Ptosis

Original article by Anthony Rimmer | Last updated on 2/6/2014
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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.
  • 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