Bell's Palsy Flashcards

1
Q

What is Bell’s palsy?

A
  • acute unilateral peripheral facial nerve palsy
  • physical examination and history are otherwise unremarkable
  • consisting of deficits affecting all facial zones equally
  • symptpms fully evolve within 72 hours.
  • remains a clinical diagnosis of exclusion
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2
Q

In what % of pts with Bell’s palsy does complete recovery to normal facial function occur?

A

70%

small % are left with permanently impaired facial function

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3
Q

How long does it take for clinical recovery (Bell’s palsy)?

A
  • 4 to 6 months of symptom onset;

lack of any return of hemi-facial tone / movement by this time is highly suggestive of an alternative diagnosis

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4
Q

Are the following symptoms in line with Bell’s palsy?

a) progressive palsy
b) waxing and waning palsy
c) palsy affecting facial zones in an uneven fashion,

A

a, b, c = NO

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5
Q

What is the cause of Bell’s palsy?

A

reactivation of HSV-1 within geniculate ganglion

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6
Q

What are the classifications of Bell’s palsy according to House-Brackmann scale (HBS)?

A
  • Grade I = normal
  • Grade II = slight weakness/asymmetry
  • Grade III = obvious weakness with movement but absence of disfigurement at rest; intact ability to close the eye
  • Grade IV = obvious weakness with movement and disfigurement at rest; inability to fully close the eye
  • Grade V = barely perceptible movement
  • Grade VI = no movement.
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7
Q

What are the risk factors for Bell’s palsy?

A
  • intranasal inactivated flu vaccine - now discontinued
  • pregnancy
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8
Q

What are the primary investigations for ?Bell’s palsy?

A
  • thorough Hx and examination –> clinical diagnosis
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9
Q

What investigations should be conducted if the primary investigations are inconclusive for ?Bell’s palsy

A

if uncertainty about diagnosis:

  • electroneuronography (72hrs - 14 days of symptom onset)
    • >90% decrease in amplitude of compound muscle action potential vs non-affected side –>
  • needle electromyography (EMG)
    • if absence of voluntary motor unit potentials found

–> REFER TO NEURO team for possible nerve decompression

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10
Q

What investigation should be routinely conducted in pts with recent travel Hx and symptoms of Bell’s palsy?

A
  • serology for Borrelia burgdorferi
    • (organism causing Lyme disease)
    • should be negative for confirmation of Bell’s palsy
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11
Q

Which investigations should be ordered if:

a) primary investigation suggests alternative diagnosis?
b) neoplasm is suspected?
c) otoscopy suggests middle ear disease/facial or head trauma?

A

a) pure tone audiometry & tympanometry and stapedius reflex
b) MRI (gadolinium-enhanced fine-cut of facial nerve course)
c) CT head

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12
Q

What is the management plan for Bell’s palsy?

A

reducing recovery time

  • Oral corticosteroids (within 72hrs of symptoms)
    • anti-inflammatory effect: reduced nerve oedema & minimised nerve insult
  • antiviral therapy
    • decreased viral load & subsequent axonal & Schwann cell injury

preventing exposure keratopathy

  • DAY: glasses protection (not a patch)
  • DAY: artificial tears used as needed
  • Overnight: ophthalmological lubricant ointment
  • Overnight: lid taped closed

preventing severe facial synkinesis (compl.)

  • only indicated in those w 90+% degeneration on electroneuronography (ENoG),*
  • Surgical decompression of the bony fallopian canal from the internal auditory canal to the stylomastoid foramen
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13
Q

In which patients should caution be exercised before prescribing high dose corticosteroids?

A
  • poorly-controlled DM
  • immunodeficiency
  • poorly-controlled HTN
  • prior history of psychosis.
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14
Q

Which factors are indicators of poor prognosis for early return of function?

A
  • complete flaccid paralysis on presentation
  • older adult
  • taste disturbance
  • diabetes mellitus
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15
Q

What is the rationale behind surgical nerve decompression as a treatment for severe Bell’s palsy?

A

surgical decompression of the facial nerve

  • removal of approx. 180 degrees of confining fallopian canal bone
    • incision of epineurium from porus acousticus to stylomastoid foramen
  • –> provides space for facial nerve to swell
  • –> reducing progression of virally-triggered compressive neuropathy & subsequent ischaemic neural insult.
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16
Q

What is the criteria for patients to be considered for surgical nerve decompression as a treatment for Bell’s palsy?

A
  • Clinically undetectable unilateral facial movement
  • Facial palsy onset within 14 days
  • ENoG (eEMG) performed between 72 hours and 14 days of facial palsy onset demonstrates >90% reduction in the amplitude of the compound muscle action potential (CMAP) using a supra-threshold neural stimulus as compared to the normal side
  • Needle EMG confirms absence of voluntary motor unit potentials in facial musculature.
17
Q

What is Bell’s phenomenon?

A

protective reflex in which eye globe rotates upwards + outwards with attempts at eye closure

(see image - patients’ right eye = affected)

18
Q

What are the indications for an ophthalmological consulation in pts with Bell’s palsy?

A
  • only seeing eye affected (i.e. blind in unaffected eye)
  • suspicion of exposure keratitis
  • decreased or absent corneal sensation.
19
Q

Opthalmologists may consider:

  • early upper eyelid weight placement OR
  • tarsorrhaphy (eyelids are partially sewn together to narrow the eyelid opening)

for which patients?

A
  • patients who lack Bell’s phenomenon
  • prognosis for early rapid return of function is poor
20
Q

Name some complications of Bells palsy

A

1) keratoconjunctivitis sicca (dry eye)

  • due to ineffective lubricating tear film
    • ineffective cornea-protective blink response
    • reduced parasympathetic function to lacrimal gland

2) exposure keratopathy (damaged cornea due to increased exposure to outside environment)
* (via physical/infectious mechanisms)

~ –> ulcerative keratitis (corneal ulcer) AND blindness

3) ectropion (sagging eyelid)

  • (rarely persists, only in flaccid stage)
    4) contracture & synkinesis (= eye muscle moves simultaneously w other facial muscles)
  • due to increased neural irritability
  • and aberrant regeneration of motor axons
  • can be treated w botox to overactive muscle

5) Gustatory hyperlacrimation

  • nasal cavity + palate: aberrant regeneration of pre-ganglionic parasympathetic fibres carried within facial nerve supplying lacrimal gland and mucosal glands (via the greater superficial petrosal nerve)
  • oral cavity: “” supplying submaxillary, sublingual, and minor salivary glands
  • can be treated w botox to lacrimal gland
21
Q

Which parameter is the most predictive of ultimate recovery outcome from Bell’s palsy/

A

extent of facial palsy following complete evolution of Bell’s palsy (i.e., within 72 hours of onset)

22
Q

What is the prognosis for patients with Bell’s palsy?

A
  • present w incomplete paralysis: 94% fully recover
  • present w complete paralysis:61% fully recover
  • if electroneuronography (ENoG) = >95% difference between sides <14 days of symptom onset spontaneous return of (near) normal facial function (i.e., HBS I or II) = reduced by 50%

worse outcomes in those w/who are:

  • pregnant
  • uncontrolled HTN/DM
  • old age
  • taste disturbance