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<meta name="DC.Title" content="Developmental Differences of the Major Forebrain Commissures in Lissencephalies" />
<meta name="DC.Identifier" content="10.3174/ajnr.A2133" />
<meta name="DC.Date" content="2010-10-01" />
<meta name="DC.Publisher" content="American Journal of Neuroradiology" />
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Indicates open access to non-subscribers at www.ajnr.org" />
<meta name="DC.AccessRights" content="open-access" />
<meta name="DC.Description" content="BACKGROUND AND PURPOSE: Changes of the major forebrain commissures in lissencephaly have not been systematically studied. We investigated the developmental differences of the commissures in patients with varying types of lissencephaly to determine whether specific commissural features may help in distinguishing lissencephaly phenotypes.

MATERIALS AND METHODS: MR imaging of 124 patients was retrospectively reviewed. Patients were classified as having cLIS, vLIS, and CBSC, according to cortical phenotype; few patients had genetic diagnoses. Abnormalities of the CC, AC, and HC were recorded, and the overall shape was regarded as hypogenetic, hypoplastic, dysmorphic, a thin flat callosal body with a vertical splenium, and a convex upward callosal body, compared with age-matched controls. Correlations between commissural characteristics and cortical patterns were analyzed by using the Monte Carlo simulation of χ2, extension to m × n table, and Fisher exact tests as appropriate ( P &lt; .05).

RESULTS: Patients were classified as having cLIS (57.4%), vLIS (38.4%), or CBSC (4.2%). The most common callosal developmental anomaly was hypogenesis with an absent rostrum, a small inferior genu, and a small splenium. An angled (90°) splenium was found to be significantly associated with cLIS, as was an excessively convex upward callosal body with VLDLR. ACC with an enlarged AC was found in all cases of ARX.

CONCLUSIONS: Specific patterns of the commissure anomalies were associated with certain types of lissencephaly. Callosal anomalies were more common than those of the AC or HC. Developmental variations of commissures may be useful as an imaging criterion in differentiating the groups of lissencephalies and may give insight into the processes causing these malformations.

