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Insights into Migraine Treatments : Towards Personalized Medicine.
- Format:
- Book
- Author/Creator:
- Filippi, M. (Massimo), 1961-
- Language:
- English
- Subjects (All):
- Migraine.
- Precision medicine.
- Physical Description:
- 1 online resource (457 pages)
- Edition:
- 1st ed.
- Place of Publication:
- Chantilly : Elsevier Science & Technology, 2025.
- Summary:
- Insights into Migraine Treatments offers a comprehensive overview to guide the selection of the most appropriate therapy for each patient within the landscape of migraine care.It explores the full spectrum of available treatments and their mechanisms of action, while addressing the challenges of individualized therapeutic decision-making.
- Contents:
- Front Cover
- Insights Into Migraine Treatments: Towards Personalized Medicine
- Copyright Page
- Contents
- List of contributors
- 1 Clinical manifestations of migraine
- 1.1 Introduction
- 1.2 Epidemiology
- 1.3 Diagnostic criteria
- 1.3.1 Migraine without aura
- 1.3.2 Migraine with aura
- 1.3.3 Episodic versus chronic migraine
- 1.3.4 Migraine subtypes
- 1.3.5 Migraine with brainstem aura
- 1.3.6 Hemiplegic migraine
- 1.3.7 Retinal migraine
- 1.3.8 Other migraine subtypes
- 1.4 Phases of migraine
- 1.5 Diagnosis
- 1.5.1 Clinical features
- 1.6 Triggers
- 1.7 Differential diagnosis
- 1.8 Conclusion
- References
- 2 Why, when, and how to treat migraine patients?
- 2.1 Why to treat migraine patients
- 2.1.1 The burden of migraine
- 2.1.2 The interictal burden of migraine
- 2.1.3 The psychological, social, and economic impact of migraine
- 2.2 When to treat migraine patients
- 2.3 How to treat migraine patients
- 2.3.1 Nonpharmacological treatment
- 2.3.1.1 Education, behavioral, and relaxation techniques
- 2.3.1.2 Neuromodulation techniques
- 2.3.1.3 Acupuncture
- 2.3.2 Pharmacological treatments
- 2.3.2.1 Treatment for acute attacks
- 2.3.2.2 Preventive treatments
- 2.3.2.2.1 Stopping preventive treatment
- 3 Acute treatments: nonsteroidal anti-inflammatory drugs, ergot alkaloids, triptans, and ditans
- 3.1 Principles of acute treatment
- 3.2 Acetaminophen
- 3.3 Nonsteroidal anti-inflammatory drugs
- 3.3.1 Acetylsalicylic acid
- 3.3.2 Ibuprofen
- 3.3.3 Naproxen
- 3.3.4 Other nonsteroidal anti-inflammatory drugs
- 3.3.5 Common side effects of nonsteroidal anti-inflammatory drugs
- 3.4 Ergot alkaloids, triptans, and ditans
- 3.4.1 Ergot alkaloids
- 3.4.2 Triptans
- 3.4.2.1 Almotriptan
- 3.4.2.2 Eletriptan
- 3.4.2.3 Frovatriptan
- 3.4.2.4 Naratriptan
- 3.4.2.5 Rizatriptan.
