Causes Of Injuries

Unilateral palsy or paralysis of the face can be divided into damage above the upper motor neuron and damage involving the lower motor neuron and its distal termination on the facial musculature. Supranuclear palsy spares the frontalis muscle because of the bilateral innervation of the nucleus from both cerebral hemispheres. In these supranuclear palsies, the facial involvement is often the most minor part of the patient’s problems.

Lesions of the lower motor neuron usually involve the entire face. Nuclear lesions usually involve adjacent brainstem structures (abducens, trigeminal nerve). The part of the nerve most commonly damaged appears to lie within the facial canal and at each end of the canal.

The largest etiological category of facial palsy is idiopathic facial palsy (Bell’s palsy), which is often diagnosed by exclusion of other etiologies. It is characterized by a rapid onset of unilateral facial palsy including movements of the forehead, orbicularis oculi, perioral muscles, and platysma. Defective taste sense (anterior two thirds of the tongue) and hyperacusis may additionally be present. The etiology of Bell’s palsy is unknown. There are a number of other causes of facial nerve palsies, which are listed in Box 28-1 .

Central upper facial nerve injuries may occur as a result of tumor surgery at the cerebellopontine angle or from skull base fractures or trauma. In its extracranial course, the facial nerve is most often injured by sharp lacerations. However, the most frequent cause of injury is iatrogenic, occurring during resection of tumors in the parotid gland. Under these conditions, immediate microsurgical repair, including the use of grafts, is indicated. Resection of malignant parotid gland or skull base tumors may necessitate resection of branches of the facial nerve or the nerve itself. It must be decided on an individual basis whether a primary reconstruction of the facial nerve using nerve grafts is indicated. In trauma situations with obvious separation of the facial nerve or its branches, an immediate coaptation must be performed. If during primary trauma care, injury is only suspected or not proved, an expectant attitude should be preferred.

Investigation Of Facial Nerve Functions

In the clinical investigation of a patient with a facial palsy, determination of onset characteristics is very important. In patients with Bell’s palsy, an acute onset (e.g., on waking in the morning after normal facial motion the night before) is typical. Sudden onset may also be present in infectious or inflammatory conditions affecting the facial nerve (e.g., herpes zoster oticus, multiple sclerosis). Patients with tumors usually demonstrate progressive paresis over long periods with initially mild symptoms (e.g., weakness of the labial depressor muscle).

In trauma patients, a delayed onset of facial palsy carries a significantly better prognosis than immediate onset. Associated symptoms may also indicate certain diseases. Oral pain, respiratory infections, and hearing loss may accompany acute otitis media, whereas initial fever, arthritis, and neuropathies may be indicative of Lyme disease. Herpes zoster oticus shows typical additional symptoms (i.e., vesicular eruptions, severe pain).

Temporal bone neoplasms may cause other cranial nerve involvements (cochlear/vestibular nerves and cranial nerves IX, X, and XI → jugular foramen; cranial nerves V, VI, and VII → temporal bone). Lesions of the second, third, fourth, and sixth cranial nerves may suggest multiple sclerosis.

First, a careful observation of voluntary facial movements is undertaken. The symmetry of forehead wrinkling is investigated when the patient is asked to raise the brows. A functioning orbicularis oculi muscle allows for complete closure of the eyelids and absence of visible upward rotation and exposure of the sclera (Bell’s phenomenon).

A forced wide smile distinguishes symmetries of the perioral muscles depending on the buccal and marginal mandibular branches. Comparison of the depth of the nasolabial folds and the symmetrical contraction of the platysma muscle is also important. The Schirmer test measures tear production over a 5-minute period.

Objective methods of determining the secretory function of the parotid and submandibular glands exist. Pure taste sensation may be investigated by using samples of sweet, bitter, acid, and salty substances on the anterior tongue. An audiological investigation may reveal the dysacusis caused by a nonfunctional stapedius muscle, which usually moves the tympanic membrane inward for sound absorption. Laboratory tests of sedimentation rate, treponemal antibody titer, and Lyme disease titer are scheduled. High-resolution computed tomography (CT) is indicated for patients with suspected temporal bone disease (e.g., skull base fracture). Magnetic resonance imaging (MRI) is indicated to detect lesions at the cerebellopontine angle. The typical symptoms of facial nerve injuries are listed in Box 28-2 .

The House-Brackmann classification is often used for rating facial palsy. Grade I refers to normal function without weakness; slight facial asymmetry with a minor degree of synkinesis is classified as grade II. Obvious but not disfiguring asymmetry (e.g., with contracture or hemifacial spasm but residual forehead movement) is judged as grade III. Grade IV represents obvious, disfiguring asymmetry with lack of forehead motion and incomplete eye closure. Asymmetry at rest and only slight facial movement is rated as grade V. Complete absence of tone or motion is grade VI.

Electromyography (EMG) and electroneurography are routinely employed. In cases of acute injury, nerve excitability tests are used, but normal results are less reliable than abnormal results, because functional deficits may occur at a later time. EMG analyzes the function of the muscles during needle insertion and gives information on the existence of spontaneous activity (action potentials) arising from voluntary muscle contraction. Spontaneous activity indicates a pathological process within the nerve, whereas fibrillation potentials may be a sign of nerve disruption.

