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textless pages(2)

Rob Sargent

2012-05-08


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Admin note: I have just recently registered with old nabble and that somehow un-iisted me. Not wanting to wait I'm re-posting (again).  Hope this doesn't show up too many times.  Apologies in advance, but I'm anxious...

Thanks to a pointer from Chris Bowditch I'm using the fop trunk as of 2 days ago to see if I can pull this off.

His hint on how to get the flow to skip a page:
<fo:simple-page-master master-name="nocontent">
<fo:region-body region-name="doesntexist"/>
</fo:simple-page-master>

My result:
The textless page is fine but it affects the next page(s).  Unfortunately I get little or no text on the immediate following page(s) The correct textual content is picked up a page(s) later. I'm wondering if anyone else out there is using region-name like this in production (or plans to) or has seen my problem and dealt with it at all.

I have one case where the output is perfect-pages, textless-page, unintentional-textless page, another-one, textless-page, perfectly-fine-pages-of-text.  Almost as if the textless-page is toggling off-on the addition of text to the flow.

Or Vincent will get another nasty fo from me. :)

Since first send didn't work I now have a test case, attached

Thanks.
<?xml version="1.0" encoding="UTF-8"?>
<fo:root xmlns:fo="http://www.w3.org/1999/XSL/Format" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:xalan="http://xml.apache.org/xslt" xmlns:ec="xalan://com.amirsys.utilities.ElementConversion">
<fo:layout-master-set>
  <fo:simple-page-master margin="0.0in 0.0in 0.6in 0.833in" page-width="8.5in" page-height="11in" master-name="chapter-open">
   <fo:region-body column-gap="0.4in" margin-right="0.7in" margin-top="3in" column-count="2" />
   <fo:region-before extent="3in" margin-right="0.7in" column-gap="0.4in" column-count="2" region-name="chapter-title" />
  </fo:simple-page-master>
  <fo:simple-page-master margin="0.0in 0.0in 0.6in 0.833in" page-width="8.5in" page-height="11in" master-name="chapter-refs-right">
   <fo:region-body column-gap="0.4in" margin-left="0.7in" margin-top="0.750in" margin-right="0.70in" column-count="2" background-color="yellow" />
   <fo:region-before extent="0.50in" column-gap="0.4in" column-count="2" region-name="default-right-header" />
  </fo:simple-page-master>
  <fo:simple-page-master margin=" 0.0in 0.833in 0.6in 0.0in" page-width="8.5in" page-height="11in" master-name="chapter-refs-left">
   <fo:region-body column-gap="0.4in" margin-left="0.7in" margin-right="0.7in" margin-top="0.75in" column-count="2" background-color="blue" />
   <fo:region-before extent="0.5in" column-gap="0.4in" column-count="2" region-name="default-left-header" />
  </fo:simple-page-master>
  <fo:simple-page-master page-width="8.5in" page-height="11in" master-name="two-up-page-2" margin=" 0.0in 0.833in 0.6in 0.0in">
   <fo:region-body margin-left="0.70in" margin-top="4.81in" column-gap="0.40in" column-count="2" />
   <fo:region-before precedence="true" extent="4.81in" region-name="header-two-up-page-2" />
  </fo:simple-page-master>
  <fo:simple-page-master page-width="8.5in" page-height="11in" master-name="gallery6-page-3" margin="0.0in 0.0in 0.6in 0.833in">
   <fo:region-body margin-right="0.70in" margin-bottom="0.01in" margin-top="10.0in" column-gap="0.40in" column-count="2" region-name="zero-length" />
   <fo:region-before precedence="true" extent="11.0in" region-name="header-gallery6-page-3" />
  </fo:simple-page-master>
  <fo:simple-page-master page-width="8.5in" page-height="11in" master-name="gallery4-page-4" margin=" 0.0in 0.833in 0.6in 0.0in">
   <fo:region-body margin-left="0.70in" margin-bottom="5.6in" margin-top="0.75in" column-gap="0.40in" column-count="2" background-color="orange"/>
   <fo:region-before precedence="true" extent="0.50in" region-name="default-left-header" />
   <fo:region-after extent="5.6in" region-name="footer-gallery4-page-4" />
  </fo:simple-page-master>
  <fo:page-sequence-master master-name="document-sequence">
   <fo:single-page-master-reference master-reference="chapter-open" />
   <fo:single-page-master-reference master-reference="two-up-page-2" />
   <fo:single-page-master-reference master-reference="gallery6-page-3" />
   <fo:single-page-master-reference master-reference="gallery4-page-4" />
   <fo:repeatable-page-master-alternatives>
    <fo:conditional-page-master-reference page-position="any" odd-or-even="even" master-reference="chapter-refs-left" blank-or-not-blank="any" />
    <fo:conditional-page-master-reference page-position="any" odd-or-even="odd" master-reference="chapter-refs-right" blank-or-not-blank="any" />
   </fo:repeatable-page-master-alternatives>
  </fo:page-sequence-master>
</fo:layout-master-set>
<fo:page-sequence force-page-count="end-on-even" initial-page-number="1" master-reference="document-sequence">
  <fo:static-content flow-name="chapter-title">
   <fo:block span="all">
    <fo:table table-layout="fixed">
      <fo:table-column column-width="proportional-column-width(1)" />
      <fo:table-column column-width="0.70in" />
      <fo:table-body>
       <fo:table-row height="0.8in">
        <fo:table-cell>
          <fo:block />
        </fo:table-cell>
        <fo:table-cell>
          <fo:block />
        </fo:table-cell>
       </fo:table-row>
       <fo:table-row>
        <fo:table-cell text-align="center" font-size="36pt" font-family="TimesNewRomanPSMT">
          <fo:block>24</fo:block>
        </fo:table-cell>
        <fo:table-cell>
          <fo:block />
        </fo:table-cell>
       </fo:table-row>
       <fo:table-row>
        <fo:table-cell>
          <fo:table table-layout="fixed">
           <fo:table-column column-width="proportional-column-width(1)" />
           <fo:table-column column-width="proportional-column-width(1)" />
           <fo:table-column column-width="proportional-column-width(1)" />
           <fo:table-body>
            <fo:table-row>
              <fo:table-cell>
               <fo:block />
              </fo:table-cell>
              <fo:table-cell>
               <fo:block>
                <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="middle" color="#2254D1" leader-pattern="rule" />
               </fo:block>
              </fo:table-cell>
              <fo:table-cell>
               <fo:block />
              </fo:table-cell>
            </fo:table-row>
           </fo:table-body>
          </fo:table>
        </fo:table-cell>
       </fo:table-row>
       <fo:table-row>
        <fo:table-cell height="1.3in" display-align="center" text-align="center" font-size="36pt" font-family="TimesNewRomanPSMT">
          <fo:block>Primary Effects of CNS Trauma</fo:block>
        </fo:table-cell>
        <fo:table-cell>
          <fo:block />
        </fo:table-cell>
       </fo:table-row>
       <fo:table-row>
        <fo:table-cell text-align="center" font-size="36pt" font-family="TimesNewRomanPSMT">
          <fo:block />
        </fo:table-cell>
       </fo:table-row>
      </fo:table-body>
    </fo:table>
   </fo:block>
  </fo:static-content>
  <fo:static-content flow-name="default-left-header">
   <fo:block background-color="#E6FAF5" height="0.50in" line-height="0.50in" text-indent="0.70in" white-space-collapse="false" font-size="11pt" font-family="Optima-Oblique">
    <fo:inline>
      <fo:page-number />
    </fo:inline>
   </fo:block>
  </fo:static-content>
  <fo:static-content flow-name="default-right-header">
   <fo:block white-space-collapse="false" last-line-end-indent="0.70in" text-align-last="end" text-align="right" background-color="#E6FAF5" height="0.50in" line-height="0.50in" font-size="11pt" font-family="Optima-Oblique">
    <fo:inline>
      Primary Effects of CNS Trauma
      <fo:page-number />
    </fo:inline>
   </fo:block>
  </fo:static-content>
  <fo:static-content flow-name="header-two-up-page-2">
   <fo:block background-color="#E6FAF5" height="0.50in" line-height="0.50in" text-indent="0.70in" white-space-collapse="false" font-size="11pt" font-family="Optima-Oblique">
    <fo:inline>
      <fo:page-number />
    </fo:inline>
   </fo:block>
   <fo:table padding-after="2pt" space-before="5pt" border-collapse="separate" table-layout="fixed">
    <fo:table-column column-width="0.70in" />
    <fo:table-column column-width="3.2585in" />
    <fo:table-column column-width="0.4in" />
    <fo:table-column column-width="3.2585in" />
    <fo:table-body>
      <fo:table-row height="8pt">
       <fo:table-cell number-columns-spanned="4">
        <fo:block />
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row height="3.3085in">
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="3.2585in" height="3.2585in" src="ref_4_1470095765" />
        </fo:block>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="3.2585in" height="3.2585in" src="ref_18_1804283379" />
        </fo:block>
