Saturday, December 30, 2006

Children: Fetal Alcohol Spectrum Disorder

Numbers, sequences pose problems for Fetal Alcohol Syndrome children

Children with Fetal Alcohol Spectrum Disorder (FASD) have particular difficulty understanding numbers and sequences, a University of Alberta study shows.

An assessment of 50 Canadian children diagnosed with FASD, a condition caused by the mother’s alcohol consumption while a fetus is still in the womb, revealed that the youngsters had specific deficits in memory for numbers and sequences, which may contribute to common math difficulties faced by these children.

Prenatal alcohol abuse often leaves them with losses in physical, behavioural, emotional and social functioning.

The findings of the study, published in the December issue of Child Neuropsychology, may help refine assessments of FASD children and provide a ‘neurobehavioural profile’ to ensure they receive the most effective treatment possible, said lead author Dr. Carmen Rasmussen, a professor of pediatrics at the University of Alberta in Edmonton, Canada.“Knowing this would help in classrooms with FASD children,” said Rasmussen. The typical teaching rate may be too rapid for children with FASD, resulting in large amounts of missed information, she said. “The study definitely has implications for treatment and education down the road.”

The FASD children, aged six to 15 years, scored lower than other 84 per cent of other children their age on memory tests for numbers and sequences.

The study also revealed differences among ethnicities. Aboriginal children (35 in the study) and non-aboriginal children (15) showed different patterns of strengths and weaknesses in neurobehavioural functioning. Aboriginal children had stronger visual memories than verbal memories, while non-aboriginal children showed just the opposite.This distinction offers the opportunity to adjust for subtle cultural or sociological differences in treatment and education programs, and it also gives a valuable heads-up to parents, Rasmussen suggested. “If parents know what their child’s strengths and weaknesses are, they can help work on those skills.”

Rasmussen theorizes that aboriginal children may have stronger aptitude in visual memory thanks to their culture, which focuses on holistic and hands-on interactive learning.

University of Alberta

Friday, December 29, 2006

Schizophrenia: biochemical changes

Abnormal proteins linked to schizophrenia found in body tissue
A new study suggests biochemical changes associated with schizophrenia aren’t limited to the central nervous system and that the disease could have more encompassing effects throughout the body than previously thought. The findings, scheduled for publication in the January 2007 issue of the American Chemical Society’s Journal of Proteome Research, could lead to better diagnostic testing for the disease and could help explain why those afflicted with it are more prone to type II diabetes, cardiovascular diseases and other chronic health problems.

Researcher Sabine Bahn, M.D., Ph.D., and her colleagues at Cambridge University in England and the University of Cologne in Germany, detected abnormal proteins linked to schizophrenia in the liver and red blood cells of people who have the disorder. It is the first time the same altered proteins have been detected both within brain tissue as well as in non-brain tissue, according to Bahn.

In time, Bahn says, these protein “biomarkers” could be used to trace the progression of the disease throughout the body.

“If changes in the rest of the body can be observed, and if these changes reflect what is going wrong in the brain, we can use these (findings) to learn about the cellular dysfunction that causes schizophrenia and this will allow us to develop better drugs and diagnostics,” Bahn says.

About 1 percent of the world’s population — including 2.4 million Americans — has schizophrenia, a complex and puzzling mental illness that can lead to delusions, hallucinations and disordered thinking. It is one of the world’s most common causes of psychosis, according to Bahn. Since it was first described more than 100 years ago, scientists have made little progress in unraveling the causes of the disease, and no definitive test is available to diagnosis it, she says.“We desperately need a better understanding of this illness. It is, however, difficult to study the disease, as the brain can’t easily be investigated. We can’t take multiple biopsies from patients to look at the disease-related changes,” Bahn says. “We need a new concept.”

While most scientists investigating the disease believe it only affects the brain, Bahn notes that researchers have long known that people who have schizophrenia are at higher risk than the general population for a number of chronic diseases. Some evidence suggests these health problems might be somehow tied to schizophrenia, she adds, but most studies have been inconclusive. Bahn’s latest discovery could help bridge this gap.

Recently, Bahn and her colleagues discovered a set of abnormal proteins in post-mortem brains of people who had schizophrenia. In this new study, they sought to detect similarly altered proteins in other organs and tissues of individuals living with the disease. After looking at thousands of proteins, they found that people with schizophrenia had 14 liver proteins and eight red blood cell proteins that were significantly altered compared to individuals who didn’t have the disease. These altered proteins were strikingly like those found in the post-mortem brains.

Several of these abnormal proteins appear to promote oxidative stress and disrupt energy metabolism in cells, Bahn says. She theorizes that schizophrenia is caused, at least in part, by these two problems. In her earlier work, for instance, Bahn found evidence that schizophrenic brains might have difficulty producing or using energy properly and are more susceptible to cell-damaging free radicals than healthy brains. The new findings, she says, suggest that the same sort of energy starvation, increased free-radical damage cycle could be occurring in other tissue and, in addition to schizophrenia, possibly be contributing to the onset of other chronic diseases.

American Chemical Society

Thursday, December 28, 2006

Tuberculosis bacillus: in adipose cells

Tuberculosis: The bacillus takes refuge in adipose cells

A team from the Institut Pasteur has recently shown that the tuberculosis bacillus hides from the immune system in its host’s fat cells. This formidable pathogen is protected against even the most powerful antibiotics in these cells, in which it may remain dormant for years.

Mycobacterium tuberculosis, the bacillus responsible for tuberculosis can hide, in a dormant state, in adipose cells throughout the body. The bacterium is protected in this cellular environment, to which the natural immune defences have little access, and is inaccessible to isoniazid, one of the main antibiotics used to treat tuberculosis worldwide. These results were obtained by Olivier Neyrolles* and his colleagues from the Mycobacterial Genetics Unit directed by Brigitte Gicquel at the Institut Pasteur, in collaboration with Paul Fornès, a pathologist from Hôpital Européen Georges Pompidou. They raise questions of considerable importance in the fight against tuberculosis.
Tuberculosis kills almost two million people worldwide every year and is considered by the World Health Organisation to represent a global health emergency. However, the bacillus is much more prevalent in the world’s population than the statistics would lead us to believe, because only 5 to 10% of those infected actually develop tuberculosis. The bacillus may be present in a significant proportion of the population, remaining in a “dormant” state in the body, sometimes for years, and may be “reactivated” at any time. The risk of rea ctivation is particularly high in immunocompromised individuals, such as those infected with AIDS: the HIV virus and the tuberculosis bacillus make a formidable team, with each infectious agent facilitating the progression of the other.
Neyrolles’ team first demonstrated, in cell and tissue cultures, that adipose cells served as a reservoir for Mycobacterium tuberculosis, and that this protected the bacillus against isoniazid. They then investigated whether the pathogen was present in adipose cells in humans. They did this by testing for traces of the genetic structure of the bacillus in samples from people considered not to be infected. Analyses were carried out on samples from deceased subjects from Mexico, where tuberculosis is endemic, and from Parisian districts reporting very few cases of tuberculosis.
The bacterium was detected in the adipose tissue of about a quarter of these people, all of whom were unaware they were infected, in both Mexico and France. These results suggest that the bacillus responsible for tuberculosis can remain protected in the adipose tissue of the body in the absence of any sign of disease.
This work has important implications for the prevention of this disease. It helps to explain how, many years after first testing positive for tuberculosis, people with no trace of the microbe in the lungs may develop some form of tuberculosis attacking the lungs, bones or genitals. It also suggests that isoniazid treatment, prescribed to the close friends and family of patients as a preventative measure, may in some cases not provide sufficient protection against the disease. This is particularly important for immunocompromised patients and for people with AIDS, for whom a secondary infection with tuberculosis bacillus may have very serious consequences.
This work highlights the importance of the search for new targeted therapeutic weapons, such as new antibiotics, which must be able to reach the dormant bacillus that has been hiding in adipose cells without our knowing it.
Public Library of Science

Wednesday, December 27, 2006

Risk of Parkinson disease

Body mass index and the risk of Parkinson disease
G. Hu, MD, PhD, P. Jousilahti, MD, PhD, A. Nissinen, MD, PhD, R. Antikainen, MD, PhD, M. Kivipelto, MD, PhD and J. Tuomilehto, MD, PhD
From the Department of Epidemiology and Health Promotion (G.H., P.J., A.N., J.T.), National Public Health Institute, Helsinki; Department of Public Health (G.H., J.T.), University of Helsinki, Helsinki; Tampere School of Public Health (P.J.), University of Tampere, Tampere; Oulu City Hospital (R.A.), Oulu; Department of Neuroscience and Neurology (A.N., M.K.), University of Kuopio, Kuopio; and South Ostrobothnia Central Hospital (J.T.), Seinäjoki, Finland.