During evoked EMG, a supramaximal stimulus is applied at the skin surface near the stylomastoid foramen. Intact axons will provide action potentials that can be recorded distally. In facial nerve injury, the amplitude of the action potential is defined as a percentage of the amplitude on the normal side. Magnetic transcranial and electrical stylomastoid stimulation procedures allow for differentiation of lesions and distinction between central and peripheral facial nerve palsies.

Surgical Management

If the distal facial nerve branches and musculature are intact, reinnervation from the proximal facial nerve is ideal. Reinnervation using another motor nerve may be indicated if the proximal facial nerve cannot be identified. Cases with partial return of nerve function are always problematical. The risk of destruction of functional nerve branches during surgery must be weighed against the possible advantages of reconstructive procedures.

The following basic strategies are applied most frequently for surgical correction of facial paralysis and its sequelae.

In light of the types of nerve injury and the general chance of a spontaneous regeneration in neurapraxia and axonotmesis, exact information about the mechanism of the facial nerve injury is mandatory. In cases of a sharp transection in the absence of significant adjacent soft tissue trauma or infection, immediate primary management by a well-trained operating team may be indicated.

Often, it is not known what type of nerve injury is present. Although peripheral dissected facial nerve branches may be identified under magnification or with electrical stimulation, the clinical consequences of these injuries often cannot be judged immediately. Therefore, during primary wound closure, suspected branches of the facial nerve are marked with non-resorbable sutures. The suture material is positioned at the external wound surface to help identify the nerve fibers at a later stage. This allows assessment of the clinical consequences of a nerve injury and performance of micronerve anastomosis under sterile conditions. Primary nerve grafting procedures are avoided.

Nerve reconstruction is performed immediately or within 2 months after the injury through the use of direct nerve coaptation or placement of a nerve graft.

Reconstructions of the facial nerve are limited by the atrophy of the musculature that occurs 6 to 12 months after the injury. Reanimation procedures such as faciofacial and 7th-to-12th nerve (VII-XII) anastomosis are performed not earlier than 6 to 12 months after the trauma. In long-standing facial nerve palsy, muscle grafts are often necessary due to the increasing atrophy of the facial muscles. A suggested algorithm of a staged facial reanimation is shown in Box 28-3 (modified after Volk et al. ).

Microsurgical Techniques

In all microsurgical techniques for facial nerve reconstruction, attempts should be made to get impulses from the ipsilateral facial nerve, such as by a surgical preparation of the nerve out of the tumor or by the use of nerve grafts. If these possibilities do not exist, other procedures (e.g., VII-XII procedures) may be considered.

In cases of primary or early secondary nerve reconstruction after a defined injury, direct identification and preparation of the nerve stumps is usually possible. Coaptation or grafting techniques can then be performed easily.

In secondary microsurgical nerve repair, exploration of the site of the lesion and the stumps of the facial nerve always follows a certain order, especially in cases of peripheral facial nerve palsies in which the extent of the injury is uncertain.

It is easy to identify the facial nerve stumps that have been marked with sutures beforehand. In older secondary lesions, this is not possible, and in these cases, the first step is the systematic preparation of the extratemporal course of the central facial nerve. The identification of the nerve at the stylomastoid foramen is the approach of choice, and tracing the nerve back from the periphery should be attempted only if the central approach is not possible.

The preauricular skin incision runs in an anteriorly curved fashion into the submandibular neck fold. The skin can then be dissected away from the fascia of the parotid gland. The cartilaginous auditory canal and the pointer, anterior to the tragus cartilage, are identified. The main trunk of the facial nerve lies approximately 1 cm caudal to that pointer at the transition level between the cartilaginous and the osseous auditory canal. If the origin of the sternocleidomastoid muscle at the mastoid and the biventer muscle are additionally prepared, the facial nerve trunk will be found to lie cranial to the angle created by these two muscles ( Fig. 28-2 ).

Identification of the facial nerve. 1, Facial nerve. 2, Temporofacial branch. 3, Cervicofacial branch. 4, Digastric muscle. 5, Styloid process. 6, Cartilaginous pointer.

For further preparation, the fibrous tissue fibers between the parotid gland and the osseous auditory canal are separated step by step, and crossing vessels are carefully coagulated. Fatty tissue cranial to the facial nerve is mobilized anteriorly. Then, the approximately 2-mm-thick facial nerve stump is identified with the help of a nerve stimulator. The division into its main branches usually occurs after 1 cm. With a small trunk scissors, the tissue overlying the nerve is dissected away from the nerve and elevated. With a second scissors, this tissue is transected. In this manner, the branches are traced into the periphery of the gland. Among the peripheral branches, the marginal branch may be identified most easily. It lies lateral to the superficial neck fascia and crosses the facial artery and vein. Via the submandibular skin incision, it can be identified at the lateral surface of the submandibular gland and then traced dorsally.

At the superior border of the parotid gland, the temporal and zygomatic branches leave the parotid gland and are identified below the zygomatic arch in the subcutaneous tissue. The buccal branches are found cranial to Stensen’s duct.

After identification of the nerve branches, the first procedure in surgical intervention is external neurolysis with preparation of the tissue surrounding the nerve and resection of the scarred perineurium. If the nerve itself is scarred, intraneural neurolysis is performed to remove cicatricial compression of the nerve fiber bundles caused by an epineural or paraneural scar. Healthy perineurium is left intact so as not to interrupt the blood supply to the individual nerve bundles and the exchange of fibers among the various fascicles.

After neurolysis, the nerve is moved away from the scar tissue bed and placed into healthy tissue to avoid further scar formation.

Direct Nerve Suture Nerve Grafts