New Study Finds Human Beings Were Never Meant To Wake Up From Sleep

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BOSTON—According to a new study published in The New England Journal Of Medicine this week, human beings were never meant to wake up after falling asleep, but were rather supposed to remain in a deep, peaceful slumber until eventually expiring. “Our research team of evolutionary biologists conducted an extensive and thorough examination of human physiology, past and present, and determined that human beings were, in their ideal state, supposed to be born, spend a solid 12 hours awake as an infant, and then lie down for a tranquil, dream-filled sleep from which they would then not awaken,” 

http://www.theonion.com/articles/new-study-finds-human-beings-were-never-meant-to-w,34288/

Neurologists Implore Professional Athletes To Wait Until They Are Dead To Send In Brains For Research

What  day is it?

ST. PAUL—The American Academy of Neurology issued a statement this week urging professional athletes with suspected concussions to wait until they are deceased before sending in their brains for research. "We already have numerous brains to study, so please stop prying open your skulls with chisels and crowbars and scooping your brain matter into a mailing envelopes," said AAN president Bruce Sigsbee MD, adding that neurologists have also received the decapitated heads of 200 professional athletes who could not figure out how to remove their brains from their skulls.

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Seizures in Infants. What do seizures do to brain cells?

J Neuropathol Exp Neurol. 2014 Apr;73(4):324-34. doi: 10.1097/NEN.0000000000000056.

Correlation between clinical and histologic findings in the human neonatal hippocampus after perinatal asphyxia.

Schiering IA1, de Haan TR, Niermeijer JM, Koelman JH, Majoie CB, Reneman L, Aronica E.

Author information

Abstract

Hypoxic ischemic encephalopathy after perinatal asphyxia is a major cause of mortality and morbidity in infants. Here, we evaluated pathologic changes in the hippocampi of a cohort of 16 deceased full-term asphyxiated infants who died from January 2000 to January 2009. 

Histochemical and immunocytochemical results for glial and neuronal cells were compared between cases with or without seizures and to adult and sudden infant death syndrome cases (n = 3 each). All asphyxiated infants displayed neuronal cell damage and reactive glial changes. Strong aquaporin-4 immunoreactivity was seen on astroglial cells within hippocampi in 50% of cases. 

In patients with seizures, the expression of metabotropic glutamate receptors was increased in glial cells. Cases with seizures displayed increased microglial activation and greater expression of the inflammatory markers interleukin 1β and complement 1q compared with those in cases without seizures. 

All cases with seizures displayed alterations in the blood-brain barrier, as assessed by immunohistochemistry for albumin. These findings confirm the complex cascade of cellular and molecular changes occurring in the human neonatal hippocampus after perinatal asphyxia. These changes may contribute to seizure development leading to secondary brain damage. These data may aid in the development of therapeutic targets for neonatal seizures.

Why should non-ambulatory children get botox for cerebral palsy? It improves care.

I have performed botox injections as a rehabilitation technique since 2000. As the only neurologist in Houston who is a member of the AACPDM, I am often asked why I offer this procedure?

In non-ambulant children it makes a significant difference in quality of life.  

I lament the fear-mongering about adverse effects. While these events can happen, they are very rare. Almost all families return for repeat procedures. I see families who drive from Louisiana, Dallas and San Antonio who come every 3-4 months. 

Here is another article demonstrating efficacy without major adverse effects!

Dr. R

J Pediatr. 2014 Mar 12. pii: S0022-3476(14)00078-X. doi: 10.1016/j.jpeds.2014.01.050. [Epub ahead of print]

Botulinum Toxin A for Nonambulatory Children with Cerebral Palsy: 

A Double Blind Randomized Controlled Trial.

Copeland L1, Edwards P2, Thorley M2, Donaghey S2, Gascoigne-Pees L2, Kentish M2, Cert G2, Lindsley J2, McLennan K2, Sakzewski L3, Boyd RN3.

Author information

Abstract

OBJECTIVES:

To examine the efficacy and safety of intramuscular botulinum toxin A (BoNT-A) to reduce spasticity and improve comfort and ease of care in nonambulant children with cerebral palsy (CP).

STUDY DESIGN:

Nonambulant children with CP (n = 41; Gross Motor Function Classification System level IV = 3, level V = 38; mean age 7.1 years, range 2.3-16 years, 66% male) were randomly allocated to receive either intramuscular BoNT-A injections (n = 23) or sham procedure (n = 18) combined with therapy. The analysis used generalized estimating equations with primary outcome the Canadian Occupational Performance Measure (COPM) at 4 weeks postintervention and retention of effects at 16 weeks. Adverse events (AE) were collected at 2, 4, and 16 weeks by a physician masked to group allocation.

RESULTS:

There were significant between group differences favoring the BoNT-A-treated group on COPM performance at 4 weeks (estimated mean difference 2.2, 95% CI 0.8, 3.5; P = .002) and for COPM satisfaction (estimated mean difference 2.2, 95% CI 0.5, 3.9; P = .01). These effects were retained at 16 weeks for COPM satisfaction (estimated mean difference 1.8, 95% CI 0.1, 3.5; P = .04). There were more mild AE at 4 weeks for the BoNT-A group (P = .002), however, there were no significant between-group differences in the reporting of moderate and serious AE.

