Upper Eyelid Ptosis (Blepharoptosis): Causes, Classification, and Treatment

Upper eyelid ptosis (blepharoptosis) is a pathological condition characterized by the drooping of the upper eyelid below its normal anatomical position when looking straight ahead.

The term originates from the Greek: “blepharon” meaning eyelid, and “ptōsis” meaning falling or drooping.

Etiology

Blepharoptosis is classified in multiple systems reflecting its pathogenetic, diagnostic, prognostic, and therapeutic aspects.

The etiology of upper eyelid ptosis falls into several categories:

1. Congenital Ptosis

Classically presents as non-progressive eyelid drooping. In 75% of cases, it is unilateral and, when bilateral, asymmetrical. Histopathological studies of isolated congenital myogenic ptosis show dysgenesis of the anterior portion of the levator palpebrae superioris, with loss of striated muscle fibers and proliferation of loose connective tissue, impairing the levator’s ability to contract or relax.

2. Acquired Ptosis

May arise due to various causes, including:

• Neurological Disorders. Ptosis in this category results from impaired innervation of the upper eyelid muscles. The affected pathways mainly include the oculomotor nerve (cranial nerve III) and the sympathetic nervous system. Neurogenic ptosis is often due to oculomotor nerve damage. The most common cause is microvascular ischemia associated with diabetes, hypertension, hyperlipidemia, and smoking. Other causes include posterior communicating artery aneurysm, giant cell arteritis, trauma, or malignancy.

Myasthenia Gravis. An acquired autoimmune disorder where antibodies against acetylcholine receptors disrupt neuromuscular transmission. Ptosis is a hallmark ocular symptom, with unilateral, bilateral, or alternating dysfunction of the levator muscle.

• Myogenic Etiology. Includes primary hereditary myopathies with chronic progressive levator dysfunction and secondary myopathies related to systemic diseases.

Primary hereditary myopathies involve mitochondrial and autosomal dominant/recessive disorders. Chronic Progressive External Ophthalmoplegia is the most common. Typically begins between ages 30–40, featuring bilateral ptosis, ophthalmoplegia, neurosensory hearing loss, and dysphagia.

Oculopharyngeal Muscular Dystrophy usually starts at ages 40–50 and is marked by progressive ptosis and external ophthalmoplegia. It is caused by an autosomal dominant mutation in the PABPN1 gene and presents with systemic dysphagia and proximal limb weakness.

• Traumatic ptosis results from damage to the levator muscle, its aponeurosis, Müller’s muscle, frontalis muscle, or their innervation. Mechanisms include direct or indirect trauma, neurotoxins, scarring, foreign bodies, iatrogenic injury, cranial nerve damage, or dermal fibrosis.

Classification of Upper Eyelid Ptosis

According to clinical severity:

• Mild: Eyelid droops by 1.5–2.0 mm, without covering the pupil
• Moderate: Eyelid reaches the upper pupil margin
• Severe: Drooping by ~4.0 mm, fully covering the pupil

3D Models Showing Different Stages of Ptosis:

Ptosis – Stage I

Ptosis – Stage II

Ptosis – Stage III

Anatomy

Eyelid elevation is a complex action involving three different retractors, each with its own innervation. Any direct or indirect impact on these muscles can lead to blepharoptosis.

The levator palpebrae superioris is the primary retractor of the upper eyelid and acts as the antagonist of the orbicularis oculi muscle. It originates from the lesser wing of the sphenoid bone and transforms into a broad aponeurosis at the superior orbital rim. This aponeurosis then divides into three slips: anterior, middle, and posterior. The anterior slip inserts into the skin of the upper eyelid, while the middle and posterior slips attach to the superior tarsal plate and the conjunctival fornix, respectively. The anterior and posterior slips are innervated by the superior branch of the oculomotor nerve, whereas the middle slip receives sympathetic innervation from the cervical ganglion. The middle portion of the levator is also known as Müller’s muscle, a smooth muscle that functions as an independent effector of vertical eyelid movement, working in coordination with the levator.

The structural foundation of the eyelid is provided by the tarsal plate, a dense connective tissue structure measuring approximately 29–30 mm in width, about 1 mm in thickness, and 10–12 mm in height.

