Relationship Between Migraine and PFO: A Study of 121 Migraine Patients
Relationship Between Migraine and PFO: A Study of 121 Migraine Patients
Background: Migraine is a common neurological disorder, the origins of which remain unknown. Patent foramen ovale (PFO) is considered to have a role in migraine. The relationship between migraine and patent foramen ovale may be stronger in patients suffering from migraine with aura compared to patients with common migraine.
Objectives: The aim of the study was to evaluate the frequency of PFO in patients with migraine with aura (MA+) and compare it with the prevalence of PFO in migraine patients without aura (MA-), and in a healthy age-matched control group. We investigated PFO association with migraine, considering such factors as: A type of migraine aura, frequency of attacks, familial occurrence, sex and age of patients.
Patients: 121 patients: 61 patients suffering from migraine with aura, 60 without aura and 65 normal controls. The group of patients with migraine with aura was divided into subgroups regarding to the type of aura.
Methods: In order to detect PFO the contrast transcranial Doppler was performed during Valsalva maneuver.
Results: The presence of PFO was found in 33/61 (54%) patients with MA(+) compared to 15/60 (25%) without aura and 16/65 (25%) control subjects. The difference between MA(+) patients and MA(-) patients and the difference between MA(+) patients and control group was statistically significant (P < .05). There was no association between type of migraine aura and PFO, as well as we found no association between PFO and frequency of attacks, familial occurrence, sex and age of patients and PFO.
Conclusions: Our findings suggest possible association of migraine with aura and PFO. It seems that PFO does not influence the type of aura and frequency of attacks of migraine as well as it is not associated with familial occurrence of migraine.
Migraine is a common disorder of uncertain pathogenesis characterized by distinctive headache and transient focal neurological symptoms of its aura in some patients. There are many hypotheses of migraine pathogenesis, but 2 of them (vascular and neuronal) are the most considerable.
Migraine headache may be related to slowly developing vasospasms, beginning at the peripheral ends of the brain vasculature, or to spreading neuronal changes. The focal symptoms during migraine aura may be due to transient constriction of a cerebral artery whereas the headache arises from a sterile inflammatory reaction around the walls of dilated cephalic vessels. The very orderly development of the aura makes a vascular origin less probable, while a primary disturbance of cortical nerve cell function, such as cortical spreading depression (CSD) and activation of trigeminovascular system seems now to be most probable explanation.
Aura of migraine presenting as a focal neurological deficit bears many similarities to transient ischemic attack (TIA), which is also presented as focal neurological symptoms. Migraine aura may occur in isolation, without headache. So TIAs may mimic aura, or aura may mimic TIA.
Some authors suggest that paradoxical cerebral embolism through a right-to-left blood shunt in the atrial chambers might be a possible cause of migraine attacks. Paradoxical cerebral embolism during a Valsalva maneuver might evoke transient focal neurological symptoms. As such, paradoxical cerebral embolism through a right-to-left shunt in atrial chambers may be a possible mechanism of aura of migraine. In fact a relationship between migraine and PFO has been recently suggested.
Therefore we evaluated the occurrence of PFO in patients with migraine concentrating on the possible association of PFO with different types of migraine aura, frequency of attacks, familial occurrence, sex and age of migraine patients.
Background: Migraine is a common neurological disorder, the origins of which remain unknown. Patent foramen ovale (PFO) is considered to have a role in migraine. The relationship between migraine and patent foramen ovale may be stronger in patients suffering from migraine with aura compared to patients with common migraine.
Objectives: The aim of the study was to evaluate the frequency of PFO in patients with migraine with aura (MA+) and compare it with the prevalence of PFO in migraine patients without aura (MA-), and in a healthy age-matched control group. We investigated PFO association with migraine, considering such factors as: A type of migraine aura, frequency of attacks, familial occurrence, sex and age of patients.
Patients: 121 patients: 61 patients suffering from migraine with aura, 60 without aura and 65 normal controls. The group of patients with migraine with aura was divided into subgroups regarding to the type of aura.
Methods: In order to detect PFO the contrast transcranial Doppler was performed during Valsalva maneuver.
Results: The presence of PFO was found in 33/61 (54%) patients with MA(+) compared to 15/60 (25%) without aura and 16/65 (25%) control subjects. The difference between MA(+) patients and MA(-) patients and the difference between MA(+) patients and control group was statistically significant (P < .05). There was no association between type of migraine aura and PFO, as well as we found no association between PFO and frequency of attacks, familial occurrence, sex and age of patients and PFO.
Conclusions: Our findings suggest possible association of migraine with aura and PFO. It seems that PFO does not influence the type of aura and frequency of attacks of migraine as well as it is not associated with familial occurrence of migraine.
Migraine is a common disorder of uncertain pathogenesis characterized by distinctive headache and transient focal neurological symptoms of its aura in some patients. There are many hypotheses of migraine pathogenesis, but 2 of them (vascular and neuronal) are the most considerable.
Migraine headache may be related to slowly developing vasospasms, beginning at the peripheral ends of the brain vasculature, or to spreading neuronal changes. The focal symptoms during migraine aura may be due to transient constriction of a cerebral artery whereas the headache arises from a sterile inflammatory reaction around the walls of dilated cephalic vessels. The very orderly development of the aura makes a vascular origin less probable, while a primary disturbance of cortical nerve cell function, such as cortical spreading depression (CSD) and activation of trigeminovascular system seems now to be most probable explanation.
Aura of migraine presenting as a focal neurological deficit bears many similarities to transient ischemic attack (TIA), which is also presented as focal neurological symptoms. Migraine aura may occur in isolation, without headache. So TIAs may mimic aura, or aura may mimic TIA.
Some authors suggest that paradoxical cerebral embolism through a right-to-left blood shunt in the atrial chambers might be a possible cause of migraine attacks. Paradoxical cerebral embolism during a Valsalva maneuver might evoke transient focal neurological symptoms. As such, paradoxical cerebral embolism through a right-to-left shunt in atrial chambers may be a possible mechanism of aura of migraine. In fact a relationship between migraine and PFO has been recently suggested.
Therefore we evaluated the occurrence of PFO in patients with migraine concentrating on the possible association of PFO with different types of migraine aura, frequency of attacks, familial occurrence, sex and age of migraine patients.