Product Categories
|
|
|
Welcome to the Autism, ADHD and Learning Difficulties Website
This website was created as a resource to help parents and children who are impacted by Autism, Attention-Deficit Hyperactivity Disorder (ADHD) and Learning Disabilities.
What is Autism?
Autism is a brain development disorder that impairs social interaction and communication, and causes restricted and repetitive behaviour, all starting before a child is three years old. This set of signs distinguishes autism from milder autism spectrum disorders (ASD) such as Asperger syndrome.1
Autism is highly heritable, although the genetics of autism are complex and it is generally unclear which genes are responsible. Proposed causes, such as childhood vaccines, are controversial and the vaccine hypotheses lack convincing scientific evidence.1a
Most recent reviews estimate a prevalence of one to two cases per 1,000 people for autism, and about six per 1,000 for ASD, with ASD averaging a 4.3:1 male-to-female ratio. The number of people known to have autism has increased dramatically since the 1980s, at least partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.2
Autism affects many parts of the brain; how this occurs is poorly understood. Parents usually notice signs in the first two years of their child's life. Early behavioural or cognitive intervention can help children gain self-care, social, and communication skills.
Classification
Autism is a developmental disorder of the human brain that first gives signs during infancy or childhood and follows a steady course without remission or relapse. Impairments result from maturation-related changes in various systems of the brain. Autism is one of the five pervasive developmental disorders (PDD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behaviour.
Of the other four PDD forms, Asperger syndrome is closest to autism in signs and likely causes; Rett syndrome and childhood disintegrative disorder share several signs with autism, but may have unrelated causes; PDD not otherwise specified (PDD-NOS) is diagnosed when the criteria are not met for a more specific disorder. Unlike autism, Asperger's has no substantial delay in language development.
The terminology of autism can be bewildering, with autism, Asperger's and PDD-NOS often called the autism spectrum disorders (ASD) or sometimes the autistic disorders, whereas autism itself is often called autistic disorder, childhood autism, or infantile autism. In this article, autism refers to the classic autistic disorder, while other sources sometimes use autism or the autisms to refer to ASD, or equate ASD with PDD. ASD, in turn, is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.
The manifestations of autism cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, intellectually disabled, showing hand flapping and rocking—to less impaired individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication. Sometimes the syndrome is divided into low-, medium- and high-functioning autism (LFA, MFA, and HFA), based on IQ thresholds, or on how much support the individual requires in daily life; these subdivisions are not standardized and are controversial.
Autism can also be divided into syndromal and non-syndromal autism, where the former is associated with severe or profound intellectual disability or a congenital syndrome with physical symptoms, such as tuberous sclerosis. Although individuals with Asperger's tend to perform better cognitively than those with autism, the extent of the overlap between Asperger's, HFA, and non-syndromal autism is unclear.
Some studies have reported diagnoses of autism in children due to a loss of language or social skills after 14 months of age, as opposed to a failure to make progress. Several terms are used for this phenomenon, including regressive autism, setback autism, and developmental stagnation. The validity of this distinction remains controversial; it is possible that regressive autism is a specific subtype.2a,b,c
Characteristics
Autism is distinguished by a pattern of symptoms rather than one single symptom. The main characteristics are impairments in social interaction, impairments in communication, restricted interests and repetitive behaviour. Other aspects, such as atypical eating, are also common but are not essential for diagnosis. Individual symptoms of autism occur in the general population and appear not to associate highly, without a sharp line separating pathological severity from common traits.
Social Development
People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic Temple Grandin described her inability to understand the social communication of neurotypicals as leaving her feeling "like an anthropologist on Mars".
Social impairments become apparent early in childhood and continue through adulthood. Infants with autism show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Toddlers with autism have more striking social deviance; for example, they have less eye contact and anticipatory postures. Three- to five-year-old children with autism are less likely to exhibit social understanding, approach others spontaneously, imitate and respond to emotions, communicate nonverbally, and take turns with others. However, they do form attachments to their primary caregivers. They display moderately less attachment security than usual, although this feature disappears in children with higher intellectual development or less severe ASD. Older children and adults with ASD perform worse on tests of face and emotion recognition.
Contrary to common belief, children with autism do not prefer to be alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they are.
There are many anecdotal reports, but few systematic studies, of aggression and violence in individuals with ASD. The limited data suggest that in children with intellectual disability, autism is associated with aggression, destruction of property, and tantrums. Dominick et al. interviewed the parents of 67 children with ASD and reported that about two-thirds of the children had periods of severe tantrums and about one-third had a history of aggression, with tantrums significantly more common than in children with a history of language impairment.3
Communication
About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs. Differences in communication may be present from the first year of life, and may include delayed onset of babbling, unusual gestures, diminished responsiveness, and the desynchronization of vocal patterns with the caregiver. In the second and third years, children with autism have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words.
Children with autism are less likely to make requests or share experiences, and are more likely to simply repeat others' words (echolalia) or reverse pronouns. Children with autism may have difficulty with imaginative play and with developing symbols into language. They are more likely to have problems understanding pointing; for example, they may look at a pointing hand instead of the pointed-at object.
In a pair of studies, high-functioning children with autism aged 8–15 performed equally well, and adults better than individually matched controls at basic language tasks involving vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks such as figurative language, comprehension and inference. As people are often sized up initially from their basic language skills, these studies suggest that people speaking to individuals with austism are more likely to overestimate what their audience comprehends.
Repetitive Behaviour
Individuals with autism display many forms of repetitive or restricted behaviour, which the Repetitive Behaviour Scale-Revised (RBS-R) categorizes as follows.
ˇ Stereotypy is apparently purposeless movement, such as hand flapping, head rolling, or body rocking.
ˇ Compulsive behaviour is intended and appears to follow rules, such as arranging objects in a certain way.
ˇ Sameness is resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.
ˇ Ritualistic behaviour involves the performance of daily activities the same way each time, such as an unvarying menu or dressing ritual. This is closely associated with sameness and an independent validation has suggested combining the two factors.
ˇ Restricted behaviour is limited in focus, interest, or activity, such as preoccupation with a single television program.
ˇ Self-injury includes movements that injure or can injure the person, such as biting oneself. Dominick et al. reported that self-injury at some point affected about 30% of children with ASD. 3
No single repetitive behaviour seems to be specific to autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviours.
Other Symptoms
Individuals with autism may have symptoms that are independent of the diagnosis, but that can affect the individual or the family. A small fraction of individuals with ASD show unusual abilities, ranging from splinter skills such as the memorization of trivia to the extraordinarily rare talents of prodigious autistic savants.
Unusual responses to sensory stimuli are more common and prominent in children with autism, although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders. The responses may be more common in children: a pair of studies found that children with autism had impaired tactile perception while adults with autism did not. 4
The same two studies also found that individuals with autism had more problems with complex memory and reasoning tasks such as Twenty Questions; these problems were somewhat more marked among adults. Several studies have reported associated motor problems that include poor muscle tone, poor motor planning, and toe walking; ASD is not associated with severe motor disturbances.5
Atypical eating behaviour occurs in about three-quarters of children with ASD, to the extent that it was formerly a diagnostic indicator. Selectivity is the most common problem, although eating rituals and food refusal also occur; this does not appear to result in malnutrition. Although some children with autism also have gastrointestinal (GI) symptoms, there is a lack of published rigorous data to support the theory that children with ASD have more or different GI symptoms than usual; studies report conflicting results, and the relationship between GI problems and ASD is unclear. 6
Slerep problems are known to be more common in children with developmental disabilities, and there is some evidence that children with ASD are more likely to have even more sleep problems than those with other developmental disabilities; autistic children may experience problems including difficulty in falling asleep, frequent nocturnal awakenings, and early morning awakenings. Dominick et al. found that about two-thirds of children with ASD had a history of sleep problems. 7
Parents of children with ASD have higher levels of stress. Siblings of children with ASD report greater admiration of and less conflict with the affected sibling; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.
Causes
Genetic factors for autism are the most significant cause for autism spectrum disorders. Early studies of twins estimated heritability explains more than 90% of autism cases. However, most of the mutations that increase autism risk have not been identified. Typically, autism cannot be traced to a Mendelian (single-gene) mutation or to single chromosome abnormalities such as fragile X syndrome or 22q13 deletion syndrome.
There may be significant interactions among mutations in several genes, or between the environment and mutated genes. Numerous candidate genes have been located; most encode proteins involved in neural development and function. The large number of individuals with ASD with unaffected family members may result from copy number variations (CNVs)—spontaneous deletions or duplications in genetic material during meiosis. Hence, a substantial fraction of autism may be highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.
All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, it is strong evidence that autism arises very early in development.3b
Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies, extensive searches are underway. Environmental factors that have been claimed to contribute to or exacerbate autism, or may be important in future research, include certain foods, infectious disease, heavy metals, solvents, diesel exhaust, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, and vaccines.
Although parents may first become aware of autism symptoms in their child around the time of a routine vaccination, and parental concern about vaccines has led to a decreasing uptake of childhood immunizations and an increasing likelihood of measles outbreaks, there is overwhelming scientific evidence showing no causal association between the measles-mumps-rubella vaccine and autism, and there is no scientific evidence that the vaccine preservative thiomersal helps cause autism. 3c
Mechanism
Despite extensive investigation, how autism occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviours. The behaviours appear to have multiple pathophysiologies.
