Neurobiological Basis of Migraine

Name: Neurobiological Basis of Migraine
Brand: Wiley-Blackwell
Price: 114.99 EUR
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Turgay Dalkara Michael A. Moskowitz(Herausgeber*in)

Wiley-Blackwell (Verlag)

Erschienen am 9. Juni 2017

424 Seiten

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Beschreibung

Published with the New York Academy of Sciences
A timely, broad-ranging exploration of the neurobiological basis and molecular mechanisms of migraines
Migraines impact the lives of a significant portion of the world's population, afflicting sufferers with severe pain, nausea, and often visual impairment. The WHO views migraines as an important public health issue, and ranks them in its top twenty most disabling illnesses. Neurobiological Basis of Migraine reviews the latest advances made in our understanding of the primary basic mechanisms of migraine headache and provides valuable insights into how these findings are being translated into novel treatment and prevention strategies around the world.
Written for researchers and clinicians alike, the book features edited contributions from distinguished experts in the field, taking a focused, yet wide-ranging approach to the subject. It begins by exploring the pathways and networks mediating migraine headaches, their underlying physiological mechanisms, characteristics of visceral pain, and the concept of dural neurogenic inflammation. From there the authors delve into the mechanisms sustaining the head pain and photophobia associated with migraines, and they review the pharmacology of newly discovered migraine treatments. These basic chapters are followed by clinical and genetic studies linking to key issues, including cortical spreading depression, ion channels, transporters, and epilepsy.
* Reviews of the latest advances in our understanding of the neurobiological basis of migraine
* Translates important research findings from around the globe into novel treatments strategies currently being investigated
* Provides researchers and clinicians with a deep understanding of the primary mechanisms of migraine from migraine modeling to clinical applications
* Includes contributions by many of the most respected researchers in the field, world-wide
* Discusses exciting recent developments in migraine mutations and their role in CSD, as well as the role of CSD in aura and trigeminal activation
Timely, comprehensive, and authoritative, Neurobiological Basis of Migraine is an indispensable working resource for clinicians and migraine, headache, and pain researchers, including neurobiologists, neuropharmacologists, neurologists, and vascular neurobiologists, as well as graduate students in those fields who are involved in researching migraine headaches.

