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Imaging in Acute Facial Nerve Paralysis. M Castillo, MD, FACR Department of Radiology University of North Carolina, Chapel Hill. Overview of Presentation. Introduction Review of facial nerve anatomy Clinical and Imaging features of Bell’s palsy Typical Atypical
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Imaging in Acute Facial Nerve Paralysis M Castillo, MD, FACR Department of Radiology University of North Carolina, Chapel Hill
Overview of Presentation • Introduction • Review of facial nerve anatomy • Clinical and Imaging features of Bell’s palsy • Typical • Atypical • Other causes of acute facial paralysis
Introduction • Bell’s palsy accounts for 75% of cases of acute facial nerve (7th cranial nerve) paralysis • Imaging is not needed in majority of patients unless they have atypical features • W/atypical features, MR & CT may demonstrate potentially treatable lesions affecting facial nerves • Facial nerves can be affected anywhere along their course
Anatomy Review • Facial nerve nuclei lie in reticular formation of brainstem, ventral to floor (tegmentum) of 4th ventricle(4) • Motor Nuclei: • Efferent fibers surround nuclei of CN VI & form small mounds on floor of 4th ventricle (facial colliculi) • Non-Motor Nuclei: • Salivatory • Solitary Facial colliculus
Efferent fibers surround 6th CN nucleus & exit at cerebellopontine angle (CPA) • 7th nerve courses into internal auditory canal (IAC) • Within superior anterior quadrant(6) Ant Post
FallopianCanal • Exits IAC via Fallopian canal • Narrowest point throughout entire course • Felt to be culprit in facial nerve compression in Bell’s palsy & other causes of nerve swelling
Geniculate ganglion • Progress to geniculate ganglion • Gives rise to greater superficial petrosal nerve • Contains taste axons from tongue & somatic fibers
Fibers then course posteriorly under lateral semicircular canal in middle ear (tympanic portion) • Fibers angle back & inferiorly at “second genu” diving the descending canal • Here last somatic & parasympathetic fibers separate from facial nerve via the chorda tympani nerve Mastoid segment Tympanic Portion
Facial nerve exits skull base at stylomastoid foramen • Facial nerve angles superiorly & anteriorly behind posterior margin of vertical mandibular ramus • Just before entering parotid gland, inferior branches originate • Posterior auricular, digastric & stylohyoid • Within substance of parotid gland, superior branches arise • Temporal, zygomatic, buccal, orbicularis oris, mandibular & cervical
Clinical Signs Suggesting Site of Facial Nerve Lesion • Upper facial territory is supplied by bilateral motor cortices • Lower facial territory is supplied only by contralateral motor cortex • Therefore, unilateral central lesions spare upper face • Lesions distal to geniculate ganglion • Mostly motor abnormalities • Lesions proximal to geniculate ganglion • Motor, gustatory & autonomic abnormalities
Typical Bell’s Palsy • Incidence • 15–30 per 100,000 • Usually during winter • Etiology not entirely understood • Possibly viral (Herpes Simplex Virus) or idiopathic • Viral infection of facial nerve results in demyelination, inflammation & swelling • Traps nerve in narrow confines of fallopian canal • Diagnosis of exclusion • Made only when clinical & imaging (if necessary) findings are supportive
Typical Bell’s Palsy • Usually a clinical diagnosis • Acute onset unilateral (lower or upper) facial paralysis, posterior auricular pain, decreased tearing, hyperacusis (30%) & disturbances of taste • By physical examination, Bell’s palsy divided according to classification by House and Brackman • Grades 1 & 2 have better outcomes with worse outcome as grade increases. • 80-90% recover completely • Over age 60, only 40% recover completely
Imaging in Typical Bell’s Palsy • Imaging in typical Bell’s palsy is not usually necessary • When necessary, MRI is best • Normal facial nerve distal to geniculate ganglion may enhance • Facial nerve proximal to geniculate ganglion does not normally enhance • In patients with Bell’s palsy, enhancement of facial nerve in fallopian & ICA is typical