Pathophysiology
Autism appears to result from developmental factors that affect many or all functional brain systems, and to disturb the course of brain development more than the final product. Neuroanatomical studies and the associations with teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception. 8
This localised anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors. Although many major structures of the human brain have been implicated, almost all postmortem studies have been of individuals who also had mental retardation, making it difficult to draw conclusions. Brain weight and volume and head circumference tend to be greater in autistic children.
The cellular and molecular bases of pathological early overgrowth are not known, nor is it known whether the overgrown neural systems cause autism's characteristic signs. Current hypotheses include:
ˇ An excess of neurons that causes local over connectivity in key brain regions.
ˇ Disturbed neuronal migration during early gestation.
ˇ Unbalanced excitatory-inhibitory networks.
ˇ Abnormal formation of synapses and dendritic spines.
Interactions between the immune system and the nervous system begin early during embryogenesis, and successful neurodevelopment depends on a balanced immune response. Several symptoms consistent with a poorly regulated immune response have been reported in autistic children. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD.
As autoantibodies have not been associated with pathology, are found in diseases other than ASD, and are not always present in ASD, the relationship between immune disturbances and autism remains unclear and controversial.
Several neurotransmitter abnormalities have been detected in autism, notably increased blood levels of serotonin. Whether these lead to structural or behavioural abnormalities is unclear. Also, some inborn errors of metabolism are associated with autism but probably account for less than 5% of cases.8a
The mirror neuron system (MNS) theory of autism hypothesizes that distortion in the development of the MNS interferes with imitation and leads to autism's core features of social impairment and communication difficulties.
The MNS operates when an animal performs an action or observes another animal of the same species perform the same action. The MNS may contribute to an individual's understanding of other people by enabling the modelling of their behaviour via embodied simulation of their actions, intentions, and emotions. Several studies have tested this hypothesis by demonstrating structural abnormalities in MNS regions of individuals with ASD, delay in the activation in the core circuit for imitation in individuals with Asperger's, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD.
However, individuals with autism also have abnormal brain activation in many circuits outside the MNS and the MNS theory does not explain the normal performance of children with ASD on imitation tasks that involve a goal or object.
A 2008 study of adults with autism found evidence for altered functional organization of the task-negative network, a large-scale brain network involved in social and emotional processing, with intact organization of the task-positive network, used in sustained attention and goal-directed thinking. 9 A 2008 brain-imaging study found a specific pattern of signals in the cingulate cortex which differs in individuals with ASD. 10
The under connectivity theory of autism hypothesizes that autism is marked by under functioning high-level neural connections and synchronization, along with an excess of low-level processes. Evidence for this theory has been found in functional neuroimaging studies on individuals with autism and by a brain wave study that suggested that adults with ASD have local over connectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex.11 Other evidence suggests the under connectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex. 12
Neuropsychology
Two major categories of cognitive theories have been proposed about the links between autistic brains and behaviour.
The first category focuses on deficits in social cognition. Hyper-systemizing hypothesizes that individuals with autism can systematize—that is, they can develop internal rules of operation to handle internal events—but are less effective at empathizing by handling events generated by other agents.
It extends the extreme male brain theory, which hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing. This in turn is related to the earlier theory of mind, which hypothesizes that autistic behaviour arises from an inability to ascribe mental states to oneself and others. The theory of mind is supported by autistic children's atypical responses to the Sally-Anne test for reasoning about others' motivations, and is mapped well from the mirror neuron system theory of autism.
The second category focuses on nonsocial or general processing. Executive dysfunction hypothesizes that autistic behaviour results in part from deficits in flexibility, planning, and other forms of executive function. A strength of the theory is predicting stereotyped behaviour and narrow interests; a weakness is that executive function deficits are not found in young autistic children. Weak central coherence theory hypothesizes that a limited ability to see the big picture underlies the central disturbance in autism. One strength of this theory is predicting special talents and peaks in performance in people with autism. A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals. These theories map well from the under connectivity theory of autism.
Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid and repetitive behaviours, while the nonsocial theories have difficulty explaining social impairment and communication difficulties. A combined theory based on multiple deficits may prove to be more useful.
Screening
About half of parents of children with ASD notice their child's unusual behaviours by age 18 months, and about four-fifths notice by age 24 months. Deficits in joint attention seem to distinguish infants with ASD; for example, they may not follow when a parent points and says "Look!" As postponing treatment may affect long-term outcome, any of the following signs is reason to have a child evaluated by a specialist without delay:
ˇ No babbling by 12 months.
ˇ No gesturing (pointing, waving goodbye, etc.) by 12 months.
ˇ No single words by 16 months.
ˇ No two-word spontaneous phrases (not including echolalia) by 24 months.
ˇ Any loss of any language or social skills, at any age.
The American Academy of Paediatrics recommends that all children be screened for ASD at the 18- and 24-month well-child doctor visits, using autism-specific formal screening tests. In contrast, the UK National Screening Committee recommends against screening for ASD in the general population, because screening tools have not been fully validated and interventions lack sufficient evidence for effectiveness.
Screening tools include the Modified Checklist for Autism in Toddlers (M-CHAT), the Early Screening of Autistic Traits Questionnaire, and the First Year Inventory; initial data on M-CHAT and its predecessor CHAT on children aged 18–30 months suggests that it is best used in a clinical setting and that it has low sensitivity (many false-negatives) but good specificity (few false-positives). Genetic screening for autism is generally still impractical.
Diagnosis
Diagnosis is based on behaviour, not cause or mechanism. Autism is defined in the DSM-IV-TR as exhibiting at least six symptoms total, including at least two symptoms of qualitative impairment in social interaction, at least one symptom of qualitative impairment in communication, and at least one symptom of restricted and repetitive behaviour. Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with parts of objects.
Onset must be prior to age three years, with delays or abnormal functioning in either social interaction, language as used in social communication, or symbolic or imaginative play. The disturbance must not be better accounted for by Rett syndrome or childhood disintegrative disorder. ICD-10 uses essentially the same definition.
Several diagnostic instruments are available. Two are commonly used in autism research: the Autism Diagnostic Interview-Revised (ADI-R) is a semi structured parent interview, and the Autism Diagnostic Observation Schedule (ADOS) uses observation and interaction with the child. The Childhood Autism Rating Scale (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.
A paediatrician commonly performs a preliminary investigation by taking developmental history and physically examining the child. If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated medical conditions.
A differential diagnosis for ASD at this stage might also consider intellectual disability, hearing impairment, and a specific language impairment such as Landau-Kleffner syndrome. ASD can sometimes be diagnosed by age 14 months, although diagnosis becomes increasingly stable over the first three years of life: for example, a one-year-old who meets diagnostic criteria for ASD is less likely than a three-year-old to continue to do so a few years later.
In the UK the National Autism Plan for Children recommends at most 30 weeks from first concern to completed diagnosis and assessment, though few cases are handled that quickly in practice. A 2006 U.S. study found the average age of first evaluation by a qualified professional was 48 months and of formal ASD diagnosis was 61 months, reflecting an average 13-month delay, all far above recommendations.
Clinical genetics evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause. Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes, consensus guidelines in the U.S. and UK are limited to high-resolution chromosome and fragile X testing.
As new genetic tests are developed several ethical, legal, and social issues will emerge. Commercial availability of tests may precede adequate understanding of how to use test results, given the complexity of autism's genetics. Metabolic and neuroimaging tests are sometimes helpful, but are not routine.
Under diagnosis and over diagnosis are problems in marginal cases, and much of the recent increase in the number of reported ASD cases is likely due to changes in diagnostic practices. The increasing popularity of drug treatment options and the expansion of benefits has given providers incentives to diagnose ASD, resulting in some over diagnosis of children with uncertain symptoms. Conversely, the cost of screening and diagnosis and the challenge of obtaining payment can inhibit or delay diagnosis.
It is particularly hard to diagnose autism among the visually impaired, partly because some of its diagnostic criteria depend on vision, and partly because symptoms of autism overlap with those of common blindness syndromes.
The symptoms of autism and ASD begin early in childhood but are occasionally missed. Adults may seek retrospective diagnoses to help them or their friends and family understand themselves, to help their employers make adjustments, or in some locations to claim disability living allowances or other benefits.
Management
The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. No single treatment is best and treatment is typically tailored to the child's needs. Intensive, sustained special education programs and behaviour therapy early in life can help children acquire self-care, social, and job skills; claims that intervention by age two to three years is crucial are not substantiated.
Available approaches include applied behaviour analysis, developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy. Educational interventions have some effectiveness in children; the limited research on the effectiveness of adult residential programs shows mixed results.
Medications are often used to treat problems associated with ASD. More than half of U.S. children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics. Aside from antipsychotics, there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.
A person with ASD may respond atypically to medications, the medications can have adverse side effects, and no known medication relieves autism's core symptoms of social and communication impairments.
Many alternative therapies and interventions are available. Few are supported by scientific studies. Treatment approaches lack empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance. Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.
Treatment is expensive; indirect costs are more so. A U.S. study estimated an average cost of $3.2 million in 2003 U.S. dollars for someone born in 2000, with about 10% medical care, 30% extra education and other care, and 60% lost economic productivity. Publicly supported programs are often inadequate or inappropriate for a given child, and unreimbursed out-of-pocket medical or therapy expenses are associated with likelihood of family financial problems. After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.
Prognosis
Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination. Although core difficulties remain, symptoms often become less severe in later childhood. Few high-quality studies address long-term prognosis.
