One Patient of Blepharoptosis Caused by Levator Palpebrae Superioris Aponeurosis Degeneration

Abstract

Ptosis is one of the common diseases of plastic surgery, which is caused by various causes of levator palpebrae superioris dysfunction or Müller muscle insufficiency, which is manifested by the upper eyelid margin being lower than normal when level viewed. Ptosis can be divided into congenital and acquired, and the main cause of congenital ptosis is due to congenital levator palpebrae superioris dysplasia or the motor nerve innervation that innervates it is caused by abnormal oculomotor neurodevelopment and dysfunction. Acquired ptosis can be divided into traumatic, neurogenic, myogenic, senile, mechanical, and false ptosis. At present, there are few reports of ptosis due to the degeneration of the aponeurosis of the upper eyelid muscle. We received a case of ptosis caused by degeneration of the levator palpebrae superioris aponeurotic mem-brane, we use the method of the levator palpebrae superioris high advancement. The levator palpebrae superioris-Miller muscle was folded to form a stable composite structure by the levator palpebrae superioris high advancement. During the operation, the levator palpebrae superioris was separated along the gap, and the surrounding tissues were less damaged. Therefore, postoperative adhesion was less, and the main complications of severe blepharoptosis after the operation, such as upper eyelid hysteresis and incomplete closure, almost did not occur, and after surgery, the results were good.

Oculomotor nerve palsy caused by imidacloprid at initial diagnosis: A case report

“…Recent research suggests that oculomotor nerve palsy caused by pyraclostrobin may share similar mechanisms with botulinum toxin-induced muscle paralysis, where the toxin absorbs through the conjunctiva and enters the gap between the Muller muscle and the levator palpebrae superioris synapses, inhibiting the release of acetylcholine from the presynaptic membrane of motor nerve endings, causing flaccid paralysis of the muscles. [ 13 ] Alternatively, the toxin may act on acetylcholine receptors, preventing acetylcholine from binding to acetylcholine receptors, leading to paralysis of the muscles innervated by the oculomotor nerve. Regarding the neurotoxicity of pyraclostrobin, researchers have found that it can induce neurotoxicity in rats by blocking acetylcholinesterase activity and reducing dopamine, serotonin, and γ-aminobutyric acid levels.…”