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SCIENTIFIC/RESEARCH ARTICLES
Attention-deficit/Hyperactivity Disorder - New Guidelines for Treatment The American Academy of Pediatrics (AAP) released new recommendations today for treating school-age children with attention-deficit/hyperactivity disorder (ADHD).
This guideline is intended for primary care physicians who have already accurately established an ADHD diagnosis. Last year
the AAP released guidelines for diagnosing ADHD.
ADHD is a condition of the brain that makes it difficult for children to control their behavior in school and social settings. It is one of the most common chronic conditions of childhood and affects between 4 and 12 percent of all school-age children. About 3 times more boys than girls are diagnosed with ADHD.
Children with ADHD may experience significant functional problems such as school difficulties, academic underachievement, troublesome relationships with family members and peers, and behavioral problems. Different children have different symptoms or problems with ADHD.
The new standardized AAP guidelines were developed by a panel of medical, mental health and educational experts. The AAP partnered with The Agency for Healthcare Research and Quality, and the Evidence-based Practice Center at McMaster University in Canada to develop the evidence base of literature on the topic. The recommendations were based on scientific studies that carefully evaluated treatments of school-age children with ADHD.
The new guidelines include the following recommendations:
Primary care clinicians should establish a treatment program that recognizes ADHD as a chronic condition. This implies the need for education about the condition, and a sustained monitoring system to track the effects of treatment and developmental changes in behavior.
The treating clinician, parents, and child, in collaboration with school personnel, should specify appropriate goals to guide management. Goals should relate to the specific problems of the individual child, e.g., school performance, difficulty finishing tasks, problems with interactions with schoolmates.
If appropriate, the clinician should recommend behavior therapy and/or stimulant medication to improve specific symptoms in children with ADHD. The guideline provides a review of the scientific evidence for recommending medication and behavior therapy. When the treatment for a child with ADHD has not met its goals, clinicians should re-evaluate the original diagnosis, all appropriate treatments, adherence to the treatment plan, and coexisting conditions, including learning disabilities and mental health conditions.
The clinician should provide a periodic and systematic follow-up for the child with ADHD. Monitoring should be directed to the child's individual goals, and any adverse effects of treatment, with information gathered from parents, teachers and the child. The guidelines recommend areas for future research in treatment options, long-term outcomes and other areas in the management of children with ADHD.
ADD/ADHD Disorder - New Guidelines Already one of the most common and most studied conditions of childhood, ADHD treatment has increased in recent years. Treatments, both medications and behavior therapy, improve the functioning of most children with ADHD. Long-term management of ADHD requires active teamwork among clinicians, parents and teachers to help assure the best outcomes. While there is no proven cure for ADHD at this time, and the cause is unclear,
research is ongoing to learn more about the role of the brain in ADHD and the best ways to treat the disorder.
Source: American Academy of Pediatrics, press release October 1, 2001
For more in-depth information about ADD/ADHD, please visit Medicine Net's Attention Deficit Disorder Forum http://www.medicinenet.com/script/main/forum.asp?li=MNI&articlekey=258
Patients with ADHD display increased motor activity, inattention, and impulsivity.
Although there are many models for ADHD, one that may be particularly helpful is the possibility of defective inhibitory processes in the brain.
Initial neuroimaging studies done with PET scans and glucose showed that adult ADHD patients had decreased glucose utilization compared with controls.[6] However, when adolescents were evaluated, this relationship appeared to be true for girls but not for boys. The more sexually developed the girls were, the greater difference between glucose utilization in their brains compared with utilization in controls.
In both genders, the prefrontal cortex was most affected, but the global result was not significant in boys or sexually immature girls.
When patients on stimulant medication were scanned, there seem to be very little difference in the scans before and after medication, even though there was a clinical response. With an intravenous dextroamphetamine challenge, there were some differences in striatum, and less so in the cerebellum.
Given the association of dopamine to ADHD through the effectiveness of stimulants, animal studies, and some plasma and cerebral spinal fluid studies, scans using a radioactively labeled dopamine compound were performed.
The scans showed that a decrease in dopaminergic activity in the anterior medial frontal cortex correlated with symptom severity. Adolescents also had an increase in dopaminergic activity in the midbrain that correlated with symptoms and a trend of decreased prefrontal activity, indicating that there may be a developmental process for ADHD throughout the lifecycle.
Source: Medscape
International Jubilee Congress of the World Psychiatric Association Day 1 - June 26, 2000 Functional Neuroimaging in Psychiatry Thomas AM Kramer, MD http://www.medscape.com/medscape/cno/2000/WPA/Story.cfm?story_id=1517 Attention Deficit Disorder -The Merck Manual
A Prognosis
Follow-up studies have shown that children with ADD do not outgrow their difficulties. Problems in adolescence and adulthood occur predominantly as academic failure, low self-esteem, and difficulty learning appropriate social behavior. Adolescents and adults with a history of ADD with impulsivity have a high incidence of personality trait disorders and antisocial behavior; most continue to display impulsivity, restlessness, and poor social skills. ADD persons with and without hyperactivity seem to adjust better to work than to academic and home situations.
Interpersonal and social problems often persist into adulthood; depression and suicide attempts (not related to methylphenidate) are reportedly higher than in the normal population. Low intelligence, aggressiveness, social and interpersonal problems, and parental psychopathology are predictors of poor outcomes in adolescence and adulthood.
