Neuro-ophthalmology Illustrated Chapter 17 – Disorders of the Eyelid 3

Questions:
14. What causes eyelid ptosis in Horner syndrome?
15. What happens to the ptosis from Horner syndrome after administration of topical apraclonidine 0.5% or 1.0%?
16. What happens to the pupils in Horner syndrome after administration of topical apraclonidine 0.5% or 1.0%?
17. What is apraxia of eyelid opening?
18. What is thought to cause apraxia of eyelid opening?
19. Apraxia of eyelid is associated with what 4 conditions?

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Questions with answers:
14. What causes eyelid ptosis in Horner syndrome?
Denervation of Müller muscle and inferior tarsal muscle. 

15. What happens to the ptosis from Horner syndrome after administration of topical apraclonidine 0.5% or 1.0%?
It resolves.

16. What happens to the pupils in Horner syndrome after administration of topical apraclonidine 0.5% or 1.0%?
The anisocoria is reversed.

17. What is apraxia of eyelid opening?
It is the inability to open the eyelids not explained by levator dysfunction. 

18. What is thought to cause apraxia of eyelid opening?
It is believed to be a supranuclear disorder. 
Patients often can open their eyelids after touching the orbital rim or after a sudden command. 

19. Apraxia of eyelid is associated with what 4 conditions?
1. Essential blepharospasm
2. Parkinson syndromes
3. Huntington disease
4. Cerebral lesions 

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The information below is from Neuro-ophthalmology Illustrated-2nd Edition. Biousse V and Newman NJ. 2012. Thieme

Ptosis Resulting from a Neuromuscular Transmission Disorder
Myasthenia gravis is a classic cause of unilateral or bilateral ptosis (▶Fig. 17.13). Myasthenic ptosis may be isolated, or it may be associated with oculomotor paresis. The pupils are always normal. The hallmark of myasthenic ptosis is fluctuation. The Ptosis usually reverses with a Tensilon test (see Chapter 13).

Neurogenic Ptosis
Lesions of the Oculosympathetic Pathways
Lesions of the oculosympathetic pathways produce an ipsilateral Horner syndrome, which consists of mild ptosis (reduced palpebral fissure) and impaired dilation of the pupil, with anisocoria worse in the dark and dilation lag (▶Fig. 17.14 and ▶Fig. 17.15a).The ptosis results from denervation of the Müller muscle and inferior tarsal muscle of the lower lid. It is usually mild and usually 1 to 2mm, although 3 or 4mm of ptosis can sometimes be observed. The ptosis from Horner syndrome resolves after administration of topical apraclonidine 0.5% or 1.0%. Apraclonidine drops are useful for the diagnosis of Horner syndrome (it reverses the anisocoria). It can also be used to improve the ptosis (▶Fig. 17.15b).

Lesions of the Third Nerve
Lesions of the third cranial nerve produce an ipsilateral ptosis. The ptosis results from weakness of the levator palpebrae muscle and may be complete or mild. It is never isolated: the eye movements are abnormal, and the pupil may be dilated. When the ptosis is complete, diplopia may not be noticed by the patient (▶Fig. 17.16). A lesion of the third nerve nucleus in the midbrain produces bilateral ptosis.

Apraxia of Eyelid Opening
Apraxia of eyelid opening is the inability to open the eyelid not explained by levator dysfunction. It is believed to be a supranuclear disorder. Patients can often open their eyelids after touching the orbital rim or after sudden command. Apraxia occurs in association with essential blepharospasm, Parkinson syndromes, Huntington disease, and cerebral lesions.

Cerebral Ptosis
Very rarely, a unilateral hemispheric lesion can cause unilateral or bilateral ptosis without third nerve palsy. It is called cerebral ptosis, and it is believed to be a supranuclear disorder.

Reference: 1. Neuro-ophthalmology Illustrated-2nd Edition. Biousse V and Newman NJ. 2012. Thieme

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