Causes of Blepharoptosis – fallen eyelid
Blepharoptosis is an abnormal fall of the eyelid. Unilateral or bilateral ptosis may be congenital, consecutive to dysgenesis of upper eyelid elevator or abnormal insertion of the aponeurosis of this muscle on the eyelid.
Acquired blepharoptosis may evolve so slowly that the patient does not realize the existence of the problem. Observation of old photos is useful for detection of the onset. It has to be investigated the existence of a history of trauma, ocular surgery, contact lens use, diplopia, systemic symptoms (eg, dysphagia or peripheral muscle weakness ) or the existence of a family history of ptosis. Variable ptosis which worsens towards the end of the day is typical for myasthenia gravis. The examination should be focused on the arguments for protruding, misshapen or eyelid masses, inflammation, pupillary inequality or limitation of motility. Palpebral fissure width is measured looking straight ahead to quantify the degree of ptosis. Ptosis will be underestimated if the patient raises the eyebrow with frontal muscle.
Mechanical blepharoptosis occurs in elderly patients because the increased size and excess of skin and subcutaneous adipose tissue of eyelid (dermatochalasis). Extra weight of this deformed tissues causes eyelid ptosis. Eyelid increase or deformation consecutive to infection, tumors, trauma or inflammation also causes ptosis, on a purely mechanical basis.
Aponeurotic blepharoptosis is a dehiscence or an acquired stretching of the aponeurotic tendon that connects the eyelid elevator to the back of the eyelid. Usually occurs in elderly patients, probably due to loss of tissue elasticity. Aponeurotic ptosis is also a common sequela of eyelid edema consecutive to infections or closed trauma of the orbit, cataract surgery or hard contact lenses usage.
Myogenic blepharoptosis includes myasthenia gravis and a number of rare myopathies. Chronic progressive external ophthalmoplegia term refers to a group of systemic disease caused by mutations in the DNA of mitochondria. As the name implies, the most important signs are slowly progressive symmetrical ptosis and limitation of eye movements. In general, diplopia is a late syndrome because all eye movements are reduced equally. In Kearns – Sayre version occur retinal pigmentation changes and cardiac conduction disorders. Peripheral muscle biopsy highlights ” irregular red fibers”‘ which are characteristic. Ocular-pharyngeal dystrophy is a distinct autosomal dominant disorder with onset at middle age, characterized by ptosis, limitation of eye movements and dysphagia. Myotonic dystrophy, another autosomal dominant disorder, produces ptosis, ophthalmoparesis , cataract and pigmentary retinopathy. Patients are experiencing muscle fatigue, myotonia , frontal baldness and heart abnormalities.
Neurogenic blepharoptosis occurs due to an injury affecting any of the two nerves that innervate the muscles that open the eyelid: Muller ‘s muscle or upper eyelid elevator muscle. Examination of the pupil helps to differentiate the two possibilities. In Horner syndrome the eye with ptosis has a smaller pupil and eye movements are complete. In oculomotor nerve paralysis, the eye with ptosis has a larger or normal pupil. If the pupil is normal, but adduction, up and down movements are limited, there is the possibility of oculomotor nerve paralysis with pupil sparing.