Migraine with aura

Around 15% to one-third of migraineurs experience aura. Aura is a fully reversible focal neurological phenomenon involving visual, sensory, speech, and/or motor symptoms that develops gradually and usually precedes the headache phase. The pivotal role of cortical spreading depression (CSD) as a mechanism underlying aura has been widely supported by a large body of studies. The diagnosis is based on the International Headache Classification Disorders III edition criteria. Aura is characterized by gradual development, duration of each symptom no longer than one hour, a mix of positive and negative features, and complete reversibility. Visual aura is the most common type of aura, occurring in over 90% of patients. When aura symptoms are multiple, they usually follow one another in succession, beginning with visual, then sensory, then aphasic; but the reverse and other orders have been noted. The accepted duration for most aura symptoms is one hour, but motor symptoms, which are rare, are often longer lasting. When a patient experiences for the first time a possible aura phase it's sometimes difficult to know if there was gradual or brutal onset of the symptoms. If the patient has no visual aura symptoms or simultaneous neurological symptoms, or presents neurological symptoms corresponding to a cerebral vascular territory, emergency exploration of a possible transient ischemic attack is necessary. Long duration (greater than one hour) of what may or may not be an aura phase, late onset of aura, or a dramatic increase in aura attacks should also be explored. The relative risk of ischemic stroke is significantly increased in migraine with aura. Combined hormonal contraception with estrogens significantly increases the risk of stroke in women with migraine with aura. It is recommended to start non-steroidal anti-inflammatory drugs (NSAIDs) or aspirin as soon as possible during the aura phase, not to treat the aura, but to avoid or to diminish the headache phase. In case of failure of NSAIDs or aspirin it is recommended to use a triptan when the headache begins. The prophylactic treatments for migraine with aura are those used in migraine without aura based on very few randomized clinical trials specifically dedicated to migraine with aura.     

Migraine with aura from pathophysiology to treatment: therapeutic strategies

Neurological Sciences - Migraine with aura (MwA) sufferers, at times, need specific treatments. This is the case when the auras are frequent, prolonged and cause anxiety and distress. Abnormal...     

Migraine with aura white matter lesions: preliminary data on clinical aspects

A few clinic-based magnetic resonance imaging studies report an increased risk of signal abnormalities in migraineurs brain’s white matter, especially in migraine with aura subjects. A vascular genesis has been hypnotized and migraine with aura was considered an independent risk factor for stroke. Available data of magnetic resonance imaging alterations are often nonspecific and sometimes controversial. The aim of our study is to investigate migraine with aura patients with standardized brain magnetic resonance imaging to detect and to quantify the presence of white matter lesions and to analyze their relation with clinical data. We report preliminary data about first 90 subjects. We did not recognize any clinical aspect in close relationship with these alterations. The only clinical feature that seems to play a role in the presence of alterations is the age, and only in migraineurs women.     

Migraine with visual aura: visual aura pictured by the patient

The most frequent type of migraine aura is the typical one in which the most frequently occurring aura type are visual phenomena. Types of visual aura may be different. Scintillating scotoma, fortification zigzags (teichopsiae), fragmentation of the visual image are typical illusions in visual aura. The visual illusion of a typical corona phenomenon was represented as a visual migraine aura symptom. The extra edges of the corona phenomenon are commonly seen around the perceptual images of objects. The corona phenomenon is strongly associated with visual loss and the presence of elementary geometric illusions. It is surrounding a person's head, shoulders, hands, or body. Illusory splitting can be differentiated from the fragmentation of visual images and from the geometric illusion or mosaic illusion. The pathogenesis of migraine aura remains unclear. The probable cause of migraine aura may be cortical spreading depression (CSD) and cerebral hypoperfusion. Ionic changes, activation of trigeminal nerve and release of neuropeptides seem to be secondary to CSD during the attack of migraine aura. In present article the pictures of visual aura experienced by migraine patient are presented and discussed.     

