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 8. 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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1 - Cover [Seite 1]
2 - Title Page [Seite 5]
3 - Copyright [Seite 6]
4 - Contents [Seite 9]
5 - List of Contributors [Seite 19]
6 - Foreword [Seite 25]
7 - Part I Anatomy and physiology [Seite 27]
7.1 - Chapter 1 Functional anatomy of trigeminovascular pain [Seite 29]
7.1.1 - 1.1 Anatomy of the trigeminovascular system [Seite 29]
7.1.1.1 - 1.1.1 Vascularization and innervation of the dura mater encephali [Seite 29]
7.1.1.2 - 1.1.2 Extracranial extensions of the meningeal innervation [Seite 30]
7.1.1.3 - 1.1.3 Neuropeptides and their receptors in meningeal tissues [Seite 31]
7.1.1.4 - 1.1.4 Transduction channels and receptors in the trigeminovascular system [Seite 34]
7.1.2 - 1.2 Trigeminal ganglion [Seite 35]
7.1.2.1 - 1.2.1 Types of trigeminal ganglion cells [Seite 35]
7.1.2.2 - 1.2.2 Neuropeptides and their receptors in the trigeminal ganglion [Seite 35]
7.1.2.3 - 1.2.3 Representation of intracranial structures in the trigeminal ganglion [Seite 38]
7.1.3 - 1.3 Trigeminal brainstem nuclear complex [Seite 38]
7.1.3.1 - 1.3.1 Organization of the trigeminal brainstem nuclear complex [Seite 38]
7.1.3.2 - 1.3.2 Nociceptive afferent projections to the spinal trigeminal nucleus [Seite 39]
7.1.3.3 - 1.3.3 Functional representation of meningeal structures in the spinal trigeminal nucleus [Seite 40]
7.1.3.4 - 1.3.4 Efferent projections from the spinal trigeminal nucleus [Seite 40]
7.1.3.5 - 1.3.5 Neuropeptides and their receptors in the trigeminal nucleus [Seite 41]
7.1.3.6 - 1.3.6 Channels and receptors involved in synaptic transmission in the trigeminal nucleus [Seite 42]
7.1.4 - References [Seite 43]
7.2 - Chapter 2 Physiology of the meningeal sensory pathway [Seite 57]
7.2.1 - 2.1 Role of the meningeal sensory pathway in headache [Seite 57]
7.2.2 - 2.2 Nociceptive response properties of peripheral and central neurons in the meningeal sensory pathway [Seite 58]
7.2.2.1 - 2.2.1 Primary afferent neurons [Seite 58]
7.2.2.2 - 2.2.2 Central neurons (dorsal horn and thalamus) [Seite 61]
7.2.3 - 2.3 Activity of neurons in the meningeal sensory pathway under conditions associated with headache: CSD and nitroglycerin [Seite 62]
7.2.4 - 2.4 Role of blood vessels in activation of the meningeal sensory pathway [Seite 64]
7.2.5 - 2.5 Unique neuronal properties of the meningeal sensory pathway [Seite 65]
7.2.6 - 2.6 Intracranial vs extracranial mechanisms of migraine: new findings [Seite 66]
7.2.7 - References [Seite 67]
7.3 - Chapter 3 Meningeal afferent ion channels and their role in migraine [Seite 75]
7.3.1 - 3.1 Meningeal afferents and migraine pain [Seite 75]
7.3.2 - 3.2 Transient receptor potential (TRP) channels and headache [Seite 75]
7.3.2.1 - 3.2.1 TRPA1 [Seite 76]
7.3.2.2 - 3.2.2 TRPM8 [Seite 78]
7.3.2.3 - 3.2.3 TRPV1 [Seite 78]
7.3.2.4 - 3.2.4 TRPV4 [Seite 79]
7.3.3 - 3.3 Acid-sensing ion channels [Seite 80]
7.3.4 - 3.4 Glutamate-gated channels [Seite 81]
7.3.5 - 3.5 ATP-gated channels [Seite 81]
7.3.6 - 3.6 K+ channels [Seite 82]
7.3.7 - 3.7 Other ion channels that may contribute to dural afferent signaling [Seite 83]
