In this study, we examine the role of brain inflammation in painful trigeminal neuropathy (PTN). 

Painful trigeminal neuropathy is a chronic facial pain typically caused by trigeminal nerve injuries. It is frequently refractory to medication management, and our understanding of pathophysiological mechanisms is limited. In this study, we examine the role of brain inflammation in PTN

Eleven patients with PTN, evaluated by a neurologist (HTC), completed a positron emission tomography-magnetic resonance imaging (PET/MR) scan with the radioligand [¹¹C]PBR28, which binds to the 18 kDa Translocator protein (TSPO), a marker of brain inflammation. [¹¹C]PBR28 PET maps (standard uptake value ratio; SUVR) were spatially normalized to the Montreal Neurological Institute space and smoothed (Full width at half maximum = 8 mm). For each participant, the mean [¹¹C]PBR28 signal value was extracted from three regions-of-interest (thalamus, insula, and postcentral gyrus, identified using the Harvard-Oxford Cortical and Subcortical Structural Atlases) and compared across hemispheres based on pain laterality (i.e., ipsilateral vs contralateral to the primary side of pain) using a paired t-test, separately for each region. 

Of the three regions explored, the thalamus displayed a statistically significant hemispheric difference, with the contralateral side demonstrating a higher [¹¹C]PBR28 signal compared to the ipsilateral side (p=0.006). There was no significant hemispheric difference for insula (p=0.42) and postcentral gyrus (p=0.92). On an individual level, the majority of participants (82%) show increased contralateral thalamic signal with an average of 2.87% increase in signal on the contralateral side. 

Our preliminary data provide evidence to support that increased thalamic inflammation is linked to PTN. If further confirmed, this work would provide a rationale for exploring neuroinflammation as a therapeutic target for this condition.