Attention deficit/hyperactivity disorder: characteristics, interventions and models
Identifieur interne : 001B44 ( Istex/Corpus ); précédent : 001B43; suivant : 001B45Attention deficit/hyperactivity disorder: characteristics, interventions and models
Auteurs : Merle G. Paule ; Andrew S. Rowland ; Sherry A. Ferguson ; John J. Chelonis ; Rosemary Tannock ; James M. Swanson ; F. Xavier CastellanosSource :
- Neurotoxicology and Teratology [ 0892-0362 ] ; 2000.
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Abstract
An epidemiological study of Attention Deficit/Hyperactivity Disorder (ADHD) suggests that the prevalence may be two to three times higher than the figure of 3–5% often cited. In addition, the data suggest that both underdiagnosis and overdiagnosis occur frequently. Rodent animal models of ADHD, like the Spontaneously Hypertensive Rat (SHR) and other rat models such as those with chemical and radiation-induced brain lesions and cerebellar stunting, and the Coloboma mouse model exhibit clear similarities with several aspects of the human disorder and should prove useful in studying specific traits. Operant behavioral tasks that model learning, short-term memory and simple discriminations are sensitive to ADHD and methylphenidate has been shown to normalize ADHD performance in a short-term memory task. Recent findings challenge not only the current postulate that response inhibition is a unique deficit in ADHD, but also the concepts of ADHD and its treatment, which presume intact perceptual abilities. Time perception deficits may account, in part, for the excessive variability in motor response times on speeded reaction time tasks, motor control problems and motor clumsiness associated with ADHD. The Multimodality Treatment Study of ADHD (MTA) provided data suggesting that pharmacological interventions that included systematic and frequent follow-up with parents and teachers, with or without psychosocial interventions, are superior to psychosocial interventions or standard community care alone. Additionally, the MTA was one of the first studies to demonstrate benefits of multimodal and pharmacological interventions lasting longer than 1 year. Imaging studies have demonstrated differences in brain areas in children with ADHD: anterior corpus callosum, right anterior white matter, and cerebellar volumes are all decreased in children with ADHD and there is less brain asymmetry in ADHD subjects. Additionally, functional imaging studies, coupled with pharmacological manipulations, suggest decreased blood flow and energy utilization in prefrontal cortex and striatum and the dysregulation of catecholamine systems in persons with ADHD.
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DOI: 10.1016/S0892-0362(00)00095-7
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Paule</name><affiliation><mods:affiliation>Behavioral Toxicology Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079-9502, USA</mods:affiliation></affiliation><affiliation><mods:affiliation>Corresponding author. Tel.: +1-870-543-7147/7203; fax: +1-870-543-7720</mods:affiliation></affiliation><affiliation><mods:affiliation>E-mail: mpaule@nctr.fda.gov</mods:affiliation></affiliation></author><author><name sortKey="Rowland, Andrew S" sort="Rowland, Andrew S" uniqKey="Rowland A" first="Andrew S" last="Rowland">Andrew S. Rowland</name><affiliation><mods:affiliation>Epidemiology Branch, NIEHS, A3-05, P.O. Box 12233, Research Triangle Park, NC 27709-2233, USA</mods:affiliation></affiliation></author><author><name sortKey="Ferguson, Sherry A" sort="Ferguson, Sherry A" uniqKey="Ferguson S" first="Sherry A" last="Ferguson">Sherry A. Ferguson</name><affiliation><mods:affiliation>Behavioral Toxicology Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079-9502, USA</mods:affiliation></affiliation></author><author><name sortKey="Chelonis, John J" sort="Chelonis, John J" uniqKey="Chelonis J" first="John J" last="Chelonis">John J. 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In addition, the data suggest that both underdiagnosis and overdiagnosis occur frequently. Rodent animal models of ADHD, like the Spontaneously Hypertensive Rat (SHR) and other rat models such as those with chemical and radiation-induced brain lesions and cerebellar stunting, and the Coloboma mouse model exhibit clear similarities with several aspects of the human disorder and should prove useful in studying specific traits. Operant behavioral tasks that model learning, short-term memory and simple discriminations are sensitive to ADHD and methylphenidate has been shown to normalize ADHD performance in a short-term memory task. Recent findings challenge not only the current postulate that response inhibition is a unique deficit in ADHD, but also the concepts of ADHD and its treatment, which presume intact perceptual abilities. Time perception