Table of Contents
Cover
Title Page
Copyright
Dedication
List of Contributors
Foreword
Part I: Anatomy and physiology
Chapter 1: Functional anatomy of trigeminovascular pain
1.1 Anatomy of the trigeminovascular system
1.2 Trigeminal ganglion
1.3 Trigeminal brainstem nuclear complex
References
Chapter 2: Physiology of the meningeal sensory pathway
2.1 Role of the meningeal sensory pathway in headache
2.2 Nociceptive response properties of peripheral and central neurons in the meningeal sensory pathway
2.3 Activity of neurons in the meningeal sensory pathway under conditions associated with headache: CSD and nitroglycerin
2.4 Role of blood vessels in activation of the meningeal sensory pathway
2.5 Unique neuronal properties of the meningeal sensory pathway
2.6 Intracranial vs extracranial mechanisms of migraine: new findings
References
Chapter 3: Meningeal afferent ion channels and their role in migraine
3.1 Meningeal afferents and migraine pain
3.2 Transient receptor potential (TRP) channels and headache
3.3 Acid-sensing ion channels
3.4 Glutamate-gated channels
3.5 ATP-gated channels
3.6 K
+
channels
3.7 Other ion channels that may contribute to dural afferent signaling
3.8 Conclusions
3.9 Acknowledgements
References
Chapter 4: Functional architecture of central pain pathways: focus on the trigeminovascular system
4.1 Introduction
4.2 Ascending trigeminal nociceptive pathways
4.3 Trigeminovascular pain is subject to descending control
4.4 Conclusions
References
Part II: Special features of migraine pain
Chapter 5: Visceral pain
5.1 Organization of innervation
5.2 Common features of visceral pain and headache
5.3 Summary and conclusions
5.4 Acknowledgement
References
Chapter 6: Meningeal neurogenic inflammation and dural mast cells in migraine pain
6.1 Introduction
6.2 The neurogenic inflammation hypothesis of migraine
6.3 Meningeal neurogenic plasma protein extravasation and migraine
6.4 Meningeal neurogenic vasodilatation and migraine
6.5 Neurogenic mast cell activation in migraine
6.6 Endogenous events that could promote meningeal NI in migraine
6.7 Anti-migraine drugs and meningeal NI
6.8 Is meningeal NI a pro-nociceptive event in migraine?
6.9 Conclusions
References
Chapter 7: Sensitization and photophobia in migraine
7.1 Introduction
7.2 Experimental activation of trigeminovascular pathways
7.3 Peripheral sensitization
7.4 Central sensitization: medullary dorsal horn
7.5 Central sensitization: thalamus
7.6 Temporal aspects of sensitization and their implications to triptan therapy
7.7 Modulation of central sensitization
7.8 Neural substrate of migraine-type photophobia
References
Chapter 8: Central circuits promoting chronification of migraine
8.1 Introduction
8.2 Pharmacotherapy of migraine
8.3 Medication overuse headache (MOH) and migraine chronification
8.4 Central circuits modulating pain
8.5 Evaluation of descending modulation: diffuse noxious inhibitory controls and conditioned pain modulation
8.6 Conclusions
References
Chapter 9: Triptans to calcitonin gene-related peptide modulators – small molecules to antibodies – the evolution of a new migraine drug class
9.1 Introduction
9.2 Trigeminovascular system – migraine physiology and pharmacology
9.3 Small molecule CGRP receptor antagonists
9.4 Current status of small molecule CGRP receptor antagonist programs
9.5 Unraveling the site of action of small molecule CGRP receptor antagonists using clinical pharmacology and brain imaging