7.3.8 - 3.8 Conclusions [Seite 83]
7.3.9 - 3.9 Acknowledgements [Seite 84]
7.3.10 - References [Seite 84]
7.4 - Chapter 4 Functional architecture of central pain pathways: focus on the trigeminovascular system [Seite 95]
7.4.1 - 4.1 Introduction [Seite 95]
7.4.2 - 4.2 Ascending trigeminal nociceptive pathways [Seite 95]
7.4.2.1 - 4.2.1 Ascending nociceptive pathways from the superficial laminae of the dorsal horn [Seite 96]
7.4.2.1.1 - 4.2.1.1 Spino/trigemino-bulbar projections [Seite 96]
7.4.2.1.2 - 4.2.1.2 Spino/trigemino-hypothalamic projections [Seite 99]
7.4.2.1.3 - 4.2.1.3 Spino/trigemino-thalamic projections [Seite 99]
7.4.2.2 - 4.2.2 Ascending nociceptive signals from the deep laminae of the dorsal horn [Seite 101]
7.4.2.2.1 - 4.2.2.1 Spino/trigemino-reticulo-thalamic projections [Seite 101]
7.4.3 - 4.3 Trigeminovascular pain is subject to descending control [Seite 103]
7.4.3.1 - 4.3.1 Descending modulation from the periaqueductal gray (PAG) and the rostral ventromedial medulla (RVM) [Seite 103]
7.4.3.2 - 4.3.2 Diffuse noxious inhibitory controls (DNIC) [Seite 105]
7.4.3.3 - 4.3.3 Hypothalamic links for the descending control of trigeminovascular pain [Seite 106]
7.4.3.4 - 4.3.4 The cortex as a major source of descending modulation [Seite 107]
7.4.4 - 4.4 Conclusions [Seite 108]
7.4.5 - References [Seite 109]
8 - Part II Special features of migraine pain [Seite 117]
8.1 - Chapter 5 Visceral pain [Seite 119]
8.1.1 - 5.1 Organization of innervation [Seite 119]
8.1.2 - 5.2 Common features of visceral pain and headache [Seite 122]
8.1.2.1 - 5.2.1 Referred sensations [Seite 122]
8.1.2.2 - 5.2.2 Sensitization [Seite 124]
8.1.2.3 - 5.2.3 Potential sensitizers [Seite 126]
8.1.2.4 - 5.2.4 Immune system involvement in visceral pain and migraine [Seite 126]
8.1.3 - 5.3 Summary and conclusions [Seite 127]
8.1.4 - 5.4 Acknowledgement [Seite 127]
8.1.5 - References [Seite 128]
8.2 - Chapter 6 Meningeal neurogenic inflammation and dural mast cells in migraine pain [Seite 133]
8.2.1 - 6.1 Introduction [Seite 133]
8.2.2 - 6.2 The neurogenic inflammation hypothesis of migraine [Seite 134]
8.2.3 - 6.3 Meningeal neurogenic plasma protein extravasation and migraine [Seite 134]
8.2.4 - 6.4 Meningeal neurogenic vasodilatation and migraine [Seite 136]
8.2.5 - 6.5 Neurogenic mast cell activation in migraine [Seite 137]
8.2.6 - 6.6 Endogenous events that could promote meningeal NI in migraine [Seite 139]
8.2.7 - 6.7 Anti-migraine drugs and meningeal NI [Seite 139]
8.2.8 - 6.8 Is meningeal NI a pro-nociceptive event in migraine? [Seite 140]
8.2.9 - 6.9 Conclusions [Seite 141]
8.2.10 - References [Seite 142]
8.3 - Chapter 7 Sensitization and photophobia in migraine [Seite 151]
8.3.1 - 7.1 Introduction [Seite 151]
8.3.2 - 7.2 Experimental activation of trigeminovascular pathways [Seite 151]
8.3.3 - 7.3 Peripheral sensitization [Seite 153]
8.3.4 - 7.4 Central sensitization: medullary dorsal horn [Seite 153]
8.3.5 - 7.5 Central sensitization: thalamus [Seite 155]
8.3.6 - 7.6 Temporal aspects of sensitization and their implications to triptan therapy [Seite 155]
8.3.7 - 7.7 Modulation of central sensitization [Seite 157]