Source: The Merck Manual
http://www.merck.com/pubs/mmanual/section19/chapter262/262d.htm ADD-areas of brain affected same as HD
Paying Attention to ADD~Dana Foundation Article 1999 Deb - I'm copying you on this message because I think this would be an excellent questionfor the HDSA to ask a physician (Dr. Nance?) specializing in juvenile HD. Is there reason for concern with JHD's being misdiagnosed with ADHD's and what are the affects of Ritalin on JHD's? Kelly was diagnosed with ADHD when she was 5 and was on medication (Dextrine) until she was 12. Since Kelly's CAG count was only 16 and 56 (low for juvenile HD) I wondered, after this article, if the medication accelerated her HD symptoms or even contributed to her later (pre-teen) co-dependency on drugs?
After reading this article a lady in Texas took her at-risk son to the neurologist since he was on Ritalin for ADHD. The neurologist did some researching and decided that Ritalin should not be given to JHD's or those children at risk and prescribed another medication which is less harmful.
The key here is where their findings show:
"They have found very small -5 to 10 percent-but consistent differences in the sizes of three distinct brain regions in ADHD children: the frontal lobe, basal ganglia, and the cerebellum. These regions are significant, says Giedd, because their individual jobs in the brain are to control the functions, such as cognition and movement, that have gone a little haywire in kids with ADHD.
Researchers are discovering that when children-and in one study, mice-with ADHD are given Ritalin they respond differently (and their brains look different) than normal children who are given the same drug."
Looking at the same dopamine rich brain regions as the NIMH investigators-the frontal lobes and structures of the basal ganglia-they found that activity between the two groups was very different.
Even more interesting were the images after each group of children took Ritalin; the ADHD kids showed increased brain activity in two regions of the basal ganglia-the putamen and caudate-while the kids without
the disorder showed decreased activity in these regions. My concern after reading this when it first came out was that children with Juvenile HD most likely already have some damage to those regions of the brain which is probably the underlying cause of the behavior therefore the medications prescribed for ADHD's, such as Ritalin, may be doing more harm to a JHD then a child who only has ADHD.
Love
Jean UPDATE: Please see response from Dr. Nance elsewhere on this site, 2002
ADD-areas of brain affected same as HD Paying Attention to ADD~Dana Foundation Article 1999 Volume 9 No.2 March/April 1999
The Charles A. Dana Foundation http://www.dana.org/articles/bwn_0499.cfm By Terri Rutter Any parent confronted with an unruly child must wonder, at some point, if he or she has attention deficit hyperactivity disorder, ADHD. Affecting an estimated 3 to 5 percent of all school-age children, ADHD is the single most commonly diagnosed behavioral disorder of childhood.
The prevalence of ADHD is partly explained by its wide variability; some children are wildly uninhibited while others are quiet, albeit inattentive, daydreamers. The symptoms of ADHD are simply-or complexly-the inability to sit still and pay attention. Yet, because the disorder is seemingly so widespread and it displays so much variability among those affected,
many professionals and parents have questioned whether ADHD is even a valid brain-related disorder. This question was debated in November at a National Institutes of Health Consensus Conference on the diagnosis and treatment of ADHD. But the attendants' only consensus opinion was that there is a need for more research. Adding fuel to the doubters' fire is that there is no clear cause of ADHD, so, in some people's minds, the diagnosis itself is dubious. Although an early term for the disorder is "minimal brain dysfunction," an anomaly, such as a lesion, in the brain that can account for the disorder has not yet been identified.
"When we first started, we were looking for the hole in the brain," says Jay Giedd, a staff scientist in the Child Psychiatry Branch of the National Institute of Mental Health, NIMH. "But there's no damage. There are biological differences," he says, "but the brain is not broken."
Giedd is among a handful of neuroscientists who are searching for an elusive-although scientists believe certain-neurological basis for ADHD. Their work will lead to better diagnoses and, hopefully, better treatments.
Giedd and his colleague F. Xavier Castellanos, as part of the ADHD Imaging Project at the NIMH, are using magnetic resonance imaging to study the brains of children diagnosed with ADHD. They have found very small-5 to 10 percent-but consistent differences in the sizes of three distinct brain regions in ADHD children: the frontal lobe, basal ganglia, and the cerebellum. These regions are significant, says Giedd, because their individual jobs in the brain are to control the functions, such as cognition and movement, that have gone a little haywire in kids with ADHD.
These are also brain regions rich in the neurotransmitter dopamine, which has a role in cognition as well as movement. The imaging studies seem to suggest, therefore, that smaller dopamine regions might mean fewer dopamine circuits in the brain, which means less available dopamine to fire the functions that depend on it.
Other research is using Ritalin, a psychostimulant drug that is the most common-although controversial-treatment for ADHD. Like other stimulants, Ritalin makes more dopamine available to the brain. The drug has also become a key component in research into the neurological basis of the disorder. Researchers are discovering that when children-and in one study, mice-with ADHD are given Ritalin they respond differently (and their brains look different) than normal children who are given the same drug.
