A lesion of the oculomotor nerve, by paralyzing the levator muscle, causes ptosis, that is, drooping of the upper eyelid. In contrast, a lesion of the facial nerve, as in Bell palsy, impairs the ability to close the eyelids because of weakness of orbicularis oculi (lagophthalmos). In some instances of Bell palsy, even after nearly full recovery of facial movements, blink frequency and amplitude may be reduced on the previously paralyzed side. A trigeminal nerve lesion on one side, by reducing corneal sensation, interferes with the blink reflex on both sides, whereas Bell palsy reduces the ipsilateral blink but does not affect the contralateral blink. Aberrant regeneration of the third nerve after an injury may result in a condition wherein the upper lid retracts on lateral or downward gaze (pseudo-von Graefe sign). Aberrant regeneration of the facial nerve after Bell palsy has an opposite effect—closure of the lid with jaw movements or speaking (one of the Marcus Gunn phenomena, the other being an afferent pupillary defect to light). There is also a congenital and sometimes hereditary anomaly in which a ptotic eyelid retracts momentarily when the mouth is opened or the jaw is moved to one side. In other cases, inhibition of the levator muscle and ptosis occurs with opening of the mouth (“inverse Marcus Gunn phenomenon,” or Marin Amat syndrome).
Unilateral ptosis is a notable feature of third nerve lesions (see above) and of sympathetic paralysis, namely, the Horner syndrome. With the former, weakness of the levator palpebrae can produce marked, or even complete ptosis, whereas with the latter, weakness of the Müller muscle produces only 1 to 2 m of ptosis. In some cases of Horner syndrome, there is also “inverse ptosis” with a slight elevation of the lower eyelid contributing to the illusion that the eye is slightly retracted (pseudo-enophthalmos). A common cause of unilateral static ptosis is a dehiscence of the tarsal muscle attachment; it can be identified by the loss of the upper lid fold just below the brow.
Ptosis may be accompanied by an overaction (compensation) of the frontalis and the contralateral levator palpebrae muscles. In patients with myasthenia, Cogan has described a “lid twitch” phenomenon, in which there is a transient retraction of the upper lid when the patient moves visual fixation from the down position to straight ahead. Brief fluttering of the lid margins upon moving the eyes vertically is also characteristic of myasthenia. Another useful clinical rule is that a combined paralysis of the levator, and orbicularis oculi muscles (i.e., the muscles that open and close the lids) indicates myasthenia gravis or a myopathic disease such as myotonic dystrophy. This is because the third and seventh cranial nerves are rarely affected together in peripheral nerve or brainstem disease.
Bilateral ptosis is a characteristic feature of myasthenia gravis and certain muscular dystrophies; congenital ptosis and progressive sagging of the upper lids in the elderly are other common forms. Botulism also produces ptosis, whether naturally acquired of occurring iatrogenically after botulinum toxin treatments. An effective way of demonstrating that mild, ostensibly unilateral ptosis is in fact bilateral is to lift the ptotic side and observe that the opposite lid promptly droops. This reflects the enhanced effort required to maintain patency of the lids.