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Facial-onset sensory-motor neuronopathy (FOSMN) first manifests with trigeminal sensory loss and pain, then spreads to bulbopontine and spinal motoneurons, sometimes with a fatal outcome.1,2

Objective: In this clinical and neuroimaging study, we sought information on the possible role of neurovascular compression in multiple sclerosis (MS)–related trigeminal neuralgia (TN). Methods: After screening 1,628 consecutive patients with MS, we enrolled 28 patients with definite unilateral MS-related TN. In these patients, we acquired dedicated 3T MRI scans, identified pontine demyelinating plaques, and, using highly specific diagnostic criteria, distinguished possible neurovascular compression. Results: MRI scans in most patients showed a demyelinating plaque in the pontine trigeminal root entry zone on the affected side. The frequency of the neurovascular compression and its association with the pontine demyelinating plaque were higher on the affected than on the unaffected side (54% vs 0%; p = 0.0001). Conclusions: Our observation that in many patients with MS-related TN a pontine demyelinating plaque and neurovascular compression coexist should prompt neurologists to seek possible neurovascular compression in patients with MS-related TN.

Editors' Note: In WriteClick this week, Dr. Tenser, referencing “A dual concurrent mechanism explains trigeminal neuralgia in patients with multiple sclerosis,” argues that vascular compression has been overemphasized as an etiology in trigeminal neuralgia (TN) and hypothesizes a CNS etiology. Authors Truini and Cruccu disagree with his reasoning and reemphasize the importance of root entry zone demyelination in pathogenesis. In reference to “Neurologic signs and symptoms frequently manifest in acute HIV infection,” Drs. Kamtchum-Tatuene et al. and authors Hellmuth et al. agree that neurologic symptoms in acute HIV infection are typically mild and possibly underestimated. Both groups stress the importance of timely HIV diagnosis and rapid initiation …

A 65-year-old man presented with a 2-month history of paroxysmal, stabbing pain at the base of the tongue and the left tonsillar fossa, triggered by swallowing and yawning. The remaining clinical and neurologic examinations were unremarkable. We diagnosed glossopharyngeal neuralgia and prescribed oxcarbazepine 300 mg 3 times a day that consistently relieved pain.1 Cerebral MRI showed juxtaposition of the left glossopharyngeal nerve and the vertebral artery, with abnormal glossopharyngeal nerve contrast enhancement (figure). The abnormal glossopharyngeal nerve contrast enhancement suggests inflammatory changes, possibly induced by irritation secondary to arterial pulsations on the nerve.