deficits may account, in part, for the excessive variability in motor response times on speeded reaction time tasks, motor control problems and motor clumsiness associated with ADHD. The Multimodality Treatment Study of ADHD (MTA) provided data suggesting that pharmacological interventions that included systematic and frequent follow-up with parents and teachers, with or without psychosocial interventions, are superior to psychosocial interventions or standard community care alone. Additionally, the MTA was one of the first studies to demonstrate benefits of multimodal and pharmacological interventions lasting longer than 1 year. Imaging studies have demonstrated differences in brain areas in children with ADHD: anterior corpus callosum, right anterior white matter, and cerebellar volumes are all decreased in children with ADHD and there is less brain asymmetry in ADHD subjects. Additionally, functional imaging studies, coupled with pharmacological manipulations, suggest decreased blood flow and energy utilization in prefrontal cortex and striatum and the dysregulation of catecholamine systems in persons with ADHD.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Merle G Paule</name><affiliations><json:string>Behavioral Toxicology Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079-9502, USA</json:string><json:string>Corresponding author. Tel.: +1-870-543-7147/7203; fax: +1-870-543-7720</json:string><json:string>E-mail: mpaule@nctr.fda.gov</json:string></affiliations></json:item><json:item><name>Andrew S Rowland</name><affiliations><json:string>Epidemiology Branch, NIEHS, A3-05, P.O. Box 12233, Research Triangle Park, NC 27709-2233, USA</json:string></affiliations></json:item><json:item><name>Sherry A Ferguson</name><affiliations><json:string>Behavioral Toxicology Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079-9502, USA</json:string></affiliations></json:item><json:item><name>John J Chelonis</name><affiliations><json:string>Department of Psychology, University of Arkansas at Little Rock, 2801 South University Avenue, Little Rock, AR 72204, USA</json:string></affiliations></json:item><json:item><name>Rosemary Tannock</name><affiliations><json:string>Brain and Behaviour Research Programme (Psychiatry Research), The Research Institute of the Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8</json:string></affiliations></json:item><json:item><name>James M Swanson</name><affiliations><json:string>Child Development Center, University of California at Irvine, 19722 MacArthur Boulevard, Irvine, CA 92612, USA</json:string></affiliations></json:item><json:item><name>F.Xavier Castellanos</name><affiliations><json:string>Child Psychiatry Branch, National Institute of Mental Health, Room 3B-19, 10 Center Drive, Bethesda, MD 20892-1251, USA</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Attention deficit disorder</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Epidemiology</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Prevalence</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Rodent models</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cerebellar stunting</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Short-term memory</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Cognitive markers</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Treatment</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Stimulant medication</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Multimodal interventions</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neuroimaging</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Prefrontal cortex</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Dopaminergic dysfunction</value></json:item></subject><language><json:string>eng</json:string></language><originalGenre><json:string>Full-length article</json:string></originalGenre><abstract>An epidemiological study of Attention Deficit/Hyperactivity Disorder (ADHD) suggests that the prevalence may be two to three times higher than the figure of 3–5% often cited. In addition, the data suggest that both underdiagnosis and overdiagnosis occur frequently. Rodent animal models of ADHD, like the Spontaneously Hypertensive Rat (SHR) and other rat models such as those with chemical and radiation-induced brain lesions and cerebellar stunting, and the Coloboma mouse model exhibit clear similarities with several aspects of the human disorder and should prove useful in studying specific traits. Operant behavioral tasks that model learning, short-term memory and simple discriminations are sensitive to ADHD and methylphenidate has been shown to normalize ADHD performance in a short-term memory task. Recent findings challenge not only the current postulate that response inhibition is a unique deficit in ADHD, but also the concepts of ADHD and its