CONCLUSIONS:

In a double-blind randomized sham-controlled trial, intramuscular BoNT-A and therapy were effective for improving ease of care and comfort for nonambulant children with CP. There was no increase in moderate and severe AE in the children who had BoNT-A injections compared with the sham group.

Crown Copyright © 2014. Published by Mosby, Inc. All rights reserved.

Brain impairment and Restless Legs Syndrome

Those who have Restless Legs Syndrome also seem to have implicated early brain development.

In a study published online in Genome Research, researchers of the Helmholtz Zentrum München und the Technische Universität München have demonstrated that a common genetic variant associated with Restless Legs Syndrome (RLS) alters the expression of a critical gene during fetal development of the brain. This leads to alterations of the developing forebrain indicating an anatomical region involved in RLS.

Restless Legs Syndrome (RLS), a neurological disorder characterized by unpleasant sensations in the legs and the urge to move them, is not caused by a single genetic defect, but rather is a complex disorder influenced by many genetic and environmental components. Previously, researchers identified genetic variants in RLS patients; however, how these variants, each of which only has a small effect, contributed to RLS was unclear.

MEIS1 gene variant leads to altered development of the brain

In this new study, authors from the Helmholtz Zentrum München (HMGU) and Technische Universität München as well as the Stanford Center for Sleep Medicine and Sciences demonstrate how one of these variants may contribute to RLS. The RLS-associated variant is located in a non-coding region of the MEIS1 gene and led to decreased ability to activate gene expression. Specifically, the authors observed the reduced gene expression in the future basal ganglia in the forebrain. "Here we have pinpointed down to an anatomical region for RLS," says lead author of the study, Prof. Juliane Winkelmann from HMGU, who is currently doing research at the Stanford University.

"The RLS-associated variant is located in an intron of MEIS1, a transcription factor involved in organ development and maintenance. The risk variant binds more strongly to the transcriptional regulator CREB1, which may lead to the reduced MEIS1 expression," explains Prof. Dr. Wolfgang Wurst from HMGU. Furthermore, screening analyses in animal models with reduced MEIS1 expression, conducted by the Institute of Experimental Genetics at the HMGU, led by Prof. Dr. Martin Hrabě de Angelis, showed hyperactivity, which resembles the human condition of RLS.

Reduced gene activity predisposition for RLS

Interestingly, the non-coding region only seems to be active during early brain development, suggesting that RLS, which is associated with aging, may have fetal origins. "Minor alterations in the developing forebrain during early embryonic development are probably leading to a predisposition to RLS," Winkelmann said. "Later in life, during aging, and together with environmental factors, these may lead to the manifestation of the disease."

In further studies researchers aim to investigate the affected cells in the forebrain. Based on their findings new treatment strategies for RLS may be developed.

This study provides one of the first in-depth examinations of a genetic variant identified in a genome-wide association study, which examines many individuals for genetic variants that are linked to a trait. Although many variants are often reported in these studies, it has been difficult understand how variants contribute to disease because they often lie in non-coding regions of the genome and have small effect sizes. This work also reveals that combinatorial use of multiple approaches will be likely required to unravel the physiological causes most of human diseases.

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Rise in autism cases may be due to rising awareness

This article claims that the rise seen in autism cases may be due to rising awareness of the condition.

Young boys continue to have the highest rate of autism diagnoses, but Danish doctors are diagnosing more girls, teenagers and adults with the disorder than they did in the mid-1990s. That's the finding from a 16-year study published 20 February in the Journal of Autism and Developmental Disorders.

Many studies look at the prevalence of autism, akin to taking a snapshot of the number of diagnoses in a given population. The new study instead examined the disorder's incidence, or newly reported diagnoses, each year.

Between 1995 and 2010, nearly 15,000 people received a new diagnosis of autism in Denmark, the study found. During that time, the incidence of autism overall increased from 9 diagnoses per 100,000 people to 38.6.

"We know that the incidence rates of autism spectrum disorders have increased in the last two decades, so we weren't actually surprised about the increases," says principal investigator Marlene Lauritsen, associate professor of child and adolescent psychiatry at Aalborg University in Denmark. "But we were surprised about most of the patients we saw the largest increases in."

For instance, the number of males with a new autism diagnosis quadrupled from 13.2 per 100,000 people in 1995 to 58 in 2010. In the same time period, female diagnoses increased sevenfold from 2.6 to 18.6 per 100,000 people.

The greatest increase in incidence among girls came from diagnoses of two subcategories of autism, Asperger syndrome and pervasive developmental disorder-not otherwise specified (PDD-NOS). Both categories are being subsumed into the autism diagnosis in the newest edition of the Diagnostic and Statistical Manual (DSM-5), the American Psychiatric Association's guidelines for diagnosis. And both are generally thought to represent the higher-functioning end of the autism spectrum.

"That is in a way interesting because it goes against the idea that girls are always more severely afflicted [than boys]," says Eric Fombonne, professor of psychiatry at Oregon Health and Science University, who was not involved in the research.

