Clinical NeuroscienceResearch PaperAbnormal expression of voltage-gated sodium channels Nav1.7, Nav1.3 and Nav1.8 in trigeminal neuralgia
Section snippets
Subject's selection
This was a randomized case×control study. Ten patients with TN according to the IASP (International Association for the Study of Pain) criteria (Merskey and Bogduk, 1994) were randomized for this study. In the moment of diagnosis, all had made computed tomography with contrast and/or magnetic resonance imaging and we did not find any abnormalities in the entry zone of the trigeminal root or other findings in any patient. All patients had been followed at the Orofacial Pain Clinic of a General
Patients' characteristics
The characteristics of the groups can be observed in Table 2 (n=23). TN ages were lower than in previous studies possibly because in general these patients need neurosurgery after some years with pain and we wanted to include only patients with recent pain onset and no surgery's history. In general, TN studies do not exclude previous operation. All TN patients had paroxysmal shock-like pain and all of them reported the maximum pain intensity (visual analogic scale—VAS=10). In the neurological
Discussion
The interest in the last decade in studying the role of voltage-gated sodium channels in chronic pain have grown, mainly because of the recent findings about single mutations that can cause pain disorders or indifference to pain (Ahmad et al 2007, Cox et al 2006, Goldberg et al 2007). Subtype Nav1.7 is particularly important, but also Nav1.8 and Nav1.3 are expressed in many chronic pain conditions (Cummins et al 2007, Dib-Hajj et al 2007, Rogers et al 2006, Rush et al 2006). In our study, we
Conclusion
There was a reduction in the expression of Nav1.7 and an increase in the expression of Nav1.3 when compared to controls; TN can be, at least in part, a channelopathy.
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