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E-raamat: Neurobiological Basis of Migraine

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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.

List of Contributors xvii
Foreword xxiii
Part I Anatomy and physiology 1(90)
1 Functional anatomy of trigeminovascular pain
3(28)
Karl Messlinger
Maria Dux
1.1 Anatomy of the trigeminovascular system
3(6)
1.1.1 Vascularization and innervation of the dura mater encephali
3(1)
1.1.2 Extracranial extensions of the meningeal innervation
4(1)
1.1.3 Neuropeptides and their receptors in meningeal tissues
5(3)
1.1.4 Transduction channels and receptors in the trigeminovascular system
8(1)
1.2 Trigeminal ganglion
9(3)
1.2.1 Types of trigeminal ganglion cells
9(1)
1.2.2 Neuropeptides and their receptors in the trigeminal ganglion
9(3)
1.2.3 Representation of intracranial structures in the trigeminal ganglion
12(1)
1.3 Trigeminal brainstem nuclear complex
12(5)
1.3.1 Organization of the trigeminal brainstem nuclear complex
12(1)
1.3.2 Nociceptive afferent projections to the spinal trigeminal nucleus
13(1)
1.3.3 Functional representation of meningeal structures in the spinal trigeminal nucleus
14(1)
1.3.4 Efferent projections from the spinal trigeminal nucleus
14(1)
1.3.5 Neuropeptides and their receptors in the trigeminal nucleus
15(1)
1.3.6 Channels and receptors involved in synaptic transmission in the trigeminal nucleus
16(1)
References
17(14)
2 Physiology of the meningeal sensory pathway
31(18)
Andrew M. Strassman
Agustin Melo-Carrillo
2.1 Role of the meningeal sensory pathway in headache
31(1)
2.2 Nociceptive response properties of peripheral and central neurons in the meningeal sensory pathway
32(4)
2.2.1 Primary afferent neurons
32(3)
2.2.2 Central neurons (dorsal horn and thalamus)
35(1)
2.3 Activity of neurons in the meningeal sensory pathway under conditions associated with headache: CSD and nitroglycerin
36(2)
2.4 Role of blood vessels in activation of the meningeal sensory pathway
38(1)
2.5 Unique neuronal properties of the meningeal sensory pathway
39(1)
2.6 Intracranial vs extracranial mechanisms of migraine: new findings
40(1)
References
41(8)
3 Meningeal afferent ion channels and their role in migraine
49(20)
Gregory Dussor
3.1 Meningeal afferents and migraine pain
49(1)
3.2 Transient receptor potential (TRP) channels and headache
49(5)
3.2.1 TRPA1
50(2)
3.2.2 TRPM8
52(1)
3.2.3 TRPV1
52(1)
3.2.4 TRPV4
53(1)
3.3 Acid-sensing ion channels
54(1)
3.4 Glutamate-gated channels
55(1)
3.5 ATP-gated channels
55(1)
3.6 K± channels
56(1)
3.7 Other ion channels that may contribute to dural afferent signaling
57(1)
3.8 Conclusions
57(1)
3.9 Acknowledgements
58(1)
References
58(11)
4 Functional architecture of central pain pathways: focus on the trigeminovascular system
69(22)
Rodrigo Noseda
Luis Villanueva
4.1 Introduction
69(1)
4.2 Ascending trigeminal nociceptive pathways
69(8)
4.2.1 Ascending nociceptive pathways from the superficial laminae of the dorsal horn
70(1)
4.2.1.1 Spino/trigemino-bulbar projections
70(1)
4.2.1.2 Spino/trigemino-hypothalamic projections
73(1)
4.2.1.3 Spino/trigemino-thalamic projections
73(2)
4.2.2 Ascending nociceptive signals from the deep laminae of the dorsal horn
75(1)
4.2.2.1 Spino/trigemino-reticulo-thalamic projections
75(2)
4.3 Trigeminovascular pain is subject to descending control
77(5)
4.3.1 Descending modulation from the periaqueductal gray (PAG) and the rostral ventromedial medulla (RVM)
77(2)
4.3.2 Diffuse noxious inhibitory controls (DNIC)
79(1)
4.3.3 Hypothalamic links for the descending control of trigeminovascular pain
80(1)
4.3.4 The cortex as a major source of descending modulation
81(1)
4.4 Conclusions
82(1)
References
83(8)
Part II Special featurs of migrain pain 91(98)
5 Visceral pain
93(14)
Michael S. Gold
G.F. Gebhart
5.1 Organization of innervation
93(3)
5.2 Common features of visceral pain and headache
96(5)
5.2.1 Referred sensations
96(2)
5.2.2 Sensitization
98(2)
5.2.3 Potential sensitizers
100(1)
5.2.4 Immune system involvement in visceral pain and migraine
100(1)
5.3 Summary and conclusions
101(1)
5.4 Acknowledgement
101(1)
References
102(5)
6 Meningeal neurogenic inflammation and dural mast cells in migraine pain
107(18)
Dan Levy
6.1 Introduction
107(1)
6.2 The neurogenic inflammation hypothesis of migraine
108(1)
6.3 Meningeal neurogenic plasma protein extravasation and migraine
108(2)
6.4 Meningeal neurogenic vasodilatation and migraine
110(1)
6.5 Neurogenic mast cell activation in migraine
111(2)
6.6 Endogenous events that could promote meningeal NI in migraine
113(1)
6.7 Anti-migraine drugs and meningeal NI
113(1)
