Sensory aspects of movement disorders

Abstract

Movement disorders, which include disorders such as Parkinson’s disease, dystonia, Tourette’s syndrome, restless legs syndrome, and akathisia, have traditionally been considered to be disorders of impaired motor control resulting predominantly from dysfunction of the basal ganglia. This notion has been revised largely because of increasing recognition of associated behavioural, psychiatric, autonomic, and other non-motor symptoms. The sensory aspects of movement disorders include intrinsic sensory abnormalities and the effects of external sensory input on the underlying motor abnormality. The basal ganglia, cerebellum, thalamus, and their connections, coupled with altered sensory input, seem to play a key part in abnormal sensorimotor integration. However, more investigation into the phenomenology and physiological basis of sensory abnormalities, and about the role of the basal ganglia, cerebellum, and related structures in somatosensory processing, and its effect on motor control, is needed.

Botulinum Toxin Type A and Physiokinesiterapy in the Treatment of Pisa Syndrome

“…Joint receptors (Golgi tendon organs, free endings, Pacinian corpuscles and Ruffini endings) operate as proprioceptors monitoring constantly the range of motion forces. This makes conscious the subject about the body's position in space contributing to the perception of verticality and drive the motor response [30,31]. The reduction of joints' ranges of motion in PD, due to rigidity and bradykinesia, changes the information coming from the periphery to the cortex about the body position and participates to developing of the PS through the impaired motor response [32].…”

Promoting plasticity in the somatosensory cortex to alter motor physiology

“…In addition to FHD, alterations in touch perception in Parkinson's disease [53,54], abnormal sensory gating in Tourette's [55], and reduced SAI sensorimotor circuitry in restless legs syndrome [56] all provide evidence for a role for somatosensory processing in the control of movement. We refer the reader to excellent in-depth reviews detailing somatosensory abnormalities in movement disorders [57,58].…”

Treatment of Dystonia

“…With the observation that young-onset dystonia appeared to be hereditary, coupled with advances in genetic techniques, several genes associated with dystonia have been identified (Table 1) [2]. Underlying mechanisms of disease that have been suggested include loss of cortical inhibition, increased cortical and subcortical neuroplasticity, and abnormal sensory processing with impaired spatial and temporal discrimination [3][4][5]. Despite a greater understanding of the disease process, treatment for dystonia remains symptomatic, rather than targeted at underlying pathophysiology.…”