{{infobox disease | name

Autism | Image Autism-stacking-cans 2nd edit.jpg | Alt Young red-haired boy facing away from camera, stacking a seventh can atop a column of six food cans on the kitchen floor. An open pantry contains many more cans. | Caption Repetitively stacking or lining up objects is a behavior occasionally associated with individuals with autism. | DiseasesDB 1142 | ICD10 | ICD9 299.00 | ICDO | OMIM 209850 | MedlinePlus 001526 | eMedicineSubj med | eMedicineTopic 3202 | eMedicine_mult | MeshID D001321 | GeneReviewsID autism-overview | GeneReviewsName Autism overview }}

Autism is a disorder of neural development characterized by impaired social interaction and communication, and by restricted and repetitive behavior. These signs all begin before a child is three years old. Autism affects information processing in the brain by altering how nerve cells and their synapses connect and organize; how this occurs is not well understood. It is one of three recognized disorders in the autism spectrum (ASDs), the other two being Asperger syndrome, which lacks delays in cognitive development and language, and Pervasive Developmental Disorder-Not Otherwise Specified (commonly abbreviated as PDD-NOS), which is diagnosed when the full set of criteria for autism or Asperger syndrome are not met.

Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations, or by rare combinations of common genetic variants. In rare cases, autism is strongly associated with agents that cause birth defects. Controversies surround other proposed environmental causes, such as heavy metals, pesticides or childhood vaccines; the vaccine hypotheses are biologically implausible and lack convincing scientific evidence. The prevalence of autism is about 1–2 per 1,000 people worldwide; however, the Centers for Disease Control and Prevention (CDC) reports approximately 9 per 1,000 children in the United States are diagnosed with ASD. The number of people diagnosed with autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.

Parents usually notice signs in the first two years of their child's life. The signs usually develop gradually, but some autistic children first develop more normally and then regress. Early behavioral or cognitive intervention can help autistic children gain self-care, social, and communication skills. Although there is no known cure, there have been reported cases of children who recovered. Not many children with autism live independently after reaching adulthood, though some become successful. An autistic culture has developed, with some individuals seeking a cure and others believing autism should be accepted as a difference and not treated as a disorder.

Characteristics

Autism is a highly variable neurodevelopmental disorder that first appears during infancy or childhood, and generally follows a steady course without remission. Overt symptoms gradually begin after the age of six months, become established by age two or three years, and tend to continue through adulthood, although often in more muted form. It is distinguished not by a single symptom, but by a characteristic triad of symptoms: impairments in social interaction; impairments in communication; and restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis. Autism's individual symptoms occur in the general population and appear not to associate highly, without a sharp line separating pathologically severe from common traits.

Social development

Social deficits distinguish autism and the related autism spectrum disorders (ASD; see ''Classification'') from other developmental disorders. 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, or people with normal neural development, as leaving her feeling "like an anthropologist on Mars".

Unusual social development becomes apparent early in childhood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers differ more strikingly from social norms; for example, they have less eye contact and turn taking, and do not have the ability to use simple movements to express themselves, such as the deficiency to point at things. Three- to five-year-old autistic children 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. Most autistic children display moderately less attachment security than non-autistic children, although this difference disappears in children with higher mental development or less severe ASD. Older children and adults with ASD perform worse on tests of face and emotion recognition.

Children with high-functioning autism suffer from more intense and frequent loneliness compared to non-autistic peers, despite the common belief that children with autism 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 feel. Functional friendships, such as those resulting in invitations to parties, may affect the quality of life more deeply.

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 mental retardation, autism is associated with aggression, destruction of property, and tantrums. A 2007 study interviewed 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 non-autistic children with language impairments. A 2008 Swedish study found that, of individuals aged 15 or older discharged from hospital with a diagnosis of ASD, those who committed violent crimes were significantly more likely to have other psychopathological conditions such as psychosis.

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 vocal patterns that are not synchronized with the caregiver. In the second and third years, autistic children have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Autistic children are less likely to make requests or share experiences, and are more likely to simply repeat others' words (echolalia) or reverse pronouns. Joint attention seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD: for example, they may look at a pointing hand instead of the pointed-at object, and they consistently fail to point at objects in order to comment on or share an experience. Autistic children may have difficulty with imaginative play and with developing symbols into language.

In a pair of studies, high-functioning autistic children aged 8–15 performed equally well as, 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 autistic individuals are more likely to overestimate what their audience comprehends.

Repetitive behavior

Autistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R) categorizes as follows.

Stereotypy is repetitive movement, such as hand flapping, making sounds, head rolling, or body rocking.

Compulsive behavior is intended and appears to follow rules, such as arranging objects in stacks or lines.

Sameness is resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.

Ritualistic behavior involves an unvarying pattern of daily activities, such as an unchanging menu or a dressing ritual. This is closely associated with sameness and an independent validation has suggested combining the two factors.

Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a single television program, toy, or game.

Self-injury includes movements that injure or can injure the person, such as eye poking, skin picking, hand biting, and head banging. A 2007 study reported that self-injury at some point affected about 30% of children with ASD. No single repetitive or self-injurious behavior seems to be specific to autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviors.

