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The prevalence and frequency of interictal microembolic signals (MES) were higher in migraine patients with higher cortical dysfunction (HCD) during aura, as compared with migraine patients without HCD during aura and with healthy controls, according to a study published in the journal Cephalalgia (2015 Sep 29. doi: 10.1177/0333102415607191).
Dr. Jasna Zidverc-Trajkovic of the Neurology Clinic, Clinical Center of Serbia, Belgrade, and her colleagues used transcranial Doppler ultrasound to test their hypothesis that the complexity of migraine aura is dependent on hypoperfusion caused by microemboli that occur in different regions of the brain. The goal was to evaluate the prevalence and clinical impact of interictal MES in migraine patients with HCD during aura.
The investigators enrolled 34 individuals with migraines who experienced language and memory impairment during aura (HCD group), 31 patients who had migraines with only visual or visual and somatosensory symptoms during aura (control group I), and 34 healthy individuals who comprised a control group (control group II). A Doppler instrument was used to detect microemboli, and the researchers also analyzed demographic data, disease features, and the detection of MES between these groups, as well as the predictors of HCD during the aura.
The duration of aura (34.71 plus or minus 18.05 minutes vs. 23.87 plus or minus 13.64 minutes; P = .002) was significantly longer and the frequency of aura per year (16.29 plus or minus 14.21 vs. 10.10 plus or minus 11.00; P = .029) was significantly higher in the HCD group, as compared with control group I. The presence of somatosensory symptoms during the aura was also significantly higher in the HCD group as well (P less than .001).
A binary logistic regression identified three independent predictors of HCD occurrence in patients with migraine aura. These were longer duration of the aura, presence of somatosensory symptoms during the aura, and positive MES detection.
MES were interictally detected in 29% of patients with migraines who experienced migraines with HCD during the aura, but in only 3% of those with visual and/or somatosensory aura. In addition, the number of detected MES in a single patient was as high as 85 among those in the HCD group, as compared with only 8 that were detected in other examined patients and healthy controls.
The detection of MES and investigating of the origin of microembolism could be a valuable tool for screening individuals with migraines with aura for ischemic stroke risk, as well as investigating links between migraine with aura and ischemic stroke, Dr. Zidverc-Trajkovic and her colleagues wrote.
The investigators speculated that in patients who have memory and language impairment during migraine aura, the cerebral cortex may be affected by cortical spreading depression (CSD) in regions beyond the occipital lobe, and microemboli may trigger CSD. This in turn might contribute to the pathophysiology of migraine aura.
“Further research should include analysis of the influence of microemboli on the neuron-glial interaction or the network modulation and pathophysiology of cortical spreading depression,” the investigators wrote.
Cortical spreading depression has been shown to occur in humans in ischemic stroke, severe traumatic brain lesions, and following hypoxia, and the scientifically relevant question is how spreading depression is triggered in patients who suffer from migraines with aura. The current study proposes that microemboli are a potential trigger.
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Dr. Hans-Christoph Diener |
Microembolic signals, or MES, were detected in 29.4% of patients with higher cortical aura, which was much higher than in the other two groups. But what does this finding implicate? The nature of MES is unknown in patients without atherosclerotic plaques, and one assumed mechanism is right-left shunt either through a patent foramen ovale or through pulmonary shunts. Patent foramen ovale is associated with a higher prevalence of migraine with aura.
The major shortcoming of the study is the recording of MES outside migraine attacks. It is difficult to understand how MES occurring outside migraine attacks should play a role in the rare events of complex auras, and many of the assumptions and implications of the authors in the discussion are not supported by scientific evidence.
In summary, this is an interesting observation with very limited relationship to the pathophysiology of migraine aura, and further research is needed.
Dr. Hans-Christoph Diener is from the department of neurology, University of Essen (Germany), and has disclosed a number of financial relationships with industry. These remarks were taken from his editorial accompanying Dr. Zidverc-Trajkovic’s report (Cephalalgia. 2015 Sep 28. doi: 10.1177/0333102415607177).