Some adults show modest improvement in communication skills, but a few decline; no study has focused on autism after midlife. Acquiring language before age six, having IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism. 13 A 2004 British study of 68 adults who were diagnosed before 1980 as children with ASD with IQ above 50 found that 12% achieved a high level of independence as adults, 10% had some friends and were generally in work but required some support, 19% had some independence but were generally living at home and needed considerable support and supervision in daily living, 46% needed specialist residential provision from facilities specializing in ASD with a high level of support and very limited autonomy, and 12% needed high-level hospital care. 14
Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children. 15
Epidemiology
Most recent reviews tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD2; because of inadequate data, these numbers may underestimate ASD's true prevalence. PDD-NOS is the vast majority of ASD, Asperger's is about 0.3 per 1,000 and the remaining ASD forms are much rarer. The number of reported cases of autism increased dramatically in the 1990s and early 2000s.
This increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness, though as-yet-unidentified contributing environmental risk factors cannot be ruled out. It is unknown whether autism's prevalence increased during the same period. An increase in prevalence would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.
The risk of autism is associated with several prenatal and perinatal risk factors. A 2007 review of risk factors found associated parental characteristics that included advanced maternal age, advanced paternal age, and maternal place of birth outside Europe or North America, and also found associated obstetric conditions that included low birth weight and gestation duration, and hypoxia during childbirth. 16
Autism is associated with several other conditions:
Genetic drisorders. About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome, and ASD is associated with several genetic disorders.
Intellectual disability. A 2001 British study of 26 children with autism found about 30% with intelligence in the normal range (IQ above 70), 50% with mild to moderate intellectual disability, and about 20% with severe to profound intellectual disability (IQ below 35). For ASD other than autism the association is much weaker: the same study reported about 94% of 65 children with PDD-NOS or Asperger's had normal intelligence. 17
Maleness. Boys are at higher risk for autism than girls. The ASD sex ratio averages 4.3:1 and is greatly modified by cognitive impairment: it may be close to 2:1 with intellectual disability and more than 5.5:1 without.
Eprilepsy, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder.
Several metabolic defects, such as phenylketonuria, are associated with symptoms of autism.
References
1. World Health Organization (2006). "F84. Pervasive developmental disorders", International Statistical Classification of Diseases and Related Health Problems, 10th ed. (ICD-10). Retrieved on 2007-06-25.
1a. Rutter M (2005). "Incidence of autism spectrum disorders: changes over time and their meaning". Acta Paediatr 94 (1): 2–15. PMID 15858952.
2. Newschaffer CJ, Croen LA, Daniels J et al. (2007). "The epidemiology of autism spectrum disorders". Annu Rev Public Health 28: 235–58. doi:10.1146/annurev.publhealth.28.021406.144007. PMID 17367287.
2a Landa RJ (2008). "Diagnosis of autism spectrum disorders in the first 3 years of life". Nat Clin Pract Neurol 4 (3): 138–47. doi:10.1038/ncpneuro0731. PMID 18253102.
2b Landa R (2007). "Early communication development and intervention for children with autism". Ment Retard Dev Disabil Res Rev 13 (1): 16–25. doi:10.1002/mrdd.20134. PMID 17326115.
2c Volkmar F, Chawarska K, Klin A (2005). "Autism in infancy and early childhood". Annu Rev Psychol 56: 315–36. doi:10.1146/annurev.psych.56.091103.070159. PMID 15709938.
3. Dominick KC, Davis NO, Lainhart J, Tager-Flusberg H, Folstein S (2007). "Atypical behaviors in children with autism and children with a history of language impairment". Res Dev Disabil 28 (2): 145–62. doi:10.1016/j.ridd.2006.02.003. PMID 16581226.
3b Arndt TL, Stodgell CJ, Rodier PM (2005). "The teratology of autism". Int J Dev Neurosci 23 (2–3): 189–99. doi:10.1016/j.ijdevneu.2004.11.001. PMID 15749245.
3c Doja A, Roberts W (2006). "Immunizations and autism: a review of the literature". Can J Neurol Sci 33 (4): 341–6. PMID 17168158.
3c B (Taylor 2006). "Vaccines and the changing epidemiology of autism". Child Care Health Dev 32 (5): 511–9. doi:10.1111/j.1365-2214.2006.00655.x. PMID 16919130.
4. Williams DL, Goldstein G, Minshew NJ (2006). "Neuropsychologic functioning in children with autism: further evidence for disordered complex information-processing". Child Neuropsychol 12 (4–5): 279–98. doi:10.1080/09297040600681190. PMID 16911973.
5. Ming X, Brimacombe M, Wagner GC (2007). "Prevalence of motor impairment in autism spectrum disorders". Brain Dev 29 (9): 565–70. doi:10.1016/j.braindev.2007.03.002. PMID 17467940.
6. Erickson CA, Stigler KA, Corkins MR, Posey DJ, Fitzgerald JF, McDougle CJ (2005). "Gastrointestinal factors in autistic disorder: a critical review". J Autism Dev Disord 35 (6): 713–27. doi:10.1007/s10803-005-0019-4. PMID 16267642.
7. Dominick KC, Davis NO, Lainhart J, Tager-Flusberg H, Folstein S (2007). "Atypical behaviors in children with autism and children with a history of language impairment". Res Dev Disability 28 (2): 145–62. doi:10.1016/j.ridd.2006.02.003. PMID 16581226.
8. Arndt TL, Stodgell CJ, Rodier PM (2005). "The teratology of autism". Int J Dev Neurosci 23 (2–3): 189–99. doi:10.1016/j.ijdevneu.2004.11.001. PMID 15749245
8a Manzi B, Loizzo AL, Giana G, Curatolo P (2008). "Autism and metabolic diseases". J Child Neurol 23 (3): 307–14. doi:10.1177/0883073807308698. PMID 18079313.
9. Kennedy DP, Courchesne E (2008). "The intrinsic functional organization of the brain is altered in autism". Neuroimage 38 (4): 1877–85. doi:10.1016/j.neuroimage.2007.10.052. PMID 18083565.
10. Chiu PH, Kayali MA, Kishida KT et al. (2008). "Self responses along cingulate cortex reveal quantitative neural phenotype for high-functioning autism". Neuron 57 (3): 463–73. doi:10.1016/j.neuron.2007.12.020. PMID 18255038. Lay summary – Technol Rev (2007-02-07).
11. Murias M, Webb SJ, Greenson J, Dawson G (2007). "Resting state cortical connectivity reflected in EEG coherence in individuals with autism". Biol Psychiatry 62 (3): 270–3. doi:10.1016/j.biopsych.2006.11.012. PMID 17336944.
12. Minshew NJ, Williams DL (2007). "The new neurobiology of autism: cortex, connectivity, and neuronal organization". Arch Neurol 64 (7): 945–50. PMID 17620483.
13. Tidmarsh L, Volkmar FR (2003). "Diagnosis and epidemiology of autism spectrum disorders". Can J Psychiatry 48 (8): 517–25. PMID 14574827.
14. Howlin P, Goode S, Hutton J, Rutter M (2004). "Adult outcome for children with autism". J Child Psychol Psychiatry 45 (2): 212–29. doi:10.1111/j.1469-7610.2004.00215.x. PMID 14982237.
15. Newschaffer CJ, Croen LA, Daniels J et al. (2007). "The epidemiology of autism spectrum disorders". Annu Rev Public Health 28: 235–58. doi:10.1146/annurev.publhealth.28.021406.144007. PMID 17367287.
16. Kolevzon A, Gross R, Reichenberg A (2007). "Prenatal and perinatal risk factors for autism". Arch Pediatr Adolesc Med 161 (4): 326–33. PMID 17404128.
17. Chakrabarti S, Fombonne E (2001). "Pervasive developmental disorders in preschool children". JAMA 285 (24): 3093–9. PMID 11427137.
Copyright (c) Life Skills 4 Kids.
Permission is granted to copy, distribute and/or modify this document
under the terms of the GNU Free Documentation License, Version 1.2
or any later version published by the Free Software Foundation;
with no Invariant Sections, no Front-Cover Texts, and no Back-Cover Texts.
A copy of the license is included in the section entitled "GNU
Free Documentation License".
What is Attention Deficit Hyperactivity Disorder (ADHD)
Attention-Deficit Hyperactivity Disorder (ADHD) is a neurobehavioural developmental disorder affecting about 3-5% of the world's population under the age of 19. It typically presents itself during childhood, and is characterized by a persistent pattern of inattention and/or hyperactivity, as well as forgetfulness, poor impulse control or impulsivity, and distractibility.
ADHD is currently considered to be a persistent and chrornic condition for which no medical cure is available. ADHD is most commonly diagnosed in children and, over the past decade, has been increasingly diagnosed in adults.
About 60% of children diagnosed with ADHD retain the condition as adults. It appears to be highly heritable, although one-fifth of all cases are estimated to be caused from trauma or toxic exposure. Methods of treatment usually involve some combination of medications, behaviour modifications, life style changes, and counselling.
The scientific consensus in the field, and the consensus of the national health institutes of the world, is that ADHD is a disorder, which impairs functioning, and that many adverse life outcomes are associated with ADHD. It has been frequently said by some news sources, social critics, certain religions, and individual medical professionals, to be a controversial disorder.
These critics question its classification as a single syndrome, its causes, its treatment, and even the existence of ADHD. See Controversy about ADHD.
Classification
ADHD is a developmental disorder, in that, in the diagnosed population, certain traits such as impulse control significantly lag in development when compared to the general population. Using magnetic resonance imaging, this developmental lag has been estimated to range between 3 years, to 5 years in the prefrontal cortex of those with ADHD patients in comparison to their peers; consequently, these delayed attributes are considered an impairment.
