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Cases of retinal vein occlusion with migraine have been described since 1882.1 An interesting case of central retinal vein occlusion (CRVO) which coincided with complete cessation of longstanding, severe migraines is reported.
A 44 year old lady developed classic migraine at the age of 11 years. Her symptoms comprised a visual aura of flashing lights followed by severe headache (not localised to one side), photophobia, and nausea, which generally lasted for two days. There were no identifiable triggers. Her management consisted of sumatriptan, which she took on experiencing the visual aura. This considerably reduced the severity of her headache and usually limited the duration of her symptoms to one day. The migraines occurred frequently and randomly with the longest migraine-free period being one month.
One morning, she awoke with visual loss in her right eye. She assumed this to be the visual aura of a migraine (although it was atypical since there was no photopsia or subsequent headache), and took her normal dose of sumatriptan. The visual loss occurred before taking the medication. The visual defect fragmented into black patches followed by gradual visual improvement over the next few days. She then consulted her general practitioner who referred her to the eye department.
At presentation to the eye department one week after the initial visual loss, her visual acuity was 6/9 right and 6/4 left. There was a right relative afferent pupillary defect. Funduscopy revealed retinal haemorrhages in all four quadrants with a swollen optic disc. A diagnosis of non-ischaemic CRVO was made. She was advised to take aspirin 75 mg daily.
On follow up, her visual acuity continued to improve with resolution of the retinal haemorrhages and the disc oedema. The following investigations were normal: full blood count, erythrocyte sedimentation rate, electrolytes, fasting glucose, fasting cholesterol, and plasma protein electrophoresis. General medical examination was normal. She is a non-smoker with no family history of cardiovascular disease. At the 18 month follow up her visual acuity was 6/5 right and 6/4 left. There was no relative afferent pupillary defect. The fundal appearance returned to normal.
Follow up to date is two years and she has not experienced a single migraine since developing the CRVO. There have been no other factors to account for the cessation of her migraines during this period.
There have been numerous reports of retinal vaso-occlusion and migraine in the context of “complicated migraine”.1 We have presented an interesting patient who instead experienced complete cessation of migraine in association with the development of a CRVO. In the natural history of migraine there is a gradual reduction in severity and frequency of attacks with age.2 The abrupt cessation of migraine following development of a CRVO suggests a causal relationship. She had no risk factors for a retinal vascular event.
It has been proposed that prophylactic use of platelet antagonists, such as aspirin, may reduce the occurrence of migraine. Serotonin is released locally in cerebral tissue shortly before the onset of a migraine attack. Since platelets contain all of the plasma serotonin platelet function has been implicated as a factor in migraine.3 The role of serotonin in migraine is complex. To the best of our knowledge there is no report of platelet antagonists causing complete cessation of migraine. It seems unlikely that aspirin was solely responsible for the cessation of migraine in our patient, however this remains a possibility.
The pathophysiology of migraine is complex but involves neuronal events linked to alterations in the calibre of intracerebral blood vessels. During a migraine aura cerebral blood flow decreases. The subsequent hyperaemia leads to headache by activation of fibres originating in the trigeminal ganglion. These trigeminovascular afferents reside primarily within the ophthalmic division of the trigeminal nerve.4 The retinal vasculature is very similar to the cerebral vasculature both in structure and response to vasoactive substances.3 This probably accounts for cases of “complicated migraine” leading to retinal vein occlusion.
We postulate that an initial neuronal event occurred in our patient that resulted in a functional alteration in her trigeminovascular system leading to the complete cessation of migraine. This neuronal event also produced a temporary decrease in central retinal artery perfusion and the subsequent development of a CRVO.5 This case therefore demonstrates the potential for intracerebral events to influence the retinal vasculature.
Competing interests: none declared
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