Sensory and autonomic measurements in idiopathic trigeminal neuralgia before and after radiofrequency thermocoagulation: differentiation from some other causes of facial pain

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Abstract
Quantitative measurements of somatosensory thresholds and skin temperature were made before (24 cases), 3-5 days after (12 cases), and 6 months after (11 cases) successful radiofrequency thermocoagulation of the proximal root and gasserian ganglion in 24 cases of idiopathic trigerminal neuralgia (TGN), 18 of whom had not previously undergone any interventional procedure; and in 3 cases of compressive non-TGN neural and 4 of non-neural facial pain at presentation. There were no differences in somatosensory thresholds between the skin innervated by the affected divisions and the unaffected mirror-image areas in previously unoperated cases of TGN and non-neutral facial pain (''atypical facial pain'') prior to operative intervention; but there were significant differences in tactile (von Frey) thresholds in the cases of non-TGN facial pain of neural origin. In TGN immediately after operation, thresholds for all modalities except cold sensation were significantly raised. Six months later, tactile and tragus pinch pain thresholds had returned to normal; but thresholds for warmth, hot pain, and pinprick remained elevated. However, in cases who had had previous procedures for TGN between 9 months and 5 years earlier, all thresholds except pinprick and possibly hot pain had returned to normal. Prior to operation for TGN, the skin temperature in the affected division was significantly lower than that in the contralateral unaffected division, presumably due to vasoconstriction. In previously operated cases in whom TGN had re-appeared, cutaneous vasoconstriction was also demonstrated. This was also true of the 3 non-TGN cases suffering from neurogenic pains presumably due to nerve compression, but not of the non-neural cases (''atypical facial pain''). In parallel with pain relief of TGN by radiofrequency thermocoagulation, skin temperatures had risen by the first postoperative examination to equal those on the normal side and remained so 6 months later provided pain remained absent. It is suggested that cutaneous vasoconstriction plays a role in the pathophysiology of TGN, and that the origin of this and other changes is central rather than peripheral; but certain questions remain to be answered before this hypothesis can be definitely established.