ADHD has also been classified as a behaviour disorder and a neurological disorder or combinations of these classifications such as neurobehavioural or neurodevelopmental disorders.
Symptoms
The most common symptoms of ADHD are distractibility, difficulty with concentration and focus, short-term memory slippage, procrastination, problems organizing ideas and belongings, tardiness, impulsivity, and weak planning and execution. Not all people with ADHD have all the symptoms. Most ordinary people exhibit some of these behaviours but not to the point where they seriously interfere with the person's work, relationships, or studies or cause anxiety or depression.
Children do not often have to deal with deadlines, organization issues, and long term planning so these types of symptoms often become evident only during adolescence or adulthood when life demands become greater. Hyperactivity is common among children with ADHD but tends to disappear during adulthood. However, over half of children with ADHD continue to have symptoms of inattention throughout their lives.
One of the things said by parents/teachers of children with ADHD is that it is very much like "Having twenty televisions lined around oneself and having them all turned to a different channel. The volume on each is constantly changing, and one finds it hard to focus on any one thing." Also, noticing things that some non-ADHD people might not notice is not uncommon.
Causes
According to a majority of medical research in the United States, as well as other countries, ADHD is today generally regarded as a chronic disorder for which there is some effective treatments, but no true cure. 18
Evidence suggests that hyperactivity has a strong heritable component, and in all probability, ADHD is a heterogeneous disorder, meaning that several causes could create very similar symptomology.
Candidate genes include dopamine transporter (DAT), dopamine receptor D4 (DRD4), dopamine beta-hydroxylase (DBH), monoamine oxidase A (MAOA), catecholamine-methyl transferase (COMT), serotonin transporter promoter (SLC6A4), 5-hydroxytryptamine 2A receptor (5-HT2A), and 5-hydroxytryptamine 1B receptor (5-HT1B).
Researchers believe that a large majority of ADHD arises from a combination of various genes, many of which affect dopamine transporters. Suspect genes include the 10-repeat allele of the DAT1 gene, the 7-repeat allele of the DRD4 gene, and the dopamine beta hydroxylase gene (DBH TaqI).
Genome wide surveys have shown linkage between ADHD and loci on chromosomes 7, 11, 12, 15, 16, and 17. If anything, the broad selection of targets indicates the likelihood that ADHD does not follow the traditional model of a "genetic disease" and is better viewed as a complex interaction among genetic and environmental factors.
As the authors of a review of the question have noted, "Although several genome-wide searches have identified chromosomal regions that are predicted to contain genes that contribute to ADHD susceptibility, to date no single gene with a major contribution to ADHD has been identified.” 20a
Studies show that there is a familial transmission of the disorder, which does not occur through adoptive relationships. Twin studies indicate that the disorder is highly heritable and that genetics contribute about three quarters of the total ADHD population. While the majority of ADHD is believed to be genetic in nature, roughly one-fifth of all ADHD cases are thought to be acquired after conception due to brain injury caused by either toxins or physical trauma prenatally or postnatally. 20b
Additionally, SPECT scans found people with ADHD to have reduced blood circulation, and a significantly higher concentration of dopamine transporters in the striatum, which is in charge of planning ahead. A study by the U.S. Department of Energy’s Brookhaven National Laboratory in collaboration with Mount Sinai School of Medicine in New York suggest that it is not the dopamine transporter levels that indicate ADHD, but the brain's ability to produce dopamine itself.
The study was done by injecting 20 ADHD subjects and 25 control subjects with a radiotracer that attaches itself to dopamine transporters.
The study found that it was not the transporter levels that indicated ADHD, but the dopamine itself. ADHD subjects showed lower levels of dopamine across the board.20c
They speculated that since ADHD subjects had lower levels of dopamine to begin with, the number of transporters in the brain was not the telling factor. In support of this notion, plasma homovanillic acid, an index of dopamine levels, was found to be inversely related not only to childhood ADHD symptoms in adult psychiatric patients, but to "childhood learning problems" in healthy subjects as well.
Although there is evidence for dopamine abnormalities in ADHD, it is not clear whether abnormalities of the dopamine system are the molecular abnormality of ADHD or a secondary consequence of a problem elsewhere. Researchers have described a form of ADHD in which the abnormality appears to be sensory overstimulation resulting from a disorder of ion channels in the peripheral nervous system.
An early PET scan study found that global cerebral glucose metabolism was 8.1% lower in medication-naive adults who had been diagnosed as ADHD while children.20d
Additionally, the regions with the greatest deficit of activity in the ADHD patients (relative to the controls) included the premotor cortex and the superior prefrontal cortex.
These findings strongly imply that lowered activity in specific regions of the brain, rather than a broad global deficit, is involved in ADHD symptoms. However, these readings are of subjects doing an assigned task. They could be found in ADHD diagnosed patients because they simply were not attending to the task. Hence, the parts of the brain used by others doing the task would not show equal activity in the ADHD patients.
The estimated contribution of non-genetic factors to the contribution of all cases of ADHD is 20 percent. The environmental factors implicated are common exposures and include alcohol, in utero tobacco smoke and lead exposure. Lead concentration below the Centre for Disease Control's action level account for slightly more cases of ADHD than tobacco smoke (290 000 versus 270 000, in the USA, ages 4 to 15). Complications during pregnancy and birth—including premature birth—might also play a role. It has been observed that women who smoke while pregnant are more likely to have children with ADHD. This could be related to the fact that nicotine is known to cause hypoxia (lack of oxygen) in utero, but it could also be that ADHD women have more probabilities to smoke both in general and during pregnancy, being more likely to have children with ADHD due to genetic factors.
Head injuries can cause a person to present ADHD-like symptoms, possibly because of damage done to the patient's frontal lobes. Because these types of symptoms can be attributable to brain damage, one earlier designation for ADHD was "Minimal Brain Damage".
There is no compelling evidence that social factors alone can create ADHD. Many researchers believe that attachments and relationships with caregivers and other features of a child's environment have profound effects on attentional and self-regulatory capacities. It is noteworthy that a study of foster children found that an inordinate number of them had symptoms closely resembling ADHD.
An editorial in a special edition of Clinical Psychology in 2004 stated that "our impression from spending time with young people, their families and indeed colleagues from other disciplines is that a medical diagnosis and medication is not enough”. 19
In our clinical experience, without exception, we are finding that the same conduct typically labelled ADHD is shown by children in the context of violence and abuse, impaired parental attachments and other experiences of emotional trauma." Furthermore, Complex Post Traumatic Stress Disorder can result in attention problems that can look like ADHD, as can Sensorry Integration Disorders.
Despite the lack of evidence that nutrition causes ADHD, studies have found that malnutrition is correlated with attention deficits.
Complicating Factors
Many studies point to synthetic preservatives and artificial colouring agents aggravating ADD & ADHD symptoms in those affected.20e Older studies were inconclusive quite possibly due to inadequate clinical methods of measuring offending behaviour.20f
Parental reports were more accurate indicators of the presence of additives than clinical tests. Several major studies show academic performance increased and disciplinary problems decreased in large non-ADD student populations when artificial ingredients, including artificial colours were eliminated from school food programs.
Diagnosis
Many of the symptoms of ADHD occur from time to time in everyone. In those with ADHD, the frequency of these symptoms occurs frequently and impairs regular life functioning typically at school or at work. Not only will they perform poorly in task-oriented settings but they will also have difficulty with social functioning with their peers. No objective physical test exists to diagnose ADHD in a patient.
As with many other psychiatric and medical disorders, the formal diagnosis is made by a qualified professional in the field based on a set number of criteria. In the USA, these criteria are laid down by the American Psychiatric Association in their Diagnostic and Statistical Manual of Mental Disorders (DSM-IV ), 4th edition. Based on the DSM-IV criteria listed below, three types of ADHD are classified:
1. ADHD, Combined Type: if both criteria 1A and 1B are met for the past 6 months
2. ADHD Predominantly Inattentive Type: if criterion 1A is met but criterion 1B is not met for the past six months
3. ADHD, Predominantly Hyperactive-Impulsive Type: if Criterion 1B is met but Criterion 1A is not met for the past six months.
The terminology of ADD expired with the revision of the most current version of the DSM. Consequently, ADHD is the current nomenclature used to describe the disorder as one distinct disorder which can manifest itself as being a primary deficit resulting in hyperactivity/impulsivity (ADHD, predominately hyperactive-impulsive type) or inattention (ADHD predominately inattentive type) or both (ADHD combined type).
DSM-IV Criteria for ADHD
A. Six or more of the following symptoms of inattention have been present for at least 6 months to a point that is disruptive and inappropriate for developmental level:
1. Often does not give close attention to details or makes careless mistakes in schoolwork, work, or other activities.
2. Often has trouble keeping attention on tasks or play activities.
3. Often does not seem to listen when spoken to directly.
4. Often does not follow instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behaviour or failure to understand instructions).
5. Often has trouble organizing activities.
6. Often avoids, dislikes, or doesn't want to do things that take a lot of mental effort for a long period of time (such as schoolwork or homework).
7. Often loses things needed for tasks and activities (e.g. toys, school assignments, pencils, books, or tools).
8. Is often easily distracted.
9. Often forgetful in daily activities.
B. Six or more of the following symptoms of hyperactivity-impulsivity have been present for at least 6 months to an extent that is disruptive and inappropriate for developmental level:
1. Often fidgets with hands or feet or squirms in seat.
2. Often gets up from seat when remaining in seat is expected.
3. Often runs about or climbs when and where it is not appropriate (adolescents or adults may feel very restless).
4. Often has trouble playing or enjoying leisure activities quietly.
5. Is often "on the go" or often acts as if "driven by a motor".
6. Often talks excessively.
Impulsiveness
1. Often blurts out answers before questions have been finished.
2. Often has trouble waiting one's turn.
3. Often interrupts or intrudes on others (e.g., butts into conversations or games).
Some symptoms that cause impairment were present before age 7 years.