Atypical Bell’s Palsy • Clinical features • Slower onset of symptoms • Bilateral • Recurrence • Numbness is not unusual • Progression beyond seven days suggests another cause
Imaging in Atypical Bell’s Palsy C/o Dr. M. Michel, Wisconsin
Alternative Causes of Acute Facial Nerve Paralysis • Atypical signs & symptoms which suggest etiology other than Bell’s palsy require imaging • Clinical history is crucial in distinguishing etiologies • Choice of imaging technique depends on clinical suspicion
Lyme Disease • Lyme disease (borreliosis) • Endemic areas (Northeast USA, central Europe, Scandinavia, Canada) • Consider in children w/atypical facial palsy • Imaging: small white matter lesions similar to multiple sclerosis, enhancement of facial & other cranial nerves • Bilateral facial paralysis: 25% • Important to make diagnosis early because it is curable early w/antibiotics
Ramsay Hunt Syndrome • Caused by reactivation varicella zoster virus (herpes virus type 3) • Facial paralysis + hearing loss +/- vertigo • Herpes zoster oticus • Two-thirds of patients have rash around ear • Other cranial nerves, particularly trigeminal nerves (5th CN) often involved • Worse prognosis than Bell’s (complete recovery: 50%) • Important cause of facial paralysis in children 6-15 years old
Infectious causes • Acute facial paralysis may result from bacterial or tuberculous infection of middle ear, mastoid & necrotizing otitis externa • Incidence of facial paralysis with otitis media: 0.16% • Infection extends via bone dehiscences to nerve in fallopian canal leading to swelling, compression & eventually vascular compromise & ischemia • Immune compromised patients are at risk for pseudomona infection • Poor prognosis (complete recovery is < 50%)
Trauma • Most acute post traumatic facial palsies are due to t-bone fractures • Historically fractures classified as longitudinal or transverse with transverse carrying risk of permanent paralysis • Longitudinal fracture usually leads to temporary paralysis from concussion & swelling of nerve • Transverse fracture can lead to transection of nerve • In all types of paralysis due to fracture, usually the region of geniculate ganglion is involved
Neoplasms • 27% of patients with tumors involving the facial nerve develop acute facial paralysis • Most common causes: schwannomas, hemangiomas (usually near geniculate ganglion) & perineural spread such as with head and neck carcinoma, lymphoma & leukemia • Other neoplasms can also involve the facial nerve • Adults: metatstatic disease, glomus tumors, vestibular schwannomas & meningiomas • Children: eosinophilic granuloma & sarcomas
Glomus Tumor • Glomus tumors arising from jugular bulb (jugulare) and/or middle ear (tympanicum) may involve the facial nerve M
Other tumors Rhabdomyosarcoma & squamous cell carcinoma of the EAC
Vestibular Schwannoma • Common tumor • However, facial nerve is resistant to compression • Therefore, tends to produce facial paralysis mostly when they attain a large size
Vestibular Schwannoma -Common tumor -However, facial nerve is resistant to compression, thus, tends to produce facial paralysis mostly when they attain a large size
Meningioma • Second most common primary tumor of cerebellopontine angle • Rarely results in facial paralysis
Hypertrophic Polyneuropathy • Hypertrophic polyneuropathies occasionally lead to facial paralysis
Other Causes • Guillain-Barre Syndrome • Ascending paralysis • Iatrogenic • Temporal bone surgery • Excision of vestibular schwannoma has <10% chance of paralysis • Middle ear surgeries • Babies who required forceps delivery • >90% recovery
Melkersson-Rosenthal Syndrome • Acute episodes of facial paralysis • Facial swelling • Fissured tongue • “Scrotal” tongue • Very rare • Familial but sporadic • Usually begins in adolescence • Leads to facial disfigurement • No definite therapy
Conclusion • While Bell’s palsy does not typically require imaging for diagnosis, imaging evaluation is important in the work-up of patients with atypical or unusual presentations of acute facial nerve paralysis, identification of discreet lesions may lead to a change in management of these patients.