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block-container overflow="hidden" height="0.6in">
          <fo:block height="0.5in" font-style="italic" font-size="9pt" font-family="TimesNewRomanPSMT">
           <fo:inline font-weight="bold">(Fig. 24.1)</fo:inline>
           <fo:inline font-weight="normal" margin-left="2pt" />
          </fo:block>
        </fo:block-container>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block-container overflow="hidden" height="0.6in">
          <fo:block height="0.5in" font-style="italic" font-size="9pt" font-family="TimesNewRomanPSMT">
           <fo:inline font-weight="bold">(Fig. 24.2)</fo:inline>
           <fo:inline font-weight="normal" margin-left="2pt" />
          </fo:block>
        </fo:block-container>
       </fo:table-cell>
      </fo:table-row>
    </fo:table-body>
   </fo:table>
  </fo:static-content>
  <fo:static-content flow-name="header-gallery6-page-3">
   <fo:block white-space-collapse="false" last-line-end-indent="0.70in" text-align-last="end" text-align="right" background-color="#E6FAF5" height="0.50in" line-height="0.50in" font-size="11pt" font-family="Optima-Oblique">
    <fo:inline>
      Primary Effects of CNS Trauma
      <fo:page-number />
    </fo:inline>
   </fo:block>
   <fo:table padding-after="2pt" space-before="5pt" border-collapse="separate" table-layout="fixed">
    <fo:table-column column-width="2.5in" />
    <fo:table-column column-width="0.156in" />
    <fo:table-column column-width="2.5in" />
    <fo:table-column column-width="0.150in" />
    <fo:table-column column-width="1.60in" />
    <fo:table-body>
      <fo:table-row height="8pt">
       <fo:table-cell number-columns-spanned="5">
        <fo:block />
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_10_1002108221" />
        </fo:block>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_11_1352112764" />
        </fo:block>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block-container overflow="hidden" text-align="left" font-style="italic" height="2.62in">
          <fo:block padding-before="1pt" font-size="9pt" font-family="TimesNewRomanPSMT">
           <fo:inline font-weight="bold">(Fig. 24.3)</fo:inline>
           <fo:inline font-weight="bold">(Fig. 24.4)</fo:inline>
          </fo:block>
        </fo:block-container>
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row height="8pt">
       <fo:table-cell number-columns-spanned="5">
        <fo:block />
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_9_1524570701" />
        </fo:block>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_8_2104571103" />
        </fo:block>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block-container overflow="hidden" text-align="left" font-style="italic" height="2.62in">
          <fo:block padding-before="1pt" font-size="9pt" font-family="TimesNewRomanPSMT">
           <fo:inline font-weight="bold">(Fig. 24.5)</fo:inline>
           <fo:inline font-weight="bold">(Fig. 24.6)</fo:inline>
          </fo:block>
        </fo:block-container>
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row height="8pt">
       <fo:table-cell number-columns-spanned="5">
        <fo:block />
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_2_679161368" />
        </fo:block>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_3_1081836686" />
        </fo:block>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block-container overflow="hidden" text-align="left" font-style="italic" height="2.62in">
          <fo:block padding-before="1pt" font-size="9pt" font-family="TimesNewRomanPSMT">
           <fo:inline font-weight="bold">(Fig. 24.7)</fo:inline>
           <fo:inline font-weight="bold">(Fig. 24.8)</fo:inline>
          </fo:block>
        </fo:block-container>
       </fo:table-cell>
      </fo:table-row>
    </fo:table-body>
   </fo:table>
  </fo:static-content>
  <fo:static-content flow-name="footer-gallery4-page-4">
   <fo:table padding-after="2pt" space-before="5pt" border-collapse="separate" table-layout="fixed">
    <fo:table-column column-width="0.70in" />
    <fo:table-column column-width="1.49in" />
    <fo:table-column column-width="0.150in" />
    <fo:table-column column-width="2.5in" />
    <fo:table-column column-width="0.156in" />
    <fo:table-column column-width="2.5in" />
    <fo:table-body>
      <fo:table-row height="8pt">
       <fo:table-cell number-columns-spanned="5">
        <fo:block />
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block-container overflow="hidden" text-align="left" font-style="italic" height="2.62in">
          <fo:block padding-before="1pt" font-size="9pt" font-family="TimesNewRomanPSMT">
           <fo:inline font-weight="bold">(Fig. 24.9)</fo:inline>
           <fo:inline font-weight="bold">(Fig. 24.10)</fo:inline>
          </fo:block>
        </fo:block-container>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_17_1821839899" />
        </fo:block>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_5_790954838" />
        </fo:block>
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row height="8pt">
       <fo:table-cell number-columns-spanned="5">
        <fo:block />
       </fo:table-cell>
      </fo:table-row>
      <fo:table-row>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block-container overflow="hidden" text-align="left" font-style="italic" height="2.62in">
          <fo:block padding-before="1pt" font-size="9pt" font-family="TimesNewRomanPSMT">
           <fo:inline font-weight="bold">(Fig. 24.11)</fo:inline>
           <fo:inline font-weight="bold">(Fig. 24.12)</fo:inline>
          </fo:block>
        </fo:block-container>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_12_120170241" />
        </fo:block>
       </fo:table-cell>
       <fo:table-cell>
        <fo:block />
       </fo:table-cell>
       <fo:table-cell>
        <fo:block>
          <fo:external-graphic border-collapse="separate" border="0.5pt solid black" content-width="scale-to-fit" content-height="scale-to-fit" width="2.5in" height="2.5in" src="ref_1_2108060176" />
        </fo:block>
       </fo:table-cell>
      </fo:table-row>
    </fo:table-body>
   </fo:table>
  </fo:static-content>
  <fo:flow font-size="10.5pt" font-family="TimesNewRomanPSMT" flow-name="xsl-region-body">
   <fo:block font-size="10pt" font-family="GillSansMTPro" border="0.6pt solid black" background-color="#E6FAF5">
    <fo:list-block padding-after="5pt" padding-before="6pt" provisional-label-separation="3pt" provisional-distance-between-starts="0.135in">
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        <fo:block />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify">
          Skull and Scalp Injuries
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="group-Skull and Scalp Injuries" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
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       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Scalp Injuries
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Scalp Injuries" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Skull Fractures
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Skull Fractures" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
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       <fo:list-item-label end-indent="label-end()">
        <fo:block />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify">
          Extraaxial Hemorrhage
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="group-Extraaxial Hemorrhage" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Acute Epidural Hematoma
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Acute Epidural Hematoma" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Acute Subdural Hematoma
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Acute Subdural Hematoma" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Subacute Subdural Hematoma
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Subacute Subdural Hematoma" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Chronic/Mixed Subdural Hematoma
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Chronic/Mixed Subdural Hematoma" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Traumatic Subarachnoid Hemorrhage
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Traumatic Subarachnoid Hemorrhage" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
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       <fo:list-item-label end-indent="label-end()">
        <fo:block />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify">
          Parenchymal Injuries
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="group-Parenchymal Injuries" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Cerebral Contusion
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Cerebral Contusion" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Diffuse Axonal Injury
