Article
Neuromagnetic brain responses as a predictive marker for the outcome of microvascular decompression in trigeminal neuralgia
Neuromagnetische Hirnantworten als Prädiktor für das Outcome der mikrovaskulären Dekompression bei der Trigeminusneuralgie
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Published: | June 26, 2020 |
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Objective: While some patients with trigeminal neuralgia (TN) respond to drug treatment, there are still patients with refractory symptoms. The most common cause of classical TN is assumed to be a neurovascular conflict of the trigeminal nerve and the superior cerebellar artery. Current imaging techniques show low specificity for relevant nerve compressions since neurovascular conflicts can also be observed in healthy individuals. Information on the functional aspect of nerve damage is still lacking. Electro- and magnetoencephalography (EEG/MEG) allow the functional investigation of the nociceptive system by means of laser-evoked brain responses. In an effort to find specific patterns of neural damage we disentangled cortical generators and assessed frequency-specific oscillations in patients before and after microvascular decompression (MVD) using MEG.
Methods: We applied 30 noxious laser pulses (Nd:YAP, ƛ 1340nm, 3 ms, 5mm, 1.75/2.00J) at the affected trigeminal dermatoma (V2/V3) and its corresponding contralateral region in patients with classic, drug-refractory TN before and after MVD (n=8, 2 were excluded due to strong muscle artifacts). After each single pulse, patients were instructed to evaluate the perceived pain intensity on a numerical rating scale. Gradients of magnetic fields were recorded using a 122-channel whole-head MEG system inside a magnetic shielded room. For source analysis of the evoked fields we used a distributed source model and evaluated nociceptive-induced oscillations using a wavelet analysis. Non-responders with persistence of pre-existing symptoms (2/8) were identified by evaluation of the German pain questionnaire.
Results: The cortical reconstruction revealed pronounced bilateral activity in the primary and secondary cortex (S1/S2) as well as in the posterior and anterior insula (pIC/aIC). The spectrotemporal analysis mainly showed changes in the low frequency range in contralateral S1. At the control site we observed an oscillatory response in the theta/alpha range within a time interval of 200–500ms after stimulus onset. In the group of responders, this activation was delayed or attenuated to the control site and, interestingly, resembled the contralateral site postoperatively again. Nonresponders showed theta/alpha activation already preoperatively.
Conclusion: Our results elucidate the functional dynamics of neural damage in S1 and might serve as a promising marker for the development of novel diagnostic concepts in the future.