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Inhalt

Cover
Title Page
Copyright
Contents
List of Contributors
Foreword
Part I Anatomy and physiology
Chapter 1 Functional anatomy of trigeminovascular pain
1.1 Anatomy of the trigeminovascular system
1.1.1 Vascularization and innervation of the dura mater encephali
1.1.2 Extracranial extensions of the meningeal innervation
1.1.3 Neuropeptides and their receptors in meningeal tissues
1.1.4 Transduction channels and receptors in the trigeminovascular system
1.2 Trigeminal ganglion
1.2.1 Types of trigeminal ganglion cells
1.2.2 Neuropeptides and their receptors in the trigeminal ganglion
1.2.3 Representation of intracranial structures in the trigeminal ganglion
1.3 Trigeminal brainstem nuclear complex
1.3.1 Organization of the trigeminal brainstem nuclear complex
1.3.2 Nociceptive afferent projections to the spinal trigeminal nucleus
1.3.3 Functional representation of meningeal structures in the spinal trigeminal nucleus
1.3.4 Efferent projections from the spinal trigeminal nucleus
1.3.5 Neuropeptides and their receptors in the trigeminal nucleus
1.3.6 Channels and receptors involved in synaptic transmission in the trigeminal nucleus
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
2.2.1 Primary afferent neurons
2.2.2 Central neurons (dorsal horn and thalamus)
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
3.2.1 TRPA1
3.2.2 TRPM8
3.2.3 TRPV1
3.2.4 TRPV4
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
4.2.1 Ascending nociceptive pathways from the superficial laminae of the dorsal horn
4.2.1.1 Spino/trigemino-bulbar projections
4.2.1.2 Spino/trigemino-hypothalamic projections
4.2.1.3 Spino/trigemino-thalamic projections
4.2.2 Ascending nociceptive signals from the deep laminae of the dorsal horn
4.2.2.1 Spino/trigemino-reticulo-thalamic projections
4.3 Trigeminovascular pain is subject to descending control
4.3.1 Descending modulation from the periaqueductal gray (PAG) and the rostral ventromedial medulla (RVM)
4.3.2 Diffuse noxious inhibitory controls (DNIC)
4.3.3 Hypothalamic links for the descending control of trigeminovascular pain
4.3.4 The cortex as a major source of descending modulation
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
5.2.1 Referred sensations
5.2.2 Sensitization
5.2.3 Potential sensitizers
5.2.4 Immune system involvement in visceral pain and migraine
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
9.6.1 Early experimental studies with CGRP antibodies
9.6.2 CGRP antibody therapeutics
9.6.3 Comparing the CGRP modulators clinically
9.6.4 Safety and tolerability of the CGRP antibodies
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?
10.4.1 CGRP ligand mouse models
10.4.2 CGRP receptor mutant mouse models: CLR, CTR, and the RAMPs
10.4.2.1 Calcitonin receptor-like receptor (CLR)
10.4.2.2 Calcitonin receptor (CTR)
10.4.2.3 hRAMP1 overexpressing mice
10.4.2.4 RAMP1 knockout
10.4.2.5 RAMP2 overexpression
10.4.2.6 RAMP2 knockout
10.4.2.7 RAMP3 knockout
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
11.4.1 Visual aura
11.4.2 Sensory aura
11.4.3 Language aura
11.4.4 Duration of typical aura
11.4.5 Motor aura or hemiplegic migraine
11.5 Proposed aura types
11.5.1 Brainstem aura
11.5.2 Retinal aura
11.5.3 Migraine aura versus other causes of neurological deficit
11.6 Postdrome
11.7 Status migrainosus
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
13.4.1 Classification and co-prevalence
13.4.2 Timing
13.4.3 Migraine aura and headache arise from distinct pathways and triggers
13.4.4 Gender, estrogen, and interictal excitability phenotype in migraine aura and epilepsy
13.4.5 Pharmacological overlap
13.5 Acquired and genetic etiologies of migraine with aura and epilepsies
13.5.1 Epilepsy
13.5.2 Migraine
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
14.7.1 Future avenues of genetic research
14.7.2 Novel sequencing strategy for gene identification
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 in migraine
Chapter 17 Mathematical modeling of human cortical spreading depression
17.1 Introduction
17.2 Microscopic models: cellular and cytoarchitectonic detail
17.2.1 Physiological observations: persistent depolarization
17.2.2 Working model: sustained inward currents
17.2.3 Physiological mechanism: excitability
17.2.4 Results, modeling iterations, and interpretation
17.2.4.1 Increasing physiological detail
17.2.4.2 Model reconciliation
17.3 Macroscopic models: large scale spatiotemporal phenomenology
17.3.1 Clinical manifestation: march of migraine aura symptoms
17.3.2 Working model: activator inhibitor type description in two spatial dimensions
17.3.3 Physiological mechanism: spatiotemporal self-organization
17.3.4 Results of modeling iterations: from fronts to pulses to solitary localized structures
17.3.4.1 The speed of the front
17.3.4.2 Propagation and zigzag percepts
17.3.4.3 Propagation of solitary localized patterns
17.3.5 Interpretation of pattern formation principles
17.3.6 Clinical predictions
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 Ca2+ in neurons and astrocytes
18.4 NADH autofluorescence: an endogenous marker of energy metabolism
18.5 Direct imaging of molecular O2 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
19.3.1 In vivo preparations
19.3.2 In vitro 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
19.7.1 Anesthesia
19.7.2 Systemic physiology
19.7.3 Surgical preparation and maintenance
19.7.4 Pharmacokinetic factors
19.7.5 Induction and recording considerations
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)
20.4.1 Prostaglandin model
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
21.2.1 Headache
21.2.2 Aura
21.2.3 Allodynia and hyperalgesia
21.2.4 Photophobia, phonophobia, and olfactory discomfort
21.2.5 Habituation
21.2.6 Autonomic dysfunction and other non-pain symptoms
21.2.7 Cerebrovascular and metabolic dysfunction
21.3 Structural brain changes in migraine
21.3.1 Grey matter alterations in migraine
21.3.2 White matter alterations in migraine
21.4 Insights from orofacial pain
21.5 Conclusions
References
Index
EULA

List of Contributors

Isamu Aiba
Developmental Neurogenetics Laboratory
Department of Neurology
Baylor College of Medicine
Houston
Texas
USA

Messoud Ashina
Danish Headache Center, Department of Neurology
Rigshospitalet, Glostrup
Faculty of Health and Medical Sciences
University of Copenhagen
Copenhagen
Denmark

Christopher W. Atcherley
Department of Collaborative Research and Neurology
Mayo Clinic
Scottsdale
Arizona
USA

Cenk Ayata
Stroke Service and Neuroscience Intensive Care Unit
Department of Neurology
Massachusetts General Hospital
Harvard Medical School
Boston
Massachusetts
USA

David A. Boas
Martinos Center for Biomedical Imaging
MGH
Harvard Medical School
Charlestown
Massachusetts
USA

David Borsook
P.A.I.N. Group
Department of Anesthesiology
Perioperative & Pain Medicine
Boston Children's Hospital, Harvard Medical School
Boston
Massachusetts
USA

K.C. Brennan
Headache Physiology Laboratory
Departments of Neurology
University of Utah
Utah
USA

Rami Burstein
Department of Anesthesia
Critical Care and Pain Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School
Boston
Massachusetts
USA

