Stimulation of morphofunctional repair of the facial nerve with photobiomodulation, using the end-to-side technique or a new heterologous fibrin sealant.

This research evaluated the influence of Photobiomodulation Therapy (PBMT) on lesions of the facial nerve repaired with the end-to-side technique or coaptation with a new heterologous fibrin sealant. Thirty-two Wistar rats were separated into 5 groups: Control group (CG), where the buccal branch of the facial nerve was collected; Experimental Suture Group (ESG) and Experimental Fibrin Group (EFG), in which the buccal branch was end-to-side sutured to the zygomatic branch on the right side of the face or coaptated with fibrin sealant on the left side; Experimental Suture Laser Group (ESLG) and Experimental Fibrin Laser Group (EFLG), in which the same procedures were performed as the ESG and EFG, associated with PBMT (wavelength of 830nm, energy density 6.2J/cm2, power output 30mW, beam area of 0.116cm2, power density 0.26W/cm2, total energy per session 2.16J, cumulative dose of 34.56J). The laser was applied for 24s/site at 3 points on the skin's surface, for a total application time of 72s, performed immediately after surgery and 3 times a week for 5weeks. A statistically significant difference was observed in the fiber nerve area between the EFG and EFLG (57.49±3.13 and 62.52±3.56µm2, respectively). For the area of the axon, fiber diameter, axon diameter, myelin sheath area and myelin sheath thickness no statistically significant differences were found (p<0.05). The functional recovery of whisker movement occurred faster in the ESLG and EFLG, which were associated with PBMT, with results closer to the CG. Therefore, PBMT accelerated morphological and functional nerve repair in both techniques.

[Effect of electroacupuncture on ultrastructural changes of facial nerve in rabbits with facial nerve injury].

OBJECTIVE: To observe the effect of electroacupuncture (EA) on ultrastructure of facial nerve and Schwann cells in facial nerve injury rabbits so as to explore its mechanism underlying improving facial palsy. METHODS: A total of 60 Japanese white rabbits were randomly assigned to normal control (normal, n = 6), sham-operation (sham, n = 18), model (n = 18) and EA (n = 18) groups. The facial nerve injury model was established by clamping the right facial nerve for 5 min by using a pair of forceps. EA (1.5 V, 3 Hz/60 Hz) was applied to "Yifeng" (TE 17)-"Hegu" (LI 4), and "Dicang" (ST4)-"Jiache" (ST6) on the affected side for 30 min, respectively, once daily for 3 weeks. Morphologic changes of the myelin sheath and Schwann cells of the facial nerve were observed by using electron microscope after 1, 2 and 3 weeks' treatment. RESULTS: Compared with the normal control group, the number of the myelin sheaths and the thickness values of the facial nerve after treatment of 1, 2 and 3 weeks in the model group were decreased significantly (P < 0.01, P < 0.05). While in comparison with the model group, the thickness value of the facial nerve 2 weeks after modeling in EA group was increased considerably (P < 0.01). In the model group, there were many vacuoles in the cytoplasm of Schwann cells instead of organells in the facial nerve. In the sham group, the demyelination was milder than that of the model group, and majority of myelin sheaths showed integral structure after 2 and 3 weeks, being similar to the normal group. Compared with the model group, the extent of demyelination was less distinct, with relatively more abundant organells in the facial nerve of the EA group, especially after 1 week of treatment. Among the three time points in the EA group, demyelination was milder in the 1st week not in the other time points. In contrast, along with the continuous EA treatment, the situation became worse after 3 weeks of treatment in the EA group. CONCLUSION: In the acute stage of facial nerve injury, EA intervention can play a positive effect on the repair of the nerve and Schwann cells. However, continuous 3- weeks' EA intervention may worsen the facial nerve injury.

Subthreshold continuous electrical stimulation facilitates functional recovery of facial nerve after crush injury in rabbit.

We sought to determine whether electrical stimulation (ES) with subthreshold, continuous, low-frequency impulses is a viable clinical method for improving functional recovery after facial nerve crush injury. In 10 rabbits, bilateral crush injuries were made on the facial nerve by compression for 30 s with mosquito forceps, causing complete facial paralysis. Subthreshold continuous direct current ES with 20-Hz square-wave pulses was applied to the proximal stump on one side for 4 weeks. Vibrissae movement returned significantly earlier on the ES side, with a less variable recovery time. Electrophysiologically, the stimulated side had a significantly shorter latency, longer duration, and faster conduction velocity. Light and transmission electron microscopy revealed that the electrical stimulation also markedly decreased Wallerian degeneration. The average numbers of fluorescent, double-labeled nerve cells were significantly different between the ES and non-ES sides. This study shows that subthreshold, continuous, low-frequency ES immediately after a crush injury of the facial nerve results in earlier recovery of facial function and shorter overall recovery time.

[Experimental study of mailuoning injection on therapy of hemifacial spasm].