treatment, which presume intact perceptual abilities. Time perception deficits may account, in part, for the excessive variability in motor response times on speeded reaction time tasks, motor control problems and motor clumsiness associated with ADHD. The Multimodality Treatment Study of ADHD (MTA) provided data suggesting that pharmacological interventions that included systematic and frequent follow-up with parents and teachers, with or without psychosocial interventions, are superior to psychosocial interventions or standard community care alone. Additionally, the MTA was one of the first studies to demonstrate benefits of multimodal and pharmacological interventions lasting longer than 1 year. Imaging studies have demonstrated differences in brain areas in children with ADHD: anterior corpus callosum, right anterior white matter, and cerebellar volumes are all decreased in children with ADHD and there is less brain asymmetry in ADHD subjects. Additionally, functional imaging studies, coupled with pharmacological manipulations, suggest decreased blood flow and energy utilization in prefrontal cortex and striatum and the dysregulation of catecholamine systems in persons with ADHD.</abstract><qualityIndicators><score>8</score><pdfVersion>1.2</pdfVersion><pdfPageSize>594 x 792 pts</pdfPageSize><refBibsNative>true</refBibsNative><keywordCount>13</keywordCount><abstractCharCount>2162</abstractCharCount><pdfWordCount>18282</pdfWordCount><pdfCharCount>112630</pdfCharCount><pdfPageCount>21</pdfPageCount><abstractWordCount>305</abstractWordCount></qualityIndicators><title>Attention deficit/hyperactivity disorder: characteristics, interventions and models</title><pii><json:string>S0892-0362(00)00095-7</json:string></pii><genre><json:string>research-article</json:string></genre><serie><editor><json:item><name>J. Grafman</name></json:item><json:item><name>K.J. 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Tel.: +1-870-543-7147/7203; fax: +1-870-543-7720</affiliation></author><author xml:id="author-2"><persName><forename type="first">Andrew S</forename><surname>Rowland</surname></persName><affiliation>Epidemiology Branch, NIEHS, A3-05, P.O. Box 12233, Research Triangle Park, NC 27709-2233, USA</affiliation></author><author xml:id="author-3"><persName><forename type="first">Sherry A</forename><surname>Ferguson</surname></persName><affiliation>Behavioral Toxicology Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079-9502, USA</affiliation></author><author xml:id="author-4"><persName><forename type="first">John J</forename><surname>Chelonis</surname></persName><affiliation>Department of Psychology, University of Arkansas at Little Rock, 2801 South University Avenue, Little Rock, AR 72204, USA</affiliation></author><author xml:id="author-5"><persName><forename type="first">Rosemary</forename><surname>Tannock</surname></persName><affiliation>Brain and Behaviour Research Programme (Psychiatry Research), The Research Institute of the Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8</affiliation></author><author xml:id="author-6"><persName><forename type="first">James M</forename><surname>Swanson</surname></persName><affiliation>Child Development Center, University of California at Irvine, 19722 MacArthur Boulevard, Irvine, CA 92612, USA</affiliation></author><author xml:id="author-7"><persName><forename type="first">F.Xavier</forename><surname>Castellanos</surname></persName><affiliation>Child Psychiatry Branch, National Institute of Mental Health, Room 3B-19, 10 Center Drive, Bethesda, MD 20892-1251, USA</affiliation></author></analytic><monogr><title level="j">Neurotoxicology and Teratology</title><title level="j" type="abbrev">NTT</title><idno type="pISSN">0892-0362</idno><idno type="PII">S0892-0362(00)X0033-5</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="2000"></date><biblScope unit="volume">22</biblScope><biblScope unit="issue">5</biblScope><biblScope unit="page" from="631">631</biblScope><biblScope unit="page" to="651">651</biblScope></imprint></monogr><idno type="istex">4B4DF0D930A18CB563C7A804CDA5DFF36B1B4AA9</idno><idno type="DOI">10.1016/S0892-0362(00)00095-7</idno><idno type="PII">S0892-0362(00)00095-7</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>2000</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>An epidemiological study of Attention Deficit/Hyperactivity Disorder (ADHD) suggests that the prevalence may be two to three times higher than the figure of 3–5% often cited. In addition, the data suggest that both underdiagnosis and overdiagnosis occur frequently. Rodent animal models of ADHD, like the Spontaneously Hypertensive Rat (SHR) and other rat models such as those with chemical and radiation-induced brain lesions and cerebellar stunting, and the Coloboma mouse model exhibit clear similarities with several aspects of the human disorder and should