Showing posts with label treatment. Show all posts
Showing posts with label treatment. Show all posts

Wednesday, August 20, 2014

Autism: ASU experts follow gut reaction in digestion treatment study

Clostridium difficile in the gut. The overgrowth of this dangerous bacteria can cause serious, life-threatening infections. 

About half of all children and adults with autism suffer from chronic gastrointestinal problems, causing frequent pain, discomfort and irritability.

Research out of Arizona State University suggests these gastrointestinal (GI) complications may be due, in part, to abnormal gut bacteria.

A new study approved by the U.S. Food and Drug Administration and led by Arizona State University will examine a novel treatment, called fecal microbiota transplant (FMT), for GI problems in children with autism.

The treatment involves transferring about 1,000 different species of live gut bacteria from a healthy donor that then act like a broad-spectrum probiotic treatment to restore normal gut bacteria.

FMT has been used to treat serious Clostrium difficle infections that kill up to 15,000 people each year in the United States.

Determining the safety and tolerability of using FMT to treat GI problems in children with autism is driving the study.

The FDA has approved a pilot treatment study of 20 children with autism, ages 7 to 17 years, and moderate to severe gastrointestinal problems.

Missing bacteria
Led by professor Rosa Krajmalnik-Brown, an expert on evaluating the composition of gut bacterial communities, and professor James Adams, director of the ASU Autism/Asperger's Research Program, the ASU research team published a scientific paper last year demonstrating that children with autism were missing several hundred species of gut bacteria compared to typical children.

"Our initial work found major differences in the gut bacteria of children with autism compared to typical children, and our subsequent work has confirmed those findings," said Krajmalnik-Brown.

"Children with autism seem to be missing hundreds of beneficial gut bacteria."

"Many children and adults with autism have chronic gut problems, sometimes lasting for many years and seriously affecting their quality of life," said Adams. "We think this treatment may be helpful."

The team's hypothesis is that FMT will "reseed" the gut with beneficial bacteria that will help diminish GI problems and possibly reduce autistic symptoms.

Several studies show that FMT may also be helpful in treating other GI problems, such as ulcerative colitis, Crohn's disease, inflammatory bowel disease, irritable bowel syndrome and chronic constipation.

Beneficial versus harmful
The human gut typically contains more than 1,000 different species of bacteria – most of them beneficial.

These bacteria help with digesting food, making certain vitamins, improving GI function and protecting against pathogenic bacteria.

However, there are a few dangerous bacteria, such as Clostidium difficile (C. difficile), which can cause serious, life-threatening infections.

C. difficile kills about 15,000 people per year in the U.S., but a single dose of FMT has been shown to cure C. difficile with 92 percent effectiveness, usually within a few days.

Collaborating with Northern Arizona University and University of Arizona, the ASU team will lead the treatment portion of the study, with the help of Sharon McDonough-Means, a developmental pediatrician involved in the care of children with autism and previous research studies.

Greg Caporaso at NAU, an expert in computational and statistical methods for studying communities of microorganisms, will analyze the effect of FMT on gut bacterial communities, and Matthew Sullivan at UA will investigate the viruses that infect gut bacteria, and thereby affect bacterial populations in the gut.

The new initiative is a follow-up to a previous study that demonstrated that treatment with a powerful oral antibiotic, vancomycin, led to a temporary improvement in both gut symptoms and symptoms of autism, presumably because it killed off harmful bacteria in the gut.

However, when the treatment was stopped, the benefits were lost, presumably because there was insufficient "reseeding" of the gut with beneficial bacteria.

Friday, April 18, 2014

Autism: Diagnosis and Treatment

In the US April is National Autism Awareness Month.

The Child Development Clinic at Children's Hospital of Richmond at VCU (CHoR) provides comprehensive assessment for pediatric patients with developmental delays or disabilities, including those with autism spectrum disorders.

The medical, psychological, social work and educational testing offered by the clinic leads to a diagnosis and recommendations to help patients and their health care providers with care planning, referrals, follow-up care coordination and treatments.

Pasquale Accardo
We sat down with Pasquale Accardo, M.D., professor and chief of the Division of Developmental Pediatrics at CHoR, to learn more about autism, including symptoms, diagnosis and treatment.

What is autism?

Autism is a neurodevelopmental disorder, this means that it is a chronic brain problem, a difficulty that the brain has with processing certain kinds of information.

In the case of autism, typically the greatest difficulty is dealing with social interaction.

What are the common signs and symptoms of autism?

Common signs of autism vary with age:

  • Young children often first present with language issues.
  • Preschool and school-age children often exhibit attention deficit hyperactivity disorder (ADHD) symptoms and other challenging behaviours.
  • Older children have significant socialization problems, repetitive and obsessive compulsive behaviours.

Symptoms of autism do change with time; certain delays are more common in younger children whereas socialization and processing problems are more common in older children and adults.

How is autism diagnosed?

Autism is diagnosed using a variety of approaches:


How is autism treated?

Autism is best treated with a variety of Early Intensive Behavioural Interventions (EIBI); speech language therapy and occupational therapy can also be used.

Applied Behaviour Analysis (ABA) is considered the standard for behavioral intervention, but most other effective behavioral programs are variants on ABA.

Tuesday, March 4, 2014

Dyslexia: Ranking the effectiveness of a range of interventions

How can we best treat dyslexia? 

A new meta-analysis of published data, carried out by researchers at Ludwig Maximilian University of Munich (LMU), now provides a means of ranking the effectiveness of a range of current interventions.

Gerd Schulte-Körne
A research group led by Professor Gerd Schulte-Körne, Director of the Clinic of Child and Adolescent Psychiatry at LMU Munich, has systematically evaluated data from published randomized controlled treatment studies of dyslexia.

The results of their investigation were recently been published in the online journal PLoS One.

