The 3rd edition of the International Classification of Headache Disorders (ICHD-3) may be reproduced freely for scientific, educational or clinical uses by institutions, societies or individuals. Otherwise, copyright belongs exclusively to the International Headache Society. Reproduction of any part or parts in any manner for commercial uses requires the Society’s permission, which will be granted on payment of a fee. Please contact the publisher at the address below. International Headache Society 2013–2018. Applications for copyright permissions should be submitted to Sage Publications Ltd, 1 Oliver’s Yard, 55 City Road, London EC1Y 1SP, United Kingdom (tel: þ44 (0) 207 324 8500; fax: þ44 (0) 207 324 8600; permissions@sagepub.co.uk) (www.uk.sagepub.com). Translations

Headache Classification Committee of the International Headache Society (IHS) The International Classification of Headache Disorders, 3rd edition

Sex, Gender, and Pain: A Review of Recent Clinical and Experimental Findings

4 CLINICAL PARTICULARS 4.1 Therapeutic Indications Trimetazidine is indicated in adults as add-on therapy for the symptomatic treatment of patients with stable angina pectoris who are inadequately controlled by or intolerant to first-line antianginal therapies. 4.2 Posology and method of administration Oral administration. Posology The dose is one tablet of 35mg of trimetazidine twice daily during meals. Special populations Renal impairment In patients with moderate renal impairment (creatinine clearance [30-60] ml/min) (see sections 4.4 and 5.2), the recommended dose is 1 tablet of 35mg in the morning during breakfast. Elderly Elderly patients may have increased trimetazidine exposure due to age-related decrease in renal function (see section 5.2). In patients with moderate renal impairment (creatinine clearance [30-60] ml/min), the recommended dose is 1 tablet of 35mg in the morning during breakfast. Dose titration in elderly patients should be exercised with caution (see section 4.4). Health Products Regulatory Authority

Summary of product characteristics

Plaguing humans for more than two millennia, manifest on every continent studied, and with more than one billion patients having an attack in any year, migraine stands as the sixth most common cause of disability on the planet. The pathophysiology of migraine has emerged from a historical consideration of the "humors" through mid-20th century distraction of the now defunct Vascular Theory to a clear place as a neurological disorder. It could be said there are three questions: why, how, and when? Why: migraine is largely accepted to be an inherited tendency for the brain to lose control of its inputs. How: the now classical trigeminal durovascular afferent pathway has been explored in laboratory and clinic; interrogated with immunohistochemistry to functional brain imaging to offer a roadmap of the attack. When: migraine attacks emerge due to a disorder of brain sensory processing that itself likely cycles, influenced by genetics and the environment. In the first, premonitory, phase that precedes headache, brain stem and diencephalic systems modulating afferent signals, light-photophobia or sound-phonophobia, begin to dysfunction and eventually to evolve to the pain phase and with time the resolution or postdromal phase. Understanding the biology of migraine through careful bench-based research has led to major classes of therapeutics being identified: triptans, serotonin 5-HT1B/1D receptor agonists; gepants, calcitonin gene-related peptide (CGRP) receptor antagonists; ditans, 5-HT1F receptor agonists, CGRP mechanisms monoclonal antibodies; and glurants, mGlu5 modulators; with the promise of more to come. Investment in understanding migraine has been very successful and leaves us at a new dawn, able to transform its impact on a global scale, as well as understand fundamental aspects of human biology.

Pathophysiology of Migraine: A Disorder of Sensory Processing

https://www.ahajournals.org/doi/pdf/10.1161/STR.0000000000000375

2021 Guideline for the Prevention of Stroke in Patients With Stroke and Transient Ischemic Attack: A Guideline From the American Heart Association/American Stroke Association

Objective
To develop and validate a questionnaire for assessing cutaneous allodynia (CA), and to estimate the prevalence and severity of CA in the migraine population.

Cutaneous allodynia in the migraine population.

