Patent Foramen Ovale and Cerebrovascular Diseases
Patent Foramen Ovale and Cerebrovascular Diseases
Several studies have demonstrated a strong association between patent foramen ovale (PFO) and migraine headache with aura (MHA). Preliminary data have shown substantial improvements in MHA severity after transcatheter PFO closure. Giardini and colleagues, from Bologna University in Italy, sought to establish which factors lead to MHA in patients with PFO and assess the mechanisms through which MHA is resolved after PFO closure.
Their study comprised 131 consecutive patients with PFO and at least one documented stroke. A total of 35 (27%) of patients from this group were diagnosed as having MHA; the incidence and severity of their symptoms was evaluated by use of a Migraine Disability Assessment (MIDAS) questionnaire.
Patients with MHA were more likely to be female (P = 0.001), have a more complex atrial septal anatomy (P = 0.001) and have associated thrombophilia (P = 0.007), than those without MHA. Transesophageal echocardiography and transcranial Doppler scanning revealed that spontaneous right-to-left shunts, and large shunts, were more prevalent in patients with MHA than in those without.
For most patients with MHA (91%), transcatheter closure of the PFO completely or substantially resolved their MHA symptoms. Furthermore, these improvements generally lasted for more than 1 year after the procedure.
These findings lend support to the theory that MHA could be triggered in patients with PFO by persistent right-to-left shunting, which permits small venous thrombus or platelet aggregate to enter the cerebral circulation. Transcatheter closure of the defect seems to resolve MHA by abolishing the right-to-left shunt.
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Several studies have demonstrated a strong association between patent foramen ovale (PFO) and migraine headache with aura (MHA). Preliminary data have shown substantial improvements in MHA severity after transcatheter PFO closure. Giardini and colleagues, from Bologna University in Italy, sought to establish which factors lead to MHA in patients with PFO and assess the mechanisms through which MHA is resolved after PFO closure.
Their study comprised 131 consecutive patients with PFO and at least one documented stroke. A total of 35 (27%) of patients from this group were diagnosed as having MHA; the incidence and severity of their symptoms was evaluated by use of a Migraine Disability Assessment (MIDAS) questionnaire.
Patients with MHA were more likely to be female (P = 0.001), have a more complex atrial septal anatomy (P = 0.001) and have associated thrombophilia (P = 0.007), than those without MHA. Transesophageal echocardiography and transcranial Doppler scanning revealed that spontaneous right-to-left shunts, and large shunts, were more prevalent in patients with MHA than in those without.
For most patients with MHA (91%), transcatheter closure of the PFO completely or substantially resolved their MHA symptoms. Furthermore, these improvements generally lasted for more than 1 year after the procedure.
These findings lend support to the theory that MHA could be triggered in patients with PFO by persistent right-to-left shunting, which permits small venous thrombus or platelet aggregate to enter the cerebral circulation. Transcatheter closure of the defect seems to resolve MHA by abolishing the right-to-left shunt.
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