The term dyslexia refers to a specific difficulty in learning to read and spell. It affects 5-10% of school children and although it is one of the most common learning disorders of childhood and adolescence, it also affects adults.

Indeed, the condition is often diagnosed relatively late. "Up to 40% of children who show signs of dyslexia also have psychological problems, which often result from discrimination provoked by their learning difficulties.

They are often confronted with comments such as: 'You're just too lazy' or 'You have to work harder'", says Prof. Schulte-Körne.

Furthermore, affected children and their families are often left to cope with the problem on their own, because nobody is responsible for providing support for them beyond the confines of the classroom.

Many popular 'therapies' are, at best, ineffective and some are downright bogus.

"Early intervention and appropriate therapeutic measures that take into account the specific nature of each individual case are urgently needed", says Prof. Schulte-Körne, pointing out that the curriculum offered in normal schools is often insufficient in helping children with severe dyslexia to overcome their disability.

"These children do not receive the necessary attention because school resources are inadequate and teachers are not sufficiently well trained to deal with the problem."

Katharina Galuschka
"More than 20 different 'treatment' methods have been developed which purport to help dyslexic children but in fact very few of them have any real effect," says Katharina Galuschka, who carried out the meta-analysis.

"Systematic training of the very basic process of relating the sound of a word to its orthographic form turns out to be particularly important."

The new study also shows that long-term interventions are significantly more effective than short-term training measures.

In addition, the study reveals that many popular methods which concentrate on single factors such as enhancing visual scanning of text, or improving auditory perception, are ineffective.

"Cognition-enhancing medication or the use of tinted lenses are also unable to improve the reading ability of dyslexic subjects."

"This the first meta-analysis of its kind and it provides a basis for formulating urgently needed guidelines for dyslexia treatment and therapy", Prof. Schulte-Körne explains.

He and his research group are now coordinating a set of medical guidelines for the treatment of dyslexia in Germany, due to be released shortly.

More information: Galuschka K, Ise E, Krick K, Schulte-Körne G (2014) "Effectiveness of Treatment Approaches for Children and Adolescents with Reading Disabilities: A Meta-Analysis of Randomized Controlled Trials." PLoS ONE 9(2): e89900. DOI: 10.1371/journal.pone.0089900

Sunday, May 19, 2013

Preschoolers With ADHD: 90 Percent of Pediatric Specialists Not Following Treatment Clinical Guidelines

A recent study by pediatricians from the Cohen Children's Medical Center of New York examined to what extent pediatric physicians adhere to American Academy of Pediatrics (AAP) clinical guidelines regarding pharmacotherapy in treating young patients with Attention Deficit Hyperactivity Disorder (ADHD).

The results showed that more than 90 percent of medical specialists who diagnose and manage ADHD in preschoolers do not follow treatment guidelines recently published by the AAP.

Andrew Adesman
"It is unclear why so many physicians who specialize in the management of ADHD -- child neurologists, psychiatrists and developmental pediatricians -- fail to comply with recently published treatment guidelines," said Andrew Adesman, MD, senior investigator and chief of developmental and behavioral pediatrics at Cohen Children's Medical Center in New Hyde Park.

"With the AAP now extending its diagnosis and treatment guidelines down to preschoolers, it is likely that more young children will be diagnosed with ADHD even before entering kindergarten.

Primary care physicians and pediatric specialists should recommend behavior therapy as the first line treatment."

Current clinical guidelines for pediatricians and child psychiatrists associated with the American Academy of Child & Adolescent Psychiatry (AACAP) recommend that behaviour therapy be the initial treatment approach for preschoolers with ADHD, and that treatment with medication should only be pursued when counseling in behavior management is not successful.

The study also found that more than one-in-five specialists who diagnose and manage ADHD in preschoolers recommend pharmacotherapy as a first-line treatment alone or in conjunction with behavior therapy.

Although the AAP recommends that pediatricians prescribe methylphenidate when medication is indicated, more than one-third of specialists who prescribe medication for preschool ADHD said they 'often' or 'very often' choose a medication other than methylphenidate initially (19.4 percent amphetamines; 18.9 percent non-stimulants).

"Although the AAP's new ADHD guidelines were developed for primary care pediatricians, it is clear that many medical subspecialists who care for young children with ADHD fail to follow recently published guidelines," said Jaeah Chung, MD, the study's principal investigator who also practices at Cohen Children's.

"At a time when there are public and professional concerns about over-medication of young children with ADHD, it seems that many medical specialists are recommending medication as part of their initial treatment plan for these children."

Saturday, March 30, 2013

Facial Palsy in Children: Bell's Palsy


About 40,000 people in the United States develop facial paralysis each year with children comprising a small percentage of that population.

There are more than 50 known causes of facial paralysis but the most common in children is “Bell’s palsy,” the cause of which is not certain.

This disorder effects one side of the facial muscles due to dysfunction of the seventh cranial nerve, usually thought to stem from a viral infection; Bell’s palsy is found in 20 out of 100,000 Americans, with the incidence increasing with each decade of life.

What causes Bell’s palsy?
In Bell’s palsy, facial paralysis results from damage (e.g., possibly from viral infection) to the facial nerve.

Adults and children will either wake up to find they have facial paralysis or palsy, or have symptoms such as a dry eye or tingling around their lips that progress to Bell’s palsy during that same day.

Occasionally symptoms may take a few days to progress to facial weakness or paralysis. Physical trauma to the head and neck region at birth and during childhood may cause facial paralysis.