Incidence inquiry:

The researchers examined records from the Danish Psychiatric Central Research Registry, which contains reports on inpatient and outpatient care and diagnoses in Denmark.

To standardize the definition of autism spectrum disorders in the study, the researchers included only people up to 65 years of age who were diagnosed by a doctor using the tenth edition of the International Classification of Diseases, a publication of the World Health Organization and the DSM-5's international counterpart. The ICD-10 was last revised in 1994 and still lists Asperger syndrome and PDD-NOS as diagnoses independent of autism. Its next edition is expected in 2017.

Boys are diagnosed more often than girls and at younger ages, the study found. On average, boys receive a diagnosis at 9 years versus an average of 11 years for girls.

In boys, the sharpest uptick over the study period is in childhood autism -- a subtype of the disorder in which symptoms appear before 3 years of age -- from 2.1 cases for every 100,000 people in 1995 to 17.6 in 2010. Another spike is in rates for PDD-NOS, which increased fivefold to 25.8 per 100,000.

In girls, new cases of PDD-NOS showed the steepest gains, jumping 11-fold from 0.8 cases to 9.3 per 100,000 people. Diagnoses of Asperger syndrome increased from 0.6 cases per 100,000 in 1995 to 5.8 in 2010.

Better diagnostic practices may explain these large hikes in incidence, says Maureen Durkin, professor of population health sciences and pediatrics at the University of Wisconsin in Madison.

"There's much more awareness of autism," say Durkin, who was not involved in the study. "There's much more screening going on. And the newer generation of clinicians are being trained in this so they are more likely to see it."

This increased attention to autism and its symptoms may also explain the rise in diagnoses of teenagers and adults.

An age-stratified analysis shows that children between the ages of 4 and 13 make up about 63 percent of the new autism cases. The fastest acceleration in new cases is in those diagnosed between 14 and 20 years of age.

Individuals diagnosed between 21 and 65 years of age account for about 9 percent of the new cases -- but their proportion also significantly increased over the time frame of the study. Like girls, many of the adults are diagnosed with higher-functioning forms of autism, such as Asperger syndrome and PDD-NOS.

"If the incidence [in adults] is increasing, it just has to do with recognition of cases that have been missed up to that age," Fombonne says. "It cannot be that you develop autism at age 50."

Overall, PDD-NOS diagnoses show steep growth, just behind childhood autism. However, Lauritsen says, PDD-NOS is not as well defined as other autism subtypes such as Asperger syndrome.

"In [PDD-NOS], you can have children that we think are on the border of the autism spectrum," she says. "We could think they are socially impaired, but it's not quite clear that it's autistic behavior."

Individuals diagnosed with PDD-NOS often have social deficits but lack repetitive behaviors, a core symptom of autism. Studies suggest that under DSM-5 guidelines, some people with PDD-NOS would fall into a new category called social communication disorder rather than autism.

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In rats, brain damage occurs with no signs of concussion

Brain damage is seen in rats after repeated "subconcussive" brain trauma, or a head injury that shows no concussion symptoms.

A standard experimental model of concussion in rats causes substantial brain damage -- but no behavioral changes comparable to those seen in patients with concussion, reports a study in the April issue of Neurosurgery, official journal of the Congress of Neurological Surgeons. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.

The results highlight the "disconnect" between preclinical and clinical studies of concussion, according to the report by Dr. Charles L. Rosen of West Virginia University, Morgantown, and colleagues. The study also adds to concerns over the possible long-term effects of repeated, "subconcussive" brain trauma -- causing no concussion symptoms -- in humans.

Despite Diffuse Brain Damage, No Signs of 'Concussion' in Rats

Concussions are thought to be a form of "mild traumatic brain injury." However, there is no definitive diagnostic test to determine when a concussion has occurred. Instead, concussion is diagnosed on the basis of symptoms such as headache, nausea, dizziness, and confusion.

In contrast, animal studies of concussion have focused on directly observed injury to brain tissues, with little attention to the possible behavioral and functional consequences of the brain trauma. Thus there is a "clear disconnect" between experimental and clinical studies of concussion, according to Dr. Rosen and colleagues.

To address this discrepancy, they used a standard technique, called the "impact-acceleration model," to induce brain injury in rats. As reported by previous studies, this technique caused "diffuse axonal injury" to the brain, with visible evidence of damage on the cellular level.

The researchers also compared injured and uninjured animals on a wide range of functional and behavioral tests. The tests were chosen to reflect symptoms and functions similar to those used to diagnose concussion in humans -- for example, locomotor activity, coordination/balance, cognitive function, and anxiety- and depression-like behaviors.

But despite a rather extensive pattern of brain injury, the rats had no significant abnormalities on any of the tests. That was so on the day after brain injury as well as up to one week afterward. "The lack of functional deficits is in sharp contrast to neuropathological findings indicating neural degeneration, astrocyte reactivity, and microglial activation." Dr. Rosen and colleagues write.

Findings Support Concerns about 'Subconcussive Injury'

The new study comes at a time when new researchers are finding evidence of long-term neurodegenerative changes in the brains of people who have never been diagnosed with a concussion. One key study in high school football players found changes in neurological function and health in athletes who never had concussion symptoms, but had sustained "repetitive subconcussive blows."

