Abstract
Perioperative bilateral medial medullary infarction (BMMI) cases mimicking acute motor axonal neuropathy (AMAN) under general anesthesia have not been reported. We describe a patient who suffered flaccid quadriplegia and could not wean from mechanical ventilation after emergence from general anesthesia in cardiac surgery. A diagnosis of AMAN was considered, but intravenous immunoglobulin showed little efficacy. Magnetic resonance imaging of the patient later revealed BMMI with “snake eyes appearance,” and he was found to have severe vertebral artery stenosis. Considering the association between severe coronary heart disease and cerebrovascular stenosis, we highlight the significance of preoperative evaluation and comprehensive management of the cerebrovascular system for certain patients.
Highlights
Bilateral medial medullary infarction (BMMI) is a rare but devastating subtype of cerebrovascular accident that may lead to acute-onset quadriplegia and respiratory failure [1]
It is clinically significant to differentiate between BMMI and acute motor axonal neuropathy (AMAN), a subtype of Guillain-Barré syndrome (GBS), due to their similar clinical manifestations
Vertebral artery stenosis in our patient was so disproportionately severe that it might serve as an etiologic factor of post-coronary artery bypass grafting (CABG) posterior circulation stroke, instead of just a marker for the general atherosclerotic burden, especially when intraoperative hypotension and impaired cerebral autoregulation caused by previous lacunar stroke [15] were present
Summary
Bilateral medial medullary infarction (BMMI) is a rare but devastating subtype of cerebrovascular accident that may lead to acute-onset quadriplegia and respiratory failure [1]. He managed to wean from mechanical ventilation 8 months after admission, which allowed him to be transferred to a rehabilitation institution His axial T2-weighted fluidattenuated inversion recovery images 9 months after onset of quadriplegia showed lesions with low signal intensity presenting as SEA at rostral medulla level; axial T1-weighted images revealed similar lesions with low intensity at the same location (Figure 2). These findings indicated that the patient suffered BMMI. Abnormal electromyography findings of the patient might be attributed to diabetic peripheral neuropathy, because his blood glucose levels during hospitalization met the diagnostic criteria for diabetes mellitus
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