Migraine/Headache

Most primary headaches can be diagnosed using the history and examination. Judicious use of neuroimaging and other testing, however, is indicated to distinguish primary headaches from the many secondary causes that may share similar features. This article evaluates the reasons for diagnostic testing and the use of neuroimaging, electroencephalography, lumbar puncture, and blood testing. The use of diagnostic testing in adults and children who have headaches and a normal neurologic examination, migraine, trigeminal autonomic cephalalgias, hemicrania continua, and new daily persistent headache are reviewed.

The term vestibular migraine designates recurrent vertigo that is caused by migraine. Vestibular migraine presents with episodes of spontaneous or positional vertigo lasting seconds to days that are accompanied by migraine symptoms. Because headache is often absent during acute attacks, other migraine features have to be identified by thorough history taking. In contrast, vestibular testing serves mainly for the exclusion of other diagnoses. Treatment still lacks solid evidence. It is targeted at the underlying migraine and comprises explanation and reassurance, lifestyle modifications, and drugs.

Migraine can be regarded as a conserved, adaptive response that occurs in genetically predisposed individuals with a mismatch between the brain's energy reserve and workload. Given the high prevalence of migraine, genotypes associated with the condition seem likely to have conferred an evolutionary advantage. Technological advances have enabled the examination of different aspects of cerebral metabolism in patients with migraine, and complementary animal research has highlighted possible metabolic mechanisms in migraine pathophysiology. An increasing amount of evidence – much of it clinical – suggests that migraine is a response to cerebral energy deficiency or oxidative stress levels that exceed antioxidant capacity and that the attack itself helps to restore brain energy homeostasis and reduces harmful oxidative stress levels. Greater understanding of metabolism in migraine offers novel therapeutic opportunities. In this Review, we describe the evidence for abnormalities in energy metabolism and mitochondrial function in migraine, with a focus on clinical data (including neuroimaging, biochemical, genetic and therapeutic studies), and consider the relationship of these abnormalities with the abnormal sensory processing and cerebral hyper-responsivity observed in migraine. We discuss experimental data to consider potential mechanisms by which metabolic abnormalities could generate attacks. Finally, we highlight potential treatments that target cerebral metabolism, such as nutraceuticals, ketone bodies and dietary interventions.

Transient disturbances in neurologic function are disturbing features of migraine attacks. Aura types include binocular visual, hemi-sensory, language and unilateral motor symptoms. Because of the gradual spreading quality of visual and sensory symptoms, they were thought to arise from the cerebral cortex. Motor symptoms previously included as a type of migraine aura were reclassified as a component of hemiplegic migraine. ICHD-3 criteria of the International Headache Society, added brainstem aura and retinal aura as separate subtypes. The susceptibility to all types of aura is likely to be included by complex and perhaps epigenetic factors.

The clinical picture, but also neuroimaging findings, suggested the brainstem and midbrain structures as possible driving or generating structures in migraine.