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Keywords:

  • stroke;
  • patent foramen ovale;
  • migraine

Abstract

  1. Top of page
  2. Abstract
  3. CASE REPORT
  4. DISCUSSION
  5. REFERENCES

The association between patent foramen ovale, ischemic stroke, and migraine with aura is well known. It is, however, complicated and generates a considerable debate about the features and clinical consequences of the phenomenon. We report a case of a woman for whom patent foramen ovale has possibly acted as an inducer of both migraine attacks and ischemic stroke.

The comorbidity of migraine with aura (MA) with ischemic stroke and patent foramen ovale (PFO) as well as its implications for clinical management has been a topic of considerable controversy. The epidemiological association of these conditions is well documented.1-5 Transcranial Doppler and transesophageal echocardiography studies have demonstrated significantly increased prevalence of right-to-left shunt (RLS) in patients with MA compared with the migraine-free control population,1,2 and it has been hypothesized that MA and PFO might share a common genetic background.3 Young patients with cryptogenic stroke have been reported to have a higher prevalence of PFO than healthy controls,4 while MA has been associated with increased risk of ischemic stroke in several epidemiological studies.5 However, the nature of the connection as well as the actual triggering event remains open.

CASE REPORT

  1. Top of page
  2. Abstract
  3. CASE REPORT
  4. DISCUSSION
  5. REFERENCES

We report a case of a 35-year-old right-handed woman with a history of asthma and migraine with visual aura since the age of 13. The patient is an ex-smoker with no other known cardiovascular risk factors. The frequency of her migraine attacks has been roughly 1 per year. The latest attack before the current incident was a little over a year ago and featured a prolonged visual aura that lasted for 5 hours.

Then, while brushing her hair soon after waking up in the morning, she developed a sudden dysphasia, right upper limb weakness, and right sensory hemiparesis and was admitted to a stroke unit where she underwent an extensive etiological workup. Most of the symptoms alleviated in the next few hours and the patient was discharged after 3 days of hospitalization with aspirin, dipyridamol, and simvastatin medications. After 6 weeks, she still suffers from a mild sensory loss and neuropsychological defects.

Brain magnetic resonance imaging performed the day after admission demonstrated a small, acute ischemic stroke in the left occipital lobe. Intracranial and extracranial magnetic resonance angiography showed no abnormalities. Chest X-ray, blood pressure, transthoracic echocardiography and electrocardiography were normal. Blood tests did not reveal any signs of prothrombotic condition. Lumbar puncture demonstrated a slightly elevated leukocyte count of 4 × 109/mm. Total cholesterol concentration was 4.0 mmol/L and low-density lipoprotein-cholesterol concentration was 2.3 mmol/L.

Examination using a dye dilution method was carried out 1 month after the stroke in order to detect a possible PFO. At first, there was no sign of RLS, but during Valsalva maneuver, a 5% RLS was observed. About 15 minutes after the Valsalva maneuver, she experienced her typical, but unusually strong visual aura – a right-sided scintillating scotoma. The aura lasted 10 minutes and was followed by a typical migraine headache. Transesophageal echocardiography was performed a few weeks later and confirmed the existence of PFO.

DISCUSSION

  1. Top of page
  2. Abstract
  3. CASE REPORT
  4. DISCUSSION
  5. REFERENCES

It has been hypothesized that PFO might predispose to both MA and ischemic stroke through paradoxical microscopic emboli through RLS. Also, passage of chemical substances normally eliminated in the lungs has been suggested to be a possible trigger of migraine. In our patient, the close temporal association of the onset of aura and the Valsalva maneuver suggests that opening of RLS acted as a trigger for migraine attack. It is also plausible, though impossible to verify afterward, that the stroke itself was caused by an embolus traversing the same RLS. A previous study has reported that paradoxical emboli frequently end up in the posterior circulation6 and, recently, it was demonstrated that MA patients with massive RLS tend to report Valsalva-provoking activities to trigger their MA attacks.7 Therefore, it is possible that visual auras are triggered by emboli which have traveled across the PFO, found their way to occipital areas through posterior circulation, and caused cortical spreading depression.

Randomized studies on closure of PFO in both ischemic stroke and MA are presently ongoing. However, according to the current guidelines, it might be good practice to consider closure of PFO only in young patients with recurrent ischemic strokes and not in those with MA without ischemic episodes.

REFERENCES

  1. Top of page
  2. Abstract
  3. CASE REPORT
  4. DISCUSSION
  5. REFERENCES