Objective: To examine the association between body mass index (BMI) and the risk of Parkinson disease (PD).
Methods: Study cohorts included 22,367 Finnish men and 23,439 women 25 to 59 years of age without a history of PD at baseline. Hazards ratios (HRs) of incident PD were estimated for different levels of BMI.
Results: During a mean follow-up period of 18.8 years, 272 men and 254 women developed incident PD. After adjustment for confounding factors (age, study years, systolic blood pressure, total cholesterol, education, leisure-time physical activity, smoking, and alcohol, coffee, and tea consumption), the HRs of PD at different levels of BMI (<23, 23 to 24.9, 25 to 26.9, 27 to 29.9, and 30 kg/m2) were 1.00, 1.97 (95% CI: 1.21 to 3.22), 1.83 (95% CI: 1.12 to 2.99), 2.34 (95% CI: 1.45 to 3.78), and 2.44 (95% CI: 1.44 to 4.15) in men, and 1.00, 1.50 (95% CI: 0.95 to 2.37), 1.65 (95% CI: 1.05 to 2.59), 1.79 (95% CI: 1.15 to 2.80), and 1.77 (95% CI: 1.12 to 2.78) in women, and 1.00, 1.70 (95% CI: 1.23 to 2.37), 1.70 (95% CI: 1.23 to 2.37), 2.02 (95% CI: 1.46 to 2.79), and 2.03 (95% CI: 1.44 to 2.85) in men and women combined (adjusted also for sex). In both sexes combined, the multivariate-adjusted direct association between BMI and the risk of PD was present both in subjects aged 25 to 49 years and 50 to 59 years, in never smokers and smokers and in participants diagnosed PD before and after 65 years of age.
Conclusion: Body mass index is associated with a risk of Parkinson disease. The effect is graded and independent of other risk factors.
NEUROLOGY 2006;67:1955-1959
© 2006 American Academy of Neurology

Chronic Hepatitis B: Emerging Therapeutics

Mark E. Mailliard1 and ­John L. Gollan1,2­
1Department of Internal Medicine and 2Office of the Dean, University of Nebraska College of Medicine, Omaha, Nebraska 68198;

Hepatitis B is a global health problem. Patients with chronic hepatitis B (CHB) carry a significant risk to eventually develop cirrhotic liver disease. Recent therapeutic advances against CHB offer excellent potential for long-term suppression of hepatitis B virus (HBV) replication during antiviral therapy, and occasionally a durable remission off medication. Selection of appropriate patients for antiviral therapy depends on identification of HBV replication and an elevated alanine aminotransferase level or histologic liver injury. Pegylated interferon alpha offers potent immunomodulatory and antiviral activity with the potential for durability, but also with adverse effects and significant cost. The nucleoside or nucleotide analogs, lamivudine, adefovir, and entecavir, suppress HBV replication and are extremely well-tolerated, but long-term or even lifelong therapy is required. Most experience has been gained with lamivudine, but viral resistance occurs frequently. Newer analogs appear to be relatively free of this problem. Approaches using a combination of agents have promise, but have yet to be proven superior to individual drugs alone. Full Text
Annual Review of MedicineVol. 57: 155-166

Tuesday, December 26, 2006

Diabetes and Alzheimer disease

Diabetes is related to cerebral infarction but not to AD pathology in older persons

Z. Arvanitakis, MD, J. A. Schneider, MD, MS, R. S. Wilson, PhD, Y. Li, PhD, S. E. Arnold, MD, Z. Wang, MD and D. A. Bennett, MD
From Rush Alzheimer's Disease Center (Z.A., J.A.S., R.S.W., Z.W., D.A.B.), Department of Neurological Sciences (Z.A., J.A.S., R.S.W., D.A.B.), Department of Pathology (J.A.S.), Department of Behavioral Sciences (R.S.W.), Rush Institute for Healthy Aging (Y.L.), and Department of Internal Medicine (Y.L.), Rush University Medical Center, Chicago, IL; and Center for Neurobiology and Behavior (S.E.A.), University of Pennsylvania, Philadelphia.

Objective: To examine the potential relation of diabetes to common neuropathologic causes of dementia, cerebral infarction and Alzheimer disease (AD) neuropathology.
Methods: Subjects were 233 older Catholic clergy in the Religious Orders Study, who underwent detailed annual evaluations, including neuropsychological testing, and brain autopsy at time of death (mean age 86 years, 45% men). Diabetes was identified by annual direct medication inspection and history. Cognitive function proximate to death was summarized into five cognitive domains, based on 19 neuropsychological tests. Macroscopic cerebral infarctions were recorded from 1 cm coronal slabs. Neuritic plaques, diffuse plaques, and neurofibrillary tangles were counted in Bielschowsky silver-stained sections and summarized to yield composite measures of neuritic plaques, diffuse plaques, tangles, and overall AD pathology. We also used immunohistochemistry with antibodies to amyloid-ß and PHF-tau to obtain quantitative measures of amyloid burden and neurofibrillary tangle density. Multiple logistic and linear regression analyses were used to examine the relation of diabetes to cerebral infarctions and AD pathology, controlling for age, sex, and education.
Results: AD pathology was related to all five cognitive domains (p < 0.01) and infarctions were related to perceptual speed (p < 0.001). Diabetes (present in 15% subjects) was associated with an increased odds of infarction (OR = 2.47, 95% CI: 1.16, 5.24). Diabetes was not related to global AD pathology score, or to specific measures of neuritic plaques, diffuse plaques or tangles, or to amyloid burden or tangle density.
Conclusion: We found a relation between diabetes and cerebral infarction but not between diabetes and Alzheimer disease pathology in older persons. Full Text
NEUROLOGY 2006;67:1960-1965
© 2006 American Academy of Neurology

Monday, December 25, 2006

Christmas Blessings for all!

Antiepileptic drugs: Psychotropic effects

Psychotropic effects of antiepileptic drugs
Alan B. Ettinger, MD
From North Shore-LIJ Comprehensive Epilepsy Centers, New Hyde Park, NY.

Background: Mood disorder symptoms are common in patients with epilepsy. Since antiepileptic drugs (AEDs) can affect these symptoms, knowledge of the psychotropic properties of AEDs is crucial. We review most studies of the psychotropic effects of AEDs that have involved potential psychiatric applications and have been reported in the psychiatric literature.
Methods: We conducted a comprehensive literature search to identify relevant clinical trial reports on the efficacy of AEDs for mood disorders.
Results: There have been few randomized controlled trials studying AED psychotropic properties in patients with epilepsy, but some randomized controlled trials of potential psychiatric indications for AEDs have been published. Data from these studies suggest that specific AEDs have mood stabilizing, anxiolytic, and antidepressant properties, while others may elicit depression, agitation, or psychosis.
Conclusion: Antiepileptic drug selection should consider potential effects on mood and behavior. Full Text

Friday, December 22, 2006

ADHD: Coexisting Conditions

ADHD - Coexisting Conditions

As part of the diagnosis, your pediatrician will look for other conditions that show the same types of symptoms as Attention-Deficit/Hyperactivity Disorder (ADHD). Your child may simply have a different condition or ADHD and another condition. Many children who have been diagnosed with ADHD have at least one coexisting condition.

