29 Hypofunctioning of the SMA in PD patients during movements has been demonstrated

by studies using functional magnetic resonance imaging (fMRI).30 The basal ganglia-SMA motor system, which regulates the elaboration of internally driven motor sequences, may be responsible for the adequate scaling of motor activity in normal movement. PD patients fail in this process because of the basal ganglia-SMA dysfunction. 31 Figure 2. Scheme of motor circuits involved in the pathophysiology of movement disturbances in schizophrenic patients. Inhibitors,research,lifescience,medical PMC, premotor cortex; SMA, supplementary motor area; CMA, angular motor area. fMRI studies on motor activation in schizophrenic patients have also revealed decreased activation of the SMA.7,32,33 Thus, reduction in SMA activity during motor tasks seems to be a common characteristic in PD and schizophrenia. Reduced SMA activity could be caused by disturbed functioning, either of the cortico-cortical

circuit, via the basal ganglia and the thalamus, or of the cortico-cerebellar-thalamic-cortical Inhibitors,research,lifescience,medical circuit (CCTCC). Both defects would lead to a deficient, thalamic output toward the SMA. Evidence from various research methodologies supports the suggestion that a disordered function of neural circuits containing the basal ganglia and the Inhibitors,research,lifescience,medical thalamus has a role in the pathophysiology of schizophrenia.34,35 Studies have revealed a disturbed basal ganglia output in schizophrenic patients who were treated with antipsychotic medication.36-38 Additionally, dysfunction of the CCTCC Inhibitors,research,lifescience,medical leading to poorly coordinated mental activity and altered excitability of the motor cortex have been demonstrated in untreated schizophrenic patients.39,40. Problems with the regularity and smoothness of the movement might, also be caused by basal ganglia dysfunction, but they are more likely to be caused by Inhibitors,research,lifescience,medical deficiencies in monitoring and optimization of movement by the use of sensory feedback information. As the cerebellum is mainly involved in these processes, cerebellar

dysfunctions in schizophrenic patients could also contribute to the observed disturbances in regularity and smoothness. In PD, hypokinesia Dacomitinib may improve under exposure to sensory or emotional stimuli. Many studies have demonstrated that PD patients can use diverse external cues or attentional strategies to enhance motor performance.27,41 Our results indicate that the normalizing effect, of external sensory stimuli on motor parameters in schizophrenic patients is similar to that, in PD patients, whereas the effect, of attentional stimuli is much less pronounced. The pathophysiological basis for this finding remains unclear. According to cerebral blood flow studies, activity in the PMC and SMA is Nutlin-3a mechanism elevated in patients with PD when external cues or attentional strategies are used to enhance motor performance.