Some impairment from the symptoms is present in two or more settings (e.g. at school/work and at home).
There must be clear evidence of significant impairment in social, school, or work functioning.
The symptoms do not happen only during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder. The symptoms are not better accounted for by another mental disorder (e.g. Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder).
In the tenth edition of the International Statistical Classification of Diseases and Related Health Problems (ICD-10) the symptoms of ADD are given the name "Hyperkinetic disorders". When a conduct disorder (as defined by ICD-10) is present, the condition is referred to as "Hyperkinetic conduct disorder". Otherwise the disorder is classified as "Disturbance of Activity and Attention", "Other Hyperkinetic Disorders" or "Hyperkinetic Disorders, Unspecified". The latter is sometimes referred to as, "Hyperkinetic Syndrome".
The American Academy of Paediatrics Clinical Practice Guideline for children with ADHD emphasizes that a reliable diagnosis is dependent upon the fulfilment of three criteria:
1. The use of explicit criteria for the diagnosis using the DSM-IV-TR.
2. The importance of obtaining information about the child’s symptoms in more than one setting.
3. The search for coexisting conditions that may make the diagnosis more difficult or complicate treatment planning.
The first criterion can be satisfied by using an ADHD-specific instrument such as the Conners' Rating Scale. The second criterion is best fulfilled by examining the individual's history. This history can be obtained from parents and teachers, or a patient's memory. The requirement that symptoms be present in more than one setting is very important because the problem may not be with the child, but instead with teachers or parents who are too demanding.
The use of intelligence testing, psychological testing, and neuropsychological testing (to satisfy the third criterion) is essential in order to find or rule out other factors that might be causing or complicating the problems experienced by the patient.
The Centres for Disease Control and Prevention (CDC) state that a diagnosis of ADD should only be made by trained health care providers, as many of the symptoms may also be part of other conditions, such as bodily illness or other physiological disorders, such as hypothyroidism. It is not uncommon that physically and mentally nonpathrological individuals exhibit at least some of the symptoms from time to time. Severity and pervasiveness of the symptoms leading to prominent functional impairment across different settings (school, work, social relationships) are major factors in a positive diagnosis.
Adults often continue to be impaired by ADD. Adults with ADD are diagnosed under the same criteria, including the stipulation that their symptoms must have been present prior to the age of seven. Adults face some of their greatest challenges in the areas of self-control and self-motivation, as well as executive functioning, usually having more symptoms of inattention and fewer of hyperactivity or impulsiveness than children do.
Common comorbid conditions are Oppositional Defiance Disorder (ODD). About 20% to 25% of children with ADD meet criteria for a learning disorder. Learning disorders are more common when there are inattention symptoms.
Treatment
There are several effective and clinically proven options to treat people with attention-deficit hyperactivity disorder (ADHD). The most popular and best (both effectively, and cost efficiently) way to treat ADHD has been with stimulant medication. The most common stimulant medications are methylphenidate, dextroamphetamine, and mixed amphetamine salts. Treatment costs vary greatly depending on the severity of ADHD. Medication management is the least expensive, followed by behavioral treatment, and combined treatment. Medical management was more effective, yet more costly than community care, and more cost effective than combination treatment alone and behavioral treatment alone. Co morbid (relating to two diseases that occur together, i.e. depression and ADHD) disorders make finding the right treatment and diagnosis much more costly and time consuming than a non comorbid disorder. Having a comorbid disorder complicates the treatment and diagnosis of ADHD so it is better to treat a comorbid disorder as soon as possible. Some cases of comorbidities, including depression or an anxiety disorder, are best treated with the combined treatment of psychosocial therapies and medication and are better then when only present is ADHD.
Singularly, stimulant medication is the most effective and cost efficient method of treating ADHD. Over 200 controlled studies have shown that stimulant medication is an effective way to treat ADHD. Methods of treatment usually involve some combination of medications, behaviour modifications, life style changes, and counselling. Behavioural parent training, behaviour therapy aimed at parents to help them understand ADHD has also shown short-term benefits. Omega-3 fatty acids, zinc and magnesium may have benefits with regard to ADHD symptoms.
Co morbid disorders or substance abuse can make finding the proper diagnosis and the right overall treatment more costly and time-consuming. Psychosocial therapy is useful in treating some co morbid conditions.
Prognosis
The diagnosis of ADHD implies an impairment in life functioning. Many adverse life outcomes are associated with ADHD.
During the elementary years an ADHD student will have more difficulties with work completion, productivity, planning, remembering things needed for school, and meeting deadlines.
Epidemiology
A review of 102 studies estimated ADHD's worldwide prevarlence in people under the age of 19 to be 5.29%. There was wide variability in prevalence estimates, mostly due to the methodological characteristics of studies (for example, diagnostic criteria used) and, to a lesser extent, geographic location (North America having a significantly higher rate of ADHD than Africa and the Middle East).20 10% of males, and (only) 4% of females have been diagnosed in the U.S. This apparent sex difference may reflect either a difference in susceptibility or that females with ADHD are less likely to be diagnosed than males.
18. NINDS Attention Deficit-Hyperactivity Disorder Information Page. National Institute of Neurological Disorders and Stroke (NINDS/NIH) February 9, 2007. Retrieved on 2007-08-13.
19. Adam James (2004) Clinical psychology publishes critique of ADHD diagnosis and use of medication on children published on Psychminded.co.uk Psychminded Ltd
20. Polanczyk G, de Lima MS, Horta BL, Biederman J, Rohde LA (2007). "The worldwide prevalence of ADHD: a systematic review and metaregression analysis". Am J Psychiatry 164 (6): 942–48. doi:10.1176/appi.ajp.164.6.942. PMID 17541055.
20a. M. T. Acosta, M. Arcos-Burgos, M. Muenke (2004). "Attention deficit/hyperactivity disorder (ADHD): Complex phenotype, simple genotype?". Genetics in Medicine 6 (1): 1–15.
20b Barkley, Russell A. Attention-Deficit/Hyperactivity Disorder: Nature, Course, Outcomes, and Comorbidity. ContinuinedEdCourse.Net. Retrieved on 2007-08-12.
20c Coccaro EF, Hirsch SL, Stein MA (2007). "Plasma homovanillic acid correlates inversely with history of learning problems in healthy volunteer and personality disordered subjects". Psychiatry research 149 (1–3): 297–302. doi:10.1016/j.psychres.2006.05.009. PMID 17113158.
20d Zametkin AJ, Nordahl TE, Gross M, et al. "Cerebral glucose metabolism in adults with hyperactivity of childhood onset." N Engl J Med. 1990 November 15;323(20):1361–6. PMID 2233902
20e Food additives and hyperactive behaviour in 3-year-old and 8/9-year-old children in the community: a randomized, double-blinded, placebo-controlled trial”, Lancet, Sept 2007
20f The Impact of a Low Food Additive and Sucrose Diet on Academic Performance in 803 New York City Public Schools, Schoenthaler SJ, Doraz WE, Wakefield JA, Int J Biosocial Res., 1986, 8(2); 185-195
Copyright (c) Life Skills 4 Kids.
Permission is granted to copy, distribute and/or modify this document
under the terms of the GNU Free Documentation License, Version 1.2
or any later version published by the Free Software Foundation;
with no Invariant Sections, no Front-Cover Texts, and no Back-Cover Texts.
A copy of the license is included in the section entitled "GNU
Free Documentation License".
What Are Learning Disabilities?
The term learning disability (LD) refers to a group of disorders that affect a broad range of academic and functional skills including the ability to speak, listen, read, write, spell, reason and organize information.
A learning disability is not indicative of low intelligence. People with learning disabilities sometimes have difficulty achieving at their intellectual level because of a deficit in one or more of the ways the brain processes information.
Overview
The National Joint Committee on Learning Disabilities (NJCLD) defines the term learning disability as:
A heterogeneous group of disorders manifested by significant difficulties in the acquisition and use of listening, speaking, reading, writing, reasoning or mathematical abilities. These disorders are intrinsic to the individual and presumed to be due to Central Nervous System Dysfunction. Even though a learning disability may occur concomitantly with other handicapping conditions (e.g. sensory impairment, intellectual disability, social and emotional disturbance) or environmental influences (e.g. cultural differences, insufficient/inappropriate instruction, psychogenic factors) it is not the direct result of those conditions or influences.
The NJCLD uses the term to refer to a discrepancy between a child’s apparent capacity to learn and his or her level of achievement.
Types of Learning Disabilities
Learning disabilities can be categorized either by the type of information processing that is affected or by the specific difficulties caused by a processing deficit.
Information Processing Deficits
Learning disabilities fall into broad categories based on the four stages of information processing used in learning: input, integration, storage, and output.
ˇ Input
This is the information perceived through the senses, such as visual and auditory perception. Difficulties with visual perception can cause problems with recognizing the shape, position and size of items seen. There can be problems with sequencing, which can relate to deficits with processing time intervals or temporal perception. Difficulties with auditory perception can make it difficult to screen out competing sounds in order to focus on one of them, such as the sound of the teacher's voice. Some children appear to be unable to process tactile input. For example, they may seem insensitive to pain or dislike being touched.
