Transient visual loss
Transient loss of vision is a fully reversible episode of visual loss lasting less than 24 hours. It often causes concern to the clinician for fear as a harbinger of imminent stroke. Patients often present after resolution of the episode and may have a normal ocular and systemic examination.
Differential diagnoses
The most important distinction in the assessment of TVL is vascular (amaurosis fugax) vs non-vascular aetiology.
| Acute angle-closure glaucoma
Uncontrolled diabetes Optic nerve dysfunction
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Vascular causes
- Emboli
- TVL can occur due to embolic occlusion of the retinal, optic disc, and choroidal blood vessels.
- Often, the emboli may be visible on ophthalmoscopic examination.
- Ocular ischaemic syndrome
- Ocular ischemic syndrome (OIS) is a disorder of ocular function that occurs subsequent to the stenosis of the carotid artery.
- TVL occurs over seconds to minutes.
- The eye may be red from dilated conjunctival and episcleral vessels.
- There is usually a slow, progressive decline in visual acuity over weeks to months.
- Characteristic features include episodes precipitated by bright light and dull ocular pain often relieved by lying down (‘ocular angina’).
- Migraine
- May cause transient monocular visual loss due to retinal vasospasm.
- Episodes may last minutes to hours, and there may be a history of stereotyped events.
- An associated headache is common.
- Mostly, the visual loss is transient, lasting 5 to 20 minutes, and may recur several times during the day.
- Other visual disturbances include monocular positive visual phenomena (flashing lights or scintillating scotoma).
- Haematological abnormalities
- Severe anaemia, sickle cell disease, and hypercoagulable states may cause episodes of transient visual loss.
- Vasculitis
- vision loss in GCA may be heralded by TVL.
- Examination reveals a swollen optic disc.
- There may be concomitant systemic symptoms (See above section on GCA)
Investigations
All patients should undergo routine haematological testing. In patients under the age of 50 without atherosclerotic risk factors, further investigation is not required.
- Haematological evaluation: FBC, CRP, ESR, cholesterol and lipid profile. Thrombophilia screening should be guided by history and concomitant symptoms.
- Cardiac investigations: ECG +/- 24-hour Holter monitor; ECHO; carotid Doppler scanning.
- Neuroimaging to exclude a haemorrhagic lesion in the brain. Angiographic imaging (CTA/ MRA) may also be utilised in imaging the head and neck.
Management
Management of TVL is directed at the underlying cause.
The North American Symptomatic Carotid Endarterectomy Trial (NASCET) demonstrated that patients with ocular TIA had a 2-year stroke incidence of 17%. This risk may be reduced in patients who have carotid stenosis greater than 70%, reducing future risks of stroke. Individuals with <75% ipsilateral internal carotid artery stenosis or complete carotid occlusion are treated with anti-platelet agents. Those with >75% stenosis should be referred to a vascular surgeon for consideration of endarterectomy or carotid artery stenting.
Ischaemic heart disease is the most common cause of death following an episode of amaurosis fugax. Vascular risk factors, such as hypertension, diabetes, and hyperlipidaemia should be addressed.
References
- Ahmed R, Foroozan R. Transient monocular vision loss. Neurol Clin 2010;28:619-629.
- Barnett HJ, Taylor W, Eliasziw M et al. Benefit of Carotid Endarterectomy in Patients with Symptomatic Moderate or Severe Stenosis. N Engl J Med 1998; 339:1415-1425
- Poole CJ, Ross Russell RW Mortality and stroke after amaurosis fugax. Journal of Neurology, Neurosurgery & Psychiatry 1985;48:902-905.
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