Cortical spreading depression has been shown to occur in humans in ischemic stroke, severe traumatic brain lesions, and following hypoxia, and the scientifically relevant question is how spreading depression is triggered in patients who suffer from migraines with aura. The current study proposes that microemboli are a potential trigger.
|
Dr. Hans-Christoph Diener |
Microembolic signals, or MES, were detected in 29.4% of patients with higher cortical aura, which was much higher than in the other two groups. But what does this finding implicate? The nature of MES is unknown in patients without atherosclerotic plaques, and one assumed mechanism is right-left shunt either through a patent foramen ovale or through pulmonary shunts. Patent foramen ovale is associated with a higher prevalence of migraine with aura.
The major shortcoming of the study is the recording of MES outside migraine attacks. It is difficult to understand how MES occurring outside migraine attacks should play a role in the rare events of complex auras, and many of the assumptions and implications of the authors in the discussion are not supported by scientific evidence.
In summary, this is an interesting observation with very limited relationship to the pathophysiology of migraine aura, and further research is needed.
Dr. Hans-Christoph Diener is from the department of neurology, University of Essen (Germany), and has disclosed a number of financial relationships with industry. These remarks were taken from his editorial accompanying Dr. Zidverc-Trajkovic’s report (Cephalalgia. 2015 Sep 28. doi: 10.1177/0333102415607177).
Cortical spreading depression has been shown to occur in humans in ischemic stroke, severe traumatic brain lesions, and following hypoxia, and the scientifically relevant question is how spreading depression is triggered in patients who suffer from migraines with aura. The current study proposes that microemboli are a potential trigger.
|
Dr. Hans-Christoph Diener |
Microembolic signals, or MES, were detected in 29.4% of patients with higher cortical aura, which was much higher than in the other two groups. But what does this finding implicate? The nature of MES is unknown in patients without atherosclerotic plaques, and one assumed mechanism is right-left shunt either through a patent foramen ovale or through pulmonary shunts. Patent foramen ovale is associated with a higher prevalence of migraine with aura.
The major shortcoming of the study is the recording of MES outside migraine attacks. It is difficult to understand how MES occurring outside migraine attacks should play a role in the rare events of complex auras, and many of the assumptions and implications of the authors in the discussion are not supported by scientific evidence.
In summary, this is an interesting observation with very limited relationship to the pathophysiology of migraine aura, and further research is needed.
Dr. Hans-Christoph Diener is from the department of neurology, University of Essen (Germany), and has disclosed a number of financial relationships with industry. These remarks were taken from his editorial accompanying Dr. Zidverc-Trajkovic’s report (Cephalalgia. 2015 Sep 28. doi: 10.1177/0333102415607177).
The prevalence and frequency of interictal microembolic signals (MES) were higher in migraine patients with higher cortical dysfunction (HCD) during aura, as compared with migraine patients without HCD during aura and with healthy controls, according to a study published in the journal Cephalalgia (2015 Sep 29. doi: 10.1177/0333102415607191).
Dr. Jasna Zidverc-Trajkovic of the Neurology Clinic, Clinical Center of Serbia, Belgrade, and her colleagues used transcranial Doppler ultrasound to test their hypothesis that the complexity of migraine aura is dependent on hypoperfusion caused by microemboli that occur in different regions of the brain. The goal was to evaluate the prevalence and clinical impact of interictal MES in migraine patients with HCD during aura.
The investigators enrolled 34 individuals with migraines who experienced language and memory impairment during aura (HCD group), 31 patients who had migraines with only visual or visual and somatosensory symptoms during aura (control group I), and 34 healthy individuals who comprised a control group (control group II). A Doppler instrument was used to detect microemboli, and the researchers also analyzed demographic data, disease features, and the detection of MES between these groups, as well as the predictors of HCD during the aura.
The duration of aura (34.71 plus or minus 18.05 minutes vs. 23.87 plus or minus 13.64 minutes; P = .002) was significantly longer and the frequency of aura per year (16.29 plus or minus 14.21 vs. 10.10 plus or minus 11.00; P = .029) was significantly higher in the HCD group, as compared with control group I. The presence of somatosensory symptoms during the aura was also significantly higher in the HCD group as well (P less than .001).
A binary logistic regression identified three independent predictors of HCD occurrence in patients with migraine aura. These were longer duration of the aura, presence of somatosensory symptoms during the aura, and positive MES detection.
