Quantitative sensory testing in classical trigeminal neuralgia-a blinded study in patients with and without concomitant persistent pain

The diagnostic criteria of the third International Classification of Headache Disorders state that there should be no neurological deficits in patients with classical trigeminal neuralgia (TN) at clinical examination. However, studies demonstrating sensory abnormalities at bedside examination in TN patients have questioned this. Our aim was to examine whether TN patients without sensory abnormalities at neurological examination have sensory abnormalities at quantitative sensory testing (QST) and whether there were any QST differences between TN with and without concomitant persistent pain. Thirty-six TN patients were investigated with the standardized QST protocol by the German Research Network on Neuropathic Pain. The investigators were blinded to presence of concomitant persistent pain and symptomatic side. Based on comparison to the German Research Network on Neuropathic Pain controls, z scores were calculated to process frequency analyses and Z-profiles. We found increased mechanical detection threshold on the symptomatic side (47.2% vs 0%, P = 0.008), asymptomatic side (33.3% vs 0%, P = 0.011), and hand (36% vs 0%, P < 0.001) in TN compared with controls. The Z-profiles demonstrated increased mechanical detection threshold on the symptomatic side compared with the asymptomatic side (-2.980 vs -2.166, P = 0.040). Thermal and mechanical hyperalgesia was detected bilaterally in the face and the hand. Trigeminal neuralgia patients with concomitant persistent pain tended to have higher mean z score values compared to TN with purely paroxysmal pain indicative of decreased detection thresholds. Trigeminal neuralgia patients with no sensory abnormalities at neurological examination had generalized subclinical hypoesthesia, which was more pronounced on the symptomatic side, and thermal and mechanical hyperalgesia. This could indicate pain-induced hypoesthesia and sensitization induced by central mechanisms.