Changes Of Function, Morphology And Neurotrophic Factor â…¢ Of Facial Nerve In Three Injured Patterns

ObjectiveFacial palsy resulted from trauma is common in all peripheral facial paralysis, approximately account to 1/3. 80% of the reason for facial palsy is temporal bone fractures, and mastoid surgery, secondly. Different injuries cause different severity and the extent of involvement of the facial nerve, And the extent of damage are directly related with the prognosis. Therefore, we should first determine the location and the degree of injury, then select reasonable and appropriate treatment prescription. In clinical, we usually contrast injured side and uninjured compound action potential (CAP), through electro-neurogram (ENoG), then calculating the percentage of nerve degeneration. In fact, facial nerve fibers are not completely cut off in most traumatic facial paralysis. Because nerve conduction of surviving fibers was destroyed by extrusion, pull, fracture, temperature and other forms injury, these fibers' CAP can not be measured at this time. Since this block is reversible, their function can be fully restored when causes were eliminated or after an appropriate time. So we can only speculate the number of injury nerve fibers by this method, but not find out the degree and nature of injury from the perspective of histopathology. Because the facial nerve trunk travels in the narrow facial nerve canal, it is difficult to understand directly the pathological and physiological changes of the facial nerve after temporal bone trauma or iatrogenic injury in clinical. This study attempts to create three different facial nerve injury models, to observe the changes of function, morphology and neurotrophic factorâ…¢(NT-3) after injury, and to discuss the function and structure of facial nerve. According this we can provide a theoretical and experimental basis for choosing and evaluating the surgery in traumatic facial paralysis.MethodsChanges of facial nerve function were assessed in 45 rats by observing their blink reflex (BF), vibrissae movement (VM) and position of nasal tip in response to three injured patterns, i.e., partial extratemporal segment lesion (group i), partial facial canal segment lesion (group ii) and complete facial canal segment lesion (groupiii). Subsequently, all facial nerves were cut into two parts at the site of the lesion after being taken off at 1st, 7th and 21st post-surgery-days(PSD). Changes of morphology and NT-3 expression were evaluated using the improved trichrome stain and immunohistochemistry techniques, respectively.Results1. Changes in facial nerve function: In group i, all animals had no blink reflex (BF) and little vibrissae movement (VM) at the 1st PSD; The blink reflex in 80% of the rats recovered partly and the vibrissae movement in 40% of the rats returned to normal at the 7th PSD; The facial nerve function in 60% of the rats was almost normal at the 21st PSD. In group ii, all left facial nerve paralyzed at the 1st PSD; The blink reflex partly recovered in 40% of the rats and the vibrissae movement was little in 80 % of the rats at the 7th PSD; 80% of the rats' BF were almost normal and 40% of the rats' VM completely recovered at the 21st PSD. In groupiii, no recovery happened at anytime.2. Changes in morphology: In group i, the size of nerve fiber differed in facial canal segment and some of myelin sheath and axons degenerated at the 7th PSD; The fibers' degeneration turned into regeneration at the 21st PSD; In group ii, what we saw in this group was familiar with the group 1 while the degenerated fibers were more and dispersed in cross-section at the 7th PSD; Regeneration of nerve fibers happened at the 21st PSD. In groupiii, most of the fibers crumbled at the 7th PSD and no regeneration was seen at the 21st PSD. 3. Changes in NT-3: Positive staining of NT-3 was largely observed in axons at the 7th PSD, although little NT-3 was seen in the normal fibers.ConclusionsFacial palsy of the rats in group ii is more extensive than that in group i and their function partly recovers at the 21st PSD. The fibers' degeneration occurs not only at the lesion site but also at both side of the lesion and disperses in cross-section. NT-3 immunoreactivity increases in activated fibers after partial facial nerve injury.