Common coexisting conditions include the following:

Oppositional Defiant Disorder or Conduct Disorder
Up to 35 percent of children with ADHD also have oppositional defiant disorder or conduct disorder. Children with oppositional defiant disorder tend to lose their temper easily and annoy people on purpose and are defiant and hostile toward authority figures. Children with conduct disorder break rules, destroy property, and violate the rights of other people. Children with coexisting conduct disorder are at much higher risk for getting into trouble with the law than children who have only ADHD. Studies show that this type of coexisting condition is more common among children with the primarily hyperactive/impulsive and combination types of ADHD. Your pediatrician may recommend counseling for your child if she has this condition.

Mood Disorders/Depression
About 18 percent of children with ADHD also have mood disorders such as depression. There is frequently a family history of these types of disorders. Coexisting mood disorders may put children at higher risk for suicide, especially during the teenage years. These disorders are more common among children with inattentive and combined types of ADHD. Children with mood disorders or depression often require a different type of medication than those normally used to treat ADHD.
Anxiety Disorders
These affect about 25 percent of children with ADHD. Children with anxiety disorders have extreme feelings of fear, worry or panic that make it difficult to function. These disorders can produce physical symptoms such as racing pulse, sweating, diarrhea and nausea. Counseling and/or medication may be needed to treat these coexisting conditions.
Learning Disabilities
Learning disabilities are conditions that make it difficult for a child to master specific skills such as reading or math. ADHD is not a learning disability. However, ADHD can make it hard for a child to do well in school. Diagnosing learning disabilities requires evaluations such as IQ and academic achievement tests.

Common Conditions Co-Existing with ADHD
American Academy of Pediatrics

Thursday, December 21, 2006

Children: Trauma and spirituality


Family Life Development Center, Cornell University

This article reviews research and theory dealing with the intersection of the developmental psychology of trauma and spirituality. The central hypothesis is that the experience of childhood traumatization functions as a kind of `reverse religious experience', a process combining overwhelming arousal and overwhelming cognitions that threatens core `meaningfulness' for the child. In addition to reviewing the role of religion in spiritual development, it offers some general principles for action and action research to understand better the role of spirituality in the traumatization and healing of children. Research implications include the need to study the life path of violent youth as a strategy for understanding the role of spirituality in preventing social problems among high risk children. The discussion is based upon the authors' formal and informal fieldwork and research with children in war zones, violent youth and street children in several regions of the world over the last 10 years, in which trauma and spiritual development have been a major focus.
Key Words: children • intervention • spiritual • development • trauma • youth
Childhood, Vol. 3, No. 4, 467-478 (1996)
© 1996 SAGE Publications

Wednesday, December 20, 2006

Human Influenza


David B. Lewis­
Department of Pediatrics and Program in Immunology, Stanford University School of Medicine, Stanford, California

Influenza A viral infection causes substantial annual morbidity and mortality worldwide, particularly for infants, the elderly, and the immunocompromised. The virus mainly replicates in the respiratory tract and is spread by respiratory secretions. A growing concern is the recent identification of H5N1 strains of avian influenza A in Asia that were previously thought to infect only wild birds and poultry, but have now infected humans, cats, pigs, and other mammals, often with fatal results, in an ongoing outbreak. A human pandemic with H5N1 virus could potentially be catastrophic because most human populations have negligible antibody-mediated immunity to the H5 surface protein and this viral subtype is highly virulent. Whether an H5N1 influenza pandemic will occur is likely to hinge on whether the viral strains involved in the current outbreak acquire additional mutations that facilitate efficient human-to-human transfer of infection. Although there is no historical precedent for an H5N1 avian strain causing widespread human-to-human transmission, some type of influenza A pandemic is very likely in the near future. The possibility of an H5N1 influenza pandemic has highlighted the many current limitations of treatment with antiviral agents and of vaccine production and immunogenicity. Future vaccine strategies that may include more robust induction of T-cell responses, such as cytotoxic T lymphocytes, may provide better protection than is offered by current vaccines, which rely solely or mainly on antibody neutralization of infection.
Annual Review of MedicineVol. 57: 139-154

Tuesday, December 19, 2006

Migraine symptoms

How often do migraine attacks occur?Migraine frequency can vary widely, from fewer than six to more than 100 attacks per year. Duration can also vary widely, from less than 4 hours to several days. The intensity of migraine attacks is more predictable, with most attacks resulting in severe headache pain.

What are the symptoms of a migraine attack?

About 15% of people who experience migraine also experience symptoms of aura. Auras are symptoms originating from the brain and usually occur about 20 minutes to one hour before the headache attack. The symptoms include problems with vision, such as flashing lights, zig-zag lines or greying vision.

There may also be hearing or speech problems, disorientation or confusion and ‘pins and needles’ feelings in certain parts of the body. The aura may disappear before the headache begins or may last into the headache phase.

The headache itself, is, for most people, the worst part of the migraine. It is usually throbbing, painful, and typically occurs on one side of the head. The pain usually becomes worse with physical activities like walking or climbing stairs.

Many people also experience nausea and some actually vomit during a migraine attack. Other symptoms that often accompany migraines include sensitivity to light, sound and smells.

Migraine Quiz: Play the Migraine Quiz 'Every Day Counts' and test your knowledge of this disorder. Migraine effectively ‘steals’ time from those who suffer from the disorder – time at work, and at play. In this quiz, the answers to the questions may help you to reduce the burden of your migraine, and allow you to get on with your life! Click here to play the Quiz

Migraine Disability Website:

Genetic map: for malaria research

Genetic map offers new tool for malaria research

An international research team announced today the completion of a genome-wide map that charts the genetic variability of the human malaria parasite Plasmodium falciparum.
Published in the December 10 advance online edition of Nature Genetics, the study reveals striking variation within the pathogen’s genome, including an initial catalog of nearly 47,000 specific genetic differences among parasites sampled worldwide. These differences lay the foundation for dissecting the functions of important parasite genes and for tracing the global spread of malaria. Led by scientists at the Harvard School of Public Health and the Broad Institute of MIT and Harvard, together with researchers in Senegal, the work has already unearthed novel genes that may underlie resistance to current drugs against the disease.
“Malaria remains a significant threat to global public health, driven in part by the genetic changes in the parasite that causes the disease,” said senior author Dyann Wirth, a professor and chairman of the department of immunology and infectious diseases at the Harvard School of Public Health and the co-director of the Broad Institute’s Infectious Disease Initiative. “This study gives us one of the first looks at genetic variation across the entire malaria parasite genome — a critical step toward a comprehensive genetic tool for the malaria research community.”
Plasmodium falciparum — the deadliest of the four parasites that cause malaria in humans — kills one person every 30 seconds, mostly children living in Africa. Despite decades of research, the genetic changes that enable it to escape the body’s natural defenses and to overcome malaria drugs remain largely unknown.
To gain a broad picture of genetic variability — worldwide and genome-wide — the scientists analyzed more than 50 different P. falciparum samples from diverse geographic locations. This includes the complete genome sequencing of two well-studied samples as well as extensive DNA analyses of 16 additional isolates. The work is one of three large-scale studies of the parasite’s DNA that appear together in Nature Genetics, and it represents a collaborative effort among Boston area researchers and a scientific team led by Souleymane Mboup, a professor at the Cheikh Anta Diop University in Senegal where malaria is endemic. “We are grateful for the contributions of our colleagues in Senegal. They are a crucial part of this collaboration,” said Wirth.
By comparing the DNA sequences to each other and to the P. falciparum genome sequenced in 2002, the researchers uncovered extensive differences, including ~ 47,000 single letter changes called single nucleotide polymorphisms (SNPs). This represents more than double the expected level of diversity in the parasite’s DNA. Although there are probably many more SNPs to be found, this initial survey — like the recent HapMap project in humans — provides a launching point for future systematic efforts to identify parasite genes that are essential to malaria.
“The roles of most of the malaria parasite’s genes are still not known,” said first author Sarah Volkman, a research scientist at the Harvard School of Public Health. “An important application of this new tool will be in pinpointing the genes that are vital to the development and spread of malaria.”
One of the tool’s strengths is its ability to reveal evolutionary differences among parasites. This information can shed light on the genes responsible for malaria drug resistance — a major obstacle to adequate control of the disease. Using the genetic map to compare parasites exposed to different anti-malarial drugs, the scientists identified a novel region that is strongly implicated in resistance to the drug pyrimethamine, and also confirmed a region of the genome known to be involved in chloroquine drug resistance.
“The same genetic principles used to study human evolution can provide important clues about malaria,” said first author Pardis Sabeti, a postdoctoral fellow at the Broad Institute. “This tool has already yielded insights into the genetic changes that correlate with different drug treatments, pointing us to genes that may contribute to drug resistance.”The map can also define the genetic landscapes of different parasite populations. Applying it to parasites from various continents, the scientists discovered greater DNA variability among P. falciparum samples from Africa relative to those from Asia and the Americas. This knowledge guides the selection of genetic markers to track the transmission of distinct parasites, particularly ones that are virulent or drug resistant. It also lays the groundwork for connecting parasite genes with traits that vary geographically and bolster malaria’s foothold in many parts of the world.“Genomic tools have largely been applied to first-world diseases up to now. This project underscores the power and importance of applying them to the devastating diseases of the developing world,” said Eric Lander, one of the study’s authors and the director of the Broad Institute. “By joining forces among scientists in the U.S., Africa and elsewhere, it should be possible to rapidly reveal the genetic variation in malaria around the world. Knowing the enemy will be a crucial step in fighting it.”
Broad Institute of MIT and Harvard

