The management of facial paralysis continues to evolve. Understanding the facial nerve anatomy and the different methods of evaluating the degree of facial nerve injury are crucial for successful management. When the facial nerve is transected, direct coaptation leads to the best outcome, followed by interpositional nerve grafting. In cases where motor end plates are still intact but a primary repair or graft is not feasible, a nerve transfer should be employed. When complete muscle atrophy has occurred, regional muscle transfer or free flap reconstruction is an option.
Nose Symptomatic stenosis of the nasal valve can be easily corrected with suturing techniques, though there are concerns that the benefits of trsuma procedures may be temporary. We usually treat Bell's palsy with a course of steroids and advice on looking after your eyes, oral hygiene and facial rehabilitation. If you continue to Facial nerve damage from eye trauma this site we will assume that you are happy frlm it. The case for oblique temporal Breast pain pinched nerve fractures. Facial nerve palsy includes both paralysis and weakness of the seventh cranial nerve. There is left lagophthalmos present during eyelid closure. In some cases, new techniques which make use of nerve grafts and tissue transfers are being studied as ways to correct facial nerve injuries. Facial nerve damage from eye trauma facial nerve controls the motor aspect of the muscles of facial expression, taste, hearing, and some sensory areas. Central facial palsy is induced by a brain disorder, whereas peripheral facial palsy is induced by a disorder merve the facial nerve pathway emanating from the brain.
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Professional Reference Facial nerve damage from eye trauma are designed for health professionals to use. Baldness and Hormone-Related Skin Disorders. I would give it a week or two, but ensure that Sadie is able to drink and eat properly in the meantime. Guillain-Barre syndrome or a peripheral neuropathy damage to nerves in your extremities such as hands, feet or arms may present with weakness on both sides of your face. Diagnosing Facial Nerve Trauma Regardless of the cause of the facial nerve disorder, the workup of the seventh cranial nerve involves looking at the face and checking on the symmetry of the muscles of facial Facial nerve damage from eye trauma. IV Trochlear : controls the movement of the eyes downward and inward toward the nose. Surgery Dorki bbs ls island sometimes needed if a collection of blood, called a hematoma, is squeezing the nerve and leading to paralysis or dysfunction. The facial nerve controls the motor aspect of the muscles of facial expression, taste, hearing, and some sensory areas. Neurologists and neurosurgeons have specialized assessments and interventions that address this type of nerve damage and should be consulted. Chronic Inflammation of the Anus. She is J Trauma. Add a comment to Miss's experience. Physical therapy may help her if there is nerve involvement to the muscles that is causing her imbalance, to keep those muscles as strong as possible. Neuropathy nerve damage Caused by Trauma.
Skull fracture to the temporal bone through which the facial nerve travels is responsible for causing facial palsy.
- Professional Reference articles are designed for health professionals to use.
- It can have a short duration or long term or permanent dysfunction.
- Neuropathy nerve damage Caused by Trauma.
The management of facial paralysis continues to evolve. Understanding the facial nerve anatomy and the different methods of evaluating the degree of facial nerve injury are crucial for successful management. When the facial nerve is transected, direct coaptation leads to the best outcome, followed by interpositional nerve grafting.
In cases where motor end plates are still intact but a primary repair or graft is not feasible, a nerve transfer should be employed. When complete muscle atrophy has occurred, regional muscle transfer or free flap reconstruction is an option. When dynamic reanimation cannot be undertaken, static procedures offer some benefit. Adjunctive tools such as botulinum toxin injection and biofeedback can be helpful. Several new treatment modalities lie on the horizon which hold potential to alter the current treatment algorithm.
Facial paralysis can be a devastating consequence resulting from blunt and penetrating trauma to the head and neck, as well as surgical injury, either accidental or due to involvement by tumor. In addition, the etiology can be attributed to a variety of other causes, ranging from infectious to metabolic and is frequently idiopathic in nature.
Treatment of the injured intratemporal facial nerve is historically controversial. Reanimation of the paralyzed face is an interesting and frequently evolving field. In this review, we will discuss the anatomy of the facial nerve, the etiology of facial nerve injury, the management of the traumatized facial nerve, and the assessment and treatment strategies for the patient suffering from facial paralysis.
The course of the facial nerve is divided into six segments Fig. Originating within the pons in the facial nucleus, the motor fibers of cranial nerve VII are joined by those of the nervus intermedius before entering the temporal bone through the internal auditory meatus.
