A.2 - The Facial nerve Flashcards

1
Q

what is the facial nerve?

A
  • The facial nerve = CN 7
  • contains:
    1. mainly motor fibers supplying the muscles of facial expressio
    2. visceral efferent parasympathetic
    3. visceral afferent (taste) fibers.
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2
Q

where does the facial nerve exists?

A

Both nerves leave the brainstem adjacent to the vestibular nerve, between the inferior cerebellar peduncle and the olive

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3
Q

what are the facial nerve fibers?

A

Sensory
gustatory sensation
Autonomic
motor

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4
Q

where is the motor nucleus of the facial nerve located?

A

lies in the lower pons,
medial to the descending nucleus and tract of the Vth cranial nerve.

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5
Q

where does the facial nerve branch off?

A

The facial nerve gives off several branches before exiting from the skull through the stylomastoid
foramen.

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6
Q

what is nervus intermedius?

A

The facial nerve and its visceral root

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7
Q

route of nervous intermedius

A

exit from the lateral aspect of the
brainstem and cross the cerebellopontine angle immediately adjacent to the VIII cranial nerve →
internal auditory meatus → facial canal of the temporal bone (lie in close proximity to the inner ear and tympanic membrane)

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8
Q

route of Visceral efferent and visceral afferent fibres

A

They run together as the nervus intermedius and accompany the facial nerve to the internal auditory meatus.

arise and terminate in the superior salivary nucleus and solitary nucleus/tract respectively

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9
Q

route of facial nerve visceral efferent fibers

A

The parasympathetic fibres (visceral efferent) pass in the greater petrosal nerve
→ sphenopalatine /pterygopalatine ganglion
→ lacrimal gland (producing tears) + in the chorda tympani nerve
→ submandibular ganglion.

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10
Q

what does the chorda tympani nerve contain?

A

parasympathetic efferent and visceral afferent fibres.

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11
Q

what are chorda tympani parasympathetic fibers responsible for?

A

salivation.

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12
Q

what sensations Visceral afferent fibres of the chorda tympani convy?

A

taste from the anterior two-thirds of the tongue.

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13
Q

where are the cell bodies of the visceral afferent fibers of the chorda tympani?

A

geniculate ganglion contains the bipolar cell bodies

visceral afferent fibers = taste

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14
Q

Supranuclear control of facial muscles

A

● Upper face:
both hemispheres (bilateral representation)

● Muscles of lower face:
contralateral hemisphere

● Lower motor neuron lesion → paralyses all facial muscles on that side

● Upper motor neuron (supranuclear) lesion → paralyses the muscles in the lower half of the face
on the opposite side.

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15
Q

Clinical examination of the facial nerve?

A

facial weakness
taste impairment
reduced lacrimation on one side
reduced salivation on one side
hyperacusis (exaggeration of sounds -loss of the stapedius reflex-).

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16
Q

Facial weakness is due to?

A
  1. lesion in pons : VI nerve palsy
  2. lesion at cerebellopontine angle/ IAM):
    V, VIII, (IX, X, XI) nerve palsies
  3. lesion in facial canal:
    Loss of taste and salivation, hyperacusis
  4. facial nerve lesions : diabetes, infectious mononucleosis
  5. peripheral nerve lesion :
    Lacrimation, taste and salivation retained, weakness localized to specific muscle group
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17
Q

where is the lesion localised in case of VI nerve palsy, contralateral limb weakness

-what are the causes

A

→ Pons

→ Causes:
-vascular
-demyelination
-tumor
-encephalitis
-syringobulbia
-motor neuron disease

18
Q

where is the lesion localised in case of V, VIII, (IX, X, XI) nerve palsies, where there is loss of:
- taste, salivation
- lacrimation
- and hyperacusis

A

→ Cerebellopontine angle/internal auditory meatus

Causes:
-acoustic tumors
-meningioma
-epidermoid
-glomus jugulare tumor

19
Q

where is the lesion localised in case of:
1. Loss of taste and salivation (proximal to nerve to stapedius)
2. hyperacusis
3. but retained lacrimation retained lacrimation

???

A

→ Facial canal

→ Causes: f
- racture of skull base
- spread of middle ear infection
- herpes zoster
- Ramsay-Hunt synd (geniculate ggl)
- petrous-temporal carcinoma
- Bell’s palsy
- leukemia deposits

20
Q

where is the lesion localised in case of:
Lacrimation, taste and salivation are all retained but weakness may be localized to a specific muscle group

A

→ Peripheral nerve

→ Causes: parotid gland lesion (eg. uveoparotid fever of sarcoidosis), parotid operations,
facial trauma

21
Q

what could be Other causes of facial nerve lesions?