Monday, December 18, 2006

Botulinum toxin: Study helps

Study helps explain why botulinum toxin is so deadly

MADISON–A pilot without a map can locate an airport by first finding a nearby landmark, like a big river, and then searching for the airport.
New research from the University of Wisconsin School of Medicine and Public Health (SMPH) and Scripps Research Institute shows how the astonishingly powerful botulinum toxin uses a similar strategy to latch onto nerve cells, the first step in inactivating them.
The research helps explain how the toxin first attaches to a receptor on the surface of a nerve cell, then looks for a second type of receptor that is nearby. Once the toxin links to this second receptor, it can enter the nerve cell and break a protein needed to deliver molecules that can signal other nerve cells.By blocking this signaling molecule, tiny amounts of botulinum toxin can cause paralysis and even death through respiratory failure. The bacteria that makes this toxin grows in soil, and can be found inside cans of food that were improperly processed. Botulinum toxin is the reason for the extreme danger from bulging cans of food.
Researchers have been working on the unique nerve-blocking ability of the seven individual botulinum toxins for decades, says botulinum expert Edwin Chapman, UW-Madison professor of physiology and a Howard Hughes Medical Institute investigator. “A major question is how the toxin enters neurons,” he says.
The research was a close collaboration with Ray Stevens of Scripps, who crystallized the structure that forms when botulinum toxin links to the protein receptor on a nerve cell.
“This is the first paper to show in atomic detail the structure of botulinum neurotoxin touching the receptor on the surface of the neuron,” Chapman says. “The toxin has to bind to the neuron it wants to poison. This is a snapshot of the first stage of that poisoning.”
The report on the work, in the journal Nature this week, identified a short section on the protein receptor as the exact spot where botulinum toxin grips the cell immediately before entering it.UW-Madison has long been a center of botulism research. In 2003, Min Dong, a post-doctoral fellow in Chapman’s lab, showed that a known protein receptor for one botulinum toxin was a key point of entry into the nerve cell. Dong shares first authorship on the current study along with Qing Chai and Joseph Arndt of Scripps.
The Nature paper is an elaboration on that 2003 discovery, which was published in The Journal of Cell Biology. Stevens’s lab bombarded a crystal of the toxin bound to a small sub-region of the primary receptor with X-rays, then measured the reflections to portray the toxin and the receptor bound in deadly embrace.
The research could have several practical applications. Botulinum toxin is a potential biological weapon, so the U.S. military is interested in finding anti-toxins to protect soldiers — molecules that attach to the binding site on the toxin or on the cell. The search for such a blocking molecule becomes easier now that the exact structure of the link between the toxin and the nerve cell are known.
Better knowledge of botulinum toxin’s structure could also enhance the growing number of treatments that use the toxin to block nerve signals. The medical treatments “are not just for wrinkles,” Chapman says. “People with paralysis get spasms in the muscles that are shut off, and this could solve that. In a wide variety of dystonias, where spasms can cause really severe pain, this can relax the muscles.”
A third potential benefit is further down the line. After the researchers found the binding site on the protein receptor, they varied it until the toxin could no longer bind to it. If a mutated toxin was made to attach to the mutated receptor, the combination might target botulinum toxin against over-active cells in the body, Chapman suggests.
Using genetic engineering, “you might be able to sensitize whatever cell you want to the toxin,” he says. Theoretically, such a treatment could be used to slow mucus production in the lungs of cystic fibrosis patients, or to attack hyperactive cells in a wide range of other disorders.
Overall, the research improves our knowledge of a devilishly clever toxin, says Dong. Botulinum is an enzyme–a biological catalyst — that can move through a cell, breaking one protein molecule and quickly attacking another. Botulinum toxin attacks communications between nerve cells, “one of the most sensitive parts of the animal physiology,” Dong says. “That provides an efficient way to immobilize an animal, far easier than targeting muscles directly.”
Another reason for botulinum toxin’s extraordinary power becomes clear from this study, Dong says. The toxin is only able to attach to a nerve cell that is working. “If the synapse between two nerve cells is not active, all the receptors will be hiding inside the cells. But a synapse that controls a very important muscle must be firing all the time, and it will be exposing more receptors, and the toxin will therefore target them.”
Botulinum toxin, he says, “Only goes where it can be effective. It’s like a smart bomb.”

University of Wisconsin-Madison

Treat heroin addiction

Study highlights new and cheaper way to treat heroin addiction

Costly methadone treatment for heroin addicts could be replaced by a substitute painkiller that is half the price, safer and less toxic.
In a study spanning three and a half years, researchers found that the prescription painkiller dihydrocodeine is equally as effective as methadone to help drug users kick the habit.
The research by the Universities of Edinburgh, Napier and Adelaide could have major implications for treatment programmes for drug users, which have proved controversial not least because of the high costs involved.
In contrast to methadone –which comes in liquid not tablet form – dihydrocodeine is much easier to store and comes under less stringent regulations because it is not as toxic and less likely to cause a fatal overdose. It is estimated that whereas methadone treatment can cost almost £1,500 annually per patient, the cost of dihydrocodeine is £713.
Dihydrocodeine has been used by GPs and specialists for many years to treat drug users . It is often preferred in situations where methadone is seen as hazardous, such as police custody or prison. Its effectiveness has, however, never been tested before.
Dr Roy Robertson, a Reader at the University of Edinburgh, who is the study’s main author, said: “Heroin addiction is a chronic condition requiring long-term medication. Just as with other chronic conditions, such as diabetes or arthritis, there should be a number of treatments available so that doctors and nurses can tailor medication to the needs of each patient.”
Methadone should still be used to treat the majority of patients withdrawing from heroin and requiring maintenance treatment, but dihydrocodeine offers an alternative treatment for those who can’t tolerate methadone, or find it hard to deal with the stigma of having to take their dose – sometimes every day – in a pharmacy. It is also much cheaper.
“The study, the first of its kind in the world, assessed 235 people requiring treatment for opiate dependency in Edinburgh and found that dihydrocodeine was just as effective as methadone.
Dr Roberston, who also works as a GP, added that while there were less restrictions attached to prescribing dihydrocodeine tablets, it is still essential that treatment regimes are controlled and tailored to the individual.
”We want to engage young people in a treatment programme which stops them from injecting drugs and running the risk of infection,“ he said.”
Apart from the danger of contracting AIDS, drug users run the real risk of exposure to the potentially fatal liver disease, Hepatitis C. We face an epidemic of Hepatitis C in Scotland, with 40% of young people who have been injecting drugs for more than two years being infected with this serious illness.
University of Edinburgh