The narrowest segment of the intratemporal facial nerve, the labyrinthine segment, extends from the internal auditory meatus to the geniculate ganglion, where the cell bodies of special visceral afferent neurons carrying taste from the anterior two-thirds of the tongue are located. It is at the geniculate where the nervus intermedius joins the facial nerve proper, and the greater superficial petrosal and lesser petrosal nerves exit the facial nerve.
The tympanic segment of the nerve extends posteriorly from the geniculate ganglion to the second genu, where the facial nerve turns inferiorly, transitioning to the vertical or mastoid segment. The nerve to the stapedius and the chorda tympani can be found exiting the vertical segment. The nerve exits the temporal bone through the stylomastoid foramen, yielding the extratemporal portion of the nerve, which proceeds to innervate all muscles of facial expression from their deep surfaces except for the levator anguli oris, buccinator, and mentalis, which are innervated from their superficial aspects.
Surgical landmarks that aid in identification of the main trunk of the facial nerve are the tympanomastoid suture, the tragal pointer, the posterior belly of the digastric muscle, and the styloid process.
The nerve lies inferior and medial to the tragal pointer, and its depth can be approximated by that of the posterior belly of the digastric muscle, lying lateral to the styloid process. The facial nerve then enters the parotid gland, where the main trunk branches into the upper and lower divisions at the pes anserinus Fig. The nerve further divides into five main branches: the temporal, zygomatic, buccal, marginal mandibular, and cervical.
Extratemporal facial nerve branches temporal, zygomatic, buccal, marginal mandibular and cervical branches. Facial nerve branches generally innervate deep to the facial muscles with the exceptions of levator anguli oris, buccinators, and mentalis muscles.
The temporal branch lies within the superficial muscular aponeurotic system SMAS at the level of the zygomatic arch. Facial paralysis can result from a wide range of causes. A list of causes can be found in Table 1. Facial paralysis can result in significant disfigurement, having severe implications for both the patient's emotional and physical well-being. Ophthalmologic consequences include diminished effectiveness of lacrimation, brow ptosis, ectropion, epiphora, and lagophthalmos.
These may lead to corneal damage from exposure keratopathy, potentially proceeding to blindness or even globe rupture.
Ineffective contraction of the perioral musculature can result in insufficient oral competence, poor swallowing function, dysarthria, and ptyalism. Precise characterization of facial nerve paralysis must be accomplished to provide proper patient counseling regarding prognosis and treatment. Careful assessment and documentation of facial nerve function should include a detailed description of the status of motion of the upper, middle, and lower face.
Special attention should be paid to the eye not only in terms of eyelid closure, lower lid laxity, and brow height but also to visual acuity, presence of Bell phenomenon, and corneal irritation. Aside from overall symmetry, other important functional considerations include nasal valve collapse and oral competence.
Injury to the intratemporal portion of the facial nerve can result in total facial paralysis, as well as dysgeusia.
Damage to the geniculate and proximal to this region can lead to decreased lacrimation due to injury to the preganglionic parasympathetic fibers that supply the lacrimal gland carried in the greater superficial petrosal nerve.
Damage to the nerve proximal to the take-off of the nerve to the stapedius can result in hyperacusis in the affected ear. ENog is an objective test that measures evoked compound muscle action potentials using skin electrodes.
EMG measures voluntary muscle response with needle electrodes placed in the target muscles that detect action potentials during muscle contraction with a functioning nerve.
Muscle that has been denervated displays fibrillation potentials, while muscle that is in the process of reinnervation demonstrates polyphasic potentials.
Temporal bone fractures are traditionally classified into longitudinal, transverse, or mixed types, depending on their orientation relative to the petrous ridge. Immediate complete paralysis warrants surgical exploration. Cases of complete paralysis in which the onset of paralysis is indeterminate should be treated as immediate in nature. Some advocate exploration based on the conditions earlier when ENog is performed within 6 days of the onset of paralysis.
Transection is treated with primary neurorrhaphy using fine suture or fibrin glue, or an interpositional nerve graft when primary anastomosis is not possible. Decompressive surgery is frequently delayed for reasons including the treatment of life threatening injuries suffered in the original trauma, referral delay, or poor neurological status.
The initial management of acute idiopathic facial paralysis, or Bell palsy, traditionally consists of corticosteroids, antiviral agents, observation, or surgical decompression. The treatment of facial paralysis must be tailored to the individual patient, and the surgeon must select the appropriate course of action based on the circumstances surrounding nerve dysfunction. Similarly, the duration of paralysis is of paramount importance in selecting treatment, as the complete degradation of motor end plates after 2 years usually renders reinnervation procedures futile.
