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Management of Facial Paralysis after Intracranial Surgery

by Mack Chen, MD and Michael McKenna, M.D
Stephen B. Tatter, M.D., Ph.D., HTML editor


Despite improvements in microsurgical techniques and intraoperative facial nerve monitoring, it is often impossible to preserve normal facial nerve function when removing tumors with intrinsic facial nerve involvement. This is especially true for large acoustic tumors and posterior fossa meningiomas. Although the facial nerve is anatomically preserved in many cases, the function may be completely lost, resulting in a complete facial paralysis. In this circumstance, full facial paralysis is often physiologically and psychologically devastating to the patient. Associated problems include painful corneal irritation, visual loss, difficulties in eating and speaking and in the worse circumstance, self-imposed social isolation. The successful management of this problem is best accomplished by a multi-disciplinary approach utilizing ihe expertise of neurosurgeons, oculoplastic surgeons, otolaryngologists, psychologists, psychiatrists, and facial reconstructive surgeons. Successful facial reanimation requires careful analysis of the patient's deficits, appropriate reconstructive procedures, and a concentrated period of rehabilitation following surgical reconstruction.

Although a variety of reconstructive methods for the management of facial paralysis have been described, the great majority of patients can be successfully managed with a few relatively simple and reliable techniques. Patient age, general health, skin laxity, neurological deficits, and expected nerve recovery must all be taken into consideration. Even under the best of circumstances, it is impossible to restore perfect dynamic facial symmetry. For this reason, it is essential to accurately assess the patient's expectations and counsel them as to reasonable expected results. The use of patient pre- and post-operative video tapes and discussion with other patients who have undergone similar procedures can be extremely useful.

Numerous scales for the assessment of facial nerve paralysis and recovery have been proposed. Although they are useful for purposes of discussion, pre- and post-operative photographic documentation is essential in patient evaluation and in the evaluation of surgical results.

In the past it has been common practice to allow for up to two years of complete recovery after complete paralysis before contemplating surgical reanimation. With this approach, it is often three to four years before rehabilitation occurs. This unnecessary delay may be significantly reduced by offering patients early reanimation procedures that do not adversely affect normal facial nerve regeneration and potential facial movement. We have found the temporalis muscle transposition in conjunction with a gold-weight implant and lower lid tightening to be the most useful combination of techniques in achieving this goal. Although it is difficult to predict the overall long-term recovery in many cases, the length of time for recovery to occur can usually be predicted by certain clinical criteria. Early surgical rehabilitation should be considered in cases where prolonged recovery is expected or when the overall recovery is uncertain. This approach can reduce the period of facial disability from years to weeks.

Patients with complete facial paralysis require immediate attention to the eye to prevent problems associated with corneal exposure. These patients should undergo oculoplastic surgery for corneal protection. This may be in the form of tarsorrhaphy, gold-weight implantion, placement of an ocular spring, or a combination of these procedures. All of these procedures are reversible if facial nerve recovery occurs. Aggressive corneal protection is especially important if a fifth cranial nerve deficit is present in conjunction with a full facial paralysis For this reason, if patients are reluctant to consider full facial reanimation, surgical protection of the eye must be encouraged. Preoperative patient counseling of the possible need for surgery to correct the eye should be included in the discussion concerning the potential for postoperative facial paralysis.

Predicting Facial Nerve Recovery

Accurate prediction of the long-term facial nerve recovery with complete paralysis after intracranial surgery is difficult, and although general guidelines are useful, the long-term results are not always uniform. Facial movement in the immediate postoperative period is the best prognostic sign for long term recovery, even if complete paralysis ensues. The ability to stimulate the facial nerve at the brain stem with a low voltage is another good prognostic sign. However, inability to stimulate the nerve at low voltage does not always correspond to poor recovery.

Table 1.

Ancillary procedures.

Facial nerve is transected at surgery and grafted.

