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Clinical Review

Recent advances in the diagnosis and management of migraine

BMJ 2006; 332 doi: https://doi.org/10.1136/bmj.332.7532.25 (Published 05 January 2006) Cite this as: BMJ 2006;332:25

Rapid Response:

Migraine: an ophthalmologist’s view.

As a footnote to the article on migraines by Goadsby (BMJ 2006;332:25
-9), I would like to add an Ophthalmologist’s perspective.
Patients are often referred to ophthalmologists with headache associated
with eye pain or headache associated with visual disturbances. To add our
penny’s worth, ocular causes of headache should not be overlooked, such as
acute angle closure glaucoma, iritis in younger patients or temporal
arteritis in older patients. Clearly ocular signs, such as a red eye or
swollen disc, should be sought. Although ophthalmic causes are frequently
diagnosed, other causes such as trigeminal neuralgia, dental, sinus or ear
pathology can also be made.
Photopsia is a presenting complaint seen several times per day in our eye
casualty. The most common diagnosis made after examination is posterior
vitreous detachment but the concern is always of a retinal tear or
detachment. New floaters or a shadow across the visual field, like a
curtain are other features of retinal detachments. Retinal problems can be
excluded by using the slit lamp biomicroscope and indirect ophthalmoscope
with indentation (to visualise the ora serrata) to examine the retina, and
also by excluding the presence of pigmented cells (“tobacco dust,
Shaffer’s sign) in the vitreous.

Acephalgic migraine is a diagnosis of exclusion, and by definition
not associated with headache[1]. The nature of flashes due to acephalgic
migraine has been well described: coloured rather than merely white
lights, affecting both eyes, like a kaleidoscope, and gradually moving in
from the periphery to the centre [2]. The temporal course of such flashes
can be a fairly good indication that the basis for the symptoms is not in
the eyeball, i.e. symptoms last 20 to 30 minutes and then completely
resolve.

“Retinal migraine” is a rare primary headache disorder, most commonly
reported in women of childbearing age who have a history of migraine with
aura (3). This tends to cause monocular visual loss for 10–20 minutes
which is be associated with diffuse or unilateral headache(4). Exercise
may precipitate retinal migraine attacks(5). The International Headache
Society diagnostic criteria for retinal migraine state that the visual
loss must be reversible. Otherwise further investigation would be
required, particularly if other neurological signs develop, in order to
exclude underlying cerebral pathology. Vasospasm of the retinal
circulation or ophthalmic artery is traditionally thought to be the cause
of the amaurosis-like episode of ocular migraine (4,5,6,7,8). Retinal
vasospasm may also be associated with low protein C and S levels; positive
antinuclear antibodies; underlying systemic diseases such as SLE (8) and
antiphospholipid syndrome (8,9); giant cell arteritis or polyarteritis
nodosa (4).

A relationship between glaucoma and migraine has been hypothesized by
some authors. A study of 460 "glaucoma suspects" (with raised intraocular
pressure, but without optic disc and visual field abnormalities) and 460
controls, found a higher prevalence of migraine in the glaucoma suspects
(13%), particularly in women (17%), than in controls (7%). Attacks of
"ocular pain" were found to occur in 51% of those who were both "glaucoma
suspects" and had migraine. (10).

There have been other claims of a relationship between migraine
headaches and refractive errors and also with binocular vision anomalies,
but little supporting evidence. However the evidence to suggest a
relationship between migraine headache and pupil anomalies, visual field
defects and pattern glare is stronger. The therapeutic use of precision-
tinted spectacles to reduce pattern glare (also called “visual stress”)
may help some migraine sufferers (11).

References:

1. Pradhan S. Chung SM. Retinal, ophthalmic, or ocular migraine. Current
Neurology & Neuroscience Reports. 4(5):391-7, 2004 Sep.

2. Kanski JJ. Clinical ophthalmology. A systemic approach. Butterworth
Heinemann publishing group.

3. Grosberg BM. Solomon S. Lipton RB. Retinal migraine. Current Pain &
Headache Reports. 9(4):268-71, 2005 Aug

4. Burger SK, Saul RF, Selhorst JB, et al. Transient monocular blindness
caused by vasospasm. N Engl J Med 1991;325:870–3.

5. Jehn A, Dettwiler B, Fleischhauer J, et al. Exercise-induced
vasospastic amaurosis fugax. Arch Ophthalmol 2002;120:220–2.

6. Glaser JS. Topical diagnosis: prechiasmal visual pathways. retinal
artery occlusions. Duane’s ophthalmology 2002; CD-ROM ed. Philadelphia:
Lippincott Williams and Wilkins, 2002.

7. Wolter JR, Birchfield WJ. Ocular migraine in a young man resulting in
unilateral blindness and retinal oedema. J Pediatric Ophthalmol
1971;8:173–6.

8. Winterkorn JMS, Kupersmith MJ, Wirtschafter JD, et al. Brief report:
treatment of vasospastic amaurosis fugax with calcium channel blockers. N
Engl J Med 1993;329:396–9.

9. Levine SR, Deegan MJ, Futrell M, et al. Cerebrovascular and neurologic
disease associated with antiphospholipid antibodies:48 cases. Neurology
1990;40:1181–9.

10. De Marinis M. Giraldi JP. de Feo A. Rinalduzzi S. De Benedetti G.
Mollicone A. Accornero N. Migraine and ocular pain in "glaucoma suspect".
Cephalalgia. 19(4):243-7, 1999 May.

11. Harle DE. Evans BJ. The optometric correlates of migraine. Ophthalmic
& Physiological Optics. 24(5):369-83, 2004 Sep.

Competing interests:
None declared

Competing interests: No competing interests

10 January 2006
Tanya N Moutray
ophthalmology LATS
Royal Victoria Hospital, Grosvenor Rd, Belfast,BT12 6BA