Sir,

We have observed three cases of isolated cotton-wool spot (CWS) accompanied by a history of migraine, and would suggest a pathophysiological association between these two clinical entities.

CWS are believed to result from acute retinal arteriolar occlusion leading to hypoperfusion and ischaemia of the retinal nerve fibre layer (RNFL). Subsequent impairment of axoplasmic flow causes accumulation of axoplasmic debris in the retinal ganglion cell axons, impairing signal conduction and producing a characteristic CWS lesion. Isolated CWS are usually asymptomatic although may produce a localised non-arcuate or arcuate scotoma.1, 2

All three patients presented with a new visual disturbance associated with recent migraine. In each case an isolated CWS was identified, corresponding to an area of scotoma. Optical coherence tomography (OCT), fundus fluorescein angiography (FFA), and Goldmann visual field assessment were performed in each case. Blood pressure examination and serum biochemistry/haematology analysis were unremarkable. In all three patients the symptoms and the CWS resolved within 6 months. We describe one example case in further detail.

Case report

A 38-year-old man presented ten days after a severe migraine associated with slightly blurry central vision. Although the migraine and blurriness had quickly resolved, the patient reported a residual right temporal–paracentral field defect. His medical history included recurrent migraines, often involving visual symptoms. He had no other ophthalmic history and took no regular medications.

An isolated CWS between the right macula and optic disc was detected and further investigated (Figure 1a and b). The patient reported a recent increase in coffee consumption and was advised to reduce this. At 6 months the patient’s symptoms and the CWS had resolved.

Figure 1
figure 1

Results of various investigations. (a) Right retinal colour photography of an isolated CWS which is lying between the macula and optic disc and is equidistant to both. Corrected visual acuity was 6/5 and Goldmann visual field assessment highlighted a region of reduced sensitivity immediately inferior to the physiological blind spot. (b) OCT reveals localised swelling of the RNFL at the location of the CWS. FFA showed no signs of retinal vasculitis or ischaemia. Blood pressure measurements, serum biochemistry, and haematology analysis were normal.

Full size image

Comment

The clinical manifestations of migraine are believed to result from transient vasospasm of the cerebral vasculature, inducing cerebral hypoperfusion. Our case series suggests vasospasm may also occur within the retinal microvasculature, although the exact mechanism of this may differ. Retinal vasospasm has been observed directly during a migrainous episode, and has also been implicated as a possible cause of branch retinal arteriolar occlusion in the presence of migraine.3, 4 Furthermore, studies have shown patients with migraine to have reduced RNFL thickness, suggesting that, although vasospasm is in itself a transient occurrence, the chronic natural history of migraine may lead to permanent structural changes.5

This small case series highlights an association between migraine and CWS, and emphasises the importance of taking a full medical history when assessing patients with sudden onset of visual field defect secondary to CWS.