Childhood cognitive development in 22q11.2 deletion syndrome: case-control study
22q11.2 deletion syndrome (22q11.2DS) is associated with a high risk of childhood as well as adult psychiatric disorders, in particular schizophrenia. Childhood cognitive deterioration in 22q11.2DS has previously been reported, but only in studies lacking a control sample. To compare cognitive traje...
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| Veröffentlicht in: | British journal of psychiatry 2017-10, Vol.211 (4), p.223-230 |
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| creator | Chawner, Samuel J R A Doherty, Joanne L Moss, Hayley Niarchou, Maria Walters, James T R Owen, Michael J van den Bree, Marianne B M |
| description | 22q11.2 deletion syndrome (22q11.2DS) is associated with a high risk of childhood as well as adult psychiatric disorders, in particular schizophrenia. Childhood cognitive deterioration in 22q11.2DS has previously been reported, but only in studies lacking a control sample.
To compare cognitive trajectories in children with 22q11.2DS and unaffected control siblings.
A longitudinal study of neurocognitive functioning (IQ, executive function, processing speed and attention) was conducted in children with 22q11.2DS (
= 75, mean age time 1 (
) 9.9, time 2 (
) 12.5) and control siblings (
= 33, mean age
10.6,
13.4).
Children with 22q11.2DS exhibited deficits in all cognitive domains. However, mean scores did not indicate deterioration. When individual trajectories were examined, some participants showed significant decline over time, but the prevalence was similar for 22q11.2DS and control siblings. Findings are more likely to reflect normal developmental fluctuation than a 22q11.2DS-specific abnormality.
Childhood cognitive deterioration is not associated with 22q11.2DS. Contrary to previous suggestions, we believe it is premature to recommend repeated monitoring of cognitive function for identifying individual children with 22q11.2DS at high risk of developing schizophrenia. |
| doi_str_mv | 10.1192/bjp.bp.116.195651 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_5623878</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2315618066</sourcerecordid><originalsourceid>FETCH-LOGICAL-c427t-8cf93c68f4f182f04f78f341324fe587c3e1795844f31d657fa4e5b843c18ff33</originalsourceid><addsrcrecordid>eNpdUU1r3DAQFaWh2Xz8gF6CoZdevPHo2z0UwtKmgUByaM_ClqVdLbbkSPbC_vsq7HZJc5o3M28eb3gIfYZqCVDj23Y7LtsxY76EmnEGH9ACqMAlUM4-okVVVaIEzKpzdJHSNreEYvEJnWMpJZa4XqDn1cb13SaErtBh7d3kdqbozM70YRyMnwrnC4xfAJY4j3szueCLtPddDIP5VugmmVIHP8XQF2mau_0VOrNNn8z1sV6iPz9__F79Kh-f7h9Wd4-lzhamUmpbE82lpRYkthW1QlpCgWBqDZNCEwOiZpJSS6DjTNiGGtZKSjRIawm5RN8PuuPcDqbT2WtsejVGNzRxr0Lj1P8b7zZqHXaKcUykkFng61EghpfZpEkNLmnT9403YU4KaiIYFgReqV_eUbdhjj6_pzABxkFWnGcWHFg6hpSisSczUKnXvFTOS7Vjxlwd8so3N2-_OF38C4j8BVRDkfw</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2315618066</pqid></control><display><type>article</type><title>Childhood cognitive development in 22q11.2 deletion syndrome: case-control study</title><source>Applied Social Sciences Index & Abstracts (ASSIA)</source><source>Cambridge Journals Online</source><source>MEDLINE</source><source>EZB-FREE-00999 freely available EZB journals</source><source>Alma/SFX Local Collection</source><creator>Chawner, Samuel J R A ; Doherty, Joanne L ; Moss, Hayley ; Niarchou, Maria ; Walters, James T R ; Owen, Michael J ; van den Bree, Marianne B M</creator><creatorcontrib>Chawner, Samuel J R A ; Doherty, Joanne L ; Moss, Hayley ; Niarchou, Maria ; Walters, James T R ; Owen, Michael J ; van den Bree, Marianne B M</creatorcontrib><description>22q11.2 deletion syndrome (22q11.2DS) is associated with a high risk of childhood as well as adult psychiatric disorders, in particular schizophrenia. Childhood cognitive deterioration in 22q11.2DS has previously been reported, but only in studies lacking a control sample.