The patient's age and comorbidities factor into the decision making process as well. Many of the surgical options for facial reanimation are complex, lengthy operations, ill suited for elderly and frail individuals, who are unlikely to tolerate such procedures without a high risk of perioperative morbidity.
Finally, the expectations and goals of the patient must be reconciled with those of the surgeon to ensure that appropriate care is given. The goal of treatment is the restoration of symmetry in all three facial zones; upper, middle, and lower face. This is accomplished through modifying either the affected side, the contralateral, normal side of the face, or both.
Generally speaking, surgical options for the treatment of facial paralysis consist of primary neurorrhaphy, interpositional nerve grafting, nerve transfers, muscle transfers, free-tissue flaps with micro-neurovascular anastomosis, and static slings, weights, and tissue rearrangement. Primary nerve repair should be performed whenever possible, with the exception to this being long standing facial paralysis with degeneration of motor end plates. In cases of immediate injury due to penetrating trauma in the intraparotid region, surgical exploration should be undertaken.
The wound should be copiously irrigated and appropriate antibiotics should be administered. The proximal and distal portions of the nerve must be identified. The use of an electric nerve stimulator can be useful in identification of distal branches. Ragged edges should be freshened and the neurorrhaphy performed. If there is insufficient length of nerve for primary repair, an interpositional graft from the great auricular nerve, sural nerve, or other suitable donor nerve should be performed.
The section that follows will delineate treatment options for facial paralysis according to each anatomic region. Management of the upper third of the face centers around the protection of the eye, and the restoration of brow symmetry. The primary goal in addressing the eye in facial paralysis is the preservation of vision. Exposure keratopathy can be avoided initially by instituting supportive measures, such as the use of lubricating eyedrops, and ointment.
Botulinum toxin can be injected into Muller muscle and the levator palpebrae superioris to counteract lagophthalmos in a temporary fashion. The implantation of a static weight to load the upper lid and achieve eye closure has been successfully performed, since the s Fig.
Platinum may confer a greater benefit than gold due to the higher density and superior biocompatibility of platinum. The development of ectropion in patients with facial paralysis contributes to exposure keratitis by leading to corneal desiccation through worsened lagophthalmos and lacrimal dysfunction. Lateral ectropion can be surgically addressed by a lateral tarsal strip procedure or a lateral transorbital canthopexy, while laxity in the medial portion of the lower lid can be corrected by performing a transcutaneous, transcaruncular, or precaruncular medial canthopexy.
Decreased morbidity has been noted with the medial canthopexy. Dynamic reanimation of the eye may be accomplished by nerve transfers, such as cross-facial nerve grafting CFNG , hypoglossal nerve transfer, and direct orbicularis oculi neurotization, or by muscle transfer procedures, borrowing from the frontalis, temporalis, or free muscle flaps.
Brow ptosis leads to cosmetic deformity as well as functional derangements by exacerbating dermatochalasis, thereby encroaching upon the upper visual field. This can be successfully mitigated with surgical brow elevation. Treatment of the midface aims to alleviate the obstruction of the nasal airway and to counteract the forces of gravity on the malar soft tissues.
Paralysis of the midface is of concern, mainly as it relates to nasal valve stenosis and the exacerbation of ectropion by dependent stretching of the canthal ligaments. Surgical procedures to counteract this are aimed at lifting the soft tissues of the middle and lower face. The extended minimal access cranial suspension lift, described by Verpaele et al, is a simple technique that was designed to improve the aging neck and lower two-thirds of the face.
In the study by Elner et al, mobilization of the suborbicularis oculi fat and periosteum was performed to provide midfacial lifting and to minimize ectropion. Symptomatic stenosis of the nasal valve can be easily corrected with suturing techniques, though there are concerns that the benefits of these procedures may be temporary. Other procedures have shown benefit in terms of their ability to improve nasal breathing.
While clearly improving facial symmetry, rhytidectomy has the potential to augment the nasal airway as well. Disability in the lower face resulting from facial paralysis consists mainly of oral incompetence, manifesting as ptyalism, and difficulty with eating and drinking, poor articulation, and loss of smile and expressivity.
Static slings, suspended from the zygomatic arch or deep temporal fascia to support the oral commissure and upper lip, lead to the elevation of these structures and the recreation of the nasolabial fold Fig. An inferior displacement of the affected oral commissure, oral incompetence, upper and lower lip asymmetry are commonly seen with facial paralysis. Upper lip philtral ridge is also commonly displaced to the unaffected side. Static suspension of lower lip can be used to address gross lip asymmetry, drooling and oral incompetence.