Other causes are:

  • Chicken pox: Chicken pox and shingles are both caused by a single virus of the herpes family known as varicella-zoster virus (VZV). Varicella is the primary infection that causes chickenpox; Herpes zoster is the reactivation of the virus that causes shingles. Research studies suggest that Bell’s palsy may be due to a reactivation of herpes simplex virus (HSV). Between 75 percent and 90 percent of chickenpox cases occur in children under 10 years of age. According to a 2001 study, about 10 percent of children between ages five and nine and about two percent of 10 to 14 year olds get chicken pox each year.
  • Infectious mononucleosis: This condition, with a peak incidence in the 15- 17 age group, can be caused by several different viruses. The leading causes are the Epstein-Barr virus and cytomegalovirus, both members of the herpes virus family. The infection is transmitted by saliva, sexual contact, respiratory droplets, and blood transfusions.
  • Lyme disease: Lyme disease is an infection that’s spread by Ixodes ticks (black-legged or deer ticks in the eastern United States, and western black-legged ticks in the west). The second stage of Lyme disease usually appears two to three months after the tick bite, and may include facial palsy or paralysis among other symptoms.

Treatments for Facial Paralysis:
If infection is the cause, then an antibiotic to fight bacteria (as in middle ear infections) or antiviral agents (to fight syndromes caused by viruses like herpes zoster (Ramsay Hunt Syndrome) may be used.

The prognosis for children with facial paralysis is generally very good. The extent of nerve damage determines the extent of recovery.

With or without treatment, studies indicate that most pediatric patients with the disorder begin to get better within two weeks after the initial onset of symptoms and recover completely within three to six months. Adults may find residual symptoms remaining for an indefinite period of time.

What happens during the diagnosis?
After an examination, the otolaryngologist- head and neck surgeon may conduct a hearing test to determine if the cause of damage to the nerve has involved the hearing nerve, inner ear, or delicate hearing mechanism.

Additional tests in the physician’s office include a balance test and a tear test, to measure the eye’s ability to produce tears.

Eye drops may be necessary to prevent drying of the surface of the eye cornea. In some circumstances, the physician may recommend a CT (computerized tomography) or MRI (magnetic resonance imaging) test to determine if there is infection, tumor, bone fracture, or other abnormality in the area of the facial nerve.

An additional diagnostic tool is the Electro neuronography (ENOG), which stimulates the facial nerve to assess how badly the nerve is damaged. This test may have to be repeated at frequent intervals to see if the disease is progressing.

Sources:
National Institute of Neurological Disorders and Stroke
Bell’s Palsy Research Foundation (US)
Bell's Palsy Association (UK)

Thursday, March 7, 2013

Anorexia Nervosa: Deep Brain Stimulation offers Hope

Scientists have raised the prospect that deep brain stimulation could help people suffering from severe anorexia nervosa.

In the small Canadian study three people were able to gain weight and had improvements in their overall mood after undergoing the procedure.

The researchers say larger trials are now needed to show whether this therapy could provide a last resort for people with difficult-to-treat anorexia.

The study is published in the Lancet.

Researchers from the Krembil Neuroscience Centre and University Health Network in Canada conducted the study primarily to find out whether this procedure is safe in people with severe cases of the eating disorder anorexia nervosa.

Deep brain stimulation - which involves implanting electrodes into the brain - has previously been used for people with Parkinson's disease, Alzheimer's disease and obsessive compulsive disorder.

'Flipping a switch' 
But this is the first time researchers have implanted the device into brains of people with such severe forms of anorexia.

They treated six women, aged between 24-57, for whom most conventional therapy had failed.

The researchers chose to implant the electrodes in an area of the brain which influences how people regulate their mood and anxiety.

They then switched on the device to deliver continuous electrical stimulation over the nine months of the study.

Lead author of the research, Dr Nir Lipsman, said this was not a study about simply flipping a switch to make people eat more.

"Anorexia nervosa has many layers and we need to address the root causes. In many people with the condition this is related to difficulties in regulating mood and anxiety.

"So we wanted to see if influencing this area of the brain could help people with the condition," he said.

And after nine months three of the women felt their quality of life had improved and they had gained weight.

Crucially they were able to stick to this weight - something they hadn't been able to do since developing the condition, the researchers said.

Kim Rollins, who took part in the study and has suffered from anorexia nervosa for 20 years said: "It has really turned my life around. It has lifted my mood and lowered my anxiety... and lessened the compulsion I had to almost destroy my body.

"But it is not a miracle - I have to put a lot of work into changing my thinking and I go to therapy and see a dietitian. But it has enabled everything to be much easier for me."

Dr Lipsman said: "We think deep brain stimulation may have helped people view their illness in a different way and meant they felt more encouraged to engage in other therapy."

But the procedure was not without serious and unwanted effects.

'Unwanted effects' 
One person involved had a seizure two weeks after the device was implanted and another suffered a panic attack during the operation to insert the device.

And for one person there were no improvements in mood, anxiety levels or weight by the end of the study.

The authors caution this procedure is not suitable for everyone.

"We worked very hard to identify a group of patients who had reached the limits of conventional treatment - for whom there is currently no effective therapy and therefore are at the greatest risk of death from the condition," Dr Lipsman said.

Prof Janet Treasure, of the Institute of Psychiatry, King's College London, who was not involved in the study but wrote a linked comment, said: "What we know is that if you can get effective treatment within three years of diagnosis, the chances of short and long-term recovery are much increased, but it is more difficult as time goes on. This is what makes this study so interesting."

She said the findings of the small study must be interpreted with caution, however.

Susan Ringwood, the chief executive of the national organisation, Beat, said: "When treatments fail to work, people with eating disorders can feel it is their fault, and that can make them very more reluctant to accept the help desperately they need.

"We are learning so much more about the brain and its role in eating disorders, and this study indicates an important new aspect that may lead to improved treatment."


Monday, March 4, 2013

US Infant born with HIV 'is cured' - Dr

Dr Hannah Gay
A baby born with the virus that causes Aids appears to have been cured, scientists have announced.

