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3P: Neuro > Eyelid And Facial Nerve Disorders > Flashcards

Eyelid And Facial Nerve Disorders Flashcards

1
Q

Contraction of the palpebral portion of orbicularis oculi

A

Closes the eyelid gently

  • spontaneous blinking
  • reflex blinking
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2
Q

Contraction of the orbital portion of orbicularis oculi muscle

A

Closes the eyelid tightly

  • voluntary blinking (winking)
  • reflex blepharospasm (benign essential blepharospasm)
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3
Q

Inferior limit of eyelids

A

Nasojugal sulcus

Malar sulcus

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4
Q

Medial canthus

A

Caruncle

Police semilunaris

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5
Q

Sensory innervation of the upper eyelid

A 
Trigeminal (CNV)
-supraorbital
Supratrochelar 
Infratrochlear 
Lacrimal
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6
Q

Lower eyelid sensory

A

CNV (V2)

  • infratrochelear )branch of ophthalmic nerve)
  • infraorbital nerve (branch of maxillary nerve)
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7
Q

Motor innervation of eyelids

A

Orbicularis oculi
=branches of facial nerve CN VII
-zygomatic and temporal

Levator
-superior division of CN III

Muller muscle
-sympathetic

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8
Q

Supranuclear pathways of facial nerve for eyelids

A
  • axon from the precentral gurus of the frontal lobe descend within the corticobulbar tracts
  • at the of the facial nerve nucleus in the pons, most supranuclear fibers cross over the opposite site to innervate the contralateral facial nerve nucleus
  • other cortobulbar fibers innervat the ipsilateral facial nerve nucleus
  • thus, the upper face is innervate by both hemispheres
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9
Q

Facial weakness (CN VII) tests to do

A

raise eyebrows

- if he can on the right, its located on the left central part

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10
Q

Contralateral lower facial weakness

A

Supranuclear (central) contralateral

  • usually assocaited with weakness of the ipsilateral arm
  • supranuclear paralysis of voluntary eyelid closure
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11
Q

Nuclear and infranuclear (central) facial nerve

A

CNVII loops around CNVI nucleus in the pons
-travel out laterally
-

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12
Q

Mobius sybdrome

A
  • congenital facial diplegia is the hallmark
  • bilateral abducents palsy is the most commonly associated feature, occurring in 82% of cases
  • also assocaited with external ophthalmoplegia, oculomotor palsy, bilateral ptosis
  • uncommonly the disorder is inherited
  • drug induced in some cases
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13
Q

Facial colliculus syndrome

A

the CN VII nerve fascicles may be disrupted dorsally

  • characterized by an ipsilateral peripheral facial palsy and conjugate gaze paresis
  • in combination with ipsilateral deafness, facial numbness, and a Horner sybdrome

The CNVII nerve fascicles may be disrupted ventrally

  • lead to ipsilateral facial paresis
  • in combination with contralateral hemiparesis (Millard-Gubler syndrome)
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14
Q

Acoustics neuroma

A
  • happens on the cerebellopontine angle (peripheral)
  • ipsilateral upper and lower facial weakness
  • CN VII palsy either late in their course as the facial nerve is displaced and compressed by an expanding cerebellopointine tumor or as a postop complication after neurosurgical rresection
  • common symptoms: tinnitus, hearing loss, and cererbellar and vestibular signs
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15
Q

Facial weakness on extrancranial nerve course (peripheral)

A

Subarachnoid

  • Lyme disease (bialteral or unilateral weakness)
  • neurosarcoidosis
  • metastatic lesions

Transtemporal bone

  • truama
  • Bell’s palsy
  • Ramsay hunt syndrome (cephalic herpes zoster)
  • otitis media
  • congential facial palsy
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16
Q

Bell’s palsy

A
  • ipsilateral upper and lower facial palsy
  • idiopathic facial palsy that may have a viral cause
  • in combination with ipsilateral ear pain, numbness, or jhyperacusis
  • excelled prognosis (84% fully recover)
  • prognosis for recovery is worse in patients with hyperacusis, decreased tearing, age greater than 60, diabetes, HTN, and psychiatric disease
  • may recur in 10-20% of affected people
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17
Q

Facial weakness at the NMJ, myopathic (peripheral)

A
  • MG
  • botulism
  • Guillain-Barre syndrome and Miller Fisher syndrome
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18
Q

GB syndrome and Miller Fisher syndrome

A
  • acute inflammatory demyelination of peripheral nerves (AIDP)
  • patients present with motor weakness affecting the limbs and trunk
  • eye movement abnormalities are prominent in the MIller Fisher syndrome (diplopia is often toe first complaint)
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19
Q

Central facial palsy eval

A

Brain MRI

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20
Q

Peripheral facial palsy: bialteral palsy eval

A

Brain MRI
Lumbar puncture
EMG (exclude GB, myotonia), edrophonium test or AchRAb level (exclude myasthenia)

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21
Q

Peripheral facial palsy: progressive palsy, dizziness, or associated hearing loss eval

