By Barbara Casolla, MD, PhD,
Degenerative and Vascular Cognitive Disorders, CHU Lille, Department of Neurology, France
The World Brain Day, an initiative of the World Federation of Neurology, is bringing global attention to Parkinson’s disease (PD). In 1999, Winikates and Jankovic first proposed clinical criteria for the diagnosis of vascular parkinsonism (VP) but, since then, this term has remained controversial (1).
Signs and symptoms of PD may be induced by strategic infarcts in the basal ganglia, that increase the basal ganglia motor output or decrease the thalamo-cortical drive, and by diffuse white matter lesions, caused by small vessel disease, that result in a cortical-subcortical disconnection. Clinicopathological diagnostic criteria were published in 2004, and recently updated (2, 3).
Observational and population-based studies reported that VP accounts for about 2.5–5% of parkinsonisms (4). In clinical practice the accurate diagnosis could be difficult because of phenotypic variability and remarkable overlap. The main clinical characteristics distinguishing VP from PD are the age at symptom onset (patients with VP are, on average, 4–10 years older than patients with PD), predominant lower limb parkinsonism, symmetrical gait difficulties, postural instability, falls, dementia, executive dysfunction, pyramidal signs, pseudobulbar palsy and urinary incontinence (5, 6). Importantly, patients with VP have fewer motor fluctuations or dyskinesias typically seen in PD. From a neuroimaging point of view, most of the patients with VP had lacunar strokes and extensive white matter disease, whereas PD patients have mild atrophy or non-specific periventricular white matter changes (6). Orienting clinicians for making the differential diagnosis is important for therapeutic and prognostic implications: VP is unresponsive to Levodopa, and is characterized by rapid progression, higher incidence of dementia, and worse prognosis. Alzheimer disease (AD), another neurodegenerative condition and the most common cause of dementia, 2 shares risk factors and neuropathological features with cerebrovas-cular disease.
Furthermore, emerging evidence suggests that cerebrovascular risk factors and cerebrovascular dysfunction are associated with PD, raising the question of other neuropathological degenerative pathway triggered by vascular pathology (7-10). Because many cerebrovascular risk factors are modifiable, and PD is responsible of a major public health burden, unraveling the pathobiological mechanisms of these connections represents a considerable challenge for future research.
Acknowledgments: Pr Caroline Moreau, Lille University Hospital, France
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