How to differentiate oculomotor nerve palsy

In clinical practice, different examination and differential diagnosis methods are used to confirm different diseases. Among them, the following methods are often used for differential diagnosis of oculomotor nerve palsy.

1. Oculomotor nerve palsy regeneration misdirection syndrome

When regeneration is disordered after oculomotor nerve paralysis, the extraocular muscles are innervated by nerve fibers that regenerate in the wrong direction. Various eye movements may occur, and there may be strange eyelid movements, such as eyelid retraction or pupil constriction when the affected eye attempts to turn down or inward. Generally, there is no change in automatic rhythm. In some cases, periodic spasms and regeneration errors occur together. It is more common in the acute or recovery period of congenital or traumatic oculomotor nerve paralysis.

2. Marcus-Gunn syndrome

Also known as mandibular blink syndrome, it was named after Marcus Gunn who first described it. Periodic oculomotor nerve palsy is common in patients with congenital ptosis and superior rectus paralysis. It manifests as a special joint movement of congenital ptosis and the pterygoid muscle, that is, when the ipsilateral pterygoid muscle is stimulated, the affected eye droops and the eyelid retracts. This eyelid retraction often occurs during movements such as opening the mouth, protruding the mandible, chewing, and sticking out the tongue. There is no abnormal change in the pupil. The cause may be related to the misdirection of the trigeminal nerve branch to the position of the levator palpebrae superioris muscle innervated by the III cranial nerve.

3. Marin-Amat syndrome

Also known as reverse jaw blink syndrome. Periodic oculomotor nerve palsy is characterized by ptosis when the mouth is opened and the jaw moves. The ptosis disappears when the mouth is closed or chewing stops.

4. Ocular myasthenia gravis

Periodic oculomotor nerve palsy is an autoimmune disease that affects the acetylcholine receptors on the postsynaptic membrane at the neuromuscular junction, leading to impaired nerve-muscle excitation transmission and a tendency to relapse and remit. The symptoms include early onset of ptosis in one or both eyes, which is milder in the morning and more severe in the afternoon, with the pupillary sphincter affected later. The severity of paralysis of the paralyzed muscles and the degree of strabismus vary greatly, and diplopia is often present. These symptoms can be alleviated or disappear after injection of neostigmine or tensilon.