Fascia lata, Gore-Tex and Alloderm can be used to suspend in a superoposterior vector as seen in the right image. Facial lifting procedures mentioned earlier, such as the extended minimal access cranial suspension can serve a similar purpose. Lower lip reanimation can also be accomplished by means of a Palmaris longus tendon transfer, which is easily performed in the outpatient setting.
The decision to perform a dynamic reconstruction over static repositioning hinges mainly on the timeframe of the paralysis. For acute traumatic injuries, such as iatrogenic nerve sectioning or penetrating wounds, primary repair of the nerve renders the best outcome. Common donor sites include the great auricular or sural nerves. When primary repair or interpositional nerve grafting are not feasible, nerve transfers represent the next rung on the ladder of facial reanimation in cases less than 2 years out from injury.
The CFNG, first introduced by Scaramella, 74 relies on peripheral branches of the contralateral, intact facial nerve to innervate corresponding areas of the paralyzed hemiface to produce spontaneous and purposeful facial movement.
Trauma whether by a physical Injury or surgery is a common cause of neuropathy, nerve damage. None of the various neuropathy treatments will build healthy nerves. Compression neuropathy - pressure on an area can result in an inability to transmit nerve impulses because compression has damaged nerve fibers either directly or indirectly by restricting their supply of oxygen. Book me a walkiee? In severe cases, we might need to repair the nerve. Indian Journal Of Neurotrauma , 9 2 ,
Facial nerve damage from eye trauma. Specific fractures
Types of facial nerve disorder
Facial nerve palsy includes both paralysis and weakness of the seventh cranial nerve. Ocular signs and symptoms of facial nerve palsy include inability to close the eye, dry eye syndrome, as well as eye redness, tearing, burning, and foreign body sensation.
Conservative management of ophthalmic complications of facial nerve palsy include instilling artificial tears, applying lubricating ointment, and taping the eyelids closed, while surgery is reserved for refractory cases with limited potential for recovery. Overall, the prognosis of facial nerve palsy depends on the cause of the palsy, and ophthalmologists have an important role in managing the symptoms and limiting the sequelae of this condition.
Facial nerve palsy includes both paralysis complete loss of function and paresis weakness of the seventh cranial nerve CN 7. CN 7 is a mixed nerve providing both sensory afferents and motor efferent fibers. Of significance to ophthalmologists, CN 7 has both a visceral motor branch that responds to parasympathetic stimuli and a somatic motor branch.
The visceral motor fibers of CN 7 innervates the lacrimal gland, stimulating reflexive tearing of the ipsilateral eye. The somatic motor fibers of CN 7 innervates all three parts of the obicularis oculi muscle palpebral, orbital, and lacrimal that functions to close the ipsilateral eyelid and draw tears towards the lacrimal punctum. Additionally, patients may present with unilateral or bilateral facial nerve palsy. Three nuclei make up the facial nerve including the facial nerve nucleus somatic motor fibers , the superficial salivary nucleus parasympathetic fibers , and the nucleus tractus solitarius special sensory fibers.
CN7 then follows a complex course that is both intra- and extra-cranial in location. The intracranial portion of the nerve consists of both a motor and sensory root and travels through the internal acoustic meatus through the temporal bone and becomes the geniculate ganglion. It also gives rise to the greater petrosal nerve that travels through the stylomastoid foramen and is responsible for the sensory functions of CN 7. Upon exiting the stylomastoid foramen, the facial nerve becomes extra-cranial, and travels through the parotid gland, giving off five terminal branches that provide the somatic motor functions of CN7 responsible for facial expression.
Typically, the combination of sensory and motor symptoms correlate to intra-cranial CN 7 pathology, while isolated motor symptoms are associated with extra-cranial CN 7 lesions. There are numerous possible etiologies of facial nerve palsy that can be broadly classified into the following areas: idiopathic, congenital, infectious, traumatic, inflammatory, neoplastic, and an iatrogenic. For a complete list of such etiologies, see Jackson C, von Doersten.
Otolaryngology for the Internist. The overall prevalence of facial nerve palsy has been estimated at cases per 10 people in the general population. Patients may seek ophthalmologic attention because of eye redness, tearing, burning, and foreign body sensation. Non-ophthalmic complaints may include: facial asymmetry, overall facial muscle weakness, difficulty chewing, increased sensitivity to sound, altered taste sensation, and decreased salivation.
