Understanding and evaluating diplopia

Abstract

Diplopia or double vision is a frequent reason for ophthalmology consultation. Monocular diplopia is usually ocular or retinal in origin, whereas binocular diplopia is often due to neurological causes. Detailed history beginning with any childhood visual disorders or head tilt and covering comorbid conditions and drug intake is essential. The alignment of images and direction of maximum separation point to the muscle(s) are involved. Temporal profile including onset, progression, and fluctuations along with comorbid conditions helps to narrow down the etiology. Refraction, ocular examination, and fundoscopy can identify ocular and retinal conditions; meticulous examination of ocular ductions and versions is mandatory to localize the cause of diplopia and to initiate investigations for the underlying disease process. Isolated ocular motor palsies are mostly due to microvascular ischemia; in the absence of red flags, investigation may be deferred for 6–8 weeks. Large vertical fusional amplitudes may be a clue to a decompensated congenital trochlear palsy. A partial third nerve palsy with early pupillary involvement, progressive signs, involvement of multiple cranial nerves, and elderly patients with rapid Erythrocyte Sedimentation Rate (ESR) are some situations warranting early imaging and other investigation. Myasthenia gravis and thyroid disease may present with diplopia and ophthalmic manifestations alone without systemic symptomatology. Immunoglobulin G4-related orbital myositis and anti-GQ1b antibody-mediated ocular neuropathies are relatively recently recognized immune-mediated conditions that may present with diplopia to an ophthalmologist. Ophthalmoplegic migraine has been renamed recurrent ophthalmoplegic neuropathy and is a diagnosis of exclusion at initial presentation.