Sunday, December 17, 2006

Alcoholism: Sleep Problems

Sleep problems — real and perceived — get in the way of alcoholism recovery

ANN ARBOR, Mich. — The first few months of recovery from an alcohol problem are hard enough. But they’re often made worse by serious sleep problems, caused by the loss of alcohol’s sedative effects, and the long-term sleep-disrupting impact that alcohol dependence can have on the brain.
Now, a new study gives further evidence that insomnia and other sleep woes may actually get in the way of recovery from alcohol problems. In fact, a person’s perception of how bad their sleep problems are may be just as important as the actual sleep problems themselves, the study suggests.
The study is published in the new issue of the journal Alcoholism: Clinical and Experimental Research, by a team from the University of Michigan’s Department of Psychiatry. They report the results of a small but thorough evaluation of sleep, sleep perception and alcohol relapse among 18 men and women with insomnia who were in the early stages of alcohol recovery.
The authors say their results show how important it is for alcohol recovery patients, and those who are helping them through their recovery, to discuss sleep disturbances and seek help. Often, sleep isn’t discussed in alcohol recovery programs – but it should be, they stress.In fact, members of the U-M team have now launched a new study that aims to help those who have just entered treatment for alcohol problems, and are having trouble sleeping. Instead of using sleep medications, which can carry their own risk of addiction, it’s based on a series of “talk therapy” sessions with a trained sleep therapist who can help patients change behaviors and patterns of thinking that contribute to sleep problems.
In the meantime, the newly published results add to the understanding of how alcohol and sleep intertwine.
“What we found is that those patients who had the biggest disconnect between their perception of how they slept and their actual sleep patterns were most likely to relapse,” says lead author Deirdre Conroy, Ph.D., who led the study as a fellow in the U-M Addiction Research Center. “This suggests that long-term drinking causes something to happen in the brain that interferes with both sleep and perception of sleep. If sleep problems aren’t addressed, the risk of relapse may be high.”
Conroy and her former mentor, U-M alcoholism researcher Kirk Brower, M.D., conducted the study in cooperation with the sleep researchers of the U-M Sleep and Chronophysiology Laboratory, the U-M Sleep Disorders Center, and U-M Addiction Treatment Services. She is now at the McLaren Sleep Diagnostic Center.
“We are now interested in what brain mechanisms are involved in the disrupted sleep of alcohol-dependent individuals,” says Brower, who has previously led studies illustrating the prevalence of sleep disorders among people with alcohol dependence and abuse issues, and their correlation with relapse back into drinking. He is the executive director of the U-M Addiction Treatment Services, which provides alcohol and drug treatment to hundreds of patients each year.
The new study involved women who had volunteered for a randomized clinical trial of gabapentin, an experimental treatment for alcohol dependence. Each one started the trial when they had been off alcohol for about a week.
The volunteers spent two separate nights in the sleep-monitoring area of the U-M General Clinical Research Center, wearing electrodes on their head and body that measured their brain waves during sleep, as well as their breathing, muscle activity and heart rhythm. The detailed measurements, which together make up a procedure called polysomnography, allowed the researchers to determine when the volunteers were sleeping, when they were awake, and which stage of sleep they were in.
These sleep data were compared with the participants’ answers on morning evaluations of how they slept – including how long they thought it took them to fall asleep, how long they were awake in the night, and other measures. The two nights of sleep monitoring were done several weeks apart. The researchers also asked the participants to report any alcohol they drank during the six weeks following each sleep test.
In all, the patients overestimated how long it took them to fall asleep, but thought they had been awake in the middle of the night for far less time than they actually were. These perceptions about how they slept were actually more accurate in predicting their potential for relapse to alcohol use than were the actual sleep measurements.
“Our study suggests that in early recovery from alcoholism, people perceived that it took them a long time to fall asleep and that they slept through the night,” says Conroy. “The reality was that it did not take them as long to fall asleep as they thought it did, and their brain was awake for a large portion of the night. On average, the participants that were less accurate about how they were sleeping were more likely to return to drinking.”
Conroy explains that poor sleep quality can lead to mood disturbances. “If recovering alcoholics are irritable because they are not getting quality sleep at night, they might be more vulnerable to return to drinking,” she says. “Previous studies show that nonalcoholics with insomnia actually think they are sleeping worse than they are, so they may be more likely to seek appropriate treatment. Our study shows that an alcoholic in early recovery has a lot of wakefulness in the night but they are not necessarily picking up on this. It is important for the clinician working with the alcohol-dependent patient to have a differential of poor sleep quality in the back of their mind as a potential challenge for the patient throughout alcohol recovery.”

University of Michigan Health System

Osteoarthritis and Smoking

Smoking worsens knee osteoarthritis

New findings from a study led by a Mayo Clinic rheumatologist indicate that men with knee osteoarthritis who smoke experience greater cartilage loss and more severe pain than men who do not smoke.
Knee osteoarthritis is one of the leading causes of disability in elders.
“This is a novel finding,” says Shreyasee Amin, M.D., Mayo Clinic rheumatologist and lead study researcher. “Previous studies showed no association between cigarette smoking and knee osteoarthritis or even a protective effect of smoking.”
The finding that cigarette smoking plays a role in the worsening of knee osteoarthritis is important, says Dr. Amin, as it is a potentially modifiable risk factor.
To conduct this study, the researchers examined 159 men with symptomatic knee osteoarthritis who participated in a prospective study on the natural history of the condition, the Boston Osteoarthritis of the Knee Study. The current study focused on men, as there were too few women in the original group studied who smoked (4 percent). The researchers took MRIs (magnetic resonance images) of the more symptomatic knee of each patient at the study beginning, and also 15 and 30 months later. Cartilage loss over follow-up, based on knee MRIs, was determined at the tibiofemoral joint (the connection between the thighbone and shinbone) and the patellofemoral joint (the junction of the knee cap and the thigh bone) in the knees, and a scoring tool was used to assess knee pain severity. Nineteen, or 12 percent, of the men were current smokers at the study’s start. These men also were leaner and younger than other study participants, so the researchers adjusted for these factors. The investigators found current smokers had a 2.3 fold increased risk of cartilage loss at the medial tibiofemoral joint and a 2.5 fold increased risk of cartilage loss at the patellofemoral joint compared to the men who had quit smoking or never smoked. Current smokers also had higher pain scores than men who were not current smokers, at the beginning of the study (60.5 vs. 45.0, with 100 as the highest possible pain score) and at follow up (59.4 vs. 44.3).
The association between smoking and cartilage loss in knee osteoarthritis could be explained by one or more of the following theories, according to the researchers:
- Smoking may disorder the cells and inhibit cell proliferation in the knee cartilage
- Smoking may increase oxidant stress, which contributes to cartilage loss
- Smoking may raise carbon monoxide levels in arterial blood, contributing to tissue hypoxia
(insufficient blood oxygenation), which could impair cartilage repair.
Dr. Amin and colleagues believe that the increased pain experienced by smokers with knee osteoarthritis may not be due to the effect of smoking on cartilage loss, as cartilage does not have pain fibers. They have several theories for the link:
- Smoking may affect other knee joint structures mediating knee pain
- Smoking may affect one’s pain threshold for knee or other musculoskeletal pain.
Dr. Amin says these findings are provocative and deserve further study, especially given the number of potential ways in which cigarette smoking could have a negative effect on knee joint cartilage.
Osteoarthritis, sometimes called degenerative joint disease or osteoarthrosis, is the most common form of arthritis. Osteoarthritis is characterized by the breakdown of joint cartilage and may affect any bodily joint, including those in the fingers, hips, knees, lower back and feet, though weight-bearing joints such as the knees are most susceptible. As cartilage slowly deteriorates over the years, chronic pain or varying amounts of discomfort can arise when standing and walking, and swelling also may occur with knee osteoarthritis. Over time, the cartilage deteriorates, and its smooth surface roughens. Eventually, if the cartilage wears down completely, bone may rub on bone, causing the ends of the bones to become damaged and the joints to become more painful. There is no known cause or cure for osteoarthritis, but available treatments can relieve pain and help patients remain active.