Chandan Vaidya and her colleagues at Stanford University keyed in on dopamine when they used functional magnetic resonance imaging, fMRI, to look at the brains of a small cohort of ADHD boys while they performed a series of especially designed video games. The investigators compared these images with those of the brains of normal children doing the same activity. Looking at the same dopamine rich brain regions as the NIMH investigators-the frontal lobes and structures of the basal ganglia-they found that activity between the two groups was very different. Even more interesting were the images after each group of children took Ritalin; the ADHD kids showed increased brain activity in two regions of the basal ganglia-the putamen and caudate-while the kids without the disorder showed decreased activity in these regions. "Our study is unique," says Vaidya, "because it is the first to use MRI to look at the brains of normal children on Ritalin." While further research is expected in this area, Vaidya suggests that this study may provide evidence that there are distinct differences in the dopamine receptors
in ADHD kids. They published their findings in the November 1998 issue of the Proceedings of the National Academy of Sciences. Marc Caron, on the other hand, believes that serotonin may be a more significant factor than dopamine in ADHD children; he also uses Ritalin to help explain why. In the January 15 issue of Science, Caron and his colleagues at Duke University present research that suggests a
reason for why Ritalin has a paradoxical calming effect in children with ADHD: because it reacts on the brain's serotonin pathways, as well as the dopamine. Serotonin, another neurotransmitter, is involved in regulating moods, particularly depression and anxiety, and emotional states. Caron's group of investigators looked at a strain of specially bred mice called "knockout" mice that were missing the gene for the dopamine transporter, a kind of valve that tightly controls the amount of dopamine available in the brain; thus, these mice had high levels of dopamine. But, contrary to what would be expected, the mice exhibited all the behaviors that look like ADHD in humans: hyperactivity, agitated response to novel environments, and so forth.
The investigators injected these hyperactive mice with Ritalin and they calmed down. But, their dopamine levels remained high. Because the control mice also showed both high levels of dopamine and high activity when given Ritalin, the researchers surmised that it couldn't be
dopamine that was causing the knockout mice to calm down. The researchers then gave the knockout mice fluoxetine, or Prozac, which acts on the serotonin pathway, and the mice calmed down.
"The interesting prospect in these findings," says Caron, "is that serotonin uses 15 different receptors to mediate its effects on the brain. If we can find which one of these 15 is responsible for the calming effects of Ritalin in the knockout mice, then it is likely that we will be able to mimic, in at least a subset of ADHD patients, these effects with a selective and much safer drug."
Better treatments and diagnostics will help quiet the chaos surrounding ADHD, for children and their parents.
Terri Rutter is senior editor at Dana.
ADHD Current Diagnosis Oct. 2000
ADHD Brains also show reduction in size From Medscape 2000 American Academy of Pediatrics Annual Meeting Day 1 - October 28, 2000 Attention Deficit Hyperactivity Disorder: Current Diagnosis and Treatment http://www.medscape.com/medscape/cno/2000/AAP/Story.cfm?story_id=176 Etiology
Although ADHD remains a heterogeneous condition for which no one etiology has emerged,there has been growing evidence for the explanation that the condition is caused by a complex interaction between biologic and environmental factors -a phenomenon similar to that of other mental disorders, such as depression and anxiety.
There is evidence that both morphologic and functional brain differences are present in individuals with ADHD compared to a normative sample. Individuals with ADHD have a consistent but moderate reduction in average size of the corpus callosum, basal ganglia (caudate and globus pallidus), and frontal lobes, compared with normal controls.[7-10]
Functionally, there is striatal hypoperfusion in individuals with ADHD compared with normal controls.[11-13]
Studies have identified the most common etiology to be heredity. Twin studies[14-18] reveal that 75% of the statistical variance between those with ADHD and normative samples can be attributed to genetic factors.
There is also an increased risk for ADHD in first-degree relatives.[19-21] Most recently, molecular genetic studies have identified errors in the dopamine transporter (DAT1) gene, [22,23] the D4 receptor gene (DRD4)[24] and the human thyroid receptor beta gene.[25]
Diagnosis While there are statistical differences in the size and function of the brains of individuals with ADHD compared with normal controls, there are such wide variations in both normal individuals and those with ADHD that neuroimaging is not yet a useful clinical diagnostic tool.
Furthermore, despite the major genetic contribution to the etiology, the diagnosis of ADHD remains dependent on the reports of observed behaviors from those most closely supervising children, ie, their parents and teachers. Based on the recent AAP guidelines for the diagnosis of ADHD,[4] pediatricians are expected to:
Comorbid Disorders
A large proportion of children with clinical features of ADHD have other developmental and/ or mental disorders as well. Comorbid conditions of ADHD include: -Learning disabilities
-Oppositional-defiant or conduct disorder -Anxiety or mood disorder -Language and communication disorders -Developmental coordination disorder (dyspraxia) -Tourette's syndrome or chronic tic disorder -Generalized unresponsiveness to thyroid hormone -Personality disorders (in adolescence)
ADHD symptoms can be seen in other conditions, such as the pervasive developmental disorders (PDD,) but children with these disorders are not considered to have a separate diagnosis of ADHD. ADHD-Perspectives from 154th Annual Meeting
Atomoxetine studies 154th Annual Meeting of the American Psychiatric Association Day 4 - May 8, 2001 Perspectives on ADHD Jerrold Rosenbaum, MD Medical Writer: Allison Kienke There has been a great deal of interest over the years in attention-deficit hyperactivity disorder (ADHD). Current thinking about ADHD is changing and clinicians and researchers are beginning to view this disorder as one that appears across the life cycle and may present in many different ways.
The topics explored at the 154th Annual Meeting of the American Psychiatric Association include the symptoms of ADHD throughout the life cycle, substance abuse issues in ADHD, cognitive features of ADHD, and a potential new medication for ADHD treatment.
Symptomatology of ADHD
In reviewing ADHD symptomatology across the life cycle, Thomas Spencer, MD,[1] of Massachusetts General Hospital, Boston, explained that the controversy regarding the persistence of ADHD over a lifetime derives from the inherent waxing and waning its various categories of symptoms. The core symptoms -- inattention, restlessness and impulsivity-- are defining symptoms of ADHD at all ages.
