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MRCP PACES Neurology > Approach to Ptosis and Horner's Syndrome > Flashcards

Approach to Ptosis and Horner's Syndrome Flashcards

1
Q

Approach to ptosis

A 
_5 questions to ask:_
1. Unilateral or bilateral?
2. Partial or complete ptosis?
3. Fatigability
4. Pupil function
5. Extraocular motility
  1. Unilateral or bilateral?
    - Unilateral: focal pathology - LPS (CN3) or tarsal failure (oculosympathetic failure in Horner)
    - Bilateral: diffuse/systemic (MG, myopathy)
    (Careful of asymmetric involvement in MG)
  2. Partial or complete ptosis?
    - Complete: eyes fully closed - complete paralysis of LPS due to CN3 palsy
  3. Fatigability
    - MG - fatigable with use, improves with rest
  4. Pupil function
    - Miosis (constricted) - ipsilateral Horner’s syndrome
    - Mydriasis (dilated) - CN3 palsy
  5. Extraocular motility
    - CN3 palsy, MG, CPEO, thyroid ophthalmopathy
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2
Q

What are the muscles that elevate the eyelids?

A
  1. Levator palpabrae superioris (LPS) - CN3
  2. Superior tarsal muscle - oculosympathetic fibres (Horner)
  3. Frontalis muscle - CN7
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3
Q

What are the causes of ptosis?

A 
Commonest causes of unilateral ptosis
1. Third nerve palsy - nuclear or nerve
2. Horner’s syndrome
3. MG (masking as asymmetric ptosis)
4. Myopathies
5. To mention Botox, rare cerebral ptosis, rare congenital

Congenital - Marcus-Gun Jaw Winking syndrome

Acquired
A. Neurogenic
1. CN3 palsy
2. Horner’s syndrome
3. Cerebral ptosis (rare)
4. GBS / MFS (unstable, won’t come out in exam)

B. NMJ
4. Myasthenia gravis
5. Botulism or botox injection

C. Muscle myopathy
6. Myotonic dystrophy
7. Ocular myopathy
8. Oculo-pharyngeal dystrophy

D. Aponeurotic and others
9. Senile ptosis - levator dehiscence with stretching
10. Post-operative ptosis
11. Blepharochalasis (eyelid inflammation_
12. Periorbital soft tissue swelling, trauma, tumour

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4
Q

CN3 palsy
- Oculomotor nerve: nucleus, fascicle, nerve
- Unilateral vs bilateral depends on site of involvement

A 
Nuclear CN3: bilateral ptosis, impaired pupil, EOM, brainstem syndromes
Fascicle CN3: unilateral ptosis, impaired pupil, EOM, brainstem syndromes
CN3 nerve: unilateral ptosis, impaired pupil, EOM, no brainstem syndromes
  1. Unilateral or bilateral? can be both
    - Unilateral: nerve or fascicle CN3 palsy
    - Bilateral: nuclear CN3 palsy
    (levator palpabrae superioris subnucleus sharing)
  2. Partial or complete ptosis? Variable
  3. Fatigability - No
  4. Pupil function
    - Pupil sparing (medical CN3)
    - Loss of reactivity in impaired parasympathetic pathway to ipsilateral eye (surgical CN3) such as tumours, aneurysm, pituitary apoplexy, DM
  5. Extraocular motility - impaired, weakness of medial rectus, superior rectus and inferior oblique muscles
  6. Others - long tract signs in nuclear and fascicular CN3 palsy (midbrain brainstem involvement)
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5
Q

Horner’s syndrome

A
  1. Unilateral or bilateral? unilateral upside-down ptosis
    Oculosympathetic denervation results in superior and inferior tarsal weakness (spares LPS)
    - Partial/mild ptosis of upper eyelid
    - Inverse ptosis (elevated lower eyelid)
    - Anisocoria
  2. Partial or complete ptosis? partial, mild, inverse
  3. Fatigability - No
  4. Pupil function - ipsilateral miosis (constriction)
  5. Extraocular motility - normal in isolated Horner
  6. Others
    - Other CN palsies and long tract sign in 1st order Horner’s syndrome.
    - Lower cervical radiculopathy, brachial plexopathy in 2nd order Horner’s syndrome
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6
Q

Myasthenia gravis
- Once confirmed, to shift to MG dance

A

Immune mediated impairment of NMJ transmission
Involves fatigability, weakness of eye opening (LPS) AND eye closure (orbicularis oculi)

  1. Unilateral or bilateral? bilateral, cautious for asymmetry masking as unilateral
  2. Partial or complete ptosis? Variable
  3. Fatigability - YES
    - Look upwards, count to 25
  4. Pupil function - intact
  5. Extraocular motility - ophthalmoparesis due to fatigability, mimics CN neuropathy, gaze palsy or INO
  6. Others
    - Orbicularis oculi muscles are weak - eye closure weak
    - Facial weakness
    - Dysarthria, dysphagia
    - Neck and truncal weakness
    - Respiratory difficulties
    - Limb weakness and fatigability
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7
Q

Myopathies
- Myotonic dystrophy
- Mitochondrial myopathy (CPEO)

A

Ptosis if facial and LPS affected
Usually with other facial weakness - expressionless appearance, tented mouth

