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make the analysis of an SSEP amplitude impossible. Such disturbances were regularly noticed by us after installation of a large CT scanner close to the operating theater. Furthermore, some patients have poor data collection due to poor transmission or unusual cortical processing of median nerve stimulation. Typical artifacts occurring during coagulation for hemostasis are variable. SSEP amplitude can nevertheless be adequately assessed during clamping, although the irregular curve during dissection and wound closure cannot go unnoticed.
According to our experience, in most cases (76.1%), of SSEP amplitudes do not change significantly during the main phases of operation, especially during clamping of the carotid artery due to collateral blood flow via the circle of Willis. This example shows the SSEP curve of a 76-year-old patient who was treated for his high-grade symptomatic internal carotid artery stenosis. During carotid endarterectomy, there were no alterations in his SSEP amplitudes. Surgery ended with still no SSEP abnormalities, and the patient awoke from his general anesthesia without any neurologic deficit. In 16.1% of cases, the SSEPs are abnormal because of insufficient collateral blood flow. The loss of SSEP amplitude or an amplitude reduction of more than 50% is registered. Figure 7 shows the intraoperative SSEP curve of a 77-year-old patient who underwent surgery for a high-grade symptomatic stenosis. During the 60-second test clamping, an SSEP loss was noticed. After shunt insertion, the SSEP amplitude recovered completely. During the second clamping phase of 2 minutes duration, the amplitude once again was reduced and then was completely lost. After restoring blood flow through the internal carotid artery, the potentials again recovered. The patient awoke without any neurologic deficit.
A typical case of embolus is demonstrate in Figure 8. While dissecting a highly stenotic ulcerated internal carotid artery, an irreversible loss of the SSEPs was registered. A thrombolytic maneuver was attempted, but the SSEPs did not improve. The patient showed a complete neurologic deficit with a Severe paresis of his right arm postoperatively. The SSEPs are usually abnormal within 60 to 80 seconds after clamping of the carotid artery. In some cases (2.8% according to our experience), the SSEPs only decline after a latency period of a few minutes. The example in Figure 9 shows the SSEP curve of a 66-year-old patient who underwent surgery for an asymptomatic left-sided stenosis. He also had an occlusion of the contralateral internal carotid artery and had suffered a stroke from this with a residual mild paresis of his arm. As seen in Figure 9, a late drop in the SSEPs was detected, despite a rather difficult curve to assess. Sixteen minutes after clamping, potentials were lost. The second short clamping of the circulation did not alter N20/P25 amplitude. This patient had a new ischemic neurologic deficit postoperatively.
Occasionally, despite uneventful SSEP curves, patients have a neurologic deficit directly following surgery. We observed a 0.1% (Continued on page 112)
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