OBJECTIVE: To explore the mechanism of electroacupuncture (EA) in promoting recovery of the facial function with the involvement of autophagy, glial cell line-derived neurotrophic factor (GDNF), and phosphatidylinositol-3-kinase (PI3K)/mammalian target of rapamycin (mTOR) signaling pathway. METHODS: Seventy-two male Sprague-Dawley rats were randomly allocated into the control, sham-operated, facial nerve injury (FNI), EA, EA+3-methyladenine (3-MA), and EA+GDNF antagonist groups using a random number table, with 12 rats in each group. An FNI rat model was established with facial nerve crushing method. EA intervention was conducted at Dicang (ST 4), Jiache (ST 6), Yifeng (SJ 17), and Hegu (LI 4) acupoints for 2 weeks. The Simone's 10-Point Scale was utilized to monitor the recovery of facial function. The histopathological evaluation of facial nerves was performed using hematoxylin-eosin (HE) staining. The levels of Beclin-1, light chain 3 (LC3), and P62 were detected by immunohistochemistry (IHC), immunofluorescence, and reverse transcription-polymerase chain reaction, respectively. Additionally, IHC was also used to detect the levels of GDNF, Rai, PI3K, and mTOR. RESULTS: The facial functional scores were significantly increased in the EA group than the FNI group (P<0.05 or P<0.01). HE staining showed nerve axons and myelin sheaths, which were destroyed immediately after the injury, were recovered with EA treatment. The expressions of Beclin-1 and LC3 were significantly elevated and the expression of P62 was markedly reduced in FNI rats (P<0.01); however, EA treatment reversed these abnormal changes (P<0.01). Meanwhile, EA stimulation significantly increased the levels of GDNF, Rai, PI3K, and mTOR (P<0.01). After exogenous administration with autophagy inhibitor 3-MA or GDNF antagonist, the repair effect of EA on facial function was attenuated (P<0.05 or P<0.01). CONCLUSIONS EA could promote the recovery of facial function and repair the facial nerve damages in a rat model of FNI. EA may exert this neuroreparative effect through mediating the release of GDNF, activating the PI3K/mTOR signaling pathway, and further regulating the autophagy of facial nerves.
Rats ; Male ; Animals ; Rats, Sprague-Dawley ; Electroacupuncture ; Phosphatidylinositol 3-Kinase/metabolism* ; Facial Nerve Injuries/therapy* ; Phosphatidylinositol 3-Kinases/metabolism* ; Beclin-1 ; Glial Cell Line-Derived Neurotrophic Factor ; Signal Transduction ; TOR Serine-Threonine Kinases/metabolism* ; Autophagy ; Mammals/metabolism*

The paper summarizes the academic thought and clinical experience of professor LI De-hua in treatment of facial nerve injury after total parotidectomy with blade needle based on jingjin (muscle region of meridian, sinew/fascia) theory. This disease is located at muscle regions of hand-/foot-three yang meridians; and the sinew/fascia adhesion is its basic pathogenesis, manifested by "transversely-distributed collaterals" and "knotted tendons". In treatment, the knotted tendons are taken as the points. Using the relaxation technique of blade needle, the lesions of sinews/fascia are dissected and removed to release the stimulation or compression to the nerves and vessels so that the normal function of sinews/fascia can be restored.
Humans ; Facial Nerve Injuries/surgery* ; Fascia ; Foot ; Hand ; Lower Extremity

It is well known that trigeminal nerve injury causes hyperexcitability in trigeminal ganglion neurons, which become sensitized. Long after trigeminal nerve damage, trigeminal spinal subnucleus caudalis and upper cervical spinal cord (C1/C2) nociceptive neurons become hyperactive and are sensitized, resulting in persistent orofacial pain. Communication between neurons and non-neuronal cells is believed to be involved in these mechanisms. In this article, the authors highlight several lines of evidence that neuron-glial cell and neuron macrophage communication have essential roles in persistent orofacial pain mechanisms associated with trigeminal nerve injury and/or orofacial inflammation.
Cell Communication ; Cervical Cord ; Facial Pain ; Inflammation ; Macrophages ; Neurons ; Nociceptors ; Trigeminal Ganglion ; Trigeminal Nerve ; Trigeminal Nerve Injuries ; Trigeminal Nucleus, Spinal

Trigeminal neuralgia is caused by compression of trigeminal nerve root and it leads to demyelination gradually. It was almost idiopathic and occurred unexpected. The upper cervical spinal cord contains the spinal trigeminal tract and nucleus. Fibers with cell bodies in the trigeminal ganglion enter in the upper pons and descend caudally to C2 level. We experienced a rare patient with facial pain, which was paroxysmal attack with severe pain after a clear event, cervical spinal injury (C2). So, this case reminds us of a possible cause of trigeminal neuralgia after a trauma of the head and neck.
Cell Body ; Cervical Cord ; Demyelinating Diseases ; Facial Pain ; Head ; Humans ; Neck ; Odontoid Process ; Pons ; Spinal Cord ; Spinal Injuries ; Trigeminal Ganglion ; Trigeminal Nerve ; Trigeminal Neuralgia

OBJECTIVETo investigate the optimal timing for the repair of persistent incomplete facial paralysis by hypoglossal-facial 'side'-to-side neurorrhaphy in rats.