Specialists at a major Aids meeting in Atlanta, Georgia, described the case of a child from Mississippi who is now two-and-a-half and has been off medication for about a year with no signs of infection.

There is no guarantee the child will remain healthy, although sophisticated testing uncovered just traces of the virus' genetic material still lingering. If so, it would be only the world's second reported cure.

"I just felt like this baby was at higher-than-normal risk, and deserved our best shot," Dr Hannah Gay, a paediatric HIV specialist at the University of Mississippi, said.

Experts say the announcement offers promising clues for efforts to eliminate HIV infection in children, especially in Aids-plagued African countries where too many babies are born with the virus.

Dr Fauci of NIH
"You could call this about as close to a cure, if not a cure, that we've seen," Dr Anthony Fauci of the National Institutes of Health said.

A doctor gave the baby faster and stronger treatment than usual, starting a three-drug infusion within 30 hours of birth. That was before tests confirmed the infant was infected and not just at risk from a mother whose HIV was not diagnosed until she was in labour.

That fast action apparently knocked out HIV in the baby's blood before it could form hideouts in the body.

Those so-called reservoirs of dormant cells usually rapidly reinfect anyone who stops medication, said Dr Deborah Persaud of Johns Hopkins Children's Centre.

Dr Deborah Persaud
She led the investigation that deemed the child "functionally cured", meaning in long-term remission even if all traces of the virus have not been completely eradicated.

Dr Persaud's team is now planning a study to try to prove that, with more aggressive treatment of other high-risk babies. "Maybe we'll be able to block this reservoir seeding," she said.

Thursday, January 31, 2013

Ampligen: Treatment for Chronic Fatigue Syndrome and ME rejected by FDA

Ampligen, the first drug ever seeking approval to treat chronic fatigue syndrome /myalgic encephalomyelitis (CFS/ME), recently hit another roadblock with the U.S. Food and Drug Administration (FDA).

In its long quest to treat 1 million Americans suffering from this debilitating illness, the FDA advisory panel did not recommend the drug to be sold on the market, largely because CFS/ME doesn't have clear biomarkers such as blood tests to define patients who most likely to respond to the drug.

Data from clinical trials of Ampligen has not convinced the FDA so far.

Nancy Klimas, M.D., one of the world’s leading researchers and clinicians in chronic fatigue syndrome/myalgic encepahalomyelitis (CFS/ME), is the director the NSU Institute for Neuro Immune Medicine.

"The real loser is not Ampligen, but CFS/ME patients whose daily suffering continues to be unabated," she says. "CFS/ME feels like you've been run over by a truck -- pain, inflammation, utter exhaustion and trouble concentrating."

Klimas has been caring for patients with CFS/ME for 26 years now. "It's heartbreaking seeing them struggle and suffer from this serious illness that has been trivialized by science and society. One of the early controversies quickly disproven suggested that CFS/ME is a form of depression. This led to enduring public policies that allowed insurance companies to limit coverage to CFS/ME to either mental health or exercise therapy, neither get to the root cause of CFS/ME," she explains.

"CFS/ME researchers, including myself, have seen major advances in our understanding of the biology of CFS/ME. It seems to resemble an illness we know how to treat like multiple sclerosis (MS), chronic viral diseases and autoimmune diseases."

Around since the late 1980s, this drug is not new to science and medicine. Two phase 3 clinical studies have been completed. The data shows that a subgroup of CFS/ME patients showed marked improvement, even recovery on the drug.

"Yet, that's not enough evidence for the FDA advisory committee to approve because they would like to see a conclusive biomarker," notes Klimas. "As a physician, I could live with this decision if I had other effective therapies to treat my CFS/ME patients. But I do not. Moreover, it defies common logic in used in drug approval for other complex immune mediated diseases."

The above story is reprinted from materials provided by Nova Southeastern University, via Newswise.

Friday, July 27, 2012

PreDICT-TB: European Develop a new Technique to deal with Pulmonary TB

A European team of scientists is working on making new tuberculosis treatments a reality by developing better diagnostic imaging technology. 
The study is supported by the PREDICT-TB ('Model-based preclinical development of anti-tuberculosis drug combinations') project, which has clinched almost EUR 14.8 million from the Innovative Medicines Initiative (IMI) under the EU's Seventh Framework Programme (FP7). IMI is a public-private partnership between the EU and the European Federation of Pharmaceutical Industries and Associations (EFPIA). The PREDICT-TB team is working together with the European pharmaceutical industry; the project's coordinator is the United Kingdom-based GlaxoSmithKline, one of the world's leading pharmaceutical companies. Results will help the many patients suffering from this airborne infectious disease: almost 9 million people worldwide currently have tuberculosis. The researchers are developing a set of in vitro and in vivo trials that will give them the information they need to make key decisions about effective treatments. They also plan to optimise the clinical studies of novel combinations of drugs to fight this disease.
'These data will, first, offer us an early evaluation of the efficiency of the combinations of drugs used to treat tuberculosis, and second, they will allow us to optimise the clinical studies with patients,' said Juan José Vaquero from the Bioengineering and Aerospace Engineering Department at the Carlos III University of Madrid (UC3M) in Spain, one of the PREDICT-TB partners. The UC3M group is researching and developing the new preclinical imaging technology, and is working on methods for processing and analysing images for the assessment and follow-up of illness in animal models. 'We are going to develop new in vivo molecular image devices and also work on the synthesis of very specific probes for the biomarkers of this illness that have been identified by other partners in the consortium,' Professor José Vaquero said.
'We are collaborating very closely with GlaxoSmithKline, whose laboratories are going to use our equipment, as well as with specialists from the Infectious Disease and Microbiology Service of Gregorio Marañón University General Hospital in Madrid, who have a great deal of experience working with both the biology and the clinical aspects of tuberculosis. This facilitates the transformation of our results into clinical applications.' The objective of UC3M, in the short term, is to develop a tomographic X-ray technique that screens quickly yet inexpensively. This technique will give researchers the opportunity to keep an eye on the evolution of the disease and to determine how effective the treatments are in animal models. The team's long-term objective team is to perfect this technique and make it more sensitive and specific. Positron emission tomography (PET) will be included, a nuclear medicine imaging technique that generates a three-dimensional image for pictures of functional processes in the body. Quantitative measurements can be taken with this more sensitive technique. The group also plans to introduce changes in imaging technology to ensure that better resolution is obtained. 'This way, with just one examination, we will be able to visualise the complete lung of a rat or guinea pig, with enough detail to detect the disease at its earliest possible stage,' Professor José Vaquero explained. The PREDICT-TB project is pioneering research in tuberculosis by investigating the use of quantitative molecular imaging. Each year, tuberculosis affects 5 million patients in developing countries. A cure is possible for only 60 % of them, and one of the biggest challenges in fighting tuberculosis is to ensure that patients are treated for 6 to 24 months. Both support and financing for trials are limited. For more information, please visit: Innovative Medicines Initiative (IMI): http://www.imi.europa.eu/

