Trigeminal neuralgia with enlarged suprameatal tubercle: A case report.

According to the International Classification of Orofacial Pain (ICOP), secondary trigeminal neuralgia can result from various conditions such as tumors in the cerebellopontine angle, arteriovenous malformation, and multiple sclerosis. This case report describes a 41-year-old woman with trigeminal neuralgia caused by narrowing of the cerebellopontine cistern due to an enlarged suprameatal tubercle. Carbamazepine treatment was initially effective, but became inadequate within a few months. Magnetic resonance imaging revealed compression of the trigeminal nerve by the superior cerebellar artery and an enlarged suprameatal tubercle. Microvascular decompression surgery was done to alleviate the neurovascular compression. Dentists should be aware of such anatomical factors contributing to trigeminal neuralgia, particularly in younger patients. Key words:Trigeminal neuralgia, enlarged suprameatal tubercle, microvascular decompression.

Involvement of interferon gamma signaling in spinal trigeminal caudal subnucleus astrocyte in orofacial neuropathic pain in rats with infraorbital nerve injury.

Background: Trigeminal nerve injury causes orofacial pain that can interfere with activities of daily life. However, the underlying mechanism remains unknown, and the appropriate treatment has not been established yet. This study aimed to examine the involvement of interferon gamma (IFN-γ) signaling in the spinal trigeminal caudal subnucleus (Vc) in orofacial neuropathic pain. Methods: Infraorbital nerve (ION) injury (IONI) was performed in rats by partial ION ligation. The head-withdrawal reflex threshold (HWT) to mechanical stimulation of the whisker pad skin was measured in IONI or sham rats, as well as following a continuous intracisterna magna administration of IFN-γ and a mixture of IFN-γ and fluorocitrate (inhibitor of astrocytes activation) in naïve rats, or an IFN-γ antagonist in IONI rats. The IFN-γ receptor immunohistochemistry and IFN-γ Western blotting were analyzed in the Vc after IONI or sham treatment. The glial fibrillary acid protein (GFAP) immunohistochemistry and Western blotting were also analyzed after administration of IFN-γ and the mixture of IFN-γ and fluorocitrate. Moreover, the change in single neuronal activity in the Vc was examined in the IONI, sham, and IONI group administered IFN-γ antagonist. Results: The HWT decreased after IONI. The IFN-γ and IFN-γ receptor were upregulated after IONI, and the IFN-γ receptor was expressed in Vc astrocytes. IFN-γ administration decreased the HWT, whereas the mixture of IFN-γ and fluorocitrate recovered the decrement of HWT. IFN-γ administration upregulated GFAP expression, while the mixture of IFN-γ and fluorocitrate recovered the upregulation of GFAP expression. IONI significantly enhanced the neuronal activity of the mechanical-evoked responses, and administration of an IFN-γ antagonist significantly inhibited these enhancements. Conclusions: IFN-γ signaling through the receptor in astrocytes is a key mechanism underlying orofacial neuropathic pain associated with trigeminal nerve injury. These findings will aid in the development of therapeutics for orofacial neuropathic pain.

Association Between Anxiety and Descending Pain Modulation of Thermal Stimuli in Patients with Burning Mouth Syndrome: A Cross-Sectional Study.

AIMS: To investigate the predictive power of depression and anxiety for conditioned pain modulation (CPM) and to examine the relationships of CPM at 40°C and CPM at 47°C with age, disease-related pain, pain duration, and psychosocial factors in burning mouth syndrome (BMS). METHODS: A total of 22 patients with BMS and 22 healthy female controls participated in this study. Temporal summation was used as the test stimulus for CPM, and subsequent exposure either to a nonpainful (40°C) or a painful (47°C) Peltier thermode was used as the conditioning stimulus. CPM was calculated as the difference in pain perception following the conditioning stimulus. Psychosocial factors were examined using the Profile of Mood States (POMS) and the State-Trait Anxiety Inventory (STAI). RESULTS: State anxiety and tension-anxiety scores were significantly higher for patients with BMS than for control participants. Multiple regression analyses showed that CPM47°C was affected by vigor, fatigue, confusion, and trait anxiety (adjusted R2 = 0.685, F = 5.147, P = .098). The corresponding analysis for CPM40°C showed that the model was not predictive for the following variables: disease-related pain, pain duration, or components of the POMS or STAI. A significant positive correlation was found between CPM47°C and trait anxiety, suggesting that trait anxiety negatively affected the endogenous pain modulation system. CONCLUSION: Increases in trait anxiety reduced the CPM effect. These findings suggest that CPM impairments and increases in trait anxiety are involved in the development of BMS.