Pathophysiology of Parkinson disease

Abstract

Pathophysiology of motor symptoms, cognitive impairments, and psychosis in Parkinson's disease (PD) was reviewed. To understand pathophysiology of motor symptoms in PD, two major models have been proposed. In firing rate model, depletion of striatal dopamine decreases neural activity in the direct pathway from striatum to GPi/SNr and increases neural activity in the indirect pathway via GPe and STN, resulting in greater inhibition of motor thalamus that facilitate corticospinal motor output. This model has led to a new surgical treatment for PD, though there is emerging evidence that criticize the model. In a new model, called oscillation (firing pattern) model, loss of dopamine develops or enhances pathological oscillations in the beta band in STN and GPi, leading to suppression of movement. This model explains treatment effect of STN stimulation at 130Hz used in the deep brain stimulation since the stimulation should suppress the pathological beta band oscillation and improve motor symptom in PD. Cognitive impairments in PD affect various domains while deficits in visuospatial and executive function are frequent. PD psychosis represents a spectrum of illusions, passage/presence hallucinations, formed visual hallucinations and delusions that often progress over the course of PD.