8.3.8 - 7.8 Neural substrate of migraine-type photophobia [Seite 159]
8.3.9 - References [Seite 161]
8.4 - Chapter 8 Central circuits promoting chronification of migraine [Seite 165]
8.4.1 - 8.1 Introduction [Seite 165]
8.4.2 - 8.2 Pharmacotherapy of migraine [Seite 166]
8.4.3 - 8.3 Medication overuse headache (MOH) and migraine chronification [Seite 167]
8.4.4 - 8.4 Central circuits modulating pain [Seite 169]
8.4.5 - 8.5 Evaluation of descending modulation: diffuse noxious inhibitory controls and conditioned pain modulation [Seite 171]
8.4.6 - 8.6 Conclusions [Seite 174]
8.4.7 - References [Seite 175]
8.5 - Chapter 9 Triptans to calcitonin gene-related peptide modulators - small molecules to antibodies - the evolution of a new migraine drug class [Seite 183]
8.5.1 - 9.1 Introduction [Seite 183]
8.5.2 - 9.2 Trigeminovascular system - migraine physiology and pharmacology [Seite 183]
8.5.3 - 9.3 Small molecule CGRP receptor antagonists [Seite 185]
8.5.4 - 9.4 Current status of small molecule CGRP receptor antagonist programs [Seite 187]
8.5.5 - 9.5 Unraveling the site of action of small molecule CGRP receptor antagonists using clinical pharmacology and brain imaging [Seite 188]
8.5.6 - 9.6 Biologic approaches to CGRP modulation [Seite 189]
8.5.6.1 - 9.6.1 Early experimental studies with CGRP antibodies [Seite 189]
8.5.6.2 - 9.6.2 CGRP antibody therapeutics [Seite 190]
8.5.6.3 - 9.6.3 Comparing the CGRP modulators clinically [Seite 191]
8.5.6.4 - 9.6.4 Safety and tolerability of the CGRP antibodies [Seite 193]
8.5.7 - 9.7 Summary and conclusion [Seite 193]
8.5.8 - References [Seite 194]
8.6 - Chapter 10 Lessons learned from CGRP mutant mice [Seite 201]
8.6.1 - 10.1 Introduction [Seite 201]
8.6.2 - 10.2 Modeling migraine [Seite 201]
8.6.3 - 10.3 Calcitonin gene-related peptide (CGRP) in migraine [Seite 202]
8.6.4 - 10.4 What has CGRP manipulation in mice taught us about migraine? [Seite 203]
8.6.4.1 - 10.4.1 CGRP ligand mouse models [Seite 203]
8.6.4.2 - 10.4.2 CGRP receptor mutant mouse models: CLR, CTR, and the RAMPs [Seite 206]
8.6.4.2.1 - 10.4.2.1 Calcitonin receptor-like receptor (CLR) [Seite 206]
8.6.4.2.2 - 10.4.2.2 Calcitonin receptor (CTR) [Seite 206]
8.6.4.2.3 - 10.4.2.3 hRAMP1 overexpressing mice [Seite 206]
8.6.4.2.4 - 10.4.2.4 RAMP1 knockout [Seite 208]
8.6.4.2.5 - 10.4.2.5 RAMP2 overexpression [Seite 208]
8.6.4.2.6 - 10.4.2.6 RAMP2 knockout [Seite 208]
8.6.4.2.7 - 10.4.2.7 RAMP3 knockout [Seite 208]
8.6.5 - 10.5 Conclusions [Seite 209]
8.6.6 - References [Seite 209]
9 - Part III Clinical characteristics of migraine [Seite 215]
9.1 - Chapter 11 The clinical characteristics of migraine [Seite 217]
9.1.1 - 11.1 Overview of migraine [Seite 217]
9.1.2 - 11.2 Migraine prodrome [Seite 217]
9.1.3 - 11.3 The migraine headache is the centerpiece of the syndrome [Seite 218]
9.1.4 - 11.4 Migraine aura [Seite 220]
9.1.4.1 - 11.4.1 Visual aura [Seite 220]
9.1.4.2 - 11.4.2 Sensory aura [Seite 220]
9.1.4.3 - 11.4.3 Language aura [Seite 221]
9.1.4.4 - 11.4.4 Duration of typical aura [Seite 222]
9.1.4.5 - 11.4.5 Motor aura or hemiplegic migraine [Seite 222]
9.1.5 - 11.5 Proposed aura types [Seite 223]
9.1.5.1 - 11.5.1 Brainstem aura [Seite 223]
