Disease relevance of Migraine with Aura

• Point mutations of the CACNA1A gene coding for the alpha 1A voltage-dependent calcium channel subunit are responsible for familial hemiplegic migraine (FHM) and episodic ataxia type 2 (EA2) [1].
• Alternating hemiplegia of childhood or familial hemiplegic migraine? A novel ATP1A2 mutation [2].
• Attacks of familial hemiplegic migraine (FHM) can be triggered by minor head trauma and are sometimes accompanied by coma [3].
• Delayed cerebral edema and fatal coma after minor head trauma: role of the CACNA1A calcium channel subunit gene and relationship with familial hemiplegic migraine [3].
• The ability of flunarizine to reduce the frequency of migraine attacks in patients with common and classical migraine is well documented; its effect on attack duration and intensity is less well established [4].

High impact information on Migraine with Aura

• Haploinsufficiency of ATP1A2 encoding the Na+/K+ pump alpha2 subunit associated with familial hemiplegic migraine type 2 [5].
• Although the clinical and neuroimaging features of familial hemiplegic migraine differ markedly from CADASIL, we hypothesized that the same gene could be involved in the pathogenesis of both conditions [6].
• The existence of slots generates predictions for how neurotransmission might be affected by changes in Ca2+ channel properties, which we tested by studying alpha1A mutations that are associated with familial hemiplegic migraine type 1 (FHM1) [7].
• Novel mutations in the Na+, K+-ATPase pump gene ATP1A2 associated with familial hemiplegic migraine and benign familial infantile convulsions [8].
• Acetazolamide responsiveness in familial hemiplegic migraine [9].

Chemical compound and disease context of Migraine with Aura

• Nifedipine in the prophylaxis of classic migraine: a crossover, double-masked, placebo-controlled study of headache frequency and side effects [10].
• Aura in some patients with familial hemiplegic migraine can be stopped by intranasal ketamine [11].
• Familial hemiplegic migraine and its abortive therapy with intravenous verapamil [12].
• These findings indicate that ascending serotonergic neurons play an important modulatory role in the regulation of thalamocortical glucose use, observations that may be of value in the understanding of the etiology and expression of classic migraine [13].
• Platelet-dense bodies, the storage organelles for serotonin, were increased in both migraine groups, particularly in classic migraine [14].

Biological context of Migraine with Aura

• Mutations of the alpha1A calcium channel subunit have been shown to cause such human neurological diseases as familial hemiplegic migraine, episodic ataxia-2, and spinocerebellar ataxia 6 and also to cause the murine neurological phenotypes of tottering and leaner [15].
• A number of missense mutations in the ATP1A2 gene, which encodes the Na,K-ATPase alpha2 subunit, have been identified in familial hemiplegic migraine with aura [16].
• Recently, different types of mutation in the brain-specific P/Q type calcium channel alpha 1A subunit gene (CACNA1A) on chromosome 19p13 were shown to be involved in three human disorders: familial hemiplegic migraine (FHM), episodic ataxia type 2 (EA2), and chronic spinocerebellar ataxia type 6 (SCA6) [17].
• Interest in ion channels in migraine has been spurred by molecular genetic findings in familial hemiplegic migraine, since familial hemiplegic migraine type 1 is caused by mutations in the calcium channel gene CACNA1A [18].

Anatomical context of Migraine with Aura

• To investigate this possibility we measured glutamic and aspartic acid level in plasma and cerebrospinal fluid (CSF) of patients with common and classic migraine during attacks, making comparisons with controls suffering stress [19].

Gene context of Migraine with Aura

• Familial hemiplegic migraine, a rare Mendelian form of MA, can be caused by mutations in the calcium channel gene, CACNA1A or in the ATP1A2 gene, a Na+/K+ pump [20].
• BACKGROUND: Familial hemiplegic migraine (FHM) is an autosomal dominant disorder, which can result from mutations in the CACNA1A (FHM1) and ATP1A2 (FHM2) genes [21].
• Mutation in the neuronal voltage-gated sodium channel SCN1A in familial hemiplegic migraine [22].
• In the group of 15 patients affected by classic migraine, basal plasma levels of beta-TG and PF4 were significantly higher than control subjects [23].
• Migraine attacks with vomiting and cerebral infarctions, most often in the posterior cerebral regions, which are reminiscent of complicated migraine, are typical features of MELAS [24].

Analytical, diagnostic and therapeutic context of Migraine with Aura

• The present study is a placebo-controlled, double-blind study concerning metoprolol in classic migraine [25].
• A clinical EEG should be performed in patients with acute headache attacks when either epilepsy, basilar migraine, migraine with prolonged aura or alternating hemiplegia is suspected [26].
• In a double-blind crossover study, 8 patients with classical migraine received disulfiram (400 mg/day) for 6 days, alternating with matched placebo tablets at 2 weekly intervals [27].
• Both CBF and CBV were evaluated by gamma-camera SPECT in 14 patients with classic migraine, all studied while symptom-free [28].

References