Traditionally, concussion has been regarded as a temporary problem that resolves with no long-term effects. But that view has changed in recent years, with studies in athletes and others showing chronic traumatic encephalopathy linked to repetitive head injury -- both the concussive and subconcussive types.

The new experiments support the concept that significant brain damage may be present in individuals who have completely normal results on symptom-based assessments currently used to diagnose concussions. Dr. Rosen and coauthors write, "It appears that even subconcussive injury, or injury below the current clinical threshold for detection using standard measures, may have lasting neurological effects."

The researchers emphasize that their short-term study in rats provides no direct evidence of long-term changes caused by "mild" traumatic brain injury in humans. They discuss the need for further research to clarify the effects of traumatic brain injury over time, and to develop new models for understanding the long-term impact of repeated head trauma.

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Girls naturally more protected from autism development

This article explains why boys are four times more likely to develop autism and explains why girls may be naturally more protected from developing autism.

It takes more mutations to trigger autism in women than in men, which may explain why men are four times more likely to have the disorder, according to a study published 26 February in the American Journal of Human Genetics.

The study found that women with autism or developmental delay tend to have more large disruptions in their genomes than do men with the disorder. Inherited mutations are also more likely to be passed down from unaffected mothers than from fathers.

Together, the results suggest that women are resistant to mutations that contribute to autism.

"This strongly argues that females are protected from autism and developmental delay and require more mutational load, or more mutational hits that are severe, in order to push them over the threshold," says lead researcher Evan Eichler, professor of genome sciences at the University of Washington in Seattle. "Males on the other hand are kind of the canary in the mineshaft, so to speak, and they are much less robust."

The findings bolster those from previous studies, but don't explain what confers protection against autism in women. The fact that autism is difficult to diagnose in girls may mean that studies enroll only those girls who are severely affected and who may therefore have the most mutations, researchers note.

"The authors are geneticists, and the genetics is terrific," says David Skuse, professor of behavioral and brain sciences at University College London, who was not involved in the study. "But the questions about ascertainment are not addressed adequately."

Genetic burden:

The new study draws from the Simons Simplex Collection (SSC), a database of families that have one child with autism and unaffected parents and siblings. (This project is funded by the Simons Foundation, SFARI.org's parent organization.) In a 2011 study, researchers found that girls with autism in the SSC tend to have more large duplications or deletions of regions of the genome, called copy number variants (CNVs), than do boys with the disorder, although this disparity does not reach statistical significance2.

For the new study, Eichler and his colleagues cataloged the number of CNVs in 109 girls and 653 boys with autism from the SSC. They found that females are twice as likely as males to carry CNVs that are at least 400 kilobases long. (The larger the CNV, the more likely it is to disrupt important genes.)

When the researchers analyzed only CNVs that encompass risk genes for neurodevelopmental disorders, they found that females with autism are three times as likely as males with the disorder to carry CNVs that encompass these genes.

Females with autism also carry slightly more rare mutations that change a single DNA nucleotide than the men do. These are the "nastiest of nasty mutations," says Eichler, because they interfere with the protein's function.

The researchers saw a similar but smaller effect for CNVs in a larger group of 9,206 males and 6,379 females referred for genetic testing: 75 percent of this group turned out to have developmental delay, intellectual disability or autism.

Women in this group are 1.28 times more likely than men to carry large CNVs that include risk factors for these disorders.

Many autism-linked mutations arise spontaneously, or de novo, and about 80 percent of these come from the father.

Eichler and his colleagues found that women are far more likely than men to transmit the inherited mutations that confer autism risk.

Of the 27 large CNVs the researchers identified in the SSC group, 70 percent, or 19, were inherited from the mother. Mothers had similarly passed down about 57 percent of the 3,561 CNVs detected in the neurodevelopmental group.

Eichler intends to extend this work in a bigger study to assess whether certain mutations are more likely than others to be inherited.

"I think it's really critical to identify these inherited components," he says. "We know they're there, but we need to really focus on identifying the specific genes so we can advise [parents] a little more about recurrence."

However, it's unclear whether this gender bias is the result of genetics or reflects differences in diagnosis or the way females manifest symptoms of the disorder. Girls with autism tend to actively compensate for their symptoms in ways that boys don't, which may account for the discrepancy, says Skuse.

As a result, the females enrolled in studies may tend to be severely affected and carry multiple mutations. "There is some suggestion that higher-functioning females are out there in the general population, but they're not being referred," he says.

The study also does not address why women with autism transmit more mutations, or how they are protected from autism.

"We need to ask what it is about brain development that makes it such that females are protected -- because ultimately that is what we want know," says Aravinda Chakravarti, director of the Center for Complex Disease Genomics at the Johns Hopkins University School of Medicine in Baltimore. "We need to re-create that developmental environment."

The most obvious explanation for autism's gender bias is that because men have only one X chromosome, they are hypersensitive to mutations in this chromosome. In line with this theory, several autism-linked genes are located on the X chromosome. However, most of the mutations that show a gender bias in the new study are not on the X chromosome, suggesting that other factors must be involved.