To compare cognitive trajectories in children with 22q11.2DS and unaffected control siblings.
A longitudinal study of neurocognitive functioning (IQ, executive function, processing speed and attention) was conducted in children with 22q11.2DS (
= 75, mean age time 1 (
) 9.9, time 2 (
) 12.5) and control siblings (
= 33, mean age
10.6,
13.4).
Children with 22q11.2DS exhibited deficits in all cognitive domains. However, mean scores did not indicate deterioration. When individual trajectories were examined, some participants showed significant decline over time, but the prevalence was similar for 22q11.2DS and control siblings. Findings are more likely to reflect normal developmental fluctuation than a 22q11.2DS-specific abnormality.
Childhood cognitive deterioration is not associated with 22q11.2DS. Contrary to previous suggestions, we believe it is premature to recommend repeated monitoring of cognitive function for identifying individual children with 22q11.2DS at high risk of developing schizophrenia.</description><identifier>ISSN: 0007-1250</identifier><identifier>ISSN: 1472-1465</identifier><identifier>EISSN: 1472-1465</identifier><identifier>DOI: 10.1192/bjp.bp.116.195651</identifier><identifier>PMID: 28882829</identifier><language>eng</language><publisher>England: Cambridge University Press</publisher><subject>Adolescent ; Age ; Attention deficit hyperactivity disorder ; Case-Control Studies ; Child ; Child Development ; Childhood ; Children ; Cognition ; Cognition & reasoning ; Cognition Disorders - complications ; Cognition Disorders - psychology ; Cognitive ability ; Cognitive development ; Cognitive functioning ; Deterioration ; DiGeorge Syndrome - complications ; DiGeorge Syndrome - psychology ; Executive function ; Female ; High risk ; Humans ; Hypotheses ; Intelligence ; Intelligence tests ; Longitudinal Studies ; Male ; Mental disorders ; Neurocognition ; Neuropsychological Tests ; Psychiatry ; Schizophrenia ; Siblings</subject><ispartof>British journal of psychiatry, 2017-10, Vol.211 (4), p.223-230</ispartof><rights>The Royal College of Psychiatrists 2017.</rights><rights>2017 This article is published under (https://creativecommons.org/licenses/by/3.0/) (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Royal College of Psychiatrists 2017. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c427t-8cf93c68f4f182f04f78f341324fe587c3e1795844f31d657fa4e5b843c18ff33</citedby><cites>FETCH-LOGICAL-c427t-8cf93c68f4f182f04f78f341324fe587c3e1795844f31d657fa4e5b843c18ff33</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,12825,27901,27902,30976</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28882829$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chawner, Samuel J R A</creatorcontrib><creatorcontrib>Doherty, Joanne L</creatorcontrib><creatorcontrib>Moss, Hayley</creatorcontrib><creatorcontrib>Niarchou, Maria</creatorcontrib><creatorcontrib>Walters, James T R</creatorcontrib><creatorcontrib>Owen, Michael J</creatorcontrib><creatorcontrib>van den Bree, Marianne B M</creatorcontrib><title>Childhood cognitive development in 22q11.2 deletion syndrome: case-control study</title><title>British journal of psychiatry</title><addtitle>Br J Psychiatry</addtitle><description>22q11.2 deletion syndrome (22q11.2DS) is associated with a high risk of childhood as well as adult psychiatric disorders, in particular schizophrenia. Childhood cognitive deterioration in 22q11.2DS has previously been reported, but only in studies lacking a control sample.
To compare cognitive trajectories in children with 22q11.2DS and unaffected control siblings.
A longitudinal study of neurocognitive functioning (IQ, executive function, processing speed and attention) was conducted in children with 22q11.2DS (
= 75, mean age time 1 (
) 9.9, time 2 (
) 12.5) and control siblings (
= 33, mean age
10.6,
13.4).
Children with 22q11.2DS exhibited deficits in all cognitive domains. However, mean scores did not indicate deterioration. When individual trajectories were examined, some participants showed significant decline over time, but the prevalence was similar for 22q11.2DS and control siblings. Findings are more likely to reflect normal developmental fluctuation than a 22q11.2DS-specific abnormality.