Other symptoms

Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family. An estimated 0.5% to 10% 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. Many individuals with ASD show superior skills in perception and attention, relative to the general population. Sensory abnormalities are found in over 90% of those with autism, and are considered core features by some, although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders. Differences are greater for under-responsivity (for example, walking into things) than for over-responsivity (for example, distress from loud noises) or for sensation seeking (for example, rhythmic movements). An estimated 60%–80% of autistic people have motor signs that include poor muscle tone, poor motor planning, and toe walking; deficits in motor coordination are pervasive across ASD and are greater in autism proper.

Unusual eating behavior 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 autistic children have more or different GI symptoms than usual; studies report conflicting results, and the relationship between GI problems and ASD is unclear.

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 than siblings of unaffected children or those with Down syndrome; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.

Classification

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 behavior. These symptoms do not imply sickness, fragility, or emotional disturbance.

Of the five 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; also called ''atypical autism'') is diagnosed when the criteria are not met for a more specific disorder. Unlike with autism, people with Asperger syndrome have no substantial delay in language development. The terminology of autism can be bewildering, with autism, Asperger syndrome 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; in clinical practice, though, ''autism'', ''ASD'', and ''PDD'' are often used interchangeably. ASD, in turn, is a subset of the broader autism phenotype, 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, mentally disabled, and locked into hand flapping and rocking—to high functioning individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication. Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary. Sometimes the syndrome is divided into low-, medium- or 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; the syndromal autism is associated with severe or profound mental retardation or a congenital syndrome with physical symptoms, such as tuberous sclerosis. Although individuals with Asperger syndrome tend to perform better cognitively than those with autism, the extent of the overlap between Asperger syndrome, 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, as opposed to a failure to make progress, typically from 15 to 30 months of age. The validity of this distinction remains controversial; it is possible that regressive autism is a specific subtype, or that there is a continuum of behaviors between autism with and without regression.

Research into causes has been hampered by the inability to identify biologically meaningful subpopulations and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics. Newer technologies such as fMRI and diffusion tensor imaging can help identify biologically relevant phenotypes (observable traits) that can be viewed on brain scans, to help further neurogenetic studies of autism; one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects. It has been proposed to classify autism using genetics as well as behavior.

Causes

It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism's characteristic triad of symptoms. However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.

Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations with major effects, or by rare multigene interactions of common genetic variants. Complexity arises due to interactions among multiple genes, the environment, and epigenetic factors which do not change DNA but are heritable and influence gene expression. Studies of twins suggest that heritability is 0.7 for autism and as high as 0.9 for ASD, and siblings of those with autism are about 25 times more likely to be autistic than the general population. 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 a single chromosome abnormality like fragile X syndrome, and none of the genetic syndromes associated with ASDs have been shown to selectively cause ASD. Numerous candidate genes have been located, with only small effects attributable to any particular gene. The large number of autistic individuals with unaffected family members may result from copy number variations—spontaneous deletions or duplications in genetic material during meiosis. Hence, a substantial fraction of autism cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.

Several lines of evidence point to synaptic dysfunction as a cause of autism. Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion. Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes. 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.

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, vaccines, and prenatal stress, although no links have been found, and some have been completely disproven.

Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. This has led to unsupported theories blaming vaccine "overload", a vaccine preservative, or the MMR vaccine for causing autism. The latter theory was supported by a litigation-funded study that has since been shown to have been "an elaborate fraud". Although these theories lack convincing scientific evidence and are biologically implausible, parental concern about a potential vaccine link with autism has led to lower rates of childhood immunizations, outbreaks of previously controlled childhood diseases in some countries, and the preventable deaths of several children.

Mechanism

Autism's symptoms result from maturation-related changes in various systems of the brain. 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 behaviors. The behaviors appear to have multiple pathophysiologies.

Pathophysiology

Unlike many other brain disorders such as Parkinson's, autism does not have a clear unifying mechanism at either the molecular, cellular, or systems level; it is not known whether autism is a few disorders caused by mutations converging on a few common molecular pathways, or is (like intellectual disability) a large set of disorders with diverse mechanisms. Autism appears to result from developmental factors that affect many or all functional brain systems, and to disturb the timing 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. This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors. Just after birth, the brains of autistic children tend to grow faster than usual, followed by normal or relatively slower growth in childhood. It is not known whether early overgrowth occurs in all autistic children. It seems to be most prominent in brain areas underlying the development of higher cognitive specialization. Hypotheses for the cellular and molecular bases of pathological early overgrowth include the following: An excess of neurons that causes local overconnectivity in key brain regions. Disturbed neuronal migration during early gestation. Unbalanced excitatory–inhibitory networks. Abnormal formation of synapses and dendritic spines, for example, by modulation of the neurexin–neuroligin cell-adhesion system, or by poorly regulated synthesis of synaptic proteins. Disrupted synaptic development may also contribute to epilepsy, which may explain why the two conditions are associated.

Interactions between the immune system and the nervous system begin early during the embryonic stage of life, and successful neurodevelopment depends on a balanced immune response. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD. Although some abnormalities in the immune system have been found in specific subgroups of autistic individuals, it is not known whether these abnormalities are relevant to or secondary to autism's disease processes. As autoantibodies are found in conditions other than ASD, and are not always present in ASD, the relationship between immune disturbances and autism remains unclear and controversial.