9.1.5.2 - 11.5.2 Retinal aura [Seite 223]
9.1.5.3 - 11.5.3 Migraine aura versus other causes of neurological deficit [Seite 224]
9.1.6 - 11.6 Postdrome [Seite 224]
9.1.7 - 11.7 Status migrainosus [Seite 225]
9.1.8 - Summary [Seite 225]
9.1.9 - References [Seite 225]
9.2 - Chapter 12 The premonitory phase of migraine [Seite 227]
9.2.1 - 12.1 What is the premonitory phase? Towards a definition [Seite 227]
9.2.2 - 12.2 How common are premonitory symptoms? [Seite 228]
9.2.3 - 12.3 Do premonitory symptoms reliably predict a migraine attack? [Seite 228]
9.2.4 - 12.4 Premonitory symptoms in individuals [Seite 229]
9.2.5 - 12.5 Intra-patient variability of the premonitory phase [Seite 229]
9.2.6 - 12.6 Difference between patients with and without premonitory symptoms [Seite 230]
9.2.7 - 12.7 Premonitory symptoms in children [Seite 230]
9.2.8 - 12.8 Premonitory symptoms and migraine triggers [Seite 230]
9.2.9 - 12.9 Premonitory symptoms and pathophysiological studies [Seite 231]
9.2.10 - 12.10 Treatment during the premonitory phase [Seite 232]
9.2.11 - 12.11 Conclusion [Seite 232]
9.2.12 - References [Seite 233]
10 - Part IV Migraine genetics and CSD [Seite 235]
10.1 - Chapter 13 The genetic borderland of migraine and epilepsy [Seite 237]
10.1.1 - 13.1 Introduction [Seite 237]
10.1.2 - 13.2 Gene-linked comorbidity [Seite 237]
10.1.3 - 13.3 The challenge of dissecting seizure and aura excitability defects [Seite 238]
10.1.4 - 13.4 Clinical overlap of migraine with aura and epilepsy phenotypes [Seite 240]
10.1.4.1 - 13.4.1 Classification and co-prevalence [Seite 240]
10.1.4.2 - 13.4.2 Timing [Seite 240]
10.1.4.3 - 13.4.3 Migraine aura and headache arise from distinct pathways and triggers [Seite 241]
10.1.4.4 - 13.4.4 Gender, estrogen, and interictal excitability phenotype in migraine aura and epilepsy [Seite 241]
10.1.4.5 - 13.4.5 Pharmacological overlap [Seite 242]
10.1.5 - 13.5 Acquired and genetic etiologies of migraine with aura and epilepsies [Seite 242]
10.1.5.1 - 13.5.1 Epilepsy [Seite 242]
10.1.5.2 - 13.5.2 Migraine [Seite 243]
10.1.6 - 13.6 Migraine aura is linked to specific genes with locus and allelic heterogeneity [Seite 244]
10.1.7 - 13.7 Correspondence of regional brain susceptibility for migraine in genetic epilepsy syndromes [Seite 245]
10.1.8 - 13.8 Are SD thresholds plastic? [Seite 246]
10.1.9 - 13.9 Spreading depolarization in cardiorespiratory brainstem regions, a candidate mechanism of SUDEP [Seite 247]
10.1.10 - 13.10 Brainstem SD is a "second hit" leading to SUDEP [Seite 248]
10.1.11 - 13.11 Tau ablation prevents seizures, SUDEP and brainstem SD threshold in models of SUDEP [Seite 249]
10.1.12 - 13.12 Conclusion [Seite 249]
10.1.13 - 13.13 Acknowledgements [Seite 249]
10.1.14 - References [Seite 249]
10.2 - Chapter 14 Genetics of monogenic and complex migraine [Seite 259]
10.2.1 - 14.1 Migraine is a genetic disease [Seite 259]
10.2.2 - 14.2 How to identify genes for migraine? [Seite 260]
10.2.3 - 14.3 Gene identification in monogenic Familial Hemiplegic Migraine [Seite 260]
10.2.4 - 14.4 Functional studies of gene mutations in monogenic Familial Hemiplegic Migraine [Seite 262]
