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127 Cards in this Set
- Front
- Back
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Embryology
The fascioacoustic primordium appears at which week of gestation? |
3rd (it eventually gives rise to the seventh and eighth cranial nerves)
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Embryology
At which week of gestation do the seventh and eighth cranial nerves become distinguishable? |
4th week of gestation
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Embryology
At which week of gestation does the facial nerve split into the chorda tympani and the main trunk? |
4th week
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Embryology
At which week of gestation do the muscles of facial expression develop? |
6th to 7th week; They develop within the second arch
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Embryology
At which week of gestation do the 5 major branches of the facial nerve formed? At which week are they completely developed? |
Week 8 of gestation
Developed completently at 12th week |
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The facial nerve is the nerve to the _________ branchial arch
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second; thus any malformations in the derivatives of Reichert cartilage make the nerves suspect for variations of it
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External ear formation
At which week of gestation do the first and second branchial arch. |
6th week
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External ear formation
At which week of gestation do the EAC and tympanic membrane appear? |
28th week
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How many functional components does the facial nerve have?
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four - two efferent and two afferent
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What do the efferent components of the facial nerve innervate?
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posterior belly of digastric
stylohyoid muscle stapedius muscle muscles of facial expression |
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Efferent parasympathetic fibers originating from the _______________________________ are responsible for lacrimation and salivation
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superior salivatory nucleus
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Which branch of the facial nerve provides efferent parasymp innervation to the salivary glands?
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chorda tympani
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Which branch of the facial nerve provides efferent parasymp innervation to the lacrimation glands?
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greater superficial petrosal nerve (the fibres have synapses in the pterygopalatine ganglion.)
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List the afferent pathways of taste & touch from the anterior 2/3 of the tongue.
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taste fibers --> chorda tympani --> facial nerve
general touch --> lingual nerve --> mandibular branch of CNV |
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How many segments of the facial nerve are there? What are the segments called?
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SIX sigments
1) Intracranial segment 2) Meatal segment (IAC) 3) Labyrinthine segment 4) Tympanic segment 5) Mastoid (vertical) segment 6) Exstratemporal segment "IML TME" |
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How long is the intracranial segment of CN7?
Where does it start and end? |
23-24mm
Brain stem to fundus of the IAC |
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How long is the meatal segment of CN7?
Where does it start and end? |
8-10mm
fundus of IAC to the meatal foramen Remember the 7UP diagram here and know where all the nerves are within the IAC (facial nerve runs anterior to the superior vestibular n and superior to the cochlear n) |
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How long is the labyrinthine segment of CN7?
Where does it start and end? |
3-5mm
meatal foramen to geniculate ganglion The nerve gives rise to its first branch, the greater superficial petrosal nerve |
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How long is the tympanic segment of CN7?
Where does it start and end? Also trace it's way on the way to the end |
8-11mm
from geniculate ganglion to the pyramidal eminence. (from the GG, the nerve makes a 40-80* turn to proceed posteriorly across the medial wall of the tympanic cavity, medial to the cochleariform process, then above the oval window, and then under the lateral semicirc canal to the pyramidal eminence; pyramidal eminence is a hollow canal for the stapedius muscle) |
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How long is the mastoid (vertical) segment of CN7?
Where does it start and end? |
10-14mm
pyramidal process/eminence to the stylomastoid foramen (pyramidal eminence is a hollow canal for the stapedius muscle, which attach to the neck of the stapes) Three branches arise from the mastoid segment: nerve to the stapedius muscle, chorda tympani nerve, and nerve from auricular branch of the vagus (Arnold's) |
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Where does the extratemporal segment of CN7 start and end? Trace it's course
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from stylomastoid foramen to the facial muscles.
After exiting the stylomastoid foramen, the nerve courses anteriorly and inferiorly, lateral to the styloid process and external carotid artery, to enter the posterior surface of the parotid gland. |
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After the facial nerve enters the parotid gland, it splits into which two segments?
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1) Temporozygomatic division
2) Cervicofacial division pes anserinus is the extensive network of anastomoses between the various limbs |
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What are the surgical landmarks of the extratemporal facial nerve?
