Abstract Details

Title Temporal Mapping of Trigeminal Neuralgia Lesions to Symptom Onset in Multiple Sclerosis: When Do the Lesions Occur and What Do They Tell Us?

Topic Multiple Sclerosis

Presentation(s) P16 - Poster Session 16 (8:00 AM-9:00 AM)

Poster/Presentation
Number 12-001

Objective To conduct a case series to evaluate if multiple sclerosis (MS) associated trigeminal neuralgia (TN) lesions have a latency between formation and symptom onset.

Background TN is one of the most difficult to treat neuropathic pain conditions in MS. The understanding of the biological processes underlying the conversion from relapsing remitting to secondary progressive MS (SPMS) remains limited. Unravelling the temporal relationship of trigeminal sensory fiber demyelination and injury, as represented by new lesions, to symptom onset may provide insight into MS pathophysiology.

Design/Methods Retrospective case series of MS patients with TN seen at a tertiary referral center. After identifying cases via a keyword search in the electronic medical record system, we calculated the time difference between TN symptom onset and the oldest MRI showing a correlative lesion. Axial T2 and T2-FLAIR sequences were used and the findings were independently verified by a neuroradiologist.

Results We identified 64 MS patients with TN; 25 had sufficient data to be included. At TN symptom onset, mean age was 57 +/-11 years, 64% were female, and 44% had SPMS. The latency between likely culprit TN lesion detection on MRI and clinical symptom onset was 54 +/- 58 months. Only 5 patients had new corresponding MS lesions noted at or after symptom onset; remainder did not have obvious change in lesion imaging characteristics around the time of TN symptom onset or additional evidence of vascular compression.

Conclusions Our study highlights a substantial latency between TN lesion formation and symptom onset in most patients, suggestive of alternative explanations than a typical relapse. TN onset could rather be due to disease progression such as conversion to SPMS related to neurodegeneration or insidious lesion enlargement, eventually meeting threshold for ectopic neuronal excitation or ephaptic transmission.

Authors/Disclosures
Sonam Mohan, MD, PhD (UCSF Neurology) PRESENTER	Dr. Mohan has nothing to disclose.
	No disclosure on file
Emmanuelle Waubant, MD, PhD, FAAN (USCF MS Center)	The institution of Dr. Waubant has received research support from NIH. The institution of Dr. Waubant has received research support from NMSS. The institution of Dr. Waubant has received research support from PCORI. The institution of Dr. Waubant has received research support from Race to Erase MS. The institution of Dr. Waubant has received research support from Roche. The institution of Dr. Waubant has received research support from Department of Defense. Dr. Waubant has received publishing royalties from a publication relating to health care.

��ɫ��

��ɫ��