OBJECTIVE: To investigate the protective effect of Mailuoning on the facial nerve demyelination of Hemifacial spasm and provide the data for therapy of Hemifacial spasm. METHOD: 24 New Zealand white rabbits were divided into control group, Saline group and Mailuoning group, on the latter two groups the models of Hemifacial spasm were made by the temporal superficial artery closely contacting the main trunk of facial nerve at stylomastoid foramen. From the 5th week, the Saline and Mailuoning were injected intravenously into ear margin for 2 weeks on Saline and Mailuoning group respectively. At the 7th week, the MDA and SOD in serum were measured, mean while the microstructure and ultrastructure of facial nerve were observed on 3 animal groups. RESULT: The MDA decreased obviously (P < 0.05) and SOD increased significantly (P < 0.01) in Mailuoning group comparing with that of Saline group, while the MDA and SOD showed insignificant changes of Mailuoning group and control group. The facial nerve severely demyelinated and axons retrogressively changed in Saline group but mild in Mailuoning group. CONCLUSION: Mailuoning injection has a significant protective effect on the facial nerve demyelination of Hemifacial spasm and the very important applied value for therapy of Hemifacial spasm.

[Effect of mailuoning injection on calcitonin gene-related peptide expression in facial nerve of rabbits with facial spasm].

OBJECTIVE: To investigate the mechanism of Mailuoning injection (MLN) in protecting facial nerve from injury. METHODS: The New Zealand white rabbit model with facial spasm was established by compressing superficial temporal artery to make artificial demyelinated lesion of the main peripheral facial nerve trunk. The successful establishment was confirmed by using electrophysiological technique to determine abnormal muscle response (AMR) which is a characteristic for facial spasm. MLN was injected continuously through ear marginal vein for 2 weeks. The change of CGRP expression in facial nerve was detected by immunohistochemical technique. RESULTS: As compared with the model group, CGRP expression in facial nerve was significantly increased in the MLN group (P <0.01), and CGRP immunoreactive positive fibers were not seen in the shamoperation group. In the model group, the facial nerve fibers degenerated obviously, myelin sheath loosened and dissociated, the turgent axons with vacuole or even completely disappeared. But the facial nerve lesion was lessened in the MLN group. CONCLUSION: MLN has a significant protective effect on facial nerve demyelination in rabbits with facial spasm, which is closely related with its effect in improving CGRP expression in the facial nerve.

Localization of the Na+-activated K+ channel Slick in the rat central nervous system.

Na+-activated K+ currents (K(Na)) have been reported in multiple neuronal nuclei and the properties of K(Na) vary in different cell types. We have described previously the distribution of Slack, a Na+-activated K+ channel subunit. Another recently cloned Na+-activated K+ channel is Slick, which differs from Slack in its rapid activation and its sensitivity to intracellular ATP levels. We now report the localization of Slick in the rat central nervous system using in situ and immunohistochemical techniques. As for Slack, we find that Slick is widely distributed in the brain. Specifically, strong hybridization signals and immunoreactivity were found in the brainstem, including auditory neurons such as the medial nucleus of the trapezoid body. As has also been shown for Slack, Slick is expressed in the olfactory bulb, red nucleus, facial nucleus, pontine nucleus, oculomotor nucleus, substantia nigra, deep cerebellar nuclei, vestibular nucleus, and the thalamus. Slick mRNA and protein, however, also are found in certain neurons that do not express Slack. These neurons include those of the hippocampal CA1, CA2, and CA3 regions, the dentate gyrus, supraoptic nucleus, hypothalamus, and cortical layers II, III, and V. These data suggest that Slick may function independently of Slack in these regions. Computer simulations indicate that Slick currents can cause adaptation during prolonged stimuli. Such adaptation allows a neuron to respond to high-frequency stimulation with lower-frequency firing that remains temporally locked to individual stimuli, a property seen in many auditory neurons. Although it is not yet known if Slick and Slack subunits heteromultimerize, the existence of two genes that encode K(Na), that are widely expressed in the nervous system, with both overlapping and nonoverlapping distributions, provides the basis for the reported heterogeneity in the properties of K(Na) from various neurons.

Normal evoked otoacoustic emissions with a profound hearing loss due to a juvenile pilocytic astrocytoma.

An interesting case is reported of an 11-year-old girl who experienced a sudden, profound right-sided hearing loss at the age of 5 years after hearing a "pop" and the sound of rushing water in her right ear. At that time the patient was thought to have Mondini's deformity, and a perilymphatic fistula of the oval window in the right ear. Six years later she was diagnosed with a juvenile pilocytic astrocytoma of the pons with an exophytic component extending into the cerebellopontine angle. Of particular interest in this case is the presence of evoked otoacoustic emissions in the right ear with a profound neural hearing loss. The presence of transient evoked and distortion product otoacoustic emissions confirmed normal sensory outer hair cell function and an intact peripheral auditory system in a clinically deaf ear, thus indicating hearing loss due to a neural component instead of a sensory component, which was previously assumed.