6.8 Is meningeal NI a pro-nociceptive event in migraine?
114(1)
6.9 Conclusions
115(1)
References
116(9)
7 Sensitization and photophobia in migraine
125(14)
Aaron Schain
Rami Burstein
7.1 Introduction
125(1)
7.2 Experimental activation of trigeminovascular pathways
125(2)
7.3 Peripheral sensitization
127(1)
7.4 Central sensitization: medullary dorsal horn
127(2)
7.5 Central sensitization: thalamus
129(1)
7.6 Temporal aspects of sensitization and their implications to triptan therapy
129(2)
7.7 Modulation of central sensitization
131(2)
7.8 Neural substrate of migraine-type photophobia
133(2)
References
135(4)
8 Central circuits promoting chronification of migraine
139(18)
Christopher W. Atcherley
Kelsey Nation
Milena De Felice
Jennifer Y. Xie
Michael H. Ossipov
David W. Dodick
Frank Porreca
8.1 Introduction
139(1)
8.2 Pharmacotherapy of migraine
140(1)
8.3 Medication overuse headache (MOH) and migraine chronification
141(2)
8.4 Central circuits modulating pain
143(2)
8.5 Evaluation of descending modulation: diffuse noxious inhibitory controls and conditioned pain modulation
145(3)
8.6 Conclusions
148(1)
References
149(8)
9 Triptans to calcitonin gene-related peptide modulators - small molecules to antibodies - the evolution of a new migraine drug class
157(18)
Richard J. Hargreaves
9.1 Introduction
157(1)
9.2 Trigeminovascular system - migraine physiology and pharmacology
157(2)
9.3 Small molecule CGRP receptor antagonists
159(2)
9.4 Current status of small molecule CGRP receptor antagonist programs
161(1)
9.5 Unraveling the site of action of small molecule CGRP receptor antagonists using clinical pharmacology and brain imaging
162(1)
9.6 Biologic approaches to CGRP modulation
163(4)
9.6.1 Early experimental studies with CGRP antibodies
163(1)
9.6.2 CGRP antibody therapeutics
164(1)
9.6.3 Comparing the CGRP modulators clinically
165(2)
9.6.4 Safety and tolerability of the CGRP antibodies
167(1)
9.7 Summary and conclusion
167(1)
References
168(7)
10 Lessons learned from CGRP mutant mice
175(14)
Levi P. Sowers
Annie E. Tye
Andrew F. Russo
10.1 Introduction
175(1)
10.2 Modeling migraine
175(1)
10.3 Calcitonin gene-related peptide (CGRP) in migraine
176(1)
10.4 What has CGRP manipulation in mice taught us about migraine?
177(6)
10.4.1 CGRP ligand mouse models
177(3)
10.4.2 CGRP receptor mutant mouse models: CLR, CTR, and the RAMPS
180(1)
10.4.2.1 Calcitonin receptor-like receptor (CLR)
180(1)
10.4.2.2 Calcitonin receptor (CTR)
180(1)
10.4.2.3 hRAMP1 overexpressing mice
180(1)
10.4.2.4 RAMP1 knockout
182(1)
10.4.2.5 RAMP2 overexpression
182(1)
10.4.2.6 RAMP2 knockout
182(1)
10.4.2.7 RAMP3 knockout
182(1)
10.5 Conclusions
183(1)
References
183(6)
Part III Clinical characteristics of migraine 189(20)
11 The clinical characteristics of migraine
191(10)
F. Michael Cutrer
Ryan Smith
David W. Dodick
11.1 Overview of migraine
191(1)
11.2 Migraine prodrome
191(1)
11.3 The migraine headache is the centerpiece of the syndrome
192(2)
11.4 Migraine aura
194(3)
11.4.1 Visual aura
194(1)
11.4.2 Sensory aura
194(1)
11.4.3 Language aura
195(1)
11.4.4 Duration of typical aura
196(1)
11.4.5 Motor aura or hemiplegic migraine
196(1)
11.5 Proposed aura types
197(1)
11.5.1 Brainstem aura
197(1)
11.5.2 Retinal aura
197(1)
11.5.3 Migraine aura versus other causes of neurological deficit
198(1)
11.6 Postdrome
198(1)
11.7 Status migrainosus
199(1)
Summary
199(1)
References
199(2)
12 The premonitory phase of migraine
201(8)
Michele Viana
Peter J. Goadsby
12.1 What is the premonitory phase? Towards a definition
201(1)
