## 1 Introduction  
Parkinson's disease (PD) is the second most common neurodegenerative disease, due to a progressive degeneration of the nigrostriatal dopaminergic pathway with loss of substantia nigra pars compacta (SNpc) neurons and depletion of dopamine [1]. PD causes several motor impairments such as slow movements, rigidity, reduced mobility, disturbances of balance, impaired gait, recurrent falls, and postural abnormalities [1, 2, 3, 4]. Posture is the position of the human-body segments in space, physiologically placed within normal ranges in upright standing [5] and during walking [6]. The central nervous system (CNS) regulates postural stability via processing the peripheral sensory afferents (visual, stomatognathic, vestibular, and somatosensory) and modulating neuromuscular adaptations of the myofascali chains [7] with biomechanical strategies against gravity [7; 8; 9], trying to ensure balance in the most unstable postural conditions [10]. Axial postural abnormalities are not uncommon in PD [4; 11; 12], and are defined as involuntary, reversible postures including bending of the trunk on the frontal and sagittal plane as well as anterior bending of the neck [13]. The pathophysiology of these conditions is still largely obscure [14]; however a recent Task Force Consensus by the International Movement Disorder Society clarified nosology and cut-off values to classify the six main axial postural abnormalities in PD [13]. On the sagittal plane, the term \"camptocormia\" was defined as an anterior trunk bending >45\({}^{\circ}\) (with thoracic fulcrum) or >30\({}^{\circ}\) (with lumbar fulcrum), whereas the term \"Anterior trunk flexion\" was proposed with the thoracic (\(\geq\)25\({}^{\circ}\) to \(\leq\)45\({}^{\circ}\)) or lumbar fulcrum (>15\({}^{\circ}\) to \(\leq\)30\({}^{\circ}\)). With regards to the neck bending, \"antecollis\" was used to define an anterior neck bending of >45\({}^{\circ}\), whereas \"anterior neck flexion\" was used for alterations of > 35\({}^{\circ}\) to \(\leq\)45. Finally, on the frontal plane, the term \"Pisa syndrome\" was used to define a lateral bending of the trunk >10\({}^{\circ}\), whereas \"lateral trunk flexion\" was chosen for angles of \(\geq\) 5\({}^{\circ}\) to \(\leq\)10 [13]. Among axial postural abnormalities, camptocormia is present in over 10% of the general PD population and over 50% of PD patients presenting with at least one postural abnormality [11]. Moreover, postural alterations are linked to motor impairment and loss of functional independence [15] as well as increased risk of fall [4]. Trunk postural abnormalities on the sagittal plane can be classified as higher or lower on the basis of whether the fulcrum is located at the thoracic (C7 to T12-L1) or lumbar level (L1-Sacrum, hip flexion), respectively [4; 16; 17]. According to several previous studies [4; 16; 17; 18; 19; 20], one of the main hallmarks of these alterations is the reversibility, namely the occurrence during standing and walking with the dramatic reduction in supine position or when leaning against a wall [13]. When the postural abnormality did not resolve during the supine position of the patient or when he is leaning against a wall, it could be considered non-reversible structured postural deformity. From a clinical point of view, the abnormalities can be classified as non-structural or structural [21]. The term \"structural\" indicates the presence of morphological abnormalities within the bones and soft tissues (fascia, muscles, ligaments, tendons). In addition, structural misalignments reveal a more severe clinical problem because they are less flexible and less prone to correction compared to the non-structural disorders. One of various tests used as a clinical measure to screen structural thoracic hyper-kyphesis, with moderate diagnostic properties, is occupit to wall distance (OWD), revealing the presence of a structured hyper-kyphesis when the OWD \(\geq\) 6.5 cm (cut-off point) [22].