  1. Unilateral or bilateral? bilateral, symmetric
  2. Partial or complete ptosis? variable
  3. Fatigability - No
  4. Pupil function - intact
  5. Extraocular motility - CPEO presents with ophthalmoparesis
  6. Others
    - Facial weakness
    - Dysarthria, dysphagia
    - Neck and truncal weakness
    - Respiratory difficulties
    - Limb weakness and fatigability

(Dermatomyositis and polymyositis rarely present with facial weakness or ptosis)

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8
Q

What is Horner’s Syndrome?
Describe the pathway orders of Horner’s Syndrome

A

Failure of sympathetic innervation of head and neck region

Triad of: ptosis, miosis, anhidrosis
(depending on the order of involvement)

  1. First order (central) - from hypothalamus to brainstem to cervical cord at C8/T1
  2. Second order (pre-ganglionic) - leaves cord, ascend within sympathetic chain until lung apex, including cervical rib
  3. Third order (post-ganglionic) - until superior cervical ganglion, splits and follows ECA and ICA
    - Vasomotor and sudomotor follows ECA
    - Oculosympathetic follows ICA, which eventually enters orbit to supply pupil dilators and tarsal muscles
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9
Q

What are the causes of different orders of Horner’s Syndrome?

A 
1st - hypothalamic, brainstem, cervical cord
> stroke, tumour, MS, trauma, myelitis, syringomyelia, AVM

2nd - brachial plexus, lung apex, vascular
> trauma, tumour, pancoast, mediastinal, aneurysm, dissection

3rd - superior cervical ganglion, ICA, cavernous sinus
> trauma, aneurysm, dissection, arteritis, tumour, CVT

First Order - central
A. Hypothalamus
- Stroke
- Tumour

B. Brainstem
- Brainstem strokes
- Demyelinating disease (MS)
- Brainstem tumours

C. Cervical cord
- Trauma
- Syringomyelia
- Spinal cord tumours
- Myelitis
- Vascular malformation

Second Order - pre-ganglionic
D. Brachial plexus
- Trauma
- Inflammation
- Malignancy metastasis
- Radiation

E. Pulmonary apex
- Pancoast tumour
- Mediastinal tumour
- Cervical rib compression

F. Vascular abnormalities
- Carotid dissection, aneurysm
- Subclavian artery aneurysm

Third Order - post-ganglionic
G. Superior cervical ganglion disorders
- Trauma or iatrogenic from surgical neck dissection

H. ICA disease
- Aneurysm, dissection
- Giant cell arteritis

I. Cavernous sinus, SOF, orbital apex
- Pituitary tumours
- NPC
- Cavernous sinus thrombosis or inflammation

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10
Q

Horner’s Syndrome Dance

A
  1. Confirmation of ptosis, miosis
    - Upside down ptosis
    - Miosis with dilatory lag in darkness
    - Anisocoria worsens in darkness
  2. Explore pattern of anhidrosis (may be difficult in air-conditioned room - try to feel for ?greasiness)
    - 1st: ipsilateral hemiface and body
    - 2nd: ipsilateral hemiface only
    - 3rd: no anhidrosis
  3. Localising order of dysfunction
    A. 1st order - brainstem dysfunction
    - Altered consciousness
    - CN neuropathies
    - Long tract signs - spasticity, hyperreflexia, Hoffman’s sign

B. 2nd order
> C8/T1 radiculopathy
- Wasting of hand muscles
- Hand weakness, numbness

> Brachial plexopathy
- Monolimbic sensorimotor deficit

> Supraclavicular fossa fullness (cervical rib), cervical LN

C. 3rd order
- CN neuropathies of CVT
- GCA - tender palpable temporal arteries

  1. Complete examination with:
    - 0.5%/1% apraclonidine
    - 4% cocaine
    - 1% hydroxyamphetamine
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11
Q

How do you test for oculosympathetic failure?

A

Theory: oculosympathetic tract relies on noradrenaline secretion at synaptic cleft to produce response

  1. Apraclonidine - weak alpha 1 receptor agonist
    > normal: unchanged
    > abnormal: upregulated alpha 1 receptor from chronic sympathetic denervation -> supersensitive, marked dilatation of pupils
    –> reversed anisocoria (++ dilation of abnormal eye)
  2. 4% cocaine - inhibits reuptake of noradrenaline at synaptic cleft
    > normal: secretes NA -> accentuate sympathetic tone, increases dilation of pupils in 45-60 minutes
    > abnormal: unable to secrete NA, thus failure of dilation
    –> worsened anisocoria (++ dilation of normal eye)
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12
Q

How to localise 1st/2nd vs 3rd order Horner’s syndrome?

A

1% hydroxyamphetamine - potentiates release of NA in 3rd order neurons leading to pupil dilation

1st/2nd order defect: abnormal eye dilates
3rd order defect: no dilation of abnormal eye
(failure to stimulate 3rd order neuron)

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13
Q

What are the investigations for Horner’s Syndrome?

A

First order
1. MRI brain and MRI cervical cord

Second order
2. MRI cervical cord, neck, brachial plexus
3. CT thorax
4. CXR

Third order
5. MRI brain
6. MRI posterior nasal space
7. MRA or invasive angiogram of head and neck arteries
8. Ultrasound of carotid arteries

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MRCP PACES Neurology (28 decks)

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