Migraine Aura Research Articles

КЛІНІЧНИЙ ВИПАДОК МОЖЛИВОЇ МІГРЕНІ З АУРОЮ, УСКЛАДНЕНОЇ МІГРЕНОЗНИМ ІНФАРКТОМ

We present a clinical case of ischemic stroke in a man with a new-onset migraine attack. Clinical case. A 25-year-old man was admitted to the acute cerebrovascular department due to severe throbbing headache in the left temporal area, vomiting, impaired vision on the right and numbness of the right leg. Complaints appeared abruptly in the form of scotoma in the right visual field. 20 minutes later, severe throbbing headache, nausea and numbness of the right leg developed. The event was preceded by sleep deprivation for 2 days. The patient’s mother has migraine with aura. Previously, the patient never had such attacks. On examination: right-sided homonymous upper-quadrant hemianopsia, hypoesthesia of the right leg. Brain MRI - focal hyperintensity at T2 and DWI in the left occipital region (acute ischemic stroke). The patient took aspirin at a dose of 300 mg for the first day, then 100 mg per day and valproic acid at a dose of 1200 mg per day. Two days after hospitalization, the patient experienced recovery of sensitivity in the right leg and regression of right-sided homonymous upper quadrant hemianopsia to small scotoma. The patient was discharged on the 5th day with a small right scotoma. It is recommended to continue taking aspirin 100 mg/day and valproic acid 1200 mg/day for the secondary prevention of migraine attacks and stroke. Discussion. The peculiarities of this case include the lack of history of migraine (at least 5 or more migrainous headache attacks) and the development of severe migraine attack with prolonged aura symptoms, which was triggered by sleep deprivation and eventually evolved into ischemic stroke. Conclusions. It is necessary to consider the possibility of ischemic stroke even in the cases of a new-onset migraine attack. If migrainous aura duration exceeds 60 minutes, it is necessary to perform a brain MRI to detect the early signs of cerebral ischemia.

Olfactory acuity based on Brief Smell Identification Test (BSITⓇ) in migraine patients with and without aura: A cross-sectional, controlled study

ObjectiveThe aim of this study was to evaluate olfactory acuity in migraine patients with and without aura (MwA and MwoA) Material and methodsThe study included 30 MwA patients, 30 MwoA patients, and 30 age- and gender-matched controls. Demographic features and odor-related symptoms (osmophobia, odor offensiveness, and odor-triggered attack status) were noted. Olfactory acuity was measured using the Brief Smell Identification Test (BSIT®), a 12-item derivative of the University of Pennsylvania Smell Identification Test (UPSIT®). BSIT® scores were compared between the migraine patients and controls. ResultsThe mean BSIT® score did not differ significantly between the MwA patients (8.7 ± 0.9) and MwoA (9.17 ± 0.9) patients (P = 0.094); however, the mean score in the control group was higher (10.4 ± 0.6) than in the MwA and MwoA patients (P < 0.001). The mean BSIT® score did not differ significantly between patients with and without odor-triggered migraine attacks (9 ± 0.9 and 8.8 ± 0.8, respectively) (P = 0.4). Osmophobia and odor-triggered attacks were more common in the MwA patients than in the MwoA patients (odor-triggered attacks: 66% vs. 40% [P = 0.04]; osmophobia: 76.6% vs. 60% [P = 0.16]) ConclusionOlfactory acuity is lower during attack-free periods in migraine patients, as compared to controls. Migraine aura status does not affect olfactory acuity. Odor-triggered attacks, osmophobia, and offensive odors between attacks were more common in the MwA patients than in the MwoA patients.

From "Transient Hemiopsia" to Migraine Aura.

This paper outlines the historical development of the concept of the visual aura of migraine, from the first comprehensive published description by the physician Hubert Airy, in 1870. Airy’s description of the phenomenon he called “transient hemiopsia” became widely copied and highly influential as a consequence of the language and images that he used in his presentation. This paper outlines the subsequent development of theories of aura from the time of Airy’s publication to the first demonstration of spreading oligaemia by Lautitzen and Olesen in the 1980s.

Aura Mapping: Where Vision and Somatosensation Meet.