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Diffuse Axonal Injury" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Diffuse Vascular Injury
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Diffuse Vascular Injury" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Subcortical Injury
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Subcortical Injury" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item space-before="2pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify">
          Miscellaneous Injuries
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="group-Miscellaneous Injuries" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Pneumocephalus
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Pneumocephalus" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Child Abuse
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Child Abuse" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Missile and Penetrating Injuries
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Missile and Penetrating Injuries" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
      <fo:list-item margin-left="9pt">
       <fo:list-item-label end-indent="label-end()">
        <fo:block line-height="1.0" font-size="9pt" />
       </fo:list-item-label>
       <fo:list-item-body start-indent="body-start()">
        <fo:block margin-right="10pt" text-align-last="justify" font-weight="normal" font-size="9pt">
          Post-Traumatic Hypopituitarism
          <fo:leader leader-pattern="dots" />
          <fo:page-number-citation ref-id="Post-Traumatic Hypopituitarism" />
        </fo:block>
       </fo:list-item-body>
      </fo:list-item>
    </fo:list-block>
   </fo:block>
   <fo:block-container language="en" hyphenate="true" padding-after="18pt" space-before="12pt" font-size="10.5pt" font-family="TimesNewRomanPSMT">
    <fo:block text-align="justify" space-before="6pt">Primary head injuries occur at the time of initial trauma. Primary injuries discussed in this chapter include scalp lesions, skull fractures, extra-axial hemorrhages, and parenchymal injuries (such as cortical contusion, diffuse axonal injury, and subcortical injuries).</fo:block>
    <fo:block text-align="justify" space-before="6pt">Brain injury can also be classified by etiology into direct and indirect trauma.</fo:block>
    <fo:block text-align="justify" space-before="6pt">Direct trauma involves a blow to the head. Direct trauma can be caused by blunt injury (i.e., hammer or baseball bat) or so-called "contact loading" in high-speed motor vehicle accidents (MVAs). Indirect trauma is caused by angular kinematics. Significant forces of acceleration/deceleration, linear translation, and rotational loading may occur without direct head blows. Here the brain undergoes deformation and distortion. Depending on the site and direction of the force applied, significant injury to axons and deep gray nuclei may occur.</fo:block>
   </fo:block-container>
   <fo:block keep-with-next="always">
    <fo:block space-before="12pt" keep-with-next="always" margin-left="-15pt">
      <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
    </fo:block>
    <fo:block language="en" hyphenate="false" margin-left="-15pt" keep-with-next="always" space-before="12pt" font-size="18pt">Skull and Scalp Injuries</fo:block>
    <fo:block space-before="12pt" keep-with-next="always" margin-left="-15pt">
      <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
    </fo:block>
   </fo:block>
   <fo:block-container language="en" hyphenate="true" font-family="TimesNewRomanPSMT" font-size="10.5pt" id="group-Skull and Scalp Injuries">
    <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
      <fo:block text-align="justify" space-before="6pt">Scalp and skull injuries are common manifestations of cranial trauma. While brain injury is usually the most immediate concern, superficial lesions such as scalp swelling and subgaleal hematoma are helpful in identifying the location of direct head trauma.</fo:block>
      <fo:block text-align="justify" space-before="6pt">Skull fractures are a common--but not invariable--finding in patients with significant intracranial injuries. Before discussing intracranial traumatic lesions we briefly review scalp and skull injuries, delineating their typical imaging findings and clinical significance.</fo:block>
    </fo:block>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Scalp Injuries">Scalp Injuries</fo:block>
      <fo:block margin-left="-15pt" space-before="5pt" keep-with-next="always" font-weight="normal" font-size="14pt">Scalp Trauma</fo:block>
      <fo:block text-align="justify" space-before="6pt">Scalp swelling, lacerations, and subgaleal hematoma commonly accompany head trauma. Other than indicating impact site, these lesions may be cosmetically important but in themselves are clinically insignificant.</fo:block>
      <fo:block text-align="justify" space-before="6pt">Scalp lacerations and contusions are often seen in the absence of skull fracture although it is very uncommon to have a skull fracture without overlying scalp injury.</fo:block>
      <fo:block text-align="justify" space-before="6pt">A scalp "bump" without other imaging abnormalities is generally of no concern. At the opposite end of the spectrum, a cranial "burst fracture" lacerates the dura and cerebrum can be extruded outside the calvaria under an intact scalp and galea.</fo:block>
      <fo:block margin-left="-15pt" space-before="5pt" keep-with-next="always" font-weight="normal" font-size="14pt">Facial Soft Tissue Injuries</fo:block>
      <fo:block text-align="justify" space-before="6pt">Facial fractures are commonly overlooked on initial imaging (typically head CT scan). Important soft tissue markers can be identified that correlate with facial fractures and may merit a dedicated CT of the facial bones. These include periorbital contusions and subconjunctival hemorrhage as well as lacerations of the lips, mouth, and nose.</fo:block>
      <fo:block text-align="justify" space-before="6pt">Holmgren et al have proposed the acronym LIPS-N (Lip laceration, Intraoral laceration, Periorbital contusion, Subconjunctival hemorrhage, and Nasal laceration) be used in conjunction with physical examination when determining whether a traumatized patient having a head CT should also get a dedicated facial CT.</fo:block>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Skull Fractures">Skull Fractures</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">Skull fractures are present on initial CT scans in about two-thirds of patients with acute head injury although between 25-35% of severely injured patients have no identifiable fracture at all. Remember: Calvarial fractures rarely occur in the absence of overlying soft tissue swelling or scalp laceration.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Three types of acute skull fracture are identified: Linear, depressed, and diastatic fractures. Fractures can involve the calvarium, skull base, or both. A fourth type of skull fracture, a "growing" skull fracture, is a rare but important long-term complication of skull trauma.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Skull fractures can also be simple or comminuted and closed or open. In open fractures, skin laceration results in communication between the external environment and intracranial cavity. Infection risk is high in this type of fracture, as well as with fractures that cross the mastoids and paranasal sinuses.</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        A
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">linear skull fracture</inline>
        is a sharply-marginated linear defect that typically involves both the inner and outer tables of the calvarium.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">
        A
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">depressed skull fracture</inline>
        is a fracture (usually comminuted) where the fragments are displaced inward. A rare variation, an elevated skull fracture, is where the fragments are displaced outwards. In depressed fracture, comminution of the fracture fragments starts at the point of maximum impact and spreads centrifugally.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">
        A
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">diastatic skull fracture</inline>
        is a fracture that extends into a suture and widens it.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">
        A
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">growing skull fracture</inline>
        is also termed a leptomeningeal cyst and is a calvarial fracture that slowly widens over time. Here brain tissue and CSF extend between the bony edges of the fracture through torn dura and arachnoid. Most growing fractures are adjacent to post-traumatic encephalomalacia of the underlying brain.