The relationship of neurochemicals to autism is not well understood; several have been investigated, with the most evidence for the role of serotonin and of genetic differences in its transport. Others have pointed to a role for group I metabotropic glutamate receptors (mGluR) in the pathogenesis of one type of autism, Fragile X. Some data suggest an increase in several growth hormones; other data argue for diminished growth factors. Also, some inborn errors of metabolism are associated with autism but probably account for less than 5% of cases.

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 perform the same action. The MNS may contribute to an individual's understanding of other people by enabling the modeling of their behavior 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 syndrome, 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 autistic children on imitation tasks that involve a goal or object.

ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks. In autism there is evidence for reduced functional connectivity of the default network, a large-scale brain network involved in social and emotional processing, with intact connectivity of the task-positive network, used in sustained attention and goal-directed thinking. In people with autism the two networks are not negatively correlated in time, suggesting an imbalance in toggling between the two networks, possibly reflecting a disturbance of self-referential thought. A 2008 brain-imaging study found a specific pattern of signals in the cingulate cortex which differs in individuals with ASD.

The underconnectivity theory of autism hypothesizes that autism is marked by underfunctioning 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 autistic individuals and by a brainwave study that suggested that adults with ASD have local overconnectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex. Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.

From studies based on event-related potentials, transient changes to the brain's electrical activity in response to stimuli, there is considerable evidence for differences in autistic individuals with respect to attention, orientiation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for non-social stimuli. For example, magnetoencephalography studies have found evidence in autistic children of delayed responses in the brain's processing of auditory signals.

In the genetic area, relations have been found between autism and schizophrenia based on duplications and deletions of chromosomes; research showed that schizophrenia and autism are significantly more common in combination with 1q21.1 deletion syndrome. Research on autism/schizophrenia relations for chromosome 15 (15q13.3), chromosome 16 (16p13.1) and chromosome 17 (17p12) are inconclusive.

Neuropsychology

Two major categories of cognitive theories have been proposed about the links between autistic brains and behavior.

The first category focuses on deficits in social cognition. The empathizing–systemizing theory postulates that autistic individuals can systemize—that is, they can develop internal rules of operation to handle events inside the brain—but are less effective at empathizing by handling events generated by other agents. An extension, the extreme male brain theory, hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing; this extension is controversial, as many studies contradict the idea that baby boys and girls respond differently to people and objects.

These theories are somewhat related to the earlier theory of mind approach, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others. The theory of mind hypothesis is supported by autistic children's atypical responses to the Sally–Anne test for reasoning about others' motivations, and the mirror neuron system theory of autism described in ''Pathophysiology'' maps well to the hypothesis. However, most studies have found no evidence of impairment in autistic individuals' ability to understand other people's basic intentions or goals; instead, data suggests that impairments are found in understanding more complex social emotions or in considering others' viewpoints.

The second category focuses on nonsocial or general processing. Executive dysfunction hypothesizes that autistic behavior results in part from deficits in working memory, planning, inhibition, and other forms of executive function. Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels. A strength of the theory is predicting stereotyped behavior and narrow interests; two weaknesses are that executive function is hard to measure and that executive function deficits have not been 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 autistic people. 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 underconnectivity theory of autism.

Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid and repetitive behaviors, 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 behaviors by age 18 months, and about four-fifths notice by age 24 months. According to an article in the ''Journal of Autism and Developmental Disorders'', failure to meet any of the following milestones ''"is an absolute indication to proceed with further evaluations. Delay in referral for such testing may delay early diagnosis and treatment and affect the long-term outcome."''

No babbling by 12 months.

No gesturing (pointing, waving bye-bye, etc.) by 12 months.

No single words by 16 months.

No 2-word spontaneous (''not just echolalic'') phrases by 24 months.

''Any'' loss of ''any'' language or social skills, ''at any age''.

US and Japanese practice is to screen all children for ASD at 18 and 24 months, using autism-specific formal screening tests. In contrast, in the UK, children whose families or doctors recognize possible signs of autism are screened. It is not known which approach is more effective. 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). It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders. Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture. Although genetic screening for autism is generally still impractical, it can be considered in some cases, such as children with neurological symptoms and dysmorphic features.

Diagnosis

Diagnosis is based on behavior, 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 behavior. 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 semistructured 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 pediatrician 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 pediatric neuropsychologist is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions. A differential diagnosis for ASD at this stage might also consider mental retardation, hearing impairment, and a specific language impairment such as Landau–Kleffner syndrome. The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as depression.

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 US and UK are limited to high-resolution chromosome and fragile X testing. A genotype-first model of diagnosis has been proposed, which would routinely assess the genome's copy number variations. 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.

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 2009 US study found the average age of formal ASD diagnosis was 5.7 years, far above recommendations, and that 27% of children remained undiagnosed at age 8 years. Although the symptoms of autism and ASD begin early in childhood, they are sometimes missed; years later, adults may seek 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.

Underdiagnosis and overdiagnosis 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 overdiagnosis 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 autistic symptoms overlap with those of common blindness syndromes or blindisms.

