Beyond Neuromonitoring: Spinal Cord Perfusion, Autonomic Dysregulation, and Neurological Risk During Complex Spinal Deformity Correction

Background: Advances in spinal deformity surgery have expanded treatment options for pediatric and adolescent patients, but neurological complications remain among the most serious adverse events. Intraoperative neuromonitoring (IONM) enables early detection of spinal cord dysfunction, while preservation of adequate spinal cord perfusion remains an important component of perioperative neurological protection. Objective: This narrative review examines current evidence regarding neurological protection during complex spinal deformity surgery, with emphasis on spinal cord perfusion, IONM interpretation, hemodynamic management, and the potential interaction between mechanical and autonomic factors. An illustrative case of recurrent IONM deterioration associated with profound hemodynamic instability is included. Methods: A narrative review of contemporary literature was conducted, focusing on spinal cord perfusion, mechanisms of neurological injury, IONM, perioperative blood pressure management, corrective strategies, and postoperative neurological surveillance. Pediatric deformity studies were prioritized, while adult and mixed-population studies were included when relevant mechanistic or technical information was provided. The clinical case was analyzed separately from the literature synthesis. Results: Current evidence supports maintaining adequate systemic perfusion and promptly evaluating reversible physiological and mechanical contributors when IONM deterioration occurs. Blood pressure augmentation may restore signals in a subset of patients, but IONM changes cannot be assumed to be purely ischemic, and improved perfusion may not overcome persistent mechanical compromise. In the illustrative case, recurrent IONM signal loss occurred during corrective maneuvers and was associated with profound hypotension and bradycardia during a subsequent correction attempt. Motor and somatosensory evoked potentials were comparable to baseline by the end of surgery after release of corrective forces, hemodynamic management, and vasopressor support; they had recovered to 50% of baseline immediately before correction was resumed. Because these interventions were performed concurrently, the relative contribution of mechanical release, improved systemic perfusion, and possible autonomic mechanisms could not be determined. Motor and sensory function remained intact postoperatively, although she later reported sweating and temperature asymmetry during follow-up. Conclusions: Neurological protection during complex spinal deformity correction requires an integrated perioperative approach combining individualized surgical strategy, multimodal IONM, hemodynamic optimization, and postoperative surveillance. When IONM deterioration occurs, mechanical, hemodynamic, anesthetic, and technical causes should be assessed concurrently. The presented case supports consideration of a possible autonomic contribution to severe intraoperative hemodynamic instability, but does not establish a specific autonomic syndrome or causal pathway.