This article has been modified from the original. An earlier version incorrectly stated that 80 percent of the genetic risk factors for autism arise spontaneously. The exact contribution of spontaneous genetic variants to autism is not known.

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ADHD medication use leads to BMI rebound

A study of ADHD stimulant medication shows that its use is associated with BMI rebound later in adolescence.

A new study from researchers at Johns Hopkins Bloomberg School of Public Health found that children treated with stimulants for attention deficit hyperactivity disorder (ADHD) experienced slower body mass index (BMI) growth than their undiagnosed or untreated peers, followed by a rapid rebound of BMI that exceeded that of children with no history of ADHD or stimulant use and that could continue to obesity.

The study, thought to be the most comprehensive analysis of ADHD and stimulant use in children to date, found that the earlier the medication began, and the longer the medication was taken, the slower the BMI growth in earlier childhood but the more rapid the BMI rebound in late adolescence, typically after discontinuation of medication. Researchers concluded that stimulant use, and not a diagnosis of ADHD, was associated with higher BMI and obesity. The study was published in Pediatrics.

"Our findings should motivate greater attention to the possibility that longer-term stimulant use plays a role in the development of obesity in children," said Brian S. Schwartz, MD, MS, Professor of Environmental Health Sciences, Epidemiology, and Medicine at the Bloomberg School of Public Health and lead author of the study. "Given the dramatic rise in ADHD diagnosis and stimulant treatment for it in recent decades, this is an interesting avenue of research regarding the childhood obesity epidemic, because the rises in each of these roughly parallel one another."

Previous research has found substantial evidence that stimulant use to treat ADHD is associated with growth deficits, and some evidence of growth delays. However, the reported associations of ADHD with obesity in both childhood and adulthood was paradoxical and somewhat unexplained. The results of this study suggest it is likely due to the strong influence that stimulants have on BMI growth, with delays in early childhood and a strong rebound in late adolescence. The study also found longitudinal evidence that unmedicated ADHD is associated with higher BMIs, but these effects were small.

ADHD is one of the most common pediatric disorders, with a 9% prevalence among children in the U.S., and ADHD medication is the second most prescribed treatment among children. Over the past 30 years, treatment for ADHD with stimulants has increased rapidly. From 2007 to 2010, 4.2.% of children under age 18 had been prescribed stimulants in the past 30 days, more than five times the amount prescribed to the same-aged children between 1988 and 1984.

The study analyzed the electronic health records of 163,820 children, ages 3 to 18, in the Geisinger Health System, a Pennsylvania-based integrated health services organization. The research geographic area included 37 counties in central and northeastern Pennsylvania. There were an equal number of boys and girls. Nearly 7% -- 11,080, or 6.8% -- had an order for stimulants. (13,789, or 8.4%, received a diagnosis of ADHD. A total of 15,473 were prescribed stimulants, some for other reasons.) There were 201,854 orders for the ADHD medications used in the analysis. The median age at first stimulant use was 8.5 years. Median use was 183 days, with 50% of children taking stimulants for less than 6 months and 50% of children for more than 6 months.

The researchers compared the BMI trajectories of those who had never had a diagnosis or prescription (the "controls") with three groups: 1.) those with a diagnosis but no stimulant prescription; 2.) those with orders for stimulants without an ADHD diagnosis and 3.) those with both an ADHD diagnosis and stimulant orders.

Those in group 3 had slower rates of BMI growth in early childhood, with more rapid rates during adolescence that eventually exceeded those of the controls. Those with a diagnosis of ADHD but no stimulant orders had more rapid BMI growth after age 10 versus the controls, but the effects were small.

"Stimulant use was strongly implicated," said Dr. Schwartz. "The earlier stimulants were started and the longer they were used, the stronger was their influence on the degree of both the delayed BMI growth in early childhood and the rebound BMI growth in late adolescence. This is an important unintended consequence of stimulant use in childhood."

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Sleep necessary for mental health and well-being

This article discusses how crucial good sleep is for a person's mental health and well-being, and the consequences of not having good quality sleep.

Having a good quality and restorative sleep is essential for one to be able to function well throughout the day. Failure to do so will lead to numerous impacts to health, both long- and short-term.

According to the Sleep Disorder Society Malaysia (SDSM) president Dr Muhammad Muhsin Ahmad Zahari, some of the short-term negative impacts include short attention span, memory recall and learning; while its long-term effects have long been associated with hypertension, ischaemic heart disease, stroke, obesity, diabetes, weakened immune system, and cancer.

Dr Muhammad Muhsin added that sleep disorder can also increase the risk of accidents.

"People who suffer from insomnia are seven times more likely to become involved in an accident which then resulted in death or serious injury," he said at the launch of the `World Sleep Day Celebration and Sleep 2014 Conference' at Cititel Hotel, here, today.

He revealed that sleep disorder actually constitute a global epidemic that threatens health and quality of life for up to 45% of the world's population, thus it is essential for everyone to have a better understanding of sleep conditions.