prove useful in studying specific traits. Operant behavioral tasks that model learning, short-term memory and simple discriminations are sensitive to ADHD and methylphenidate has been shown to normalize ADHD performance in a short-term memory task. Recent findings challenge not only the current postulate that response inhibition is a unique deficit in ADHD, but also the concepts of ADHD and its treatment, which presume intact perceptual abilities. Time perception deficits may account, in part, for the excessive variability in motor response times on speeded reaction time tasks, motor control problems and motor clumsiness associated with ADHD. The Multimodality Treatment Study of ADHD (MTA) provided data suggesting that pharmacological interventions that included systematic and frequent follow-up with parents and teachers, with or without psychosocial interventions, are superior to psychosocial interventions or standard community care alone. Additionally, the MTA was one of the first studies to demonstrate benefits of multimodal and pharmacological interventions lasting longer than 1 year. Imaging studies have demonstrated differences in brain areas in children with ADHD: anterior corpus callosum, right anterior white matter, and cerebellar volumes are all decreased in children with ADHD and there is less brain asymmetry in ADHD subjects. Additionally, functional imaging studies, coupled with pharmacological manipulations, suggest decreased blood flow and energy utilization in prefrontal cortex and striatum and the dysregulation of catecholamine systems in persons with ADHD.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Attention deficit disorder</term></item><item><term>Epidemiology</term></item><item><term>Prevalence</term></item><item><term>Rodent models</term></item><item><term>Cerebellar stunting</term></item><item><term>Short-term memory</term></item><item><term>Cognitive markers</term></item><item><term>Treatment</term></item><item><term>Stimulant medication</term></item><item><term>Multimodal interventions</term></item><item><term>Neuroimaging</term></item><item><term>Prefrontal cortex</term></item><item><term>Dopaminergic dysfunction</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="2000">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api.istex.fr/document/4B4DF0D930A18CB563C7A804CDA5DFF36B1B4AA9/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla" xml:lang="en"><item-info><jid>NTT</jid><aid>5306</aid><ce:pii>S0892-0362(00)00095-7</ce:pii><ce:doi>10.1016/S0892-0362(00)00095-7</ce:doi><ce:copyright type="full-transfer" year="2000">Elsevier Science Inc.</ce:copyright></item-info><head><ce:dochead><ce:textfn>Symposium overview</ce:textfn></ce:dochead><ce:title>Attention deficit/hyperactivity disorder: characteristics, interventions and models</ce:title><ce:author-group><ce:author><ce:given-name>Merle G</ce:given-name><ce:surname>Paule</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref><ce:cross-ref refid="CORR1">*</ce:cross-ref><ce:e-address>mpaule@nctr.fda.gov</ce:e-address></ce:author><ce:author><ce:given-name>Andrew S</ce:given-name><ce:surname>Rowland</ce:surname><ce:cross-ref refid="AFF2"><ce:sup>b</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Sherry A</ce:given-name><ce:surname>Ferguson</ce:surname><ce:cross-ref refid="AFF1"><ce:sup>a</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>John J</ce:given-name><ce:surname>Chelonis</ce:surname><ce:cross-ref refid="AFF3"><ce:sup>c</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>Rosemary</ce:given-name><ce:surname>Tannock</ce:surname><ce:cross-ref refid="AFF4"><ce:sup>d</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>James M</ce:given-name><ce:surname>Swanson</ce:surname><ce:cross-ref refid="AFF5"><ce:sup>e</ce:sup></ce:cross-ref></ce:author><ce:author><ce:given-name>F.Xavier</ce:given-name><ce:surname>Castellanos</ce:surname><ce:cross-ref refid="AFF6"><ce:sup>f</ce:sup></ce:cross-ref></ce:author><ce:affiliation id="AFF1"><ce:label>a</ce:label><ce:textfn>Behavioral Toxicology Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079-9502, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF2"><ce:label>b</ce:label><ce:textfn>Epidemiology Branch, NIEHS, A3-05, P.O. Box 12233, Research Triangle Park, NC 27709-2233, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF3"><ce:label>c</ce:label><ce:textfn>Department of Psychology, University of Arkansas at Little Rock, 2801 South University Avenue, Little Rock, AR 72204, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF4"><ce:label>d</ce:label><ce:textfn>Brain and Behaviour Research Programme (Psychiatry Research), The Research Institute of the Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8</ce:textfn></ce:affiliation><ce:affiliation id="AFF5"><ce:label>e</ce:label><ce:textfn>Child Development Center, University of