MES were interictally detected in 29% of patients with migraines who experienced migraines with HCD during the aura, but in only 3% of those with visual and/or somatosensory aura. In addition, the number of detected MES in a single patient was as high as 85 among those in the HCD group, as compared with only 8 that were detected in other examined patients and healthy controls.
The detection of MES and investigating of the origin of microembolism could be a valuable tool for screening individuals with migraines with aura for ischemic stroke risk, as well as investigating links between migraine with aura and ischemic stroke, Dr. Zidverc-Trajkovic and her colleagues wrote.
The investigators speculated that in patients who have memory and language impairment during migraine aura, the cerebral cortex may be affected by cortical spreading depression (CSD) in regions beyond the occipital lobe, and microemboli may trigger CSD. This in turn might contribute to the pathophysiology of migraine aura.
“Further research should include analysis of the influence of microemboli on the neuron-glial interaction or the network modulation and pathophysiology of cortical spreading depression,” the investigators wrote.
The prevalence and frequency of interictal microembolic signals (MES) were higher in migraine patients with higher cortical dysfunction (HCD) during aura, as compared with migraine patients without HCD during aura and with healthy controls, according to a study published in the journal Cephalalgia (2015 Sep 29. doi: 10.1177/0333102415607191).
Dr. Jasna Zidverc-Trajkovic of the Neurology Clinic, Clinical Center of Serbia, Belgrade, and her colleagues used transcranial Doppler ultrasound to test their hypothesis that the complexity of migraine aura is dependent on hypoperfusion caused by microemboli that occur in different regions of the brain. The goal was to evaluate the prevalence and clinical impact of interictal MES in migraine patients with HCD during aura.
The investigators enrolled 34 individuals with migraines who experienced language and memory impairment during aura (HCD group), 31 patients who had migraines with only visual or visual and somatosensory symptoms during aura (control group I), and 34 healthy individuals who comprised a control group (control group II). A Doppler instrument was used to detect microemboli, and the researchers also analyzed demographic data, disease features, and the detection of MES between these groups, as well as the predictors of HCD during the aura.
The duration of aura (34.71 plus or minus 18.05 minutes vs. 23.87 plus or minus 13.64 minutes; P = .002) was significantly longer and the frequency of aura per year (16.29 plus or minus 14.21 vs. 10.10 plus or minus 11.00; P = .029) was significantly higher in the HCD group, as compared with control group I. The presence of somatosensory symptoms during the aura was also significantly higher in the HCD group as well (P less than .001).
A binary logistic regression identified three independent predictors of HCD occurrence in patients with migraine aura. These were longer duration of the aura, presence of somatosensory symptoms during the aura, and positive MES detection.
MES were interictally detected in 29% of patients with migraines who experienced migraines with HCD during the aura, but in only 3% of those with visual and/or somatosensory aura. In addition, the number of detected MES in a single patient was as high as 85 among those in the HCD group, as compared with only 8 that were detected in other examined patients and healthy controls.
The detection of MES and investigating of the origin of microembolism could be a valuable tool for screening individuals with migraines with aura for ischemic stroke risk, as well as investigating links between migraine with aura and ischemic stroke, Dr. Zidverc-Trajkovic and her colleagues wrote.
The investigators speculated that in patients who have memory and language impairment during migraine aura, the cerebral cortex may be affected by cortical spreading depression (CSD) in regions beyond the occipital lobe, and microemboli may trigger CSD. This in turn might contribute to the pathophysiology of migraine aura.
“Further research should include analysis of the influence of microemboli on the neuron-glial interaction or the network modulation and pathophysiology of cortical spreading depression,” the investigators wrote.
FROM CEPHALALGIA
Key clinical point: A higher prevalence and frequency of microembolic signals were detected in migraine patients with higher cortical dysfunction during migraine aura.
Major finding: MES were detected in 29.4% of patients in the HCD group, which was significantly higher than was 3.2% and 5.9% in the control groups.
Data source: The study included 34 persons with migraines with language and memory impairment during aura, 31 with only visual or visual and somatosensory symptoms during aura, and 34 healthy controls.
Disclosures: This work was supported by a grant from the Ministry of Education, Science, and Technological development of the Republic of Serbia. The authors have no disclosures.
