Because of complicated neuronal circuits, the oculomotor nerves (cranial nerve pairs III, IV and VI) coordinate the action of the extraocular muscle, which are responsible for moving the eyeball towards the object of interest so that the images perceived by each eye merge in a single image in the visual brain. The term oculomotor nerve paralysis refers to the decreased strength of a muscle, which translates to reduced rotational movement of the eyeball in the direction corresponding to the paralysed muscle.
- Strabismus: The deviation may be vertical, horizontal, torsional or mixed, depending on the muscle affected. If the affected eye is the sixth cranial nerve, which innervates the lateral rectus, then the patient’s eye will deviate inward with limited external rotation. In the cases of the fourth cranial nerve, which enervates the superior oblique muscle exclusively, the eye will deviate upward. The third cranial nerve “controls” the medial rectus, superior rectus, inferior rectus, inferior oblique muscle, the upper eyelid levator, iris sphincter and ciliary muscle, therefore if the affectation is complete, the eye is deviated outward and downward, the eyelid is droopy (ptosis), the patient will have a dilated pupil and will be unable to focus. If the affectation is incomplete, the case will depend on the muscles affected.
- Diplopia (double vision)/Amblyopia (lazy eye): The rate of diplopia in children under the age of 8 is low as their visual system is still developing, meaning the brain tends to erase the image of the deviated eye leading to lazy eye.
- Torticollis: This is the anomalous position of the head adopted by the patient to make up for double vision.
The term oculomotor nerve paralysis refers to the decreased strength of a muscle, which translates to reduced rotational movement of the eyeball in the direction corresponding to the paralysed muscle.
The aetiology of paralyses is varied and may manifest itself at any age. There are congenital paralyses that can be side effects of neurological or anatomical anomalies, birth canal trauma or neonatal asphyxia. In terms of acquired causes, there are benign forms, generally with spontaneous resolution, which occur after infectious or inflammatory processes and vaccines, plus there are others that are side effects of tumours, trauma or intracranial hypertension.
Before deciding on treatment, it's fundamental to assess the patient's systemic involvement. Once the cause has been identified, if the paralysis is in the acute stage (first 6 months), treatment is conservative and includes observation, occluding one eye and/or a Botulinum toxin injection. After more than 6 months (chronic phase) and if the patient has partially recovered and the residual deviation is small, prism lenses will be incorporated into the glasses. If the magnitude is greater, surgery is indicated.
There is no single technique to repair on cases, so surgery will depend on the affected muscle. The objective is to obtain maximum parallelism of the eyes in primary gaze position (looking straight in front), to eliminate diplopia, avoid amblyopia, correct torticollis and obtain the maximum possible field of binocular vision. Surgery will not restore the function of the paralysed nerve, and on occasions, more than one procedure may be necessary.