Author(s): Nurmikko T.J.

Source: Journal of Headache and Pain; 2017; vol. 18 (no. 1)

Publication Date: 2017

Publication Type(s): Conference Abstract

Available  at Journal of Headache and Pain –  from SpringerLink – Medicine

Available  at Journal of Headache and Pain –  from Europe PubMed Central – Open Access

Available  at Journal of Headache and Pain –  from ProQuest (Hospital Premium Collection) – NHS Version

Available  at Journal of Headache and Pain –  from EBSCO (MEDLINE Complete)

Abstract:An underlying concept in the new ICHD-3 classification of trigeminal neuralgia is the postulation that clinical presentations matter because they reflect distinct pathophysiological mechanisms. Previous attempts to establish the connection between the two have yielded uncertain results as the authors have paid limited attention to individual clinical symptoms and signs. Yet, the relatively strict criteria for trigeminal neuralgia and its subgroups yield homogenous populations that allow advantage to be taken of the advances in neurophysiological and imaging methods. It is now possible to conduct subgroup-specific pathophysiological studies aimed at biomarkers that pave the way for precision diagnosis of TN and individualised therapy. An example of how this might be done comes from recent studies based on sensory profiling of peripheral neuropathic pain. In a large group of patients with three different diagnoses, cluster analysis of detailed sensory testing revealed three main sensory phenotypes [1], with the potential to allocate individual patients to these sensory groups [2]. For TN, a stratification based on the new classification and linked to patients’ symptoms, somatosensory profiles, and neurophysiological and neuroimaging data provides a unique opportunity to explore clinical questions that are even more ambitious than those for other neuropathic pains. In my presentation I will suggest a pathway as to how to accomplish this. I will start by arguing that the existing data are sufficient to recommend preferred treatment in selected cases. I will then highlight a number of clinically relevant research questions that can be answered by largepopulation multi-centre studies applying established methods ranging from QST and evoked potentials to structural and functional neuroimaging of the trigeminal system and linking them with clinical signs and symptoms. Alongside this, I will discuss the challenges of phenotype profiling that could guide pharmacotherapy with, e.g., Nav 1.7 channel blockers or identifying genes that could make a subject susceptible to the development of TN.

Database: EMBASE