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Year 3 > Bell's palsy (N) > Flashcards

Bell's palsy (N) Flashcards

1
Q

Define Bell’s palsy.

A

Acute, unilateral, idiopathic, peripheral facial nerve palsy (paralysis) in patients for whom physical examination and history are otherwise unremarkable

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2
Q

Deficits in Bell’s palsy affect which facial zones?

A

Affects all facial zones equally - no forehead sparing

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3
Q

How long does it take for deficits in Bell’s palsy to fully evolve?

A

Deficits affecting all facial zones equally fully evolve within 72 hours

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4
Q

Is Bell’s palsy an UMN or LMN condition?

A

LMN condition - unlike UMN conditions of the face, LMN conditions affect the entire side of the face - in this case ipsilateral CN VII affected

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5
Q

Which demographics is Bell’s palsy most common in? (2)

A
  • 15-45y/o
  • pregnant women
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6
Q

What condition are most cases of Bell’s palsy preceded by?

A

URTI - suggests viral or post-viral aetiology

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7
Q

Which virus has a strong correlation with Bell’s palsy?

A

Herpes simplex virus type 1 (HSV-1) - affects the geniculate ganglion

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8
Q

Describe the aetiology of Bell’s palsy.

A
  • reactivation of HSV-1 within the geniculate ganglion
  • infection of Schwann cells –> demyelination and neural inflammation
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9
Q

How can you tell whether a lesion is UMN or LMN?

A
  • assess for forehead sparing on affected side
  • if no forehead sparing: LMN lesion
  • if forehead sparing: UMN (i.e. stroke) - because forehead innervated by both sides of cerebral cortex, so a unilateral stroke will not paralyse the forehead as ipsilateral UMN still functions
  • forehead sparing = can wrinkle forehead, raise eyebrow and close eye on affected side, but cheeks and mouth still affected
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10
Q

What are the clinical features of Bell’s palsy? (11)

A
  • single episode
  • unilateral acute facial weakness and droop
  • absence of constitutional symptoms (fever, malaise, myalgia, arthralgia, headache, rash)
  • non-forehead sparing = ipsilateral LMN lesion
    • forehead sparing = contralateral UMN lesion
  • all branches of facial nerve involved
  • keratoconjunctivitis sicca (dry eyes and mouth) - lack of adequate blink function + parasympathetic dysfunction of lacrimal gland
    • may later progress to epiphora and gustatory hyperlacrimation
  • hyperacusis - hypersensitivity to loud noises
  • dysgeusia - loss of taste in anterior 2/3 of tongue
  • synkinesis - involuntary and abnormal movements of face
  • speech impairment
  • pain - post-auricular pain and mild-mod otalgia
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11
Q

What might you see on examination of Bell’s palsy? (3)

A
  • involvement of all facial nerve branches - equal distribution of facial weakness
  • hyperacusis - hypersensitivity to loud noises
  • dysgeusia - taste disturbance anterior 2/3 of tongue
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12
Q

What might the face of a patient with Bell’s palsy look like? (7)

A
  • inability to wrinkle forehead
  • inability to raise brow
  • droopy eyelid + inability to close eye (–> irritation)
  • inability to puff cheek
  • asymmetrical smile
  • asymmetrical facial muscle tone
  • ‘sagging’ face
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13
Q

Describe the Bell phenomenon seen in patients with Bell’s palsy.

A

When asked to close eyes, unaffected eye closes but affected side does not, with eyeball rolling upwards

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14
Q

What are some risk factors for Bell’s palsy? (10)

A
  • intranasal influenza vaccination
  • pregnancy (3x risk)
  • HSV exposure (infection or vaccination)
  • URTI
  • arid/cold climate
  • hypertension
  • diabetes
  • Fx
  • Black/Hispanic ancestry
  • dental procedures
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15
Q

What is the main method of diagnosis of Bell’s palsy?

A

Clinical diagnosis of exclusion - acute unilateral facial palsy with otherwise normal physical examination

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16
Q

What other investigations can be done for Bell’s palsy? (3)

A
  • electroneuronography (ENoG AKA evoked EMG) - if near-complete/complete facial paralysis o/e, should be done 72h-14d after onset
  • needle electromyography (EMG) - used to confirm absence of voluntary motor unit potentials in facial musculature of one side
  • serology for Borrelia burgdorferi - indicated in all patients with recent travel to Lyme disease-endemic area
17
Q

When can Bell’s palsy NOT be diagnosed? (3)

A
  • facial palsy of an otherwise known aetiology (e.g. Lyme disease-associated facial palsy)
  • facial palsy that is progressive, waxing and waning
  • affects facial zones in an uneven fashion / forehead sparing
18
Q

What are some differential diagnoses for Bell’s palsy? (8)

A
  • Herpes Zoster oticus (Ramsay Hunt Syndrome)
  • stroke - sparing of upper 1/3 of face, presence of other neurological deficits if cortical
  • Lyme disease - skin rash, frontal headache, bilateral
  • facial nerve tumour - progressive
  • chronic otitis media or cholesteatoma
  • necrotising otitis media
  • idiopathic orofacial granulomatosis
  • uveoparotid fever
19
Q

What scale is used to measure the severity of facial nerve damage or paralysis in Bell’s palsy?

A

House-Brackmann score:

  • 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
20
Q

What is the 1st-line management for acute Bell’s palsy?

A

Corticosteroid (prednisolone PO) within 72hrs (careful in patients with DM, immunodeficiency, poorly controlled hypertension, Hx psychosis)

PLUS eye protection (glasses, artificial tears, ophthalmic lubricant, eye taping at night) - eye will dry out –> corneal damage

21
Q

How do we manage severe palsy/complete palsy on presentation of Bell’s palsy? (3)

A
  • corticosteroid (prednisolone) + eye protection
  • concurrent antiviral therapy (valaciclovir, acyclovir)
  • surgical decompression:
    • clinical undetectable unilateral facial movement
    • facial palsy onset within 14d
    • ENoG performed 72h-14d
    • needle EMG confirms absence of voluntary motor unit potentials in facial musculature
22
Q

What do you do if no signs of improvement after 3 weeks of Bell’s palsy?

A

Immediate urgent ENT referral

23
Q

What are some complications of Bell’s palsy? (6)

A
  • keratoconjunctivitis sicca
  • exposure keratopathy
  • ulcerative keratitis (eye ulcers)
  • ectropion (sagging eyelid)
  • contracture and synkinesis
  • gustatory hyperlacrimation
24
Q

Describe the prognosis of Bell’s palsy.

A

85-90% recover function with 2-12 weeks with/without treatment

Some develop permanent weakness/paralysis

Year 3 (145 decks)

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