Authors: Zach Fiore
Mentors: Jared Nielsen
Insitution: Brigham Young University
Gait apraxia is a type of apraxia that affects lower limb use in walking. It is characterized by difficulty initiating gait, freezing of gait, and other gait disturbances that cannot be attributed to complications affecting sensory, motor, or cerebellar function, psychiatric disease, nor ataxia. Symptoms often present following brain trauma. Previous research has indicated that gait apraxia may be linked to lesions in the frontal lobes, basal ganglia and supplementary motor area. However, the specific cerebral location has been debated with minimal research done on the symptom’s implicated neural circuits. The purpose of this study is to determine the networks in the brain that are involved in the pathophysiology of gait apraxia. To determine this, we used the lesion network mapping method. A systematic literature review was performed, with specific inclusion criteria, to find case studies of patients presenting with gait apraxia stemming from acquired brain injury (n=15). Lesion network mapping analysis (Fox et al., 2018) was performed on 15 cases with a large cohort of healthy control resting-state scans (n=1000). The analysis showed that lesions exhibited functional connectivity to the bilateral medial dorsal and pulvinar nuclei of the thalami (n=15), which supports previous associations of basal ganglia damage contributing to gait apraxia. A novel region, the cingulate cortex (n=15), was also found to be functionally connected to the lesion networks. This region is a part of the cingulo-opercular network, responsible for many functions, including action. This network has recently been found to display strong functional connectivity with the somato-cognitive action network, responsible for coordinating movements with cognitive processes. Further research is necessary to determine the mechanism of how these networks interact in contributing to gait apraxia.