AC
:   anterior commissure
ACC
:   agenesis of the CC
ARX
:   lissencephaly with ARX mutation
ARX-XLAG
:   lissencephaly with ARX mutation, and an absent callosum, ambiguous genitalia
CBSC
:   cobblestone complex
CC
:   corpus callosum
cLIS
:   classic lissencephaly
CMD
:   congenital muscular dystrophies
DCX
:   lissencephaly with mutated DCX gene
FCMD
:   Fukuyama CMD
FKRP
:   lissencephaly with FKRP mutation
HC
:   hippocampal commissure
LARGE
:   lissencephaly with LARGE mutation
LIS1
:   lissencephaly with mutated LIS1 gene
ND
:   not determined
(p)
:   presumed
POMT1, POMT2, and POMGnT1
:   lissencephalies with POMT1 , POMT2 , POMGnT1 mutations
RELN
:   lissencephaly with RELN mutation
TUBA1A
:   lissencephaly with TUBA1A mutation
VLDLR
:   lissencephaly with VLDLR mutation
vLIS
:   variant lissencephaly" />
<meta name="DC.Contributor" content="S. Kara" />
<meta name="DC.Contributor" content="P. Jissendi-Tchofo" />
<meta name="DC.Contributor" content="A.J. Barkovich" />
<meta name="article:published_time" content="2010-10-01" />
<meta name="article:section" content="Pediatrics" />
<meta name="citation_title" content="Developmental Differences of the Major Forebrain Commissures in Lissencephalies" />
<meta name="citation_abstract" lang="en" content="&lt;h3&gt;BACKGROUND AND PURPOSE:&lt;/h3&gt;
&lt;p&gt;Changes of the major forebrain commissures in lissencephaly have not been systematically studied. We investigated the developmental differences of the commissures in patients with varying types of lissencephaly to determine whether specific commissural features may help in distinguishing lissencephaly phenotypes.&lt;/p&gt;&lt;h3&gt;MATERIALS AND METHODS:&lt;/h3&gt;
&lt;p&gt;MR imaging of 124 patients was retrospectively reviewed. Patients were classified as having cLIS, vLIS, and CBSC, according to cortical phenotype; few patients had genetic diagnoses. Abnormalities of the CC, AC, and HC were recorded, and the overall shape was regarded as hypogenetic, hypoplastic, dysmorphic, a thin flat callosal body with a vertical splenium, and a convex upward callosal body, compared with age-matched controls. Correlations between commissural characteristics and cortical patterns were analyzed by using the Monte Carlo simulation of χ&lt;sup&gt;2&lt;/sup&gt;, extension to m × n table, and Fisher exact tests as appropriate (&lt;i&gt;P&lt;/i&gt; &amp;lt; .05).&lt;/p&gt;&lt;h3&gt;RESULTS:&lt;/h3&gt;
&lt;p&gt;Patients were classified as having cLIS (57.4%), vLIS (38.4%), or CBSC (4.2%). The most common callosal developmental anomaly was hypogenesis with an absent rostrum, a small inferior genu, and a small splenium. An angled (90°) splenium was found to be significantly associated with cLIS, as was an excessively convex upward callosal body with VLDLR. ACC with an enlarged AC was found in all cases of ARX.&lt;/p&gt;&lt;h3&gt;CONCLUSIONS:&lt;/h3&gt;
&lt;p&gt;Specific patterns of the commissure anomalies were associated with certain types of lissencephaly. Callosal anomalies were more common than those of the AC or HC. Developmental variations of commissures may be useful as an imaging criterion in differentiating the groups of lissencephalies and may give insight into the processes causing these malformations.&lt;/p&gt;" />
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<meta name="twitter:title" content="Developmental Differences of the Major Forebrain Commissures in Lissencephalies" />
<meta name="twitter:card" content="summary_large_image" />
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<meta name="twitter:description" content="BACKGROUND AND PURPOSE: Changes of the major forebrain commissures in lissencephaly have not been systematically studied. We investigated the developmental differences of the commissures in patients with varying types of lissencephaly to determine whether specific commissural features may help in distinguishing lissencephaly phenotypes.

MATERIALS AND METHODS: MR imaging of 124 patients was retrospectively reviewed. Patients were classified as having cLIS, vLIS, and CBSC, according to cortical phenotype; few patients had genetic diagnoses. Abnormalities of the CC, AC, and HC were recorded, and the overall shape was regarded as hypogenetic, hypoplastic, dysmorphic, a thin flat callosal body with a vertical splenium, and a convex upward callosal body, compared with age-matched controls. Correlations between commissural characteristics and cortical patterns were analyzed by using the Monte Carlo simulation of χ2, extension to m × n table, and Fisher exact tests as appropriate ( P &lt; .05).

RESULTS: Patients were classified as having cLIS (57.4%), vLIS (38.4%), or CBSC (4.2%). The most common callosal developmental anomaly was hypogenesis with an absent rostrum, a small inferior genu, and a small splenium. An angled (90°) splenium was found to be significantly associated with cLIS, as was an excessively convex upward callosal body with VLDLR. ACC with an enlarged AC was found in all cases of ARX.

CONCLUSIONS: Specific patterns of the commissure anomalies were associated with certain types of lissencephaly. Callosal anomalies were more common than those of the AC or HC. Developmental variations of commissures may be useful as an imaging criterion in differentiating the groups of lissencephalies and may give insight into the processes causing these malformations.