9.6 Biologic approaches to CGRP modulation
9.7 Summary and conclusion
References
Chapter 10: Lessons learned from CGRP mutant mice
10.1 Introduction
10.2 Modeling migraine
10.3 Calcitonin gene-related peptide (CGRP) in migraine
10.4 What has CGRP manipulation in mice taught us about migraine?
10.5 Conclusions
References
Part III: Clinical characteristics of migraine
Chapter 11: The clinical characteristics of migraine
11.1 Overview of migraine
11.2 Migraine prodrome
11.3 The migraine headache is the centerpiece of the syndrome
11.4 Migraine aura
11.5 Proposed aura types
11.6 Postdrome
11.7 Status migrainosus
11.8 Summary
References
Chapter 12: The premonitory phase of migraine
12.1 What is the premonitory phase? Towards a definition
12.2 How common are premonitory symptoms?
12.3 Do premonitory symptoms reliably predict a migraine attack?
12.4 Premonitory symptoms in individuals
12.5 Intra-patient variability of the premonitory phase
12.6 Difference between patients with and without premonitory symptoms
12.7 Premonitory symptoms in children
12.8 Premonitory symptoms and migraine triggers
12.9 Premonitory symptoms and pathophysiological studies
12.10 Treatment during the premonitory phase
12.11 Conclusion
References
Part IV: Migraine genetics and CSD
Chapter 13: The genetic borderland of migraine and epilepsy
13.1 Introduction
13.2 Gene-linked comorbidity
13.3 The challenge of dissecting seizure and aura excitability defects
13.4 Clinical overlap of migraine with aura and epilepsy phenotypes
13.5 Acquired and genetic etiologies of migraine with aura and epilepsies
13.6 Migraine aura is linked to specific genes with locus and allelic heterogeneity
13.7 Correspondence of regional brain susceptibility for migraine in genetic epilepsy syndromes
13.8 Are SD thresholds plastic?
13.9 Spreading depolarization in cardiorespiratory brainstem regions, a candidate mechanism of SUDEP
13.10 Brainstem SD is a “second hit” leading to SUDEP
13.11 Tau ablation prevents seizures, SUDEP and brainstem SD threshold in models of SUDEP
13.12 Conclusion
13.13 Acknowledgements
References
Chapter 14: Genetics of monogenic and complex migraine
14.1 Migraine is a genetic disease
14.2 How to identify genes for migraine?
14.3 Gene identification in monogenic Familial Hemiplegic Migraine
14.4 Functional studies of gene mutations in monogenic Familial Hemiplegic Migraine
14.5 Genetic studies in monogenic disorders in which migraine is a prominent part of the clinical phenotype
14.6 Genome-wide association studies in common polygenic migraine
14.7 Future directions in genetic migraine research
References
Chapter 15: Lessons from familial hemiplegic migraine and cortical spreading depression
15.1 Introduction
15.2 FHM genes and functional consequences of FHM mutations
15.3 Insights into the mechanisms underlying susceptibility to cortical spreading depression and initiation of migraine attacks from the functional analysis of FHM mouse models
15.4 Acknowledgements
References
Chapter 16: From cortical spreading depression to trigeminovascular activation in migraine
16.1 CSD causes the visual aura
16.2 SD may underlie transient neurological dysfunctions preceding attacks
16.3 Does SD cause headache?
16.4 Human data supporting the parenchymal inflammatory signaling
16.5 Meningeal neurogenic inflammation amplifies the parenchymal signal
16.6 Understanding human CSD and migraine without aura
16.7 Potential of CSD models to understand migraine and drug development
References
Part V: Modeling and imaging inmigraine
Chapter 17: Modeling and imaging in migraine
17.1 Introduction
17.2 Microscopic models: cellular and cytoarchitectonic detail
17.3 Macroscopic models: large scale spatiotemporal phenomenology
References
Chapter 18: Tools for high-resolution in vivo imaging of cellular and molecular mechanisms in cortical spreading depression and spreading depolarization
18.1 Introduction
18.2 Large-scale imaging of vascular dynamics with microscopic resolution
18.3 Combining measurements of single-vessel diameter with imaging and quantification of intracellular Ca
2+
in neurons and astrocytes
18.4 NADH autofluorescence: an endogenous marker of energy metabolism
18.5 Direct imaging of molecular O
2
in blood and tissue
18.6 Employing optogenetics to study inter-cellular communication
18.7 Conclusions and outlook
References
Chapter 19: Animal models of migraine aura
19.1 Introduction: spreading depression and migraine
19.2
In vivo
and
in vitro
models of SD susceptibility
19.3 Experimental preparations
19.4 Methods to trigger SD
19.5 Methods to detect CSD
19.6 SD susceptibility attributes
19.7 Recommended quality measures for experimental models of migraine aura
19.8 Future directions
References
Chapter 20: Human models of migraine
20.1 Introduction
20.2 The first steps: GTN and the NO-hypothesis
20.3 Calcitonin gene-related peptide (CGRP)
20.4 Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating polypeptide (PACAP)
20.5 Can we gain from the use of experimental models to study functional consequences of migraine mutations?
20.6 Conclusion
References
Chapter 21: Imaging pain and headache
21.1 Introduction
21.2 Functional brain changes in migraine
21.3 Structural brain changes in migraine
21.4 Insights from orofacial pain
21.5 Conclusions
References
Index
End User License Agreement
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Guide
Cover
Table of Contents
Foreword
Part I: Anatomy and physiology
Begin Reading