Oculomotor (III) nerve lesions are pathological processes which negatively affect the nerve’s function.
The exact aetiology of most cases of oculomotor nerve palsies is idiopathic. There is a hereditary component to this condition, where the usual causative factor is either an aplasia or hypoplasia of one or more of the muscles supplied by the oculomotor nerve, or a partial palsy of the nerve itself. Oculomotor nerve palsies have also been recorded as a consequence of severe birth trauma.
Broadly speaking, this condition can be divided into acquired and inherited. Below is a list of the acquired forms of oculomotor nerve palsies:
- Inflammation, and infections
- Vascular disorders, including diabetes
- Space occupying lesions
- Multiple sclerosis
- Autoimmune disorders, e.g: myasthenia gravis
The oculomotor nerve supplies the levator palpabrae superioris muscle, the sphincter pupillae and three eye muscles: the medial and inferior rectus muscles, and the inferior oblique muscle.
Damage to the oculomotor nerve will result in the affected individual being unable to move their eye normally, ptosis of the eyelid on the affected side, and the eye typically takes a â€œDOWN AND OUTâ€ appearance. Other signs and symptoms include strabismus and diplopia.
The cranial nerves III, IV, and VI and usually tested together as the examiner instructs the patient to hold his/her head still and follow only with the eyes a finger that circumscribes a large “H” in front of the patient. The examiner is looking out for any signs of strabismus, and whether eye movement is smooth, synchronous and that both the patient’s eye are able to fix on the same point.
Because the oculomotor nerve also controls pupillary constriction, the examiner should also perform the accommodation reflex by moving a finger toward a person’s face, looking for pupil constriction and synchronous eye movement. Pupillary constriction should also be assessed with a light, checking for left/right symmetry.