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1) Tragal pointer - nerve identified 1cm inferior and deep to this
2) Tympanomastoid fissure - nerve can be identified at 6 to 8 mm below the inferior "drop off" of the fissure 3) Posterior belly of digastric muscle at its insertion to the mastoid process: nerve exits stylomastoid foramen just anterior to this 4) Proximal dissection of peripheral facial nerve branches through the parotid gland: allows the surgeon to localize the nerve when anatomy is distorted or parotid neoplasm present. |
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What are the landmarks for the identification of the intratemporal facial nerve?
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1) Cochleariform process: tympanic segment located deep to this
2) Lateral semicirc canal: second genu of tympanic segment lies inferior to this 3) Digastric ridge: stylomastoid foramen located at anterior end of ridge |
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What is the most common site of facial nerve injury during mastoid surgery?
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A prominence of the nerve posterior and lateral to the lateral semicirc canal (pyramidal turn) makes the nerve more susceptible to injury in this area.
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What is the incidence of fallopian canal dehiscence?
What is the most common congenital location and also the most common site of iatrogenic injury during middle ear surgery? |
30%
tympanic segment over the oval window |
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What is the facial canal?
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The canal that the facial nerve runs through in the temporal bone; starts at the IAC meatus to the stylomastoid foramen.
AKA the fallopian canal |
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Name some idiopathic causes of facial nerve paralysis
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Bell's palsy
Recurrent facial palsy |
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Name some congenital causes of facial nerve paralysis
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Mobius syndrome
Congenital unilateral lower lip paralysis Melkersson-Rosenthal syndrome Dystrophic myotonia |
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Name some traumatic causes of facial nerve paralysis
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Temporal bone fx
Birth trauma Facial contusions/lacerations Penetrating wounds to the face or temporal bone Iatrogenic injury Barotrauma |
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Name some infectious causes of facial nerve paralysis
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Hepes zoster oticus (Ramsey Hunt syndrome)
Otitis media with effusion Acute mastoiditis Malignant otitis externa Acute suppurative otitis media Tuberculosis Lyme disease Acquired immunodeficiency syndrome Infectious mononucleosis Influenza Encephalitis Sarcoidosis |
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Name some neoplastic causes of facial nerve paralysis
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Cholesteatoma
Carcinoma (primary or metastatic) Acoustic neuroma Meningioma Facial neuroma Ossifying hemangioma Glomus jugulare or tympanicum Schwannoma of lower cranial nerves Benign and malignant parotid tumors Leukemia Hemangioblastoma Histiocytosis Rhabdomyosarcoma |
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Name some metabolic/systemic causes of facial nerve paralysis
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Diabetes mellitus
Hyperthyroidim/hypothyroidism Pregnancy Autoimmune disorders |
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Name some neurologic causes of facial nerve paralysis
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Guillain-Barre syndrome
Multiple sclerosis Millard-Gubler syndrome |
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Any palsy demonstrating progression beyond a ___ week period of lack of improvement after ____ months should be considered a neoplasm until proven otherwise.
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progression beyond 3 weeks & lack of improvement after 4 months
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What grading system is used for standardized documentation of facial nerve functional recovery?
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House-Brackmann grading system
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What happens to the upper eyelid movement in facial nerve paralysis?
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Levator palpebrae muscle is innervated by the oculomotor nerve, which will remain intact despite a total facial nerve paralysis
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Is there a correlation between signal intensity of the facial nerve seen on MRI with gadiolinium between the severity of paralysis in Bell's palsy or Ramsey Hunt syndrome?
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While most agree that the increased signal intensity observed in both conditions is similar, there is no correlation between the level of enhancement and the severity of the paralysis, electrophysiologic test results, intraoperative finds, and prognosis for functional recovery.
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Nerve injury classification and prognostic implications:
Describe neurapraxia |
Neurapraxia: blockage of axonal transport due to local compression. The nerve does not sustain permanent damage and no Wallerian degeneration occurs.
Normal fnct will be restored when the compression is relieved. All electrophysiologic tests will be within normal limits. |
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Nerve injury classification and prognostic implications:
Describe axonotmesis |
Axonotmesis: axonal integrity has been disrupted, but endoneural sheaths are preserved. Wallerian degeneration distal to the lesion occurs. Electrophysiologic tests will reveal rapid and complete degeneration. As long as the endoneurium is preerved there will be complete recovery with return of normal function.
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Nerve injury classification and prognostic implications:
Describe neurotmesis |
Neurotmesis: destruction of the axon and surrounding support tissue. Characterize by Wallerian degeneration, and unpredictable regeneration potential, and the likelihood of significant resultant dysfunction and synkinesis. Early electrophysiologic testing mimics that of axonotmesis.