METHODSA total of 30 adult rats with crushed and bulldog-clamped facial nerve injury were randomly divided into 5 groups (n = 6 each) that were subjected to injury without nerve repair or with immediate repair, 2-week-delayed repair, 4-week-delayed repair, or 8-week-delayed repair. Three months later, the effects of repair in each rat were evaluated by facial symmetry assessment, electrophysiological examination, retrograde labeling, and axon regeneration measurement.

RESULTSAt 3 months after injury, the alpha angle significantly increased in the group of rats with 4-week-delayed repair compared with the other four groups. Upon stimulation of the facial nerve or Pre degenerated nerve, the muscle action potentials MAPs were recorded in the whisker pad muscle, and the MAP amplitude and area under the curve in the 4-week-delayed repair group were significantly augmented at 3 months post-injury. Similarly, the number of retrograde-labeled motor neurons in the facial and hypoglossal nuclei was quantified to be significantly greater in the 4-week-delayed repair group than in the other groups, and a large number of regenerated axons was also observed.

CONCLUSIONThe results of this study demonstrated that hemiHN-FN neurorrhaphy performed 4 weeks after facial nerve injury was most effective in terms of the functional recovery of axonal regeneration and activation of facial muscles.

Animals ; Disease Models, Animal ; Facial Nerve ; surgery ; Facial Nerve Injuries ; complications ; surgery ; Facial Paralysis ; etiology ; surgery ; Hypoglossal Nerve ; surgery ; Nerve Regeneration ; Neurosurgical Procedures ; methods ; Rats, Sprague-Dawley ; Treatment Outcome

BACKGROUND AND OBJECTIVES: Controversy related to the choice of surgical approach for vestibular schwannoma (VS) resection remains. Whether the retrosigmoid (RS) or translabyrinthine (TL) approach should be performed is a matter of debate. In the context of a lack of clear evidence favoring one approach, we conducted a retrospective study to compare the morbidity rate of both surgical approaches. SUBJECTS AND METHODS: 168 patients underwent surgical treatment (2007-2013) for VS at our tertiary care center. There were no exclusion criteria. Patients were separated into two groups according to the surgical approach: TL group and RS group. Signs and symptoms including ataxia, headache, tinnitus, vertigo and cranial nerve injuries were recorded pre- and postoperatively. Surgical complications were analyzed. Perioperative facial nerve function was measured according to House-Brackmann grading system. RESULTS: Tumor resection was similar in both groups. Facial paresis was significantly greater in RS group patients preoperatively, in the immediate postoperative period and at one year follow-up (p < 0.05). A constant difference was found between both groups at all three periods (p=0.016). The evolution of proportion was not found to be different between both groups (p=0.942), revealing a similar rate of surgically related facial paresis. Higher rate of ataxic gait (p=0.019), tinnitus (p=0.039) and cranial nerve injuries (p=0.016) was found in RS group patients. The incidence of headache, vertigo, vascular complications, cerebrospinal fluid leak and meningitis was similar in both groups. No reported mortality in this series. CONCLUSIONS: Both approaches seem similar in terms of resection efficacy. However, according to our analysis, the TL approach is less morbid. Thus, for VS in which hearing preservation is not considered, TL approach is preferable.
Ataxia ; Cerebrospinal Fluid Leak ; Cranial Nerve Injuries ; Facial Nerve ; Facial Paralysis ; Follow-Up Studies ; Gait ; Headache ; Hearing ; Humans ; Incidence ; Meningitis ; Mortality ; Neuroma, Acoustic ; Postoperative Period ; Retrospective Studies ; Tertiary Care Centers ; Tinnitus ; Vertigo

A sialocele is a subcutaneous cavity containing saliva, most often caused by facial trauma or iatrogenic complications. In subcondylar fractures, most surgeons are conscious of facial nerve injury; however, they usually pay little attention to the parotid duct injury. We report the case of a 41-year-old man with a sialocele, approximately 5×3 cm in size, which developed 1 week after subcondylar fracture reduction. The sialocele became progressively enlarged despite conservative management. Computed tomography showed a thin-walled cyst between the body and tail of the parotid gland. Fluid leakage outside the cyst was noted where the skin was thin. Sialography showed a cutting edge of the inferior interlobular major duct before forming the common major duct that seemed to be injured during the subcondylar fracture reduction process. We decided on prompt surgical treatment, and the sialocele was completely excised. A duct from the parotid tail, secreting salivary secretion into the cyst, was ligated. Botulinum toxin was administrated to block the salivary secretion and preventing recurrence. Treatment was successful. In addition, we found that parotid major ducts are enveloped by the deep lobe and extensive dissection during the subcondylar fracture reduction may cause parotid major duct injury.
Adult ; Botulinum Toxins ; Facial Nerve Injuries ; Humans ; Intraoperative Complications ; Mandibular Fractures ; Parotid Gland ; Recurrence ; Saliva ; Sialography ; Skin ; Surgeons ; Tail