The functional impairments (eg, occupational failure and social and intellectual deficits), on the other hand, also occur in other disorders such as dyslexia. He described a third symptom group -- those with comorbid disorders that are often present with ADHD.
Dr. Spencer highlighted the shift in ADHD symptomatology that often occurs between childhood (ages 6-12 years) and adolescence (ages 13-18 years). Although symptoms of carelessness, poor organization and poor follow through on tasks is seen at all ages, blurting out, intruding, disrupting, poor peer relations, and inability to wait turns are seen mainly
in children. By adolescence, however, there is less structure and often more demand for independent work and multitasking, therefore, symptoms including restlessness (rather than hyperactivity), failure to complete independent work, and engaging in 'risky' behavior appear. Adolescents with ADHD are at risk for school failure, poor social relationships, car accidents, delinquency, drug/alcohol abuse, and poor vocational outcome.
The controversy over whether ADHD persists or resolves over time is sustained, in part, by the fact that some symptoms (eg, hyperactivity and impulsiveness) diminish over time, whereas inattention tends to persist.
As the patient with ADHD ages from childhood to adolescence to adulthood, the disorder becomes less of a hyperactive-behavioral problem and more of a cognitive difficulty. In early childhood, children are asked for limited responses in a very structured, sheltered environment. As children grow and begin to enter adolescence, there are increasing demands, such as multitasking and independent organization.
Executive functions, especially associated with the prefrontal cortex -- such as working memory, self-regulation of affect motivation and arousal, error detection, and choice-making -- become increasingly important with age.
Dr. Spencer argued that ADHD is not variable but persists over time, unless it diminishes. Many individuals develop adaptive habits, such as rigid organization, impulse delay, organizational aids, and inner fidgeting with outward calm. These compensatory mechanisms often confuse or hide the presence of ADHD; chronicity and follow-up studies report the ADHD "lifetime" as ranging from 8-34 years. He noted, however, that the way ADHD is defined greatly affects the measured persistence of the disorder.
Studies which use ADHD criteria of hyperactivity, learning disabilities, and Diagnostic and Statistical Manual of Mental Disorders, Second Edition (DSM-II) hyperkinesis, report that ADHD goes away quickly. But when ADHD is defined using the DSM-III, DSM III-R or DSM-IV, the persistence is much longer.
The continuance of ADHD into adolescence and adulthood is associated with school and work failure and low self-esteem, as well as increased risk for antisocial and substance abuse disorders. Studies of ADHD children who have reached adulthood, after controlling for IQ, show worse scores on standardized achievement tests,[2] significantly more academic problems in school[3] and lower occupational attainment[4] than those who don't have ADHD.
Data from an adult ADHD study of occupational impairment[5] show that employers reported worse performance in regards to completion of tasks, independent work, and relationships with supervisors compared with healthy individuals.
In addition, motor vehicle driving studies using computer-simulated driving tests report that ADHD drivers have more crashes, scrapes, and erratic steering. And, official driving records show that individuals with ADHD have more speeding citations, license suspensions and crashes (including more which caused bodily injury).[6]
People with ADHD also have trouble with organizing and maintaining the home, managing finances, and remaining health conscious.
Results from twin studies comparing ADHD heritability in monozygotic dizygotic twins, and indicate that ADHD is one of the more heritable psychiatric conditions, with heritability rates ranging from 0.60 to 0.91[7,8]
Family-genetic studies report that biological relatives of children with ADHD are at increased risk for ADHD. It was also noted that 11 or 12 family-genetic studies report a greater risk of ADHD in parents of children who are ADHD.[9] In addition, adoptive relatives have a lower risk of ADHD than biologic relatives.[10,11]
Dr. Spencer concluded by reiterating the striking continuity of ADHD throughout the life cycle, although symptoms change slightly in executive function. Neuroimaging studies and studies of impairment, treatment effectiveness, family genetics, gene candidates, comorbidity, and
neuropsychological testing converge to describe a disorder (ADHD) that persists throughout the life cycle. ADHD and Substance Abuse
The clinical presentation of comorbid substance abuse disorders and ADHD is common, and research has shown a high prevalence of ADHD in substance abusers as well as ADHD to be a risk factor for substance abuse.[12]
Timothy E. Wilens, MD,[13] from Massachusetts General Hospital, described 2 ongoing studies of ADHD and substance abuse, the first of which introduced preliminary data from an ongoing open trial which seeks to determine whether bupropion SR will effectively treat both ADHD
and substance abuse in adults. Subjects were outpatient adults, aged 18-60 years, and diagnosed by structured interview inclusion for ADHD and substance abuse. Potential subjects were excluded if they suffered from severe substance abuse; medical conditions; had a history of cardiac arrhythmias, seizures,
eating disorders, or organic brain disorders; or were on psychotropics. Although there was a high attrition rate, nevertheless 16 of 28 subjects completed the trial. The preliminary findings show bupropion SR to be an effective treatment for ADHD as well as substance abuse. Using last-observation-carried-forward data, there was a significant reduction of 57% in the DSM-IV ADHD symptom checklist after 6 weeks of bupropion treatment. In addition, at the end of 6 weeks, there was a 31% reduction in substance use, which wasmeasured by both urine chemistry and self-report. Dr. Wilens noted that many of these individuals have continued to maintain sobriety and have indicated an "anticraving" effect of the medication gave them power to abstain.
Bupropion was well tolerated and there were no reports of interaction between bupropion and substances of abuse. He emphasized the necessity to first stabilize the addiction and afterward address the ADHD.
