Long term decline of P100 amplitude in migraine with aura.
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OBJECTIVES: To investigate visual function in migraine using visual evoked potentials. METHODS: Electroretinograms (ERGs) and visual evoked potentials (VEPs) to single flash (SF) and pattern reversal (PR) stimuli were studied in 92 migraine subjects and 62 controls. RESULTS: In subjects with migraine, ERGs to single flash were normal. Mean latencies of the P1 and P2 waves in the SFVEP were increased at the occiput by 6% and 4% respectively, but normal at the vertex. Mean latency of the P100 wave in the PRVEP was increased by 5%. These increases were not related to the presence or absence of an aura or to the duration of migraine. P100 amplitude showed a more complex abnormality. It was increased in migraine without aura by 23% compared with controls, regardless of duration of migraine. In migraine with aura it was similarly increased, by 23%, in cases of short duration, but in addition it showed a sharp decline with duration. In cases with a duration of 30 or more years it was 36% less than in cases of short duration, and 21% less than in controls. CONCLUSIONS: Subjects with migraine have constitutionally prolonged VEP latencies and increased P100 amplitude, but the latter declines to below normal in cases with a long history of migraine with aura. This decline may reflect subtle neuronal damage within the visual system from repeated transient ischaemia experienced during the aura. Future electrophysiological and other studies will need to be controlled for duration of migraine history. (+info)
Alternate numbness in the upper extremities as the initial symptom of basilar migraine: an electrophysiological evaluation using EEG power topography.
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A case of basilar migraine (BM) with alternate numbness as the initial symptom is described. The patient's chief complaint was alternate numbness in the right and left upper extremities. After angiography the patient fell into a drowsy state, followed by excitation, and finally confusion. The EEG power topography showed slow alpha, theta and delta power in the right occipital area, and alternatively in the right and left parietal area. These findings suggest that the cause of BM is not only based on a vasoconstriction mechanism, but also cortical spreading depression. BM should be suspected as a cause of sensory symptoms. (+info)
Relationship between migraine and cardiac and pulmonary right-to-left shunts.
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A relationship between migraine with aura and the presence of right-to-left shunts has been reported in two studies. Right-to-left shunts are also associated with some forms of decompression illness. While conducting research in divers with decompression illness, it was our impression that divers with a large shunt often had a history of migraine with aura in everyday life and after dives. Therefore we routinely asked all divers about migraine symptoms. The medical records of the last 200 individuals referred for investigation of decompression illness were reviewed to determine the association between right-to-left shunts and migraine aura after diving, and migraine in daily life unconnected with diving. Migraine with aura in daily life unconnected with diving occurred significantly more frequently in individuals who had a large shunt which was present at rest (38 of 80; 47.5%) compared with those who had a shunt which was smaller or only seen after a Valsalva manoeuvre (four of 40; 10%) or those with no shunt (11 of 80; 13.8%) (P<0.001). Hemiplegic migraine occurred in 10 divers, each of whom had a shunt that was present at rest; in eight of these cases the shunt was large. The prevalence of migraine without aura was similar in all groups. Post-dive migraine aura was significantly more frequent in individuals who had a large shunt present at rest (21 of 80; 26.3%) compared with those who had a shunt that was smaller or only seen after a Valsalva manoeuvre (five of 40; 12.5%) or no shunt (one of 80; 1.3%) (P<0.001). Thus individuals with a large right-to-left shunt have an increased prevalence of migraine with aura in daily life unconnected with diving, and they also have an increased incidence of migraine aura after dives, but only when the dives liberate venous bubbles. These data suggest the possibility that, in some individuals, right-to-left shunts have a role in the aetiology of migraine with aura. The observations suggest that paradoxical gas embolism may precipitate migraine with aura. (+info)
Visual dysfunction between migraine events.
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PURPOSE: To evaluate interictal visual dysfunction in persons with migraine in terms of spatiotemporal selectivity and location within the visual pathways. METHODS: The vision of a group of 15 persons who had experienced migraine with aura was compared with that of 15 normal age-matched control subjects. A range of thresholds was measured to evaluate precortical (background modulation, contrast thresholds for static, and moving stimuli), area V1 (orientation discrimination and motion discrimination thresholds), and higher order (global dot motion thresholds) visual processes. Testing was performed centrally and at 10 degrees in the superior visual field. For each of the tests, the spatial and temporal parameters of the stimuli were selected to bias detection toward either parvocellular or magnocellular visual mechanisms. RESULTS: No defects were found for parvocellular processes. Significant (P: < 0.05) losses were apparent with the temporal background modulation method (16 Hz), orientation discrimination (0.5 cyc/deg), and global dot motion tasks. CONCLUSIONS: Both cortical and precortical visual dysfunction were identified in migraine group 7 days after the headache. This loss was selective for targets with temporal modulation of approximately 16 Hz. (+info)
Mechanisms of migraine aura revealed by functional MRI in human visual cortex.