- 3.4.2.6 Sumatriptan
- 3.4.2.7 Zolmitriptan
- 3.4.3 Common side effects and contraindications for triptans
- 3.4.4 Recommendations for choosing the triptan for daily clinical practice
- 3.5 Ditans
- 3.6 Combination therapies
- 3.7 Medication overuse headache
- 3.8 Regional differences in use of acute migraine therapies worldwide
- 4 Acute treatments: neuromodulation and peripheral nerve blocks
- 4.1 Introduction
- 4.2 Transcutaneous supraorbital nerve stimulation
- 4.2.1 Efficacy in clinical studies
- 4.2.2 Proposed mechanism of action
- 4.2.3 Tolerability, safety, and contraindications
- 4.3 Sphenopalatine ganglion block and neuromodulation
- 4.3.1 Efficacy in clinical studies
- 4.3.2 Proposed mechanism of action
- 4.3.3 Tolerability, safety, and contraindications
- 4.4 Transcranial magnetic stimulation
- 4.4.1 Efficacy in clinical studies
- 4.4.2 Proposed mechanism of action
- 4.4.3 Tolerability, safety, and contraindications
- 4.5 Noninvasive vagus nerve stimulation
- 4.5.1 Efficacy in clinical studies
- 4.5.2 Proposed mechanism of action
- 4.5.3 Tolerability, safety, and contraindications
- 4.6 Remote electric neuromodulation
- 4.6.1 Efficacy
- 4.6.2 Proposed mechanism of action
- 4.6.3 Tolerability, safety, and contraindications
- 4.7 Greater occipital nerve block
- 4.7.1 Efficacy in clinical studies
- 4.7.2 Proposed mechanism of action
- 4.7.3 Tolerability, safety, and contraindications
- 5 Oral preventive treatments: antidepressants, antihypertensives, anticonvulsants, betablockers, and calcium channel blockers
- 5.1 Introduction
- 5.2 Antidepressants
- 5.3 Anticonvulsants
- 5.4 Beta blockers
- 5.5 Calcium channel blockers
- 5.6 Antihypertensives
- 6 Preventive treatments: onabotulinumtoxinA and peripheral nerve blocks
- 6.1 Introduction.
- 6.2 Botulinum neurotoxin
- 6.2.1 Characteristics and mechanisms of action of botulinum neurotoxin
- 6.2.2 Injection procedure
- 6.2.3 Clinical trials of botulinum toxins in migraine
- 6.2.4 Real-world studies
- 6.2.5 Advantages and disadvantages of onabotulinumtoxinA in migraine
- 6.2.6 Future directions and opportunities for personalized medicine
- 6.2.7 Nerve blocks
- 6.2.8 Clinical trials
- 6.2.9 Real-world studies
- 6.2.10 Advantages and disadvantages of peripheral nerve blocks for migraine
- 6.2.11 The place of peripheral nerve blocks in the treatment of migraine
- 6.2.12 Future directions and opportunities for personalized medicine
- 6.3 Conclusions
- 7 Nonpharmacological approaches in migraine prevention: neuromodulation, nutraceuticals, and behavioral approaches
- 7.1 Introduction
- 7.2 Neuromodulation
- 7.2.1 Trigeminal nerve stimulation
- 7.2.2 Occipital nerve stimulation
- 7.2.3 Noninvasive vagal nerve stimulation
- 7.2.4 Single-pulse transcranial magnetic stimulation
- 7.2.5 Repetitive transcranial magnetic stimulation
- 7.2.6 Transcranial direct current stimulation
- 7.2.7 Remote electrical neuromodulation
- 7.2.8 Cervical spinal cord stimulation
- 7.3 Nutraceuticals
- 7.3.1 Riboflavin
- 7.3.2 Coenzyme Q10
- 7.3.3 Butterbur (Petasites hybridus)
- 7.3.4 Magnesium
- 7.3.5 Omega-3
- 7.3.6 Feverfew (Tanacetum parthenium)
- 7.3.7 Melatonin
- 7.3.8 Cannabis sativa
- 7.3.9 Combination of nutraceuticals
- 7.4 Behavioral approaches
- 7.4.1 Cognitive behavioral therapy
- 7.4.2 Relaxation training
- 7.4.3 Biofeedback training
- 7.4.4 Exercise
- 7.4.5 Acupuncture
- 7.4.6 Emerging behavioral therapies
- 8 Why target the calcitonin gene-related peptide pathway: Receptors, intracellular pathways, and its role in migraine pathophysiology
- 8.1 Introduction.