Childhood cognitive deterioration is not associated with 22q11.2DS. Contrary to previous suggestions, we believe it is premature to recommend repeated monitoring of cognitive function for identifying individual children with 22q11.2DS at high risk of developing schizophrenia.</description><subject>Adolescent</subject><subject>Age</subject><subject>Attention deficit hyperactivity disorder</subject><subject>Case-Control Studies</subject><subject>Child</subject><subject>Child Development</subject><subject>Childhood</subject><subject>Children</subject><subject>Cognition</subject><subject>Cognition & reasoning</subject><subject>Cognition Disorders - complications</subject><subject>Cognition Disorders - psychology</subject><subject>Cognitive ability</subject><subject>Cognitive development</subject><subject>Cognitive functioning</subject><subject>Deterioration</subject><subject>DiGeorge Syndrome - complications</subject><subject>DiGeorge Syndrome - psychology</subject><subject>Executive function</subject><subject>Female</subject><subject>High risk</subject><subject>Humans</subject><subject>Hypotheses</subject><subject>Intelligence</subject><subject>Intelligence tests</subject><subject>Longitudinal Studies</subject><subject>Male</subject><subject>Mental disorders</subject><subject>Neurocognition</subject><subject>Neuropsychological Tests</subject><subject>Psychiatry</subject><subject>Schizophrenia</subject><subject>Siblings</subject><issn>0007-1250</issn><issn>1472-1465</issn><issn>1472-1465</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>7QJ</sourceid><sourceid>8G5</sourceid><sourceid>BENPR</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNpdUU1r3DAQFaWh2Xz8gF6CoZdevPHo2z0UwtKmgUByaM_ClqVdLbbkSPbC_vsq7HZJc5o3M28eb3gIfYZqCVDj23Y7LtsxY76EmnEGH9ACqMAlUM4-okVVVaIEzKpzdJHSNreEYvEJnWMpJZa4XqDn1cb13SaErtBh7d3kdqbozM70YRyMnwrnC4xfAJY4j3szueCLtPddDIP5VugmmVIHP8XQF2mau_0VOrNNn8z1sV6iPz9__F79Kh-f7h9Wd4-lzhamUmpbE82lpRYkthW1QlpCgWBqDZNCEwOiZpJSS6DjTNiGGtZKSjRIawm5RN8PuuPcDqbT2WtsejVGNzRxr0Lj1P8b7zZqHXaKcUykkFng61EghpfZpEkNLmnT9403YU4KaiIYFgReqV_eUbdhjj6_pzABxkFWnGcWHFg6hpSisSczUKnXvFTOS7Vjxlwd8so3N2-_OF38C4j8BVRDkfw</recordid><startdate>201710</startdate><enddate>201710</enddate><creator>Chawner, Samuel J R A</creator><creator>Doherty, Joanne L</creator><creator>Moss, Hayley</creator><creator>Niarchou, Maria</creator><creator>Walters, James T R</creator><creator>Owen, Michael J</creator><creator>van den Bree, Marianne B M</creator><general>Cambridge University Press</general><general>Royal College of Psychiatrists</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>0-V</scope><scope>3V.</scope><scope>7QJ</scope><scope>7TK</scope><scope>7XB</scope><scope>88G</scope><scope>88J</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ALSLI</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>HEHIP</scope><scope>M2M</scope><scope>M2O</scope><scope>M2R</scope><scope>M2S</scope><scope>MBDVC</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201710</creationdate><title>Childhood cognitive development in 22q11.2 deletion syndrome: case-control study</title><author>Chawner, Samuel J R A ; Doherty, Joanne L ; Moss, Hayley ; Niarchou, Maria ; Walters, James T R ; Owen, Michael J ; van den Bree, Marianne B M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c427t-8cf93c68f4f182f04f78f341324fe587c3e1795844f31d657fa4e5b843c18ff33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adolescent</topic><topic>Age</topic><topic>Attention deficit hyperactivity disorder</topic><topic>Case-Control Studies</topic><topic>Child</topic><topic>Child Development</topic><topic>Childhood</topic><topic>Children</topic><topic>Cognition</topic><topic>Cognition & reasoning</topic><topic>Cognition Disorders - complications</topic><topic>Cognition Disorders - psychology</topic><topic>Cognitive ability</topic><topic>Cognitive development</topic><topic>Cognitive functioning</topic><topic>Deterioration</topic><topic>DiGeorge Syndrome - complications</topic><topic>DiGeorge Syndrome - psychology</topic><topic>Executive function</topic><topic>Female</topic><topic>High risk</topic><topic>Humans</topic><topic>Hypotheses</topic><topic>Intelligence</topic><topic>Intelligence tests</topic><topic>Longitudinal