Diplopia differential diagnosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief:

Overview

Diplopia may be caused by disorders of the orbit, extraocular muscles, neuromuscular junction dysfuntion, paralysis of the oculomotor, trochlear and abducens nerves, and injuries affecting the central nervous system (CNS). Given the various causes of diplopia, it is important to differentiate between the different causes that lead to diplopia.

Differentiating Diplopia From Other Diseases

Diplopia may be caused by disorders of the orbit, extraocular muscles, neuromuscular junction dysfuntion, paralysis of the oculomotor, trochlear and abducens nerves, and injuries affecting the central nervous system (CNS). Given the various causes of diplopia, it is important to differentiate between the different causes that lead to diplopia. The following table differentiates between various causes of diplopia:

Dilopia causing disorder	Subcategory	Mechanism	Distinguising Features	Exam Findings
Orbital disorder	Trauma	Direct injury to the orbit or eye	Ecchymosis Bone fracture Hematoma formation Altered mental status
	Orbital apex mass	Inflitration or mass effect in the orbital apex or cavernous sinus Compression of the oculomotor nerve	Palsies of oculomotor, trochlear and/or abducens nerves Periorbital or facial numbness Retro-orbital pain Proptosis Signs of venous congestion	Multi-directional horizantal and vertical diplopia Down and out pupil Pupillary dilation Deterioration of visual acuity Exophthamos Prominent choroidal folds Optic atrophy Bone destruction
	Orbital cellulitis	Spread of infection from contiguous sinuses (especially ethmoidal suinus) Culprit organisms include S. aureus and S. pneumoniae	Proptosis Eyelid edema Ophthalmoplegia Ocular pain Presence of risk factors: Recent upper respiratory illness Sinus infection Younger age Retained foreign bodies within the orbit Trauma Immunosuppression Systemic infection Dental infections	Eyelid swelling Conjunctival chemosis Axial proptosis Restriction of eye movements Retinal venous congestion Papilledema
	Thyroid-associated ophthalmopathy (Grave's disease)	Autoimmune	Proptosis Restriction of elevation and abduction of the eyes Tachycardia Intolerance to heat Weight loss Insomnia Fatigue Diarrhea	Dysthyroid orbitopathy (involvement of medial and inferior rectii muscles) Von Grafe's sign (lid lag on downward gaze) Joffroy sign (Absent creases on forehead on upward gaze) Stellwag sign (Infrequent and incomplete blinking) Boston sign (jerky irregular movements on downward gaze) Vigouroux sign (eyelid fullness) Dalrymple’s sign Optic disc edema Choroidal folds Optic disc paleness
Extraocular muscle disorder	Extraocular muscle injury or hematoma	Facial trauma Sinus surgery Extreme strabismus
	Mitochondrial myopathies	Dominant Optic Atrophy (OPA1 gene mutation) Leber Hereditary Optic Neuropathy (point mutation in mitochondrial DNA) Chronic Progressive External Ophthalmoplegia (TYMP, ANT1, PEO1, POLG, POLG2, and even OPA1 gene mutations)	Retinal ganglion cells and nerve fiber layer of the retina affected in dominant optic atrophy (may lead to blindness) Acute and painless central vision loss of both eyes in Leber hereditary optic neuropathy (days to months) Extraocular muscle mobility impairment in chronic progressive external ophthalmoplegia	Chronic Progressive External Ophthalmoplegia: Restriction of eye movements Visual acuity is spared Ptosis Leber Hereditary Optic Neuropathy: Disc pseudoedema Thickening of the retinal nerve fiber layers Dominant optic atrophy: Blindness Thinning of the neuroretinal rim Cup to disc ratio > 0.5 Peripapillary atrophy Sectoral pallor of the optic nerve
	Muscular dystrophy
Neuromuscular junction dysfunction	Myasthenia gravis	Auto-antibodies against nicotinic acetylcholine receptors	Fluctuating muscular weakness Ptosis Diplopia and weakness worsens with activity and improves with rest	Ptosis Incommitant strabismus or/and external ophthalmoplegia Cogan’s lid-twitch sign Weakness of the orbicularis oculi muscle
	Botulism	Inhibition of acetylcholine release due to toxin at cholinergic synapse and pre-synaptic myoneural junction	Dysathria Dysphagia Autonomic dysreflexia Pupillary dysfunction	Ptosis Blurred vision Ophthalmoplegia
Palsies of the third, fourth or sixth cranial nerves	Oculomotor nerve palsy	Microvascular ischemia: Diabetic neuropathy Hemorrhage Tumor Vascular malformation Aneurysm Meningitis Multiple sclerosis	Muscles affected: Medial, inferiorn superior rectii Inferior oblique muscle Levator palpebrae muscle Ciliary and constrictor pupillae muscles	Multi-directional horizantal and vertical diplopia No diplopia on lateral gaze to the affected side Eyelid droop (ptosis) Down and out pupil Pupillary dilation
	Trochlear nerve palsy		Muscles affected: Superior oblique muscle	Rotational diplopia that is worse on looking downwards and towards the nose Extorsion on downward gaze
	Abducens nerve palsy		Muscles affected: Lateral rectus muscle	Horizontal diplopia on gaze towards the affected side Lateral gaze palsy
Central nervous system injury (pathways and cranial nerve nuclei)	Basilar artery thrombosis	Occlusive thrombosis of the basilar artery Brainstem ischemia	Dysarthria Vertigo Cranial nerve palsies Presence of risk factors for ischemic stroke	Nystagmus Visual field defects Restriction of eye movements (maybe internuclear ophthalmoplegia)
	Vertebral dissection	Vertebrobasilar insufficiency	Acute onset Neck pain Vertigo Presence of risk factors for vertebral dissection	Occipital and nuchal pain Monocular blindness Hemianopsia Bilateral visual field defects Amaurosis fugax Ptosis Miosis
	Aneurysm	Enlarging aneurysm causes direct compression of the cranial nerves	Oculomotor nerve palsy Pupillary involvement	Aneurysm visible on fundoscopy
	Wernicke's encephalopathy	Thiamine deficiency leads to metabolic failure and tissue injury	Nystagmus Ataxia Altered mental status Ophthalmoplegia Malnutrition History of alcoholism	Optic disc edema Preretinal hemorrhage