A painful CN III palsy with pupil involvement is a posterior communicating artery aneurysm until proven otherwise — rupture risk is high and outcome is fatal without urgent intervention. Giant Cell Arteritis can cause permanent blindness within hours of diplopia onset — starting steroids urgently prevents bilateral visual loss. Posterior circulation strokes frequently present with diplopia and vertigo and are missed without a structured neurological assessment.

Monocular diplopia is almost always benign and ophthalmic. Binocular diplopia always indicates failure of ocular motor alignment — cranial nerve palsy, extraocular muscle disease, or brainstem pathology — and requires neurological assessment. Pupil involvement in CN III palsy is the key distinguishing feature: the pupilloconstrictor fibres travel on the outside of CN III and are compressed first by aneurysms but spared in ischaemic (microvascular) palsies.

Isolated CN VI palsy in a hypertensive or diabetic patient aged 50–70 is usually microvascular and resolves in 8–12 weeks. However, CN VI palsy can be a false localising sign of raised ICP — urgent MRI is needed if there is no vascular risk factor. Myasthenia gravis is frequently missed (mean diagnostic delay 2 years) — fatiguability is the key clue. Internuclear ophthalmoplegia in a young patient is MS until proven otherwise.

Pupil examination is the single most important element in CN III palsy — pupil involvement changes management from watchful waiting to emergency neurosurgical referral. A full neuro examination allows detection of brainstem signs that would mandate immediate imaging. Temporal artery examination takes 30 seconds and prevents bilateral blindness from missed GCA. Examining eye movement in all 9 positions of gaze localises the affected muscle and cranial nerve.

ESR and CRP must be checked urgently in any patient over 50 with new diplopia and headache — GCA is a treatable emergency. Steroids should not wait for biopsy results if clinical suspicion is high. CT angiography is preferred over MRI angiography for acute PComm aneurysm detection because it is faster and more widely available. Isolated microvascular CN VI/IV palsies do not require imaging if there are clear vascular risk factors — this avoids unnecessary CT radiation and waiting times.

GCA requires same-day ophthalmology assessment because visual loss can occur within hours and high-dose steroids (prednisolone 60 mg or IV methylprednisolone) must be started immediately. Delaying by even one day risks the fellow eye. Painless isolated CN VI with diabetes/hypertension can be managed expectantly in primary care with 12-week monitoring, avoiding unnecessary neurology referrals. Prisms can significantly improve quality of life in stable diplopia.

Microvascular CN palsies (CN III pupil-sparing, CN IV, CN VI in diabetics/hypertensives) resolve spontaneously in 85% of cases within 12 weeks as the ischaemic nerve recovers. During this period, occlusion of one eye eliminates diplopia functionally. DVLA regulations prohibit driving with diplopia — failure to advise patients creates medico-legal risk. GCA steroids must not be delayed: high-dose prednisolone reduces the risk of visual loss from 30% to under 5%.

Vascular risk factor management is the primary prevention of microvascular CN palsies and reduces recurrence risk by ~40%. Patients frequently underestimate the functional impact of diplopia — fall risk is doubled and driving ability is abolished. In children, occlusion of one eye without alternating risks inducing amblyopia in the occluded eye — this is an ophthalmological emergency and requires urgent referral.

The key safety-netting message: microvascular palsies should improve, not worsen. Any progression demands urgent imaging — a "reassured" patient who returns with worsening symptoms may have a compressive lesion that was missed on initial assessment. The 12-week threshold is the standard for ophthalmology/neurology referral of unresolved palsies. GCA monitoring is critical — steroid dose must be titrated to ESR/CRP response and symptoms, with relapses requiring dose increase.