Ptosis (Blepharoptosis) in Adults Clinical Presentation

Updated: Aug 14, 2017
  • Author: Adam J Cohen, MD; Chief Editor: Hampton Roy, Sr, MD  more...
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Presentation

History

Obtain a thorough medical and ophthalmic history in patients with ptosis.

More specifically, the onset of ptosis, alleviating or aggravating factors, family history of ptosis, and history of trauma or ocular surgery are important clues to the etiology.

Patients usually complain of a bedroom-eye appearance, always appearing sleepy or tired, and constriction of their visual fields.

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Physical

If the patient has not been under the care of an ophthalmologist, a complete ocular examination is required.

Quantification and qualification of the ptosis is needed for proper diagnosis and treatment. All quantitative eyelid and eyebrow measurements should be taken before the use of dilating drops.

The palpebral fissure is the distance between the upper and lower eyelid in vertical alignment with the center of the pupil.

The marginal reflex distance-1 (MRD-1) is the distance between the center of the pupillary light reflex and the upper eyelid margin with the eye in primary gaze. A measurement of greater than 2.5 mm is considered normal.

The marginal reflex distance-2 (MRD-2) is the distance between the center of the pupillary light reflex and the lower eyelid margin with the eye in primary gaze. A measurement of 5 mm is considered normal.

The margin crease distance is the distance from the upper eyelid margin to the lid crease. In white women, a central measurement of 10-11 mm is considered normal, and in white men, 8-10 mm is considered normal.

Levator function is the distance the eyelid travel from downgaze to upgaze while the frontalis muscle is held inactive at the brow. A measurement of greater than 10 mm is considered excellent, whereas 0-5 mm is considered poor.

The presence of proptosis, lagophthalmos, tear dysfunction, absence of a Bell response, and lower eyelid laxity or scleral show may affect the amount of ptosis repair.

Pseudoptosis can result from dermatochalasis, microphthalmos, enophthalmos or anophthalmos, acquired hypotropia after a blowout fracture (orbital floor fracture), superior sulcus deformity, or contralateral vertical lid retraction. Eyelid retraction may warrant thyroid function studies to exclude dysthyroid orbitopathy. Parinaud syndrome should be considered if convergence-retraction nystagmus and pupillary light-near disassociation is found in conjunction with eyelid retraction; neuroimaging should be obtained.

The margin fold distance is the distance from the upper eyelid margin to the fold of skin.

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Causes

Ptosis can be caused by problems with elevator muscles of the eyelid or the levator aponeurosis; central or peripheral nerve abnormalities, trauma, inflammation, or lesions of the lid or orbit. [4]

Aponeurotic ptosis

Aponeurotic ptosis is the most common cause of acquired ptosis.

Involutional changes, dehiscence, or disinsertion of the levator aponeurosis are common causes.

Chronic inflammation or intraocular surgery (eg, cataract surgery) necessitating speculum use can stretch the levator aponeurosis, causing dehiscence of the levator from the anterior surface of the tarsal plate.

Long-term use of contact lenses has also been implicated. Patients maintain normal or near-normal levator function, with a high upper eyelid crease. The attachments from the levator to the skin remain intact, and this forms the crease.

Neurogenic ptosis

Neurogenic ptosis may be congenital or acquired. Congenital neurogenic ptosis is usually due to Horner syndrome or third nerve dysfunction. Acquired neurogenic ptosis causes include Horner syndrome, third nerve dysfunction, or myasthenia gravis.

Congenital Horner syndrome can result in mild ptosis associated with ipsilateral miosis, iris and areola hypopigmentation, and anhidrosis. The cause is paresis of the Mueller muscle, secondary to an embryologic lesion of the sympathetic pathway.

Congenital third nerve palsy has a variety of causes. Patients can present with aberrant regeneration and a small pupil. Often, parents believe that this is secondary to birth trauma.

Acquired Horner syndrome can be secondary to trauma, neoplasms, or vascular disease of the sympathetic pathway. All stigmata of congenital Horner syndrome, excluding iris and areola hypopigmentation, are present. Raeder paratrigeminal syndrome occurs in middle-aged men who experience daily headaches and have stigmata of acquired Horner syndrome.

Dysfunction of the third cranial nerve can result from a myriad of acquired insults. Trauma, multiple sclerosis, vasculopathy, and infection are all potential etiologies. Extraocular muscle dysfunction, pupillary abnormalities, and the presence of aberrant regeneration may aid in establishing the correct diagnosis.

Synkinetic neurogenic ptosis stems from innervational anomalies. Marcus-Gunn jaw winking and posttraumatic ptosis are 2 examples of this interesting etiology. Importantly, microvascular diabetic neuropathies never result in synkinetic neurogenic ptosis.

Myogenic ptosis

Myogenic ptosis usually is congenital, but can be associated with acquired disease processes.

Congenital myogenic ptosis is secondary to levator dysgenesis.

Acquired myogenic ptosis can be found in myasthenia gravis, chronic progressive external ophthalmoplegia, oculopharyngeal dystrophy, and myotonic dystrophy.

Traumatic ptosis

Traumatic ptosis can occur after eyelid laceration with transection of the upper eyelid elevators or disruption of neural input.

Mechanical ptosis

Mechanical ptosis can stem from the presence of eyelid neoplasms, for example, neurofibromas or hemangiomas or from cicatrization secondary to inflammation or surgery.

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