Management

The main goals when treating children with autism 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. Families and the educational system are the main resources for treatment. Studies of interventions have methodological problems that prevent definitive conclusions about efficacy. Although many psychosocial interventions have some positive evidence, suggesting that some form of treatment is preferable to no treatment, the methodological quality of systematic reviews of these studies has generally been poor, their clinical results are mostly tentative, and there is little evidence for the relative effectiveness of treatment options. Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills, and often improve functioning and decrease symptom severity and maladaptive behaviors; claims that intervention by around age three years is crucial are not substantiated. Available approaches include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy.

Educational interventions can be effective to varying degrees in most children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children and is well-established for improving intellectual performance of young children. Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided. It is not known whether treatment programs for children lead to significant improvements after the children grow up, and the limited research on the effectiveness of adult residential programs shows mixed results. The appropriateness of including children with varying severity of autism spectrum disorders in the general education population is a subject of current debate among educators and researchers.

Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails. More than half of US 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 effects, and no known medication relieves autism's core symptoms of social and communication impairments. Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function, suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.

Although many alternative therapies and interventions are available, few are supported by scientific studies. Treatment approaches have little 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. Some alternative treatments may place the child at risk. A 2008 study found that compared to their peers, autistic boys have significantly thinner bones if on casein-free diets; in 2005, botched chelation therapy killed a five-year-old child with autism.

Treatment is expensive; indirect costs are more so. For someone born in 2000, a US study estimated an average lifetime cost of $}} (net present value in dollars, inflation-adjusted from 2003 estimate), 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; one 2008 US study found a 14% average loss of annual income in families of children with ASD, and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment. US states increasingly require private health insurance to cover autism services, shifting costs from publicly funded education programs to privately funded health insurance. After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.

Prognosis

There is no known cure. Children recover occasionally, so that they lose their diagnosis of ASD; this occurs sometimes after intensive treatment and sometimes not. It is not known how often recovery happens; reported rates in unselected samples of children with ASD have ranged from 3% to 25%. Most autistic children can acquire language by age 5 or younger, though a few have developed communication skills in later years. Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination. Although core difficulties tend to persist, symptoms often become less severe with age. 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 an IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism. A 2004 British study of 68 adults who were diagnosed before 1980 as autistic children 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. A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence. A 2008 Canadian study of 48 young adults diagnosed with ASD as preschoolers found outcomes ranging through poor (46%), fair (32%), good (17%), and very good (4%); 56% of these young adults had been employed at some point during their lives, mostly in volunteer, sheltered or part-time work. Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.

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 ASD; because of inadequate data, these numbers may underestimate ASD's true prevalence. PDD-NOS's prevalence has been estimated at 3.7 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, and childhood disintegrative disorder at 0.02 per 1,000. 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 unidentified environmental risk factors cannot be ruled out. The available evidence does not rule out the possibility that autism's true prevalence has increased; a real increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.

Boys are at higher risk for ASD than girls. The sex ratio averages 4.3:1 and is greatly modified by cognitive impairment: it may be close to 2:1 with mental retardation and more than 5.5:1 without. Although the evidence does not implicate any single pregnancy-related risk factor as a cause of autism, the risk of autism is associated with advanced age in either parent, and with diabetes, bleeding, and use of psychiatric drugs in the mother during pregnancy. The risk is greater with older fathers than with older mothers; two potential explanations are the known increase in mutation burden in older sperm, and the hypothesis that men marry later if they carry genetic liability and show some signs of autism. Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.

Several other conditions are common in children with autism. They include: Genetic disorders. 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. Mental retardation. The fraction of autistic individuals who also meet criteria for mental retardation has been reported as anywhere from 25% to 70%, a wide variation illustrating the difficulty of assessing autistic intelligence. For ASD other than autism, the association with mental retardation is much weaker. Anxiety disorders are common among children with ASD; there are no firm data, but studies have reported prevalences ranging from 11% to 84%. Many anxiety disorders have symptoms that are better explained by ASD itself, or are hard to distinguish from ASD's symptoms. Epilepsy, 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 autistic symptoms. Minor physical anomalies are significantly increased in the autistic population. Preempted diagnoses. Although the DSM-IV rules out concurrent diagnosis of many other conditions along with autism, the full criteria for ADHD, Tourette syndrome, and other of these conditions are often present and these comorbid diagnoses are increasingly accepted. Sleep problems affect about two-thirds of individuals with ASD at some point in childhood. These most commonly include symptoms of insomnia such as difficulty in falling asleep, frequent nocturnal awakenings, and early morning awakenings. Sleep problems are associated with difficult behaviors and family stress, and are often a focus of clinical attention over and above the primary ASD diagnosis.

History

A few examples of autistic symptoms and treatments were described long before autism was named. The ''Table Talk'' of Martin Luther, compiled by his notetaker, Mathesius, contains the story of a 12-year-old boy who may have been severely autistic. Luther reportedly thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated, although a later critic has cast doubt on the veracity of this report. The earliest well-documented case of autism is that of Hugh Blair of Borgue, as detailed in a 1747 court case in which his brother successfully petitioned to annul Blair's marriage to gain Blair's inheritance. The Wild Boy of Aveyron, a feral child caught in 1798, showed several signs of autism; the medical student Jean Itard treated him with a behavioral program designed to help him form social attachments and to induce speech via imitation.

