• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Bell's palsy

Bell's palsy



made easy

made easy



Total Views
Views on SlideShare
Embed Views



0 Embeds 0

No embeds



Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
Post Comment
Edit your comment

    Bell's palsy Bell's palsy Presentation Transcript

    • You wake up one morning, and your face feels stiff and odd. When you look in a mirror, half your face appears to droop. You can only manage half a smile, your eye is dripping tears and doesn't want to close. What in the world is going on?
    •  Charles Bell › Well known for his studies on the nervous system and the brain › In the 19th century discovered that lesions of the 7th cranial nerve causes facial paralysis
    • The 7th cranial nerve is paired with the structure that travels through a narrow, bony canal (called the Fallopian canal) in the skull beneath the ear to the muscles on each side of the face. The nerve is mostly encased in this bony shell.
    • Each nerve controls: › Eye blinking and closing › Facial expressions  Smiling and frowning › Tear glands › Saliva glands › Muscle of small bone in middle of ear called the stapes › Taste sensations
    •  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
    • Sunderland classification of nerve injury 1° damage = Compression 2° damage = Interruption of axoplasm 3° damage = Disruption of myelin 4° damage = Disruption of perineurium, myelin and axon 5° damage = Transection of nerve
    •  Characterized by: › Peripheral facial paralysis › Acute benign cranial polyneuritis Acute disorder characterized by a disruption of the motor branches of cranial nerve VII on one side of the face. (in absence of stroke)
    •  Varies from person to person › Comes on suddenly › Mild to total paralysis  Weakness, twitching on one of both sides of the face › Facial and eyelid droop › Drooling › Dryness of eye or mouth › Impairment of taste › Excessive tearing of eye
    •  Pain or discomfort in jaw and behind the ear  Ringing in one or both ears  Loss of taste  Headache  Hypersensitivity to sound  Impaired speech  Dizziness  Difficulty eating and drinking
    •  Often accompanied by an outbreak of herpes vesicles in or around the ear.  Pain around or behind the ear  Fever, tinnitus, hearing deficits  Flaccidity of the affected side of the face with drooping of the mouth accompanied by drooling DT paralysis of the facial nerve (motor branches)
    •  Inability to close the eyelids, with an upward movement of the eyeball when closure is attempted; lower lid may turn out  Wide palpebral fissure (opening between eyelids)  Flattening of the nasolabial fold  Inability to smile, frown, or whistle  Unilateral loss of taste  Altered chewing ability; loss of or excessive tearing
    •  Grade I - Normal  Grade II - Mild dysfunction, slight weakness on close inspection, normal symmetry at rest  Grade III - Moderate dysfunction, obvious but not disfiguring difference between sides, eye can be completely closed with effort  Grade IV - Moderately severe, normal tone at rest, obvious weakness or asymmetry with movement, incomplete closure of eye  Grade V - Severe dysfunction, only barely perceptible motion, asymmetry at rest  Grade VI - No movement
    •  To determine the anatomical level of a peripheral lesion  Lacrimation  Geniculate ganglion  Stapedius reflex  motor nerve of stapedius muscle  Taste  chorda tympani
    •  Geniculate ganglion & petrosal nerve function test  Schirmer’s test +ve when › Affected side shows less than half the amount of lacrimation seen on the normal side › Sum of the lengths of wetted filter paper for both eyes less than 25 mm  Lesion at or proximal to the geniculate ganglion
    •  Nerve to stapedius muscle test  Impedance audiometry can record the presence or absence of stapedius muscle contraction to sound stimuli 70 to 100 dB above hearing threshold  An absence reflex or a reflex less than half the amplitude is due to a lesion proximal to stapedius nerve
    •  Chorda tympani nerve test  Solution of salt, sugar, citrate, quinine or Electrical stimulation  Compares amount of current require for a response each side of tongue  Normal : difference < 20 uAmp (thresholds differening by more than 25%= abnormal)  Total lack of Chorda tympani : No response at 300 uAmp  Disadvantage : False +ve in acute phase of Bell’s palsy
    •  It occurs when the facial nerve is swollen, inflamed, or compressed
    •  Mostly unknown  May be caused by a viral infection › Viral meningitis › Herpes simplex  Influenza  Headaches  Chronic ear infections  High blood pressure  Diabetes  Sarcoidosis  Tumors  Lyme disease  trauma
    •  Affects 40,000 Americans each year › Men and women equally affected › Can occur at any age  Mostly after 15 and before 60 y/o  Occurs more often in people who: › Are pregnant › Are diabetic › Have an upper respiratory infection
    •  Psychological withdrawal DT changes in appearance, malnutrition or dehydration, mucous membrane trauma, corneal abrasion, muscle stretching, and facial spasms and contractures.
    •  There are no specific lab tests to confirm diagnosis  Will exam for upper and lower facial weakness  Electromyography › Confirm presence of damage and determine severity  MRI and CT › r/o causes of pressure on nerve
    •  No real Treatment › Symptoms usually subside  Anti-inflammatory and an antiviral › Prednisone and acyclovir  Increases the chance of recovery  Acupuncture and surgery › For long term paralysis
    •  Hard to close eye › Use and eye patch › Eye drops › Tape eye shut when sleeping
    •  Corticosteroids- drug of choice  Prednisone may be started immediately! › Best if initiated before paralysis is complete › Taper off over 2 weeks › Decrease edema and pain Analgesics may be needed for pain Antivirals : Acyclovir (Zovirax) and Famvir because HSV is implicated in 70% of cases.
    •  Outcome is good!!!  Total recovery depends on amount of damage to nerve  Improvement is gradual  Usually start to get better after 2 weeks of onset and most recover completely within 3 to 6 months.  In a few cases, the symptoms may never completely disappear.  In rare cases, the disorder may recur, either on the same or the opposite side of the face.
    •  Clinical features › Slower onset of symptoms › Bilateral › Recurrence  Numbness is not unusual  Progression beyond seven days suggests another cause
    •  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
    •  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
    •  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%)
    •  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
    •  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
    •  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
    •  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