Another question Dr. Wilens addressed is whether ADHD pharmacotherapy in children predisposes them to a substance abuse problem or alternatively reduces later substance abuse, a concern receiving much public health attention.
Data were available from a study conducted at Massachusetts General Hospital of children 10 and 11 years of age, who were either untreated or treated for ADHD (mostly with stimulants), and followed late into adolescence.[14] The study included 45 children with ADHD with no
medication exposure, 117 children on medications, and 344 non-ADHD controls. Both ADHD and substance abuse diagnoses were made by structured interview and consensus among investigators. The medicated and unmedicated groups were matched at baseline for predictors of substance
abuse (social class, gender, family history, rates of conduct or bipolar disorder). In contrast to some popular beliefs, the data showed a protective role of stimulant treatment in preventing the later development of substance abuse disorders. Exposure to stimulants is not putting children at a greater risk for substance abuse.
The medicated group had lower rates of marijuana, cocaine and alcohol abuse, whereas the unmedicated group appeared to be at a greater
risk for substance abuse. Dr. Wilens noted that there are at least 4 other reports in support of these data.[13] ADHD and Neuropsychological Deficits
In exploring the cognitive features of ADHD and the possibility that ADHD encompasses more than just the observable symptoms of excess activity, inattention, and hyperactive impulsivity, Rosemary Tanneck, PhD,[15] from the Hospital for Sick Children, Toronto, Ontario, considered several questions:
There are crucial elements to consider regarding cognitive impairments in ADHD. First, these cognitive impairments could be co-occurring but unrelated. Alternatively, the behavioral problems caused by ADHD could give rise to the cognitive difficulties. Or, it may be that the cognitive
problems are giving rise to the behavioral symptoms. Dr. Tanneck explained that if this last possibility is true, then the cognitive impairments need to be carefully examined and targeted treatments developed. The argument is strengthened by evidence that cognitive dysfunctions are occurring in the majority of ADHD patients, across the
lifespan and they are specific to ADHD If these deficits were seen as preceding the disorder, then predicting ADHD onset would be possible. There are 2 specific "executive function" deficits which can, in actuality, be distinguished by neuroimaging: response inhibition and working memory. In reviewing the latest findings, there is evidence of response inhibition deficits across the lifespan, as measured by the Stop Signal test.[16]
Multiple studies, conducted in various countries, report children, adolescents, and adults with ADHD as showing slower response inhibition when compared with non-ADHD matched controls.
In addition, comorbidities moderate these response inhibition impairments oppositional defiant disorder (ODD), anxiety, and dyslexia have all been shown to attenuate the impairment.
Dr. Tanneck also considered the question of a possible genetic role in the response inhibition impairments, but the studies have not been done. She also addressed the questions of whether response-inhibition deficits are universal in ADHD and/or specific to ADHD. The answer to both questions is no.
Inhibition deficits are shown in only about 30% to 40% of those with ADHD and the inhibition has been shown to be impaired in patients with dyslexia without ADHD as well as in patients with specific learning disorder but not ADHD.
The second cognitive marker described was working memory, an essential aspect of higher-level learning. It was defined as the ability to retain, associate, and manipulate on-line memory storage over a brief time period.
The more recent interpretations of working memory describe it as crucial
in the ability to focus. A recent paper in Science reported that the greater the working memory load, the more an individual will be distracted by irrelevant information.[17] It proposed that perhaps either impairments in working memory give rise to distractibility or vice versa. There is some evidence, albeit equivocal, of cognitive impairments in ADHD in terms of response inhibition, working memory, and lapses in attention as defined by variability in response time. There are also suggestions, which are limited by experimental design variability, that these cognitive
impairments may underlie and give rise to the actual symptoms of ADHD. Dr. Tanneck highlighted, the following clinical implications:
New Possibilities for Nonstimulant Treatment of ADHD
A new investigational treatment for ADHD atomoxetine (formerly tomoxetine), is thought to act by a blockade of the presynaptic norepinephrine transporter.
According to David Michelson, MD,[18] from Eli Lilly and Company, Indianapolis, Indiana, the drug has been shown to be quite selective in
that it has very low affinity for all other receptors yet a very high affinity for the norepinephrine transporter. The drug is metabolized through the cytochrome P450 2D6 pathway, and studies have closely looked at both slow and fast metabolizers. Atomoxetine's half-life is around 4 hours (and approximately 15 hours in slow metabolizers). Its single active metabolite is cleared from the
body in less than 30 minutes, and nearly all of the drug is excreted in the urine. Dosing is around 1.2 mg/kg/day, and the drug has been given twice daily in all studies. Because the medication is a nonstimulant, later-day dosing is not problematic.
Atomoxetine efficacy has been shown to be consistent across symptom domains. Dr. Michelson discussed preliminary data from a study showing atomoxetine to be more effective than methylphenidate.
According to Dr. Michelson, 4 placebo-controlled studies (3 in children, 1 in adults) have been completed and all 4 have shown robust separation between atomoxetine and placebo. In addition, there are several studies in progress, some of which are investigating long-term maintenance treatment, comorbidities, and comparisons against other treatments.
In 1998, atomoxetine for adult ADHD was assessed in a double-blind, placebo-controlled, 3-week crossover study in 22 adults with well-characterized ADHD.[19]
Treatment with atomoxetine at an average dose of 76 mg/day was well-tolerated, and 11 of 21 (52%) patients showed improvement (defined as > 30% improvement in ADHD symptoms) after receiving atomoxetine, compared with only 2 of 21 (10%) patients who improved after receiving
placebo (P < .01). Random-effects analyses revealed that response attained statistical significance by the second week of treatment and there was further improvement by week 3. Neuropsychological measures of inhibitory capacity from Stroop tests were used to assess improvement.