"Sleep is a basic human need and it is crucial not only to our health and well-being, it also plays an important role in the metabolic regulation in children," said Dr Muhammad adding that SDSM is working closely with the relevant authorities, associations and organisations in improving the quality of service of sleep medicine.

"With regards to the quality service in sleep medicine, facilities such as sleep laboratory are vital. As our population grows, there is definitely a need to increase the number of sleep laboratory in public hospitals to cater to the need of the people." he added.

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Autism and the environment

A study discusses how environmental factors may increase a person's risk of developing autism.

A large U.S. study suggests environmental pollution might be contributing to autism risk, although the specific culprit toxins remain unknown.

Researchers analyzed medical records and found a correlation between U.S. counties' autism rates and their rates of genital birth defects in boys, which could be a sign of some common environmental contributors.

However, the findings, which were reported March 13 in the journal PLoS Computational Biology, do not prove that any particular environmental exposure directly raises the risk for the developmental disorder, experts said.

There's no "smoking gun," said Alycia Halladay, senior director of environmental and clinical sciences for the advocacy group Autism Speaks.

"This study was not designed to figure out what the [environmental] factors are," said Halladay, who was not involved in the research.

Still, she said, experts believe autism arises from a combination of genetic vulnerability and any number of environmental exposures. Some suspects include infections such as flu during pregnancy, certain prescription drugs taken during pregnancy and environmental toxins.

These latest findings support the "scientific agreement that it's a mix of genes and environment," Halladay said.

The lead researcher on the study agreed. "Both genes and environment are important," said Andrey Rzhetsky, a professor of genetic medicine at the University of Chicago.

The task ahead, Rzhetsky said, is to figure out which environmental exposures matter.

Autism refers to a collection of disorders, usually diagnosed during childhood, that affect language and social skills.

For the study, Rzhetsky's team analyzed nearly 100 million U.S. health insurance claims for a county-by-county look at rates of autism and intellectual disability. They also examined rates of genital malformations in boys -- such as micropenis, undescended testicles and hypospadias (in which the urethral opening is on the underside of the penis).

Those genital malformations were used as an indicator of parents' exposure to environmental pollutants, Rzhetsky said. The exact causes of those birth defects are not clear, but some studies have suggested that certain environmental toxins -- including pesticides and lead -- might play a role, he said.

In this study, county rates of genital birth defects ranged from none to just over 2 percent. Overall, the researchers found, for every 1 percent increase in those birth defects, the rate of autism rose by close to 300 percent.

Even accounting for county demographics, a strong link existed between rates of genital defects and autism, Rzhetsky said.

But the reasons for the correlation aren't clear. Genes could play some role, Rzhetsky said, and so could environmental factors other than pollutants.

Halladay said endocrine disruptors -- chemicals found in plastics, food cans and other everyday products -- have been linked to genital birth defects. But so far, researchers haven't found a connection to autism risk.

On the other hand, some studies have found a link between high exposure to air pollution during pregnancy and an increased autism risk, Halladay said.

Researchers continue to look for the environmental players in autism, Halladay said. Autism Speaks has a program that funds research on the environmental factors -- including toxic exposures and nutrition during pregnancy -- that might affect autism risk.

Rzhetsky said he hopes his team's findings help fuel the interest in that type of research. "There is a lot of research focused on the genetics," he said. "But environment plays a big role."

But chemicals in the environment are only one potential reason autism rates vary across the United States.

Rzhetsky's team also found lower rates of autism in states where regulations require a doctor's diagnosis of autism before kids can qualify for special education.

Halladay said the finding is consistent with past studies suggesting that differences in diagnosis help explain regional differences in autism rates.

A 2012 study from the U.S. Centers for Disease Control and Prevention found that one in 88 U.S. children had an autism spectrum disorder -- up almost 25 percent from just a few years before. But the rate varied widely, from one in 47 in Utah to one in 210 in Alabama.

Experts speculated that the national increase had a lot to do with better detection, and that differences in awareness and autism services might explain the regional differences.

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Sea lions have form of epilepsy similar to humans

Researchers find that some sea lions have a form of epilepsy that is similar to epilepsy seen in humans.

California sea lions exposed to a toxin in algae develop a form of epilepsy that is similar to one in humans, according to a new study led by Stanford University School of Medicine researchers.

Every year, hundreds of sea lions wash up along the California coast, suffering seizures caused by exposure to domoic acid, a neurotoxin that can produce memory loss, tremors, convulsions and death. Domoic acid is produced by algae blooms that have been proliferating along the coast in recent years, accumulating in anchovies and other small fish that the sea lions feed on, said Paul Buckmaster, PhD, DVM, professor of comparative medicine at Stanford.

Buckmaster and his colleagues studied the brains of affected sea lions and found they had a pattern of damage in the hippocampus -- the brain's memory center -- much like that in humans with temporal lobe epilepsy.

"We found there was a loss of neurons in specific patterns that closely matched what is found in people," he said. "And there is synaptic reorganization -- a rewiring of surviving neurons. This also matches what is found in humans with temporal lobe epilepsy."

He said further studies in the animals could help in developing better treatments for them, as well as for their human counterparts.