10.2.5 - 14.5 Genetic studies in monogenic disorders in which migraine is a prominent part of the clinical phenotype [Seite 265]
10.2.6 - 14.6 Genome-wide association studies in common polygenic migraine [Seite 266]
10.2.7 - 14.7 Future directions in genetic migraine research [Seite 267]
10.2.7.1 - 14.7.1 Future avenues of genetic research [Seite 268]
10.2.7.2 - 14.7.2 Novel sequencing strategy for gene identification [Seite 269]
10.2.8 - References [Seite 269]
10.3 - Chapter 15 Lessons from familial hemiplegic migraine and cortical spreading depression [Seite 277]
10.3.1 - 15.1 Introduction [Seite 277]
10.3.2 - 15.2 FHM genes and functional consequences of FHM mutations [Seite 278]
10.3.3 - 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 [Seite 281]
10.3.4 - 15.4 Acknowledgements [Seite 286]
10.3.5 - References [Seite 286]
10.4 - Chapter 16 From cortical spreading depression to trigeminovascular activation in migraine [Seite 293]
10.4.1 - 16.1 CSD causes the visual aura [Seite 293]
10.4.2 - 16.2 SD may underlie transient neurological dysfunctions preceding attacks [Seite 295]
10.4.3 - 16.3 Does SD cause headache? [Seite 296]
10.4.4 - 16.4 Human data supporting the parenchymal inflammatory signaling [Seite 300]
10.4.5 - 16.5 Meningeal neurogenic inflammation amplifies the parenchymal signal [Seite 301]
10.4.6 - 16.6 Understanding human CSD and migraine without aura [Seite 302]
10.4.7 - 16.7 Potential of CSD models to understand migraine and drug development [Seite 304]
10.4.8 - References [Seite 304]
11 - Part V Modeling and imaging in migraine [Seite 311]
11.1 - Chapter 17 Mathematical modeling of human cortical spreading depression [Seite 313]
11.1.1 - 17.1 Introduction [Seite 313]
11.1.2 - 17.2 Microscopic models: cellular and cytoarchitectonic detail [Seite 314]
11.1.2.1 - 17.2.1 Physiological observations: persistent depolarization [Seite 314]
11.1.2.2 - 17.2.2 Working model: sustained inward currents [Seite 314]
11.1.2.3 - 17.2.3 Physiological mechanism: excitability [Seite 315]
11.1.2.4 - 17.2.4 Results, modeling iterations, and interpretation [Seite 317]
11.1.2.4.1 - 17.2.4.1 Increasing physiological detail [Seite 317]
11.1.2.4.2 - 17.2.4.2 Model reconciliation [Seite 317]
11.1.3 - 17.3 Macroscopic models: large scale spatiotemporal phenomenology [Seite 318]
11.1.3.1 - 17.3.1 Clinical manifestation: march of migraine aura symptoms [Seite 318]
11.1.3.2 - 17.3.2 Working model: activator inhibitor type description in two spatial dimensions [Seite 319]
11.1.3.3 - 17.3.3 Physiological mechanism: spatiotemporal self-organization [Seite 320]
11.1.3.4 - 17.3.4 Results of modeling iterations: from fronts to pulses to solitary localized structures [Seite 321]
11.1.3.4.1 - 17.3.4.1 The speed of the front [Seite 321]
11.1.3.4.2 - 17.3.4.2 Propagation and zigzag percepts [Seite 322]
11.1.3.4.3 - 17.3.4.3 Propagation of solitary localized patterns [Seite 324]
11.1.3.5 - 17.3.5 Interpretation of pattern formation principles [Seite 325]
11.1.3.6 - 17.3.6 Clinical predictions [Seite 326]
11.1.4 - References [Seite 327]
11.2 - Chapter 18 Tools for high-resolution in vivo imaging of cellular and molecular mechanisms in cortical spreading depression and spreading depolarization [Seite 333]