Migraine: imaging the aura

We currently conceive of a migraine attack as originating in the brain. Triggers of an attack initiate a depolarizing neuroelectric and metabolic event likened to the spreading depression of Leao. This event activates the headache and associated features of the attack by mechanisms that remain to be determined, but appear to involve either peripheral trigeminovascular or brainstem pathways, or both. The excitability of cell membranes, perhaps partly genetically determined, is the brain's susceptibility to attacks. Factors that increase or decrease neuronal excitability constitute the threshold for triggering attacks. Using a model of visual stress-induced migraine or by studying spontaneous attacks and applying advanced imaging and neurophysiological methods, results have been obtained that support spreading neuronal inhibition as the basis of aura. This neuroelectric event is accompanied by hyperoxia of the brain, possibly associated with vasodilation. Evidence has also been obtained that the spreading cortical event can activate the subcortical centers possibly involved in nociception and associated symptoms of the migraine attack. Susceptibility to migraine attacks appears to be related to brain hyperexcitability. These newer techniques of functional neuroimaging have confirmed the primary neural basis of the migraine attack with secondary vascular changes, reconciling previous theories into a neurovascular mechanism.     

Migraine with aura: conventional and non-conventional treatments

Migraine with aura (MwA) is a primary headache that affects up 30% of migraine patients. Although the frequency of MwA attacks is usually low and the majority of migraine sufferers do not need prophylactic treatment(s), same particular patients do. This occurs when the neurological symptoms, that characterize the auras, determine anxiety to the migraine sufferers and when the frequency of MwA attacks is or becomes high. In this study, we review the few therapeutic conventional options specifically devoted to cure MwA attacks present in the literature together with those, recent, non-conventional.

     

Migraine with and without aura: a single entity?

A debate has been going on for many years about whether migraine with aura and migraine without aura are part of the same disorder or should instead be considered as two separate disorders. Although no final consensus has yet been reached on this issue, many clinical and pathogenetic elements suggest that the second option is true. Clinically, migraine with aura and migraine without aura are differentiated by epidemiological features, the characteristics of the headache phase, patient behaviour during attacks, natural history, age at onset and age at resolution, the recurrence pattern of attacks, favouring circumstances and trigger factors, correlation to female reproductive events, comorbidity and preventive therapies. Moreover, several literature reports suggest a possible different pathogenetic basis for the two forms of migraine.     

Migraine with aura and white matter tract changes

We aimed to explore whether a migraine with aura (MA) is associated with structural changes in tracts of a white matter and to compare parameters of diffusivity between subgroups in migraineurs. Forty-three MA and 20 healthy subjects (HS), balanced by sex and age, were selected for this study. Analysis of diffusion tensor parameters was used to identify differences between MA patients and HS, and then between MA subgroups. A diffusion tensor probabilistic tractography analysis showed that there is no difference between MA patients and HS. However, using more-liberal uncorrected statistical threshold, we noted a trend in MA patients toward lower diffusivity indices of selected white matter tracts located in the forceps minor and right anterior thalamic radiation (ATR), superior longitudinal fasciculus (temporal part) (SLFT), cingulum-cingulate tract, and left uncinate fasciculus. Migraineurs who experienced somatosensory and dysphasic aura, besides visual symptoms, had tendency toward lower diffusivity indices, relative to migraineurs who experienced only visual symptoms, in the right inferior longitudinal fasciculus, forceps minor, and right superior longitudinal fasciculus (parietal part), SLFT, and cingulum-angular bundle. Aura frequency were negatively correlated with axial diffusivity and mean diffusivity of the right ATR (partial correlation?=???0.474; p?=?0.002; partial correlation?=???0.460; p?=?0.002), respectively. There were no significant differences between MA patients and HS, neither between MA subgroups. Migraineurs with abundant symptoms during the aura possibly have more myelinated fibers relative to those who experience only visual symptoms. Lower diffusivity indices of the right ATR are linked to more frequent migraine with aura attacks.     

Migraine with aura and white matter lesions: an MRI study

Several studies report the presence of white matter lesions on brain magnetic resonance imaging in patients with migraine. The aim of our study was to detect the entity of white matter T2-hyperintensities in 90 high selected patients affected by migraine with aura, compared to a group of 90 healthy controls. We found no significant difference of incidence of white matter alterations comparing these two groups.     