While migraine auras are most frequently visual, somatosensory auras are also relatively common. Both are characterized by the spread of activation across a cortical region containing a spatial mapping of the sensory (retinal or skin) surface. When both aura types occur within a single migraine episode, they may offer an insight into the neural mechanism which underlies them. Could they both be initiated by a single neural event, or do the timing and laterality relationships between them demand multiple triggers? The observations reported here were carried out 25 years ago by a group of six individuals with migraine with aura. They timed, described and mapped their visual and somatosensory auras as they were in progress. Twenty-nine episode reports are summarized here. The temporal relationship between the onset of the two auras was quite variable within and across participants. Various forms of the cortical spreading depression hypothesis of migraine aura are evaluated in terms of whether they can account for the timing, pattern of symptom spread and laterality of the recorded auras.

Migraine: features of pharmacotherapeutic and drug-free preventive treatment

Migraine is one of the most common forms of headache, which can lead to a significant reduction in quality of life. There is migraine with aura, migraine without aura, as well as chronic migraine, which significantly reduces the efficiency of patients and is often combined with mental disorders and drug-induced headaches. Complications of migraine include migraine status, persistent aura without a heart attack, migraine heart attack (stroke) and epileptic seizure caused by migraine aura. The diagnosis of migraine is established based on complaints, medical history, objective examination data, and diagnostic criteria of the International Headache Classification of the 3rd revision. Additional research methods are recommended only in the presence of “red flags” — symptoms that alert to the secondary nature of the headache. Migraine treatment is aimed at reducing the frequency and intensity of attacks, reducing the number of pharmatherapeutical analgesics. It includes three main approaches: seizure relief therapy, preventive therapy, and non-drug methods. Non-steroidal anti-inflammatory drugs, simple and combined analgesics, triptans, as well as anti-nausea drugs (for severe nausea or vomiting) are recommended for seizures relief. In case of frequent or severe migraine attacks, as well as in case of chronic migraine, prophylactic therapy is indicated, which includes antidepressants, topiramate, beta-blockers, angiotensin II receptor antagonists, botulinum toxin type A-hemagglutinin complex and monoclonal antibodies to calcitonin gene-related peptide receptors. Pharmacotherapy is recommended to be combined with non-drug methods, which include cognitive-behavioral therapy, the method of transcranial magnetic stimulation, the method of biological feedback, postsphygmic period, acupuncture, therapeutic exercises, block of greater occipital nerve, and stimulation of the first trigeminal nerve.

Visual Phenomena Associated With Migraine and Their Differential Diagnosis.

Visual phenomena are of many different kinds; their differential diagnosis is usually possible with directed history-taking. In this review, we describe common visual phenomena that must be distinguished from a migraine aura. This review is based on publications retrieved by a selective search in PubMed and the Web of Knowledge/Science, with special attention to the current classification of the International Headache Society and the recommendations of the German Migraine and Headache Society. The following search terms were used: "visual phenomena/phenomenon," "migraine aura," and "persistent/complication/ long-lasting/ongoing." The most helpful questions for differential diagnosis are whether the symptoms are present in one eye only or in both, whether their onset was sudden or over minutes or days, and whether the phenomenon has occurred only once or repeatedly, or is persistently present. A visual aura associated with migraine must be distinguished, in rare cases, from an isolated epileptic aura, from cerebral/retinal ischemia, or from visual snow. Further differential diagnoses include a persisting perceptual disturbance after hallucinogen use (HPPD, "hallucinogen persisting perception disorder") and the Charles Bonnet syndrome (CBS); the latter arises as a consequence of severely impaired vision. Posterior reversible encephalopathy syndrome (PRES) is rare and generally reveals itself over its further course through the appearance of additional clinical manifestations. Primary ophthalmological causes can usually be readily identified and classified by ophthalmological examination. Patients with visual phenomena typically consult physicians from various medical specialties. A correct differential diagnosis can be made based on the history if the physician views the symptoms in their overall context to determine the particular disease entity that is responsible.

Atypical auras in pediatric migraine: Clinical series and pathophysiological correlations

Aura is one of the most important symptoms of migraine and “Cortical Spreading Depression (CSD)” has been suggested as the most plausible underlying pathophysiological mechanism. However, recent reports raised doubt against the concept that CSD could account for all presentations of migraine aura. Here, we show a series of atypical paediatric aura hardly explainable by the CSD principles, suggesting partly different pathophysiological mechanisms.