ˇ Integration
This is the stage during which perceived input is interpreted, categorized, placed in a sequence, or related to previous learning. Students with problems in these areas may be unable to tell a story in the correct sequence, unable to memorize sequences of information such as the days of the week, able to understand a new concept but be unable to generalize it to other areas of learning, or able to learn facts but be unable to put the facts together to see the "big picture." A poor vocabulary may contribute to problems with comprehension.
ˇ Storage
Problems with memory can occur with short-term or working memory, or with long-term memory. Most memory difficulties occur in the area of short-term memory, which can make it difficult to learn new material without many more repetitions than is usual. Difficulties with visual memory can impede learning to spell.
ˇ Output
Information comes out of the brain either through words, that is, language output, or through muscle activity, such as gesturing, writing or drawing. Difficulties with language output can create problems with spoken language, for example, answering a question on demand, in which one must retrieve information from storage, organize our thoughts, and put the thoughts into words before we speak. It can also cause trouble with written language for the same reasons. Difficulties with motor abilities can cause problems with gross and fine motor skills. People with gross motor difficulties may be clumsy, that is, they may be prone to stumbling, falling, or bumping into things. They may also have trouble running, climbing, or learning to ride a bicycle. People with fine motor difficulties may have trouble buttoning shirts, tying shoelaces, or with handwriting.
Specific Learning Disabilities
Deficits in any area of information processing can manifest in a variety of specific learning disabilities.
ˇ Reading disability
The most common learning disability. Of all students with specific learning disabilities, 70%-80% have deficits in reading. The term "dyslexia" is often used as a synonym for reading disability; however, many researchers assert that there are different types of reading disabilities, of which dyslexia is one. A reading disability can affect any part of the reading process, including difficulty with accurate and/or fluent word recognition, word decoding, reading rate, prosody (oral reading with expression), and reading comprehension.
Common indicators of reading disability include difficulty with phonemic awareness -- the ability to blend sounds into words or break up words into their component sounds, and difficulty with matching letters or letter combinations to specific sounds (sound-symbol correspondence).
ˇ Writing disability
Speech and language disorders can also be called Dysphasia/aphasia
Impaired written language ability may include impairments in handwriting, spelling, organization of ideas, and composition. The term "dysgraphia" is often used as an overarching term for all disorders of written expression. Others, such as the International Dyslexia Association, use the term "dysgraphia" exclusively to refer to difficulties with handwriting.
ˇ Nonverbal learning disability
Nonverbal learning disabilities often manifest in motor clumsiness, poor visual-spatial skills, problematic social relationships, difficulty with math, and poor organizational skills. These individuals often have specific strengths in the verbal domains, including early speech, large vocabulary, early reading and spelling skills, excellent rote-memory and auditory retention, and eloquent self-expression.
ˇ Disorders of speaking and listening
Difficulties that often co-occur with learning disabilities include difficulty with memory, social skills and executive functions (such as organizational skills and time management).
ˇ Auditory processing disorder
Difficulties processing auditory information include difficulty comprehending more than one task at a time and a relatively stronger ability to learn visually.
Diagnosis
IQ-Achievement Discrepancy
The presence of a learning disability is sometimes suspected by a child's parents long before problems are seen at school. However, the issues typically become visible when a child begins having difficulty at school. Difficulty learning to read is often one of the first signs that a learning disability is present.
Learning disabilities are often identified by school psychologists, clinical psychologists, and neuropsychologists through a combination of intelligence testing, academic achievement testing, classroom performance, and social interaction and aptitude. Other areas of assessment may include perception, cognition, memory, attention, and language abilities. The resulting information is used to determine whether a child's academic performance is commensurate with his or her cognitive ability. If a child's cognitive ability is much higher than his or her academic performance, the student is often diagnosed with a learning disability. The DSM-IV and many school systems and government programs diagnose learning disabilities in this way.
Although the discrepancy model has dominated the school system for many years, there has been substantial criticism of this approach among researchers. Recent research has provided little evidence that a discrepancy between formally-measured IQ and achievement is a clear indicator of LD. Furthermore, diagnosing on the basis of a discrepancy does not predict the effectiveness of treatment. Low academic achievers who do not have a discrepancy with IQ (i.e. their IQ scores are also low) appear to benefit from treatment just as much as low academic achievers who do have a discrepancy with IQ (i.e. their IQ scores are higher).
Response to Intervention (RTI)
Much current research has focused on a treatment-oriented diagnostic process known as response to intervention (RTI). Researcher recommendations for implementing such a model include early screening for all students, placing students having difficulty in research-based early intervention programs, and closely monitoring the progress of identified students to determine whether increasingly intense intervention results in adequate progress.
There are still concerns about the use of RTI, particularly in that it requires a strong intervention program before students can be identified with a learning disability. If students' receive poor quality interventions, they can be judged non-responsive and thus as having a learning disability when the cause is really only poor instruction.
Assessment
Many normed assessments can be used in evaluating skills in the primary academic domains: reading, not including word recognition, fluency, and comprehension; mathematics, including computation and problem solving; and written expression, including handwriting, spelling and composition.
The most commonly used comprehensive achievement tests include the Woodcock-Johnson III (WJ III), Weschler Individual Achievement Test II (WIAT II), the Wide Range Achievement Test III (WRAT III), and the Stanford Achievement Test–10th edition. These tests include measures of many academic domains that are reliable in identifying areas of difficulty.
In the reading domain, there are also specialized tests that can be used to obtain details about specific reading deficits. Assessments that measure multiple domains of reading include Gray's Diagnostic Reading Tests–2nd edition (GDRT II) and the Stanford Diagnostic Reading Assessment. Assessments that measure reading subskills include Gray's Oral Reading Test IV – Fourth Edition (GORT IV), Gray's Silent Reading Test, Comprehensive Test of Phonological Processing (CTOPP), Tests of Oral Reading and Comprehension Skills (TORCS), Test of Reading Comprehension 3 (TORC-3), Test of Word Reading Efficiency (TOWRE), and the Test of Reading Fluency. A more comprehensive list of reading assessments may be obtained from the Southwest Edurcational Development Laboratory.
Of course, assessment of learning disabilities requires the consideration of more than test scores. The purpose of assessment is to determine what is needed for intervention, which also requires consideration of contextual variables and whether there are comorbid disorders that must also be identified and treated, such as behavioural issues or language delays.
Treatment and Intervention
Poor academic achievement can be addressed with a variety of interventions. Although the underlying processing difficulty is usually considered to be a lifelong disorder, academic skills themselves can be improved with targeted interventions. Some (adjustments, equipment and assistants) are designed to accommodate or help compensate for the disabilities while others (specialized instruction) are intended to make improvements in the weak areas. Practice is a particularly important component in developing competence, regardless of the starting point. Children who start out with a weakness in a basic skill, such as reading, may miss out on the necessary practice because of the need to catch up with their chronological age peers. Thus a small weakness can snowball into a larger problem.
Interventions include:
ˇ Mastery model:
o Learners work at their own level of mastery.
o Practice
o Gain fundamental skills before moving onto the next level
§ Note: this approach is most likely to be used with adult learners or outside the mainstream school system.
Direct Instruction:
ˇ Highly structured, intensive instruction
ˇ Emphasizes carefully planned lessons for small learning increments
ˇ Scripted lesson plans
ˇ Rapid-paced interaction between teacher and students
ˇ Correcting mistakes immediately
ˇ Achievement-based grouping
ˇ Frequent progress assessments
Classroom adjustments:
ˇ Special seating assignments
ˇ Alternative or modified assignments
ˇ Modified testing procedures
Special equipment:
ˇ Electronic spellers and dictionaries
ˇ Word processors
ˇ Talking calculators
ˇ Books on tape
Classroom assistants:
ˇ Note-takers
ˇ Readers
ˇ Proofreaders
Special Education:
ˇ Prescribed hours in a special class
ˇ Placement in a special class
ˇ Enrolment in a special school for learning disabled students
Sternberg21 has argued that early remediation can greatly reduce the number of children meeting diagnostic criteria for learning disabilities. He has also suggested that the focus on learning disabilities and the provision of accommodations in school fails to acknowledge that people have a range of strengths and weaknesses, and places undue emphasis on academic success by insisting that people should receive additional support in this arena but not in music or sports.
Causes and Risk Factors
The causes for learning disabilities are not well understood, and sometimes there is no apparent cause for a learning disability. However, some causes of neurological impairments include:
Heredity - Learning disabilities often run in the family.
Problems during pregnancy and birth - Learning disabilities can result from anomalies in the developing brain, illness or injury, foetal exposure to alcohol or drugs, low birth weight, oxygen deprivation, or by premature or prolonged labour.
Accidents after birth - Learning disabilities can also be caused by head injuries, malnutrition, or by toxic exposure (such as heavy metals or pesticides).
Impact on Affected Individuals
Individuals with a learning disability may isolate themselves from society as they may feel:
* Ashamed of the types of difficulties they struggle with, such as poor literacy skills, attention or memory difficulties
* Fear of failure, criticism, ridicule or rejection
* Fear that others may think that they are stupid or incapable
* Ashamed that they are unable to read or that they have poor handwriting
* Left out of every day discussions due to lack of understanding
* Depressed
* Alone
Gender issues
ˇ Researchers believe that there are more boys in special education programs compared to girls. Coutinho and Oswald 22 found that data was collected from the U.S. office of Civil Rights to view the under-representation of females in special education. Oswald found that 73% of learning disabled individuals in specials education programs were boys.
