Abstract
Neuropeptides and neurotransmitters act as intermediaries to transmit impulses from one neuron to another via a synapse. These neuropeptides are also related to nerve degeneration and regeneration during nerve damage. Although there are various neuropeptides, three are associated with neural regeneration in facial nerve damage: calcitonin gene-related peptide (CGRP), galanin, and pituitary adenylyl cyclase-activating peptide (PACAP). Alpha CGRP in facial motoneurons is a signaling factor involved in neuroglial and neuromuscular interactions during regeneration. Thus, it may be a marker for facial nerve regeneration. Galanin is a marker of injured axons rather than nerve regeneration. PACAP has various effects on nerve regeneration by regulating the surrounding cells and providing neurotrophic factors. Thus, it may also be used as a marker for facial nerve regeneration. However, the precise roles of these substances in nerve generation are not yet fully understood. Animal studies have demonstrated that they may act as neuromodulators to promote neurotrophic factors involved in nerve regeneration as they appear early, before changes in the injured cells and their environment. Therefore, they may be markers of nerve regeneration.
Highlights
IntroductionFacial nerve paralysis can be caused by a variety of conditions, including idiopathies, infection (such as Ramsay Hunt syndrome, otitis media with effusion, acute suppurating otitis media, chronic otitis media, malignant otitis externa, tuberculosis, Lyme disease, and AIDS), trauma (including temporal bone fracture, birth damage, facial lacerations, penetration damage, iatrogenic damage, and radiation injury), tumor (such as cholesteatoma, glomeruloma, malignant tumor, facial neurinomas, meningioma, histiocytosis, and rhabdomyosarcoma), congenital (including crush injuries, Möbius syndrome, and labialis inferior palsy), recurrent (including repetitive facial palsy and Melkersson-Rosenthal syndrome), and metabolic and systemic (such as sarcoidosis, Guillain–Barre syndrome, and autoimmune diseases) [1,2] (Table 1)
Published: 29 October 2021Facial nerve paralysis can be caused by a variety of conditions, including idiopathies, infection, trauma, tumor, congenital, recurrent, and metabolic and systemic [1,2] (Table 1).While facial paralysis is not a life-threatening condition, if recovery is incomplete, patients will experience psychological and social deterioration, which can impact social activities; complete treatment is important [3,4]
It has been reported that neuropeptides are involved in the neurophysiology of the normal facial nerve and in the regeneration process following facial nerve damage
Summary
Facial nerve paralysis can be caused by a variety of conditions, including idiopathies, infection (such as Ramsay Hunt syndrome, otitis media with effusion, acute suppurating otitis media, chronic otitis media, malignant otitis externa, tuberculosis, Lyme disease, and AIDS), trauma (including temporal bone fracture, birth damage, facial lacerations, penetration damage, iatrogenic damage, and radiation injury), tumor (such as cholesteatoma, glomeruloma, malignant tumor, facial neurinomas, meningioma, histiocytosis, and rhabdomyosarcoma), congenital (including crush injuries, Möbius syndrome, and labialis inferior palsy), recurrent (including repetitive facial palsy and Melkersson-Rosenthal syndrome), and metabolic and systemic (such as sarcoidosis, Guillain–Barre syndrome, and autoimmune diseases) [1,2] (Table 1). While facial paralysis is not a life-threatening condition, if recovery is incomplete, patients will experience psychological and social deterioration, which can impact social activities; complete treatment is important [3,4]. Various studies have been conducted on the cure of facial paralysis, no specific biomarkers or complete remedies have been established and the exploration of new materials for neuroregeneration has been slow.
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