Mechanisms of Bradykinesia—Disturbances in Sensorimotor Processing

Summary

Bradykinesia, slowness in the initiation and execution of movement, is a characteristic motor disorder in Parkinson’s disease which has been attributed to dysfunction of the striatum.

Disclosure of cognitive dysfunctions, involvement of parts of CNS other than nigrostriatal system in advanced stages of the disease, suggests involvement of the cerebral cortex which may contribute to the bradykinesia.

Reaction time studies on Parkinson’s disease disclosed that inattention, visual information processing, difficulty in concept formation and its maintenance are attributable to prolongation of the reaction time. In addition to failures in motor output systems, sensory perception and central information processing prior to motor mechanisms should be considered as neural processes responsible for bradykinesia in Parkinson’s disease.

Bradykinesia is defined as a delay in initiation and slowness in the execution of movement. It is a common symptom in Parkinson’s disease (PD) observable in daily life activities as well as in experiments, which has long been considered due to dysfunction of the basal ganglia as a motor center.

During the last decade, the neurophysiological aspects of PD have been studied to clarify dysfunctions other than motor, resulting in a disclosure of cognitive impairments in PD from various aspects (Lees and Smith 1983; Brown and Marsden 1986; Mayeux et al. 1988).

The responsible sites of lesions in cognitive dysfunctions have been attributed to the prefrontal cortex or its connections to the basal ganglia since Lees & Smith(1983), who disclosed failure in Wisconsin Card Sorting Test in early stages of PD.

On the other hand, pathological and chemical studies on the brain of PD at various stages of illness disclosed involvement of extensive regions, including cerebral cortex, as the disease advanced (Jellinger 1990). This can be related to reappearance of akinesia in the advanced stages of PD despite continuous administration of dopaminergic drugs which have continuous beneficial effects on tremor and rigidity as signs of dysfunctions of the basal ganglia per se.

In this article, possible cortical dysfunctions relevant to bradykinesia will be discussed. Inattention, failure in visual information processing and difficulty in criteria shift for motor response will be discussed, based on our experiments, as causes of delay in initiation of movement in PD.