ˇ Although, in contrast to the statement above if learning disabled students are identified by research criteria as opposed to teachers, the ratio of boys to girls (having a learning disability) is equal. In dealing with learning disabilities no significant gender differences were found in a study of more than 400 children. Bandian found that if identified by research criteria there were no differences in gender, but if learning disabilities were identified by general education teachers and/or special education teachers, there was twice as many boys identified compared to girls.23 Alongside that, there was another statement said by Bandian that supported the claim stated above “boys were twice as likely to be identified by teachers as in need of a learning disability programs [sic] [compared to girls].”
ˇ In a study 266 youth between the ages of 12-18 were voluntarily interviewed with 74 structured questions in a small classroom, question structure was based on “special education, juvenile justice, and child and adolescent development literature,” and then categorized into three parts: personal, home, and school.24 Based on the information the individuals provided to the interviewers the juvenile delinquents were put into a category, special education, or non-special education. Zabel and Nigro stated that “girls are less often viewed as disruptive and disturbing behaviour patterns that often lead to special education.” In contrast to that Zabel and Nigro also found that the “gender pattern was reversed for LD classification, with nearly 78.6% of females who had been in special education.” This study relates directly to the information provided in the welfare section because females are being identified with in the schools and are in turn receiving help from welfare programs. Although, this information provided in this section is in contrast to the gender differences section stating that boys are more identified for learning disabled programs compared to girls, this section supports the welfare section.
Contrast with Other Conditions
People with an IQ lower than 70 are usually characterized as having an intellectual disability or cognitive impairment and are not included under most definitions of learning disabilities, because their learning difficulties are related directly to their low IQ scores.
Attention-deficit hyperactivity disorder (ADHD) is often studied in connection with learning disabilities, but it is not actually included in the standard definitions of learning disabilities. An individual with ADHD may struggle with learning, but he or she can often learn adequately once successfully treated for the ADHD. A person can have ADHD but not learning disabilities or have learning disabilities without having ADHD. The conditions can co-occur (see Co morbidity). In order to understand the difference, imagine that someone with a learning disability is affected in only one or a few areas. However, people with ADHD are often affected in all areas.
Some research is beginning to make a case for ADHD being included in the definition of LDs, since it is being shown to have a strong impact on "executive functions" required for learning (planning, organization, etc). This has not as yet affected any official definitions.
Criticism of the concept of learning disabilities
Some critics of the concept of learning disabilities and of special education take the position that every child has a different learning style and pace and that each child is unique, not only capable of learning but also capable of succeeding. These critics assert that applying the medical model of problem-solving to individual children who are pupils in the school system, and labelling these children as disabled, systematically prevents the improvement of the current educational system.
Describing current instructional methods as homogenization and lockstep standardization, alternative approaches are proposed, such as the Sudbury model schools, an alternative approach in which children learn at their own pace rather than following a chronologically-based curriculum. Proponents of unschooling have also claimed that children raised in this method do not suffer from learning disabilities.
Gerald Coles asserts that there are partisan agendas behind the educational policy-makers and that the scientific research that they use to support their arguments regarding the teaching of literacy are flawed. 25 These include the idea that there are neurological explanations for learning disabilities.
21. Sternberg, R. J., & Grigorenko, E. L. (1999). Our labeled children: What every parent and teacher needs to know about learning disabilities. Reading, MA: Perseus Publishing Group
22. Coutinho, M.J. & Oswald, D.P.(2005). State variation in gender disproportionally in special education: Finding and recommendations. Remedial and Special Education, 26(1), 7-15
23. Bandian, N.A. (1999). Reading disability defined as a discrepancy between listening and reading comprehension: A longitudinal study of stability, gender differences, and prevalence. Journal of Learning Disabilities, 32(2) 138-148
24. Zabel, R.H. & Nigro, F.A. (1999). Juvenile offenders with behavioral disorders, learning disabilities, and no disabilities: Self- reports of personal, family, and school characteristics. Behavioral Disorders, 25(1), 22-40.
25. Gerald Coles (1987). The Learning Mystique: A Critical Look at "Learning Disabilities". Accessed April 4, 2008.
Copyright (c) Life Skills 4 Kids.
Permission is granted to copy, distribute and/or modify this document under the terms of the GNU Free Documentation License, Version 1.2 or any later version published by the Free Software Foundation;
with no Invariant Sections, no Front-Cover Texts, and no Back-Cover Texts.
A copy of the license is included in the section entitled "GNU Free Documentation License".
|
Useful Links
Autism Spectrum Australia (Aspect)
Autism Spectrum Australia (Aspect) is the leading provider of autism-specific services in Australia, building partnerships with people with Autism Spectrum Disorders, their families and the community to provide information, services, learning and research.
ˇ Autism Victoria
ˇ Autism
Information covering the symptoms, treatment and diagnosis of Autism the developmental disorder.
ˇ Autism
Links to information on autism spectrum disorders, including Asperger's syndrome.
ˇ Autism Queensland : Education, Therapy and Support Services
ˇ Welcome to Autism SA
ˇ Autism Collaboration - www.autism.org
ˇ Autism Society of America:
ˇ Autism - March of Dimes
Autism is a pervasive developmental disorder that affects how a child functions in several areas, including speech, social skills and behaviour.
ˇ Autism
Autism is a developmental disorder of brain function.
ˇ AutismWeb: The Parent's Guide to Autism and PDD
A parents' guide to the diagnosis, education and treatment of children with autism and Pervasive Developmental Disorder (PDD).
ˇ Autism Mercury
Generation Rescue provides information and resources for treating autism based on its cause: mercury poisoning.
ˇ Sensory Processing Disorder
Sensory Processing Disorder; the new name for Sensory Integration Dysfunction! Here you will find valuable articles, tips, and resources for identifying and treating SPD.
ˇ The SPD Network - About Sensory Processing Disorder
ˇ Sensory Integration Dysfunction
KidPower Family Support Resource, Inc. Sensory Integration Dysfunction section describes this disorder, what behaviours can manifest and how you can help your child.
ˇ Sensory Integration - FamilyEducation.com
These articles will help you learn more about SI dysfunction and how you can help your child.
ˇ The KID Foundation
The KID Foundation focuses on research, education, and advocacy related to Sensory Processing Disorder (SPD), a complex disorder of the brain.
ˇ Sensory Integration Dysfunction Signs, Symptoms and Background Information
Student programs for children struggling at school.
ˇ LD OnLine :: Understanding Sensory Integration
www.ldonline.org
Centre for Genetics Education Austalia
Fact sheets on the genetics of autism and other diagnoses.
Online Mendelian Inheritance in Man (OMIM) Peak database of disorders and conditions eg ADHD, Autism Spectrum Disorders etc.
Early Childhood Intervention Australia (ECIA) provides a national focus and forum, promotes the public profile of Early Childhood Intervention, facilitates effective liaison and advocacy in the community, and fosters quality information and service provision.
Life Skills 4 Kids. Paediatric Occupational Therapist. Helping kids with Autism, sensory processing disorders, sensory integration, sensory integration dysfunction, ADD, ADHD, mental health issues, STICKIDS, sensory diet, wheat bags, weighted blanket.
ˇ Sensory Child - Sensory Processing Disorder
Welcome to SensoryChild.com, a comprehensive resource for parents and caregivers of children with Sensory Processing Disorder ( SPD ). Created by parents of a child with SPD, SensoryChild.com is the result of six years of one family s journey to navigate the often-bewildering world their child lives in.
ˇ NationMaster - Encyclopedia: Sensory Integration Dysfunction
ˇ Vision and Sensory Processing Research - Neuroscience Research Center - The University of Texas Health Science Center at Houston
ˇ Sensory Integration www.sensorycritters.com
relationship between sensory abilities and the brain. We take in information through our senses: seeing, hearing, touching, tasting, and smelling. Unless the correct actions take place in the brain, we are not able to perceive and properly make use of the information from our senses.
ˇ Special needs, sensory and therapy equipment from Abilitations - a School Specialty Company.
Abilitations is a company whose primary focus is serving the needs of individuals with special needs. We accomplish this in a variety of ways including, but not limited to, our catalog and Thera-Talk. Our product mix focuses on movement, positioning, sensorimotor, exercise, aquatics and play.
ˇ Sensory-Motor Integration and Learning
ˇ Move to Learn - Articles and Research on Movement Programs and Learning Difficulties (LD)
Move to Learn - Articles and Research on Movement Programs and Learning Difficulties (LD) www.movetolearn.com.au
ˇ John Worthington - Educational and Developmental Psychologist
Assessment of the educational and learning related behaviours of individuals using both standardised and observational techniques to define and identify levels of skills and specific learning needs.To provide 'plain english' reports detailing the results including an individual Developmental Learning Profile (DLP) see link to DLP) and based on this information formulate specific recommendations and strategies to assist the learner.
ˇ Sensory Integration Therapy
Sensory Integration is a term that describes the brain's ability to take in information from the senses, organize it, and respond to it during experiences of daily life.
ˇ Sensory Integration and Sensory Processing Disorder - Center for Adoption Medicine
Resource for medical and developmental issues in adoption.
ˇ Autism: The heart of the disorder? Sensory processing and social engagement illustrations from autobiographical accounts and selected research findings - Early Childhood Australia
Early Childhood Australia advocates to ensure quality, social justice and equity in all issues relating to the education and care of children from birth to eight years., Elaine Keane Charles Sturt University/Vern-Barnett School for Children with Autism. Autism is currently identified by a set of diagnostic criteria which are based on observable behaviour, ...