Medial and lateral canthal ligaments extend from the ends of the upper and lower tarsal plates and serve to anchor the eyelids medially and laterally.

Diagnosis

1. Patient Complaints: Patients with upper eyelid ptosis often report a reduction in their visual field, which may interfere with everyday activities such as reading and driving. This condition frequently leads to frontal headaches and chronic fatigue caused by the constant compensatory effort to elevate the eyebrows using the frontalis muscle. Additionally, patients may develop neck strain due to persistent backward head tilting, which engages the trapezius and other neck extensor muscles.
2. Medical History Collection: During the interview with the patient, the presence or absence of the following is assessed:

• Any previous eye diseases, traumatic injuries to the eyelid, orbit, or head, as well as history of eyelid surgery;
• Diplopia, daily variability in eyelid position, increased general fatigue, chronic progressive external ophthalmoplegia, myotonic dystrophy, and family history of ptosis;
• Recent trauma, including head injuries;
• Associated systemic diseases — neurological, endocrine, cardiovascular disorders, as well as thyroid disease and diabetes mellitus;
• Details of the patient’s medication history.

3. Clinical Examinations: Assessment includes visual acuity testing (visometry), autokeratometry, intraocular pressure measurement, biomicroscopy using a slit lamp, ophthalmoscopy, and both static and kinetic perimetry for evaluating visual field boundaries.
   Diagnostic methods for upper eyelid ptosis and its severity include measuring the palpebral fissure height and the margin reflex distance, assessing the function of the levator palpebrae superioris muscle, and determining the height of the upper eyelid crease.
   Biomicroscopy is used to evaluate the condition of the conjunctiva, cornea, iris pigmentation, and the pupil’s width and mobility. Conjunctivitis and keratopathy may cause reactive blepharoptosis.
   Modern diagnostic evaluation of myasthenia gravis in patients with blepharoptosis includes preliminary tests to detect pathological fatigability of the ocular muscles (such as the sleep test and ice test), the Tensilon test, serum analysis for autoantibodies against the acetylcholine receptor, and electromyographic studies.

Treatment of Upper Eyelid Ptosis

The treatment of blepharoptosis depends on its cause, severity, and associated symptoms.

Drug therapy

Medical treatment may be appropriate for certain forms of ptosis. Ocular disorders associated with thyroid disease can present with upper eyelid drooping and should be managed with corticosteroids and/or immunomodulatory therapy to achieve and maintain eyelid stability for approximately 6–9 months before considering surgical intervention.
Given the considerable variability in levator function in patients with myasthenia gravis, it is ideal to titrate cholinesterase inhibitors and/or corticosteroids to stabilize the condition over a period of 3–4 years prior to surgical correction.

Botulinum toxin injection into the pretarsal portion of the orbicularis oculi muscle may be successfully used in the treatment of mild acquired aponeurotic ptosis or acquired neurogenic ptosis.

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Surgical treatment

Methods for correcting blepharoptosis can be divided into the following types:

• The first type involves strengthening the function of the muscle that elevates the upper eyelid;
• The second type involves suspending the upper eyelid to either the superior rectus muscle or the frontalis muscle.

In modern ophthalmic surgery, it is generally accepted that suspension-type operations are performed when levator function is weak, whereas levator resection is performed when levator function is moderate or good.

In suspension-type surgery, the function of lifting the upper eyelid is transferred to the frontalis or superior rectus muscles. This method of correcting ptosis is described in various variations using different sutures, as well as materials derived from autologous tissues such as muscle, sclera, dura mater, and the fascia lata, among others. Autologous materials, except for the fascia lata, are currently rarely used due to insufficient effectiveness and the development of blepharoptosis recurrence.

Another pathogenetic approach to treating blepharoptosis is levator resection. The anatomical effect of this surgery is the restoration of the normal position of the upper eyelid. For severe degrees of blepharoptosis, maximal levator resection is recommended, which involves complete transection of the lateral aponeurotic bands and Whitnall’s ligament.

Operations that strengthen the muscle elevating the upper eyelid can be divided into two groups: transcutaneous levator resection and transconjunctival levator resection, both of which create a fold that shortens the levator tendon.