Featuring Dr. Jim Scott, Consultant Neurologist, in conversation with Jane Wrinch
A patient in their late 30s arrives at the dental office with sharp, electric facial pain along the lower jaw. The teeth look healthy. The pain pattern is classic for trigeminal neuralgia. The question that often goes unasked: could this be the first sign of something larger? Dr. Jim Scott, a consultant neurologist with more than 30 years of experience and one of only two neurologists in Victoria, British Columbia providing specialized multiple sclerosis (MS) care, sat down with Jane Wrinch to discuss exactly that. The conversation has direct implications for dental clinicians, who are often the first to see these patients.
Why Dental Providers Are Often the First Stop
Trigeminal neuralgia (TGN) is a recognized initial manifestation of MS, and patients in pain almost always seek dental evaluation before neurological evaluation. Dr. Scott’s rule of thumb is age-based: in patients under 50 who present with TGN, MS sits at the top of the differential diagnosis. In patients over 50, TGN is much more commonly caused by an aberrant blood vessel compressing the trigeminal nerve in the posterior fossa—a structural problem rather than a demyelinating one. Either way, the imaging pathway is the same: an MRI of the brain and brainstem is non-negotiable before any definitive treatment plan is made.
Optic neuritis is the presenting event in roughly 25% of all MS patients, but trigeminal neuritis and trigeminal neuralgia are common enough that dentists, orofacial pain specialists, and oral medicine providers should treat unexplained facial pain in a younger patient as a referral trigger, not a diagnostic dead end.
What MS Actually Is—In One Paragraph
MS is an inflammatory disease of the central nervous system in which repeated attacks strip away myelin, the insulating sheath around nerve fibers in the brain and spinal cord. Symptoms depend entirely on where the inflammation lands: sensory cortex involvement produces numbness or altered sensation; motor pathways produce weakness or spasticity; the brainstem and cerebellum produce balance and gait disorders; the trigeminal nerve roots can produce facial pain. Early in the disease, demyelinated areas can remyelinate and patients recover fully between attacks. Over time, however, the underlying axons begin to break down—and axonal damage is permanent. As Dr. Scott put it, “We cannot give people back what they’ve lost neurologically. None of the medications we have can do that.”
The Four Clinical Types—and Why the Distinction Matters
Roughly 70% of patients first present with relapsing-remitting MS: discrete attacks with periods of recovery in between. Most of those patients will eventually transition to secondary progressive MS in their late 40s or 50s, where the relapses fade but a slow, smoldering axonal degeneration takes over. Primary progressive MS, more common in young males, is chronic from the outset and tends to be less responsive to immune therapies. The fourth category, progressive-relapsing, increasingly looks like part of the same spectrum—as higher-resolution MRI has shown that no relapse leaves a patient entirely unchanged.
The clinical takeaway is straightforward: time matters. Disease-modifying treatments are most effective in the early relapsing-remitting phase. Treat early, treat aggressively, and you preserve neurologic capital that cannot be recovered later.
Diagnosis: Clinical First, Imaging Second
MS remains a clinical diagnosis supported by MRI and, increasingly, cerebrospinal fluid analysis. Dr. Scott performs lumbar punctures far more often now than a decade ago, because CSF analysis helps distinguish MS from a growing list of MS mimics: neuromyelitis optica (NMO), MOGAD (myelin oligodendrocyte glycoprotein antibody disease), lupus, Sjögren’s syndrome, structural lesions, and functional neurological disorders. He also offered a useful caution about MRI: roughly 25% of the general population has scattered white matter lesions on imaging. “You can’t treat an MRI scan,” he said. “You treat the patient.”
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How MS Is Treated Today
The treatment landscape has changed dramatically. Ten years ago there were roughly four disease-modifying treatments (DMTs); today there are more than ten. Most current DMTs target central nervous system inflammation by depleting B cells, T cells, or both; blocking immune cell entry across the blood-brain barrier; or trafficking immune cells into lymph nodes and away from the CNS. The most significant advance has been the monoclonal antibodies—particularly natalizumab, ocrelizumab, and rituximab—where complete cessation of clinical relapses and new MRI lesions is now a realistic treatment goal.
Bone marrow transplantation, studied at a center in Ottawa for more than 15 years, shows promise for young patients with aggressive relapsing-remitting disease, though access is limited and the procedure carries roughly a 1% mortality risk. Dr. Scott also flagged the cautionary tale of the Zamboni procedure—a jugular vein dilatation treatment promoted in the early 2010s that was advocacy-driven rather than evidence-driven, and abandoned after several serious adverse events.
Trigeminal Neuralgia: Medical and Surgical Options
When TGN is caused by MS, open surgical decompression is not an option—there is no vascular structure to fix. First-line treatment remains carbamazepine (Tegretol), which Dr. Scott described as still the most effective medication worldwide despite requiring blood monitoring for neutropenia and liver enzyme elevation. Oxcarbazepine, a closely related metabolite, has a milder side-effect profile and is nearly as effective. Gabapentin, baclofen, lamotrigine, and phenytoin are additional options, generally as second-line or adjunctive agents.
For patients who are not adequately controlled on oral medication, minimally invasive rhizotomies—typically using alcohol to sclerose the affected trigeminal branch—can provide significant relief. The trade-off is a persistent area of facial numbness. As Dr. Scott observed, “For most people with TGN, numbness is way better than trigeminal pain.” Trigeminal neuralgia has historically been called the suicide pain for good reason.
Botox: An Emerging Off-Label Option
Perhaps the most clinically novel section of the conversation concerned botulinum toxin (Botox) for trigeminal neuralgia—still considered off-label, but increasingly part of the treatment armamentarium. Dr. Scott has been using it for TGN over the past four years, building on decades of experience injecting Botox for dystonia, hemifacial spasm, and chronic migraine. His approach is what he calls “chasing the pain”: mapping the affected dermatome from the patient’s description and injecting along that distribution.
Dosing has evolved with experience. Four years ago he was using 30 to 40 units for a maxillary (V2) division case; today he uses 80 to 100 units, with clear patient counseling about the possibility of temporary facial droop. For V2 injections, he targets pre-auricular sites, sub-zygomatic regions, and the nasolabial fold, working medially toward the superior perioral region. For mandibular (V3) injections, cosmetic risk is lower and tolerance has been excellent. Across his cohort of roughly 25 to 30 patients, results are not universal—some respond dramatically, others modestly—but the option is meaningful for patients who have failed medication.
What This Means for Dental Providers
For dentists, oral medicine specialists, and orofacial pain clinicians, the takeaways are clear. Unexplained facial pain in a patient under 50, particularly when it follows a trigeminal distribution, should prompt neurological referral with MRI—not a search for an occult dental etiology. Optic, sensory, motor, or balance symptoms reported alongside the facial pain raise the index of suspicion further. And when patients ask what their referring neurologist might offer, dental providers can now describe a treatment ladder that starts with carbamazepine or oxcarbazepine, escalates through neuropathic pain adjuncts, and increasingly includes Botox before any surgical option is considered. That kind of cross-specialty knowledge is what allows dental clinicians to give patients real options at the moment of referral, rather than pointing them toward an unknown next step.
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