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Concepts.</fo:inline>
        <fo:inline font-weight="normal">Most linear skull fractures are caused by relatively low-energy blunt trauma that is delivered over a relatively wide surface area of the skull. Depressed fractures are most often caused by high-energy direct blows to a small surface with a blunt object (i.e., hammer, baseball bat, or metal pipe). Diastatic skull fractures usually occur in association with a linear skull fracture that extends into an adjacent suture.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="4pt" font-weight="normal" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Associated Injuries.</fo:inline>
        <fo:inline font-weight="normal">Linear skull fractures may occur without any significant brain injury. They are found in the majority of epi- and subdural hematomas. Depressed skull fractures typically tear the underlying dura and arachnoid and are associated with cortical contusions and potential leakage of CSF into the subdural space. Fractures extending to a dural sinus or the jugular bulb have a 40% prevalence of associated venous sinus thrombosis.</fo:inline>
        <fo:block text-align="justify" space-before="6pt">Fractures that extend through the skull base may be associated with cranial nerve palsies, vascular injuries (such as dissection, pseudoaneurysm, and carotid-cavernous fistula) and CSF leaks. Clival fractures are strongly associated with neurovascular trauma and CTA should be obtained in these cases. Cervical spine and midface fractures are also highly associated with blunt cerebrovascular injuries and merit further investigation. Soft tissue injuries of the neck rarely result in significant vascular injury. Horner syndrome and cervical bruit are strongly associated with arterial dissection.</fo:block>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">Plain skull radiographs have no role in the modern evaluation of traumatic head injury. One-quarter of fatal injuries have no skull fracture at autopsy. CT is fast, widely available, sensitive for both bone and brain injury, and has become the world-wide diagnostic standard of care for patients with head injuries. Both bone and soft tissue reconstruction algorithms should be utilized. Soft tissue reconstructions should be viewed with both narrow ("soft tissue") and intermediate ("subdural") windows.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">New generations of multi-section CT scanners offer increasing spatial resolution. Three-dimensional (3D) reconstruction and curved MIPs of the skull have been shown to improve fracture detection over the use of axial sections alone.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal">While fractures can involve any part of the calvarium or skull base, the middle cranial fossa is most susceptible because of its thin "squamous" bones and multiple foramina and fissures</fo:inline>
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">NECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">NECT scans show a sharply-marginated lucent line. Depressed fractures are typically comminuted and show focal implosion of fracture fragments.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">CTA.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">If fractures cross the sites of major vascular structures such as the carotid canal or dural venous sinuses, CT angiography is recommended. Sagittal, coronal, and MIP reconstructions are helpful in delineating the site and extent of vascular injuries. Multiplanar reconstructions are especially useful in identifying vertex epidural hematomas, which may be difficult to detect if only axial images are obtained.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">While T2WIs and FLAIR scans are more sensitive than CT in detecting and delineating parenchymal lesions such as cortical contusions and axonal injury (see below), MR is rarely used in the setting of acute head trauma. Adding T2* sequences, especially SWI, is helpful in identifying hemorrhagic lesions.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        The major differential diagnoses of skull fracture are normal structures such as
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">vascular grooves and sutures</inline>
        . Vascular grooves have well-corticated margins and are not typically as sharp or lucent as linear skull fractures. Overlying soft tissue swelling is absent. Sutures occur in predictable locations (i.e., coronal, sagittal, and mastoid), are densely corticated, and are less distinct than fractures. Sutures wider than 2 mm that are seen in the presence of a linear skull fracture are probably diastatic.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">Venous lakes and arachnoid granulations</inline>
        are smooth, corticated, and occur in predictable locations (i.e., parasagittal and adjacent to or within dural venous sinuses).
