disease (PD): its prevalence ranges between 14% and 80% [12]. It is related to older age, severity and duration of the disease [13,14] and can be caused by autonomic dysfunction, drugs, or both causes. Few studies have evaluated the specific mechanisms of orthostatic hypotension in patients with PD. Lowering of blood pressure may be mainly due to drugs (in particular levodopa), when autonomic cardiovascular function tests are normal [15]. On the other hand, the absence of activation of compensatory chronotropic mechanisms to low blood pressure while standing may be due to autonomic failure [16]. Dopaminergic agonists (levodopa, carbidopa) frequently cause orthostatic hypotension, even at the beginning of therapy, through the activation of dopamine receptors, determining cutaneous, mesenteric and renal vasodilation, but also through other mechanisms, such as a reduced central sympathetic tone, which causes a small reduction in heart rate, and an impaired release of renin and aldosterone [17,18]. However, among antiparkinsonian drugs, selegiline seems to be more frequently involved in the onset of orthostatic hypotension, even after long-term therapy, if compared to levodopa [16,19]. Furthermore, while combined treatment with both drugs can determine severe orthostatic hypotension [20,21], levodopa alone is less often responsible for this phenomen. In fact, in additon to the peripheral vasodilatation due to dopamine agonists, the decreased reuptake of dopamine and norepinephrine in central neurvous system caused by selegiline causes a reduction in sympathetic tone [22]. Ha et al. [13] did not find a significant difference in dopaminergic agonist doses between PD patients with and without symptoms related to orthostatic hypotension, suggesting that other factors, such as age and other concomitant therapies, may be responsible for orthostatic hypotension in PD [13]. These data were further confirmed by Perez-Lloret et al.