Chronic daily headache

Chronic daily headache relates to the daily or almost daily occurrence of headache in a nonparoxysmal pattern. In this review, I discuss the presentation, development, outcome, and treatment of chronic daily headache. In the context of the development of chronic daily headache, a headache continuum is presented along with its underlying pathophysiology. The treatment section covers rebound headache, analgesic and vasoconstrictor withdrawal, and the use of long-acting opioids in intractable patients. The review concludes with a discussion of hemicrania continua, an indomethacin-responsive headache syndrome

Agrarische arbeid 2010; Themaverkenning naar arbeidsvoorziening, arbeidsomstandigheden, arbeidskosten en sociale zekerheid in de land- en tuinbouw

Kwalitatieve verkenning van de belangrijkste ontwikkelingen en knelpunten op het gebied van arbeid in de land- en tuinbouw voor de komende tien tot vijftien jaar. Het onderzoek is gericht op de onderling samenhangende thema's arbeidsvoorziening, arbeidsomstandigheden, arbeidskosten en sociale zekerheid. De ontwikkeling wordt verkend tegen de achtergrond van te verwachten veranderingen op economisch, sociaal en technologisch gebied. Bij de arbeidsvoorziening zal arbeid meer als "human capital" worden beschouwd en neemt de concurrentie met andere bedrijfstakken toe. Wat de arbeidsomstandigheden betreft, zal de psychische belasting van zowel ondernemers als het personeel eerder toe- dan afnemen. Van betekenis is eveneens de verdere invoering van combizorg. Ten aanzien van arbeidskosten is op termijn sprake van hogere kosten per uur en geleidelijke productiviteitsgroei. Op het gebied van de sociale zekerheid speelt de tendens tot privatisering en de versterking van financiële prikkels. Tenslotte wordt ingegaan op aandachtspunten voor het beleid die samenhangen met hogere kwaliteitseisen aan arbeidsinhoud en arbeidsomstandigheden, flexibilisering van de arbeid en privatisering van de sociale zekerheid

Does Aneuploidy in the Brain Play a Role in Neurodegenerative Disease?

Aneuploidy, a state in which cells exhibit copy number changes of (parts of) chromosomes, is a hallmark of cancer cells and, when present in all cells, leads to miscarriages and congenital disorders, such as Down syndrome. In addition to these well-known roles of aneuploidy, chromosome copy number changes have also been reported in some studies to occur in neurons in healthy human brain and possibly even more in Alzheimer’s disease (AD). However, the studies of aneuploidy in the human brain are currently under debate as earlier findings, mostly based on in situ hybridization approaches, could not be reproduced by more recent single cell sequencing studies with a much higher resolution. Here, we review the various studies on the occurrence of aneuploidy in brain cells from normal individuals and Alzheimer’s patients. We discuss possible mechanisms for the origin of aneuploidy and the pros and cons of different techniques used to study aneuploidy in the brain, and we provide a future perspective

2000 Families: identifying the research potential of an origins - of migration study

Despite extensive recent advances in the empirical and theoretical study of migration, certain critical areas in the analysis of European migration remain relatively underdeveloped both theoretically and empirically. Specifically, we lack studies that both incorporate an origin comparison and trace processes of intergenerational transmission across migrants over multiple generations and incorporating family migration trajectories. This paper outlines the development, data and design of such a study, the 2000 Families study, framed within a theoretical perspective of ?dissimilation? from origins and over generations. We term the study an origins-of-migration study, in that it captures the country of origin, the family origins and potentially the originating causes of migration processes and outcomes. The resulting data comprised nearly 2,000 migrant and non-migrant Turkish families with members across three or more generations, covering. 50,000 individuals. We reflect on the potential of this study for migration research

Rapid Responders to Frovatriptan in Acute Migraine Treatment: Results from a Long-Term, Open-Label Study

Background. the Chronic Nature of Migraine and the Reliance on Acute Treatment Constitute the Basis of the Present Long-Term, Open-Label Study. Objectives. First, Assessment of the Tolerability and Safety of Frovatriptan, 2.5-7.5 Mg Taken Orally over 24 Hours, for the Acute Treatment of Migraine, Repeatedly over a 12-Month Period. Second, Assessment of the Efficacy and Tolerability of a Second, Double-Blind Dose of 2.5-Mg Frovatriptan, Compared with Placebo, for Nonresponse at 2 Hours after Treatment of Moderate or Severe Headache with 2.5-Mg Frovatriptan. Results. with Regard to the First Attack Treated, 173 (36%) of the 486 Subjects in the Study Did Not Take a Second Dose at 2 Hours for Nonresponse. at 2 Hours and 4 Hours, These Rapid Responders Experienced a Decrease in Headache Intensity from Moderate or Severe to Mild or No Pain in 84% and 98%, Respectively ( Headache Response ). Six Percent of Them Experienced Recurrence of Moderate or Severe Headache within 24 Hours Following a Response at 4 Hours and 12% Took Rescue Medication. the Response, Measured in Terms of Median Time to Complete Migraine Relief, Was Maintained over 30 Subsequent Migraine Attacks, Treated from Attack 2 Onwards over the Course of 12 Months. Conclusion. Frovatriptan Provides a Remarkably Fast and High Headache Response in a Subgroup of More Than One-Third of Migraineurs, with a Very Low 24-Hour Headache Recurrence and Low Rescue Medication Intake. © 2009 American Academy of Pain Medicine

