This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Khiani, R. Articles by Mas, J.-L. Search for Related Content PubMed PubMed Citation Articles by Khiani, R. Articles by Mas, J.-L.

(Stroke. 2002;33:2149.)
© 2002 American Heart Association, Inc.

Letters to the Editor

Re: Clinical and Imaging Findings in Cryptogenic Stroke Patients With and Without Patent Foramen Ovale

Raj Khiani, MRCP; Kevin Daly, MRCS Charles McCollum, MD, FRCS

Academic Department of Surgery, South Manchester University Hospital, Manchester, UK

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

We read with interest the article by Lamy et al¹ in which they felt that their data did not support paradoxical embolism as the mechanism of stroke in patients with a patent foramen ovale (PFO). Their study excluded patients with a thrombophilia, which is the group most at risk for venous thromboembolism and hence paradoxical embolism. They therefore excluded the stroke patients most likely to have suffered paradoxical embolism. How many such patients were excluded?

They also argued that as deep vein thrombosis (DVT) was rarely detected in their stroke patients, it was unlikely that paradoxical embolism had occurred. However, in patients with a confirmed pulmonary embolism, which must have arisen from a DVT, the causative DVT usually cannot be detected despite extensive investigation.^2,3 Considering that the origin of a paradoxical embolus may be a very small DVT, even a valve cusp thrombus, failure to document a DVT after a stroke does not exclude paradoxical embolism any more than it would exclude the diagnosis of pulmonary embolism.

We were interested to see that migraine was again found to be more common in cryptogenic stroke patients with a PFO than in those without a PFO. This association has been reported previously.⁴ It is biologically plausible that showers of microemboli crossing a PFO may cause cerebral vasospasm and migraine. Sztajzel et al⁴ demonstrated that surgical closure or anticoagulant treatment in stroke patients with a PFO may cure migraine symptoms. Lamy et al do not seem to have considered the possibility that paradoxical . . . [Full Text of this Article]

Catherine Lamy, MD Jean-Louis Mas, MD

Sainte-Anne Hospital, Paris, France