These are among the least predictable group of patients. Results in this group vary from no recovery to recovery of all movement in all divisions with synkinesis. The endpoint for recovery may require 12 to 18 months. Electrical testing is of no use in predicitng recovery. Based on experience, the surgeon who has performed the repair can give the best prediction for recovery.

Facial nerve is anatommically intact but does not stimulate at the brainstem and there is no facial movement in the immediate postoperative period. Recovery in this group of patients is generally poor. If recovery does occur, the endpoint may requir 18 months. The best recovery to be reasonably hoped for is reinstutuion of resting tone and weak movement with synkinesis. Electroneurography (ENoG) in the early postoperative period generally demonstrates an absent compound action potential suggestive of sever neural degeneration.

Facial nerve is anatomically intact, stimulates at low voltage, but no movement immediately after surgery. In this group of patients, ENoG may be particularly useful in the postoperative period. If the compound action potential of the paralyzed side remains greater that 10% of that of the normal side after one week, then a good recovery usually occurs, although it may require several months.

Facial nerve is anatomically intact, there is some movement in the immediate postoperative period, but complete paralysis ensues within hours. This group generally has a satisfactory recovery. It is important that real significant movement is appreciated

ENoG is only of limited value in predicting the degree of overall recovery. It is most helpful during the first two postoperative weeks. It may be useful in distinguishing severe injuries with neural degeneration from neuropraxic irjury. Intramuscular electromyography may be useful in detecting reinnervation after injury and prolonged paralysis, before detectable motion is present. It is of no value in the late postoperative period.

Ocular Management in Facial Paralysis

Paresis of the orbicularis oculi muscle results in diminished blink, incomplete eyelid closure (lagophthalmos), impairment of the nasolacrimal pumping system, and occasional eyelid malposition (paralytic ectropion). The blink reflex and lid position are important in maintaining the ocular surface epithelial integrity. Each blink physically spreads the tear film over the ocular surface and allows for a continuous layer of moisture. The precorneal tear film continuity is also dependent on the volume of tears produced by the lacrimal gland, the surfectant properties of the tear film resulting from its biochemical composition, and the microanatomic state of the surface epithelium. Lack of blinking and incomplete eyelid closure result in increased evaporation from the ocular surface, discontinuity of the precorneal tear film, and degenerative changes in the surface erosions (exposure keratitis) and ulceration which ultimately can result in permanent visual loss. When intrinsic corneal disease coexists with paralytic lagophthalmos (e.g. neurotrophic keratitis with corneal anesthesia) or decreased tear production (e.g. autonomic facial nerve involvement), ocular surface deterioration is often accelerated.

The ophthalmic management of paralytic lagophthalmos is directed at maintaining a normal corneal epithelium which provides comfort and preserves visual acuity. Initial management would include an ocular lubricant such as a tear substitute or ointment (Lacrilube, Hypotears ointment, etc.) used at varying intervals. Ointments are more effective in corneal protection; however, they often substantially blur vision. If this is not effective or if the paralysis is expected to persist, more permanent therapy would include procedures which narrow the palpebral fissure such as tarrsorhaphy, lower-lid elevation with spacers, medial canthoplasty or procedures which increase the amplitude of the blink reflex such as gold weight or spring implant. If paralytic ectropion is present, correction of this lid malposition can be very helpful in relieving symptoms and signs of corneal exposure.

Tarsorrhaphy has been the standard method of managing exposure keratitis and is often effective if large enough. However, larger tarsorrhaphies are disfiguring and do limit peripheral vision. Generally, a lateral tarsorrhaphy of <5 mm is not noticeable and can be integrated with other procedures to obtain optimal results. Medial tarsorrhaphies are always disfiguring and should only be used as a last resort in managing surface exposure. The tarsorrhaphy should include a tongue-in-groove technique that does not disturb the lash follicles at the anterior lid margins. "Bedside" lid margin scraping procedures with suture approximation may disrupt the lash line and lead to trichiasis or heal with lateral palpebral angle webbing.