ˇ Sensory Integration.
Fun family ideas for families with children with special needs.
ˇ Learning Disabilities: Signs, Symptoms and Strategies - Learning Disabilities Association of America
The Learning Disabilities Association of America helps people with learning disabilities, their parents, teachers and other professionals. We provide support on the national, state and local levels by providing cutting edge information, practical solutions, and a comprehensive network of resources.
ˇ Tourette's-Disorder.com Tourette Links
Links for Tourette's Disorder Tourette Syndrome, the spectrum of symptoms and comorbid conditions related.
ˇ Welcome to The John Maxwell Biasco Foundation for Children with Autism - Now on the Worldwide Web!
The John Maxwell Biasco Foundation for Children with Autism - Information resource and support for families with children with Autism.
ˇ SSEPAC-Sensory Integration Links
ˇ Lesson Tutor : Sensory Integration Dysfunction
Recognition of sensory integration is easily missed. Read how one family coped with the search for answers to their child's erratic behaviour.
www.lessontutor.com
ˇ Sensory Integration Problems in Preemies
Causes and solutions for common sensory integration problems in preemies.
ˇ Services – The Dan Centre for Autism
ˇ Trauma Headquarters
You will find some of the best resources families who have children suffering from Trauma and Reactive Attachment Disorder!
ˇ The Alcott Center for Cognitive Enhancement - Home
What is the efficacy of sensory integration use in children with autism? : NLH Question Answering Service
ˇ Childhood Sensory Integration Disorder
ˇ Reading Rockets : Handwriting Club: Using Sensory Integration Strategies to Improve Handwriting
Offers effective teaching strategies, activities, lessons, lesson plans, worksheets, exercises, skills, tests, assessments for reading comprehension, language arts, literacy, fluency, phonics and phonemic awareness for children, especially those with dyslexia and other reading difficulties.
ˇ Treatment for Dysfunction in Sensory Integration
Many children with Down syndrome also experience difficulties with sensory integration or sensory processing.
ˇ Sensory Integration Dysfunction | Asperger Help
ˇ Blog | Watch Me Learn
ˇ RESCUE POST: Sensory Integration and Biochemistry
The Rescue Post offers news and opinions on autism epidemic that the mainstream media won't touch.
ˇ Sensory Integration
Sensory Integration from Discovering New Heights Therapy.
Space Coast Early Intervention Centre
ˇ SENSORYINTEGRATION, EMOTIONS AND AUTISM
ˇ ADDults with ADHD
ADDults with ADHD (NSW) Inc. is a not for profit voluntary organisation established in 1995 to address the needs of adults with ADHD and other related conditions, and their families - ADDults have Charity Status and donations are non-taxable
ˇ Adult & Child ADD / ADHD: Attention Deficit & Hyperactivity Disorder
Adult and Child ADD and ADHD information and resources. Test for attention deficit and hyperactivity disorder symptoms. Find ADD and ADHD medication, treatment and medicine
ˇ Sensory Smart
The Sensory Smart Child Ltd is a private Paediatric Occupational Therapy practice based in the south east of England, offering a comprehensive assessment and therapy service for children 0 - 16 years through fun, education and play.
ˇ Some symptoms of ADHD may instead be sensory dysfunction
ˇ Strattera.com - What is Adult ADD?
ADD in adults is the continuation of the childhood disorder into adulthood. Symptoms are similar, but not identical, to those seen in children and adolescents.
ˇ Adult ADD
This site provides information about the diagnosis and treatment of adults with Attention Deficit Disorder.
ˇ ADHD: How To Cure it Naturally
ADHD Natural, Safe Help and valuable information about Attention Deficit Disorder
ˇ Attention Deficit Disorder (ADD)
A child is given the diagnosis of Attention Deficit Disorder (ADD), also called Attention Deficit Hyperactivity Disorder (ADHD) when he is considered overactive, cannot pay attention and cannot sit still, ALL VERY subjective symptoms. ADD is diagnosed four times more frequently in boys because boys mature more slowly than girls and because boys are put in classes at school with girls of the same age, so the boys, being less mature, appear to be hyperactive.
ˇ ADHD Australia
All about ADHD and comorbid disorders
ˇ ADHD Potatoes Home
ADHD Potatoes is a new book by Melbourne author Geraldine Moore about Attention Deficit Hyperactivity Disorder. Book reviews, information about the author, how to purchase a copy of ADHD Potatoes, and sample questions for interviewers.
ˇ Fish oil helps ADHD kids
Media Doctor is a website dedicated to improving the accuracy of media reports about new medical treatments in Australia. Involving a dedicated group of academics from the Newcastle Institute of Public Health, the site reviews current news items about medical treatments, assesses their quality using a standardised rating scale, and presents reviews of good and bad examples of reports.
ˇ Home - ADHD (Attention Deficit Hyperactive Disorder) Education from Eli Lilly Canada Inc.
The symptoms of ADHD are generally divided into symptoms of inattention, hyperactivity, and impulsivity.
ˇ Attention Deficit Hyperactivity Disorder (ADHD) - ADHD info.com
Find information about attention deficit hyperactivity disorder (ADHD) for parents, caregivers, school personnel, and kids.
ˇ Death from Ritalin the Truth Behind ADHD
Info for Parents who are pressured to diagnose and drug their children for ADD or ADHD. Story behind our Sons death caused from ADHD drug, Ritalin.
ˇ Special Needs Awareness Project: ADHD Camp
To promote the academic and social success of children with disabilities so that they can reach their fullest potential
ˇ Sensory Gym at Growing Together Therapeutic Center
ˇ ADDAQ - Attention Deficit Disorder Association Queensland - Shedding light on ADD - ADHD
Attention Deficit Disorder Association Queensland, shedding light on ADD.
ˇ ADD/ADHD specific links, research & support — Relationships Australia
Support, Websites and Research for Attention Deficit Disorder (ADD) / Attention Deficit Hyperactivity Disorder (ADHD)
ˇ Kids health info for parents : ADHD - an overview
ˇ ADHD
What is ADHD?
ˇ ADHD NSW
All about ADHD and comorbid disorders
ˇ ADHD Support Website Australia
This website gives information and treatment advice for parents of children who have been diagnosed with Attention Deficit Hyperactivity Disorder (ADHD), for teenagers and adults who have been diagnosed, or for anyone who just wants to obtain more information about the condition.
ˇ Children and Adolescents with Attention-deficit/Hyperactivity Disorder, National Mental Health Information Center
Children and Adolescents with Attention-deficit/Hyperactivity Disorder
Resources on Attention Deficit/Hyperactivity Disorder - Vermont Department of Health
ˇ Child-autism-parent-café.com
Great resources for parents with a child with autism.
ˇ Child Development Conferences
Child Development Conferences, Workshops, and Events
ˇ Prader-Willi Syndrome Association of Victoria
ˇ RUCSN: Resource Unit for Children with Special Needs, Western Australia.
ˇ Federation for Children with Special Needs
ˇ RESOURCES FOR CHILDREN WITH SPECIAL NEEDS
RESOURCES FOR CHILDREN WITH SPECIAL NEEDS
ˇ Parenting Xchange
ˇ Raising Children Network | Queensland services
Parent support services in Queensland
ˇ Behaviour Management
About the EIE Behaviour Management program
ˇ Federation of Parents and Citizens' Associations - Education for Special Needs
ˇ Resources for Parents with a Mental Illness and their Support People
Resource information for young people where a parent has a mental illness
ˇ Attention/Concentration Problems
ˇ Symptom: Concentration difficulty - CureResearch.com
Conditions causing symptom Concentration difficulty including possible medical causes, diseases, disorders, and related symptoms.
ˇ LDAA - Learning Disabilities Association of Alberta
ˇ Learning Disabilities Association of Vancouver BC
ˇ We help you help your child - Smart Kids With Learning Disabilities
Smart Kids with Learning Disabilities, Inc. - Helping Parents Advocate for their Children with Learning Disabilities
ˇ Learning Disabilities from Carers.org
Many of us take learning for granted. From birth we are constantly discovering new skills and developing a better understanding of the world we live in. For those with learning problems such as Autistic...
ˇ ICEH: Learning and Developmental Disabilities Initiative
The Institute for Children's Environmental Health (ICEH) is a nonprofit educational organization working to ensure a healthy, just and sustainable future for ALL children. ICEH's primary mission is to foster collaborative initiatives to reduce and ultimately eliminate environmental exposures that can undermine the health of current and future generations. Projects include the Learning and Developmental Disabilities Initiative, the Collaborative on Health and the Environment - Washington and others.
ˇ LD Blog
Yet another Special Edventure
ˇ Activities for Kids
Learning Disabilities
ˇ Learning Difficulties Australia - Students Learning Difficulties
The Centre specialises in offering individual programs to help students learning with difficulties such as: children with ADD, dyslexia help, ADHD support, children with dyspraxia & more.
ˇ LDW -- LEARNING DISABILITIES WORLDWIDE
ˇ Gifted Learning Disabled. Helping gifted children.
ˇ Dyslexia treatment & ADD ADHD correction
Dyslexia, ADD / ADHD & learning difficulty or learning disability correction using Davis Dyslexia programs.
ˇ Learning Disabilities Disorders - LD NVLD ADD ADHD
Students with learning disabilities are more likely to drop out of school, but many experts believe it's because they're less likely to get the help they need, and so they get frustrated and quit. We're hoping that the information provided on this site will move parents to act more quickly, as that lost year is significant in the academic life of a learning disabled student.
|
This website is sponsored by
|
|