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Nerve injury classification and prognostic implications:
Describe synkinesis |
Synkinesis: defined as the loss of discrete facial movements after facial nerve injury. Results from a single axon or a small group of axons innervating motor end units of numerous and separated muscles.
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Nerve injury classification and prognostic implications:
Describe bogorad syndrome |
Bogorad syndrome (crocodile tear syndrome): occurs when regenerating nerve fibers originally destined for the submaxillary gland innervate the lacrimal gland. This causes profuse lacrimation during eating.
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Nerve injury classification and prognostic implications:
Describe topodiagnostic testing |
The concept of testing specific neuronal fnct corresponding to the numerous branches of the facial nerve in an attempt to localize the site of injury and to predict functional outcome.
Commonly used examples include Schirmer's test, the submandibular flow test and the stapedial reflex test. Experience has shown, however, that topodiagnostic tests correlate poorly with the site of injury and fail to serve as a useful prognostic tool. Rarely used in clinical practice today. |
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What are the three most common causes of acute facial paralysis?
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Bell's palsy
Trauma Infection All 3 of these produce nerve degeneration in the first 3 weeks following onset. |
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Describe the nerve excitability test
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Compares current thresholds required to elicit MINIMAL muscle contraction on the normal side of the face to those of the paralyzed side.
Measured in milliamperes (mA). Difference of 3.5 mA or greater between the normal side and paralyzed side suggests degeneration. The test is unreliable clinically and no longer used in clinical practice. |
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Desribe the maximum stimulation test
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Similar to nerve excitability test (NET), except that it uses MAXIMAL rather than minimal stimulation.
The main trunk as well as each major branch of nerve on the normal and abnormal sides are stimulated at an intensity that produces maximal muscle contraction of the non-paralyzed side without discomfort. Better prognotic indicater of muscle denervation compared to the NET, however, as with NET, results are variable and clinically unreliable. |
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Describe electroneurography (ENoG/ENG)
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ENG provides a quantitative analysis of the extent of degeneration w/o being dependent on observer quantification (like in NET & MST).
Currently the most reliable prognostic indicator of all the elctrodiagnostic tests in the first 2 weeks following onset of complete facial paralysis. Measures the compound muscle action potential (CMAP) generated. The normal side is compared to the injured side, and degree of degeneration is inferred by the difference between the amplitudes of the two. ENoG is valuable when used between 3-14 days after onset of complete facial paralysis. |
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What is test is currently the most reliable prognostic indicator of all the elctrodiagnostic tests in the first 2 weeks following onset of complete facial paralysis?
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Electroneuropgraphy
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What are fibrillation potentials?
When is the earliest evidence of nerve recovery demonstrated? |
Degeneration of a lower motor nerve is followed in 14-21 days by spontaneous electrical activity called fibrillation potentials.
However, at 6-12 weeks prior to clinical return of facial fnct, polyphasic reinnervation potentials are present and provide the earliest evidence of nerve recovery. |
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When is electromyography a valuable test?
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At anytime after the onset of complete facial paralysis. Also used in conjunction with ENoG to confirm the absence of recover (absent voluntary motor unit action potentials on EMG testing) to identify appropriate candidates for surgical decompression of the facial nerve.
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When is surgical decompression ofthe facial nerve offered?
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Surgical decompression may be offered when 90% or more degeneration has occured. Absence of early neural regeneration in these cases is confirmed on EMG testing.
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Desribe the Schirmer's test. Which nerve is it testing?
What is the Schirmer's II & III tests? |
Evaluates the greater superficial petrosal nerve function (ie, tear production).
Paper strips are placed in the conjunctival fornix of both eyes. After 5 min the length of paper moistened is compared. Positive if - if less than 5mm moistened after 5 min, or les than 10mm after 15min; Also, unilateral reduction of greater than 30% of the total amount of lacrimation of both eyes. Also if reduction of total lacrimation to less than 25mm after a 5-minute period (this is significant because a unilateral transgeniculate lesion may produce bilateral reduction of lacrimation) Schirmer's II test is a modification of the original test with the addition of nasal mucosal stimulation. Schirmer's III test uses light as a stimulation for lacrimal secretions.. |
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Describe the stapedial reflex
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The stapedius muscle contracts reflexively in BOTH ears when one ear is stimulated with a loud tone. This alters the eactive compliance of the middle ear, which can be mesured with impedance audiometry.