If a 5 mm tarsorrhaphy is not sufficient to manage the exposure keratitis, then a reanimation procedure should be considered. Gold-weight implantation is the most direct and effective method of enhancing the blink reflex. Gold was chosen for this implant because this metal best matches Caucasian skin color. The weights are supplied by the Meddev Corporation and vary from 0.6 to 1.6 grams. The weights are taped to the pretarsal portion of the upper lid to determine which size will be needed to reduce the lagophthalmos. The heavier weights can induce ptosis and patients should be warned of this complication. .1.0 to 1.2 grams are most commonly used. An incision is made at the upper lid crease exposing the anterior surface of the tarsal plate, and the weight is fixed to the anterior surface of the tarsus with at least 8-0 nylon through three separate holes (Fig 1 ). The skin-muscle flap is closed in separate layers. Edema of the upper lid often persists for several weeks. Complications include extrusion and distortion of the lid fold and crease, infection, ptosis, and persistent corneal exposure symptoms.

Figure 1. The gold weight is placed over the anterior surface of the tarsal plate and fixed with 8-0 nylon through three separate holes.

This procedure is potentiated by concomitant lateral tarsorrhaphy or lower-lid elevation with spacers. Spring implants made from orthodontic wire can increase the amplitude of the blink reflex. The orthodontic wire spring is fixed to the lateral orbital rim periosteum with the other end of the spring passed under the orbicularis muscle to the mid-tarsal position. The tension produced by the spring is also judged and adjusted by preoperatively fixing one limb of the spring to the lateral orbital rim and assessing the reduction in lagophthalmos. In order to limit extrusions, the pretarsal end of the spring is covered with a Dacron sleeve.

Paralytic ectropion often responds to horizontal lid shortening. This lid malposition is often more common in older patients with pre-existing lid laxity and canthal tendon dehiscences.

Lower lid elevations can be accomplished with cartilage or scleral spacers. The spacer is placed between the lower-lid retractor (capsulopalpebral fascia) and the inferior border of the tarsal plate. A subciliary or a transconjunctival approach can provide the surgical exposure to insert the spacer.

Ophthalmic follow-up with slit lamp examination and flourescein staining are advised to assess corneal and visual status after any lid procedure.

Reconstruction of the Paralyzed Face

Each patient with facial paralysis requires a detailed analysis of the individual's particular concerns and physical deformities. Multiple surgical techniques have been described and advocated for facial reanimation after facial nerve paralysis. In our experience the most versatile technique for early facial reanimation utilizes temporalis muscle transposition. This technique can be used to achieve early facial reanimation and improve facial symmetry without affecting potential facial nerve recovery. Because of this, it can be performed in the early postoperative period when long-term results remain uncertain. Patients can expect an immediate improvement in facial symmetry at rest, and in the majority of cases, movement in the corner of the mouth which allows the patient to produce an organized and controlled smile within six weeks of the operation. This procedure can be performed in conjunction with a hypoglossal-facial nerve anatomosis in which the hypoglossal nerve is split and anastomosed to a lower branch of the facial nerve. This results in limited problems with movement of the tongue and prevents mass facial movement which has been a recurrent problem in full hypoglossal nerve procedures. In our experience the resultant reanimation using the parital hypoglossal-facial nerve is more natural than that achieved by anastomosis of the entire hypoglossal nerve to the main trunk of the facial nerve

Preoperative Planning

Temporalis muscle transfer for reconstruction of the paralyzed face is not a difficult surgical maneuver. However, the use of this technique to create a meaningful, organized, and symmetrical smile pattern is challenging. The preoperative evaluation of the patient's smile pattern, the selection of the proper amount and orientation of the temporalis muscle, and the optimal insertion and tension of the temporalis muscle at the time of surgery all affect the final surgical result.

Figure 2: The vascular and neural supply to the temporalis muscle lies on the medial aspect of the muscle with dtstribution in an arcadian pattern from the trigeminal nerve and the internal maxillary artery.

