![]() ![]() In 1935 the German ophthalmogist, Bielschowsky stated that “in the course of healing….the nerve fibers prefer certain ‘routes’ for growing in the wrong sheaths,” leading to the synkinesis or paradoxical co-contraction of extraocular muscles. In 1928, an experiment severing the sciatic nerve of a cat showed fibers originating from the proximal end of the two trunks aberrantly regenerating without concern for their original pathways. Historical laboratory studies have provided evidence of this mechanism. Oculomotor synkinesis most commonly occurs in the process of regeneration after acute cranial nerve injury. Third Degree/Neurotmesis: Nerve and endoneurium are disrupted, may regenerate in aberrant pathway. Nerve regeneration is confined to original architecture so aberrancy does not occur. Second Degree/Axonotmesis: Crush injury, disruption of axon while endoneurial tubes are preserved. Explains why aberrancy does not usually result from ischemic injury of nerve. Most commonly microvascular in origin such as from diabetes or hypertension. Oculomotor nerve injury is categorized as follows by Seddon’s Peripheral Nerve Injury Classification: įirst Degree/Neurapraxia: Conduction block, continuity of axon is maintained. This phenomenon has been reported in a wide range of ages from infants to elderly patients, and does not appear to be limited to a specific demographic. ![]() Another case report documents a patient with oculomotor synkinesis following an episode of Miller-Fisher Syndrome. One unique report discusses a case of oculomotor misdirection secondary to aytpical Tolosa Hunt Syndrome causing inflammation of the nerve, seen clinically and proven by enhancement on magnetic resonance imaging (MRI). Rare reports have been documented showing ophthalmoplegic migraine as a cause of oculomotor synkinesis, likely secondary to major ischemic damage to peripheral nerve. The incidence of aberrant regeneration of the third nerve after acute oculomotor nerve injury is about 15%. When associated with trauma, it is more commonly the indirect effects such as hematoma formation, rather than the direct trauma which damages the nerve. However, secondary oculomotor synkinesis most commonly results weeks to months following an acquired third cranial nerve palsy (e.g., trauma, surgery, tumor, posterior communicating artery aneurysm). The primary oculomotor synkinessis is typically secondary to slow growing intracavernous lesions (e.g., meningioma, intracavernous aneurysm, or schwannoma). ![]() This phenomenon can occur with (secondary) or without (primary) preceding oculomotor nerve dysfunction. In aberrant regeneration after injury to the oculomotor nerve, fibers grow to supply muscles other than their original terminal muscle, leading to co-contraction of these muscles (lid, extraocular muscles, or pupil) on firing of the nerve. The third cranial nerve (oculomotor nerve) supplies the inferior oblique, medial rectus, superior rectus, inferior rectus, the parasympathetically innervated pupil sphincter, and levator palpebrae muscles. The term “synkinesis” refers to involuntary muscular movements that accompany voluntary movements. It is a result of persistent partial oculomotor nerve dysfunction after failure to completely recover from disruption of the nerve due to any cause. Oculomotor Synkinesis (also known as aberrant regeneration of the third cranial nerve or oculomotor nerve misdirection) refers to the abnormal response to firing of the oculomotor nerve causing paradoxical co-contraction (i.e., synkinesis) of muscles.
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