Injury to the facial nerve proximal to the branch to the stapedius muscle (which branches off of the facial nerve in the mastoid/vertical segment of the temporal bone), the muscle will not contract and no change in impedance will be recorded. |
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Describe the trigeminofacial reflex
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Percutaneous electrical stimulation of the supraorbital nerve elicits a blink reflex that is recorded by electrodes placed over the orbicularis oculi muscle.
Due to the trigeminal-facial arc, it measures central lesions and may prove to be a beneficial diagnostic tool in the future. It is currently not used routinely in the eval of facial paralysis. |
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Describe salivary flow testing
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By cannulating Wharton's papillae, a mesurement of sailvary flow to gustatory stimulation can be obtained.
A reduction of 25% as compared to the uninvolved side is considered abnormal. No longer used clinically. |
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What is the most common cause of acute facial paralysis? What is the incidence?
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Bell's Palsy AKA idiopathic facial paralysis
70% of cases |
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What is the incidence of Bell's palsy? Age groups? Males/Females?
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Incidence - 15-40 per 100,000
Occurs in any age group, but most prevalent in the 3rd decade. No sexual or racial predilection. |
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What is the recurrant paralysis % in Bell's Palsy?
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10-12% of patients, and more often occurs on the contralateral side
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Is there a positive family history in Bell's palsy?
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up to 14% of cases have a family hx
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HSV has been implied in etiopathogenesis of Bell's palsy. What is the theory behind the mechanism?
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Viral infection induces an inflammatory response that results in neural edema and vascular compromise of the facial nerve within the fallopian canal.
This entrapment neuropathy is most evident in the labyrinthine segment of the facial nerve, where the fallopian canal is narrowest in diameter. |
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What is the typical presentation of Bell's palsy?
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Unilateral facial WEAKNESS of sudden onset, involving all branches of the facial nerve, that may progress to complete PARALYSIS in 2/3rds of pt's over the course of 3-7 days
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What are the minimum diagnostic criteria for Bell's palsy?
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1) Sudden onset
2) Paralysis or paresis of all muscle groups of one side of the face 3) Absence of signs of CNS dz, ear dz or CPA dz |
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What are some other signs and symptoms demonstrated with Bell's Palsy?
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1) Viral prodrome (60%)
2) Numbness or pain of the ear, face, or neck (60%) 3) Dysgeusia (57%) 4) Hyperacusis (30%) 5) Decreaed tearing (17%) |
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Typical Bell's palsy improves within ______ months and always by ______ months after onset.
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Imrpvoes within 4-6mo, and always by 12 mo
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When would you consider imaging for Bell's palsy?
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Imaging is not routinely obtained, however, in cases of total paralysis with SNHL on the affected side, recurrent ipsilateral facial paralysis, or polyneuropathy, and the absence of any other localizing findings on physical examination, a gadolinium-enhanced MRI scan of the facial nerve is recommended.
Also, absence of any clinical recovery 4-6 mo after onset of paralysis, progressive paralysis beyond 3 weeks, and the presence of facial twitching also constitute clinical indicators for imaging of the facial nerve. |
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Describe the treatment options for Bell's palsy
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1) Steroid's administered early in the course help improve function recovery.
2) Concomitant antiviral therapy early in the course is controversial. (GI complaints are the most common side effects) 3) Surgical decompression - has been advocated for cases of complete facial paralysis with electrical evidence of extensive nerve degeneration. It was found that Bell's palsy pt's who have 90% or more degeneration on ENoG testing within the first 14 days of onset of complete paralysis and absence of motor unit action potentials on voluntary EMG testing, surgical decompression of the facial nerve at the meatal foramen, labyrinthine segment, and geniculate ganglion resulted in a 91% chance of good outcome 7 months after paralysis, compared to a 42% chance in those tx with steroids only. However, number of studies supporting surgical decompression are lacking. |
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If surgical decompression is to be performed for Bell's palsy, what are the various approaches used?
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If good hearing - a middle cranial fossa approach is used
If poor/no hearing - a translabyrinthine apprach is used |
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What is the second most common cause of facial paralysis? What are the two categories?