OBJECTIVES: To investigate neurotoxic effect of bone cement (BC) on facial nerve by using electrophysiological and histopathological methods. METHODS: This study included 20 male albino Wistar rats, divided into four equal groups. Group A was designed as the control group, while group B was sham group. In the group C, BC solution was dropped onto the facial nerve trunks of rats and washed with physiological saline after 5 seconds. In the group D, BC solution was dropped onto the facial nerve trunks of rats and after allowing 5 minutes to dry, wounds were closed. Pre- and postoperative (on 4th week) evoked electromyography (EMG) measurements were done. For histopathological assessments, the rats were euthanized and tissue samples of facial nerve and surrounding areas were collected. RESULTS: According to the wave amplitude levels of evoked EMG, postoperative amplitude levels of group D were significantly decreased, compared to preoperative amplitude levels (P=0.043). We found no statistically significant difference in inflammation among the groups. In none of the groups, foreign body reaction and granulation tissue were not detected in any of the groups. In addition, degeneration in axon, myelin, or perineural nets was not detected in any of the groups. CONCLUSION: This study results suggest that BC has no direct toxicity on facial nerve, while it has indirect effects, by decreasing amplitude. Therefore, we conclude that direct contact of BC with nerve should be avoided, and the area should be cleaned by aspiration or washing with physiological saline in case of contact.
Animals ; Axons ; Bone Cements ; Electromyography ; Facial Nerve* ; Foreign-Body Reaction ; Granulation Tissue ; Humans ; Inflammation ; Male ; Myelin Sheath ; Rats ; Rats, Wistar ; Wounds and Injuries

Facial soft tissue injury due to trauma is common. Severe damage of soft tissue causes functional and cosmetic problems. In the initial evaluation of patients with facial trauma, airway maintenance and respiratory maintenance are the most important. The principles of treatment include adequate irrigation and debridement, primary closure, or secondary wound healing. Postoperative care such as taping, silicone gel sheeting, and sun screening is important to prevent scarring. The scalp and forehead are abundant in blood and can cause severe bleeding. The eyelid is very thin and has a multi-layered structure, requiring accurate suturing and reconstruction of the layers. It is advisable to determine the presence of hematoma in the ear and treat it. When the cheek area is damaged, it is necessary to identify and treat the damage of the parotid gland and the facial nerve branch. The lips should be sewn with the white roll of lip and vermillion.
Cheek ; Cicatrix ; Debridement ; Ear ; Eyelids ; Facial Nerve ; Forehead ; Hematoma ; Hemorrhage ; Humans ; Lip ; Mass Screening ; Parotid Gland ; Postoperative Care ; Scalp ; Silicon ; Silicones ; Soft Tissue Injuries ; Solar System ; Wound Healing ; Wounds and Injuries

OBJECTIVES: The aim of this study is to investigate the efficacy of locally applied insulin-like growth factor 1 (IGF-1) on the recovery of facial nerve functions after crush injury in a rabbit model. METHODS: The rabbits were randomly assigned into three groups. Group 1 consisted of the rabbits with crush injury alone; group 2, the animals applied saline solution onto the crushed facial nerve and group 3, IGF-1 implemented to the nerve in the same manner. Facial nerve injury was first electrophysiologically studied on 10th and 42nd days of the procedure. The damage to the facial nerves was then investigated histopathologically, after sacrification of the animals. RESULTS: In the electrophysiological study, compound muscle action potential amplitudes of the crushed nerves in the second group were decreased. In pathological specimens of the first and second groups, the orders of axons were distorted; demyelination and proliferation of Schwann cells were observed. However, in IGF-1 treated group axonal order and myelin were preserved, and Schwann cell proliferation was close to normal (P < 0.05). CONCLUSION: Local application of IGF-1 in a slow releasing gel was found efficacious in the recovery of the facial nerve crush injury in rabbits. IGF-1 was considered worthy of being tried in clinical studies in facial nerve injury cases.
Action Potentials ; Animals ; Axons ; Cell Proliferation ; Demyelinating Diseases ; Facial Nerve Injuries ; Facial Nerve* ; Insulin* ; Insulin-Like Growth Factor I ; Models, Animal ; Myelin Sheath ; Rabbits ; Schwann Cells ; Sodium Chloride