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DOI 10.1016/j.clinph.2019.09.027

Медицинская библиотека · Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology · 2019

Neural correlates and gait characteristics for hypoxic-ischemic brain injury induced freezing of gait.

Yoon Seo Yeon, Lee Sang Chul, An Young-Sil, Kim Yong Wook

Сравнительное исследованиеСтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

OBJECTIVE

To investigate gait characteristics in patients with freezing of gait (FOG) after hypoxic-ischemic brain injury (HIBI) and to elucidate neural correlates for FOG using F-18 fluoro-2-deoxy-d-glucose positron emission tomography.

METHODS

We enrolled 12 patients with FOG after HIBI and 17 patients without FOG after HIBI. We performed three-dimensional gait analyses and compared each parameter and gait variability. Brain metabolism was measured, and we compared regional brain metabolism using a voxel-by-voxel-based statistical mapping analysis.

RESULTS

The FOG group revealed a significantly decreased joint range of motion (ROM), particularly in the sagittal plane for three-joint summated ROM (p < 0.0025). Spatiotemporal results demonstrated that stride length and step length were decreased in the with FOG group (p < 0.005). FOG severity was negatively correlated with brain metabolism in the left thalamus, and three-joint summated ROM in the sagittal plane was positively associated with brain metabolism in the left thalamus and midbrain (p < 0.05).

CONCLUSIONS

Central organizational level amplitude disorder may play an important role in the pathophysiology, and disturbance in the cholinergic pathway might contribute to the development of FOG in patients with HIBI.

SIGNIFICANCE: These findings contribute to understanding FOG in HIBI.

Для цитирования: Yoon Seo Yeon, Lee Sang Chul, An Young-Sil, Kim Yong Wook. Neural correlates and gait characteristics for hypoxic-ischemic brain injury induced freezing of gait.. Clinical neurophysiology : official journal of the International Federation of Clinical Neurophysiology. 2019. DOI: 10.1016/j.clinph.2019.09.027.

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