Mechanisms of signal change during intraoperative somatosensory evoked potential monitoring of the spinal cord

In scoliosis surgery, intraoperative somatosensory evoked potential (SSEP) monitoring has reduced the incidence of postoperative neurologic deficits. Many factors affect the amplitude and latency of SSEP waveforms during surgery. Somatosensory evoked potential amplitude decreases with ischemia and anoxia because of temporal dispersion of the afferent volley and conduction block in damaged axons. In conjunction with surgical manipulations, minor drops in blood pressure may result in substantial SSEP changes that reverse when perfusion pressure is increased. Irreversible anoxic injury to central nervous system white matter with loss of SSEP waveforms is dependent on calcium influx into the intracellular space. Somatosensory evoked potential monitoring may be less sensitive for detecting acute insults in the presence of preexisting white matter lesions. Increased extracellular potassium from acute barotrauma can block axonal conduction transiently even when there is no axonal disruption. Marked temperature-related drops in SSEP amplitude may occur after exposure of the spine but before instrumentation and deformity correction. Hypothermia may increase false-negative outcomes. Short-interval double-pulse stimulation may improve the sensitivity of the SSEP in detecting early ischemic changes. For neurosurgical procedures on the spinal cord the use of SSEP monitoring in improving postoperative outcome is less well established.