Increased functional connectivity between motor and sensory cortex in a patient with Lance–Adams syndrome

Abstract

Survivors from cardiorespiratory arrest may develop neurologcal complications, such as post-hypoxic myoclonus (PHM). The hronic type of PHM is known as Lance–Adams syndrome (LAS), hich begins within days to weeks following an episode of anoxia 1]. LAS is characterized by myoclonus, which is triggered by intenional action or external stimuli and relieved at resting state or leep [1]. Several investigations have been performed to determine he pathogenesis of LAS. The loss of the neurotransmitter serotonin ithin the inferior olive has been believed to be an important causal actor for LAS, and gamma-aminobutyric acid may also be involved n the genesis of LAS [2–4]. Recently, neuroimaging has been used o detail the anatomical and pathophysiological basis of LAS [2,3]. evertheless, the pathogenesis of LAS has been not determined. We encountered a patient with LAS and performed resting state unctional MRI (rs-fMRI) to investigate the pathogenesis of LAS.