Introduction
Ptosis may be unilateral or bilateral – symmetrical or asymmetrical
Upper lid lifted by contraction of levator (CN III) and sympathetic innervation of smooth muscle component
Lids closed by orbicularis oculi (CN VII) – facial nerve palsy does not cause ptosis
Enonphthalmos (e.g. orbital wall fracture) and proptosis may give the appearance of ptosis in unaffected eye.
Dermatochalasis: excess skin of upper lid, may sag below lid margin.
Causes of ptosis: involutional changes, CN III palsy, myasthenia gravis, levator trauma, Horner’s syndrpme and mitochondrial myopathies.
- Involutional changes: loss of connection between levator and eyelid skin – usually bilateral.
- CN III palsy: divergent squint and, in some cases, dilated pupil.
- Atherosclerosis, diabetes mellitus and intracranial aneurysms.
- Myasthenia gravis: antibodies to nicotinic acetylcholine receptors.
- Initial presentation may be ocular – ptosis variable and fatigable, abnormal eye movements leading to diplopia.
- Trauma: sever connections between levator and skin.
- Horner’s syndrome: sympathetic innervation of Muller’s muscle (smooth muscle of levator) disrupted, ptosis accompanied by small pupil and dryness of skin on affected side.
- Mitochondrial myopathies: rare, inherited from mother. Retinal pigmentation and cardiac conduction abnormalities.
Examination
- Confirm presence of a ptosis and determine if congenital or acquired.
- Compensation through action of frontalis (firmly press against the brow).
Management
- Surgical restoration of levator-skin connection
- Myasthenia gravis is managed with anticholinesterase inhibitors
- Simple lid-lifting devices
- In CN III palsy, elevating lid may lead to disabling diplopia