Mayo Clinic

Saturday, December 16, 2006

New biomarker predicts drugs

New biomarker predicts effectiveness of breast cancer drugs

CINCINNATI—University of Cincinnati (UC) researchers have identified a new way to predict when anti-estrogen drug therapies are inappropriate for patients with hormone-dependent breast cancer.
The team’s leader, Erik Knudsen, PhD, says the findings could help physicians more accurately predict which tumors will respond to anti-estrogen therapy and improve long-term survival for breast cancer patients.
“If we know upfront that a patient’s cancer will resist traditional anti-estrogen therapies,” Knudsen says, “physicians can immediately begin treating the patient with alternative drugs that are more likely to succeed.”
The UC researchers found that when a pathway controlling cell growth known as the retinoblastoma (RB) tumor suppressor is disrupted or “shut off,” the tumor resists anti-estrogen drugs and the cancer continues to grow in spite of the therapy. They report their findings in the January edition of the Journal of Clinical Investigation.Anti-estrogen drugs such as tamoxifen (Novaldex) are a standard treatment for hormone-dependent breast cancer. They work by blocking the estrogen action, which is required for the proliferation of most breast cancers. Although these drugs are effective in the beginning, says Knudsen, many patients who initially respond to this treatment eventually develop a resistance to it.
“Since evidence shows anti-estrogen drugs will fail in a many patients with estrogen-receptor-positive breast cancer,” says Knudsen, “our research suggests that physicians should examine both estrogen receptor status and RB tumor suppressor status during the initial diagnosis, in order to prescribe the most effective therapy for that specific patient’s cancer.
”According to the National Cancer Institute, about two-thirds of women with breast cancer have estrogen-receptor-positive breast cancer, in which tumor growth is regulated by the natural female hormone estrogen. Previous research has shown that estrogen promotes the growth of most types of breast cancer.
“The RB tumor suppressor is a fundamental regulator of cell proliferation in the body, so we can use its actions as a biomarker for how tumors will respond to anti-estrogen therapy,” explains Knudsen. “It could become the basis for deciding how patients with estrogen-receptor-positive breast cancer are treated clinically.
”In this one-year laboratory study, Knudsen and his team used a specialized technique to disrupt the RB suppression pathway in breast cancer cells and analyzed the impact on tumor growth using animal models. The researchers then compared their results with a large patient record database to determine if the same phenomenon was occurring in patients with estrogen receptor-positive breast cancer. Studies supported their hypothesis that RB may be a critical determinant of whether a tumor will respond to anti-estrogen therapy.Knudsen stresses that comprehensive clinical research is needed before this new method for predicting the success of anti-estrogen drugs is applied in daily patient care.
University of Cincinnati

Middle Childhood

Middle Childhood Friendships
Between the ages of 5 and 12, making friends is one of the most important missions of middle childhood - a social skill that will endure throughout their lives. Developmentally, school-age children are ready to form more complex relationships. They become increasingly able to communicate both their feelings and their ideas, and they can better understand concepts of time- - past, present, and future. At this age they are no longer so bound to the family or so concerned mostly about themselves but begin relying on peers for companionship, spending more time with friends than they did during the preschool years. Day by day they share with one another the pleasures and frustrations of childhood.

In the early elementary school years, friends are almost always of the same sex. During the latter years of middle childhood, however, girls and boys begin to spend a little more time together. Girls may gossip with their girlfriends - and boys with their boyfriends - about whom they like and who is cute; even so, at this age there is no real dating, even though kids may talk of "going together." Sometime during adolescence they will finally begin to pair off in a more serious way.

The natural tendency toward gender-segregated friendships in the middle years has an unfortunate consequence. It limits the opportunities for girls and boys to get to know and appreciate one another before the sexual attraction of puberty places them together. Ideally, girls need boys as friends (and vice versa) if they are to have good relationships as teenagers and good marriages as adults. You should encourage and provide opportunities for your school-age daughter to play with boys. However, you are likely to meet with some resistance. Girls of this age simply prefer to play with girls, and boys with boys.

Late in the middle years, peer influence is very evident. Friendships often evolve into highly exclusive cliques in which children strongly influence one another. At most schools there are a variety of cliques, each with its own hierarchy of members. Youngsters' attraction to particular friends may be based on anything from personality to extracurricular interests, from athletic ability to appearance. In these preadolescent years, youngsters in tightly knit inner circles may feel quite secure with one another, creating their own group identity by looking and talking alike, perhaps creating a secret handshake, and feeling much more "with it" than those on the outside looking in. These youngsters often feel a strong pressure to dress and talk in a particular way, listen to certain music, and wear their hair in a specific style. This peer pressure begins to compete (and sometimes clash) with the influence of parents and their values.

Pre-adolescents also tend to be quite judgmental, labeling others and at the same time becoming increasingly concerned about what their friends think of them. If a peer is even just a little different, they may conclude, "He's terrible; I just hate him."

Friday, December 15, 2006


Migraine - the facts

What is migraine?
Migraine is a debilitating and recurrent neurological disorder, characterized by a throbbing headache that is usually made worse by movement and is often associated with nausea, vomiting, photophobia and phonophobia. It is increasingly recognized as a disorder that seriously undermines patients’ ability to work, study and have a normal family life. Its debilitating nature and its prevalence (9-16% of the Western population, typically between the ages of 25 and 55) result in a great personal and social burden, with consequent economic effects. For example, the annual cost of lost labour due to migraine in the USA is estimated to range from $5.6 to $17.2 billion.

Who suffers from migraine?
About one in ten people suffer from migraine, although the prevalence varies with age. Most migraine sufferers experience their first attacks during childhood or as teenagers, but migraines can sometimes begin during adult life. Studies have shown that, the age of onset is earlier in boys than in girls. Migraine can affect people at any age, but it is most common from 25 to 55 years of age, when work and family commitments are maximal. Migraine prevalence also varies with gender. Migraine is two to three times more common in women than in men. The higher prevalence in women may be explained in part by hormonal factors. However, it is not just a ‘women’s disorder’; over one in every 20 men also suffer from migraine.
Estimates of migraine prevalence worldwide
Migraine is common in all races. However, current evidence suggests that migraine prevalence is higher in Caucasians than in Africans or Asians.
Migraine sufferers may experience the burden of other associated illnesses on top of the burden of their migraines. They are at an increased risk from psychiatric illnesses, particularly depression and anxiety disorders. Migraine has also been associated with stroke, epilepsy and asthma.

What causes a migraine?
The exact mechanisms that cause migraines are not known and, indeed, may be numerous. Many people believe that certain factors ‘trigger’ their attacks. These may include too much or too little sleep, strong light, weather changes and specific foods.
In women, hormonal changes at certain times of life or at the onset of menstruation can trigger migraines.
Many people mistakenly believe that migraine is a psychological disease. This is not true. Migraine is an organic neurological disease and headache is one of its symptoms.
A number of theories have been put forward to explain the biological mechanisms involved in a migraine attack.
One of the most popular theories is that a migraine is caused when a physiological trigger, or triggers, cause vasodilation (expansion of the blood vessels) in the cranial blood vessels, which activates trigeminal nerve endings in the brain. This activation of the ‘trigeminovascular system’ is thought to cause the release of chemical substances called neurotransmitters, of which the neurotransmitter serotonin (also known chemically as 5-hydroxytryptamine or 5-HT) is an important factor in the development of migraine. During a migraine attack, inflammation of the tissue surrounding the brain (neurogenic inflammation) worsens the pain.

