Non-neuronal cells act as crucial players in neuropathic orofacial pain.

BACKGROUND: Following peripheral nerve damage, various non-neuronal cells are activated, triggering accumulation in the peripheral and central nervous systems, and communicate with neurons. Evidence suggest that neuronal and non-neuronal cell communication is a critical mechanism of neuropathic pain; however, its detailed mechanisms in contributing to neuropathic orofacial pain development remain unclear. HIGHLIGHT: Neuronal and non-neuronal cell communication in the trigeminal ganglion (TG) is believed to cause neuronal hyperactivation following trigeminal nerve damage, resulting in neuropathic orofacial pain. Trigeminal nerve damage activates and accumulates non-neuronal cells, such as satellite cells and macrophages in the TG and microglia, astrocytes, and oligodendrocytes in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1-C2). These non-neuronal cells release various molecules, contributing to the hyperactivation of TG, Vc, and C1-C2 nociceptive neurons. These hyperactive nociceptive neurons release molecules that enhance non-neuronal cell activation. This neuron and non-neuronal cell crosstalk causes hyperactivation of nociceptive neurons in the TG, Vc, and C1-C2. Here, we addressed previous and recent data on the contribution of neuronal and non-neuronal cell communication and its involvement in neuropathic orofacial pain development. CONCLUSION: Previous and recent data suggest that neuronal and non-neuronal cell communication in the TG, Vc, and C1-C2 is a key mechanism that causes neuropathic orofacial pain associated with trigeminal nerve damage.

Quantitative sensory testing in trigeminal traumatic neuropathic pain and persistent idiopathic facial pain / Teste sensitivo quantitativo em dor neuropática trigeminal pós-traumática e dor facial idiopática persistente

The objective of this article was to investigate, with a systematic protocol of quantitative sensory testing, patients with persistent idiopathic facial pain (PIFP) and others with trigeminal traumatic neuropathic pain (TTN) compared to controls. Thirty patients with PIFP, 19 with TTN, and 30 controls were evaluated on subjective numbness and dysesthesia and with a systematic protocol of quantitative sensory testing for thermal evaluation (cold and warm), mechanical detection (touch and pinpricks for mechanical pain), superficial pain thresholds, and corneal reflex. We found that PIFP and TTN had numbness and dysesthesia higher than controls (p<0.001 and p=0.003), and that in both of them mechanical pain by pinpricks detection was abnormal intra and extra orally at the mandibular branch (p<0.001). Cold, warm, and tactile detections and pain thresholds were similar among the groups. Corneal reflex was abnormal in TTN (p=0.005). This study supports neuropathic mechanisms involving pain processing in PIFP and that the criterion on absence of sensorial variations in PIFP should be revised.

O objetivo deste artigo foi investigar, com um protocolo sistemático de testes sensitivos quantitativos, pacientes com dor facial idiopática persistente (DFIP) e outros com dor neuropática trigeminal traumática (DNTT) comparado aos controles. Trinta pacientes com DFIP, 19 com DNTT e 30 controles foram avaliados quanto à dormência e à disestesia subjetiva e por meio de um protocolo sistemático de testes sensitivos quantitativos, que incluiu avaliação térmica (frio e quente), detecção mecânica (táctil e alfinetes), limites de dor superficial e reflexo córneo-palpebral. Foi observado que os pacientes apresentaram mais dormência e disestesia do que os controles (p<0,001 e p=0,003), além de mais anormalidades intra e extraorais no ramo mandibular (p<0,001). As alterações de calor, frio, dor e tato foram semelhantes entre os grupos. O reflexo córneo-palpebral foi anormal somente no grupo com DNTT (p=0,005). Este estudo suporta mecanismos de dor neuropática envolvidos no processamento da DFIP, e o critério de ausência de variações sensoriais nesta deve ser revisto.