| disease | Facial Nerve Injury |
| alias | Facial Nerve Injury |
The incidence of craniocerebral injury accompanied by facial nerve injury is approximately 3%. Among patients with bleeding or fluid discharge from the external auditory canal after injury, about one-fifth may develop ipsilateral facial muscle weakness. The common cause of facial nerve injury is fractures in the petrous part of the middle cranial fossa and the mastoid region. About 50% of longitudinal fractures and 25% of transverse fractures in this area are associated with injury to the VII cranial nerve. Particularly in longitudinal fractures parallel to the long axis of the petrous pyramid, the facial nerve is most susceptible to traction, contusion, or compression by fracture fragments, leading to early-onset or delayed-onset facial nerve palsy.
bubble_chart Clinical Manifestations
Early-onset cases present with immediate facial muscle paralysis after injury, where the affected side loses expression, has incomplete eyelid closure, and the mouth corners deviate toward the healthy side, especially noticeable during crying or laughing. The affected eye often develops exposure keratitis. If the facial nerve injury is proximal to the chorda tympani nerve, the ipsilateral anterior two-thirds of the tongue also loses taste sensation. Delayed-onset cases typically develop facial muscle paralysis 5–7 days post-injury, mostly due to hemorrhage, ischemia, edema, or compression, and have a better prognosis.
The severity of facial nerve injury can be assessed based on the timing and degree of post-injury paralysis, as well as electrical excitability and electromyography tests. If both nerve electrical responses and electromyography are negative, it indicates an interruption in nerve conduction, but it cannot yet determine whether it is an anatomical discontinuity or a physiological block. Over time, repeated testing often allows for an accurate judgment.
bubble_chart Treatment MeasuresThe treatment of facial nerve injury. Since there is a high possibility of recovery after facial nerve injury, early management should primarily involve non-surgical treatment. Dexamethasone and appropriate dehydration measures are used to reduce traumatic reactions and local edema. Neurotrophic drugs and calcium channel blockers are administered to improve nerve metabolism and vascular blood supply, often promoting the recovery of nerve function. Surgical treatment is only employed for patients whose nerves have been severed or who exhibit severe deviation of the mouth and show no improvement after 4–6 months of non-surgical treatment. The goal is not only to restore the motor function of facial muscles but also to correct facial appearance and alleviate psychological stress in patients. Successful reports exist for intracranial reconstruction of facial nerve injuries caused by intraoperative errors; however, no reports exist for the reconstruction of traumatic deviation of the mouth. Early decompression of the facial nerve canal not only yields poor results but may also worsen nerve injury, so it should be approached with caution. In otoneurosurgery, for injuries near the genu of the facial nerve, early exploration of the facial nerve via the middle ear or mastoid approach is often performed. If the nerve is severed, anastomosis is performed. If the nerve is compressed and ischemic, decompression is carried out, and the connective tissue sheath of the nerve's outer membrane is opened. In neurosurgery, persistent complete deviation of the mouth is often treated with alternative repair surgeries, such as facial-accessory nerve anastomosis or facial-phrenic nerve anastomosis. Additionally, facial-hypoglossal nerve anastomosis, which involves using the hypoglossal nerve to repair the facial nerve, leads to atrophy of the ipsilateral tongue muscles, affecting speech and mastication, and is now rarely used.
This procedure involves end-to-end anastomosis of the central segment of the accessory nerve with the peripheral segment of the facial nerve. The surgical method is simple, with a high success rate. Most patients show recovery of facial muscle movement within 3–5 months postoperatively. The drawback is that the sternocleidomastoid and trapezius muscles originally innervated by the accessory nerve will become paralyzed and atrophy, leading to shoulder drop. However, if the sternocleidomastoid branch of the accessory nerve is used while preserving the trapezius branch, shoulder drop can be avoided. Alternatively, anastomosing the descending branch of the hypoglossal nerve with the peripheral segment of the accessory nerve can also mitigate the issue of shoulder drop.
Surgical Method: The procedure is performed under local or general anesthesia, with the patient in a supine position and the head tilted to the healthy side. An incision approximately 7 cm long is made from the root of the mastoid process behind the ear, extending along the anterior border of the sternocleidomastoid muscle to slightly below its midpoint. The subcutaneous tissue is dissected, and blunt dissection is first performed between the upper end of the sternocleidomastoid muscle and the parotid gland. Using a surgical microscope, the facial nerve is carefully identified and freed. The nerve is then traced retrograde along its trunk to the stylomastoid foramen, where the facial nerve is severed at a high position, and the stump is protected with saline-soaked cotton for later use. Next, the anterior border of the sternocleidomastoid muscle is freed, and the muscle is retracted laterally. On its deep surface near the midpoint of the posterior border, the sternocleidomastoid branch of the accessory nerve (the trapezius branch runs parallel and continues posteriorly into the trapezius muscle) is identified. This branch is severed close to the muscle and freed retrograde to ensure tension-free anastomosis. Then, end-to-end nerve anastomosis is performed using 7-0 non-traumatic sutures, with 4–5 stitches in the nerve's outer membrane. After the procedure, the incision layers are sutured as usual, and a rubber drain is placed subcutaneously for 24 hours. Postoperatively, nerve growth factors are administered to promote nerve regeneration.
This involves end-to-end anastomosis of the central segment of the phrenic nerve with the peripheral segment of the facial nerve. This procedure is more complex than facial-accessory nerve anastomosis, as the phrenic nerve must be freed from the neck and transmitted subcutaneously retrograde to the facial nerve incision for anastomosis. However, the advantage is that the phrenic nerve has strong regenerative capacity, and there are numerous anastomotic branches between the two phrenic nerves. Additionally, fibers from the 9th to 12th intercostal nerves are incorporated. Therefore, after unilateral phrenic nerve transection, only temporary ipsilateral diaphragmatic dysfunction occurs, which soon compensates and recovers spontaneously.
Surgical method: The approach to expose the facial nerve is as described above, with the incision simply shortened to the level of the mandibular angle. Additionally, a 5 cm incision parallel to the clavicle is made approximately 3–4 cm above the clavicle, centered on the posterior border of the sternocleidomastoid muscle. The subcutaneous tissue and platysma are dissected, and the posterior border of the sternocleidomastoid muscle is freed and retracted anteriorly to expose the anterior scalene muscle. Under the surgical microscope, the phrenic nerve can be seen crossing obliquely from posterosuperior to anteroinferior over the superficial surface of the anterior scalene muscle. Carefully follow the nerve to incise the fascial membrane, then bluntly dissect the nerve distally, freeing it as far down as possible to obtain sufficient length before transection. Next, dissect the central segment of the phrenic nerve proximally until it can be retrograde-transposed deep to the sternocleidomastoid muscle and introduced into the facial nerve incision. Finally, perform an end-to-end anastomosis between the central segment of the phrenic nerve and the peripheral segment of the facial nerve under no tension. Close the incisions in layers as usual, with subcutaneous drainage for 24 hours. Administer nerve growth factor postoperatively.
Most patients who recover well usually show positive electrical responses within a few days to three weeks after the injury. If there are no signs of recovery by 6 to 8 weeks post-injury, the outcome is generally poorer. Fortunately, approximately 75% of facial nerve injuries can fully recover, about 15% partially recover, and only 10% result in permanent facial muscle paralysis (Mc Hugh, 1959).
