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  • Title: Limitations of median nerve somatosensory evoked potential monitoring during carotid endarterectomy.
    Author: Okuyama S, Nishimura S, Takahashi Y, Kubota K, Hirano T, Kazama K, Tomii M, Matsuyama J, Mizuno J, Matsushima T, Sato M, Watanabe K.
    Journal: J Neurosurg; 2019 Sep 01; 131(3):750-756. PubMed ID: 30192190.
    Abstract:
    OBJECTIVE: Hypoperfusion during carotid artery cross-clamping (CC) for carotid endarterectomy (CEA) may result in the major complication of perioperative stroke. Median nerve somatosensory evoked potential (MNSSEP) monitoring, which is an established method for the prediction of cerebral ischemia, has low sensitivity in detecting such hypoperfusion. In this study the authors sought to explore the limitations of MNSSEP monitoring compared to tibial nerve somatosensory evoked potential (TNSSEP) monitoring for the detection of CC-related hypoperfusion. METHODS: The authors retrospectively analyzed data from patients who underwent unilateral CEA with routine shunt use. All patients underwent preoperative magnetic resonance angiography and were monitored for intraoperative cerebral ischemia by using MNSSEP, TNSSEP, and carotid stump pressure during CC. First, the frequency of MNSSEP and TNSSEP changes during CC were analyzed. Subsequently, variables related to stump pressure were determined by using linear analysis and those related to each of the somatosensory evoked potential (SSEP) changes were determined by using logistic regression analysis. RESULTS: A total of 94 patients (mean age 74 years) were included in the study. TNSSEP identified a greater number of SSEP changes during CC than MNSSEP (20.2% vs 11.7%; p < 0.05). Linear regression analysis demonstrated that hypoplasia of the contralateral proximal segment of the anterior cerebral artery (A1 hypoplasia) (p < 0.01) and hypoplasia of the ipsilateral precommunicating segment of the posterior cerebral artery (P1 hypoplasia) (p = 0.02) independently and negatively correlated with stump pressure. Both contralateral A1 hypoplasia (OR 26.25, 95% CI 4.52-152.51) and ipsilateral P1 hypoplasia (OR 8.75, 95% CI 1.83-41.94) were independently related to the TNSSEP changes. However, only ipsilateral P1 hypoplasia (OR 8.76, 95% CI 1.61-47.67) was independently related to MNSSEP changes. CONCLUSIONS: TNSSEP monitoring appears to be superior to MNSSEP in detecting CC-related hypoperfusion. Correlation with stump pressure and SSEP changes indicates that TNSSEP, and not MNSSEP monitoring, is a reliable indicator of cerebral ischemia in the territory of the anterior cerebral artery.
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