USMLE – Diplopia
This arises when eye movement is impaired so that the image of an object is not projected to homologous points on the two retina. Impairment may result from central disorders or from disturbance of the ocular motor nerves, muscles or the neuromuscular junction. SY0-301 The pattern of double vision, along with any associated features, usually allows localization of the lesion while the mode of onset and subsequent behavior (e.g, fatigability) suggest the etiology.
The trochlear (4th) nerve innervates the superior oblique muscle, and the lateral rectus is innervated by the abducens (6th) nerve. The oculomotor (3rd) nerve innervates the remainder of the extraocular muscles along with the levator palpebrae superioris, and the ciliary body (pupil constriction and accommodation).
Complete oculomotor nerve lesions cause ptosis and a dilated pupil and the eye tends to rest in a ‘down and out’ position due to unopposed tonic activity of the unaffected lateral rectus and superior oblique muscles. The pupil is often spared in ischemic lesions (e.g. in diabetes) and its involvement requires that compressive lesions such as aneurysm be excluded. Trochlear nerve palsy presents with vertical diplopia (especially noticeable going downstairs) and the patient may have a head tilt and double vision when looking down to the side opposite the lesion. Abducens nerve palsy causes horizontal double vision when trying to look towards the side of the lesion. In diplopia of any cause, the image projected furthest away from primary position arises from the paretic eye and this can often be determined by alternate eye cover.
Myasthenia gravis can cause diplopia by affecting any or all of the extraocular muscles. It is often associated with ptosis, and the hallmark is fatigability. Similarly, diseases of TK0-201 the extraocular muscles themselves can cause diplopia. Such diseases include thyroid eye disease, myopathies and orbital myositis.
Central lesions can also give rise to diplopia. Brain-stem lesions affecting the 3rd, 4th or 6th nerves or nuclei will cause diplopia, as will lesions of the MLF. The hallmark of an MLF lesion is an internuclear ophthalmoplegia (INO). The lateral gaze centre in the pons sends fibers to the ipsilateral 6th nerve nucleus. The nucleus contains two populations of neurons. Half the cells send their axons directly into the 6th nerve to supply the lateral rectus, while the remaining half send their fibers into the contralateral MLF and up to the contralateral 3rd nerve nucleus, where they synapse with neurons destined for the medial rectus. Hence, damage to the 6th nerve nucleus itself will prevent both eyes from moving ipsilaterally (gaze palsy) and a lesion of the MLF will interfere with adduction of the ipsilateral eye (INO). An INO may be partial or complete, and may be associated with nystagmus of the contralateral, abducting eye.