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Trauma - subdivided into iatrogenic and noniatrogenic causes
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Iatrogenic facial nerve injury
What is the incidence of facial nerve injury during mastoid or middle ear surgery? |
~ 1%
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Iatrogenic facial nerve injury
What is the most common area of iatrogenic injury in the middle ear surgery? |
Tympanic segment (remember the faical nerve courses posteriorly across the medial wall of the tympanic cavity)
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Iatrogenic facial nerve injury
What testing in the immediate postoperative setting is very valuable in determing the anatomic continuity of the facial nerve? |
EMG testing. If no voluntary motor unit action potentials are detected, a severe contusion or disruption of the nerve can be inferred and surgical exploration is warrented.
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Iatrogenic facial nerve injury
Postoperative paresis of the facial nerve is almost always the result of what? |
Minor trauma and edema. Rarely progresses to paralysis.
Systemic steroids may be administered to reduce the neural edema. |
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Noniatrogenic facial nerve injury
Usually as a result of what kind of trauma? What are the classifications? |
Temporal bone fractures.
Classified as longitudinal or transverse with respect to the long axis of the petrous ridge. |
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Noniatrogenic facial nerve injury
Desribe the longitudinal temporal bone fractures. |
80-90% of all temporal bone fractures.
Parallel to the petrous ridge Usually secondary to trauma to the temporoparietal area Almost always involve the middle ear (CHL), but only 20% will have facial nerve injury (if present, usually from compression and ischemia as opposed to neural disruption). Common presentations - bleeding from themiddle/external ear, laceration of the TM, and CHL |
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Noniatrogenic facial nerve injury
Desribe the transverse temporal bone fractures. |
Less common, 10-20%
Usually secondary to trauma to the occiput Facial nerve injury is present in up to half of cases, typically from nerve severance. Common presentations - hemotympanum, vestibular sx, and severe SNHL or mixed HL. |
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A pt presents with facial trauma and has unilateral facial weakness. You suspect injury to the facial nerve. What is the management?
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Regardless of the type of trauma, if paralysis is incomplete, conservative management is indicated since spontaneous recovery occurs in most individuals.
Delayed-onset facial paralysis associated with temporal bone trauma is also likely to recover w/o surgical intervention. |
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Should you use steroids in a pt with temporal bone trauma in whom you suspect facial nerve injury?
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Use of steroids remains controversial. As long as there are no contraindications to short-term steroid use, there is some evidence to suggest that this may assist in shortening the recovery phase.
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When do you performe surgical decompression for facial nerve paralysis secondary to trauma?
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1) ENoG testing is performed once paralysis is complete. If degeneration of >90% is identified w/in 2 wks after the injury, surgical decompression of the facial nerve at the affected site should be performed.
2) If paralysis is complete, an imaging demonstrates an obvious bone fragment impinging on the intratemporal facial nerve, surgical decompression is indicated even beyond the 2-week window period. |
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More than 90% of temporal bone fractures with complete facial paralysis involve which region?
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The region of the geniculate ganglion, especially the labyrinthine segment.
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Pt has a trauma induced facial nerve injury, and surgery is planned. Which approaches will you use in hearing and non-hearing pt's?
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Hearing pt's - middle cranial fossa approach. Often this procedure can be combined with a trasmastoid approach if decompression of the distal tympanic and mastoid segments is indicated.
Nonhearing pt - translabyrinthine approach is much easier and result in less morbidity. |
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What are some common grafting options for facial nerve reconstruction?
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Great auricular nerve. If a longer segment of nerve is required, the sural nerve is the graft of choice.
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The ability to repair the facial nerve in noniatrogenic extratemporal injury depends on what?
What are two exceptions to immediate repair of this type of injury? |
Ability to achieve a tension-free anastomosis.
Two exceptions to immediate repair include: 1) presence of significant soft tissue loss & 2) extensive gross contamination of the wound. Under these conditions, immediate exploration with wound debridement and tagging of the nerve branches is initially performed. A 2nd stage procedure is done within 30 days. |
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How can you distinguish herpes zoster from Bell's palsy? What are some associated findings?
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Associated findings: intense otalgia, vesicular eruptions involving external ear (occasionally extending onto the TM), SNHL, tinnitus, and vertigo.
Unlike facial paresis in Bell's palsy which peaks within 2 weeks, progressive paresis may occur up to 3 weeks following onset. |
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What is the syndrome?
Vesicular eruptions on the ear and facial paralysis |
Ramsay Hunt syndrome
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What is the prognosis of herpes zoster compared to Bell's palsy?