A

MRI of verebellopontine angle

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22
Q

Peripheral facial palsy: acute unilateral/bialteral palsy eval

A

Blood glucose level, syphilis serology, and CBC; Lyme titer (endemic urea or exposure history); angiotensin-converting enzyme (exclude sarcoidosis)

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23
Q

Peripheral facial palsy: chronic palsy eval

A

Chest radiography )exclude sarcoidosis, tumor), brain MRI

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24
Q

Medical treatment for poor eyelid closer and exposure keratitis

A
  • topical eye lubricant QID (primary) NPAT every hour
  • bed time coverage: petroleum ointment
  • wear goggles or a small oval of cellophane wrap
  • tape the lid (not always successful)
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25
Q

Other treatments for advanced corneal complications in facial weakness

A

Surgical
-temporary or permanent tarsorrhapy

Various prosthetic devices
-silicone bands (abandoned), eyelid springs, eyelid gold weight implants

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26
Q

DiffDx of absent or decreased blinking

A

Corneal reflexes

Blink to visual threat

27
Q

Corneal reflexes in absent or decreased blinking associated with facial weakness

A
  • with detective ophthalmic nerve, neither eye will blink to ipsilateral corneal stimulation
  • with facial nerve palsy, only the contralateral eye will blink fully, regardless of which cornea is stimulated
  • with acute unilateral hemispheric lesions, eyes may have a diminished blink reflex when the contralateral cornea is stimulated
  • contralateral hemisphere may exert supranuclear influence upon the blink reflex (not very clear)
28
Q

Blink to visual threat in DiffDx for absent or decreased blinking

A

Pateitns may not blink when approached with a menacing gesture in the defective field

29
Q

Blepharospasm: DiffDx for excessive blinking

A
  • idiopathic dystonic disorder characterized by involuntary intermittent bialteral eyelid closure
  • ranges from increased blinking frewuncy to severe, sustained spasm of the orbicularis oculi
  • women are affected more than men
  • usually begins in the 4th-6th decade of life
  • accompanied by dystonic movements of the lower face or neck is termed Meige Syndrome
30
Q

Differential Diagnosis for excessive blinking

A

Blepharospasm

Hemifacial spasm

31
Q

Hemifacial spasms: DiffDx for excessive blinking

A
  • the whole face on one side contracts, with eyelid closure and elevation of the corner of the mouth
  • maybe due to hyperexcitabiltiy of the facial motor nucleus, either idiopathically or because of ischemia lesion in the pons
  • maybe due to compression of the facial nerve near its exit from the brain stem
32
Q

Physiological facial synkineses as cause of excessive blinking

A

-following injury of the peripheral facial nerve, abnormally innervation patterns may be observed as motor function recovers

33
Q

Treatment for excessive blinking

A

Localized subcutaneous injections of Botox around the eyelids to weaken the orbicularis oculi, other muscles involved in eyelid closure, and facial movements

34
Q

Congential causes of ptosis

A

Isolated and with elevator palsy
Marcus Gunn Jae winking
Other congential causes

35
Q

Acquired causes of ptosis

A
  • myopathic
  • NMJ
  • neuropathic
  • Horner syndrome
  • cerebral ptosis
  • apraxia of eyelid opening
  • levator dehiscence-disinsertion syndromes (aponeruotic ptossi)
  • pseudo ptosis
36
Q

Congential ptosis

A

Isolated with elevator palsy

  • isolated, non progressive
  • usually due to congential maldevelopemtn of the levator or its tendon in the neotate or child
  • in some cases, myopathic or dysgenetic features in the levator muscle
  • commonly the involved eye has SR or complete elevator palsy
  • no normal upgaze
37
Q

Marcus Gunn Jaw-Winking

A
  • congential causes of ptosis
  • ptotic eyelid retracts during contraction of the external pterygoic muscle
  • presumably from anaomlous innervation of the levator by the trigeminal nucleus
  • usually unilateral but rarely patients are bilaterally affected
  • usually associated qiwth amblyopia, SR weakness, double elevator palsy, and anisometropia
38
Q

Other congenital causes of ptosis

A
  • NF and lid tumors such as hemangioma
  • birthtruama
  • neonatal myasthenia
  • congential fibrosis syndrome
39
Q

Acquired causes of ptosis at NMJ

A

MG
Lambert-Eaton syndrome
Botulism

40
Q

MG pathophysiology

A

Autoimmune attack by antibodies directed against the Ach receptors causes the blockade, accelerated degradation, and complement-mediating damage. This results in a defect in the NM transmission and muscle weakness

41
Q

Symptoms of MG

A
  • ptosis, diplopia, chewing difficulties, dysarthria, dysphasia, dispensing, and systemic weakness are the hallmark signs of MG
  • most patients symptoms exhibit diurnal variation, as they weakness is better in the Am or after sleep than at the end of the day, when they are weakest
42
Q

Common eyelid signs in ocular MG

A
  • ptosis-asymmetric or symmetric
  • Cogans lid twitch
  • curtailing (enhanced ptosis)
  • fatigue
  • weakness of eyelid closure
43
Q

Cogans lid twitch

A

If a patient with MG looks down, for 3-5 seconds, then looks up quickly into primary gaze, the eyelid appears to overshoot upwards, then quickly falls