Operative Technique

The temporalis muscle itself is broadly based, arises from the temporal line, and inserts into the coronoid process of the mandible. The vascular supply from the internal maxillary artery is of surgical importance as the preservation of this consisient blood supply is important to the viability of the muscle to be transferred for facial reanimation. The neural supply is from the trigeminal nerve and courses into the undersurface of the muscle in the area of the zygomatic arch to provide innervation to the muscle in an arcadian pattern.

(Fig. 2) The temporalis muscle has many characteristics which make it highly suitable for use in facial reanimation. The muscle is relatively short (3-5 cm), thin (2-3 mm), and has a contractual capability of 1 to 1.5 cm. The mid-portion of the muscle has sufficient strength to adequately mobilize the face and to resist the forces of soft tissue fibrosis.

Figure 3: The incisions utilized in temporalis muscle transfer reconstruction extend from the midportion of the superior auricular helix to a point above the temporal line. An extension of this incision may be executed if partial cranial nerve 7 to 12 anastomosis is performed. The vermilion incision is designed 1.5 to 2.0 cm along the upper and lower borders of the lips.

After adequately evaluating the orientation of the patient's smile on the unaffected side, temporalis muscle transposition is planned. The incision is designed to extend from the midportion of the superior auricular helix and courses above the temporal line with tangential extensions of the vertical incision above the temporal line to gain full exposure of the temporalis muscle (Fig 3). The initial incision allows for the development of a separate temporoparietal fascial flap. This flap is mobilized laterally and is used to reconstruct the secondary temporal fossa defect which is created when the temporalis muscle is used. The muscular fascia is exposed anteriorly to the temporal hairline and posteriorly for a distance of 5 to 6 cm. The incision is then extended in the pretragal area to allow access for facial disseclion. An important point is the transfer of the plane of dissection to the temporoparietal fascia. By transferring to this plane of dissection, the risks of peripheral facial nerve injury are minimized. This technical detail is especially important in those patients in whom eventual recovery of facial function is anticipated. Using sharp dissection, an area of approximately 4 to 5 cm is undermined from the zygomatic arch to the oral commissure. A vermilion incision is made at the oral commissure extending 1.5 to 2 cm along the upper and lower lip. The lateral aspect of the orbicularis oris muscle varies in its fullness and anatomical characteristics depending upon the duration of facial paralysis.

With the facial flap fully elevated and with the surgeon able to pass both index fingers comfortably from the zygomatic arch to the vermilion border at the oral conimissure (Fig. 4), determination of temporalis muscle width, orientation and elevation of the muscle flap are pursued. As a general rule approximately 2 to 2.5 cm of temporalis muscle is utilized for facial rehabilitation. It has been our experience that the muscle best suited for facial rehabilitation lies in the central one third of the temporalis muscle. The anterior one third of the muscle has a heavy tendency to be short, bulky, and poorly oriented for useful reanimation of the face. On the other hand, the posterior one third of the muscle lacks appropriate contractile properties and is poorly oriented for rehabilitation purposes. The central one third of the temporalis muscle provides adequate length and exhibtis active contractile properties, which make it the ideal donor muscle source for transfer (Fig 5). The muscle is harvested from the temporal fossa and is elevated with pericranium on its medial surface. Using blunt elevation and careful attention to the inferior aspect of the muscle in the area of ihe zygomatic arch, the vascular and neural supply to the muscle is preserved. A central incision is made in the muscle flap which represents the point of placement of the temporalis muscle to the oral commissure. Three 3-0 Prolene sutures are placed into the fascia and muscle at the disial tip using a figure-of-eight suture technique (Fig. 6). The muscle is then transferred into the lower face and suture stabilized using 3-0 Prolene at appropriate points along the lateral border of the orbicularis oris muscle. As a rule, we rely upon muscle-to-muscle contact between the temporalis muscle and the orbicularis oris muscle, as this results in increased dynamic postoperative movement (Fig 7). Overcorrection at the time of surgery is essential with an attempt made to expose the second to third molar of the upper dental arch at the time of muscle transposition. The vermilion border is closed using a horizontal mattress suture to accentuate this landmark. The donor site is reconstructed using the previously developed temporoparietal fascial flap and a silicone drain is placed in the temporal and fascial regions for 24 to 36 hours. A bulky compressive dressing is used in the first 24 hours postoperatively in an attempt to reduce the risk of hematoma formation and to reduce facial swelling.

