An increasing awareness of the interaction between gait and cognition has occurred over recent time. This interaction is even more prominent in Parkinson ' s disease (PD), where the alteration of striatal dopamine deficiency places a greater emphasis on cognition to compensate for the gait disturbances seen in PD. This dissertation aims to provide an insight into this interaction in PD and demonstrate how normal gait control mechanisms are altered in PD to more cognitive control. Evidence will be provided which demonstrates a shift between attention and automatic gait control mechanisms toward attention. In addition, it will be demonstrated that, because of the cognitive dysfunction that also occurs in PD, the capacity to normalize gait still remains impaired and becomes more subject to the effects of external environmental influences. Further, a rationale will be provided to utilize this interaction in a more beneficial manner, to assist the attention control mechanisms to return gait towards normal. This latter approach is applicable to all aspects of gait disorders in PD and forms a basis for possible intervention therapies.
- Basal ganglia
- Parkinson's disease