Sunday, July 15, 2012

Dyslexia: Recognition in Symptoms but little Progress in Treatment

Despite advances in medical treatments for dyslexia over the past five years, not enough is being done to understand the causes of the condition to help kids struggling to read, concludes a seminar published online in The Lancet today.

Most children are only diagnosed with dyslexia after they have experienced serious difficulties in school, at a time when it is much harder for them to master new skills, and this could be thwarting their ability to fully realise their potential, say the authors.

“Professionals should not wait until children are formally diagnosed with dyslexia or experience repeated failures before implementation of reading treatment, because remediation is less effective than early intervention”, explain Robin Peterson and Bruce Pennington from the University of Denver in Colorado, USA.

About 7% of the population are dyslexic, and boys are about twice as likely to have dyslexia as girls. Mounting evidence suggests that the underlying problem involves difficulty with how sounds in language are heard and mapped onto letters — phonological impairment.

“Like all behaviourally defined disorders, the cause of dyslexia is multifactorial and is associated with multiple genes and environmental risk factors”, explain the authors.

Despite the recent identification of six genes that contribute to the disorder, very little is known about how these and other possible genetic determinants might contribute to dyslexia or the role of the environment in the cause of the condition.

Further research is needed to hunt out further genes that may contribute to dyslexia, and to find which gene locations are shared and not shared with associated disorders, including attention deficit hyperactivity disorder (ADHD), say the authors.

The impact of environmental risk factors, such as the language and pre-literacy stimulus parents provide for their children also warrant further investigation, they say.

“We still need to learn more about the nature of phonological deficit and how this problem interacts with other linguistic and non-linguistic risk factors, the developmental course of neural abnormalities and how these predict treatment response, and which environmental risk factors contribute to the development of poor reading and whether these are the same across demographic groups”, they explain.

Treatment still needs to be improved, they add. “Brain-imaging studies have shown that effective intervention seems to promote normalisation of activity in the left hemisphere reading and language network that has shown reduced activity in dyslexia.”

Common coexisting conditions such as ADHD, language impairment, and speech sound disorder, which are likely to be apparent much earlier, could be used to help predict a child’s risk of later reading problems, conclude the authors, adding that: “Many effective treatments are low cost, which further draws attention to the importance of early identification, prevention, and treatment of dyslexia for public health.”

Sunday, June 17, 2012

Dietary Changes and Milk fats alter gut bacteria causing degenerative bowel diseases

The rise of inflammatory bowel diseases could be down to our shifting diets causing a "boom in bad bacteria", according to US researchers.

Mouse experiments detailed in the journal Nature linked certain fats, bacteria in the gut and the onset of inflammatory diseases.

The researchers said the high-fat diet changed the way food was digested and encouraged harmful bacteria.

Microbiologists said modifying gut bacteria might treat the disease.

Inflammatory bowel diseases (IBDs), such as Crohn's and ulcerative colitis, affect one in every 350 people in the UK. When the gut becomes inflamed it can lead to abdominal pain and diarrhoea.

The researchers at the University of Chicago said the incidence of the diseases was increasing rapidly.

They used genetically modified mice which were more likely to develop IBDs. One in three developed colitis when fed either low-fat diets or meals high in polyunsaturated fats. This jumped to nearly two in three in those fed a diet high in saturated milk fats, which are in many processed foods.

They also suggest an effective means of dealing with such diseases, by simply reshaping the microbial balance of the gut”

Dr Roy Sleator Cork Institute of Technology

These saturated fats are hard for the body to digest and it responds by pumping more bile into the gut.

This changes the gut environment and leads to a change in the bacteria growing there, the researchers said.

Treatments

One bacterium in particular, Bilophila wadsworthia, was identified. It thrives in the extra bile produced to break down the fats. It went from being incredibly rare to nearly 6% of all bacteria in the gut in the high-fat diet.

Prof Eugene Chang, of the University of Chicago, said: "Unfortunately, these can be harmful bacteria. Presented with a rich source of sulphur, they bloom, and when they do, they are capable of activating the immune system of genetically prone individuals."

However, he said this could lead to possible treatments as the gut bacteria could be "reshaped" without "significantly affecting the lifestyles of individuals who are genetically prone to these diseases".

Commenting on the research, Dr Roy Sleator, from the Cork Institute of Technology, said: "Not only do the authors provide, what is in my opinion, the first credible explanation as to how Western diet contributes to the unusually high incidence in inflammatory bowel disease; they also suggest an effective means of dealing with such diseases, by simply reshaping the microbial balance of the gut."