Stress and psychological factors before a migraine attack: A time-based analysis

<p>Abstract</p> <p>Background</p> <p>The objective of this study is to examine the stress and mood changes of Japanese subjects over the 1–3 days before a migraine headache.</p> <p>Methods</p> <p>The study participants were 16 patients with migraines who consented to participate in this study. Each subject kept a headache diary four times a day for two weeks. They evaluated the number of stressful events, daily hassles, domestic and non-domestic stress, anxiety, depressive tendency and irritability by visual analog scales. The days were classified into migraine days, pre-migraine days, buffer days and control days based on the intensity of the headaches and accompanying symptoms, and a comparative study was conducted for each factor on the migraine days, pre-migraine days and control days.</p> <p>Results</p> <p>The stressful event value of pre-migraine days showed no significant difference compared to other days. The daily hassle value of pre-migraine days was the highest and was significantly higher than that of buffer days. In non-domestic stress, values on migraine days were significantly higher than on other days, and there was no significant difference between pre-migraine days and buffer days or between pre-migraine days and control days. There was no significant difference in the values of domestic stress between the categories. In non-domestic stress, values on migraine days were significantly higher than other days, and there was no significant difference between pre-migraine days and buffer days or between pre-migraine days and control days.</p> <p>There was little difference in sleep quality on migraine and pre-migraine days, but other psychological factors were higher on migraine days than on pre-migraine days.</p> <p>Conclusion</p> <p>Psychosocial stress preceding the onset of migraines by several days was suggested to play an important role in the occurrence of migraines. However, stress 2–3 days before a migraine attack was not so high as it has been reported to be in the United States and Europe. There was no significant difference in the values of psychological factors between pre-migraine days and other days.</p

A Uniform Genomic Minor Histocompatibility Antigen Typing Methodology and Database Designed to Facilitate Clinical Applications

BACKGROUND: Minor Histocompatibility (H) antigen mismatches significantly influence the outcome of HLA-matched allogeneic stem cell transplantation. The molecular identification of human H antigens is increasing rapidly. In parallel, clinical application of minor H antigen typing has gained interest. So far, relevant and simple tools to analyze the minor H antigens in a quick and reliable way are lacking. METHODOLOGY AND FINDINGS: We developed a uniform PCR with sequence-specific primers (PCR-SSP) for 10 different autosomal minor H antigens and H-Y. This genomic minor H antigen typing methodology allows easy incorporation in the routine HLA typing procedures. DNA from previously typed EBV-LCL was used to validate the methodology. To facilitate easy interpretation for clinical purposes, a minor H database named dbMinor (http://www.lumc.nl/dbminor) was developed. Input of the minor H antigen typing results subsequently provides all relevant information for a given patient/donor pair and additional information on the putative graft-versus-host, graft-versus-tumor and host-versus-graft reactivities. SIGNIFICANCE: A simple, uniform and rapid methodology was developed enabling determination of minor H antigen genotypes of all currently identified minor H antigens. A dbMinor database was developed to interpret the genomic typing for its potential clinical relevance. The combination of the minor H antigen genomic typing methodology with the online dbMinor database and applications facilitates the clinical application of minor H antigens anti-tumor targets after stem cell transplantation

Non-adjacent dependency learning in humans and other animals

International audienc

Centrosome defects cause microcephaly by activating the 53BP1-USP28-TP53 mitotic surveillance pathway

Mutations in centrosome genes deplete neural progenitor cells (NPCs) during brain development, causing microcephaly. While NPC attrition is linked to TP53-mediated cell death in several microcephaly models, how TP53 is activated remains unclear. In cultured cells, mitotic delays resulting from centrosome loss prevent the growth of unfit daughter cells by activating a pathway involving 53BP1, USP28, and TP53, termed the mitotic surveillance pathway. Whether this pathway is active in the developing brain is unknown. Here, we show that the depletion of centrosome proteins in NPCs prolongs mitosis and increases TP53-mediated apoptosis. Cell death after a delayed mitosis was rescued by inactivation of the mitotic surveillance pathway. Moreover, 53BP1 or USP28 deletion restored NPC proliferation and brain size without correcting the upstream centrosome defects or extended mitosis. By contrast, microcephaly caused by the loss of the non-centrosomal protein SMC5 is also TP53-dependent but is not rescued by loss of 53BP1 or USP28. Thus, we propose that mutations in centrosome genes cause microcephaly by delaying mitosis and pathologically activating the mitotic surveillance pathway in the developing brain