California at Irvine, 19722 MacArthur Boulevard, Irvine, CA 92612, USA</ce:textfn></ce:affiliation><ce:affiliation id="AFF6"><ce:label>f</ce:label><ce:textfn>Child Psychiatry Branch, National Institute of Mental Health, Room 3B-19, 10 Center Drive, Bethesda, MD 20892-1251, USA</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Tel.: +1-870-543-7147/7203; fax: +1-870-543-7720</ce:text></ce:correspondence></ce:author-group><ce:date-received day="28" month="4" year="2000"></ce:date-received><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>An epidemiological study of Attention Deficit/Hyperactivity Disorder (ADHD) suggests that the prevalence may be two to three times higher than the figure of 3–5% often cited. In addition, the data suggest that both underdiagnosis and overdiagnosis occur frequently. Rodent animal models of ADHD, like the Spontaneously Hypertensive Rat (SHR) and other rat models such as those with chemical and radiation-induced brain lesions and cerebellar stunting, and the Coloboma mouse model exhibit clear similarities with several aspects of the human disorder and should prove useful in studying specific traits. Operant behavioral tasks that model learning, short-term memory and simple discriminations are sensitive to ADHD and methylphenidate has been shown to normalize ADHD performance in a short-term memory task. Recent findings challenge not only the current postulate that response inhibition is a unique deficit in ADHD, but also the concepts of ADHD and its treatment, which presume intact perceptual abilities. Time perception deficits may account, in part, for the excessive variability in motor response times on speeded reaction time tasks, motor control problems and motor clumsiness associated with ADHD. The Multimodality Treatment Study of ADHD (MTA) provided data suggesting that pharmacological interventions that included systematic and frequent follow-up with parents and teachers, with or without psychosocial interventions, are superior to psychosocial interventions or standard community care alone. Additionally, the MTA was one of the first studies to demonstrate benefits of multimodal and pharmacological interventions lasting longer than 1 year. Imaging studies have demonstrated differences in brain areas in children with ADHD: anterior corpus callosum, right anterior white matter, and cerebellar volumes are all decreased in children with ADHD and there is less brain asymmetry in ADHD subjects. Additionally, functional imaging studies, coupled with pharmacological manipulations, suggest decreased blood flow and energy utilization in prefrontal cortex and striatum and the dysregulation of catecholamine systems in persons with ADHD.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Attention deficit disorder</ce:text></ce:keyword><ce:keyword><ce:text>Epidemiology</ce:text></ce:keyword><ce:keyword><ce:text>Prevalence</ce:text></ce:keyword><ce:keyword><ce:text>Rodent models</ce:text></ce:keyword><ce:keyword><ce:text>Cerebellar stunting</ce:text></ce:keyword><ce:keyword><ce:text>Short-term memory</ce:text></ce:keyword><ce:keyword><ce:text>Cognitive markers</ce:text></ce:keyword><ce:keyword><ce:text>Treatment</ce:text></ce:keyword><ce:keyword><ce:text>Stimulant medication</ce:text></ce:keyword><ce:keyword><ce:text>Multimodal interventions</ce:text></ce:keyword><ce:keyword><ce:text>Neuroimaging</ce:text></ce:keyword><ce:keyword><ce:text>Prefrontal cortex</ce:text></ce:keyword><ce:keyword><ce:text>Dopaminergic dysfunction</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Attention deficit/hyperactivity disorder: characteristics, interventions and models</title></titleInfo><titleInfo type="alternative" lang="en" contentType="CDATA"><title>Attention deficit/hyperactivity disorder: characteristics, interventions and models</title></titleInfo><name type="personal"><namePart type="given">Merle G</namePart><namePart type="family">Paule</namePart><affiliation>Behavioral Toxicology Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079-9502, USA</affiliation><affiliation>Corresponding author. Tel.: +1-870-543-7147/7203; fax: +1-870-543-7720</affiliation><affiliation>E-mail: mpaule@nctr.fda.gov</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Andrew S</namePart><namePart type="family">Rowland</namePart><affiliation>Epidemiology Branch, NIEHS, A3-05, P.O. Box 12233, Research Triangle Park, NC 27709-2233, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Sherry A</namePart><namePart type="family">Ferguson</namePart><affiliation>Behavioral Toxicology Laboratory, Division of Neurotoxicology, HFT-132, National Center for Toxicological Research, 3900 NCTR Road, Jefferson, AR 72079-9502, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">John J</namePart><namePart type="family">Chelonis</namePart><affiliation>Department of Psychology, University of Arkansas