(P80) Seeing Double!

A 42 year old healthy female woke up and noted double vision only with extreme leftward and downward gaze. Sent to emergency department by ophthalmologist with concern for acute fourth nerve palsy of the right eye.

On exam, patient found to have diplopia when gazing at the lower left visual field with improvement when occluding one eye. Pupils were equally round and reactive to light. Extraocular movements intact. No gross strabismus or hyperopia, nystagmus. Rest of neurologic exam normal.

Workup: MRI brain showed acute/subacute infarct in the left thalamus. MRA head/neck showed no large vessel occlusion, no significant stenosis. Hypercoagulable workup revealed elevated anti-thrombin III.

▪ Case

Discussion: Monocular diplopia reflects a problem with the eye itself. Binocular diplopia, which occurs when both eyes are open and resolves with one eye closed, typically reflects a lesion either along the pathway of a cranial nerve, at the neuromuscular junction (for example myasthenia gravis), or at the extraocular muscles (orbital myositis, infection, trauma, or mechanical restriction).
▪ Oculomotor nerve (CN III) pathology will involve limitation of elevation, depression and adduction, with an eye deviated “down and out”. If an aneurysm or other compressive lesion is the cause of third nerve palsy, the pupil will almost always be involved given the arrangement of parasympathetic fibers located at the periphery of the third nerve bundle. Microvascular disease may cause pupil sparing third nerve palsy, as the fibers that innervate the muscles are located towards the center of the nerve bundle.
▪ The abducens nerve (CN VI) turns the eye laterally; pathology involving this nerve will give horizontal binocular diplopia most pronounced in the direction of the palsy. If you have a right CN VI palsy, that eye cannot look rightward when the left can, causing double vision.

Case discussion: This patient was sent in by ophthalmologist to rule out a trochlear nerve (CN IV) palsy. The trochlear nerve emerges from the dorsal brainstem near cranial nerves III and V, and decussates to innervate the contralateral superior oblique muscle. The superior oblique muscle is responsible for intorsion, depression, and abduction of the eye. Patients with trochlear nerve pathology may notice diplopia looking downwards, for example walking down stairs. They may compensate by tilting their head away from the affected side to correct.

This patient was found to have a thalamic infarct, her sole finding on imaging. The thalamus has its own independent function in regulation of visual movements. The thalamus itself contains different nuclei that independently help coordinate eye movements involving saccades, fixation, and eye or gaze position. The frontal and supplementary eye fields receive many projections from the central thalamus.

• If our patient had isolated trochlear nerve palsy due to thalamic stroke, the area of infarct would somehow have to involve the dorsal territory but bypass the rest of the cranial nerves. Ischemia involving the midbrain would likely involve the ipsilateral CN III, since its nucleus is located between the thalamus and CN IV nucleus. In the case of a stroke, this is such a small area that typically multiple cranial nerves are affected. Thus it is possible that the patient’s symptoms may be due to direct dysregulation of the thalamic function in coordinating eye movement, presenting similarly to a trochlear nerve palsy.