Whole brain surface-based morphometry study in subtypes of migraine with aura patients

Little is known about the pathophysiologic basis of the clinical variability of migraine aura presentation. We were aimed to study intracerebral white matter fiber bundles, using a tract-based spatial statistics (TBSS) analysis of diffusion tensor imaging (DTI), and grey matter cortical thickness from structural magnetic resonance imaging data in migraine patients with pure visual auras (MA), and in patients with complex neurological auras (MA+), i.e. with the addition of at least one of sensory and language symptoms.

Continuous long-term recording and triggering of brain neurovascular activity and behaviour in freely moving rodents.

A minimally invasive, microchip-based approach enables continuous long-term recording of brain neurovascular activity, heart rate, and head movement in freely behaving rodents. This approach can also be used for transcranial optical triggering of cortical activity in mice expressing channelrhodopsin. The system uses optical intrinsic signal recording to measure cerebral blood volume, which under baseline conditions is correlated with spontaneous neuronal activity. The arterial pulse and breathing can be quantified as a component of the optical intrinsic signal. Multi-directional head movement is measured simultaneously with a movement sensor. A separate movement tracking element through a camera enables precise mapping of overall movement within an enclosure. Data is processed by a dedicated single board computer, and streamed from multiple enclosures to a central server, enabling simultaneous remote monitoring and triggering in many subjects. One application of this system described here is the characterization of changes in of cerebral blood volume, heart rate and behaviour that occur with the sleep-wake cycle over weeks. Another application is optical triggering and recording of cortical spreading depression (CSD), the slowly propagated wave of neurovascular activity that occurs in the setting of brain injury and migraine aura. The neurovascular features of CSD are remarkably different in the awake vs. anaesthetized state in the same mouse. With its capacity to continuously and synchronously record multiple types of physiological and behavioural data over extended time periods in combination with intermittent triggering of brain activity, this inexpensive method has the potential for widespread practical application in rodent research. KEY POINTS: Recording and triggering of brain activity in mice and rats has typically required breaching the skull, and experiments are often performed under anaesthesia A minimally invasive microchip system enables continuous recording and triggering of neurovascular activity, and analysis of heart rate and behaviour in freely behaving rodents over weeks This system can be used to characterize physiological and behavioural changes associated with the sleep-wake cycle over extended time periods This approach can also be used with mice expressing channelrhodopsin to trigger and record cortical spreading depression (CSD) in freely behaving subjects. The neurovascular responses to CSD are remarkably different under anaesthesia compared with the awake state. The method is inexpensive and straightforward to employ at a relatively large scale. It enables translational investigation of a wide range of physiological and pathological conditions in rodent models of neurological and systemic diseases.

Relationships between migraine and epilepsy: Pathophysiological mechanisms and clinical implications.

Migraine and epilepsy are distinct neurological diseases with specific clinical features and underlying pathophysiological mechanisms. However, numerous studies have highlighted the complex and multifaceted relationships between the two conditions. The relationships between headache and epilepsy manifest themselves in different ways. Firstly, the clinical diagnosis of these disorders may be challenging in view of possible overlapping. While post-ictal headache is a frequent condition, ictal epileptic headache is a rare but challenging diagnosis. Both situations raise the question of the pathophysiological mechanism of headache triggered by seizures. Migraine aura and epilepsy can also exhibit overlapping symptoms leading to their misdiagnosis, in particular in the case of visual aura. Secondly, migraine with aura and epilepsy can occur as a co-morbid condition, particularly in familial hemiplegic migraine (FHM). From a pathophysiological perspective, the identification of genetic mutations in FHM has brought significant advances in the understanding of dysfunctions of neuronal networks leading to hyperexcitability. The purpose of this review is to present clinical situations encompassing headache and epilepsy that can be challenging in neurological practice and to discuss the underlying pathophysiological mechanism of such interactions.

The 2021 American Headache Society Meeting.

The American Headache Society held its Annual Meeting June 3–6, 2021, virtually. Although it was virtual, it was anything but boring. There was plenty for neuro-ophthalmologists to learn as well. There were 920 attendees from 45 states and 33 countries. The format was a modified zoom platform with prerecorded lectures and live question and answer sessions. Although there were many highlights, one was an award lecture, the Graham Award, given by our own Dr. Deborah Friedman. Her talk Practicing Headache Medicine on the Ground in 2021 highlighted many of the challenges neuro-ophthalmologists have faced not only during the pandemic but also to our medical system including insurance companies, billing, and access to care. It is a real classic in only the way Dr. Friedman could present. Each topic was first introduced from a basic science point of view and then there were clinical correlates. Topics included cortical spreading depression and its relationship to pain and sleep. Many lessons were there for neuro-ophthalmologic patients who have aura and sleep disturbances. Another session highlighted sex and gender differences in pain thresholds in laboratory animals and then explored clinical correlates. One amazing talk by Dr. Huda Akil, PhD, University of Michigan, Genes Stress and Resilience highlighted how our genetics and epigenetics can affect our health and disease. There were lots of posters too and even a talent show (like our 2021 NANOS show). If you are interested, you can still register and view content until June 2022! Register at: http://bit.ly/2021ASM-Registration. There is a registration fee to access the content. For those of us who see a lot of patients with eye pain, migraine aura, and headache—this meeting was a real gem.

