Objective Idiopathic Parkinson’s disease (IPD) is the second most common neurodegenerative disorder, often complicated by dementia. Cardiovascular risk factors and spontaneous cerebral emboli (SCE) are strongly associated with Alzheimer’s (AD) and vascular dementia (VaD). We measured SCE in the middle cerebral artery and arterial wall volume in the extracranial arteries in patients with IPD and controls, and explored the relationships with structural and physiological MRI brain neurovascular measures. Patients and Methods Arterial wall volume over 2cm of the axillary and internal carotid arteries (ICA) bilaterally was measured by 3-D tomographic ultrasound in 15 IPD patients and 16 age/gender matched controls. SCE were counted by Transcranial Doppler (TCD) using international consensus criteria. Venous to arterial circulation shunting (v-aCS), usually through a patent foramen ovale (PFO), was measured using a TCD technique with intravenous microbubble contrast. Structural and physiological MRI brain neurovascular measures, acquired separately, comprised white matter lesion volume (WMLV), cerebral blood flow (CBF) and arterial arrival time (AAT). Results Mean (95% CI) axillary and ICA wall volume was higher in IPD patients at 523 mm3 (446, 600) and 455 mm3 (374, 536) respectively compared with 412 mm3 (342, 483) and 408 mm3 (362, 454) in controls being significant for the axillary artery (p = 0.04). Cerebral WMLV was related to mean arterial wall volume for both axillary (r = 0.555, p = 0.009) and ICA (r = 0.559, p = 0.026) in all participants. SCE were detected in four IPD patients and three controls (p = 1.00). Two IPD patients and three controls were positive for a v-aCS equivalent to PFO (p = 0.477). Conclusion Although frequent in AD and VaD, neither SCE nor v-aCS were associated with IPD. This is the first study to demonstrate arterial wall volume is increased in IPD and relates to WMLV.
This is the author’s version of a work that was accepted for publication in Clinical Neurophysiology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Clinical Neurophysiology, 167, 2018 DOI: 10.1016/j.clineuro.208.02.013