Saturday, June 16, 2012

Childhood Obstructive Sleep Apnea (OSA): Treatment reverses brain abnormalities

Treatment of obstructive sleep apnea (OSA) in children normalizes disturbances in the neuronal network responsible for attention and executive function, according to a new study.

“OSA is known to be associated with deficits in attention, cognition, and executive function,” said lead author Ann Halbower, MD, Associate Professor at the Children’s Hospital Sleep Center and University of Colorado Denver.

“Our study is the first to show that treatment of OSA in children can reverse neuronal brain injury, correlated with improvements in attention and verbal memory in these patients.”

The results will be presented at the ATS 2012 International Conference in San Francisco.

In the study, children (ages 8-11) with moderate-severe OSA were compared to healthy controls.

Brain imaging with magnetic resonance spectroscopy imaging was performed at baseline in 15 OSA patients and seven controls, along with neuro-psychological testing.

OSA treatment consisted of adenotonsillectomy followed by monitored continuous positive airway pressure (CPAP) or nasal treatments. Brain imaging and neuropsychological testing was performed again in 11 OSA patients and the seven controls six months after treatment.

Compared with controls at baseline, children with OSA exhibited significantly decreased N-acetyl aspartate to choline ratios (NAA/Cho) in the left hippocampus and left frontal cortex, along with significant decreases in the executive functions of verbal memory, and attention.

Following treatment, both left and right frontal cortex neuronal metabolites normalized, and hippocampal metabolites improved with a medium effect size (0.5).

More complete reversal of hippocampal abnormalities was seen in children with milder OSA when apnea-hypopnea index (AHI) improved (although this is very preliminary data).

Verbal memory and attention improved with medium to large effect sizes. Improvements in attention and verbal memory were correlated with normalization of NAA/Cho in the right and left frontal cortex (p=0.5).

“We have demonstrated for the first time that treatment of OSA in children normalizes brain metabolites in portions of the neuronal network responsible for attention and executive function,” concluded Dr. Halbower.

“We speculate that if OSA is treated earlier, there may be a more brisk improvement in the hippocampus, a relay station for executive function, learning, and memory.”

“Our results point to the importance of early diagnosis and treatment of OSA in children, as it could potentially have profound effects on their development.”

Monday, June 11, 2012

Receptor may hold key to Multiple Sclerosis treatment

This image shows the A2A adenosine receptor (in red) abundantly expressed in the central nervous system (CNS). The blue colour identifies the nuclei of cells in the CNS.

A receptor recently discovered to control the movement of immune cells across central nervous system barriers (including the blood-brain barrier) may hold the key to treating multiple sclerosis (MS), a neuroinflammatory disease of the central nervous system.
 
In MS, immune cells enter the central nervous system and attack and destroy the myelin sheath surrounding the axons of nerve cells in the brain and spinal cord, resulting in blindness, paralysis, incontinence and many more symptoms.

The research, appearing last month online and in print June 1 in the Journal of Immunology, reveals how the A2A adenosine receptor expressed on blood-brain barrier cells acts as a gateway, allowing immune cells to enter the brain, where they can cause havoc in people with MS.

The blood-brain barrier is composed of specialized cells that selectively prevent substances from passing from the bloodstream into the brain.

"We found that expression of this A2A adenosine receptor is important for regulating the entry of cells into the brain; whereby its activation allows immune cell entry and its inhibition blocks entry," said Margaret Bynoe, associate professor of immunology at Cornell's College of Veterinary Medicine and senior author of the paper, which was also selected as a featured publication in the "In This Issue" section of the journal, where the top 10 percent of manuscripts are featured. Jeffrey Mills, a postdoctoral associate in Bynoe's lab, is the paper's lead author.

In this study, the researchers used mice where the A2A adenosine receptor was knocked out and then infused those mice with normal immune cells from wild-type mice expressing the A2A adenosine receptor.

This produced chimeric mice expressing the A2A receptor on immune cells, but not on blood-brain barrier cells.

Without A2A receptor on blood-brain barrier cells, the normal immune cells failed to effectively infiltrate the central nervous system, and thus, these mice were protected and developed less severe symptoms of MS-like disease.

"The absence of the A2A receptor on blood-brain barrier cells is similar to the effect of pharmacologically blocking the receptor with antagonists [drugs], which also protected mice from MS-like disease," Bynoe said.

"The implications of these findings are that, potentially, modulation of this receptor can be beneficial for future treatment of MS," she added.

Journal reference: Journal of Immunology  
Provided by Cornell University

Thursday, November 10, 2011

SAD: Take your light therapy, and stick it in your ear

Many readers in the Northern Hemisphere are likely already starting to experience seasonal affective disorder, appropriately enough known as SAD.

For those people fortunate enough not to be familiar with it, SAD is a mood disorder that is brought on by the shorter day-length experienced in winter - less sunlight results in gloomier people.

One of the most common treatments involves regular exposure to bright artificial lights, that appear to psychologically serve the same purpose as sunlight.

Now, one might assume that such light therapy would require that people see the light. According to the Finnish designers of the Valkee device, however, light also does the trick if you shine it up your ears.

The invention is based around the assertion that not only are our visual systems photosensitive, but so are our brains themselves.

More specifically, there are apparently 18 sites in our brains, where OPN3 photoreceptor proteins are located. These regions will supposedly react favourably to exposure to light, even when that light is filtered through tissue and bone.


The Valkee itself looks a lot like a personal music player, complete with earbuds. Instead of emitting music, however, these buds contain fiber optic lights.

By turning the device on and sticking the glowing fibers in your ears for about ten minutes a day, it is claimed that your brain will receive enough light to send the SAD packing.

Does it sound like quackery? A great deal of people would certainly say so.

Not among those people, however, would be a group of scientists from Finland's University of Oulu.

In two clinical trials, they had people with severe SAD use the device daily, for 8 to 12 minutes a day.

