Abnormal Eye Movements (Diplopia)

Usually acute in onset and distressing. Establish first whether it is monocular (problem within the eye itself — e.g. cataract, refractive error, corneal irregularity) or binocular (problem with the extraocular muscles/their innervation — resolves when either eye is covered).

Differential diagnosis

Common:

• Ocular cranial nerve palsies (III/IV/VI)
• CVA/TIA
• Ophthalmoplegic migraine
• Alcohol/benzodiazepines
• Monocular causes: cataract, refractive error, corneal pathology

By category:

Category	Causes
Vascular	Stroke/TIA, microvascular ischaemia (diabetes, hypertension, atherosclerosis), aneurysm, carotid-cavernous fistula
Infective	Intraocular abscess, syphilis, mastoiditis, meningitis, herpes zoster
Neoplastic	Slow-growing tumour, raised ICP, skull-base tumours, infiltrative disease (e.g. leukaemia)
Autoimmune	Giant cell arteritis, multiple sclerosis, myasthenia gravis, orbital myositis, sarcoidosis, vasculitides, Guillain-Barré (a late sign)
Traumatic	Orbital wall fracture
Endocrine	Thyroid eye disease — see thyroid-eye-disease.md
Congenital	Decompensated childhood strabismus — see strabismus.md

Malignancy should be considered in any patient with new-onset diplopia and a history of cancer — arrange prompt neuroimaging.

Giant cell arteritis — do not miss this

GCA must be excluded in any patient aged over 50 with diplopia. Diplopia occurs in up to 19% of GCA patients and can precede severe, potentially bilateral visual loss — treating the diplopia-causing episode promptly can prevent that outcome. Diplopia in GCA may be central (ischaemia of cranial nerve nuclei/supranuclear gaze centres) or peripheral (ischaemic cranial nerve or extraocular muscle insult) — sixth nerve palsy is a recognised isolated presentation, not just amaurosis fugax or vision loss.

• Systemic clues: constitutional symptoms (fever, night sweats, weight loss, fatigue, myalgia) in up to 50%; headache in ~60%; scalp tenderness, jaw claudication, temporal artery tenderness
• Investigate: ESR/CRP/platelets (elevated in most GCA, individual sensitivity 65–71%); temporal artery ultrasound (a “halo sign” — less invasive than biopsy, though biopsy remains gold standard: 77% vs 54% sensitivity, 100% vs 81% specificity)
• Do not delay steroids awaiting investigation results if clinical suspicion is high — refer urgently
• Treatment: IV methylprednisolone 3–5 days then a prolonged oral prednisolone taper over 1–2 years; tocilizumab (anti-IL-6) is increasingly used as a steroid-sparing agent with superior sustained-remission outcomes vs prednisolone alone

Examination

• Test the direction of gaze in which diplopia occurs, both monocularly (to exclude monocular diplopia) and binocularly
• Diplopia on lateral gaze → 6th nerve (abducens) palsy
• Diplopia on downward gaze (eye deviates upward) → 4th nerve (trochlear) palsy
• Eye deviated down and out → 3rd nerve (oculomotor) palsy

Investigations

• Screen for diabetes
• ESR/CRP for GCA (as above)
• TFTs for hyperthyroidism/thyroid eye disease
• Lipids for microvascular disease (more common with isolated abducens/CN VI palsies)
• MRI (preferred) or CT brain if MRI unavailable — for microvascular disease, TIA/CVA, and tumour identification

Management

• Discuss with ophthalmology or neurology
• Microvascular 6th nerve palsies typically resolve spontaneously in 3–6 months
• Surgery or botulinum toxin for a permanent deviation
• Patching one eye or an occluder gives symptomatic relief while a cause is identified/ treated — see vision-and-fitness-to-drive.md for the driving implications of diplopia