The New Latin word ''autismus'' (English translation ''autism'') was coined by the Swiss psychiatrist Eugen Bleuler in 1910 as he was defining symptoms of schizophrenia. He derived it from the Greek word ''autós'' (αὐτός, meaning ''self''), and used it to mean morbid self-admiration, referring to "autistic withdrawal of the patient to his fantasies, against which any influence from outside becomes an intolerable disturbance".

The word ''autism'' first took its modern sense in 1938 when Hans Asperger of the Vienna University Hospital adopted Bleuler's terminology ''autistic psychopaths'' in a lecture in German about child psychology. Asperger was investigating an ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate diagnosis until 1981. Leo Kanner of the Johns Hopkins Hospital first used ''autism'' in its modern sense in English when he introduced the label ''early infantile autism'' in a 1943 report of 11 children with striking behavioral similarities. Almost all the characteristics described in Kanner's first paper on the subject, notably "autistic aloneness" and "insistence on sameness", are still regarded as typical of the autistic spectrum of disorders. It is not known whether Kanner derived the term independently of Asperger.

Kanner's reuse of ''autism'' led to decades of confused terminology like ''infantile schizophrenia'', and child psychiatry's focus on maternal deprivation led to misconceptions of autism as an infant's response to "refrigerator mothers". Starting in the late 1960s autism was established as a separate syndrome by demonstrating that it is lifelong, distinguishing it from mental retardation and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy. As late as the mid-1970s there was little evidence of a genetic role in autism; now it is thought to be one of the most heritable of all psychiatric conditions. Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD, parents continue to feel social stigma in situations where their autistic children's behaviors are perceived negatively by others, and many primary care physicians and medical specialists still express some beliefs consistent with outdated autism research.

The Internet has helped autistic individuals bypass nonverbal cues and emotional sharing that they find so hard to deal with, and has given them a way to form online communities and work remotely. Sociological and cultural aspects of autism have developed: some in the community seek a cure, while others believe that autism is simply another way of being.

References

External links

Category:Pervasive developmental disorders Category:Communication disorders Category:Neurological disorders Category:Neurological disorders in children Category:Mental and behavioural disorders

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Name	Tommy Hilfiger
Nationality	American
Birth date	March 24, 1951
Birth place	Elmira, New York, U.S.
Education	Elmira Free Academy
Label name	Tommy Hilfiger }}

Thomas Jacob "Tommy" Hilfiger (born March 24, 1951) is an American fashion designer and founder of the premium lifestyle brand Tommy Hilfiger.

Early life

Hilfiger born in Elmira, New York. The second of nine children, he grew up in an Irish-American family; he claims direct descendence from Scottish poet Robert Burns. His parents originally intended for him to be an engineer. He attended Elmira Free Academy for high school. Rather than furthering his education, he started to work in retail at the age of 18. Hilfiger would go to New York City to buy jeans and bell-bottom pants, which he customized and resold at a local downtown Elmira store, Brown's.

He later opened his own store, named The People's Place, around the block in downtown Elmira. Although the store was a hot spot for teens with frequent contests and live DJ appearances, there were often more people hanging out than shopping. Over the years, a number of stores closed in downtown Elmira as shopping traffic shifted to the new Arnot Mall in Horseheads, New York. It wasn't long before The People's Place became another casualty. After seven years, The People's Place went bankrupt, when Hilfiger was 25. The site of the original store has since been demolished to make room for First Arena, home of the Elmira Jackals Hockey team.

Career

After turning to the design of clothing by designing for the rest of his stores in upstate New York, Hilfiger moved to New York City with his now estranged wife, Susie. Although he was offered design assistant positions with designers Calvin Klein and Perry Ellis, and was broke, he turned them both down with greater plans in mind.

In 1984, he founded the Tommy Hilfiger Corporation,'' (NYSE:TOM)'', with support from The Murjani Group, which went public in 1992, introducing his signature menswear collection. By 2004 the company had 5,400 employees and revenues in excess of $1.8 billion. Hilfiger was named Menswear Designer of the Year by the Council of Fashion Designers of America in 1995..

In 1998, Hilfiger gave singer Aaliyah her endorsement deal, in which he honored her in his Summer 1998 fashion show in Jamaica.

In 2005, a CBS TV reality show called ''The Cut'' tracked the progress of sixteen contestants as they competed for a design job with Hilfiger in similar fashion to Donald Trump's ''The Apprentice''. In the end Hilfiger chose Chris Cortez.

Largely due to declining sales, in 2006, Tommy Hilfiger sold his company for $1.6 billion, or $16.80 a share, to Apax Partners, a private investment company.

In March 2010, Phillips-Van Heusen, owner of Calvin Klein, bought the Tommy Hilfiger Corporation for $3 billion.

Personal life

Hilfiger has four children with his ex-wife, Susie: Alexandria ("Ally"), Richard, Elizabeth, and Kathleen. His daughter Ally was featured in the MTV reality show ''Rich Girls'' and his son, Rich, was signed to hip hop super producer Swizz Beatz' label Full Surface. Rich, who goes by the hip-hop stage name Rich Hil, was arrested on August 1, 2010 in West Hollywood for possession of marijuana and intent to sell.

Hilfiger put his Greenwich, Connecticut, mansion on the market in the summer of 2008 for an asking price of $27 million.