       </fo:block>
      </fo:block-container>
    </fo:block-container>
   </fo:block-container>
   <fo:block keep-with-next="always">
    <fo:block space-before="12pt" keep-with-next="always" margin-left="-15pt">
      <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
    </fo:block>
    <fo:block language="en" hyphenate="false" margin-left="-15pt" keep-with-next="always" space-before="12pt" font-size="18pt">Extraaxial Hemorrhage</fo:block>
    <fo:block space-before="12pt" keep-with-next="always" margin-left="-15pt">
      <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
    </fo:block>
   </fo:block>
   <fo:block-container language="en" hyphenate="true" font-family="TimesNewRomanPSMT" font-size="10.5pt" id="group-Extraaxial Hemorrhage">
    <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
      <fo:block text-align="justify" space-before="6pt">Extra-axial hemorrhages and hematomas are common manifestations of head trauma. They can occur in any intracranial compartment, within any space--potential or actual--and between any layers of the cranial meninges.</fo:block>
      <fo:block margin-left="-15pt" space-before="5pt" keep-with-next="always" font-weight="normal" font-size="14pt">Terminology</fo:block>
      <fo:block text-align="justify" space-before="6pt">There are three basic types of intracranial extraaxial bleeds. Only one, an epidural hematoma (EDH), lies completely outside the cranial meninges. EDHs arise between the inner table of the skull and outer (periosteal) layer of the dura. Subdural hematomas (SDHs) are located between the inner (meningeal) layer of the dura and the arachnoid. Traumatic subarachnoid hemorrhage (tSAH) is found within the sulci and subarachnoid cisterns, between the arachnoid and the pia. Of these, only the subarachnoid spaces exist normally. All the other spaces are potential spaces and occur only under pathological conditions.</fo:block>
    </fo:block>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Acute Epidural Hematoma">Acute Epidural Hematoma</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">Epidural hematomas (EDHs) are an uncommon but potentially lethal complication of head trauma. Mortality and morbidity can be low if an EDH is promptly recognized and appropriately treated.</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">An epidural hematoma is a collection of blood between the calvarium and outer (periosteal) layer of the dura.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Most EDHs arise from direct trauma to the skull that lacerates an adjacent artery or dural venous sinus. The vast majority (90%) are caused by arterial injury, most commonly to the middle meningeal artery. Approximately 10% of EDHs are venous, usually secondary to a fracture that crosses a dural venous sinus.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">A dark purple "currant jelly" clot underlies a calvarial fracture, usually the squamous portion of the temporal bone.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">EDHs are much less common than either traumatic subarachnoid hemorrhage (tSAH) or subdural hematoma (SDH). EDHs are found in between 1-4% of patients imaged for craniocerebral trauma although EDHs represent up to 10% of fatal injuries in autopsy series.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">EDHs are uncommon in infants and the elderly. Most are found in older children and young adults. The male:female ratio is 4:1.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">The prototypical "lucid interval," where a traumatized patient has an initial brief loss of consciousness followed by a variable asymptomatic period prior to onset of coma and/or neurologic deficit, occurs in only 50% of EDH cases. Headache, nausea, vomiting, symptoms of intracranial mass effect (e.g., pupil-involving third cranial nerve palsy) followed by somnolence and coma are common.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">Outcome depends on size and location of the hematoma, whether the EDH is arterial or venous, and if there is active bleeding (see below). Overall mortality rate with prompt recognition and treatment is under 5%.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Patients with mixed-density EDHs tend to present earlier than patients with hyperdense hematomas, have a lower mean GCS score, larger hematoma volumes, and poorer prognosis.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Delayed development or enlargement of an EDH occurs in 10-15% of cases, usually within 24-36 hours following trauma.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">Most EDHs are surgically evacuated. Mixed density EDHs expand rapidly in size and require even earlier and more aggressive treatment.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Occasionally a small hyperdense EDH that does not exhibit a "swirl sign" and has minimal or no mass effect is managed nonoperatively with close clinical observation and follow-up imaging within 24-36 hours.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">Over 90% of EDHs are unilateral, supratentorial, and biconvex in shape. Tight adherence of the periosteal dura to the inner calvarium explains this typical configuration. As EDHs expand, they strip the dura away from the inner table of the skull, forming the classic "lens-shaped" hematoma. EDHs compress the underlying subarachnoid space and displace the cortex medially, "buckling" the gray-white matter interface. Between 90-95% are associated with skull fracture.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">EDHs, especially in adults, typically do not cross sutures unless a fracture or sutural diastasis is present. In children, 10% of EDHs cross suture lines, typically the coronal or sphenosquamous suture.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Other co-morbid lesions such as contrecoup injuries, tSAH, and secondary brain herniations are common with EDHs.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal">NECT scan is the procedure of choice for initial imaging in patients with head injury. Both soft tissue and bone reconstruction algorithms should be obtained.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">NECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">
          The classic imaging appearance of
          <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">arterial EDHs</inline>
          is that of a hyperdense (60-90 Hounsfield units), lentiform-shaped extra-axial collection. Presence of a hypodense component ("swirl sign") is seen in about one-third of cases and indicates active, rapid bleeding with unretracted clot.
        </fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Air in an EDH occurs in approximately 20% of cases and is usually--but not invariably--associated with a sinus or mastoid fracture.</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">Venous EDHs</inline>
        are often small, develop more slowly than arterial EDHs and are easily overlooked. Most are caused by skull fracture that crosses a dural venous sinus and therefore occur near the vertex (superior sagittal sinus) or skull base (transverse/sigmoid sinus). Venous EDHs can "straddle" intracranial compartments, crossing both sutures and lines of dural attachment. Coronal and sagittal reformatted imaging is helpful in their detection and delineation.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">MR generally plays a minor role in the diagnosis and management of acute head trauma. Acute EDHs are typically isointense with underlying brain, especially on T1WIs. The displaced dura is seen as a definite "black line" between the hematoma and the brain.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Angiography.</fo:inline>
        <fo:inline font-weight="normal">DSA may show a lacerated middle meningeal artery with "tram-track" fistulization of contrast from the MMA into the paired middle meningeal veins. Mass effect with displaced cortical arteries and veins is seen.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        In the appropriate setting, imaging findings of EDH are pathognomonic. The major differential diagnosis is
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">subdural hematoma</inline>
        , which is usually (although not invariably) crescentic and frequently crosses suture lines but is confined by dural attachments of the falx or tentorium. Co-existence of both an EDH and SDH is common. Other hyperdense extra-axial collections on NECT scan include both primary and metastatic neoplasms such as meningioma, lymphoma, and metastases. Occasionally infections (such as dural tuberculoma) and extramedullary hematopoiesis present as a hyperdense extra-axial mass.
       </fo:block>
      </fo:block-container>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Acute Subdural Hematoma">Acute Subdural Hematoma</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">Subdural hematomas are much more common than epidural hematomas. Most SDHs do not occur as isolated injuries. The vast majority are associated with traumatic subarachnoid hemorrhage as well as significant parenchymal injuries such as cortical contusions, brain lacerations, and diffuse axonal injuries. Acute SDHs are one of the leading causes of death and disability in severe traumatic brain injury.</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">An acute subdural hematoma (aSDH) is a collection of acute blood products that lies between the inner (meningeal) layer of the dura and the arachnoid.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Trauma is the most common cause of aSDH. Direct blows to the head as well as nonimpact injuries may result in formation of an aSDH. Tearing of bridging cortical veins as they cross the subdural space to enter a dural venous sinus (usually the superior sagittal sinus) is the most common etiology. Cortical vein lacerations can occur with either a skull fracture or the sudden changes in velocity and brain rotation that occur during nonimpact closed-head injury.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Blood from ruptured vessels spreads quickly through the potential space between the dura and the arachnoid. Large SDHs may spread over an entire hemisphere, extending into the interhemispheric fissure and along the tentorium.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Tearing of cortical arteries from a skull fracture may also give rise to an aSDH. The arachnoid itself may also tear, creating a pathway for leakage of CSF into the subdural space, resulting in admixture of both blood and CSF.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Less common causes of aSDH include aneurysm rupture, skull/dura-arachnoid metastases from vascular extracranial primary neoplasms, and spontaneous hemorrhage in patients with severe coagulopathy. Rarely, an acute spontaneous SDH of arterial origin occurs without any traumatic history or vascular anomaly. These patients usually have sudden serious disturbance of consciousness and have a poor outcome unless recognized and treated promptly.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">The gross appearance of an aSDH is that of a soft, purplish "currant jelly" clot beneath a tense, bulging dura. More than 95% are supratentorial. Most aSDHs spread diffusely over the affected hemisphere and are therefore typically crescent-shaped.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">An aSDH is the second most common traumatic extra-axial hematoma, exceeded only by traumatic subarachnoid hemorrhage (tSAH). An aSDH is found in 10-20% of all head-injured patients and is observed in 30% of autopsied fatal injuries.