Cortical excitability in migraine: Contributions of magnetic resonance imaging.

Migraine is characterized by symptoms related to cortical hyperexcitability such as photophobia, phonophobia, osmophobia and allodynia. One-third of migraineurs experience aura, whose neurophysiological substrate is thought to be cortical spreading depression (CSD). Functional magnetic resonance imaging (MRI) has shown the migraine aura to be characterized by cerebral hyperactivity/hyperperfusion followed by hypometabolism/hypoperfusion spreading along the occipital cortex with the same spatiotemporal organization as the experimentally triggered CSD. The link between migraine aura and headache remains undetermined. Neuroimaging studies have failed to show a leakage of the blood-brain barrier, which was suspected to occur during CSD and to cause the stimulation of trigeminal nociceptive receptors. However, recent studies have highlighted the involvement of neuroglial inflammation and other studies have suggested that a common central network plays a role in the link between CSD and migraine pain. Finally, MRI has made it possible to study the contribution of metabolites such as glutamic acid, γ-amino-butyric acid and sodium in the pathophysiology of hyperexcitability in migraine.

Editors' Note: The Index Vein Pointing to the Origin of the Migraine Aura Symptom: A Case Series

Dr. Slavova et al. presented a case series of 6 patients with acute migraine aura who had a prominent draining sulcal vein on emergency MRI susceptibility-weighted imaging (SWI) initially performed for suspected stroke. The vein pointed toward the cortical area that correlated with the clinical presentation. In response, Drs. Bugnicourt and Godefroy raise several concerns regarding the “index vein” finding reported by the authors, including the fact that only 1 patient had demonstrated reversibility of the SWI abnormality, adding to 3 previous case reports that demonstrated reversible venous dilatation in migraine aura; the inclusion of only 6 patients over 7 years, raising questions about the frequency of this finding; the absence of 3D time-of-flight magnetic resonance angiography (MRA) findings in the results; and uncertainty about the underlying mechanism of this finding. Responding to these comments, the authors agree that there are enduring questions regarding the mechanism, reversibility, and potentially low prevalence of the index vein finding, but note that their intention was to introduce this phenomenon and propose a definition that could then be used in future studies to evaluate its diagnostic accuracy for migraine aura. They report that time-of-flight MRA was normal in all reported patients. In summary, the appearance of a prominent vein potentially associated with a culprit cortical area in patients with migraine aura is a phenomenon that requires validation in larger studies of consecutive patients. Dr. Slavova et al. presented a case series of 6 patients with acute migraine aura who had a prominent draining sulcal vein on emergency MRI susceptibility-weighted imaging (SWI) initially performed for suspected stroke. The vein pointed toward the cortical area that correlated with the clinical presentation. In response, Drs. Bugnicourt and Godefroy raise several concerns regarding the “index vein” finding reported by the authors, including the fact that only 1 patient had demonstrated reversibility of the SWI abnormality, adding to 3 previous case reports that demonstrated reversible venous dilatation in migraine aura; the inclusion of only 6 patients over 7 years, raising questions about the frequency of this finding; the absence of 3D time-of-flight magnetic resonance angiography (MRA) findings in the results; and uncertainty about the underlying mechanism of this finding. Responding to these comments, the authors agree that there are enduring questions regarding the mechanism, reversibility, and potentially low prevalence of the index vein finding, but note that their intention was to introduce this phenomenon and propose a definition that could then be used in future studies to evaluate its diagnostic accuracy for migraine aura. They report that time-of-flight MRA was normal in all reported patients. In summary, the appearance of a prominent vein potentially associated with a culprit cortical area in patients with migraine aura is a phenomenon that requires validation in larger studies of consecutive patients.

Author Response: The Index Vein Pointing to the Origin of the Migraine Aura Symptom: A Case Series.

