Association between lifestyle factors and headache

Modification of lifestyle habits is a key preventive strategy for many diseases. The role of lifestyle for the onset of headache in general and for specific headache types, such as migraine and tension-type headache (TTH), has been discussed for many years. Most results, however, were inconsistent and data on the association between lifestyle factors and probable headache forms are completely lacking. We evaluated the cross-sectional association between different lifestyle factors and headache subtypes using data from three different German cohorts. Information was assessed by standardized face-to-face interviews. Lifestyle factors included alcohol consumption, smoking status, physical activity and body mass index. According to the 2004 diagnostic criteria, we distinguished the following headache types: migraine, TTH and their probable forms. Regional variations of lifestyle factors were observed. In the age- and gender-adjusted logistic regression models, none of the lifestyle factors was statistically significant associated with migraine, TTH, and their probable headache forms. In addition, we found no association between headache subtypes and the health index representing the sum of individual lifestyle factors. The lifestyle factors such as alcohol consumption, smoking, physical activity and overweight seem to be unrelated to migraine and TTH prevalence. For a judgement on their role in the onset of new or first attacks of migraine or TTH (incident cases), prospective cohort studies are required

Bed sharing when parents do not smoke: is there a risk of SIDS? An individual level analysis of five major case-control studies.

OBJECTIVE: To resolve uncertainty as to the risk of Sudden Infant Death Syndrome (SIDS) associated with sleeping in bed with your baby if neither parent smokes and the baby is breastfed. DESIGN: Bed sharing was defined as sleeping with a baby in the parents' bed; room sharing as baby sleeping in the parents' room. Frequency of bed sharing during last sleep was compared between babies who died of SIDS and living control infants. Five large SIDS case-control datasets were combined. Missing data were imputed. Random effects logistic regression controlled for confounding factors. SETTING: Home sleeping arrangements of infants in 19 studies across the UK, Europe and Australasia. PARTICIPANTS: 1472 SIDS cases, and 4679 controls. Each study effectively included all cases, by standard criteria. Controls were randomly selected normal infants of similar age, time and place. RESULTS: In the combined dataset, 22.2% of cases and 9.6% of controls were bed sharing, adjusted OR (AOR) for all ages 2.7; 95% CI (1.4 to 5.3). Bed sharing risk decreased with increasing infant age. When neither parent smoked, and the baby was less than 3 months, breastfed and had no other risk factors, the AOR for bed sharing versus room sharing was 5.1 (2.3 to 11.4) and estimated absolute risk for these room sharing infants was very low (0.08 (0.05 to 0.14)/1000 live-births). This increased to 0.23 (0.11 to 0.43)/1000 when bed sharing. Smoking and alcohol use greatly increased bed sharing risk. CONCLUSIONS: Bed sharing for sleep when the parents do not smoke or take alcohol or drugs increases the risk of SIDS. Risks associated with bed sharing are greatly increased when combined with parental smoking, maternal alcohol consumption and/or drug use. A substantial reduction of SIDS rates could be achieved if parents avoided bed sharing

Leptomeningeal neurons are a common finding in infants and are increased in sudden infant death syndrome

Developmental abnormalities of the brain, in particular, the brainstem potentially affecting centers for breathing, circulation and sleep regulation, are thought to be involved in the etiology of sudden infant death syndrome (SIDS). In order to investigate whether leptomeningeal neurons could serve as morphological indicators for a developmental failure or retardation in cerebral maturation, we evaluated the density of isolated leptomeningeal neurons (without associated glia) in 15 brain regions of 24 SIDS and 8 control cases, representing part of the German Study on sudden infant death. Leptomeningeal neurons were encountered in 79% of SIDS and 68% of control cases. More leptomeningeal neurons in SIDS versus control cases were found in lower pons (p = 0.002), upper pons (p = 0.016), cerebellar hemispheres (p = 0.012), lower medulla oblongata (p = 0.039), and temporal lobe (p = 0.041). Summarizing the data according to gross anatomical region of origin (i.e., brainstem, cerebellum or cerebrum), higher numbers of leptomeningeal neurons in SIDS cases were only found in the brainstem (p = 0.006 vs. 0.13 and 0.19, respectively). Our data show that single leptomeningeal neurons are present in most normal infantile brains. The age-dependent increase of leptomeningeal neurons among SIDS cases may either (a) represent a delayed maturation or retardation, i.e., a later or slower reduction of neurons or a delayed peak in occurrence (shift toward an older age), or (b) may be interpreted as a generally increased occurrence of leptomeningeal neurons among SIDS cases as a result of a diffuse developmental abnormality during central nervous system maturation

Proposal for an international classification of SUDI : a response to Blair, Byard and Fleming

In 2009, Blair, Byard and Fleming, drawing on discussions between SIDS (sudden infant death syndrome) researchers and practitioners, proposed an international classification scheme for SUDI (sudden unexpected death in infancy) (Blair et al., 2009). as indicated in their proposal, the term SUDI incorporates a range of causes of death, both apparent and hidden. Whilst the proportion of SUDI for which a cause is found has risen, at least 50% remain unexplained in all published studies. Blair, Byard and Fleming point outthat, although an internationally agreed definition of SIDS exists, use of the term is inconsistent, and both practitioners and researchers often resort to alternative labels for those deaths that remain unexplained. Furthermore, approaches to the investigation of SUDI vary both between and within countries. These inconsistencies complicate research in the field, and potentially hamper our search for understanding of these deaths. Nevertheless they are a reality which will not go away

International comparison of sudden unexpected death in infancy rates using a newly proposed set of cause-of-death codes.

BackgroundComparing rates of sudden unexpected death in infancy (SUDI) in different countries and over time is difficult, as these deaths are certified differently in different countries, and, even within the same jurisdiction, changes in this death certification process have occurred over time.AimsTo identify if International Classification of Diseases-10 (ICD-10) codes are being applied differently in different countries, and to develop a more robust tool for international comparison of these types of deaths.MethodsUsage of six ICD-10 codes, which code for the majority of SUDI, was compared for the years 2002–2010 in eight high-income countries.ResultsThere was a great variability in how each country codes SUDI. For example, the proportion of SUDI coded as sudden infant death syndrome (R95) ranged from 32.6% in Japan to 72.5% in Germany. The proportion of deaths coded as accidental suffocation and strangulation in bed (W75) ranged from 1.1% in Germany to 31.7% in New Zealand. Japan was the only country to consistently use the R96 code, with 44.8% of SUDI attributed to that code. The lowest, overall, SUDI rate was seen in the Netherlands (0.19/1000 live births (LB)), and the highest in New Zealand (1.00/1000 LB). SUDI accounted for one-third to half of postneonatal mortality in 2002–2010 for all of the countries except for the Netherlands.ConclusionsThe proposed set of ICD-10 codes encompasses the codes used in different countries for most SUDI cases. Use of these codes will allow for better international comparisons and tracking of trends over time.</jats:sec