Afterward, when those people completed a BDI-21 questionnaire (a standard for assessing depression), it was found that 92 percent of the subjects in the first trial had completely recovered.

The information presented by the company is definitely somewhat difficult to sort out, although it appears that the results of the second trial were similarly encouraging.

A placebo group was included in at least one of the trials, to ensure that people weren't feeling better merely because they expected to.

To read more about the Valkee device visit their website

Sunday, October 30, 2011

Children with diabetes -Healthy halloween advice

While there are challenges, Halloween can still be fun for children with diabetes, an expert says

"They can enjoy Halloween and enjoy some of the sweets the holiday offers -- within reason," Dr. Kenneth McCormick, a pediatric endocrinologist and senior scientist at the University of Alabama at Birmingham Comprehensive Diabetes Center, said in a university news release.

"We give parents and kids three options and let them decide how they want to handle Halloween and the sweets that come with it," he explained.

The first option: Count the carbohydrates. 
A child tracks how many carbohydrates he or she consumes and takes, for example, one unit of insulin for every 15 to 20 grams of carbs.

"This is an easy option for kids on an insulin pump because they can just dial in an extra dose of insulin to compensate for what they are about to eat, but for kids that take shots, this could prove to be more difficult or inconvenient, especially if they have to go to the school nurse for an extra dose," McCormick said.

The second option: Exchange candy for other goodies.
"Parents can trade the child a gift, money or low-carb snack for their candy. Parents also can provide a substitute snack for their child if a Halloween party at school is an issue," McCormick said.

"We have been advising parents to do this for many, many years, and it is a solution that continues to work."

The third option: Save Halloween treats for an after-dinner dessert.
"By incorporating a sugary treat into mealtime, when a child would normally get a dose of insulin, it eliminates the need for adding doses to their regimen," McCormick said.

We wish you and your children a very merry, safe and enjoyable festival!

Tuesday, October 11, 2011

Selling you the Brain Balance Programme

Hearing that your child is dyslexic, is on the autism spectrum, or has ADHD can be very hard for a parent. After that diagnosis, parents want to be in control and feel that decisions must be made, but the choices are often confusing.

What’s best for the child: a drug, a special school program, therapy, all of the above? It is reported that these diagnoses are becoming more common, some studies indicate that autism spectrum disorders now affect 1 out of 64 children in the US. In the midst of this how do parents find effective treatment for their children?

Dr. Mark Smith claims to be the only active board-certified chiropractic neurologist in central Virginia. He is now opening a Brain Balance Achievement Center Richmond (http://www.brainbalancecenters.com) this month. He claims that this method helps parents and children who are working to overcome these learning and neurologigal behavioural difficulties.

The revolutionary Brain Balance Achievement Center approach offers an integrated and comprehensive non-drug, whole-child approach that includes academic performance, social abilities, cognitive function, sensory/motor skills, visual/spatial organisation skills, and nutritional diets.

Their overall goal is commendable and simple: to help kids literally change the connections in their brains, working on the basis that there is something wrong with the existing connections.

Dr. Smith says “I’ve worked with children in the Autistic Spectrum for the past 20 years, and it has become my passion to help these families heal."

He claims that; "People need to know that there are effective methods available to actually get to the underlying cause of these problems, that they are not doomed to just endure and ‘live with it’."

He also claims that; "We have seen tremendous improvement using these research based protocols and are thrilled with the results and excited to offer this program to the greater community.“

The Brain Balance Program was developed by Dr. Robert Melillo, based on his research on Hemispheric Integration Therapy (H.I.T.).

HIT claims to be a multi-modal approach to the treatment of ADHD, dyslexia, autism, Asperger’s, Tourette’s, learning disabilities, and other neurobehavioural disabilities found in children.

His research was the precursor to and foundation for the program, which was founded in 2003 to help children with neurobehavioural deficits improve their academic, social and behavioural functions.

We do not reccommend or condemn this research or subsequent 'treatment' and provide this article on it, purely for information. Caveat Emptor! Let the buyer beware!

Thursday, March 10, 2011

Benlysta® - A Breakthrough in Lupus Treatment

Scientific advances at The Scripps Research Institute were key to laying the foundation for the new drug Benlysta® (belimumab), approved today by the U.S. Food and Drug Administration.

Benlysta®, which treats the most common type of lupus, is the first in a new class of pharmaceuticals that prevents the body from attacking its own critical tissues.


“I am deeply gratified that our scientific findings have proven so valuable to drug discovery,” said Richard A. Lerner, MD, president of Scripps Research. “This development underlines the importance of basic academic science in laying important groundwork for life-saving medical advances.”

Benlysta®, developed by GlaxoSmithKline and Human Genome Sciences, is the first new drug treatment for lupus in 50 years.

Short-Circuiting the Cycle of Lupus
Benlysta® was approved for systemic lupus erythematosus, a chronic, life-threatening inflammatory disease affecting the joints, skin, kidneys, blood, heart, and lungs. It is often simply referred to as “lupus” (although there are other types of lupus, including one that affects solely the skin).

Estimates of the number of Americans affected by sytemic lupus erythematosus range from 161,000 to 1.5 million, according to the U.S. Centers for Disease Control. Lupus can occur at any age, but first appears largely in 15- to 40-year-olds, the majority of whom are women.

Lupus is an autoimmune disease, which occurs when a person’s body produces an immune response against its own tissues instead of solely attacking foreign invaders such as viruses, bacteria, and other toxins.

Symptoms can include debilitating fatigue, painful and swollen joints, fever, skin rash, and kidney problems.

The disease can also lead to arthritis, kidney failure, heart and lung inflammation, central nervous system abnormalities, inflammation of the blood vessels, and blood disorders.