Pooled data from the 4 studies (atomoxetine n = 270; placebo n = 340) show the following:
Atomoxetine would be the first nonstimulant agent approved for the treatment of ADHD, and it shows promise as an alternative treatment for this disorder. Summary
In conclusion, it is important to take a broad view of ADHD because it affects people of all ages and in many different ways. Differentiating the various cognitive features of ADHD, comorbid disorders, and the clinical presentations throughout the life cycle is important for clinicians. By delineating the various aspects of the disorder, appropriate new nonpharmacologic and pharmacologic interventions can be designed and implemented at all age levels. References
See Source Medscape Article at http://www.medscape.com/medscape/cno/2001/APACME/Story.cfm?story_id=2261 Atomoxetine for ADHD Non-Stimulant Medication Nonstimulant Therapy Shows Efficacy In ADHD
May 14, 2001 WESTPORT (Reuters Health) - An investigative drug shows promise as an effective nonstimulant alternative for treating attention deficit hyperactivity disorder (ADHD), according to Dr. David Michelson, who presented data at the 154th annual meeting of the American Psychiatric Association in New Orleans this week.
Atomoxetine is more effective than placebo for treating ADHD and may be more easily tolerated, said Dr. Michelson, the medical director at Eli Lilly responsible for the drug's development. In several double-blind, placebo-controlled studies funded by Eli Lilly that involved both adults and children, he and colleagues found that atomoxetine was superior to placebo in controlling ADHD symptoms.
In one study with a methylphenidate arm, the investigators found evidence that atomoxetine is more easily tolerated than methylphenidate. For example, atomoxetine appears not to be associated with insomnia, Dr. Michelson reported.
"Atomoxetine seems to work by blocking the norepinephrine transporter and doesn't involve the dopamine receptors directly," he told Reuters Health. "Therefore, it has a different mechanism of action than the stimulants commonly used to treat ADHD."
"Clinicians and parents have been looking for alternatives to stimulants for the treatment of ADHD for years," coinvestigator Dr. Christopher Kratochvil, of the University of Nebraska, noted in a separate interview with Reuters Health. "There are concerns about side effects, and about reports of children and adolescents using [methylphenidate] recreationally."
"We're looking for an alternative class of medications that will be effective and have a different side-effects profile than stimulants," he continued. "Indications are that atomoxetine is not an abusable drug; therefore, it's likely not to be a scheduled drug."
Children with ADHD who have other comorbidities, such as anxiety disorder, may be more effectively treated with a nonstimulant alternative, Dr. Kratochvil added.
In his experience, atomoxetine has been a safe and effective treatment for ADHD. Phase III studies are ongoing, he said, and Eli Lilly is preparing to submit an application to the US Food and Drug Administration for approval of atomoxetine for ADHD later this year.
Pooled data from the 4 studies (atomoxetine n = 270; placebo n = 340) show the following:
Atomoxetine would be the first nonstimulant agent approved for the treatment of ADHD, and it shows promise as an alternative treatment for this disorder. See file for:
Symptomatology of ADHD 154th Annual Meeting of the American Psychiatric Association Day 4 - May 8, 2001 One a day pill for ADHD
Concerta, a new ADHD medication that's only taken once a day. The surface of the pill is absorbed immediately. Then the containers inside the pill release more medication over the following 12 hours.
Child psychiatrist Peter Jensen, M.D., says the constant dosing eliminates the ups and downs that often come with traditional medications. "Concerta lasts 10 to 12 hours and is designed to give a very smooth sustained release for maximum benefit and then shut off, at 10 to 12 hours, so that the child's appetite and sleep are fine later at the end of
the day," says Dr. Jensen, of the Center for the Advancement of Children's Mental Health at Columbia University in New York. The once a day dosing also helps erase the stigma that often goes with ADHD.For Dianelli, it means acceptance from teachers and friends.
Concerta is the first of the slow-release medications to be created for ADHD. Several others are expected to be introduced in the next year.
If you would like more information, please contact:
Center for the Advancement of Children's Mental Health
1051 Riverside Drive, Unit 78 New York, NY 10032 (212) 543-5334 Source Ivanhoe
http://www.ivanhoe.com/stream/longlastingadhdhelp.shtml Long-Lasting ADHD Help
Television News Service/Medical Breakthroughs Ivanhoe Broadcast News General Practioners "not qualified" to prescribe Ritalin
13 August 2001, 16:31
LONDON - By Deirdre Lee - GPs are the first port of call when a
parent is concerned about their child's behavioral health, but a new survey suggests they are not adequately trained to deal with such problems. Despite the fact that 85 per cent of GPs questioned in the survey
had at least one child in their practice with a diagnosis of attention-deficit hyperactivity disorder (ADHD), only 6 per cent said they had received formal training on the condition. Many had instead gained their information from medical journals, television and magazines. Eighty-four per cent of GPs said they would value further training
in ADHD and 88 per cent wanted training in the use of medication to treat the disorder,according to the research team from Trehafod Child and Adolescent Mental Health Service in Swansea. The findings, published in this month's Psychiatric Bulletin,
highlight the lack of GP confidence in tackling ADHD. None of the GPs surveyed felt they should initially start a child on Ritalin, a drug commonly prescribed for ADHD, and 65 per cent believed a child psychiatrist should have this responsibility. While most GPs had prescribed Ritalin with specialist supervision,
11 per cent said they did not prescribe it, many because they did not have training. System for Measuring Attention Shifts improve the accuracy of ADHD tests
I am elated that they are developing more accurate testing for this condition to help determine the correct course of treatment but still caution parents of a child at-risk for JHD to let the physician know this if the child has been diagnosed with ADHD. Jean
System for Measuring Attention Shifts Developed For Diagnosis of ADHD WESTPORT, CT (Reuters Health) May 10 - A system that measures attention shifts may improve the accuracy of diagnosis of attention deficit hyperactivity disorder (ADHD) in children, according to Dr. Martin H. Teicher
of Harvard Medical School, who spoke Thursday at the 154th annual meeting of the American Psychiatric Association. The new screening method, dubbed OPTAx (OPtical Tracking and Attention test), consists of two components: a 15-minute challenge test of attention and video documentation of the child's head movements.