Migraine Disability Website

ADHD: Diagnosis

Attention-deficit/hyperactivity disorder (ADHD) is a condition of the brain that makes it hard for children to control their behavior. It is one of the most common chronic conditions of childhood. All children have behavior problems at times. Children with ADHD have frequent, severe problems that interfere with their ability to live normal lives.

ADHD — Making the Diagnosis
Your pediatrician will determine whether your child has Attention-Deficit/Hyperactivity Disorder (ADHD) using standard guidelines developed by the American Academy of Pediatrics. These diagnosis guidelines are for children 6 to 12 years of age.
It is difficult to diagnose ADHD in children 5 years of age and younger. This is because many preschool children have some ADHD symptoms in various situations. In addition, children change very rapidly during the preschool years. It is also difficult to diagnose ADHD once a child becomes a teenager.
There is no single test for ADHD. The process requires several steps and involves gathering a lot of information from multiple sources. You, your child, your child's school, and other caregivers should be involved in assessing your child's behavior.
Children with ADHD show signs of inattention, hyperactivity, and/or impulsivity in specific ways. Your pediatrician will look at how your child's behavior compares to that of other children his own age, based on the information reported about your child.

To confirm a diagnosis of ADHD these behaviors must:

- Occur in more than one setting, such as home, school and social situations.
- Be more severe than in other children the same age.
- Start before the child reaches 7 years of age. (However, these may not be recognized as ADHD
symptoms until a child is older.)
- Continue for more than six months.
- Make it difficult to function at school, at home, and/or in social situations.
In addition to looking at your child's behavior, your pediatrician will do a physical examination. A full medical history will be needed to put your child's behavior in context and screen for other conditions that may affect your child's behavior. Your pediatrician also will talk to your child about how he acts and feels.

Your pediatrician may refer your child to a pediatric sub-specialist if there are concerns in one of the following areas:
- Mental retardation
- Developmental disorder, such as speech problems, motor problems or a learning disability
- Chronic illness being treated with a medication that may interfere with learning
- Trouble seeing and/or hearing
- History of abuse
- Major anxiety or major depression
- Severe aggression
- Possible seizure disorder
As a parent, you will provide crucial information about your child's behavior and how it affects her life at home, in school and in other social settings. Your pediatrician will want to know what symptoms your child is showing, how long the symptoms have occurred, and how the behavior affects your child and your family. You may need to fill in checklists or rating scales about your child's behavior.

In addition, sharing your family history can offer important clues about your child's condition.
For an accurate diagnosis, your pediatrician will need to get information about your child directly from your child's classroom teacher or another school professional. Children 6 to 12 years of age spend many of their waking hours at school. Teachers provide valuable insights. Your child's teacher may write a report or discuss the following with your pediatrician:

-Your child's behavior in the classroom
-Your child's learning patterns
-How long the symptoms have been a problem
-How the symptoms are affecting your child's progress at school
-Ways the classroom program is being adapted to help your child
-Whether other conditions may be affecting the symptoms

In addition, your pediatrician may want to see report cards and samples of your child's schoolwork. Other caregivers also may provide important information about your child's behavior. Former teachers, religious leaders or coaches may have valuable input. If your child is homeschooled, it is especially important to assess his behavior in settings outside of home.
Your child probably does not behave the same way at home as he does in other settings. Direct information about the way your child acts in more than one setting is required. It is important to consider other possible causes of your child's symptoms in these settings.

In some cases, other mental health care professionals also may be involved in gathering information for the diagnosis.

You may have heard theories about other tests for ADHD. There are no other proven tests for ADHD at this time. Many theories have been presented. But studies have shown that the
following tests have little value in diagnosing an individual child:

- Screening for high lead levels in the blood
- Screening for thyroid problems
- Computerized continuous performance tests
- Brain imaging studies such as CAT scans, MRI's, etc
- Electroencephalogram (EEG) or brain-wave test
While these tests are not helpful in diagnosing ADHD, your pediatrician may see other signs or symptoms in your child that warrant blood tests, brain imaging studies or an EEG.

Thursday, December 14, 2006

Religiosity: Depressive Disorder.

Religiosity and Remission of Depression in Medically Ill Older Patients

Harold G. Koenig, M.D., M.H.Sc., Linda K. George, Ph.D. and Bercedis L. Peterson, Ph.D.

OBJECTIVE: The effects of religious belief and activity on remission of depression were examined in medically ill hospitalized older patients.
METHOD: Consecutive patients aged 60 years or over who had been admitted to medical inpatient services at a university medical center were screened for depressive symptoms. Of 111 patients scoring 16 or higher on the Center for Epidemiologic Studies Depression Scale, 94 were diagnosed with depressive disorder (DSM-III major depression or subsyndromal depression) by a psychiatrist using a structured psychiatric interview. After hospital discharge, depressed patients were followed up by telephone at 12-week intervals four times. At each follow-up contact, criterion symptoms were reassessed, and changes in each symptom over the interval since last contact were determined. The median follow-up time for 87 depressed patients was 47 weeks. Religious variables were examined as predictors of time to remission by means of a multivariate Cox model, with controls for demographic, physical health, psychosocial, and treatment factors.
RESULTS: During the follow-up period, 47 patients (54.0%) had remissions; the median time to remission was 30 weeks. Intrinsic religiosity was significantly and independently related to time to remission, but church attendance and private religious activities were not. Depressed patients with higher intrinsic religiosity scores had more rapid remissions than patients with lower scores.
CONCLUSIONS: In this study, greater intrinsic religiosity independently predicted shorter time to remission. To the authors' knowledge, this is the first report in which religiosity has been examined as a predictor of outcome of depressive disorder.

Am J Psychiatry 155:536-542, April 1998
© 1998 American Psychiatric Association

Spirituality, Religion, and Pediatrics

Spirituality, Religion, and Pediatrics: Intersecting Worlds of Healing

Linda L. Barnes(a,b), Gregory A. Plotnikoff(c), Kenneth Fox (b) , and Sara Pendleton(d)

a) Spirituality and Child Health Initiative, Department of Pediatrics, Boston Medical Center and Medical Anthropology,
b)Department of Pediatrics, Boston University School of Medicine, Boston, Massachusetts;
c) Center for Medicine and Spirituality, Academic Health Center, University of Minnesota and Internal Medicine and Pediatrics, University of Minnesota Medical School, Minneapolis, Minnesota;
d) Department of Pediatrics, Wayne State University Medical School, Detroit, Michigan.

Religious practices such as prayer represent the most prevalent complementary and alternative therapies in the United States. However, biomedicine has sometimes viewed faith and related religious worldviews as relevant only when they obstruct implementation of scientifically sound biomedical care. Recent efforts to arrive at a new synthesis raise challenges for pediatricians. This article reviews theories of child faith development, and models of child spirituality from different disciplinary perspectives. It provides sources illustrating how spirituality and religion may inform children's lives; play a part in children's moral formation, socialization, and induction into a sacred worldview; and provide the child with inner resources. It also suggests some of the positive and negative effects of spiritual and religious engagement. Second, this article examines aspects of spirituality and religion that parents may bring to bear in relation to their children's health. Third, this article addresses the spiritual and/or religious identity of the provider. These topics are discussed in the context of cultural competence and the related importance of religious diversity. The authors suggest 1) some approaches for appropriate inclusion of spirituality in clinical practice, 2) challenges for medical education, and 3) areas requiring further research.

PEDIATRICS Vol. 106 No. 4 Supplement October 2000, pp. 899-908
© 2000 American Academy of Pediatrics.