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Nerve degeneration tends to be progressive and more severe in herpes zoster, and therefore the prognosis for recovery is worse.
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What are treatment options for facial paralysis caused by herpes zoster?
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Systemic steroids + antiviral meds
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Name some bacterial causes of facial nerve paralysis.
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Acute suppurative OM, chronic OM, mastoiditis, and malignant otitis externa.
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A pt has evidence of osteomyelitis from malignant otis externa. A gallium scan is performed to follow the course of the disease. There is a reduction in uptake on the gallium scan. Is this improvement or worsening?
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Reduction in gallium uptake = improvement; it detects inflammatory response by binding granulocytes.
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What are the treatments for malignant otitis externa?
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Primarily 6-week course of high-dose IV antipseudomonal ABx. (cipro + 3rd/4th gen ceph)
Surgical debridement is performed only to remove necrotic bone. |
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Facial nerve palsy occurs in ___% of pt's with Lyme dz.
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10%, but remains the most common neurologic sign of Lyme dz
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What is the prognosis for recovery of Facial fnct in Lyme dz?
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Excellent, almost 100% achieving a complete recovery
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Describe uveoparotid fever or Heerfordt dz?
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A variant of sarcoidosis, which presents as bilateral facial nerve paralysis 50% of time.
Also presents with uveitis, swelling of the parotid gland, and chronic fever. |
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In pt's presenting with new-onset facial paralysis, what percentage is neoplastic?
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5%
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Name some features of facial nerve paralysis that suggest the possibility of tumor involvement
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1) Progression of paresis beyond 3 weeks
2) Associated facial twitching 3) Absence of functional recovery 4 months after onset of paralysis 4) Ipsilateral recurrence of facial paralysis 5) Facial paralysis with cocurrent SNHL or vestibular sx 6) Presence of multiple cranial nerve deficits 7) Presence of a parotid mass 8) Hx of carcinoma |
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What are two commonest benign tumors originating from the facial nerve?
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Facial neuromas - rare, slow-growing tumors arising from the facial nerve at any point along its course, but most frequently involve the geniculate ganglion. Can present with facial paralysis and/or hearing loss
Hemangiomas - tend to cause facial paralysis early in the dz process despite their small tumor size. |
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What do Compound Muscle Action Potential (CMAP) amplitude and ENoG testing look like when there is a tumor present?
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CMAP amplitude is reduced
ENoG has a prolonged conduction latency Also, presence of both fibrillation AND polyphasic reinnervation potentials on EMG testing is characteristic of tumor dz d/t simultaneous ongoing degeneration and regeneration of the nerve. |
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Extracranial neoplasms causing facial paralysis are almost exclusively of _______ origin.
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parotid
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What is usually the initial method of evaluating a salivary gland neoplasm?
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FNAB
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Approximately ___% to ___% of malginant parotid neoplasms cause facial nerve paralysis.
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12-15%
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Which is the most common malignancy of the parotid gland?
Which parotid gland neoplasm has a predilection for facial nerve involvement? |
Mucoepidermoid carcinoma
Adenoid cystic carcinoma |
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Wha is the incidence of facial nerve paralysis in the newborn?
What is the most common cause? |
~1:2000 deliveries
birth trauma (congenital paralysis makes up the remainder) |
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What is the most common insulting agent causing facial nerve paralysis in a newborn?
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use of forceps
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Why is it that the facial nerve is move vulnerable to compression and injury in a newborn?
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The mastoid tip is poorly developed and lies in a superficial location.
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What are the two most common congenital anomalies affecting facial muscle function?
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1) Mobius syndrome
2) Agenesis/hypoplasia of the depressor anguli oris muscle |
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Describe Mobius syndrome
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1) Hereditary condition
2) Presents with congenital facial diplegia and unilateral/bilateral abducens palsy 3) May also affect CN 9, 10, 12 as well as other extraocular motor nerves 4) Extremity abnormality may occur, including absence of the pec major muscle in Poland syndrome 5) Tx - transposition of healthy muscle, along with its nerve supply. |
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Desribe the Agenesis/hypoplasia of the depressor anguli oris muscle syndrome
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1) Also turned as Congenital Unilateral Lower Lip Paralysis (CULLP)
2) Thought to be a brain stem lesion that results in a lack of development of the depressor anguli oris muscle. 3) Usually unilateral and noted by facial asymmetry when crying. 4) Associated anomalies occur in 70% of pt's, including the head, neck and CV system |
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What is the spontaneous recovery rate for traumatic neonatal facial nerve paralysis?