Shih-Pin Chen
Department of Neurology
Taipei Veterans General Hospital
Taipei
Taiwan

F. Michael Cutrer
Department of Neurology
Mayo Clinic
Rochester
Minnesota
USA

Markus A. Dahlem
Department of Physics
Humboldt University of Berlin
Berlin
Germany

Turgay Dalkara
Department of Neurology
Faculty of Medicine and Institute of Neurological Sciences and Psychiatry Hacettepe University
Ankara
Turkey

Milena De Felice
School of Clinical Dentistry
University of Sheffield
South Yorkshire
United Kingdom

Anna Devor
Departments of Neurosciences and Radiology
UCSD
La Jolla
California
USA

David W. Dodick
Mayo Clinic Hospital
Phoenix
Arizona
USA

Gregory Dussor
Behavioral and Brain Sciences
BSB-14, The University of Texas at Dallas
Richardson
Texas
USA

Mária Dux
Department of Physiology
University of Szeged
Szeged
Hungary

Else Eising
Department of Human Genetics
Leiden University Medical Center
Leiden
The Netherlands

Michel D. Ferrari
Department of Neurology
Leiden University Medical Center
Leiden
The Netherlands

G.F. Gebhart
Center for Pain Research
Department of Anesthesiology
School of Medicine
University of Pittsburgh
Pittsburgh
Pennsylvania
USA

Peter J. Goadsby
Headache Group - NIHR-Wellcome Trust
King's Clinical Research Facility
King's College London
London
UK

Michael S. Gold
Center for Pain Research
Department of Neurobiology
School of Medicine
University of Pittsburgh
Pittsburgh
Pennsylvania
USA

Jakob Møller Hansen
Danish Headache Center
Department of Neurology
Rigshospitalet
Glostrup
Faculty of Health and Medical Sciences
University of Copenhagen
Copenhagen
Denmark

Richard J. Hargreaves
Biogen
Cambridge
Massachusetts
USA

Duncan J. Hodkinson
P.A.I.N. Group
Department of Anesthesiology
Perioperative & Pain Medicine
Boston Children's Hospital, Harvard Medical School
Boston
Massachusetts
USA

Kıvılcım Kılıç
Department of Neurosciences
UCSD
La Jolla
California
USA

Jonghwan Lee
Martinos Center for Biomedical Imaging
MGH
Harvard Medical School
Charlestown
Massachusetts
USA

Dan Levy
Department of Anesthesia
Critical Care and Pain Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School
Boston
Massachusetts
USA

Agustin Melo-Carrillo
Department of Anesthesia
Critical Care and Pain Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School
Boston
Massachusetts
USA

Karl Messlinger
Institute of Physiology and Pathophysiology
Friedrich-Alexander University Erlangen-Nürnberg
Erlangen
Germany

Michael A. Moskowitz
Departments of Radiology and Neurology
Massachusetts General Hospital
Harvard Medical School
Boston
Massachusetts
USA

Kelsey Nation
Department of Pharmacology
University of Arizona
Tucson
Arizona
USA

Jeffrey Noebels
Developmental Neurogenetics Laboratory
Department of Neurology
Baylor College of Medicine
Houston
Texas
USA

Rodrigo Noseda
Department of Anesthesia
Critical Care and Pain Medicine
Beth Israel Deaconess Medical Center
Harvard Medical School
Boston
Massachusetts
USA

Michael H. Ossipov
Department of Pharmacology
University of Arizona
Tucson
Arizona
USA

Daniela Pietrobon
Department of Biomedical Sciences
University of Padova
and
CNR Institute of Neuroscience
Padova
Italy

Frank Porreca
Department of Collaborative Research and Neurology
Mayo Clinic
Scottsdale
Arizona
USA
and
Department of Pharmacology
University of Arizona
Tucson
Arizona
USA

Andrew F. Russo
Neuroscience Program
Department of Molecular Physiology and Biophysics
VA Center for the Prevention and Treatment of Visual Loss
University of Iowa
Iowa City
Iowa
USA

Payam A. Saisan
Department of Neurosciences
UCSD
La Jolla
California
USA

Sava Sakadzic
Martinos Center for Biomedical Imaging
MGH
Harvard Medical School
Charlestown
Massachusetts
USA

Aaron Schain
Department of Anesthesia
Critical Care and Pain Medicine
Beth Israel Deaconess Medical Center, Harvard Medical School
Boston
Massachusetts
USA

Ryan Smith
Department of Molecular Physiology and Biophysics
VA Center for the Prevention and Treatment of Visual Loss
Iowa City
Iowa
USA

Levi P. Sowers
Department of Molecular Physiology and Biophysics
VA Center for the Prevention and Treatment of Visual Loss
University of Iowa
Iowa City
Iowa
USA

Andrew M. Strassman
Department of Anesthesia
Critical Care and Pain Medicine
Beth Israel...

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