With these two components, the test can help clinicians differentiate ADHD from several other conditions that can have similar symptoms, such as anxiety disorders, bipolar disorder and post-traumatic stress disorder, Dr. Teicher told Reuters Health during the meeting.
He noted that, while children with other disorders can be abnormally active, children with ADHD have characteristic head motions that the camera in this testing system detects.
"Although most professionals feel that they're doing a good job at diagnosing and treating ADHD, parents and society perceive a need for more objectivity in ADHD testing," he continued. "Some parents are concerned that the diagnosis is arrived at so quickly. When you have something that adds objective information, parents are very
relieved. The test can show parents the severity of the problem and the degree of the child's response to medication. Conversely, the test will sometimes show parents that the child does not have ADHD."
In his meeting presentation, Dr. Teicher said that another use of OPTAx is to determine more accurately whether ADHD patients on methylphenidate are responding to treatment. Untreated, ADHD patients were "on-task" for
42.6% of the testing segments, compared with 82.4% of segments for controls. A total of 120 minutes after a dose of methylphenidate, the patients' on-task rate increased to 75.4% of the segments. OPTAx is manufactured by OPTAx Systems, Inc., Nashville, Tennessee. Dr. Teicher has no financial interest in this company.
Medscape
The Treatment of Learning Disabilities - Differences between LD and ADHD
Discussess differences between learning disabilities and ADHD
Doesn't say too much new except that physician's shouldn't be so quick to lump all childhood ADHD/LD into one catagory for medical treatments (DUH). What I did find interesting was the conclusion discussing where it's possible to alter the brain's physiology with some of these treatments. Jean The Treatment of Learning Disabilities
Roberto Touchman International Pediatrics Volume 15, Number 2, 2000 http://www.int-pediatrics.org/Volume%2015/15-2-toc.htm Medications states, in part:
There is a significant overlap between ADHD and LD. The usual figure of
overlap between these two disorders is 20 to 25% but some estimates that AD and HD disorder coexists in 40% of the population of children with learning disabilities. Treatment with medications such as neurostimulants (methylphenidate or
dexedrine) may allow a child with LD to be less impulsive and more able to receive remediation through educational interventions. Furthermore affective disorders such as anxiety disorders, depression,
mania or phobias may coexist with LD. These comorbid conditions can then be targeted with appropriate medications, which will open a window of opportunity to allow effective educationsl interventions to take place. Another treatable condition in a child with LD is clinical seizures. In
addition, despite the fact that the EEG in the majority of children with LD does not usually demonstrate epileptiform activity there is increasing evidence that in some children subclinical epileptiform discharges do cause transient cognitive impairment (TCI). Transient cognitive impairment may not be clinically evident but can be documented when specific neuro-psychological testing is done simultaneously with ongoing EEG monitoring.
Specific functions such as perceptions, reaction time and scholastic
performance have been shown to be disrupted by brief epileptiform dis- charges in the absence of clinical seizures. There are reports of children with LD's and a severely epileptiform EEG but without clinical seizures in which treatment with valproic acid resulted in improvement in cognitive performance and this improvement was proportionals to the reduction in epileptiform discharges. It is also possible that medications used to treat specific disorders that
coexist with learning disabilities may have direct effects on learning. Medications such as methylphenidate, antidepressants such as Fluoxetine and mood stablizers such as lithium carbonate or valproic acid may directly enhance certain cognitive processess. The evidence for this is still scant but further research into the cognitive enhancing potential of selective medications is needed. Specifically there is ongoing conroversy both in the adult and pediatric literature on the cognitive enhancing effects if any compounds known as (can't read this clearly) nootropics. Article then goes on to discuss:
Piracetam - the most widely researched nootropic compound not approved
for clinical use in the USA. Most accepted treatment is for myoclonic seizures with several studies on use in children with LD. At the present time MEDICATIONS IN CHILDREN WITH LD SHOULD BE
USED TO TREAT SPECIFIC TARGETED SYMPTOMS SUCH AS attention, anxiety or seizures. However there is a growing interest in the direct role that medications may play in enhancing cognitive processess. CONCLUSIONS (in part)
A recent study in an adult with acquired dyslexis SUGGESTS IT IS POSSIBLE
TO ALTER BRAIN PHYSIOLOGY with therapy for acquired language disorders. Children With ADHD May Suffer From Memory Deficits
December 1999 article Key factor below....medication does NOT help children with this type of learning disability! Jean
Children With ADHD May Suffer From Memory Deficits December 8, 1999 The Medical Tribune Some children with attention-deficit hyperactivity disorder (ADHD)
also have problems with memory, according to a study by researchers at the University of Iowa (www.uiowa.edu) in Iowa City. These memory problems are unrelated to ADHD and require separate assessment. "Probably the most prominent finding of the study was that those
children who had ADHD without diagnosed learning problems also had memory deficits," said Lynn C. Richman, professor of pediatric psychology at the University of Iowa and the study's lead investigator. Memory problems reported involved short-term memory skills, such as