Objective: The authors estimated the prevalence and severity of cutaneous allodynia (CA) in individuals with primary headaches from the general population. Methods: We mailed questionnaires to a random sample of 24,000 headache sufferers previously identified from the population. The questionnaire included the validated Allodynia Symptom Checklist (ASC) as well as measures of headache features, disability, and comorbidities. We modeled allodynia as an outcome using headache diagnosis, frequency and severity of headaches, and disability as predictor variables in logistic regression. Covariates included demographic variables, comorbidities, use of preventive medication, and use of opioids. Results: Complete surveys were returned by 16,573 individuals. The prevalence of CA of any severity (ASC score ≥3) varied with headache type. Prevalence was significantly higher in transformed migraine (TM, 68.3%) than in episodic migraine (63.2%, p Conclusions: Cutaneous allodynia (CA) is more common and more severe in transformed migraine and migraine than in other primary headaches. Among migraineurs, CA is associated with female sex, headache frequency, increased body mass index, disability, and depression.

/pdf/prevalence-and-characteristics-of-allodynia-in-headache-3cf69wz2a0.pdf

Prevalence and characteristics of allodynia in headache sufferers A population study

Objective: To evaluate the association between migraine without aura (MO) and migraine with aura (MA) and 3 types of structural brain abnormalities detected by MRI: white matter abnormalities (WMAs), infarct-like lesions (ILLs), and volumetric changes in gray and white matter (GM, WM) regions. Methods: PubMed as well as the reference lists of identified studies and reviews were used to identify potentially eligible studies through January 2013. Candidate studies were reviewed and eligible studies were abstracted. Pooled odds ratios (OR) and 95% confidence intervals (CI) were calculated for WMAs and ILLs. Results: Six population-based and 13 clinic-based studies were identified. The studies suggested that structural brain changes, including WMAs, silent ILLs, and volumetric changes in GM and WM regions, were more common in migraineurs than in control groups. The results were strongest for MA. The meta-analysis of WMAs showed an association for MA (OR 1.68; 95% CI 1.07–2.65; p = 0.03) but not for MO (OR 1.34; 95% CI 0.96–1.87; p = 0.08). The association of ILLs was greater for MA (OR 1.44; 95% CI 1.02–2.03; p = 0.04) than for MO, but no association was found for MA ( p = 0.52) and MO ( p = 0.08) compared to controls. Conclusion: These data suggest that migraine may be a risk factor for structural changes in the brain. Additional longitudinal studies are needed to determine the differential influence of migraine without and with aura, to better characterize the effects of attack frequency, and to assess longitudinal changes in brain structure and function.

/pdf/migraine-and-structural-changes-in-the-brain-a-systematic-3xrt9us34u.pdf

Migraine and structural changes in the brain A systematic review and meta-analysis

Post-dural puncture headache (PDPH) is a frequent complication of dural puncture whether performed for diagnostic purposes or accidentally, as a complication of anesthesia. Because both procedures are common, clinicians interested in headache should be familiar with this entity. The differential diagnosis of PDPH is broad and includes other complications of dural puncture as well as headaches attributable to the condition which lead to the procedure. The patterns of development of PDPH depend on a number of procedure- and nonprocedure-related risk factors. Knowledge of procedure-related factors supports interventions designed to reduce the incidence of PDPH. Finally, despite best preventive efforts, PDPH may still occur and be associated with significant morbidity. Therefore, it is important to know the management and prognosis of this disorder. In this review, we will highlight diagnosis and clinical characteristics of PDPH, differential diagnosis, frequency, and risk factors as well as pathophysiology of PDPH.

Post-dural puncture headache: part I diagnosis, epidemiology, etiology, and pathophysiology.

BackgroundWe assessed the prevalence of neck pain in the population in relation to headache.MethodsIn a cross-sectional study, a total of 797 individuals completed a headache interview and provided...

Sait Ashina

Papers

Cutaneous allodynia in the migraine population.

Prevalence and characteristics of allodynia in headache sufferers A population study

Migraine and structural changes in the brain A systematic review and meta-analysis

Post-dural puncture headache: part I diagnosis, epidemiology, etiology, and pathophysiology.

Prevalence of neck pain in migraine and tension-type headache: A population study