12.2 How common are premonitory symptoms?
202(1)
12.3 Do premonitory symptoms reliably predict a migraine attack?
202(1)
12.4 Premonitory symptoms in individuals
203(1)
12.5 Intra-patient variability of the premonitory phase
203(1)
12.6 Difference between patients with and without premonitory symptoms
204(1)
12.7 Premonitory symptoms in children
204(1)
12.8 Premonitory symptoms and migraine triggers
204(1)
12.9 Premonitory symptoms and pathophysiological studies
205(1)
12.10 Treatment during the premonitory phase
206(1)
12.11 Conclusion
206(1)
References
207(2)
Part IV Migraine genetics and CSD 209(76)
13 The genetic borderland of migraine and epilepsy
211(22)
Isamu Aiba
Jeffrey Noebels
13.1 Introduction
211(1)
13.2 Gene-linked comorbidity
211(1)
13.3 The challenge of dissecting seizure and aura excitability defects
212(2)
13.4 Clinical overlap of migraine with aura and epilepsy phenotypes
214(2)
13.4.1 Classification and co-prevalence
214(1)
13.4.2 Timing
214(1)
13.4.3 Migraine aura and headache arise from distinct pathways and triggers
215(1)
13.4.4 Gender, estrogen, and interictal excitability phenotype in migraine aura and epilepsy
215(1)
13.4.5 Pharmacological overlap
216(1)
13.5 Acquired and genetic etiologies of migraine with aura and epilepsies
216(2)
13.5.1 Epilepsy
216(1)
13.5.2 Migraine
217(1)
13.6 Migraine aura is linked to specific genes with locus and allelic heterogeneity
218(1)
13.7 Correspondence of regional brain susceptibility for migraine in genetic epilepsy syndromes
219(1)
13.8 Are SD thresholds plastic?
220(1)
13.9 Spreading depolarization in cardiorespiratory brainstem regions, a candidate mechanism of SUDEP
221(1)
13.10 Brainstem SD is a "second hit" leading to SUDEP
222(1)
13.11 Tau ablation prevents seizures, SUDEP and brainstem SD threshold in models of SUDEP
223(1)
13.12 Conclusion
223(1)
13.13 Acknowledgements
223(1)
References
223(10)
14 Genetics of monogenic and complex migraine
233(18)
Else A. Tolner
Else Eising
Gisela M. Terwindt
Michel D. Ferrari
Am M.J.M. van den Maagdenberg
14.1 Migraine is a genetic disease
233(1)
14.2 How to identify genes for migraine?
234(1)
14.3 Gene identification in monogenic Familial Hemiplegic Migraine
234(2)
14.4 Functional studies of gene mutations in monogenic Familial Hemiplegic Migraine
236(3)
14.5 Genetic studies in monogenic disorders in which migraine is a prominent part of the clinical phenotype
239(1)
14.6 Genome-wide association studies in common polygenic migraine
240(1)
14.7 Future directions in genetic migraine research
241(2)
14.7.1 Future avenues of genetic research
242(1)
14.7.2 Novel sequencing strategy for gene identification
243(1)
References
243(8)
15 Lessons from familial hemiplegic migraine and cortical spreading depression
251(16)
Daniela Pietrobon
15.1 Introduction
251(1)
15.2 FHM genes and functional consequences of FHM mutations
252(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
255(5)
15.4 Acknowledgements
260(1)
References
260(7)
16 From cortical spreading depression to trigeminovascular activation in migraine
267(18)
Turgay Dalkara
Michael A. Moskowitz
16.1 CSD causes the visual aura
267(2)
16.2 SD may underlie transient neurological dysfunctions preceding attacks
269(1)