AC
:   anterior commissure
ACC
:   agenesis of the CC
ARX
:   lissencephaly with ARX mutation
ARX-XLAG
:   lissencephaly with ARX mutation, and an absent callosum, ambiguous genitalia
CBSC
:   cobblestone complex
CC
:   corpus callosum
cLIS
:   classic lissencephaly
CMD
:   congenital muscular dystrophies
DCX
:   lissencephaly with mutated DCX gene
FCMD
:   Fukuyama CMD
FKRP
:   lissencephaly with FKRP mutation
HC
:   hippocampal commissure
LARGE
:   lissencephaly with LARGE mutation
LIS1
:   lissencephaly with mutated LIS1 gene
ND
:   not determined
(p)
:   presumed
POMT1, POMT2, and POMGnT1
:   lissencephalies with POMT1 , POMT2 , POMGnT1 mutations
RELN
:   lissencephaly with RELN mutation
TUBA1A
:   lissencephaly with TUBA1A mutation
VLDLR
:   lissencephaly with VLDLR mutation
vLIS
:   variant lissencephaly" />
<meta name="og-title" property="og:title" content="Developmental Differences of the Major Forebrain Commissures in Lissencephalies" />
<meta name="og-url" property="og:url" content="http://ajnr-stage2.stage.highwire.org/content/31/9/1602" />
<meta name="og-site-name" property="og:site_name" content="American Journal of Neuroradiology" />
<meta name="og-description" property="og:description" content="BACKGROUND AND PURPOSE: Changes of the major forebrain commissures in lissencephaly have not been systematically studied. We investigated the developmental differences of the commissures in patients with varying types of lissencephaly to determine whether specific commissural features may help in distinguishing lissencephaly phenotypes.

MATERIALS AND METHODS: MR imaging of 124 patients was retrospectively reviewed. Patients were classified as having cLIS, vLIS, and CBSC, according to cortical phenotype; few patients had genetic diagnoses. Abnormalities of the CC, AC, and HC were recorded, and the overall shape was regarded as hypogenetic, hypoplastic, dysmorphic, a thin flat callosal body with a vertical splenium, and a convex upward callosal body, compared with age-matched controls. Correlations between commissural characteristics and cortical patterns were analyzed by using the Monte Carlo simulation of χ2, extension to m × n table, and Fisher exact tests as appropriate ( P &lt; .05).

RESULTS: Patients were classified as having cLIS (57.4%), vLIS (38.4%), or CBSC (4.2%). The most common callosal developmental anomaly was hypogenesis with an absent rostrum, a small inferior genu, and a small splenium. An angled (90°) splenium was found to be significantly associated with cLIS, as was an excessively convex upward callosal body with VLDLR. ACC with an enlarged AC was found in all cases of ARX.

CONCLUSIONS: Specific patterns of the commissure anomalies were associated with certain types of lissencephaly. Callosal anomalies were more common than those of the AC or HC. Developmental variations of commissures may be useful as an imaging criterion in differentiating the groups of lissencephalies and may give insight into the processes causing these malformations.

AC
:   anterior commissure
ACC
:   agenesis of the CC
ARX
:   lissencephaly with ARX mutation
ARX-XLAG
:   lissencephaly with ARX mutation, and an absent callosum, ambiguous genitalia
CBSC
:   cobblestone complex
CC
:   corpus callosum
cLIS
:   classic lissencephaly
CMD
:   congenital muscular dystrophies
DCX
:   lissencephaly with mutated DCX gene
FCMD
:   Fukuyama CMD
FKRP
:   lissencephaly with FKRP mutation
HC
:   hippocampal commissure
LARGE
:   lissencephaly with LARGE mutation
LIS1
:   lissencephaly with mutated LIS1 gene
ND
:   not determined
(p)
:   presumed
POMT1, POMT2, and POMGnT1
:   lissencephalies with POMT1 , POMT2 , POMGnT1 mutations
RELN
:   lissencephaly with RELN mutation
TUBA1A
:   lissencephaly with TUBA1A mutation
VLDLR
:   lissencephaly with VLDLR mutation
vLIS
:   variant lissencephaly" />
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      <h1 class="highwire-cite-title" id="page-title">Developmental Differences of the Major Forebrain Commissures in Lissencephalies</h1>  
    	<div class="highwire-cite-authors"><span  class="highwire-citation-authors"><span class="highwire-citation-author first" data-delta="0">S. Kara</span>, <span class="highwire-citation-author" data-delta="1">P. Jissendi-Tchofo</span> and <span class="highwire-citation-author" data-delta="2">A.J. Barkovich</span></span></div>
  