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Cortical spreading depression (CSD) has been suggested to underlie migraine visual aura. However, it has been challenging to test this hypothesis in human cerebral cortex. Using high-field functional MRI with near-continuous recording during visual aura in three subjects, we observed blood oxygenation level-dependent (BOLD) signal changes that demonstrated at least eight characteristics of CSD, time-locked to percept/onset of the aura. Initially, a focal increase in BOLD signal (possibly reflecting vasodilation), developed within extrastriate cortex (area V3A). This BOLD change progressed contiguously and slowly (3.5 +/- 1.1 mm/min) over occipital cortex, congruent with the retinotopy of the visual percept. Following the same retinotopic progression, the BOLD signal then diminished (possibly reflecting vasoconstriction after the initial vasodilation), as did the BOLD response to visual activation. During periods with no visual stimulation, but while the subject was experiencing scintillations, BOLD signal followed the retinotopic progression of the visual percept. These data strongly suggest that an electrophysiological event such as CSD generates the aura in human visual cortex. (+info)
The clinical spectrum of familial hemiplegic migraine associated with mutations in a neuronal calcium channel.
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BACKGROUND: Familial hemiplegic migraine, an autosomal dominant disorder characterized by attacks of transient hemiparesis followed by a migraine headache, is classically divided into pure familial hemiplegic migraine (affecting 80 percent of families) and familial hemiplegic migraine with permanent cerebellar signs (affecting 20 percent of families). Mutations in CACNA1A, which encodes a neuronal calcium channel, are present in 50 percent of families with hemiplegic migraine, including all those with cerebellar signs. We studied the various clinical manifestations associated with mutations in CACNA1A in families with hemiplegic migraine with and without cerebellar signs. METHODS: CACNA1A was analyzed and nine mutations were detected in 15 of 16 probands of families affected by hemiplegic migraine and cerebellar signs, in 2 of 3 subjects with sporadic hemiplegic migraine and cerebellar signs, and in 4 of 12 probands of families affected by pure hemiplegic migraine. Genotyping of probands and relatives identified a total of 117 subjects with mutations whose clinical manifestations were assessed in detail. RESULTS: Eighty-nine percent of the subjects with mutations had attacks of hemiplegic migraine. One third had severe attacks with coma, prolonged hemiplegia, or both, with full recovery. All nine mutations, including five newly identified ones, were missense mutations. Six mutations were associated with hemiplegic migraine and cerebellar signs, and 83 percent of the subjects with these six mutations had nystagmus, ataxia, or both. Three mutations were associated with pure hemiplegic migraine. CONCLUSIONS: Hemiplegic migraine in subjects with mutations in CACNA1A has a broad clinical spectrum. This clinical variability is partially associated with the various types of mutations. (+info)
A case of hemiplegic migraine in childhood: transient unilateral hyperperfusion revealed by perfusion MR imaging and MR angiography.
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We report on an 8-year-old girl with a typical attack of hemiplegic migraine, in whom MR angiography and perfusion MR imaging revealed unilateral dilation of branches of both the middle and posterior cerebral arteries and hyperperfusion of the ipsilateral hemisphere, respectively. The findings resolved spontaneously after the attack. These imaging techniques should be indicated for patients with migraine attacks and may play a role in assessing the vascular events in migraine headache. (+info)
Endothelin-1 potently induces Leao's cortical spreading depression in vivo in the rat: a model for an endothelial trigger of migrainous aura?
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According to the 'neuronal' theory, cortical spreading depression (CSD) is the pathophysiological correlate of migrainous aura. However, the 'vascular' theory has implicated altered vascular function in the induction of aura symptoms. The possibility of a vascular origin of aura symptoms is supported, e.g. by the clinical observation that cerebral angiography frequently provokes migrainous aura. This suggests that endothelial irritation may somehow initiate one of the pathways resulting in migrainous aura. Up to now, an endothelium-derived factor has never been shown to trigger CSD. Here, for the first time, we demonstrate and characterize the ability of the vasoconstrictor and astroglial/neuronal modulator endothelin-1 to trigger Leao's 'spreading depression of activity' in vivo in rats. At a concentration range between 10 nM and 1 microM, endothelin-1 induced changes characteristic of CSD with regard to the rate of propagation, steady (direct current) potential and extracellular K(+)-concentration. A spreading hyperaemia followed by oligaemia was observed similar to those in K(+)-induced CSD. Endothelin-1 did not provoke changes characteristic of a terminal depolarization. The mechanism by which endothelin-1 generated CSD involved the N-methyl-D-asparate receptor. Cerebral blood flow decreased slightly, but significantly, before endothelin-1 generated CSD. A vasodilator (NO*-donor) shifted the threshold for CSD induction to higher concentrations of endothelin-1. Endothelin-1, in contrast to K(+), did not induce CSD in rat brain slices suggesting indirectly that endothelin-1 may require intact perfusion to exert its effects. In conclusion, endothelin-1 was found in the experiment to be the most potent inducer of CSD currently known. We propose endothelin-1 as a possible candidate for the yet enigmatic link between endothelial irritation and migrainous aura. (+info)