On December 12, 2008, he married his second wife Dee Ocleppo (''née'' Erbug), former wife of Gianni Ocleppo, famous Italian tennis player of the 1980s.

On February 25, 2009, the New York Post reported that Ocleppo was three months pregnant, and Hilfiger would welcome a fifth child later in 2009.

On May 4, 2009, Hilfiger and Ocleppo announced they were expecting a boy, who was born on Tuesday, August 4, 2009, and named Sebastian Thomas Hilfiger.

Criticisms

Hilfiger has been criticized for manufacturing clothes in sweatshop conditions in the United States territory of Saipan in the Northern Mariana Islands. As a U.S. Commonwealth, clothes made there can be labeled "Made in the USA", but federal labor laws including the minimum wage do not apply. In March 2000, the company, along with other defendants, settled a class action suit brought by Saipan garment workers, which had alleged mistreatment by over 20 large U.S. clothing manufacturers.

Libelous hoax email

An email saying that Hilfiger appeared on the Oprah Winfrey television show on "28 November" and made racist remarks, and calling for a boycott of Hilfiger's merchandise, has circulated widely. It was first seen in 1996, seemed to disappear, but reappeared and was still in circulation . Winfrey made clear on her show and website in 1999 that Hilfiger had never appeared on her show until then, much less made the remarks attributed to him in the email; and Hilfiger paid investigators, who traced it to a college campus but could not identify the perpetrator. Allegations were reported to the Anti-Defamation League; they wrote to Hilfiger in 2001 "We have concluded that these rumors are completely false, and it is apparent that you never made the statements attributed to you, nor did you appear on The Oprah Winfrey Show". Hilfiger appeared on the Winfrey show on 1 January 2006, where he and Winfrey repeated that he had not appeared before. Winfrey said about the email "You're supposed to say, 'That's a big fat lie.'"

Product lines

Hilfiger Denim, a premium-upscale denim collection for men and women. Designs are inspired by American classics and finished with a modern edge.

True Star Gold, fragrance created by Hilfiger and spokeswoman Beyoncé Knowles

True Star, another fragrance created by Hilfiger and with spokesperson Beyoncé Knowles & True Star Men, a fragrance created by Hilfiger and with spokesperson Enrique Iglesias

Tommy Girl, fragrance for women

Red Label, a line of denim-themed products including jeans, t-shirts, and sweatshirts

H by Tommy Hilfiger, an upscale line which was ended after Tommy Hilfger sold his company, the same sort of style is now carried on under the Tommy Hilfiger label in their specialty stores

Tommy Hilfiger, the company line of clothes sold in department stores, company stores, and specialty stores

Tommy Sport, a defunct line that came out in the 1990s and capitalized on Hilfiger's popularity in urban areas.

Tommy Hilfiger for the Home, a line of bedding and bath products

Tommy Sailing, was due to be released in January or February 2007.

Tommy, a brightly colored casual line.

Tommy Jeans, a denim inspired clothing collection and corresponding fragrance

Hilfiger Athletics, a sport inspired clothing line and fragrance

References

External links

Official website

Urban Legends that allege false claims against Hilfiger

Anti-Defamation League; Letter to Tommy Hilfiger

Category:1951 births Category:American fashion businesspeople Category:American fashion designers Category:Companies established in 1985 Category:American people of Irish descent Category:Living people Category:People from Elmira, New York Category:People from New York City Category:Irish American history

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name	James Christopher McMurray
birth place	Joplin, Missouri
birth date	June 03, 1976
awards	2003 NASCAR Winston Cup Series Raybestos Rookie of the Year
achievements	2010 Daytona 500 Winner2010 Brickyard 400 Winner
cup car team	1 – Earnhardt Ganassi Racing
previous year	2010
prev cup pos	14th
best cup pos	11th – 2004
cup wins	6
cup top tens	94
cup poles	8
first cup race	2002 EA Sports 500 (Talladega)
first cup win	2002 UAW-GM Quality 500 (Charlotte)
last cup win	2010 Bank of America 500 (Charlotte)
prev busch year	2010
prev busch pos	38th
best busch pos	6th – 2002
busch wins	8
busch top tens	65
busch poles	3
first busch race	2000 Sam's Town 250 (Memphis)
first busch win	2002 Aaron's 312 (Atlanta)
last busch win	2010 Great Clips 300 (Atlanta)
best truck pos	22nd – 2000
truck wins	1
truck top tens	6
truck poles	3
first truck race	1999 O'Reilly Auto Parts 200 (I-70)
first truck win	2004 Kroger 200 (Martinsville)
last truck win	2004 Kroger 200 (Martinsville)
updated	January 10, 2011 }}

James Christopher "Jamie" McMurray (born June 3, 1976) is a professional American race car driver. McMurray is best known for winning the 2002 UAW-GM Quality 500 as a substitute driver in his second Winston Cup start, and is one of three drivers to win both the Daytona 500 and Brickyard 400 in the same year. He currently drives the #1 Bass Pro Shops/McDonald's Chevrolet Impala in the Sprint Cup Series for Earnhardt Ganassi Racing with crew chief Kevin Manion.