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~90%
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When is surgical intervention for congenital facial paralysis performed?
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Usually deferred until adolescence when facial development is nearly mature and the child is able to cope with the psychosocial aspects of facial reanimation
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What are some recommended criteria for surgical management of traumatic neonatal facial nerve paralysis?
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1) Unilateral complete paralysis at birth
2) Hemotympanum with displaced temporal bone fracture 3) Electrophysiologic studies demonstrating complete absence of voluntary and evoked motor unit responses in all muscles innervated by the facial nerve by 3 to 5 days. 4) No return of facial nerve fnct clinically or electrophysiologically by 5 weeks of life. |
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What is the most common cause of facial paralysis in older children? What is the tx?
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Bell's palsy
Steroids have not been shown to alter recovery in children. May use eye protection and close observation. |
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What is the most common complication of facial nerve paralysis, regardless of cause?
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Corneal desiccation and exposure keratitis.
Also may get lagophthalmos, lower lid ectropion, diminished lacrimation and often altered corneal reflex. These result in significant risk of corneal ulceration, scarring and permanant visual loss. |
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What is the only nerve crossover anastomosis that has been reproducible?
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Hypoglossal facial anastomosis
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What treatment method can be used for hemifacial spasms and hyperkinetic blepharospasms post facial nerve injury? What are side effects of this tx?
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Botox
SE are ptosis, diplopia, corneal exposure, facial weakness and epiphora. |
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Trace the blood supply to the facial nerve.
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ECA --> postauricular artery --> stylomastoid artery
ECA --> Middle meningeal artery --> greater superficial petrosal artery |
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What are the lengths of the facial nerve in these segments?
Pons to IAC (intracranial) = Meatal/IAC = Labyrinthine = Tympanic = Mastoid = Parotid before branching = |
Pons to IAC (intracranial) = 23-24mm
Meatal/IAC = 8-10mm Labyrinthine = 3-5mm Tympanic = 8-11mm Mastoid = 10-14mm Parotid before branching = 15-20mm |
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In parotid surgery, the facial nerve can be identified at 6-8mm below the inferior "drop-off" of the _______________________
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tympanomastoid fissue
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The chorda tympani branches off at about 5-7mm before the ___________________
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stylomastoid foramen
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Describe the Bell's phenomenon
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Upward and outward movement of the eye, when an attempt is made to close the eyes. It is a normal defense reflex present in about 75% of the population.
It may become noticeable in facial paralysis or when the orbicularis oris muscle becomes weak (Guillian-Barre). Absent in facial paralysis of central origin. |
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What is the most common cause of bilateral facial paralysis?
What do you suspec if there is a bilateral simultaneous facial paralysis? |
Guillain-Barre syndrome
Sign of central generalized disease |
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What does someone with facial nerve paralysis not involving the greater superficial petrosal nerve would have a "tearing" eye?
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1) Paralysis of Horner muscle that dilates the nasolacrimal duct orifice
2) Ectropion that produces malposition of the puncta 3) Absence of blinking (ie, lack of the pumping action) |
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What is Hitselberger's sign?
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Decreased sensitivity in the posterior-superior aspect of the concha (posterior EAC) corresponding to the sensory distribution of the CN7 (Arnold's nerve), suggests a space-occuping lesion in the IAC (ie. acoustic neuroma)
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The incidence of severe neural degeneration with Bell's palsy approximates ___%, whereas with herpes zoster oticus, the incidence approximates ___%
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Bell's palsy - 15%
Herpes zoster oticus - 40% |
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What is Melkersson-Rosenthal syndrome?
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Recurrent unilateral or bilateral facial palsy of unknown etiology. It is associated with chronic or recurrent edema of the face with fissuring of the tongue.
The peak age groups is the twenties. Histologically, dilated lymphatic channels, giant cells and inflammatory cells are seen. |
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Facial nerge regenerates how many mm/day?
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3 mm/day
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What are the most common motor nerves involved in herpes zoster oticus?
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Most common is CN7, then next are CN3, 4 and 6
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What is the most common site injury to the facial nerve following blunt head trauma with fracture of the temporal bone?
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Perigeniculate area
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