Trigeminal neuralgia patients have microstructural abnormalities in their trigeminal nerves and brain white matter connecting regions involved in pain perception, attention, and motor functions.
Idiopathic trigeminal neuralgia (TN) is classically associated with neurovascular compression (NVC) of the trigeminal nerve at the root entry zone (REZ), but NVC-induced structural alterations are not always apparent on conventional imaging. Previous studies report lower fractional anisotropy (FA) in the affected trigeminal nerves of TN patients using diffusion tensor imaging (DTI). However, it is not known if TN patients have trigeminal nerve abnormalities of mean, radial, or axial diffusivity (MD, RD, AD – metrics linked to neuroinflammation and edema) or brain white matter (WM) abnormalities. DTI scans in 18 right-sided TN patients and 18 healthy controls were retrospectively analyzed to extract FA, RD, AD, and MD from the trigeminal nerve REZ, and Tract-Based Spatial Statistics (TBSS) was used to assess brain WM. In patients, the affected trigeminal nerve had lower FA, and higher RD, AD, and MD was found bilaterally compared to controls. Group TBSS (P < 0.05, corrected) showed patients had lower FA and increased RD, MD, and AD in brain WM connecting areas involved in the sensory and cognitive-affective dimensions of pain, attention, and motor functions, including the corpus callosum, cingulum, posterior corona radiata, and superior longitudinal fasciculus. These data indicate that TN patients have abnormal tissue microstructure in their affected trigeminal nerves, and as a possible consequence, WM microstructural alterations in the brain. These findings suggest that trigeminal nerve structural abnormalities occur in TN, even if not apparent on gross imaging. Furthermore, MD and RD findings suggest that neuroinflammation and edema may contribute to TN pathophysiology.
aDivision of Brain, Imaging and Behaviour Systems Neuroscience, Toronto Western Research Institute, University Health Network, Toronto, ON, Canada
bInstitute of Medical Science, University of Toronto, Toronto, ON, Canada
cDivision of Neurosurgery, Toronto Western Hospital & University of Toronto, Toronto, ON, Canada
* Corresponding author. Address: Toronto Western Hospital, Room MP13-306, 399 Bathurst Street, Toronto, ON M5T 2S8, Canada. Tel.: +1 416 603 5662; fax: +1 416 603 5745.
1 These authors contributed equally to the manuscript.
Received 18 July 2013
Received in revised form 23 August 2013
Accepted 26 August 2013
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