A

diabetes
infectious mononucleosis

22
Q

what is Bell’s palsy

A

Acute idiopathic peripheral facial palsy is also known as Bell palsy

Acute paralysis of the face related to inflammation and swelling
of the facial nerve within the facial canal or at the stylomastoid
foramen.

It is usually unilateral and may occur repetitively.

A family history can sometimes be found.

23
Q

what is the etiology for Bells palsy?

A

Etiology:
* primary: idiopathic

Secondary:
* Trauma (e.g., temporal bone fracture)
* Infection:
*Herpes zoster (Ramsay Hunt syndrome)
*Borreliosis (Lyme disease)
*HSV reactivation
*HIV
*Malignant otitis externa
* Tumors (parotid gland tumors, acoustic neuroma)
* Pregnancy
* Diabetes mellitus
* Guillain-Barré syndrome
* Sarcoidosis (Heerfordt syndrome)
* Amyloidosis
* Stroke

  • epidemics of Bell’s palsy occur sporadically

-borellia can cause bilateral bells palsy

24
Q

Symptoms of bells palsy?

A

● Pain of variable intensity over the ipsilateral mastoid
precedes weakness, which develops over a 48h period

● Impairment of taste, hyperacusis and salivation depend
on the extent of inflammation and will be lost in more severe cases

● Lacrimation is rarely affected

● Bell´s phenomenon : attempt to close eyes and show teeth → one eye unable to close, eyeball rotates upward and outwards

25
Q

what does bells palsy diagnosis depends on?

A

on typical presentation and exclusion of:
- middle ear disease
- diabetes
- sarcoidosis
- Lyme disease

26
Q

bells palsy th

A

● Acute stage: Protect exposed eye during sleep

● High dose prednisolone for 10 days has shown improved recovery

● Role of antiviral therapy less clear

● Eye care (shielding and artificial tears) is important in preventing corneal abrasion.

27
Q

bells palsy prognosis?

A

● Most patients (70%) recover in 4-8 weeks w/o treatment

● Residual facial asymmetry may require corrective surgery in the remaining 30%

● Incomplete paralysis → good prognosis

● In patients with complete paralysis → electrical absence of denervation on electromyography is
an optimistic sign

28
Q

what is Ramsay Hunt syndrome?

A

Herpes zoster infection of the geniculate (facial) ggl

29
Q

the symp’s of Ramsay Hunt syndrome?

A

○ Sudden severe facial weakness with a typical zoster vesicular eruption within the external auditory meatus

○ Pain is a major feature and may precede the facial weakness

○ Serosanguinous fluid may discharge from the ear

30
Q

complications of Ramsay Hunt syndrome?

A

Deafness may result from VIII involvement, occasionally other cranial nerves from V-XII are
affected

31
Q

Treatment of Ramsay Hunt syndrome?

A

Acyclovir may help

32
Q

what are Hemifacial spasm?

A

unilateral clonic spasms beginning in the orbicularis oculi and spreading to
involve other facial muscles.

Contractions are irregular, intermittent and worsened by emotional stress and fatigue

33
Q

what happens if stapedius m is affecred in hemifacial spasm?

A

subjective ipsilateral
clicking sound

34
Q

Onset of Hemifacial spasm?

A

middle to old age, more common in females

35
Q

Cause of hemifacial spasms

A

usually vascular compression of the facial n. at the root entry zone.

Sometimes caused by tumor compressing the nerve.

36
Q

Diagnosis of hemifacial spasms?

A

exclude tics, and “focal” seizures selectively affecting the face.

MRI of posterior fossa excludes the presence of cerebellar pontine angle lesion and may show a dilation of the basilar artery

37
Q

Treatment of hemifacial spasms

A

○ Drugs:
local injection of botulinum toxin of involved muscles.
Effect only last 3 months

○ Surgery:
Post. fossa exploration and microvascular decompression (cure rate 80%), carries the risk of producing deafness and rarely brain stem damage

38
Q

mention some other facial nerve lesions?

A
  • Tonic facial spasm
  • Facial myokymia
  • Myoclonus
  • Blepharospasm
39
Q

what is Tonic facial spasm?

A

Less common than hemifacial spasm.

Occurs with cerebellar pontine angle
lesions.

It produces tonic elevation of the corner of the mouth with narrowing of the eye.

The diagnosis is confirmed by CT/MR scanning and treatment is surgical.

40
Q

what is Facial myokymia?

A
  • rare condition seen most often in multiple sclerosis.
  • Flickering of facial muscles results from spontaneous discharge in the facial motor nucleus.
  • Other brainstem signs
    are present.
  • The facial movements respond to carbamazepine.
41
Q

what is Myoclonus?

A

Rhythmic facial movement associated with similar palatal movements and
characteristic of dentate or olivary nucleus disease

42
Q

what is Blepharospasm?

A

Spasmodic closing or screwing up of eyes