44
Q

Curtaining of eyelids in MG

A

In ptosis, when the more ptotic eyelid is manually elevated, the fellow eyelid often drops (curtaining)
Due to Herring’s Law

45
Q

Weakness of eyelid closure in MG

A

Orbicularis oculi are weak, causing deficient eyelid closure

46
Q

Oculomotor abnormalities in MG

A

Can mimic any pupil sparing CN III nerve palsy, or CN IV, CN VI palsy, or supranuclear or nuclear gaze paresis

47
Q

Diagnostic testing for MG

A

Ab testing
Electromyography
Edrophonium test
Ice pack, rest, sleep tests

48
Q

Antibody testing for MG

A

Anti-ACH receptor antibodies

MuSK

49
Q

How good of a test is the ice pack test for MG

A

80% sensitivity and 1% specificity

Better than edrophonium

50
Q

Lambert Eaton myasthenic syndrome

A
  • antibodies directed against voltages gated calcium channel portion of the NMJ
  • Ach release, which is dependent on the influx of Ca into the nerve terminal, is therefore impaired
51
Q

Neuro-ophthalmic signs for lambert-Eaton

A

Have mild bialteral ptosis, usually without noticeable ophthlamoparesis

52
Q

Botulism as cause of ptosis

A
  • caused by a clostridia toxin from C botulinum that blocks the release of ACh from the presynaptic nerve terminal
  • breast-fed infants less than 1 year of age living in endemic areas are most commonly affected
53
Q

Neuro-ophthalmic signs of botulism

A
  • ophthlamiplegia, ptosis, blurry vision, bifacial weakness and diplopia
  • poorly reactive pupils are also frequently seen
  • THIS MAKES IT DIFF FROM MG
54
Q

CPEO

A

Chronic progressive external ophthlamoplegia

  • caused by mitochondrial DNA deletions
  • slowly progressive ptosis
  • usually there is no diplopia
  • historical evidence of longstanding muscle weakness, such as difficulty with running, jumping, or climbing, may be present
55
Q

KSS

A

CPEO “plus”

  • caused by mitochondrial DNS deletions
  • combination of CPEO
  • onset before age 20
  • pigmetnary retinopathy
  • at least one of the following: heart block, ataxia, or CSF protein above 100mg/dL
56
Q

Cerebral ptosis

A
  • rare
  • occurs in Pattinson with hemispheric strokes, especially in association with right hemispheric lesions.
  • suggests some supranuclear cortical control of the levator muscles perhaps with right hemispheric dominance
57
Q

Other acquired ptosis

A

Cerebral
Apraxia of eyelid opening
Levator dehiscence-disinsertion sydnrome

58
Q

Levator dehiscence-disinsertion syndrome (aponeurtic ptosis)

A
  • the most common cause of acquired ptosis in adults
  • in many elderly patients the aponeurosis of the levator muscle may spontaneously dehiscence or disinsert fromthe tarsal plate of the upper eyelid
  • in younger and middle aged patients, the most common etiology of levator dehiscence is contanct lens wear
  • can also be caused by fibrosis of mullers muscle
  • other class include truama, ocualr surgery, allergies and eyelid edema
59
Q

Treatment of ptosis

A
  • primary causes
  • taping the eyelid
  • surgical managment is more effective in chronic cases (shorten lavator or muller muscel)
60
Q

Thyroid assocaited ophthlamopathy (graves)

A
  • either unilateral or bialteral
  • often accompanied by lid lag (Von graefe sign)
  • assoaitioed with exposure K and dry eye
61
Q

Dorsal midbrain syndrome

A
  • eyelid retraction
  • also called pretectal (colliers sign) or parinauds syndrome
  • often accompanied by upgaze paresis
  • thyroid workup negative
  • history of HA, blurred vision, or ataxia
  • may also habe pupillary light near dissociation, eyelid lag in downagaze, and convergence retraction syndrome
  • result either from a unilateral lesion of the nPC or front interruption of the PC, both of which would result in decreased inhibition of levator neurons in the CCN (Schmidtke and Buttner-Ennever)
62
Q

Plus-minus eyelid syndrome

A

-contralateral lid retraction can be mimicked in an individual with ptosis who fixates with the optic eye, thereby increasing the innervation to both levator (Hering’s law)

63
Q

Levator muscel and vertical eye movements

A
  • an area called the M group which is located media lot the rostral interstitial nucleus of the MLF, appears to be important in lid eye coordination
  • this region received input from the riMLF and the interstitial nucleus of Cajal (inC)
  • the M group exerts control over thecentral caudal nucleus (CCN) in the oculomotor nuclear complex (IIIrd n)
  • the riMLF may excite the M group during upward saccades to drive the eyelids upwards
  • the M group may be inhibited by the inC during downgaze, resulting in relaxation of the eyelids
  • the nucleus of the (nPC) may also be important in control of lid eye coordination. Note that fibers from the inC mediating vertical gaze also pops thtough the PC before innercating the IIIrd and IVth nerve nucleus . This lesions of the PC may cause both vertical gaze paresis and eyelid retraction

3P: Neuro (11 decks)

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