Ophthalmologists should characterize the onset, duration, and severity of symptoms, as well as whether symptoms are present at rest or only upon voluntary movement. Gross physical examination of the face should note any facial asymmetry and whether the patient presents with unilateral or bilateral involvement of CN 7. Also, involvement of the forehead and periocular region indicates whether the lesion at the level of the upper motor neuron no involvement of the forehead or the lower motor neuron forehead involvement.
As part of a complete ophthalmic exam, assess visual acuity, extra-ocular movements, and pupillary movements. Make note of the following physical examination findings as part of the exam:   .
Thorough examination of patients with CN 7 palsy warrants assessment of involvement of other cranial nerves. CN 2, 3, 4, and 6 are assessed as part of the ophthalmic exam as above.
Sensory components of CN 5 can be evaluated by assessing sensation on the forehead and upper eyelid ophthalmic division as well as along the lower eyelid maxillary division. CN 8 travels with CN 7 through the internal acoustic meatus, so referral to otolaryngology should be considered.
Facial nerve palsy is a clinical diagnosis based on history and physical examination. Further workup of facial nerve palsy is dictated by clinical suspicion of the underlying cause of facial weakness. Complete assessment of facial nerve palsy should address the chronicity, severity, and laterality of the palsy, and comment on whether the palsy is either primary or secondary, and if lesion is likely a proximal or distal lesion.
Importantly, objective grading of the severity of facial nerve palsy remains difficult. Therefore, currently, there is no universal scale available to document and assess the complete spectrum of ophthalmic presentations of facial nerve palsy. However, features suggestive of facial nerve palsy secondary to an underlying cause may require additional workup. As a result, Clinical Practice Guidelines state that the following tests may be ordered to aid in diagnosis or prognosis of facial nerve lesions: .
The overall goal of treating facial nerve palsy is to maintain quality of life by protecting vision and retaining cosmesis. To achieve these goals, both medical and surgical options for management of facial nerve palsy are available. Typically, conservative and medical management strategies are used in patients whether there is potential for facial nerve recovery, while surgical options are typically reserved for cases in which these is no potential for recovery from facial paralysis.
Initial conservative management aims to protect the cornea as facial nerve function recovers. Additionally, overnight, patients should tape their eyelids closed and apply petroleum-jelly based lubricating ointment.
Patching and padding of the affected eye should be avoided to prevent accidental corneal abrasion. If conservative management fails, medical management should be pursued. Transcutaneous or subconjuncitval injection of botulinum toxin can paralyze the levator palpebrae superioris, thus inducing ptosis of the upper lid for approximately 6 weeks to protect the cornea.
Current practice guidelines recommend starting oral steroids with 72 hours of symptom onset in patients older than 16 years of age diagnosed with Bell's palsy. When clinical judgment suggests that there is limited likelihood of functional improvement in facial nerve function, surgery can be performed to limit corneal complications of facial nerve palsy. To reduce lag ophthalmos and its sequelae, implantation of a gold weight in the upper eyelid can be performed.
The gold weight of typically 1. Alternatives to this procedure include palpebral springs, periocular silicon slings, and facial slings. Tarsorraphy, which partially sews upper and lower eyelids together, can provide either temporary or permanent corneal protection. Tarsorraphy can be performed at either the medial or lateral canthus via canthoplasty or tarsal strip.
Alternatives include lateral canthal sling. There are multiple complications of facial nerve palsy. Conservative management aims to limit the ophthalmic complications such as exposure keratitis and corneal drying. However, preventative measures cannot be taken against other hyperkinetic complications of facial nerve palsy including synkinesis, hemifacial spasm, and facial asymmetry.
A disabling complication of facial nerve palsy is synkinesis, in which involuntary movements accompany voluntary facial movements. However, many other examples of synkinesis secondary to facial nerve palsy have been reported, including gustatory lacrimation or crocodile tear syndrome. Hemifacial spasm, or involuntary muscle contractions of one side of the face can occur as part of the post-facial paralytic syndrome secondary to axonal degeneration of the nerve.
Lastly, patients may also find the facial asymmetry associated with seventh nerve palsy to be disfiguring. Management of each of these hyperkinesias is similar, and involves a combination of facial physical therapy and use of botulinum toxin. Facial physical therapy can be used to compensate for synkinesis and to strengthen the muscles on the weaker side of the face in hemifacial spasm.
By contrast, botulinum toxin is used to paralyze muscles, and is used in the management of synkinesis, hemifacial spasm, and in weakening the stronger side of the face in hemifacial spasm.
The prognosis of facial nerve palsy depends on multiple factors. Prognosis of secondary facial facials depends on the success and management of the primary disease process.
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