Botulinum toxin in pain management of trigeminal neuralgia: literature review

Abstract

BACKGROUND AND OBJECTIVES: Inflammation is a defense response of the body to a cellular damage caused by physical, chemical or biological agents, which triggers, among other factors, pain. Although inflammation plays an important role in the protection and regeneration of tissue injury, inflammatory pain results in decreased quality of life. In view of this, the development of safe and less invasive forms for the treatment of inflammatory pain is of great importance. The objective of this study was to evaluate the antihyperalgesic potential of the culture supernatant of keratinocytes and human fibroblasts in an experimental model of inflammatory hyperalgesia. METHODS: Evaluation of carrageenan induced inflammatory hyperalgesia through the use of electronic von Frey in animal models treated with culture supernatant of keratinocytes and fibroblasts. RESULTS: Local administration of naloxone, a nonselective opioid antagonist, in peripheral tissue, has been observed to inhibit the antihyperalgesic effect of the keratinocyte culture supernatant. Fibroblast culture supernatant on days 1 and 3 reverses for 2 hours the carrageenan induced inflammatory hyperalgesia, which is mediated by µ opioid agonist. CONCLUSION: This study indicates that culture supernatant of fibroblasts and keratinocytes is capable of inducing antinociception in inflammatory hyperalgesia, mediated by the release of Evaluation of the keratinocytes or fibroblasts culture supernatant in an inflammatory hyperalgesia model Avaliação do sobrenadante da cultura de queratinócitos ou fibroblastos em modelo de hiperalgesia inflamatória

Diagnosis and Treatment of Patients with Trigeminal Neuralgia: A Review

“…Botulinum neurotoxin (BoNT) is derived from the bacterium Clostridium botulinum and characterized by a group of homologous chain proteins with seven serotypes (A, B, C1, D, E, F e G). 16 It is widely used in esthetic treatments and in cases of disorders, such as dystonia and muscle spasms. 17,18 Type A BoNT (BoNT/A) inhibits the release of acetylcholine (ACh) at the cholinergic nerve endings of the motor nerves, as it prevents ACh vesicles from binding to the membrane for the release of content and subsequent binding to receptors on the postsynaptic membrane.…”

“…17,18 Type A BoNT (BoNT/A) inhibits the release of acetylcholine (ACh) at the cholinergic nerve endings of the motor nerves, as it prevents ACh vesicles from binding to the membrane for the release of content and subsequent binding to receptors on the postsynaptic membrane. 16 This blockade leads to the desired esthetic and therapeutic effect, as it weakens the muscle for a period of three to four months. 16 BoNT/A has a beneficial effect in the treatment of neuropathic pain, [19][20][21][22] with antinociceptive and antiinflammatory activity.…”

“…16 This blockade leads to the desired esthetic and therapeutic effect, as it weakens the muscle for a period of three to four months. 16 BoNT/A has a beneficial effect in the treatment of neuropathic pain, [19][20][21][22] with antinociceptive and antiinflammatory activity. BoNT/A acts at peripheral and central sites.…”