- 1.
How is ptosis classified?
Ptosis is classified by either time of onset or etiology. By onset, ptosis is either congenital or acquired. By etiology, ptosis may be neurogenic, aponeurotic, mechanical, myogenic, or traumatic.
- 2.
What is the most common cause of acquired ptosis?
Acquired ptosis is most often the result of disinsertion or attenuation of the levator aponeurosis, which is most commonly related to aging but can be related to chronic ocular inflammation or eyelid edema ( Fig. 37-1 ).
Figure 37-1
Involutional (aponeurotic) ptosis is characteristically mild to moderate with high upper eyelid crease. Deep sulci are seen in severe cases. Levator function is essentially normal.
(From Kanski JJ: Clinical Ophthalmology: A Synopsis. New York, Butterworth-Heinemann, 2004.)
- 3.
What clinical findings help to differentiate congenital ptosis from acquired aponeurotic ptosis?
Patients with aponeurotic ptosis have a ptotic eyelid in all positions of gaze. In downgaze the ptotic eyelid remains ptotic. Patients with congenital ptosis, however, demonstrate eyelid lag in downgaze. The ptotic eyelid frequently appears higher than the normal eyelid as the patient moves toward downgaze. This is caused by the maldevelopment of the levator muscle, with poor ability to contract in elevation as well as inability to relax as the eyelid moves to downgaze.
- 1.
High eyelid crease (>10 mm)
- 2.
Moderate ptosis (3-4 mm)
- 3.
Good levator function (>10 mm)
- 4.
No eyelid lag on downgaze
- 4.
What are the features of congenital ptosis?
Congenital ptosis is caused by a dystrophy or maldevelopment in the levator muscle/superior rectus complex ( Fig. 37-2 ). Most patients demonstrate poor levator function on examination and, at surgery, have fatty infiltration of the levator muscle. This myogenic abnormality causes an inability of the levator to relax on downgaze, resulting in eyelid lag and in some cases, lagophthalmos. Patients may or may not demonstrate motility defects because of superior rectus dysfunction (double elevator palsy with ptosis, vertical strabismus, and poor Bell’s phenomenon). Approximately 75% of cases are unilateral.
Figure 37-2
Simple congenital ptosis. A, Decreased levator muscle function occurs along with an indistinct upper eyelid crease. B, The ptosis is exaggerated in upgaze because of the poor function of the levator muscle. C, In downgaze the ptosis is reduced or absent because the fibrotic levator muscle cannot stretch.
(From Custer PL: Blepharoptosis. In Yanoff M, Duker JS [eds]: Ophthalmology, ed 2, St. Louis, Mosby, 2004.)
With congenital ptosis, it is critical to evaluate visual function and refractive error as amblyopia will occur in up to 20% of cases.
- 5.
What causes pseudoptosis?
Causes of pseudoptosis ( Fig. 37-3 ) include the following:
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Hypotropia on the ptotic side
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Eyelid retraction on the opposite side
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Enophthalmos/phthisis bulbi
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Anophthalmos/microphthalmos
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Severe dermatochalasis—with skin obscuring the position of the eyelid margin
Figure 37-3
Left pseudoptosis caused by ipsilateral hypotropia.
(Kanski JJ: Clinical Ophthalmology: A Systematic Approach, ed 5, New York, Butterworth-Heinemann, 2003.)
- •
- 6.
What is the primary cause of ptosis after intraocular surgery?
It is thought that levator dehiscence causes ptosis related to previous intraocular surgery. The exact etiology is uncertain; however, it has been linked to superior rectus bridal sutures, eyelid speculums, retrobulbar and peribulbar injections, and other draping maneuvers associated with manipulation of the eyelids. Affected patients probably had a tendency toward levator dehiscence preoperatively.
- 7.
What is the anatomic cause for the eyelid crease?
The eyelid crease is formed by the levator aponeurotic attachments that travel through the orbicularis muscle to the skin. With aponeurotic ptosis, these attachments are disinserted, causing the eyelid crease to elevate.
- 8.
What neurologic conditions are associated with ptosis?
Neurologic conditions that must be considered in a ptosis evaluation include third-nerve palsy, Horner’s syndrome, myasthenia gravis, Marcus Gunn’s jaw-winking syndrome, ophthalmoplegic migraine, multiple sclerosis, and the Miller-Fisher syndrome, a variant of Guillain-Barre syndrome.
- 1.
Ptosis—mild to complete
- 2.
Decreased elevation, adduction, and depression—may not all be present, depending on superior or inferior division involvement
- 3.
Possible ipsilateral pupillary dilation—may be subtle to complete
- 9.
What are the myogenic causes of ptosis?
Muscular abnormalities associated with ptosis include myasthenia gravis, muscular dystrophies, chronic progressive external ophthalmoplegia (CPEO), oculopharyngeal dystrophy, and congenital maldevelopment of the levator.
- 1.
Slowly progressive ophthalmoplegia
- 2.
Bilateral ptosis
- 3.
Rarely have diplopia—owing to symmetry of disease
- 4.
No variability (as in myasthenia gravis)
- 10.
What are the features of blepharophimosis syndrome?
Blepharophimosis syndrome ( Fig. 37-4 ) is a congenital autosomal dominant disorder characterized by ptosis, epicanthus, blepharophimosis (narrowing of the palpebral fissure in all dimensions), and telecanthus (widening of the distance between the medial canthi). Some patients also may demonstrate a flat nasal bridge, lower eyelid ectropions, and hypoplastic orbital rims.