Racing career

Early NASCAR career

In 1999, McMurray made four starts in the Craftsman Truck Series. In 2000, he ran 15 Craftsman Truck races and posted one top-five and four top-ten finishes. During 2001 and 2002, he competed full-time in the NASCAR Busch Series, driving the #27 Williams Travel Centers Chevrolet Monte Carlo for Brewco Motorsports. The latter year was better for McMurray, as he won two races and finished sixth in the overall points standings.

Before the fall race at Richmond in 2002, Chip Ganassi announced McMurray would be the driver of a Texaco-Havoline sponsored Dodge in 2003. Ganassi planned to have Jamie drive the #42 Dodge for seven races in 2002.

2002 win at Lowe's Motor Speedway

McMurray substituted for an injured Sterling Marlin, who fractured a vertebra at the Winston Cup race at Kansas Speedway. He made his Cup debut, filling in the #40 Coors Light Dodge at [[Talladega Superspeedway| Talladega]]. One week later, in just his second career NASCAR Winston Cup start, McMurray outraced Bobby Labonte to win the UAW-GM Quality 500 at Lowe's Motor Speedway in Concord, NC. McMurray had been consistent the entire night, and led 96 of the final 100 laps to score the win. It is considered one of the biggest upsets in NASCAR history, with McMurray making his only start at Talladega Superspeedway, where upsets are common. This win set a modern era record for fewest starts before a win (breaking the record held by Kevin Harvick (who had won in his 3rd start in 2001), and most recently been tied by Trevor Bayne in the 2011 Daytona 500, and it was also the first time a driver won in his or her first start at a 1.5 mile track, the most common type of track used in the sport. McMurray drove a total of six races in the #40.

2003–2006

In 2003, McMurray became a Winston Cup regular. He won the NASCAR Winston Cup (now Sprint Cup) Rookie of the Year competition by 37 points over Greg Biffle, despite not winning a race. McMurray had five top-5 finishes for the year and finished 13th overall. He began competing part-time in the Busch Series.

In 2004, McMurray and his team were penalized 25 points after the Food City 500 for an incorrect "x-measurement," a method of comparing the center of the roof with the center of the chassis, which proved costly when later in the year McMurray missed the Chase for the Cup by 15 points. He had 23 top-10s during the season, including 12 in the last 14 races, and finished eleventh in the points standings, which earned him a $1 million bonus. In the same year, he won a Craftsman Truck Series race, joining 20 other drivers that have won a race in all three of NASCAR's top touring series (Craftsman Truck, Busch, and NEXTEL Cup).

McMurray left the #42 team after the 2005 season to drive for Roush Fenway Racing. Owner Chip Ganassi was initially adamant that McMurray would be held to his contract, but on November 7, 2005, McMurray was released. McMurray was originally to go to the #6 Ford in 2006, but since Kurt Busch was leaving for Penske Racing and Mark Martin announced he would race for another year, McMurray instead took over for Kurt Busch in the #97 Ford (which was then renumbered #26).

In April 2006, Jack Roush moved Jimmy Fennig from crew chief of the #26 Ford to head Roush's Busch operations. Bob Osbourne, who had been crew chief for Carl Edwards, moved to head the crew for McMurray. McMurray's best finish of the 2006 season came at Dover International Speedway, where he finished second after leading the most laps.

2007

McMurray began the 2007 season with crew chief Larry Carter, formerly from Michael Waltrip Racing and Penske Racing, with sponsorship from Crown Royal and IRWIN Tools. On June 22, 2007, he won his third career NASCAR NEXTEL Cup pole, for the 2007 Toyota/Save Mart 350. On July 7, 2007, McMurray won the Pepsi 400 by .005 of a second over Kyle Busch for his second career Cup win. The photo finish was the closest in Daytona International Speedway history and tied for the second closest finish (1993 DieHard 500) since the advent of electronic scoring in 1993. McMurray finished the year 17th overall in the point standings.

2008

In the beginning of the 2008 season, McMurray encountered a string of poor finishes that relegated him to 36th in points and thus not guaranteed a spot in the field when NASCAR reached the spring Martinsville race. When the current points went into effect to determine the people who were locked in the race, McMurray was required to qualify for the race based on his time around the track. He qualified 5th, locking himself into the field as the fastest of the teams not locked into the race. He earned an 8th place finish in the race, securing himself a spot in the top 35 in points and thus a guaranteed starting position for the next race. Throughout the remainder of the season, he steadily climbed in the standings and reached the top 20 in points. On October 11, 2008, McMurray rallied to finish fifth in the Bank of America 500 at Lowes Motor Speedway. It was his first top five finish since his victory at Daytona in July of the previous year. McMurray finished the 2008 season with three third-place finishes, and was 16th in the standings.

2009

McMurray re-united with former crew chief Donnie Wingo in 2009. Crew Chief Larry Carter moved to Yates Racing to be crew chief for Paul Menard. McMurray started the 2009 season by dominating the final stages of the Budweiser Shootout, but finished second when he lost the lead to Kevin Harvick on the last lap. McMurray had a excellent Speedweeks, finishing 9th in his Gatorade Duel. In the Daytona 500, McMurray ran up front and was a contender, but was eliminated after he was involved in the race's biggest crash. Roush Fenway Racing informed McMurray he would be allowed to leave the team, as they needed to cut their teams down to the NASCAR-mandated four. On November 1, 2009, McMurray won the AMP Energy 500 at Talladega Superspeedway after leading over 20 laps and passing David Stremme with 8 laps to go. He then survived a green-white checkered finish to earn his second restrictor-plate win. Roush Fenway released him and the #26 team at the end of the season due to NASCAR's four team limit and the expiration of Roush Racing's exemption that allowed a 5th team.