Migraine with and without aura: electrophysiological and functional neuroimaging evidence

The neuropathological processes believed to underlie migraine with and without aura are still widely debated in the literature. In order to arrive at a more detailed and comprehensive picture of the altered processes present in migraineurs, electrophysiological data obtained through transcranial magnetic stimulation (TMS) and electroencephalography (EEG) were combined with haemodynamic data obtained through functional magnetic resonance imaging (fMRI). Ten subjects affected by migraine (with or without aura) underwent TMS and EEG investigation prior to a visual stimulation task, studied in fMRI. Our preliminary results showed a reduced cortical silent period especially in subjects affected by migraine with aura. The fMRI BOLD response was found to be weaker in occipital areas proportionally to the frequency and severity of migraine attacks. The data obtained from our study seem to support the theory of cortical spreading depression recently observed in human subjects. Moreover, the electrophysiological data were also correlated to migraine attack frequency, thus pointing to elevated cortical excitability between attacks. Better understanding of the neuropathological processes that trigger migraine attacks will help in the selection of more adequate prophylactic therapies. The results of this preliminary study need to be confirmed in a a large sample of subjects.     

Migraine with aura and white matter abnormalities: Notch3 mutation

The authors report on an Italian family with eight affected members who show autosomal dominant migraine with prolonged visual, sensory, motor, and aphasic aura. These symptoms are associated with white matter abnormalities on brain MRI. All living affected members carry a Notch3 mutation (Arg153Cys) previously reported in cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL). White matter abnormalities occur in a variable percentage of the general migraine population; CADASIL should be suspected in migraineurs with prolonged atypical aura and white matter abnormalities.     

Migraine with a combination of aura symptoms as a clinical manifestation of cortical spreading depression

The pathomechanism of the migraine aura remains unclear. The most probable cause of the aura is cortical spreading depression with associated hypoperfusion. Both the cortical spreading depression and hypoperfusion begin in the occipital lobes and spread forward slowly (2-3 mm/min) in a wave-like mode along the brain convolutions and cross territories of brain arteries. We present a 24-year-old female patient with a combination of aura symptoms. Each migraine attack began with a bright scintillating zig-zag, which crossed the visual field. It was followed by left sided hemiparesthesiae marching from the face to the hand. The last symptom of aura was motor aphasia. Later a unilateral, pulsating headache developed with associated photo- and phonophobia. The stable pattern and duration of aura symptoms in the presented case suggest that the cortical spreading depression plays an important role in the pathomechanism of migraine with aura.     

Migraine without aura: a population-based twin study.

To investigate the importance of genetic and environmental factors to the etiology of migraine without aura and to compare the symptomatology of migraine without aura in monozygotic and dizygotic twins, 2,680 twin pairs were recruited from the population-based Danish Twin Registry. Monozygotic (MZ) and same-sex dizygotic (DZ) twin pairs, where at least one twin had self-reported migraine or self-reported severe headache with accompanying symptoms, were telephone interviewed by a physician. The participation rate in the telephone interview was 90%. The pairwise concordance rate was significantly higher in MZ than in DZ twin pairs (28% vs 18%). The probandwise concordance rate was 40% (95% CI, 33-48%) in MZ and 28% (95% CI, 23-33%) in DZ twin pairs. The pairwise concordance rates for the different pain characteristics and accompanying symptoms were not significantly different in MZ and DZ twin pairs. However, comparing all of the pairwise concordance rates of pain characteristics and accompanying symptoms together, MZ twin pairs were significantly more concordant than DZ twin pairs. Our data demonstrate a significant genetic factor in migraine without aura. The size of this factor is modest and the demonstration of susceptibility genes is predicted to be laborious and difficult.     

Migraine with and without aura share the same pathogenic mechanisms

Migraine with aura and without aura share the same clinical features with respect to the headache, and differ nosologically in the presence or absence of aura. The mechanisms of aura generation are now becoming clearer, based on imaging studies, and a common migraine pathophysiology for all subtypes of migraine headaches now seems reasonable, as it would seem implausible that all of these neurological events have different pathogenic mechanisms. Both major subtypes of migraine clearly represent a perturbation of normal physiology and employ normal anatomic pathways to generate the aura and headache, similar to aura and a seizure. So what is the mechanism of migraine aura? Do migraine without aura patients have clinically silent aura? Migraine is after all defined as a clinical disorder and is the prototypic primary headache and thus its uniform pathogenesis must underlie all that we know about migraine clinically. This presentation will take the resolve that the migraine with and without aura share the same pathogenic mechanisms.