What is it?

There are 7 extraocular muscles: four straight muscles and two oblique muscles, and the upper eyelid levator. They are responsible for moving the eyeballs toward the object of attention in the visual field, and the images perceived by each eye to merge into one in the cerebral visual cortex.

Complicated neuronal, brain circuitry and the oculomotor nerve (cranial nerves III, IV and VI) control, direct and coordinate the actions of the eye muscles. The term ocular palsy defines the decreased strength of a muscle, which produces a reduced rotational movement of the eyeball in the direction corresponding to the paralysed muscle. Partial deficit is called paresis, while full deficit is called paralysis. They may appear isolated or associated with each other.


There are a number of signs and symptoms common to all kinds of ocularmotor palsies.

Strabismus (loss of parallelism of the eyes). Oculomotor nerve palsy generates vertical-, horizontal-, torsional- or mixed-gaze deviation, depending on the muscle or muscles affected by the lack of innervation. If the affected eye is the sixth cranial nerve, which innvervates 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). It occurs because in the eye affected by the paralysis, the image of the object being looked at does not fall in the same retinal point as the healthy eye, so both eyes do not fall in a coordinated way.

Torticollis. It is the anomalous position of the head adopted by the patient to make up for double vision. The head “turns” towards the place where the paralysed muscle has greatest difficulty, in an attempt to substitute its action. Depending on the affected muscles, torticollis can be laterocollis, rotational, anterocollis and retrocollis.  Torticollis might not appear in patients with poor vision in one eye, a lazy eye, a history of strabismus from an early age.


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. Acquired causes my include vascular (because of diabetes mellitus, high blood pressure or arteriosclerosis), infectious, inflammatory, tumoral or traumatic causes.


In the case of vascular oculomotor paralyses, prevention is possible by undertaking a strict control of the cardiovascular risk factors (glycemia, cholesterol, blood pressure...).


Before deciding on treatment, it is fundamental to assess the patient’s systemic involvement by undertaking an exhaustive study that may require a multidisciplinary approach from a neurologist or neurosurgeon, a radiologist, an endocrinologist and/or oncologist. Once the cause has been identified, treatment can be decided on.

If the paralysis is at the acute stage (first 6 months), treatment must be conservative and include various therapeutic options.

  • Observation.
  • Eye occlusion (preferably alternately) to avoid double vision.
  • Non-steroid anti-inflammatory drugs if it is painful.
  • Botulinum toxin injection to minimise antagonistic muscle contracture (that which performs the opposite action to the paralysed muscle).

Once 6 months have passed from the start of the clinical picture, we talk about the chronic phase. If the patient experienced partial recovery, then there are different alternatives depending on the magnitude of the patient's residual deviation.

  • If the deviation is small, prisms are incorporated onto your glasses to prevent double vision.
  • If the deviation is greater, the prism cannot be tolerated so surgical treatment is indicated. The choice of procedure will depend on the affected muscle. There is no single technique to repair all cases, so surgery will be customised for each individual. The objective is to obtain maximum parallelism of the eyes in primary gaze position (looking from the right to the front), to eliminate diplopia, correct torticollis and obtain the maximum possible field of binocular vision. It is important to remember that surgery will not restore the function of the paralysed nerve, and on occasions, more than one procedure may be necessary.

Professionals who treat this pathology

Frequently asked questions

  • In the case of acute paralysis, it is good to wait 6 months, then in some cases (depending on the cause and age of the patient), full recuperation occurs without the need for any treatment. When it comes to deciding to add a prism to your glasses or have surgery, it is fundamental that the deviation is stable and at a chronic stage. All other underlying base pathologies must have been ruled out.

  • In these cases, surgery will not restore the muscle function, as we cannot “replace” the paralysed nerve. The aim is to obtain maximum alignment and avoid double vision in the primary gaze and reading position. After the operation, a small residual deviation may remain which, if symptomatic, means the patient will require a temporary or permanent prism on the glasses.