We thank Dr. Bugnicourt and Dr. Godefroy for their comments on our article.1 We agree with their statements on the potential release of vasoactive factors during migraine aura and on the limitations around reversibility and the potentially low prevalence of an index vein. Naturally, a case series has to deal with the data given, and only 1 patient had follow-up imaging. The aim of our study was to introduce the phenomenon of the index vein. It would be of incredible value to calculate accuracy measures of the index vein for making the diagnosis of migraine aura in the emergency setting. We therefore strongly encourage using the definition of the index vein provided in our study for future studies to obtain sensitivity, specificity, and negative or positive predictive values of this finding. The question of involvement of the cerebral arteries during migraine aura for reversible vasoconstriction—although important—has not been the focus of this case series and remains to be determined. In this respect, time-of-flight MR angiography was indeed normal in all reported patients.

Reader Response: The Index Vein Pointing to the Origin of the Migraine Aura Symptom: A Case Series

Slavova et al.1 report susceptibility-weighted MRI (SW-MRI) findings during migraine aura, namely, a hypointense signal revealing a single prominent vein draining the cortical area responsible for the patients' symptoms (the index vein). Despite the major interest of these findings, they require clarification.

Acute prolonged motor aura resembling ischemic stroke after COVID \u2212\u200919 vaccination (CoronaVac): the first case report

BackgroundWe report the first case of a patient who suffered transient focal neurological deficit mimicking stroke following CoronaVac vaccination. However, instead of an ischemic stroke, motor aura was suspected.Case presentationsA 24 year-old Thai female presented with left hemiparesis fifteen minutes after receiving CoronaVac. She also had numbness of her left arm and legs, flashing lights, and headaches. On physical examination, her BMI was 32.8. Her vital signs were normal. She had moderate left hemiparesis (MRC grade III), numbness on her left face, arms, and legs. Her weakness continued for 5 days. A brain CT scan was done showing no evidence of acute infarction. Acute treatment with aspirin was given. MRI in conjunction with MRA was performed in which no restricted diffusion was seen. A SPECT was performed to evaluate the function of the brain showing significant hypoperfusion of the right hemisphere. The patient gradually improved and was discharged.DiscussionsIn this study, we present the first case of stroke mimic after CoronaVac vaccination. After negative imaging studies had been performed repeatedly, we reach a conclusion that stroke is unlikely to be the cause. Presumably, this phenomenon could possibly have abnormal functional imaging study. Therefore, we believed that it might be due to cortical spreading depression, like migraine aura, which we had conducted a literature review.

Involvement of TRPM2 in the Neurobiology of Experimental Migraine: Focus on Oxidative Stress and Apoptosis

Excessive Ca2+ influx and mitochondrial oxidative stress (OS) of trigeminal ganglia (TG) have essential roles in the etiology of migraine headache and aura. The stimulation of TRPM2 channel via the generation of OS and ADP-ribose (ADPR) induces pain, inflammatory, and oxidative neurotoxicity, although its inhibition reduces the intensity of pain and neurotoxicity in several neurons. However, the cellular and molecular effects of TRPM2 in the TG of migraine model (glyceryl trinitrate, GTN) on the induction of pain, OS, apoptosis, and inflammation remain elusive. GTN-mediated increases of pain intensity, apoptosis, death, cytosolic reactive oxygen species (ROS), mitochondrial ROS, caspase -3, caspase -9, cytosolic Ca2+ levels, and cytokine generations (TNF-α, IL-1β, and IL-6) in the TG of TRPM2 wild-type mouse were further increased by the TRPM2 activation, although they were modulated by the treatments of GSH, PARP-1 inhibitors (PJ34 and DPQ), and TRPM2 blockers (ACA and 2APB). However, the effects of GTN were not observed in the TG of TRPM2 knockout mice. The current data indicate that the maintaining activation of TRPM2 is not only important for the quenching OS, inflammation, and neurotoxicity in the TG neurons of mice with experimental migraine but also equally critical to the modulation of GTN-induced pain.

Persistent monocular visual loss in migraine patients.

