Reversible Causes of Transitory Motor Evoked Potential Decrease During Posterior Spine Fusion in Rapidly Progressive Scoliosis Treatment: A Case Report

TL;DR

A teenage girl with severe scoliosis experienced temporary spinal cord monitoring changes during surgery, but recovered fully thanks to careful monitoring.

Contribution

This case report highlights reversible causes of motor evoked potential decreases during scoliosis surgery and the importance of multimodal neuromonitoring.

Findings

Intraoperative motor evoked potential (MEP) loss was observed during posterior spinal fusion but recovered fully or partially by the end of surgery.

Multimodal neuromonitoring detected reversible spinal cord dysfunction without permanent neurological damage.

Possible causes included temporary venous congestion or vasospasm from surgical manipulation.

Abstract

Introduction: Idiopathic adolescent scoliosis (IAS) is commonly managed non-surgically; however, patients with a Cobb angle >45° before skeletal maturity often require posterior spinal fusion. Because this procedure carries a risk of neurological complications, intraoperative neurophysiological monitoring (IONM) is essential for early detection of spinal cord compromise. Case report: We present a 13-year-old girl with rapidly progressing scoliosis (Cobb angle 78°) who developed intraoperative changes in motor evoked potentials (MEPs) during posterior fusion from L4 to Th2. Total intravenous anesthesia without muscle relaxants was used, and standard multimodal IONM with somatosensory evoked potentials (SSEPs), MEPs, and spontaneous/triggered electromyography was applied. After induction of general anesthesia and surgical exposure, pedicle preparation at Th8–Th9 was followed by increased bleeding from the vertebral bodies and an abrupt loss of MEPs in both lower limbs, most prominently in the tibialis anterior muscles, whilst SSEPs remained unchanged. Intraoperative radiography confirmed correct screw placement, and anesthetic variables were reassessed with no reversible cause identified. Because MEPs remained absent, a wake-up test was performed and demonstrated intact voluntary movement, allowing the surgery to continue. By the end of the procedure, MEPs recovered fully on the left side and partially on the right. The patient awoke without any postoperative motor deficit. Conclusion: It is well known that motor responses can show variability during surgery, including a gradual decrease due to prolonged anesthesia. After excluding anesthetic and mechanical factors, one of the hypothetical explanations for the transient MEP loss was temporary venous congestion and retrograde flow within the intravertebral and epidural/intraspinal venous networks, resulting in reversible spinal cord drainage impairment. Another hypothetical possibility was transient vasospasm from surgical manipulation without direct neural or vascular injury. This case highlights the critical role of continuous multimodal neuromonitoring in detecting reversible spinal cord dysfunction and guiding safe decision-making during complex scoliosis surgery.

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