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">An aSDH may occur at any age from infancy to the elderly. There is no gender predilection.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Even relatively minor head trauma, especially in elderly patients who are often anticoagulated, may result in an SDH. In such patients, a definite history of trauma may be lacking.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Clinical findings vary from none to loss of consciousness and coma. Most patients with aSDHs have low Glasgow Coma Scores on admission. Delayed deterioration, especially in elderly anticoagulated patients, is common.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">An aSDH may remain stable, grow slowly, or rapidly increase in size causing mass effect and secondary brain herniations. Prognosis is generally poor and varies with hematoma thickness, midline shift, and the presence of associated parenchymal injuries. An aSDH that is thicker than two centimeters correlates with poor outcome (35-90% mortality). An aSDH that occupies more than 10% of the total available intracranial volume is usually lethal.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">Presence of an aSDH in a traumatized patient is generally considered a neurosurgical emergency. Evacuation of an aSDH that has significant mass effect is typical. Small collections are sometimes managed with close clinical observation and follow-up imaging. Any sudden deterioration in the patient's condition should be evaluated with repeat CT scan.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">A supratentorial crescent-shaped extra-axial collection that displaces the gray-white matter interface medially is the classic finding of an aSDH. SDHs are typically more extensive than EDHs, easily spreading along the falx, tentorium, and around the anterior and middle fossa floors. SDHs may cross suture lines but generally do not cross dural attachments. Bilateral SDHs occur in 15% of cases. "Contrecoup" injuries such as contusion of the contralateral hemisphere are common.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Both standard soft tissue and intermediate ("subdural") windows should be used in all trauma patients as small, subtle aSDHs can be obscured by the density of the overlying calvarium.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal" />
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">NECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">Approximately 60% of aSDHs are hyperdense on NECT scan. Mixed attenuation lesions are found in 40% of cases. Pockets of hypodensity within the larger hyperdense collection ("swirl sign") usually indicate rapid bleeding. "Dots" of CSF trapped within compressed, displaced sulci are often seen underlying an aSDH.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Mass effect with an aSDH is common. In some cases, especially athletes with repeat head injury, brain swelling with unilateral hemisphere vascular engorgement occurs. Here the mass effect is disproportionate to the size of the SDH, which may be relatively small. This entity, the so-called "second impact syndrome," is probably caused by vascular dysautoregulation.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Occasionally an aSDH is nearly isodense with the underlying cortex. This unusual appearance is found in extremely anemic patients (Hgb under 8-10 g/dL) and sometimes in patients with coagulopathy. In rare cases, CSF leakage through a torn arachnoid may mix with--and dilute--the acute blood that collects in the subdural space.</fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">CECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">CECT scans show inward displacement of cortical veins and are helpful in detecting small isodense aSDHs. CTA may be useful in visualizing a cortical vessel that is actively bleeding into the subdural space.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">CT or xenon perfusion scans may demonstrate decreased cerebral blood flow (CBF) and low perfusion pressure, one of the reasons for the high mortality rate of aSDHs. The cortex underlying an evacuated aSDH may show hyperemic changes with elevated rCBF values. Persisting hyperemia has been associated with poor outcome.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">MR scans are rarely obtained in acutely brain-injured patients. In such cases, aSDHs appear isointense in the very acute stage and hypointense on T2WIs. Signal intensity on FLAIR scans is usually iso- to hyperintense compared to CSF but hypointense compared to the adjacent brain. aSDHs are hypointense on T2* scans.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">DWI shows heterogeneous signal within the hematoma but may show patchy foci of restricted diffusion in the cortex underlying the aSDH.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        In the setting of acute trauma, the major differential diagnosis is
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">epidural hematoma</inline>
        . Shape is a helpful feature as most aSDHs are crescentic while EDHs are biconvex. EDHs are almost always associated with skull fracture; SDHs frequently occur in the absence of skull fracture. EDHs may cross sites of dural attachment; SDHs do not cross the falx or tentorium.
       </fo:block>
      </fo:block-container>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Subacute Subdural Hematoma">Subacute Subdural Hematoma</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">With time, subdural hematomas (SDHs) undergo clot organization, lysis, and neomembrane formation. Within two to three days, the initial soft, loosely organized clot of an acute subdural hematoma becomes organized. Breakdown of blood products and the formation of organizing granulation tissue change the imaging appearance of subacute and chronic SDHs.</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">A subacute subdural hematoma (sSDH) is between several days and several weeks old.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        Evolution of an untreated, uncomplicated SDH follows a very predictable pattern. Density of an extraaxial hematoma decreases approximately 1-2
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-family="LucidaSansRegular" font-style="normal" font-weight="normal">μ</inline>
        each day. Therefore, an sSDH will become nearly isodense with the underlying cerebral cortex within a few days of trauma.
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">A collection of partially-liquified clot with resorbing blood products is surrounded by a "membrane" of organizing granulation tissue. The outermost membrane is closely applied to the dura and is typically thicker than the inner membrane that abuts the arachnoid. In some cases, repetitive hemorrhages of different ages arising from the friable granulation tissue may be present. In others, liquefaction of the hematoma over time produces serous, blood-tinged fluid.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">SDHs are found in 10-20% of patients imaged for brain trauma. Autopsy in fatal cases shows a 30% prevalence of SDH.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">Children and the elderly are most commonly affected.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Clinical symptoms vary from asymptomatic to loss of consciousness and hemiparesis caused by sudden rehemorrhage into an sSDH. Headache and seizure are other common presentations.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">An sSDH may slowly and spontaneously resolve. In some cases, repeated hemorrhages may cause sudden enlargement and mass effect.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">Surgical drainage may be indicated if the sSDH is enlarging or symptomatic.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">Imaging findings are related to hematoma age and the presence of encasing membranes. A crescent-shaped isodense fluid collection that spreads diffusely over the cerebral hemisphere is the classic finding. Intracranial hematomas decrease an average of 1.5H/day.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal" />
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">NECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">SSDHs are typically iso- to slightly hypodense compared to the underlying cortex. Medial displacement of the gray-white interface ("buckling") with foci of CSF in trapped, partially effaced sulci underlying the sSDH is often present. Mixed-density hemorrhages are common.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Bilateral sSDHs may be difficult to detect because of their "balanced" mass effect. Sulcal effacement with displaced GM-WM interfaces is the typical appearance.</fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">CECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">CECT scans show the enhanced cortical veins are displaced medially. The encasing membranes, especially the thicker superficial layer, may enhance.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">MR can be very helpful in identifying sSDHs, especially small lesions that are virtually isodense with underlying brain on CT scans. Signal intensity varies with hematoma age. Most sSDHs are moderately hyperintense on T1WI. Early subacute SDHs may be hypointense on T2WI but gradually become hyperintense in the late subacute stage as methemoglobin forms. Linear hypodensity that represents the encasing membranes surrounding the SDH is sometimes present. Gyral edema secondary to cortical hyperemia is seen in some cases.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">FLAIR is the most sensitive standard sequence for detecting sSDH as the collection is typically hyperintense. Because FLAIR signal intensity varies depending on the relative contribution of T1- and T2 effects, early subacute SDHs may initially appear hypointense due to their intrinsic T2 shortening.</fo:block>
       <fo:block text-align="justify" space-before="6pt">T2* scans are also very sensitive as sSDHs show distinct "blooming."</fo:block>
       <fo:block text-align="justify" space-before="6pt">Signal intensity on DWI varies with hematoma age. DWI commonly shows a crescent high intensity area with a low intensity rim close to the brain surface ("two-layered" structure). The low intensity area corresponds to a mixture of resolved clot and CSF whereas the high intensity area correlates with solid clot.</fo:block>
       <fo:block text-align="justify" space-before="6pt">T1C+ scans may show enhancing, thickened encasing membranes. The membrane surrounding an sSDH is usually thicker on the dural side of the collection. Delayed scans may show "filling in" and increasing hyperintensity of the sSDH.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        The major differential diagnosis of an sSDH is an
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">isodense acute SDH</inline>
        . These are typically seen only in an extremely anemic or anticoagulated patient. A
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">subdural effusion</inline>
        following surgery, meningitis, or occurring as a component of intracranial hypotension can also mimic an sSDH. A
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">subdural hygroma</inline>
        typically is isodense/isointense with CSF and does not demonstrate enhancing, encapsulating membranes.