remembering math facts, spelling, words and other reading-related tasks. These memory deficits may be wrongly attributed to the inattention associated with ADHD, rather than seen as a separate problem, such as a learning disability, she said. The study involved testing short-term memory of two groups of 40
children. In one group were children diagnosed with ADHD, which is characterized by inattentive and impulsive behavior. Children in the other group had been diagnosed with undifferentiated attention deficit disorder (UADD), a subset of ADHD marked only by inattention. The two groups of children were then tested to see if they had reading
disabilities. Results revealed that children in the ADHD group, whether or not they had a learning disability, had significantly more memory deficits than those in the UADD group. Because no known drug exists to improve short-term memory, doctors
rely instead on visualization, which Richman called "very effective," as well as memory strategy training. Such training includes rhymes to aid in memory, such as spelling rule of "i before e except after c," said Richman. Dr. James Perrin, associate professor of pediatrics at Harvard Medical
School, Boston and co-chair of the committee on quality improvement, subcommittee on ADHD at Harvard, called the findings "interesting," though he added he was not surprised by them. He said it was "important to realize that just a small number of children were studied." One problem, said Richman, is that it can be difficult for parents and
teachers to distinguish between behavior due to ADHD and a learning disability. "Parents often just think the child's not listening to them and may even punish the child for not doing what he or she is told," said Richman. Perrin agreed that this was a significant issue and urged parents to
avoid punishing children based on behavior resulting from either ADHD or a learning disability. Comorbidity in ADHD
also background on Kelly and ADHD Old timers on Hunt-Dis probably remember my saying this, but back in 1973 when Kelly was 5 and diagnosed with "hyperactivity" the total extent of testing her for this "condition" was (a) a teacher recommending that they felt the child demonstrated hyperactivity in school" (b) the doctor writing letters on the child's (Kelly's) back with his fingers and, when she could not identify all of them concluding the child is hyperactive and prescribed Ritalin.
After 1 week on Ritalin changing Kelly from a model child to a MONSTER, the doctor just responded "oh that happens sometimes, give her Dextrin" ......for the next 7 years. In 1980, when Kelly was 12, her then doctor said that hyperactivity medication was no longer effective once a child reached puberty! Shortly afterwards Kelly started using drugs and alcohol, had severe emotional inbalances (suicide threats,low self-esteem, etc). By 16 she had been diagnosed with JHD.
Two things that are important in our case. One Kelly had attended a Montessori pre-school for two years, doing algebra/IQ of 156, when I divorced her father (later pHD) and had to put her in public school. Not adjusting well to kindergarten finger-painting and learning her ABC's (she could already read and write), the teacher insisted she was hyperactive and had to see a doctor. (She was, obviously to me, bored in school. There were no special education classes for bright children back then.) It was either see the doctor or take her out of school in Missouri, back then.
Second is I did NOT want to put my child on ANY medications I did NOT feel that she needed. The initial doctor she saw, and a psychiatrist I consulted before allowing Kelly to take medication, advised me (remember this was '73) that if a hyperactive child was NOT helped with medication that the chances were over 80% that that child would commit suicide by the time they were 20. That was when I was gullible and believed everything a doctor told me.
Needless to say I was scared to death that if I didn't put Kelly on medication it would be my fault if she committed suicide later in life. So I put her on the medication ONLY during school hours (the school gave it to her). She never needed it at home and I know in my heart she never
needed it at all. But once a child is "labeled" in the school system you can NEVER convince them otherwise. The YEARS of frustration with that whole scenario is an entire different article! Medscape Pediatrics
Expert Column ADHD: Clinical Issues and Case Examples
Henry L. Shapiro, MD, FAAP
[Medscape Pediatrics, 2001. © 2001 Medscape, Inc.] http://www.medscape.com/medscape/pediatrics/journal/2001/v03.n02/mpe0404.shap/mpe0404.shap-01.html The criteria for ADHD have changed with updated editions of the Diagnostic and Statistical Manual of Mental Disorders (DSM),[3,5] which accoount for some of the change in the rates of ADHD.[2]
Other organizations have published guidelines and practice parameters[6-9] including the American Academy of Pediatrics,[7] (whose consensus group guidelines were based on an external subject review[10]) and the Institute for Clinical Systems Improvement.[9] (see below for these references)
Comorbidity
Rates of comorbidity are largely drawn from studies of referred patients, although there have been some community samples and prospective studies that provide valuable information on comorbidity in ADHD.[4]
Diagnoses include
The DSM-IV specifically excludes the diagnosis of ADHD in children Above references:
Medscape Diagnostic and Statistical Manual of Mental Disorders (DSM)
2000 American Academy of Pediatrics Annual Meeting Day 1 - October 28, 2000 Attention Deficit Hyperactivity Disorder: Current Diagnosis and Treatment http://www.medscape.com/Medscape/CNO/2000/AAP/Story.cfm?story_id=1769 American Academy of Pediatrics Diagnosis and Evaluation of the Child With Attention -Deficit/Hyperactivity Disorder
The Agency for Health Care Policy and Research Technical Review:
Number 3 Diagnosis of Attention-Deficit/Hyperactivity Disorder
http://www.ahrq.gov/clinic/adhdsutr.htm Institute for Clinical Systems Improvement Diagnosis and Management of ADHD in Primary Care in pdf format http://www.icsi.org/guide/ADHD.pdf |
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