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.

Dysregulation of the peripheral glutamatergic system: A key player in migraine pathogenesis?

Background Although the role of glutamate in migraine pathogenesis remains uncertain, there has been significant interest in the development of drug candidates that target glutamate receptors. Activation of trigeminovascular afferent fibers is now recognized as a crucial step to the onset of a migraine episode. New evidence suggests a dysfunction in peripheral glutamate regulation may play a role in this process. Objective To provide a narrative review of the role of peripheral glutamate dysfunction in migraine. Method A review of recent literature from neurobiological, pharmacological and genomic studies was conducted to support peripheral glutamate dysfunction as a potential element in migraine pathogenesis. Results Studies in rats suggest that elevated blood glutamate mechanically sensitizes trigeminal afferent fibers and stimulates the release of calcitonin-gene related peptide and other neuropeptides to promote and maintain neurogenic inflammation. These effects may be driven by upregulation of glutamate receptors, and modifications to reuptake and metabolic pathways of glutamate. Furthermore, genome wide association studies have found polymorphisms in glutamate receptor and transporter genes that are associated with migraine. Conclusion The role of peripheral glutamate signalling in the onset and maintenance of migraine is not completely elucidated and future studies are still needed to confirm its role in migraine pathogenesis.

Migraine and the Scope of Homeopathy

Migraine is usually a genetic disorder. In the United States, every 10 seconds someone with a migraine goes to the emergency room. Approximately 1.2 million annual visits to the emergency room occur due to acute migraine attacks. About 90% of migraine patients have a family history of this illness. More than 90% of sufferers are unable to work or function normally during their migraine episode, affecting their quality of life and medical expenditure. While the majority of patients experience attacks once or twice a month, more than four million people suffer due to a chronic migraine with at least 15 migraine days per month. Migraine is often undiagnosed and undertreated and remains a poorly understood disease. In spite of the high prevalence of migraine and its effects on patients, research into migraine is still underfunded. In this article, the author reviewed facts about migraine, the best possible suggested treatments and the scope of homeopathy for its treatment. More research and clinical trials with improved trial designs are warranted. Publications of large numbers of homeopathic case studies worldwide, long-term observational studies of treated migraine patients having no further migraine recurrences are needed to see the role of homeopathy for the complete cure.

THE SPECTRUM OF MIGRAINE IN 306 PATIENTS WITH CADASIL

Migraine is often the first manifestation of CADASIL, the commonest monogenic cause of stroke. We aimed to determine the pattern of migraine, and its relationship with other features of CADASIL. Of 314 patients seen in a national referral clinic, 71.6% reported migraines. Migraine was the first feature of CADASIL in 67.6% of symptomatic individuals. Females (81.7%) were more likely to develop migraine than males (66.9%), and suffered migraine at an earlier age (27.0±12.7 vs 32.3±13.2 years, p=0.004).89.8% of migraneurs experienced aura. Where aura occurred it was visual in 69.7% sensory 58.7%, dysphasic 30.3%, confusional 17.9%, motor 15.9% and sensorimotor 9.95%.A self-limiting encephalopathy occurred in 33 patients (10.8%); 72.7% of these evolved from a migraine episode. Patients with confusional migraines were more likely to develop encephalopathy (OR=3.93, 95% CI=1.51–9.73, p=0.0024).Non-migraneurs had a higher cumulative risk of stroke than those migraneurs (HR 2.13, 95% CI 1.53–2.96, p=6.8×10−6).In conclusion, the spectrum of migraine in CADASIL differs from that in the general population. Acute encephalopathy is a common feature of CADASIL and usually evolves from a migraine episode. Non-migraneurs have a higher risk of developing stroke, however the reasons for this are not well understood.

FAMILIAL MIGRAINE LIMB PAIN SYNDROME (MLPS): THREE GENERATIONS AND SEVEN YEAR FOLLOW-UP

We describe a family with migraine-limb pain syndrome (MLPS) in children and adults over three generations, in an autosomal dominant pattern.MLPS is intermittent pain occurring in any limb, temporally related to a migraine episode, cluster headache or cluster migraine. It is usually ipsilateral to the headache, but can alternate and may spread with a migrainous march over 20 minutes or more. Body or chest pain (corpalgia) is also described. Limb or body pain may not coincide with headache at presentation. The association may be misdiagnosed as radiculopathy, thoracic outlet syndrome or arthritis.There is one previous report of a family with childhood limb pain, followed by migraine in adulthood, in a pattern suggesting autosomal dominant inheritance.We report a second family with three generations of MLPS starting in childhood or adulthood, with variable duration, commencing in any limb. All the patients with limb pain had concurrent or associated migraine with aura. Pain intensity in the previous family was mild, but poorly responsive to treatment. In our family the symptom was treatment responsive with variable intensity.Convergence of nociceptive input from the trigeminovascular system in the cervical spinal cord, brainstem, thalamus and cortex is a possible physiological basis for MLPS.

Pressure-painful scalp arteries in children and adolescents suffering from migraine

Objective: This study aimed to evaluate the presence of pressure-painful scalp arteries in children and adolescents with migraine. Materials and methods: Pressure-painful points on scalp arteries were searched in 130 consecutive children (6–12 years old) and adolescents (>13 years old) affected with migraine, 89 females and 41 males, and in 40 age-matched controls. Results: In the absence of a migraine episode, we examined 76 patients: 54 (71.1%) reported one or more pressure-painful arteries and 22 reported none. Of the 40 controls, pressure-painful arteries were present in 11, with a highly significant difference (p < 0.0001). During a migraine attack, of the 54 patients examined, 43 (79.6 %) reported one or more pressure-painful arteries and 11 reported none. The arteries most frequently painful were the frontal branch and the superficial temporal artery. Conclusions: Scalp arteries are frequently painful on pressure in children and adolescents with migraine, both in the absence of and during a migraine attack. Painful arteries suggest hypersensitivity of periarterial nociceptive afferents.

Chocolate is a Migraine-Provoking Agent

Patients with migraine who believed that chocolate could provoke their attacks were challenged with either chocolate or a closely matching placebo. In a double-blind parallel group study, chocolate ingestion was followed by a typical migraine episode in 5 out of 12 patients, while none of the 8 patients challenged with placebo had an attack ( p = 0.051). The median time to the onset of the attack was 22 h. This brief study provides some objective evidence that chocolate is able to provoke a migraine attack in certain patients who believe themselves sensitive to it.