       </fo:block>
      </fo:block-container>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Chronic/Mixed Subdural Hematoma">Chronic/Mixed Subdural Hematoma</fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">A chronic subdural hematoma (cSDH) is an encapsulated collection of sanguineous or serosanguineous fluid confined within the subdural space. Recurrent hemorrhage(s) into a pre-existing cSDH are common and produce a mixed-age SDH (mSDH).</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">With continued degradation of blood products, a subdural hematoma becomes progressively more liquified until it is largely serous fluid tinged with blood products. Rehemorrhage, either from vascularized encapsulating membranes or rupture of stretched cortical veins as they cross the expanded subdural space, occurs in 5-10% of cSDHs.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">Blood within the subdural space incites tissue reaction around its margins. Organization and resorption of the hematoma contained within the "membranes" of surrounding granulation tissue continues. These neomembranes have fragile, easily disrupted capillaries and easily rebleed, creating an mSDH. Multiple hemorrhages of different ages are common in mSDHs.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Eventually most of the liquified clot in a cSDH is resorbed. Only a thickened dura-arachnoid layer remains with a few scattered pockets of old blood trapped between the inner and outer membranes.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">Unoperated, uncomplicated subacute SDHs eventually evolve into cSDHs. Approximately 5-10% will rehemorrhage, causing multi-loculated mixed-age SDHs.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">Chronic SDHs may occur at any age. Mixed-age SDHs are much more common in elderly patients.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Presentation varies from no/mild symptoms including headache to sudden neurologic deterioration if a preexisting cSDH rehemorrhages.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">In the absence of repeated hemorrhages, cSDHs gradually resorb and largely resolve, leaving a residue of thickened dura-arachnoid that may persist for months or even years. Older patients, especially those with brain atrophy, are subject to repeated hemorrhages</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">If follow-up imaging of an sSDH shows expected resorption and regression of the cSDH, no surgery may be required. Surgical drainage with evacuation of the cDSH and resection of its encapsulating membranes is performed if significant mass effect or repeated hemorrhages causes neurologic complications.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">Chronic SDHs have a spectrum of imaging appearances. Uncomplicated cSDHs show relatively homogeneous density/signal intensity with slight gravity-dependent gradation of its contents. Mixed SDHs with acute hemorrhage into an otherwise uncomplicated cSDH show an hematocrit level, with distinct layering of the old (top) and new (bottom) hemorrhages. Trabecular or loculated cSDHs are septated extra-axial collections with thickened internal septae that contain hemorrhages of different ages. Dependent layering of blood within the loculated collections may appear quite bizarre. Extremely old cSDHs with virtually complete resorption of all liquid contents are seen as pachymengiopathies with diffuse dura-arachnoid thickening.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal" />
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">NECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">A hypodense crescentic fluid collection extending over the surface of one or both cerebral hemispheres is the classic finding. Uncomplicated cSDHs approach CSF in density. A slight gradation in density that increases slightly from top to bottom is common.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Trabecular or loculated cSDHs show internal septations, often with evidence for repeated hemorrhages. With age, the encapsulating membranes surrounding the cSDH become thickened and may appear moderately hyperdense. Eventually, some cSDHs show peripheral calcifications that persist for many years. In rare cases, a cSDH may densely calcify or even ossify, a condition aptly termed "armored brain."</fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">CECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">The encapsulating membranes around a cSDH contain fragile neocapillaries that lack endothelial tight junction. Therefore the membranes show strong enhancement following contrast administration.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">As with all intracranial hematomas, signal intensity of a cSDH or mSDH is quite variable and depends on age of the blood products. On T1WIs, uncomplicated cSDHs are typically iso- to slightly hyperintense compared to CSF. Depending on the stage of evolution, cSDHs are iso- to hypointense compared to CSF on T2WIs. Most cSDHs are hyperintense on FLAIR and may show blooming on T2* scans if subacute-chronic blood clots are still present. In about a quarter of all cases, superficial siderosis can be identified over the gyri underlying a CSH.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">The encapsulating membranes of a cSDH enhance following contrast administration. Typically the outer layer is thicker than the inner layer.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Chronic SDHs typically do not restrict on DWI. A "double layer" effect with a nonrestricting fluid collection and a crescent of hyperintensity, indicates rehemorrhage.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        A mixed SDH is difficult to mistake for anything else. In older patients, a small uncomplicated cSDH may be difficult to distinguish from simple
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">brain atrophy</inline>
        with enlarged bifrontal CSF spaces. However, cSDHs exhibit mass effect. cSDHs flatten the underlying gyri, often extending around the entire hemisphere and into the interhemispheric fissure. The increased extra-axial spaces in patients with cerebral atrophy are predominately frontal and temporal.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">
        A traumatic
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">subdural hygroma</inline>
        (TSHy) is an accumulation of CSF in the subdural space after head injury, probably secondary to an arachnoid tear. tSDHs are early lesions and can usually be detected in the first 24 hours after trauma although the mean time for appearance of a tSDH is 9 days after injury.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">A classic uncomplicated subdural hygroma is a hypodense, CSF-like crescentic extra-axial collection that consists purely of CSF, has no blood products, lacks encapsulating membranes, and shows no enhancement following contrast administration. Recent evidence indicates that CSF leakage into the subdural space is also present in the vast majority of patients with cSDH. Therefore, many--if not most--cSDHs contain a mixture of both CSF and blood products.</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        A
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">subdural effusion</inline>
        is an accumulation of clear fluid over the cerebral convexities or in the interhemispheric fissure. Subdural effusions are generally complications of meningitis an a history of prior infection, not trauma, is typical.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">
        A
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">subdural empyema</inline>
        (SDE) is a hypodense extraaxial fluid collection that contains pus. Most SDEs are secondary to sinusitis or mastoiditis, have strongly enhancing membranes and often co-exist with findings of meningitis. A typical SDE restricts strongly and uniformly on DWI.
