Right posterior hypometabolism in Pisa syndrome of Parkinson's disease: A key to explain body schema perception deficit?

Abstract

Background: Pisa syndrome (PS) is a trunk postural abnormality in Parkinson's disease (PD). Its pathophysiology is still debated: peripheral and central mechanisms have been hypothesized.

Objective: To investigate the role of nigrostriatal dopaminergic deafferentation and of brain metabolism impairment in the onset PS in PD patients.

Methods: We retrospectively selected 34 PD patients who developed PS (PS+) and who had previously undergone dopamine transporter (DaT)-SPECT and/or brain F-18 fluorodeoxyglucose PET (FDG-PET). PS + patients were divided considering leaning body side in left ((l)PS+) or right ((r)PS+). DaT-SPECT specific-to-non-displaceable binding ratio (SBR) of striatal regions (BasGan V2 software) were compared between 30 PS+ and 60 PD patients without PS (PS-) as well as between 16 (l)PS+ and 14 (r)PS + patients. Voxel-based analysis (SPM12) was used to compare FDG-PET among 22 PS+, 22 PS- and 42 healthy controls (HC) and between 9 (r)PS+ and 13 (l)PS+.

Results: No significant DaT-SPECT SBR differences were found between PS+ and PS- groups or between (r)PD+ and (l)PS + subgroups. Compared to HC, significant hypometabolism in PS+ was found in bilateral temporal-parietal regions, mainly in the right hemisphere, whereas the right Brodmann area 39 (BA39) was relatively hypometabolic both in the (r)PS+ and in the (l)PS+. BA39 and bilateral posterior cingulate cortex were significantly hypometabolic in PS + than in PS- group.

Conclusions: As a hub of the network supervising the body schema perception, the involvement of the right posterior hypometabolism supports the hypothesis PS is a result of a somatosensory perceptive deficit rather than a nigrostriatal dopaminergic unbalance.