at Little Rock, 2801 South University Avenue, Little Rock, AR 72204, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Rosemary</namePart><namePart type="family">Tannock</namePart><affiliation>Brain and Behaviour Research Programme (Psychiatry Research), The Research Institute of the Hospital for Sick Children, University of Toronto, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">James M</namePart><namePart type="family">Swanson</namePart><affiliation>Child Development Center, University of California at Irvine, 19722 MacArthur Boulevard, Irvine, CA 92612, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">F.Xavier</namePart><namePart type="family">Castellanos</namePart><affiliation>Child Psychiatry Branch, National Institute of Mental Health, Room 3B-19, 10 Center Drive, Bethesda, MD 20892-1251, USA</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">2000</dateIssued><copyrightDate encoding="w3cdtf">2000</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">An epidemiological study of Attention Deficit/Hyperactivity Disorder (ADHD) suggests that the prevalence may be two to three times higher than the figure of 3–5% often cited. In addition, the data suggest that both underdiagnosis and overdiagnosis occur frequently. Rodent animal models of ADHD, like the Spontaneously Hypertensive Rat (SHR) and other rat models such as those with chemical and radiation-induced brain lesions and cerebellar stunting, and the Coloboma mouse model exhibit clear similarities with several aspects of the human disorder and should prove useful in studying specific traits. Operant behavioral tasks that model learning, short-term memory and simple discriminations are sensitive to ADHD and methylphenidate has been shown to normalize ADHD performance in a short-term memory task. Recent findings challenge not only the current postulate that response inhibition is a unique deficit in ADHD, but also the concepts of ADHD and its treatment, which presume intact perceptual abilities. Time perception deficits may account, in part, for the excessive variability in motor response times on speeded reaction time tasks, motor control problems and motor clumsiness associated with ADHD. The Multimodality Treatment Study of ADHD (MTA) provided data suggesting that pharmacological interventions that included systematic and frequent follow-up with parents and teachers, with or without psychosocial interventions, are superior to psychosocial interventions or standard community care alone. Additionally, the MTA was one of the first studies to demonstrate benefits of multimodal and pharmacological interventions lasting longer than 1 year. Imaging studies have demonstrated differences in brain areas in children with ADHD: anterior corpus callosum, right anterior white matter, and cerebellar volumes are all decreased in children with ADHD and there is less brain asymmetry in ADHD subjects. Additionally, functional imaging studies, coupled with pharmacological manipulations, suggest decreased blood flow and energy utilization in prefrontal cortex and striatum and the dysregulation of catecholamine systems in persons with ADHD.</abstract><note type="content">Section title: Symposium overview</note><subject lang="en"><genre>Keywords</genre><topic>Attention deficit disorder</topic><topic>Epidemiology</topic><topic>Prevalence</topic><topic>Rodent models</topic><topic>Cerebellar stunting</topic><topic>Short-term memory</topic><topic>Cognitive markers</topic><topic>Treatment</topic><topic>Stimulant medication</topic><topic>Multimodal interventions</topic><topic>Neuroimaging</topic><topic>Prefrontal cortex</topic><topic>Dopaminergic dysfunction</topic></subject><relatedItem type="host"><titleInfo><title>Neurotoxicology and Teratology</title></titleInfo><titleInfo type="abbreviated"><title>NTT</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">200009</dateIssued></originInfo><identifier type="ISSN">0892-0362</identifier><identifier type="PII">S0892-0362(00)X0033-5</identifier><part><date>200009</date><detail type="volume"><number>22</number><caption>vol.</caption></detail><detail type="issue"><number>5</number><caption>no.</caption></detail><extent unit="issue pages"><start>607</start><end>772</end></extent><extent unit="pages"><start>631</start><end>651</end></extent></part></relatedItem><identifier type="istex">4B4DF0D930A18CB563C7A804CDA5DFF36B1B4AA9</identifier><identifier type="DOI">10.1016/S0892-0362(00)00095-7</identifier><identifier type="PII">S0892-0362(00)00095-7</identifier><accessCondition type="use and reproduction" contentType="copyright">©2000 Elsevier Science Inc.</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science Inc., ©2000</recordOrigin></recordInfo></mods></metadata></istex></record>Pour manipuler ce document sous Unix (Dilib)
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