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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 baro-trauma 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.

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Fenestration of vertebral arteries has been reported in association with thromboembolic brain infarctions. However, few cases have been reported in which recurrent infarction occurred in spite of adequate anticoagulation. We report a young man with fenestrated vertebral arteries and stroke who failed to respond to standard anticoagulation therapy but did well with angiographic coil obliteration of an abnormal vertebral segment. An 18-year-old left-handed man presented with acute onset of dizziness and headache. No trauma or other stroke risk factors were identified. Left cerebellar infarction was seen on CT, but the cause could not be identified by brain and neck MRI, MRA, or CTA. Bilateral fenestrated vertebral arteries were identified with conventional angiography. Although the patient recovered fully and was treated with anticoagulation, he suffered a recurrent stroke 1 month later involving the right cerebellum while he was on a therapeutic dose of warfarin. Repeat arteriography showed a spontaneous dissection within one of the fenestrated vertebral segments. Since receiving angiographic coil obliteration of the pathologic segment, he has been free of all symptoms. We conclude that the patient sustained recurrent thromboembolic events in his posterior circulation due to spontaneous dissection within a fenestrated vertebral artery segment. Conventional angiography and emergent interventional embolization were essential to his diagnostic evaluation and therapeutic intervention.