Buckmaster is lead author of the study, which will be published online March 19 in the Journal of Comparative Neurology.

Temporal lobe epilepsy is one of the most common forms of epilepsy in humans and has no cure. It typically begins with a seizure caused by an insult to the brain, such as head trauma, high fever or lack of oxygen. Months or years later, it progresses into epilepsy, with periodic seizures that may be treated with anti-convulsive medication or, in some cases, surgery.

There is one documented case of a patient who was found to have developed temporal lobe epilepsy following exposure to domoic acid. The 84-year-old Canadian was one of more 250 people who became ill in 1987 after eating mussels from Prince Edward Island that were found to be contaminated with domoic acid. The man, who suffered nausea, vomiting, coma and convulsions, initially recovered but was diagnosed a year later with temporal lobe epilepsy; he died some two years later of pneumonia. Three other Canadians died in the mussel incident as a result of domoic acid poisoning.

In sea lions, the first link between domoic acid and epilepsy was established in 1998, when some 400 animals washed ashore in California's Monterey Bay on Memorial Day weekend. Some had died, while others were in the throes of seizures, weaving their heads, flailing about and scratching themselves in an odd way. About 100 of the animals were rescued by the Marine Mammal Center in Sausalito, where experts were at a loss to explain the animals' bizarre behavior, said Frances Gulland, PhD, DVM, senior scientist at the center and co-author of the current study.

She contacted Christopher Scholin, PhD, now president of the Monterey Bay Aquarium Research Institute, who discovered the bay waters had the highest levels of domoic acid ever recorded, she said. Blood and urine samples from the sea lions confirmed they had domoic acid poisoning. The researchers documented their findings in a 2000 Nature paper.

Since then, Gulland said a few hundred sea lions with epilepsy have been rescued every year by the mammal center, and about half respond to treatment with anti-convulsive therapy. But some suffer from seizures that may continue for hours, causing extensive brain damage. These animals have no hope for recovery and have to be euthanized.

In these cases, mammal center officials turn to Buckmaster, a veterinarian who is an expert in epilepsy in animals. For the past four years, he has been working on studies of the epileptic sea lions, examining samples of their brain tissue to better understand what underlies the disease.

In the current study, he and his colleagues retrieved samples of tissue from the hippocampus, which they cut into thin slices and then stained so that the neurons could be viewed under a microscope. They collected tissues from 14 sea lions with epilepsy and compared them with similar samples from nine without epilepsy who had died of other causes, such as cancer, infection or shark bite wounds.

The animals with epilepsy had lost about 50 percent of the neurons in the hippocampus, similar to what is seen in people with temporal lobe epilepsy, Buckmaster said. The researchers observed another striking similarity: In most cases, the hippocampus on only one side of the brain in the sea lions showed any signs of damage.

"That was really surprising," Buckmaster said. "That is what you find in people -- 80 percent of the time the damage is just on one side."

In rats and mice, which are the models typically used in epilepsy studies, injury is seen in the hippocampus of both sides of the brain, he said.

The results are curious, as sea lions ingest the toxin throughout their bodies, he said. "Why would there be damage only on one side?"

He speculated that it could be related to the size and structure of the brain. Like the human brain, the sea lion brain is significantly larger than a rodent brain -- 700 times larger than a mouse brain and 180 times larger than a rat brain -- and contains many more neurons. However, the average number of synapses -- connections between nerve cells -- per neuron is roughly the same in rodents and humans. Without more synapses for each neuron, the probability of any two neurons in the large brain being connected must be lower than it is in the small brain, Buckmaster surmised. So this relative lack of interconnectivity in human and sea lion brains could be why damage remains localized to a specific area, he said. (The number of synapses hasn't been measured in sea lions, though it seems reasonable to speculate that they would have a similar ratio of synapses per neuron, he said.)

The researchers also noticed a pattern of rewiring in the brains of the epileptic sea lions that is similar to that in humans with temporal lobe epilepsy. Among the neurons that survived the assault by domoic acid, some of the axons -- the nerve fibers that carry electrical impulses away from the neuron -- extended into a region of the hippocampus where they don't normally grow. That creates a kind of positive feedback loop in which the cells are exciting themselves, which might contribute to more seizure activity, Buckmaster said.

"We see this in people with temporal lobe epilepsy," he said. "It's one of the key neuropathological features of the disease."

Because of these similarities, he said the sea lions could serve as good models for developing new treatments for the disease. Patients typically are treated with daily, anti-convulsive drugs, or in some cases with surgery in which doctors remove a portion of the hippocampus -- an invasive procedure that often causes some memory loss.

The ultimate goal, he said, is to develop a therapy that could be used early on to forestall brain damage and prevent further seizures.

"What we need is an interventional treatment -- both in humans and sea lions," he said. "You'd give the treatment right after the brain injury, and that would prevent them from developing epilepsy. That's the dream, but we are not there yet."

Gulland said the research has been a valuable contribution to the field. "For us, the work Dr. Buckmaster has done is really important because it shows the sea lions are really epileptic," she said. "We used to think if they had just a small amount of the poison, they could recover and be fine. But if the seizure has gone on for any length of time, they become permanently affected. It's very distressing to the animals and to the people who work with them to see them coming back having seizure after seizure."