Figure 4: A facial flap is created that extends from the temporal region to the oral commissure. This flap is elevated to allow for both index fingers of the surgeon to pass comfortably from the zygomatic arch to the oral commissure.

Figure 5: The central one third of the temporalis muscle is best suited for rehabilitation of the paralyzed face. The orientation of the muscle can be varied to individualize the muscular repair.

Figure 6: Temporalis muscle is harvested from the temporal fossa mobilzed to the zygomatic arch, and transferred into the midface with 3-0 Prolene suture.

Figure 7: The temporalis rnuscle is sutured to the lateral border of the orbicularis orbis muscle with 3-0 Prolene.

Partial hypoglossal-facial nerve anastomosis

The partial hypoglossal-facial nerve anatomosis is utilized in specific clinical circumstances in which ihe facial nerve has been sacrificed at the time of surgery and the surgeon is unable to immediately graft the neural defect. This technique is utilized in conjunction with the temporalis transposition flap and is important in providing resting tone and improving facial symmetry of the lower lip, commissure, and the nasolabial fold regions. In keeping with our philosophy of dividing ihe face into three zones of reconstruction, the partial hypoglossal-facial nerve anastomosis directs its neural input to the middle and lower zones of the facial nerve. The incision is an extension of the incision used for the temporalis muscle transposition technique. The pretragal incision is carried around the auricular lobule and into the cervical region 2 to 2.5 cm below the angle of the mandible (Fig 3). The facial nerve is identified as it courses from the stylomastoid foramen and is dissected peripherally distal to the point where the two major divisions of the faciai nerve are clearly identified. At this point the surgical dissection is carried into the neck where the posterior belly of the digastric muscle and the anterior border of the sternocleidomastoid muscle are utilized for hypoglossal nerve identification. Rather than a complete transection of the hypoglossa1 nerve, this technique utilizes a 30% selected neural graft which is mobilized distal to the takeoff of the ansa hypoglossal nerve and is superiorly rotated for microsurgical anastomosis with the lower division of the facial nerve. The superior division of the facial nerve is ligated. An epineural anastomosis is then performed to approximate the partial hypoglossal nerve to the lower division of the facial nerve. In our sreies of patients this technique has provided improve resing tone to the loer division of the face and has eliminated the donor defect of hemiparesis of the tongue, which has been associated with the full resection of the hypoglossal nerve.

Aberrant Regeneration of the Facial Nerve

Following prolonged facial paralysis, facial nerve regeneration can often be associated with misdirected axonal regrowth, which can cause abnormal synkinetic movements of the facial muscles, epiphora, and barying degrees of hemifacial contracture. The most troubling of the synkiectic movements in involuntary eyelid closure with movements of the jaw and lower face. The clinician will observe internittent ptosis at the patient speaks with return to a resting state (reverse Marcus-Gunn sign). The eyelid closure is often associated with distortion in the nasolabial fold and lip position, or asymmetric dimpling near the lateral angle of the mouth.

Therapy with botulinum A toxin injection is directed at relieving the involuntary blepharospasm. Injections are given in the mideial and lateral extremes of the pretarsal orbicularis muscle with tow additional injections along the lateral orbicularis. the total dose in each injeciton site probably should not exceed four international unite (IU) as excessive weakening of the orbicularis oculi muscle may result in lagophthalmos and exposure keratitis. The injection results in a substantial reduction in the degree of involuntary eyelid closure for a periof of four to five months. It is especially important not to exceed 15 IU on initial injection because the orbicularis already is partially denervated and is exceptionally sensitive to botulinum toxin injection. Patient acceptance of this therapy is excellent and injections can be repeated without reduction of efficacy.


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