Exploring the link between essential tremor and Parkinson’s disease

Epidemiological studies have reported a link between essential tremor (ET) and Parkinson’s disease (PD). Recent studies have suggested ET as a possible neurodegenerative disease whose subgroup contained Lewy bodies in the brainstem, as in PD. PD with antedated ET (PD(conv)) might exhibit traits different from those of the pure form of ET or PD. This study aimed to unveil the interplay between PD and premorbid ET, which might be the core pathobiology that differentiates PD(conv) from PD. The study included 51 ET, 32 PD(conv), and 95 PD patients who underwent positron emission tomography using (18)F-N-(3-fluoropropyl)-2beta-carbon ethoxy-3beta-(4-iodophenyl) nortropane and (123)I-meta-iodobenzylguanidine myocardial scintigraphy to analyze central dopaminergic and peripheral noradrenergic integrity. The results show that PD(conv) group followed the typical striatal pathology of PD but with a delay in noradrenergic impairment as it caught up with the denervating status of PD a few years after PD diagnosis. Whereas the two PD subtypes displayed similar patterns of presynaptic dopamine transporter deficits, ET patients maintained high densities in all subregions except thalamus. Presynaptic dopaminergic availability decreased in a linear or quadratic fashion across the three groups (ET vs. PD(conv) vs. PD). The age at onset and duration of ET did not differ between pure ET and PD(conv) patients and did not influence the striatal monoamine status. The myocardium in PD(conv) patients was initially less denervated than in PD patients, but it degenerated more rapidly. These findings suggest that PD(conv) could be a distinctive subclass in which the pathobiology of PD interacts with that of ET in the early phase of the disease.