Evolving concepts on bradykinesia

Abstract

Bradykinesia is one of the cardinal motor symptoms of Parkinson's disease and other parkinsonisms. The various clinical aspects related to bradykinesia and the pathophysiological mechanisms underlying bradykinesia are, however, still unclear. In this article, we review clinical and experimental studies on bradykinesia performed in patients with Parkinson's disease and atypical parkinsonism. We also review studies on animal experiments dealing with pathophysiological aspects of the parkinsonian state. In Parkinson's disease, bradykinesia is characterized by slowness, the reduced amplitude of movement, and sequence effect. These features are also present in atypical parkinsonisms, but the sequence effect is not common. Levodopa therapy improves bradykinesia, but treatment variably affects the bradykinesia features and does not significantly modify the sequence effect. Findings from animal and patients demonstrate the role of the basal ganglia and other interconnected structures, such as the primary motor cortex and cerebellum, as well as the contribution of abnormal sensorimotor processing. Bradykinesia should be interpreted as arising from network dysfunction. A better understanding of bradykinesia pathophysiology will serve as the new starting point for clinical and experimental purposes.

Keywords: Parkinson’s disease; bradykinesia; clinical neurophysiology; motor control; transcranial magnetic stimulation.

Figure 1

The Network hypothesis for bradykinesia pathophysiology. Basal ganglia dysfunction is responsible for altered movement selection. The altered movement scaling at basal ganglia level may also arise from a fault in the sensory loop, responsible for sensorimotor integration. Other mechanisms involve sensorimotor areas. Cerebellar structures likely play a role in movement feedback, particularly important for continued and repetitive movements. The energy for all basal ganglia, sensorimotor areas, and the cerebellar functions appear to come from dopamine. With dopamine loss, the system slows down, reaction times increase, movement speed and amplitude decrease, and the sequence effect develops. Dotted lines indicate possible compensatory mechanisms.