    	<div class="highwire-cite-metadata"><span  class="highwire-cite-metadata-journal highwire-cite-metadata">American Journal of Neuroradiology </span><span  class="highwire-cite-metadata-date highwire-cite-metadata">October 2010,  </span><span  class="highwire-cite-metadata-volume highwire-cite-metadata">31 </span><span  class="highwire-cite-metadata-issue highwire-cite-metadata">(9) </span><span  class="highwire-cite-metadata-pages highwire-cite-metadata">1602-1607; </span><span  class="highwire-cite-metadata-doi highwire-cite-metadata">DOI: https://doi.org/10.3174/ajnr.A2133 </span></div>
  
  
  
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<div id="hw-article-author-popups-top-node-9839--61903766191" style="display: none;"><div class="author-tooltip-0"><div class="author-tooltip-name">S. Kara </div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=S.%2BKara%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Kara%20S&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link last"><a href="/search/author1%3AS.%2BKara%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li></ul></div><div class="author-tooltip-1"><div class="author-tooltip-name">P. Jissendi-Tchofo </div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=P.%2BJissendi-Tchofo%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Jissendi-Tchofo%20P&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link last"><a href="/search/author1%3AP.%2BJissendi-Tchofo%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li></ul></div><div class="author-tooltip-2"><div class="author-tooltip-name">A.J. Barkovich </div><ul class="author-tooltip-find-more"><li class="author-tooltip-gs-link first"><a href="/lookup/google-scholar?link_type=googlescholar&amp;gs_type=author&amp;author%5B0%5D=A.J.%2BBarkovich%2B" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on Google Scholar</a></li><li class="author-tooltip-pubmed-link"><a href="/lookup/external-ref?access_num=Barkovich%20A&amp;link_type=AUTHORSEARCH" target="_blank" class="" data-icon-position="" data-hide-link-title="0">Find this author on PubMed</a></li><li class="author-site-search-link last"><a href="/search/author1%3AA.J.%2BBarkovich%2B" rel="nofollow" class="" data-icon-position="" data-hide-link-title="0">Search for this author on this site</a></li></ul></div></div></div>  </div>

