An eye disease characterized by the drooping or falling of the upper or lower eyelid.

Ptosis is a drooping or falling of the upper eyelid.

Ptosis is when the upper eyelid droops or sags due to weakness or paralysis of the levator muscle which is responsible for raising the eyelid, or due to damage to nerves controlling the muscle.

It can be a manifestation of the normal aging process, a congenital condition, or due to an injury or disease.

Risk factors related to ptosis include diabetes, stroke, Horner syndrome, Bell’s Palsy. myasthenia gravis, brain tumor or other cancers that can affect nerve or muscle function.

The drooping may be worse after being up longer, when the individual’s muscles are tired.

If severe and left untreated, the drooping eyelid can cause other conditions, such as amblyopia or astigmatism.

Occurs due to dysfunction of the muscles that raise the eyelid or their nerve supply, the oculomotor nerve for levator palpebrae superioris and sympathetic nerves for superior tarsal muscle.

It can affect one eye or both eyes.

More common in the elderly, as muscles in the eyelids may begin to deteriorate.

Congenital ptosis can be hereditary, and the cause remains unknown.

Ptosis may be caused by damage/trauma to the muscle which raises the eyelid, damage to the superior cervical sympathetic ganglion or damage to the 3rd cranial nerve.

The oculomotor nerve, the third cranial nerve controls this muscle.

Oculomotor nerve damage could be a sign or symptom of an underlying disease such as diabetes mellitus, brain tumor, a pancoast tumor, and diseases which may cause weakness in muscles or nerve damage, such as myasthenia gravis or oculopharyngeal muscular dystrophy.

Exposure to toxins in some snake venoms, may also cause this.

Can be caused by the aponeurosis of the levator muscle, nerve abnormalities, trauma, inflammation or lesions of the lid or orbit.

Dysfunction of the levators may occur as a result of autoimmune antibodies.

May be due to a myogenic, neurogenic, aponeurotic, mechanical or traumatic causes,but may be associated with immunological, degenerative, or hereditary disorders, tumors, or infections.

Acquired ptosis is most commonly caused by aponeurotic ptosis.

Aponeurotic ptosis is a result of senescence, dehiscence or disinsertion of the levator aponeurosis.

Chronic inflammation or intraocular surgery can lead to ptosis.

Wearing contact lenses for long periods of may be associated with development of ptosis.

Congenital neurogenic ptosis can be caused by the Horner syndrome.

An acquired Horner syndrome may result after trauma, neoplastic insult, or even vascular disease.

Ptosis due to trauma can ensue follow eyelid laceration with transection of the upper eyelid elevators or disruption of the neural input.

Other causes of ptosis include: eyelid neoplasms, neurofibromas or the scarring after inflammation or surgery.

Risk factors related to ptosis include diabetes, stroke, Horner syndrome, Bell’s Palsy, myasthenia gravis, brain tumor or other cancers that can affect nerve or muscle function.

Mild ptosis may occur with aging.

Can be one of the first signs of a third nerve palsy due to a cerebral aneurysm, that otherwise is asymptomatic.

Use of high doses of opioid drugs can cause ptosis.

Pregabalin,an anticonvulsant drug, has also been known to cause mild ptosis.

Neurogenic ptosis which includes: oculomotor nerve palsy, Horner’s syndrome, Marcus Gunn jaw winking syndrome, third cranial nerve misdirection.

Ptosis may occur in victims of Botulism.

Myogenic ptosis includes: oculopharyngeal muscular dystrophy, myasthenia gravis, myotonic dystrophy, ocular myopathy, simple congenital ptosis, blepharophimosis syndrome.

Mechanical ptosis may be due to edema or tumors of the upper lid.

Neurotoxic ptosis is a classic symptom of envenomation by snakes such as cobras, kraits, mambas and taipans.

Neurotoxic ptosis is a precursor to respiratory failure and eventual suffocation caused by complete paralysis of the thoracic diaphragm.

Neurotoxic ptosis is a medical emergency and immediate treatment is required.

Myasthenia gravis is a common neurogenic ptosis,because the site of pathology is at the neuromuscular junction.

Up to 70% of myasthenia gravis patients present with ptosis, and 90% of these patients will eventually develop ptosis.

In myasthenia gravis, ptosis can be unilateral or bilateral and its severity tends to be oscillating during the day, because of factors such as fatigue or drug effect.

This type of ptosis is distinguished from the others with the help of a Tensilon challenge test and blood tests, and the fact that coldness inhibits the activity of cholinesterase, which makes possible differentiating this type of ptosis by applying ice onto the eyelids.

Bilateral ptosis is commonly associated with diplopia, dysphagia and/or progressive muscular paralysis.

Pseudo ptosis may be related to lack of lid support due to an empty socket or atrophic globe.

The ptosis due oculomotor palsy can be unilateral or bilateral, because the subnucleus to the levator muscle is a shared, midline structure in the brainstem.

When the palsy is caused by the compression of the nerve by a tumor or aneurysm, it is highly likely to result in an abnormal ipsilateral papillary response and a larger pupil.

Surgical third nerve palsy is characterized by a sudden onset of unilateral ptosis and an enlarged or sluggish pupil to the light.

Medical third nerve palsy, contrary to surgical third nerve palsy, usually does not affect the pupil and it tends to slowly improve in several weeks.

Surgical correction of ptosis due to medical third nerve palsy is considered only if the improvement and ocular motility are unsatisfactory.

Patients with third nerve palsy tend to have diminished or absent function of the levator.

In the Horner’s syndrome, ptosis is usually accompanied by miosis and anhidrosis, and is due to the result of interruption innervations to the sympathetic, autonomic Muller’s muscle rather than the somatic levator palpebrae superioris muscle.

In the Horner’s syndrome the ptosis is generally mild, no more than 2 mm.

Chronic progressive external ophthalmoplegia is a systemic condition that usually affects the lid position and the external eye movement, without involving the movement of the pupil.

Chronic progressive external ophthalmoplegia accounts for nearly 45% of myogenic ptosis cases.

In most patients develop ptosis due to chronic progressive external ophthalmoplegia disease in their adulthood.

Aponeurotic and congenital ptosis may require surgical correction if severe or if cosmetics is a concern.

Surgical procedures include: Levator resection, Müller muscle resection, and frontalis sling operation.

Ptosis that is caused by a disease may improve if the disease is treated successfully.

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