2010

In 2010, McMurray began to drive for Earnhardt Ganassi Racing in the #1 car, replacing Martin Truex, Jr.. McMurray reunited with Chip Ganassi in the 2010 24 Hours of Daytona; it was the first time he has been with Ganassi since 2005. On February 14, McMurray won the 2010 Daytona 500. He led for only two laps, the least in Daytona 500 history. McMurray led the final stage of the Aaron's 499 but was passed in a scramble to the finish by Kevin Harvick, who beat him to the line by just .011 sec. McMurray led 27 laps.

In July, McMurray won the 2010 Brickyard 400, making him one of only three drivers to win the Daytona 500 and the Brickyard in the same year. Chip Ganassi became the first owner to win both races and the Indianapolis 500 in the same year, with Dario Franchitti's victory in that race. Although he missed the Chase in 2010, he won again in October at the site of his first win, Charlotte Motor Speedway. McMurray finished 14th in the standings with three wins and nine top 5s.

2011

On January 19, 2011, McMurray signed a multi-year extension with Earnhardt Ganassi Racing to continue driving the 1 McDonalds / Bass Pro Shops Chevrolet.

JR Motorsports

McMurray will drive nine races for JR Motorsports in the Nationwide #88 car after Kelly Bires was released due to a lack of sponsorship. In his first race with JR Motorsports, McMurray ran up front and had a top 10 finish. During the next race at Talladega, he was involved in a final lap wreck. On September 4, 2010, McMurray held off Kyle Busch to win at Atlanta.

Personal life

McMurray was born in Joplin, Missouri. He races annually at the World Karting Association's Daytona KartWeek in late December.

Jamie McMurray married Christy Futrell in July 2009. Their first child Carter Scott McMurray was born Thanksgiving morning, November 25, 2010.

Though his trouble filled 2009, and the contrasting current year, McMurray has found the power of prayer. Jamie said in the post race interview, that "As those laps were winding down I was thinking about Daytona and why I cry and the power of prayer. I had a tough year last year. I found out the power of prayer and what that can do for you. When you get to victory lane, and you get to experience this, it just makes you a believer."

Races won

Sprint Cup (6 career wins)

October 13, 2002 July 7, 2007 November 1, 2009 February 14, 2010 July 25, 2010 October 16, 2010

!Win No.!!Date!!Track!!Race Name!!Distance(laps/miles)
1	|	Charlotte Motor Speedway	Bank of America 500>UAW-GM Quality 500	334 / 501
2	|	Daytona International Speedway at Daytona Beach, FL	Pepsi 400	160 / 400
3	|	Talladega Superspeedway	AMP Energy 500	188 / 500
4	|	Daytona International Speedway at Daytona Beach, FL	Daytona 500	200 / 500
5	|	Indianapolis Motor Speedway	Brickyard 400	160 / 400
6	|	Charlotte Motor Speedway	Bank of America 500	334 / 500

Nationwide Series (8 career wins)

November 2, 2002 October 26, 2002 February 24, 2003 November 8, 2003 February 21, 2004 November 6, 2004 November 13, 2004 September 4, 2010

!Win No.!!Date!!Track!!Race Name!!Distance(laps/miles)
1	|	Rockingham Speedway	Target House 200>Sam's Club 200	197 / 200
2	|	Atlanta Motor Speedway	Aaron's 312 (Atlanta)>Aaron's 312	195 / 200
3	|	Rockingham Speedway	Goody's Headache Powder 200>Rockingham 200	197 / 200
4	|	Rockingham Speedway	Target House 200>Sam's Club 200	197 / 200
5	|	Rockingham Speedway	Goody's Headache Powder 200	197 / 200
6	|	Phoenix International Raceway	Bashas' Supermarkets 200	200 / 200
7	|	Darlington Raceway	BI-LO 200	147 / 200
8	|	Atlanta Motor Speedway	Great Clips 300	195 / 300

''*McMurray won the last four Busch Series races to be run at Rockingham Speedway.''

Craftsman Truck Series (1 career win)

October 23, 2004

!Win No.!!Date!!Track!!Race Name!!Distance(laps/miles)
1	|	Martinsville Speedway	Kroger 200 (NCTS)>Kroger 200	197 / 200

References

External links

JamieMcMurray.com – Official Site

}} }}

Category:1976 births Category:American racecar drivers Category:American people of Scottish descent Category:Living people Category:NASCAR drivers Category:NASCAR Rookies of the Year Category:People from Joplin, Missouri Category:Roush Racing drivers Category:Texaco Category:24 Hours of Daytona drivers Category:Daytona 500 winners Category:Brickyard 400 winners

de:Jamie McMurray fr:Jamie McMurray nl:Jamie McMurray ja:ジェイミー・マクマレー no:Jamie McMurray pt:Jamie McMurray simple:Jamie McMurray sv:Jamie McMurray