Have double vision is to see two images instead of one, or we have two eyes and yet we see simple. This binocular vision is not a passive phenomenon, it involves highly complex neural circuits, still poorly understood, leading to the merger of our two images.
The generator center of the ocular motor is located in the brain stem. He sits in the nuclei of III (nerve oculomotor), IV trochlear nerve (nerve pathetic old), and VI (abducens) giving rise to the corresponding nerves. The latter provide the innervation of the eye muscles.
III innervates the levator of the upper eyelid, upper right, the inferior oblique, medial right, lower right and the constrictor of the pupil (intrinsic motility). The IV supplies the superior oblique. The VI innervate the superior oblique. The VI supplies the right side.
Damage to the muscles, nerves, oculomotor nuclei breaks the static eye and causes diplopia.
The action of the eye muscles diagram is essential to the understanding of diplopia.
A oculomotor palsy removes the alignment of optical axes and no longer allows two images to merge: diplopia moved.
Binocular diplopia is a phenomenon: it goes to the occlusion of one eye. This simple test, eliminates the outset a monocular diplopia, frequent clinical trap; diplopia persistent occlusion of an eye is monocular, not neurological: it reflects a corneal eye disease or cristallinienne (severe astigmatism, corneal edema, cataract).
The first step of the examiner before a recent diplopia is to identify pathological muscle: this purpose, the study tour of both eyes in all directions of gaze highlights when the paralysis is massive, a limitation of an eye in a direction. There may also be a deviation of a globe: the patient is strabismus.
Paralysis Lateral Law Law sets a limit to the abduction of the right eye and convergent strabismus (by action of hyper Right Medial ipsilateral).
If the oculomotor palsy is minimal, both visual axes appear perfectly aligned and the study of globes excursion shows no limitation or deviation, however, the patient complained of diplopia. The red glass test and review Hess-Lancaster to determine the paralyzed muscle.
These two eye tests are based on the same principle. They dissociate the image of each eye by interposing in front of one of them a colored glass. During eye movements, increasing the gap between the normal image and the color image determines the direction of action of the paralyzed muscle. Both tests achievable in ophthalmic community, are the first step of the analysis of diplopia.
Diplopia can be horizontal or vertical, easy to identify (suffering from a muscle) or complex (unilateral involvement of several muscles, bilateral involvement). It can exist in one way or another, be intermittent or permanent, be variable in the day and night to increase the fatigue; it can appear suddenly or develop slowly, worsening by the day.
The signs are associated to carefully search for the inspection and examination. They are either eye (proptosis, ptosis, anisocoria) or neurological (headaches, dizziness). Moreover, the existence of diabetes, thyroid dysfunction, helps guide etiological research.
Diplopia arising in the aftermath of Graves’ disease is the first symptom of a dysthyroid ophthalmopathy and the presence of large eye muscle imaging confirms the diagnosis.
A horizontal diplopia upper bound in the look right, linked to a paralysis of the right VI, brutally occurred in a young woman with a history of optic neuritis, calls for multiple sclerosis; MRI requested quickly will highlight the hyper signal in the white matter, characteristics of démyélinisations.
The sudden onset of sharp pain periorbital and temporal associated with ipsilateral nerve palsy, complete (extrinsic and intrinsic, with pupil mydriasis) is an absolute emergency: immediate angio MRI aims to visualize the carotid aneurysm responsible for this particular syndrome that is a painful III.
The occurrence of a variable diplopia in the day, sometimes with a slight ptosis or paralysis of the orbicularis muscle, is highly suggestive of a myasthenic syndrome: the existence of a similar episode or prior diplopic term treatment with beta-blockers, are all diagnostic evidence for myasthenia gravis.
The causes of oculomotor paralysis diplopia officials are multiple tumor, vascular, inflammatory, traumatic, myasthenic.
They require comprehensive etiologic balance sheets still having an imaging.
The diplopia usually disappear with treatment of the causal disease or decrease to disappear spontaneously.
If diplopia sequelae (posttraumatic, postoperative myasthenic …) prismatic corrections or oculomotor surgery can be a therapeutic response to this debilitating situation is a definitive diplopia.