The Evolution of a Migraine Attack – A Review of Recent Evidence

Headache: The Journal of Head and Face Pain

Early View 
1. Andrew Charles MD^*
Article first published online: 20 DEC 2012
DOI: 10.1111/head.12026

A migraine attack is an extraordinarily complex brain event that takes place over hours to days. This review focuses on recent human studies that shed light on the evolution of a migraine attack. It begins with a constellation of premonitory symptoms that are associated with activation of the hypothalamus and may involve the neurotransmitter dopamine. Even in the premonitory phase, patients experience sensitivity to sensory stimuli, indicating that central sensitization is a primary phenomenon. The migraine attack progresses to a phase that in some patients includes aura, which involves changes in cortical function, blood flow, and neurovascular coupling. The aura phase overlaps with the headache phase, which is associated with further changes in blood flow and function of the brainstem, thalamus, hypothalamus, and cortex. Serotonin receptors, nitric oxide, calcitonin gene-related peptide, pituitary adenylate cyclase-activating polypeptide, and prostanoids are demonstrated specific chemical mediators of migraine based on therapeutic and triggered migraine studies. A number of migraine symptoms persist beyond resolution of headache into a postdromal phase, accompanied by persistent blood flow changes in several brain regions. Although these phases of migraine have substantial temporal, neurochemical, and anatomical overlap, each represents an important window onto the pathophysiology of migraine as well as a target for therapeutic intervention. A comprehensive approach to migraine requires an understanding of the entire range of mechanisms and resultant symptoms that occur throughout the evolution of an attack.

What has functional neuroimaging done for primary headache … and for the clinical neurologist?

Journal of Clinical Neuroscience
Volume 17, Issue 5 , May 2010, Pages 547-553 

Till Sprenger^a and Peter J. Goadsby^{, a,}

^a UCSF Headache Centre, Department of Neurology, University of California, 1701 Divisadero St, Suite 480, San Francisco, CA 94115, USA

Received 30 July 2009; 

accepted 23 September 2009. 

Available online 12 March 2010.

Abstract

Our understanding of mechanisms involved in primary headache syndromes has been substantially advanced using functional neuroimaging. The data have helped establish the now-prevailing view of primary headache syndromes, such as migraine and cluster headache, as brain disorders with neurovascular manifestations, not as disorders of blood vessels.

This review focuses on the results of studies applying positron emission tomography, functional MRI, and voxel-based morphometry, and attempts to synthesize the growing body of literature to provide pathophysiological concepts. We will further outline future research directions and the clinical applicability of functional imaging in headache patients.

Article Outline

1. Introduction

2. Methods of functional neuroimaging

2.1. Positron emission tomography

2.2. Functional MRI

3. What are the data?

3.1. Experimental pain

3.2. Trigeminal autonomic cephalalgias

3.2.1. Cluster headache

3.2.2. Paroxysmal hemicrania and SUNCT

3.3. Migraine without aura

3.4. Migrane with aura

3.5. Tension-type headache

4. What do the data mean?

4.1. Peripheral versus central pathogenesis and pain control mechanisms

4.1.1. Trigeminal autonomic cephalgias

4.1.2. Migraine

4.1.3. Migraine aura

4.2. Specificity of results

5. What are the consequences for the clinical neurologist

5.1. Patient education

5.2. Clinical application of imaging findings, neuroimaging as a diagnostic tool?

6. What can be expected?

Acknowledgements

References

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Fig. 2. Statistical comparison of [¹¹C]diprenorphine positron emission tomography (PET) impulse response function at 60 minutes (IRF60) in the pineal gland between patients with cluster headache and healthy volunteers. Decreases in opioidergic receptor availability are superimposed in color on an anatomic reference MRI (single-subject sagittal T1-weighted MRI provided by the statistical parametric mapping software) (p < 0.001 uncorrected). (From Sprenger T, Willoch F, Miederer M, Schindler F, Valet M, Berthele A, Spilker ME, Förderreuther S, Straube A, Stangier I, Wester HJ, Tölle TR. Opioidergic changes in the pineal gland and hypothalamus in cluster headache: a ligand PET study. Neurology 2006;66:1108–10.⁶)

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