- 8.1.1 The discovery of calcitonin gene-related peptide
- 8.2 Molecular features of calcitonin gene-related peptide
- 8.2.1 The synthesis of calcitonin gene-related peptide
- 8.2.2 The molecular structure of calcitonin gene-related peptide
- 8.2.3 Calcitonin gene-related peptide localization
- 8.2.4 The release of calcitonin gene-related peptide
- 8.2.5 The calcitonin gene-related peptide family of peptides
- 8.3 Receptors mediating calcitonin gene-related peptide actions
- 8.3.1 The canonical calcitonin gene-related peptide-receptor complex
- 8.3.2 Other noncanonical receptors
- 8.3.3 Nonpeptide calcitonin gene-related peptide receptor antagonists
- 8.4 Calcitonin gene-related peptide receptor-mediated signal transduction
- 8.4.1 GSα coupled signal transduction
- 8.4.2 Gαi/o coupled signal transduction
- 8.4.3 Gαq/11 coupled signal transduction
- 8.4.4 Mitogen-activated protein kinases cascades
- 8.5 Calcitonin gene-related peptide and migraine
- 8.5.1 Vascular effects
- 8.5.2 Neural effects
- 8.6 Summary
- 9 Gepants
- 9.1 Introduction
- 9.2 Calcitonin gene-related peptide and calcitonin gene-related peptide receptors
- 9.3 First-generation gepants
- 9.3.1 Olcegepant
- 9.3.2 Telcagepant
- 9.3.2.1
- 9.3.3 Second-generation gepants
- 9.3.4 Ubrogepant
- 9.3.5 Pharmacokinetics
- 9.3.6 Efficacy
- 9.3.7 Safety
- 9.4 Rimegepant
- 9.4.1 Pharmacokinetics
- 9.4.2 Efficacy in acute treatment
- 9.4.3 Efficacy in migraine prevention
- 9.4.4 Safety
- 9.4.5 Lactation
- 9.5 Atogepant
- 9.5.1 Pharmacokinetics
- 9.5.2 Efficacy in prevention of episodic migraine
- 9.5.3 Efficacy in prevention of chronic migraine
- 9.5.4 Safety
- 9.6 Third-generation gepants
- 9.6.1 Zavegepant
- 9.6.2 Pharmacokinetics
- 9.6.3 Efficacy
- 9.6.4 Safety
- 9.7 Gepants in comparison with other treatment options.
- 9.7.1 Acute treatment
- 9.7.2 Preventive treatment
- 9.8 Conclusions
- 10 Anti-CGRP monoclonal antibodies
- 10.1 Mechanisms of action
- 10.2 Pharmacological properties
- 10.3 Findings from randomized placebo-controlled trials
- 10.3.1 Erenumab
- 10.3.2 Fremanezumab
- 10.3.3 Galcanezumab
- 10.3.4 Eptinezumab
- 10.4 Comparison with other preventive treatments
- 10.5 Insights from real-world studies
- 10.6 Predictors of response
- 10.7 Treatment discontinuation and restart
- 10.8 Switch between antibodies
- 10.9 Combination treatments
- 10.10 Treatment recommendations and specific populations
- 10.11 Patients with cardiovascular risk factors
- 10.12 Menstrual migraine
- 10.13 Pregnancy
- 11 Biomarkers of treatment response
- 11.1 Introduction
- 11.2 Acute medications
- 11.3 First-line oral preventive treatments
- 11.3.1 Clinical biomarkers
- 11.3.2 Genetic biomarkers
- 11.4 Botulinum toxin A
- 11.4.1 Clinical biomarkers
- 11.4.2 Molecular biomarkers
- 11.5 Treatments targeting the calcitonin gene-related peptide pathway
- 11.5.1 Clinical biomarkers
- 11.5.2 Molecular biomarkers
- 11.5.3 Genetic biomarkers
- 11.5.4 Vascular biomarkers
- 11.6 Conclusions
- Refrences
- 12 Migraine treatments: what have we learned from neuroimaging?
- 12.1 Introduction
- 12.2 Neuroimaging techniques
- 12.2.1 Nuclear imaging modalities
- 12.2.2 Magnetic resonance imaging
- 12.3 Study designs
- 12.4 Imaging studies of acute treatments
- 12.5 Imaging studies of pharmacological preventive treatments
- 12.6 Imaging studies of nonpharmacological preventive treatments
- 12.7 Conclusions
- 13 Migraine treatments: what have we learned from neurophysiology?
- 13.1 Introduction
- 13.2 Methods
- 13.3 Most frequently detected electrophysiological features of the migraine brain.
- 13.4 Electroencephalography studies.
- Notes:
- Description based on publisher supplied metadata and other sources.
- Part of the metadata in this record was created by AI, based on the text of the resource.
- ISBN:
- 0-443-23650-X
- 9780443236501
- OCLC:
- 1561173907
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