Wednesday, December 13, 2006

First-time Mothers: Mental Disorders

First-time mothers at increased risk for postpartum mental disorders

Postpartum depression is a serious mental health problem for women and their families, with an estimated prevalence of about 10 percent to 15 percent among mothers. Postpartum disorders can also include more severe mental disorders, with a prevalence of about 1 per 1,000 births, according to background information in the article. There is some indication that a small percentage of men experience postpartum depression, but the possible relationship between becoming a father and first onset of mental disorders has not been established.

Trine Munk-Olsen, M.Sc., of the University of Aarhus, Denmark and colleagues conducted a study to estimate the risk of postpartum mental disorders requiring hospital admission or outpatient contact for first-time mothers and fathers up to 12 months after becoming a parent. The researchers analyzed data from Danish health and civil service registers, which for this study included a total of 2,357,942 Danish-born persons who were followed up from their 15th birthday or January 1973, whichever came later, until date of onset of the disorder in question, date of death, date of emigration from Denmark, or July 2005, whichever came first.

From 1973 to 2005, a total of 630,373 women and 547,431 men became parents for the first time. A total of 1,171 women and 658 men were admitted with a mental disorder to a psychiatric hospital during the first 12 months after parenthood, and the corresponding prevalence of severe mental disorders through the first 3 months after childbirth was 1.03 per 1,000 births for mothers and 0.37 per 1,000 births for fathers. For first-time mothers, the first weeks and months after the delivery were associated with an increased risk of first admission with any mental disorder, and the period from 10 to 19 days following the birth was associated with the highest risk (7.3 times increased risk) compared with women who had given birth 11 to 12 months previously. The increased risk of admission among mothers remained statistically significant through the first 3 months after childbirth regardless of age of the mother. Risk for mothers was also increased for psychiatric outpatient contacts through the first 3 months after childbirth, also with the highest risk occurring 10 to 19 days following the birth.

Unlike motherhood, fatherhood was not associated with any increased risk of hospital admission or outpatient contact. “This may indicate that the causes of postpartum mental disorders are more strongly linked to an altered physiological process related to pregnancy and childbirth than psychosocial aspects of motherhood.”

“Accurate estimates of the rates of and risk factors for postpartum depression are highly important for the scientific and clinical understanding of mental and behavioral disorders during the postpartum period as well as for planning mental health services for childbearing women and their families,” the authors write.

JAMA and Archives Journals

Deadly Childhood Disease

Treatment discovered for deadly childhood disease

The disorder causes profound muscle weakness and heart and breathing problems and affects as many as one in 40,000 births. The study is published in the online edition of Neurology, the scientific journal of the American Academy of Neurology.

“This form of treatment has changed the natural history of this otherwise lethal disease,” said study author Priya Sunil Kishnani, MD, with Duke University in Durham, North Carolina.

The year long study involved 18 children under the age of six months with rapidly progressing Pompe disease. Pompe disease is caused by a deficiency in the enzyme acid a-glucosidase (GAA), which is needed to break down glycogen, a complex sugar molecule which releases glucose.
The study found all 18 children who started to receive the enzyme replacement, recombinant human GAA (rhGAA), before they were six months old survived to at least 18 months of age. Fifteen of the 18 children also did not need a ventilator. The study showed that starting rhGAA before the age of six months reduced the risk of death in children by 99 percent, reduced the risk of death or invasive breathing assistance by 92 percent, and reduced the risk of death or any type of ventilation by 88 percent, compared to past patients without this treatment.

“This form of enzyme replacement therapy markedly extended survival and improved respiratory performance in these children, with a majority of them showing normal growth and substantial gains in motor development,” said Kishnani. “rhGAA is safe and the only effective treatment for Pompe disease; it is life saving.”Kishnani said the young age at which the children began treatment may have contributed to their improved response compared to previous trials with rhGAA, where patients were older.

“This study demonstrates that starting enzyme replacement therapy early, which could be facilitated by newborn screening, shows great promise to reduce the mortality and disability of babies with this devastating disorder,” said Kishnani.

The most common side effects of the rhGAA treatment included skin reactions such as rash and hives, fever, and changes in heart rate. The study was supported by the Genzyme Corporation, maker of rhGAA.

American Academy of Neurology

Tuesday, December 12, 2006

Teen's Stress - part 2

Is Stress Always Bad?
Even though stress makes us feel uncomfortable, it’s not always a bad thing. Sometimes stress can really help us deal with tough situations. A lot of stress changes our bodies quickly and helps us react to an emergency. A little stress keeps us alert and helps us work harder.
Ages ago, when people had to survive in the jungle, the emergency nervous system was a great thing to have. Imagine your great, great, great ancestors, Sam and Zelda, eating some berries and soaking up the sun. Suddenly they saw a tiger and they knew they had to run! Hormones gave them the huge burst of energy that they needed to escape.

How did their bodies react? First, Sam and Zelda got a sinking feeling in their stomachs as the blood in their bellies quickly went to their legs so they could run fast. Then, when they jumped to their feet, their hearts beat faster to pump more blood. As they ran from the tiger, they breathed faster to get more air. Their sweat cooled them as they ran. Their pupils became bigger so they could see in the dark, in case they needed to jump over a log while running away. They didn’t think about anything but running because they weren’t supposed to stop and figure out a friendly way to talk to the tiger.
Sam and Zelda would never have survived without the stress reaction, but stress helps us do more than run from tigers. It keeps us alert and prepared. (You can be sure that the next time Sam and Zelda sat down to munch on berries, they listened for the sounds of a tiger.)

Few of us need to outrun tigers today, but we all have worries that turn on some of those same stress responses. That panicky feeling you sometimes get when you’re studying for a big test comes from your body’s reaction to stress. Your heart beats almost as fast as it would if you were running from a tiger. Your breathing becomes heavier and you sweat, just as if you were getting ready to run.If Stress Is a Survival Tool,

Why Does It Make Us Feel Awful?
Good old Sam and Zelda had few choices when the tiger chased them. Either the tiger ate them or they escaped. As sick as it sounds, if they’d been eaten, they wouldn’t have had much to worry about anymore, right? If they lived, you can be sure their burst of energy allowed them to outrun the tiger or at least outrun Zok (their slower friend who was eaten by the tiger instead). In their run for survival, Sam and Zelda used up every drop of their hormones and then took a well-deserved nap.
In the modern world, our biggest worries are not usually about life or death. We don’t really have to run away from our problems. But those same stress hormones stay in our bodies because unlike Sam and Zelda, we don’t use them up by running. Instead, those hormones continue to hang around, unused and confused. They seem to be asking, “Why did my body stand still when that ‘tiger’ attacked?”

Even when there are no real emergencies, our emotions can make our bodies act like there is a huge emergency. This is because the brain controls both emotions and stress hormones. If your brain thinks something terrible is happening, your body will react as if it really is! Even a little bit of stress that never seems to go away can confuse the body. It makes the body work harder to prepare for an emergency that may not really be there.
A tiger running at you is a real crisis. If you believe a mild stress (like a math test) is an emergency, you will not be able to study. Your body will be preparing to deal with a real tiger. You won’t be able to concentrate on anything but escaping. The trick is to figure out when something really is an emergency and when your emotions are only acting as if it is one.

How Do People Deal With Stress?
Nobody can avoid all stress, but you can learn ways to deal with it. When you’re stressed, it is normal to want to feel better. Some ways to deal with problems might make you feel better for a little while, but can make stress much worse later. Think about some of the ways people might deal with stress that can really mess them up.

  • Drugs
  • Cigarettes
  • Alcohol
  • Bullying
  • Fighting

These harmful choices might feel good for a couple of minutes, but they can be dangerous. They end up messing up your life, and then you end up a lot more stressed. They’re especially dangerous if they are the only way you manage stress. This is one of the ways addictions start.
There are many healthy ways of dealing with stress. They are safe, help you feel better, and end up making you happy.

A Teen’s Personalized Guide to Managing Stress
American Academy of Pediatrics