As we know, freezing of gait is one of the most disabling symptoms in Parkinson’s disease. It is a complex phenomenon and it is yet poorly understood. In this context, we aim to assess structural and functional connectivity alteration in two key structures that may play an important role in the generation of freezing of gait that are cerebellum and amygdala given their role in motor control and emotional processing...
As we know, freezing of gait is one of the most disabling symptoms in Parkinson’s disease. It is a complex phenomenon and it is yet poorly understood. In this context, we aim to assess structural and functional connectivity alteration in two key structures that may play an important role in the generation of freezing of gait that are cerebellum and amygdala given their role in motor control and emotional processing. We found an increased volume of cerebellar vermis together with an increased functional connectivity of cerebellar vermis with the frontal and cerebellar areas and we hypothesized that this might represent an initial attempt to compensate for reduced automaticity in Parkinson’s disease that then becomes a maladaptive mechanism as suggested by correlation with the worse gait pattern. On the other hand we found an increased volume also of amygdala together with altered functional connectivity that may represent an increased impact of emotional processing on motor control and dysfunctional integration of motor cognitive and emotional networks. As I said in the beginning, we are facing a complex phenomenon and it is fundamental to try to understand it better in order to propose a new therapeutic approach and studies such as the one I just presented may be a starting point to develop new, for example, rehabilitation approaches or to study new targets for neuromodulation.
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