trials 3: 122. doi: https://doi.org/10.15344/2456-8007/2018/122

Abstract

Background: Cardiovascular autonomic failure is a frequent non-motor symptom of Parkinson’s disease (PD), its key feature being orthostatic hypotension (OH). Recent studies suggest that blood pressure deregulation in PD may be associated with increased cerebrovascular damage. Cerebral vasoreactivity (CVR) refers to the vasodilatory response of cerebral arterioles to elevation of pCO2. Reduced CVR is considered a risk factor for chronic cerebrovascular damage in the setting of hypertension or severe carotid artery stenosis. Here we evaluated CVR in PD patients with or without cardiovascular autonomic failure and age-matched healthy subjects.
Methods: Transcranial doppler ultrasound was applied to measure blood flow velocity in the middle cerebral arteries of 12 PD patients and 11 healthy subjects. CVR was quantified by means of the breath holding index (BHI). OH was identified during a standing test, and in this setting blood flow velocities were likewise recorded.
Results: PD patients displayed significantly lower BHI compared to controls, independently from the presence of OH. Patients with OH had lower mean arterial blood flow velocities compared to those without OH, both in supine and orthostatic position.
Conclusions: These preliminary results show interactions between cerebral hemodynamics and blood pressure disturbances in PD, that may contribute to chronic cerebrovascular ischemic damage in PD.