Benlysta® (itself a type of immune molecule) acts by targeting a specific protein called B-lymphocyte stimulator, or BLyS, involved in stimulating the “autoantibodies” causing lupus and certain other autoimmune disorders.

Benlysta® is the first approved drug that disables BLyS, thus preventing the immune system’s destructive attacks against the body.

The Foundation
In the 1980s the therapeutic potential of antibodies — which recognize a wide range of foreign pathogens, then alert the immune system to the presence of the invaders — was widely recognized, as they are an important part of the body’s natural system for fighting illness.

But tapping that potential had proven difficult. Researchers at the time were working mainly with short snippets of antibodies and testing their effects through a slow and painstaking petri-dish process.

But Lerner led a Scripps Research team that made two critical advances to transform the field, ultimately leading to the discovery and development of drugs such as Benlysta®.

The researchers first developed a method of combining different pieces of antibodies isolated from human or animal cells into proteins long enough to encompass natural antibodies’ most critical portions — the parts actually binding to and neutralizing infectious agents or otherwise unwanted material.

The scientists dubbed this technique “repertoire cloning,” because it allowed them to build libraries of compounds that encompassed the full repertoire of a natural immune system.

This was a game-changing development.

Eliminating the Petri-Dish Bottleneck
But even with an expansive repertoire, putting it to use was a separate problem. It was a second key Scripps Research discovery that helped eliminate the petri-dish bottleneck.

In 1991, Lerner and his colleagues pioneered a technique for employing phage display to facilitate large “combinatorial antibody libraries” to find human antibodies that could be used therapeutically.

Combinatorial antibody libraries allow human antibodies to be identified directly by searching among billions of antibody variants taken from human blood samples to find those that bind to a particular target — such as BLyS — involved in a particular disease.

In this technique, the scientists hijack the inner workings of phages (viruses that attack bacteria). By inserting genetic sequences encoding active portions of antibodies, the researchers are able to make phages displaying on their surfaces the antibody of interest.

These antibody-displaying phage particles can then be tested en masse for their ability to bind to molecules of interest. Successful binders can then be purified and identified as a target for additional research.

With the British Medical Research Council (MRC) Laboratory of Molecular Biology, Scripps Research licensed the inventions to Cambridge Antibody Technology (now part of AstraZeneca) to facilitate exploitation of the technology for creation of new medicines.

In 1999, Cambridge Antibody Technology partnered with Human Genome Sciences, which entered into a co-development and commercialization agreement with GlaxoSmithKline in 2006.

While much technology has changed over the decades, variations of combinatorial antibody libraries are still a mainstay of drug discovery research. Commercialized throughout the 1990s, the promise of this method is now beginning to be realized — today with Benlysta®, tomorrow, Lerner predicts, with other life-saving drugs.

About The Scripps Research Institute
The Scripps Research Institute is one of the world’s largest independent, non-profit biomedical research organizations.

Scripps Research is internationally recognized for its discoveries in immunology, molecular and cellular biology, chemistry, neuroscience, and vaccine development, as well as for its insights into autoimmune, cardiovascular, and infectious disease.

Headquartered in La Jolla, California, the institute also includes a campus in Jupiter, Florida, where scientists focus on drug discovery and technology development in addition to basic biomedical science.

Scripps Research currently employs about 3,000 scientists, staff, postdoctoral fellows, and graduate students on its two campuses. The institute’s graduate program, which awards Ph.D. degrees in biology and chemistry, is ranked among the top ten such programs in the nation.

For more information, see www.scripps.edu

Saturday, March 13, 2010

Sleep Deficit and ADHD, which came first?

Researchers have long since found that children with ADHD demonstrate significantly more difficulty sleeping at night than their undiagnosed peers.

Unfortunately, too many psychiatrists have overlooked sleep disturbances as a possible cause of the ADD/ADHD because previous studies on the subject provided mixed evidence.

Recent finding that children with ADD/ADHD do have more sleep disturbances, however, means that future studies are needed and should be aimed at the possibility of separating the causes, from the condition.

This would mean that the treatment and reduction of sleep disturbances and poor sleep behaviour, may improve daytime ADHD symptoms.

Parents and guardians know that children with ADD/ADHD demonstrate more bedtime resistance, e.g. refusing to get ready for bed, refusing to remain in their own bed, difficulty with falling asleep, restless and disturbed sleep, etc.

ADHD children are also more likely to have other sleep orientated or sleep disordered symptoms e.g. snoring, long pauses in breathing, sleep apnea, etc. This has the added issue of the children not being able to wake properly, or on time.

We all know the detrimental effects of not sleeping well and not feeling refreshed from a night spent sleeping. We feel grouchy, are more clumsy and later in the day we will experience increased daytime sleepiness and be looking for a catch-up nap.

Resolving Sleep Disorders
Children with ADD/ADHD are reported to take longer to transition from full wakefulness, through sleepiness to finally falling asleep, as well as experiencing more shallow breathing and a lower respiratory rate while sleeping.

We learn good bedtime routines from our parents and family. Good sleep behaviour is a learned experience and it needs to be taught to modern children, living in a 24 hour always-on society.

We need to teach them how to withdraw at the right time, how to relax and calm the senses before preparing for bed. The bedroom is a place for sleeping, so no TV, no computer games or other stimulating activities. It should be warm, not hot. A safe, secure place to fall comfortably asleep.

Seek Help
Sleep problems with ADHD children can be addressed separately from their other ADHD symptoms and once this hurdle is overcome it will have a calming effect on the child and a beneficial effect on their behaviour generally.

The skills learned in treating sleep deficits can be expanded into everyday life and will have added beneficial effects on the whole family. The need to improve the difficult relationships inside a family affected by ADHD is essential if everyone is to get the best out of their lives.

For more invaluable information on sleep behaviour training and bedtime parenting skills click on the link to Dream-Angus.com