Buckmaster is now planning new studies of the sea lions using the entire brain, fully preserved right after the animals' death so the "beautiful anatomy" of various structures is visible.

"We will be able to see areas of brain damage we have never seen before," he said. "Based on the hippocampus results, there's a good chance it will be similar to people."

He also has a grant to study the effects of in utero exposure to domoic acid. Some of the sea lions in the study were younger animals thought to be exposed before birth, as domoic acid can concentrate in amniotic fluid at a time when the nervous system is developing, Buckmaster said. The mammal center has treated three pups from mothers that were exposed to domoic acid in pregnancy, two of whom developed epilepsy later in life. It's believed that humans could be susceptible to in utero damage from the toxin as well, he said.

Meanwhile, the problem of marine mammal exposure to domoic acid is not likely to go away anytime soon. The harmful algae blooms, believed to be produced by micronutrients contained in agricultural runoff, have been increasing in frequency along the California coast and are lasting longer, sometimes for months at a time, Gulland said.

And while sea lions may be the most visible victims, it's believed that other marine mammals, such as whales and dolphins, are affected by the toxin and may have seizures and drown in the open ocean, though the extent of the problem isn't known, Gulland said. William van Bonn, DVM, formerly of the Marine Mammal Center and now at the Shedd Aquarium in Chicago, was senior author of the paper.

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Headaches in children

This article gives a lot of information on headaches in children.

Why do children get headaches?

Headaches in children are common and usually not serious.  Causes include migraines, stress and tension headaches, trauma, sinus disease and eye problems.  Certain foods with nitrate preservatives and MSG (monosodium glutamate) can trigger headaches.  Brain tumors in children as a cause for headaches are extremely rare, and are usually associated with additional neurologic symptoms such as dizziness and lack of coordination.

How are children with headaches evaluated?

Children should have a thorough physical examination with a pediatrician.  He/she may order additional tests or refer to a neurologist.  It is helpful to keep a headache diary so that possible triggers (certain foods or activities) can be discovered.

If no obvious medical cause for the headaches is found by the pediatrician, a referral to an ophthalmologist is required to perform a complete eye exam.  The entire visual system should be examined.  This includes refractive error (the need for glasses), eye alignment, and binocularity (the ability to use both eyes together).  During this examination the pupils should be dilated.

 How do eye problems cause headaches in children?

Hyperopia (farsightedness) requires extra effort to focus clearly while reading.  This can sometimes lead to fatigue and headache.  Glasses can reduce the effort required to see clearly at near and improve the headache.

The decreased ability to pull the eyes toward each other when viewing near objects (convergence), particularly while reading, may cause headaches.  This is called convergence insufficiency, and symptoms include the doubling of images or words, blurred vision, fatigue, and headaches which worsen with prolonged reading.  Glasses are sometimes prescribed.  At home eye exercises, sometimes with the help of computer software, can help treat convergence insufficiency.  Expensive in office eye exercises are rarely indicated.

 Acute infections and inflammatory diseases of the eyes can cause headaches.  These problems are often accompanied by redness of the eye and/or eyelid and light sensitivity (photophobia).  Acute glaucoma can cause headaches, but rarely affects children.  A complete exam by an ophthalmologist can rule out these conditions.

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The link between childhood obesity and sleep apnea

This article discusses the link between childhood obesity and sleep apnea.

Sleep apnea is a disorder where a person’s breathing is interrupted and may stop during the sleep schedule. Recent reports claim that this disorder may afflict not only adults, but also children. Previous research has focused on behavioral issues for children suffering from sleep apnea as well as other health concerns such as diabetes.

CHEO Research Institute’s principal investigator Dr. Sherri Katz claims that there is a direct link between obesity and sleep apnea. “In the past we used to see predominantly preschool-age children who had large tonsils and large adenoids, that was the basis for their obstructive sleep apnea. As time goes on we are seeing a second wave of children with obstructive sleep apnea, predominantly over the age of eight, where obesity is the major factor contributing to their sleep disorder.” Dr. Katz said before adding, “Rates of sleep apnea are about three to 10 times higher in children with obesity. There aren’t sufficient pediatric sleep laboratory resources across the country to manage the growing demand.”

Dr. Indra Narang, who is the director of sleep medicine at The Hospital for Sick Children in Toronto, echoed the concerns voiced by Dr. Katz, explaining that a main determinant in children visiting the sleep medicine department that she oversees is due to obesity.

“We are inundated with referrals for obesity-related sleep apnea. We also believe that probably 60 to 70 per cent of obesity-related sleep apnea isn’t even diagnosed because of a lack of an awareness of sleep apnea associated with obesity. I think the disaster is happening as we speak. Not only do they not sleep well at night, but these children are affected during the day. They are sleeping, they are tired, they don’t learn as well, they don’t do as well at school. They can’t participate in physical activity. Our concern is 75 per cent of obese children will become obese adults and will have untreated obstructive sleep apnea and what we will see is an epidemic of premature cardiovascular death because of obesity and because of related obstructive sleep apnea,” Dr. Narang said.

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