# Visualizing nociplastic pain: functional hyperexcitability in neuropathic and idiopathic facial pain syndromes

## TL;DR

The study uses brain imaging to compare pain processing in neuropathic and idiopathic facial pain, revealing overactive brain regions in both conditions.

## Contribution

The study identifies shared and distinct patterns of brainstem activation in neuropathic and idiopathic facial pain using a consistent imaging protocol.

## Key findings

- NFP patients showed stronger activation in the spinal trigeminal nucleus and pain-related areas compared to healthy controls.
- PIFP patients exhibited a distinct network of overactive brain regions compared to NFP patients.
- Altered central pain processing is suggested as a potential nociplastic mechanism in PIFP.

## Abstract

Neuropathic facial pain (NFP) is linked to lesions of trigeminal nerves, distinguishing it from persistent idiopathic facial pain (PIFP) which is clinically similar but without neurological abnormalities and without clinically objectifiable cause. Our recent brainstem imaging studies have demonstrated that abnormal central pain processing plays a role in the pathophysiology of PIFP.

Using the identical brainstem imaging protocol this current study aims to investigate the trigeminal pain processing mechanisms in patients with peripheral NFP using functional magnetic resonance imaging (fMRI).

Twenty patients with NFP and 20 healthy control subjects (HC) participated in a well-established protocol of trigeminal nociceptive stimulation using gaseous ammonia. Functional images were acquired with a 3T MRI scanner, utilizing an optimized protocol designed for high-resolution echoplanar imaging of the brainstem. In a further step, using the same protocol, the imaging data from our database of patients with PIFP characterized by specific clinical features of persistent facial pain without detectable neurological damage, were incorporated into the analyses.

Patients with NFP exhibited stronger activation in the spinal trigeminal nucleus (sTN) and other pain transmitting areas in response to painful stimulation when compared to HC. This finding is similar to a previous study in PIFP patients using the same imaging parameters. When contrasting patients with PIFP from this earlier study with NFP patients, a network of overactive brain areas further distinguished PIFP patients.

Our findings indicate that altered central pain processing contributes to the pathophysiology of PIFP, possibly as a sign for nociplastic changes. Integrating these results into facial pain models could enhance the overall understanding of mechanisms underlying NFP and PIFP.

The online version contains supplementary material available at 10.1186/s10194-025-02133-w.