11.2.1 - 18.1 Introduction [Seite 333]
11.2.2 - 18.2 Large-scale imaging of vascular dynamics with microscopic resolution [Seite 334]
11.2.3 - 18.3 Combining measurements of single-vessel diameter with imaging and quantification of intracellular Ca2+ in neurons and astrocytes [Seite 335]
11.2.4 - 18.4 NADH autofluorescence: an endogenous marker of energy metabolism [Seite 337]
11.2.5 - 18.5 Direct imaging of molecular O2 in blood and tissue [Seite 338]
11.2.6 - 18.6 Employing optogenetics to study inter-cellular communication [Seite 340]
11.2.7 - 18.7 Conclusions and outlook [Seite 340]
11.2.8 - References [Seite 341]
11.3 - Chapter 19 Animal models of migraine aura [Seite 347]
11.3.1 - 19.1 Introduction: spreading depression and migraine [Seite 347]
11.3.2 - 19.2 In vivo and in vitro models of SD susceptibility [Seite 348]
11.3.3 - 19.3 Experimental preparations [Seite 350]
11.3.3.1 - 19.3.1 In vivo preparations [Seite 350]
11.3.3.2 - 19.3.2 In vitro preparations [Seite 350]
11.3.4 - 19.4 Methods to trigger SD [Seite 353]
11.3.5 - 19.5 Methods to detect CSD [Seite 355]
11.3.6 - 19.6 SD susceptibility attributes [Seite 357]
11.3.7 - 19.7 Recommended quality measures for experimental models of migraine aura [Seite 359]
11.3.7.1 - 19.7.1 Anesthesia [Seite 359]
11.3.7.2 - 19.7.2 Systemic physiology [Seite 359]
11.3.7.3 - 19.7.3 Surgical preparation and maintenance [Seite 359]
11.3.7.4 - 19.7.4 Pharmacokinetic factors [Seite 359]
11.3.7.5 - 19.7.5 Induction and recording considerations [Seite 360]
11.3.8 - 19.8 Future directions [Seite 360]
11.3.9 - References [Seite 361]
11.4 - Chapter 20 Human models of migraine [Seite 373]
11.4.1 - 20.1 Introduction [Seite 373]
11.4.2 - 20.2 The first steps: GTN and the NO-hypothesis [Seite 373]
11.4.3 - 20.3 Calcitonin gene-related peptide (CGRP) [Seite 377]
11.4.4 - 20.4 Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating polypeptide (PACAP) [Seite 379]
11.4.4.1 - 20.4.1 Prostaglandin model [Seite 379]
11.4.5 - 20.5 Can we gain from the use of experimental models to study functional consequences of migraine mutations? [Seite 380]
11.4.6 - 20.6 Conclusion [Seite 381]
11.4.7 - References [Seite 381]
11.5 - Chapter 21 Imaging pain and headache [Seite 389]
11.5.1 - 21.1 Introduction [Seite 389]
11.5.2 - 21.2 Functional brain changes in migraine [Seite 389]
11.5.2.1 - 21.2.1 Headache [Seite 389]
11.5.2.2 - 21.2.2 Aura [Seite 390]
11.5.2.3 - 21.2.3 Allodynia and hyperalgesia [Seite 391]
11.5.2.4 - 21.2.4 Photophobia, phonophobia, and olfactory discomfort [Seite 391]
11.5.2.5 - 21.2.5 Habituation [Seite 391]
11.5.2.6 - 21.2.6 Autonomic dysfunction and other non-pain symptoms [Seite 391]
11.5.2.7 - 21.2.7 Cerebrovascular and metabolic dysfunction [Seite 393]
11.5.3 - 21.3 Structural brain changes in migraine [Seite 393]
11.5.3.1 - 21.3.1 Grey matter alterations in migraine [Seite 394]
11.5.3.2 - 21.3.2 White matter alterations in migraine [Seite 396]
11.5.4 - 21.4 Insights from orofacial pain [Seite 396]
11.5.5 - 21.5 Conclusions [Seite 397]
11.5.6 - References [Seite 398]
12 - Index [Seite 403]
13 - EULA [Seite 424]

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