Studies</topic><topic>Male</topic><topic>Mental disorders</topic><topic>Neurocognition</topic><topic>Neuropsychological Tests</topic><topic>Psychiatry</topic><topic>Schizophrenia</topic><topic>Siblings</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Chawner, Samuel J R A</creatorcontrib><creatorcontrib>Doherty, Joanne L</creatorcontrib><creatorcontrib>Moss, Hayley</creatorcontrib><creatorcontrib>Niarchou, Maria</creatorcontrib><creatorcontrib>Walters, James T R</creatorcontrib><creatorcontrib>Owen, Michael J</creatorcontrib><creatorcontrib>van den Bree, Marianne B M</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Social Sciences Premium Collection</collection><collection>ProQuest Central (Corporate)</collection><collection>Applied Social Sciences Index & Abstracts (ASSIA)</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Psychology Database (Alumni)</collection><collection>Social Science Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Social Science Premium Collection</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>Sociology Collection</collection><collection>ProQuest Psychology</collection><collection>ProQuest Research Library</collection><collection>ProQuest Social Science Journals</collection><collection>Sociology Database</collection><collection>Research Library (Corporate)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>British journal of psychiatry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chawner, Samuel J R A</au><au>Doherty, Joanne L</au><au>Moss, Hayley</au><au>Niarchou, Maria</au><au>Walters, James T R</au><au>Owen, Michael J</au><au>van den Bree, Marianne B M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Childhood cognitive development in 22q11.2 deletion syndrome: case-control study</atitle><jtitle>British journal of psychiatry</jtitle><addtitle>Br J Psychiatry</addtitle><date>2017-10</date><risdate>2017</risdate><volume>211</volume><issue>4</issue><spage>223</spage><epage>230</epage><pages>223-230</pages><issn>0007-1250</issn><issn>1472-1465</issn><eissn>1472-1465</eissn><abstract>22q11.2 deletion syndrome (22q11.2DS) is associated with a high risk of childhood as well as adult psychiatric disorders, in particular schizophrenia. Childhood cognitive deterioration in 22q11.2DS has previously been reported, but only in studies lacking a control sample.
To compare cognitive trajectories in children with 22q11.2DS and unaffected control siblings.
A longitudinal study of neurocognitive functioning (IQ, executive function, processing speed and attention) was conducted in children with 22q11.2DS (
= 75, mean age time 1 (
) 9.9, time 2 (
) 12.5) and control siblings (
= 33, mean age
10.6,
13.4).
Children with 22q11.2DS exhibited deficits in all cognitive domains. However, mean scores did not indicate deterioration. When individual trajectories were examined, some participants showed significant decline over time, but the prevalence was similar for 22q11.2DS and control siblings. Findings are more likely to reflect normal developmental fluctuation than a 22q11.2DS-specific abnormality.
Childhood cognitive deterioration is not associated with 22q11.2DS. Contrary to previous suggestions, we believe it is premature to recommend repeated monitoring of cognitive function for identifying individual children with 22q11.2DS at high risk of developing schizophrenia.</abstract><cop>England</cop><pub>Cambridge University Press</pub><pmid>28882829</pmid><doi>10.1192/bjp.bp.116.195651</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adolescent Age Attention deficit hyperactivity disorder Case-Control Studies Child Child Development Childhood Children Cognition Cognition & reasoning Cognition Disorders - complications Cognition Disorders - psychology Cognitive ability Cognitive development Cognitive functioning Deterioration DiGeorge Syndrome - complications DiGeorge Syndrome - psychology Executive function Female High risk Humans Hypotheses Intelligence Intelligence tests Longitudinal Studies Male Mental disorders Neurocognition Neuropsychological Tests Psychiatry Schizophrenia Siblings |
| title | Childhood cognitive development in 22q11.2 deletion syndrome: case-control study |
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