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Migraine and stroke in young women

M.J. Cuadrado, M.A. Khamashta, G.R.V. Hughes
DOI: http://dx.doi.org/10.1093/qjmed/93.5.317 317-318 First published online: 1 May 2000


The association between migraine and stroke has been described in several studies.1–5 The predictive value of variables such as gender, the presence or absence of family history of migraine, use of oral contraceptives, high blood pressure, diabetes, heart disease or smoking has been analysed.

We would like to suggest a possible pathogenetic link between some cases of migraine followed by stroke not frequently mentioned in the literature—the presence of antiphospholipid antibodies (aPL).

Following the description of the antiphospholipid syndrome (APS) in 1983,6 it has become clear that headaches, including migraine, and strokes are major features of the disease.7 Our own clinical experience in the lupus unit at St Thomas Hospital points towards the juxtaposition of severe headache including migraine and the development of stroke in a number of young individuals, especially females. Table 1highlights the clinical features of eight female APS patients with migraine and subsequent stroke. In every patient, the migraine antedated the stroke (mean 29±21 months, range 9–72 months). Magnetic Resonance Imaging (MRI) before stroke was normal in six patients, while two showed multiple high‐intensity small images compatible with small‐vessel disease (patients 7 and 8). All patients were receiving treatment for migraine as shown in Table 1. Interestingly, in two patients (patients 2 and 6), severe recurrent migraine attacks improved following the use of low‐dose aspirin (75 mg/day). A further two patients (3 and 5) were treated with warfarin as therapeutic trial, showing a dramatic improvement of migraine. All patients received warfarin after developing stroke and those four who still suffered with migraine, also had a good response to warfarin.

The pathogenesis of migraine in APS is unknown.7 Possible mechanisms include the activation and aggregation of platelets8,,9 and the expression on endothelial cells of proteins such as endothelin‐1,10 or tissue factor, the major initiator of the coagulation cascade in vivo.11 The mechanism behind the reduction in migrainous headaches during warfarin treatment in some of our patients is unclear, however, the dramatic response leads us to suggest that in the very resistant patient, anticoagulants may be an alternative therapy.12

The data presented in the current literature1–5 clearly show that some young migraine patients are at increased risk of stroke. The risk for the first stroke in patients positive for aPL has been estimated at 10–26%.13 Indeed, it has been suggested that APS may be responsible for up to 18% of strokes in under 45‐year‐olds.14

The presence of aPL is a clear risk for stroke, and a risk identified by a simple, inexpensive blood test. We believe that aPL measurement should be included in the investigation of all young individuals with migraine unresponsive to conventional treatment, and all individuals under 50 with stroke. The presence of aPL should be an integral part of future epidemiological studies of these conditions.

View this table:
Table 1

Characteristics of patients

PatientAgeDiagnosisTime betweenAntiphospholipidTreatment forResponse of
migraine andantibodiesmigraine beforemigraine to
stroke (months)warfarintreatment
232PAPS9+ve+veAspirin (75 mg)Total
631SLE/APS31+ve+veAspirin (75 mg)Total
  • PAPS, primary antiphospholipid syndrome; APS, antiphospholipid syndrome; SLE, systemic lupus erythematosus; NSAIDs, non‐steroidal anti‐inflammatory drugs.


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