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  • Title: Trigeminal neuropathic pain: pathophysiological mechanisms examined by quantitative assessment of abnormal pain and sensory perception.
    Author: Eide PK, Rabben T.
    Journal: Neurosurgery; 1998 Nov; 43(5):1103-10. PubMed ID: 9802854.
    Abstract:
    OBJECTIVE: This study was undertaken to examine the pathophysiological characteristics of trigeminal neuropathic pain. METHODS: The study included 23 consecutive patients with trigeminal neuropathic pain (15 patients with pain after nerve injury and 8 patients with pain of spontaneous origin). For each patient, quantitative examination of sensory and pain perception was performed in the painful facial skin area, and results were compared with the findings for the contralateral nonpainful facial skin area. RESULTS: In the painful facial skin area of patients with neuropathic pain after nerve injury, we demonstrated increased temperature and tactile thresholds, as well as abnormal temporal summation of pain (i.e., repetitive nonpainful skin stimulation produced an abnormal progressive increase of pain intensity, with abnormal radiation of pain and aftersensation). In the painful skin area of patients with pain of spontaneous origin, temperature and tactile thresholds were not increased, but heat pain and cold pain thresholds were significantly reduced, indicating heat and cold hyperalgesia. The characteristics of temporal summation of pain were not significantly altered in the painful facial skin area in this group of patients. CONCLUSION: This clinical study provides evidence that the pathophysiological mechanisms of trigeminal neuropathic pain after nerve injury involve impaired function of both small unmyelinated fibers and large myelinated fibers. An explanation for the finding of abnormal temporal summation of pain may involve hyperexcitability of central wide-dynamic range neurons. The results suggest that other mechanisms are involved in trigeminal neuropathic pain of spontaneous origin. Reduced heat and cold pain thresholds indicate heat and cold hyperalgesia, which possibly may be explained by sensitization of peripheral C nociceptors.
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