The relationship between migraine and vision is complex. Besides migraine aura status and persistent visual aura without infarction, recognized by International Headaches Classification 3, cases of persistent monocular alterations have been described in migraineurs. To discuss the role of migraine as a risk factor for persistent monocular visual loss. We present five new cases of persistent monocular visual loss in migraineurs, discuss the differential diagnosis and possible relationship with migraine. Five young healthy patients are reported (three women) with a history of migraine (four with visual aura), that developed persistent monocular visual defects, four during an episode of migraine with aura. All patients were submitted to an extensive investigation. In three patients the scotoma was identified on automated perimetry; one of these patients had retinal hemorrhagic lesions, with fluorescein angiography revealing an isolated retinal vasculitis. In two patients fundoscopy revealed transient cotton wools spots. Except for the patient with retinal vasculitis, etiologic investigation was not conclusive. Monocular visual loss can occur in the setting of multiple pathologies that affect the eye and related structures. Although diseases requiring emergent intervention should always be excluded, we propose migraine should be considered as a contributing factor for unexplained monocular persistent scotoma.Monocular visual loss can occur in the setting of multiple pathologies that affect the eye and related structures. Although diseases requiring emergent intervention should always be excluded, we propose migraine should be considered as a contributing factor for unexplained monocular persistent scotoma.

Narrative review of neuroimaging in migraine with aura.

To improve the understanding of the role and utility of various neuroimaging modalities (clinical and research) for the evaluation of migraine aura (MA) and hemiplegic migraine during the ictal and interictal phases. MA is defined by reversible neurologic symptoms and is considered a manifestation of a primary condition. As such, most patients with MA do not require imaging. However, if there are atypical features, change in symptom pattern, or it is a first-time presentation, neuroimaging may be used to evaluate for secondary conditions. Neuroimaging includes many modalities, and it is important to consider what information is being captured by these modalities (i.e., structural vs. functional). Imaging abnormalities may be noted both during (ictal) and between (interictal) MA attacks, and it is important for clinicians to be familiar with neuroimaging findings reported in migraine with aura (MWA) compared with other conditions. With the assistance of a medical librarian, we performed a review of the literature pertaining to MWA and neuroimaging in PubMed. Search terms included were magnetic resonance imaging, positron-emission tomography, single photon-emission computed tomography, functional magnetic resonance imaging, and migraine with aura. We hand-searched these references to inform our subsequent literature review. Acute MA can be associated with several unique neuroimaging findings-reversible cortical diffusion restriction, cortical venous engorgement, and a "biphasic" transition from hypoperfusion to hyperperfusion. Imaging findings during MA tend to span more than one vascular territory. Between acute attacks, neuroimaging in people with MWA can resemble migraine without aura in terms of white matter abnormalities and "infarct-like lesions." Research imaging modalities such as volumetric analysis and functional imaging have demonstrated unique findings in migraine with aura. Although migraine is a clinical diagnosis, understanding of neuroimaging findings in MWA can help clinicians interpret imaging findings and improve patient care.

Calcitonin gene-related peptide-induced hemodynamic changes in migraine with and without aura.

Exogenous calcitonin gene-related peptide (eCGRP) can induce CGRP-induced headaches (CGRP-IH) and aura in migraine with aura (MA). This implies a common pathophysiological mechanism of trigeminovascular sensitization (TVS) in migraine headaches and aura. The aim was to assess hemodynamic changes in cerebral circulation induced by eCGRP. We predicted that cerebral hemodynamic changes may differ between migraine without aura (MO) and MA. We included twenty participants with migraine, of whom 15 (75%) had MO, and 5 (25%) had MA. An intravenous infusion of eCGRP was administered. Polymodal recording of mean arterial velocity in MCA (vm MCA) and PCA (vm PCA), end-tidal carbon dioxide partial pressure (Et-CO2 ), mean arterial pressure (MAP), and heart rate (HR) was employed using transcranial Doppler sonography (TCD). The parameters were determined at different time points with single responses vm MCAtot , vm PCAtot , Et-CO2tot , MAPtot , and HRtot . The CGRP-IH appeared in five participants with MA (100%) and in 11 participants with MO (73.3%) (p=.530). The difference of changes in vm MCAtot (p=.014) and vm PCAtot (p=.004) was significant, whereas in Et-CO2tot (p=.658), MAPtot (p=.392), and HRtot (p=.686), it appeared to be non-significant. We found significant associations between vm MCAtot and MA (p=.023; OR=0.88; 95%C.I. 0.78-0.98), and vm PCAtot and MA (p=.018; OR=0.85; 95%C.I. 0.74-0.97). Cerebral hemodynamics differs between MO and MA, indicating a pronounced vasodilatation and TVS in MA, which could induce aura.