  
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<p id="p-2"><strong>BACKGROUND AND PURPOSE:</strong> Changes of the major forebrain commissures in lissencephaly have not been systematically studied. We investigated the developmental differences of the commissures in patients with varying types of lissencephaly to determine whether specific commissural features may help in distinguishing lissencephaly phenotypes.</p>
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<p id="p-3"><strong>MATERIALS AND METHODS:</strong> MR imaging of 124 patients was retrospectively reviewed. Patients were classified as having cLIS, vLIS, and CBSC, according to cortical phenotype; few patients had genetic diagnoses. Abnormalities of the CC, AC, and HC were recorded, and the overall shape was regarded as hypogenetic, hypoplastic, dysmorphic, a thin flat callosal body with a vertical splenium, and a convex upward callosal body, compared with age-matched controls. Correlations between commissural characteristics and cortical patterns were analyzed by using the Monte Carlo simulation of χ<sup>2</sup>, extension to m × n table, and Fisher exact tests as appropriate (<em>P</em> &lt; .05).</p>
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<p id="p-4"><strong>RESULTS:</strong> Patients were classified as having cLIS (57.4%), vLIS (38.4%), or CBSC (4.2%). The most common callosal developmental anomaly was hypogenesis with an absent rostrum, a small inferior genu, and a small splenium. An angled (90°) splenium was found to be significantly associated with cLIS, as was an excessively convex upward callosal body with VLDLR. ACC with an enlarged AC was found in all cases of ARX.</p>
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<p id="p-5"><strong>CONCLUSIONS:</strong> Specific patterns of the commissure anomalies were associated with certain types of lissencephaly. Callosal anomalies were more common than those of the AC or HC. Developmental variations of commissures may be useful as an imaging criterion in differentiating the groups of lissencephalies and may give insight into the processes causing these malformations.</p>
</div></div><div class="section glossary" id="glossary-1"><h2>Abbreviations</h2><dl id="def-list-1"><dt id="def-item-1">AC<span class="def-item-dt-sep"></span></dt><dd>anterior commissure<span class="def-item-dd-sep"></span></dd><dt id="def-item-2">ACC<span class="def-item-dt-sep"></span></dt><dd>agenesis of the CC<span class="def-item-dd-sep"></span></dd><dt id="def-item-3">ARX<span class="def-item-dt-sep"></span></dt><dd>lissencephaly with <em>ARX</em> mutation<span class="def-item-dd-sep"></span></dd><dt id="def-item-4">ARX-XLAG<span class="def-item-dt-sep"></span></dt><dd>lissencephaly with <em>ARX</em> mutation, and an absent callosum, ambiguous genitalia<span class="def-item-dd-sep"></span></dd><dt id="def-item-5">CBSC<span class="def-item-dt-sep"></span></dt><dd>cobblestone complex<span class="def-item-dd-sep"></span></dd><dt id="def-item-6">CC<span class="def-item-dt-sep"></span></dt><dd>corpus callosum<span class="def-item-dd-sep"></span></dd><dt id="def-item-7">cLIS<span class="def-item-dt-sep"></span></dt><dd>classic lissencephaly<span class="def-item-dd-sep"></span></dd><dt id="def-item-8">CMD<span class="def-item-dt-sep"></span></dt><dd>congenital muscular dystrophies<span class="def-item-dd-sep"></span></dd><dt id="def-item-9">DCX<span class="def-item-dt-sep"></span></dt><dd>lissencephaly with mutated <em>DCX</em> gene<span class="def-item-dd-sep"></span></dd><dt id="def-item-10">FCMD<span class="def-item-dt-sep"></span></dt><dd>Fukuyama CMD<span class="def-item-dd-sep"></span></dd><dt id="def-item-11">FKRP<span class="def-item-dt-sep"></span></dt><dd>lissencephaly with <em>FKRP</em> mutation<span class="def-item-dd-sep"></span></dd><dt id="def-item-12">HC<span class="def-item-dt-sep"></span></dt><dd>hippocampal commissure<span class="def-item-dd-sep"></span></dd><dt id="def-item-13">LARGE<span class="def-item-dt-sep"></span></dt><dd>lissencephaly with <em>LARGE</em> mutation<span class="def-item-dd-sep"></span></dd><dt id="def-item-14">LIS1<span class="def-item-dt-sep"></span></dt><dd>lissencephaly with mutated <em>LIS1</em> gene<span class="def-item-dd-sep"></span></dd><dt id="def-item-15">ND<span class="def-item-dt-sep"></span></dt><dd>not determined<span class="def-item-dd-sep"></span></dd><dt id="def-item-16">(p)<span class="def-item-dt-sep"></span></dt><dd>presumed<span class="def-item-dd-sep"></span></dd><dt id="def-item-17">POMT1, POMT2, and POMGnT1<span class="def-item-dt-sep"></span></dt><dd>lissencephalies with <em>POMT1</em>, <em>POMT2</em>, <em>POMGnT1</em> mutations<span class="def-item-dd-sep"></span></dd><dt id="def-item-18">RELN<span class="def-item-dt-sep"></span></dt><dd>lissencephaly with <em>RELN</em> mutation<span class="def-item-dd-sep"></span></dd><dt id="def-item-19">TUBA1A<span class="def-item-dt-sep"></span></dt><dd>lissencephaly with <em>TUBA1A</em> mutation<span class="def-item-dd-sep"></span></dd><dt id="def-item-20">VLDLR<span class="def-item-dt-sep"></span></dt><dd>lissencephaly with <em>VLDLR</em> mutation<span class="def-item-dd-sep"></span></dd><dt id="def-item-21">vLIS<span class="def-item-dt-sep"></span></dt><dd>variant lissencephaly</dd></dl></div><ul class="copyright-statement"><li class="fn" id="copyright-statement-1">Copyright © American Society of Neuroradiology</li></ul><div class="license" id="license-1"><p id="p-1">Indicates open access to non-subscribers at <a href="http://www.ajnr.org">www.ajnr.org</a></p></div><span class="highwire-journal-article-marker-end"></span></div><span class="related-urls"></span></div><a href="http://ajnr-stage2.stage.highwire.org/content/31/9/1602.full" class="hw-link hw-link-article-full-text" data-icon-position="" data-hide-link-title="0">View Full Text</a></div>  </div>

  
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