16.3 Does SD cause headache?
270(4)
16.4 Human data supporting the parenchymal inflammatory signaling
274(1)
16.5 Meningeal neurogenic inflammation amplifies the parenchymal signal
275(1)
16.6 Understanding human CSD and migraine without aura
276(2)
16.7 Potential of CSD models to understand migraine and drug development
278(1)
References
278(7)
Part V Modeling and imaging in migraine 285(92)
17 Mathematical modeling of human cortical spreading depression
287(20)
Markus A. Dahlem
17.1 Introduction
287(1)
17.2 Microscopic models: cellular and cytoarchitectonic detail
288(4)
17.2.1 Physiological observations: persistent depolarization
288(1)
17.2.2 Working model: sustained inward currents
288(1)
17.2.3 Physiological mechanism: excitability
289(2)
17.2.4 Results, modeling iterations, and interpretation
291(1)
17.2.4.1 Increasing physiological detail
291(1)
17.2.4.2 Model reconciliation
291(1)
17.3 Macroscopic models: large scale spatiotemporal phenomenology
292(9)
17.3.1 Clinical manifestation: march of migraine aura symptoms
292(1)
17.3.2 Working model: activator inhibitor type description in two spatial dimensions
293(1)
17.3.3 Physiological mechanism: spatiotemporal self-organization
294(1)
17.3.4 Results of modeling iterations: from fronts to pulses to solitary localized structures
295(1)
17.3.4.1 The speed of the front
295(1)
17.3.4.2 Propagation and zigzag percepts
296(1)
17.3.4.3 Propagation of solitary localized patterns
298(1)
17.3.5 Interpretation of pattern formation principles
299(1)
17.3.6 Clinical predictions
300(1)
References
301(6)
18 Tools for high-resolution in vivo imaging of cellular and molecular mechanisms in cortical spreading depression and spreading depolarization
307(14)
Kivilcim Kilic
Hana Uhlirova
Peifang Tian
Payam A. Saisan
Mohammad Abbas Yaseen
Jonghwan Lee
Sergei A. Vinogradov
David A. Boas
Sava Sakadzic
Anna Devor
18.1 Introduction
307(1)
18.2 Large-scale imaging of vascular dynamics with microscopic resolution
308(1)
18.3 Combining measurements of single-vessel diameter with imaging and quantification of intracellular Ca2+ in neurons and astrocytes
309(2)
18.4 NADH autofluorescence: an endogenous marker of energy metabolism
311(1)
18.5 Direct imaging of molecular O2 in blood and tissue
312(2)
18.6 Employing optogenetics to study inter-cellular communication
314(1)
18.7 Conclusions and outlook
314(1)
References
315(6)
19 Animal models of migraine aura
321(26)
Shih-Pin Chen
Jeremy Theriot
Cenk Ayata
K.C. Brennan
19.1 Introduction: spreading depression and migraine
321(1)
19.2 In vivo and in vitro models of SD susceptibility
322(2)
19.3 Experimental preparations
324(3)
19.3.1 In vivo preparations
324(1)
19.3.2 In vitro preparations
324(3)
19.4 Methods to trigger SD
327(2)
19.5 Methods to detect CSD
329(2)
19.6 SD susceptibility attributes
331(2)
19.7 Recommended quality measures for experimental models of migraine aura
333(1)
19.7.1 Anesthesia
333(1)
19.7.2 Systemic physiology
333(1)
19.7.3 Surgical preparation and maintenance
333(1)
19.7.4 Pharmacokinetic factors
333(1)
19.7.5 Induction and recording considerations
334(1)
19.8 Future directions
334(1)
References
335(12)
20 Human models of migraine
347(16)
Jakob Moller Hansen
Messoud Ashina
20.1 Introduction
347(1)
20.2 The first steps: GTN and the NO-hypothesis
347(4)
20.3 Calcitonin gene-related peptide (CGRP)
351(2)
20.4 Vasoactive intestinal peptide (VIP) and pituitary adenylate cyclase activating polypeptide (PACAP)
353(1)
20.4.1 Prostaglandin model
353(1)
20.5 Can we gain from the use of experimental models to study functional consequences of migraine mutations?
354(1)
20.6 Conclusion
355(1)
References
355(8)
21 Imaging pain and headache
363(14)
Duncan J. Hodkinson
Sophie L. Wilcox
David Borsook
21.1 Introduction
363(1)
21.2 Functional brain changes in migraine
363(4)
21.2.1 Headache
363(1)
21.2.2 Aura
364(1)
21.2.3 Allodynia and hyperalgesia
365(1)
21.2.4 Photophobia, phonophobia, and olfactory discomfort
365(1)
21.2.5 Habituation
365(1)
21.2.6 Autonomic dysfunction and other non-pain symptoms
365(2)
21.2.7 Cerebrovascular and metabolic dysfunction
367(1)
21.3 Structural brain changes in migraine
367(3)
21.3.1 Grey matter alterations in migraine
368(2)
21.3.2 White matter alterations in migraine
370(1)
21.4 Insights from orofacial pain
370(1)
21.5 Conclusions
371(1)
References
372(5)
Index 377
About the Editors

Turgay Dalkara, MD, PhD is Professor of Neurology and Chair of the Institute of Neurological Sciences and Psychiatry at Hacettepe University, Ankara, Turkey. He also holds a joint appointment at the department of Radiology at the Massachusetts General Hospital, Harvard University, Boston.

Michael A. Moskowitz, MD is Professor of Neurology at Harvard Medical School and a former Member of the Harvard-MIT Division of Health Science & Technology. He is also senior neuroscientist in the Departments of Radiology and Neurology at the Massachusetts General Hospital, Boston.
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