       </fo:block>
      </fo:block-container>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Traumatic Subarachnoid Hemorrhage">Traumatic Subarachnoid Hemorrhage</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">Traumatic subarachnoid hemorrhage (tSAH) is found in virtually all cases of moderate to severe head trauma. Trauma--not ruptured saccular aneurysm--is the most common cause of intracranial subarachnoid hemorrhage. In this section we will look at the pathology and imaging manifestations of tSAH and its mimics.</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Traumatic SAH can occur with both direct trauma to the skull and nonimpact closed head injury. Tearing of cortical arteries and veins, rupture of contusions and lacerations into the contiguous subarachnoid space, and choroid plexus bleeds with intraventricular hemorrhage may all result in blood collecting within the subarachnoid cisterns. Less commonly, tSAH arises from major vessel lacerations or dissections, with or without basilar skull fractures.</fo:block>
       <fo:block text-align="justify" space-before="6pt">While tSAH occasionally occurs in isolation, it is usually accompanied by other manifestations of brain injury. Subtle tSAH may be the only clue on initial imaging that more serious injuries lurk beneath the surface....</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">Traumatic SAH is contained between the arachnoid and pia. tSAH typically occurs adjacent to cortical contusions and is therefore most commonly identified around the sylvian fissures and anterior-inferior frontal and temporal lobes, rather than concentrating in the suprasellar cisterns as is typical of aneurysmal subarachnoid bleeds. "Gliding" gyral contusions often result in tSAH into the sulci of the superolateral hemispheres. tSAH is also commonly identified under acute epi- and subdural hematomas. I</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">Traumatic SAH is found in most cases of moderate trauma and is identified in virtually 100% of fatal brain injuries at autopsy.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">The prevalence of tSAH generally follows that of other traumatic brain injuries, i.e., it is bimodal and most common in young adults (especially males) and the elderly.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Clinical symptoms are primarily related to other traumatic injuries such as extra-axial hematoma, contusions and axonal injury. In some cases, tSAH may cause delayed vasospasm and secondary ischemic symptoms.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">Breakdown and resorption of tSAH occurs gradually. Outcome is generally dictated by other injuries and is related to initial Glasgow Coma Score as well as the amount of blood in the subarachnoid cisterns at initial imaging.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">Supportive therapy is the primary treatment. In some cases, infusion of nimodipine or other calcium channel blocker such as verapamil may prevent vasospasm and its attendant complication.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">With the exception of location, the general appearance of tSAH is identical to that of aneurysmal SAH, i.e., sulcal-cisternal hyperdensity/hyperintensity. tSAH can be focal or diffuse. In contrast to aSAH (mostly in the basal cisterns), the predominant location of tSAH is perisylvian, in the anteroinferior frontal and temporal sulci, and over the hemisphere convexities. In very severe cases, tSAH spreads over most of the brain. In mild cases, blood collects in a single sulcus or the dependent portion of the interpeduncular fossa.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal" />
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">NECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">Acute tSAH appears as linear hyperdensities in sulci adjacent to cortical contusions or under EDH/ SDHs. Occasionally, isolated tSAH is identified within the interpeduncular fossa. Post-traumatic interpeduncular cistern hemorrhage is a good marker for possible brainstem lesions in patients with otherwise unexplained coma and may warrant further investigation.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Some cases of mild tSAH may have hemorrhage in a single convexity sulcus. In severe cases, tSAH spreads diffusely in the subarachnoid cisterns and layers over the tentorium. Chronic tSAH may appear as hypodense fluid that expands the affected sulci.</fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">CTA.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">CTA is typically normal for the first several days after tSAH. Vasospasm may ensue from 2-3 days to two weeks after trauma and is identified as multifocal areas of vessel narrowing or "beading."</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">As acute blood is isointense with brain, it may be difficult to detect on T1WIs. "Dirty" sulci with "smudging" of the perisylvian cisterns is typical. Subarachnoid blood is hyperintense to brain on T2WIs and appears similar in signal intensity to cisternal CSF. FLAIR scans show hyperintensity in the affected sulci.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">"Blooming" with hypointensity can be identified on T2* scans, typically adjacent to areas of cortical contusion. SWI is the most sensitive sequence. tSAH is recognized by very hypointense signal intensity surrounded by hyperintense CSF. tSAH also has a unique morphology. Compared with smooth, linear veins, SAH has a "triangle" shape with rough irregular boundaries and inhomogeneous signal intensity. Chronic tSAH causes focal superficial siderosis that appears as curvilinear hypointensity along gyri.</fo:block>
       <fo:block text-align="justify" space-before="6pt">DWI imaging may show foci of restricted diffusion in areas of frank ischemia or trauma-induced cytotoxic edema.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Angiography.</fo:inline>
        <fo:inline font-weight="normal">DSA is rarely performed in acute brain trauma unless vascular injury such as dissection or pseudoaneurysm is suspected. Vasospasm with acute tSAH is unusual but may develop several days after the initial traumatic event.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        The major differential diagnosis of tSAH is
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">nontraumatic SAH</inline>
        (ntSAH). Ruptured aneurysm causes 80-90% of all ntSAH. A saccular aneurysm can be identified in most cases with CTA or DSA. Arteriovenous malformation accounts for 10-15% of ntSAHs and is easily identified on both CT and MR. Dissections and dissecting aneurysms, especially of the vertebrobasilar system, are less common but important causes of ntSAH.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Sulcal-cisternal hyperintensity on FLAIR is nonspecific and can be caused by meningitis, neoplasm, artifact (incomplete CSF suppression), contrast leaking into the subarachnoid space (i.e., with renal failure), and high inspired oxygen during general anesthesia.</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        The term
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">"pseudosubarachnoid hemorrhage"</inline>
        has been used to describe the CT appearance of a brain with severe cerebral edema. This makes circulating blood in arteries and veins look relatively hyperdense compared to the hypodense hemispheres. The hyperdensity here is smooth and conforms to the expected shape of the vessels, not the subarachnoid spaces, and should not be mistaken for tSAH or ntSAH.
       </fo:block>
      </fo:block-container>
    </fo:block-container>
   </fo:block-container>
   <fo:block keep-with-next="always">
    <fo:block space-before="12pt" keep-with-next="always" margin-left="-15pt">
      <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
    </fo:block>
    <fo:block language="en" hyphenate="false" margin-left="-15pt" keep-with-next="always" space-before="12pt" font-size="18pt">Parenchymal Injuries</fo:block>
    <fo:block space-before="12pt" keep-with-next="always" margin-left="-15pt">
      <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
    </fo:block>
   </fo:block>
   <fo:block-container language="en" hyphenate="true" font-family="TimesNewRomanPSMT" font-size="10.5pt" id="group-Parenchymal Injuries">
    <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
      <fo:block text-align="justify" space-before="6pt">Intra-axial traumatic injuries include cortical contusions and lacerations, diffuse axonal injury (DAI), subcortical injuries, and intraventricular hemorrhages. In this section we begin with the most peripheral parenchymal injuries, cortical contusions, and end with the deepest (subcortical) injuries. In general, the deeper the brain injury, the more serious the consequences.</fo:block>
    </fo:block>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Cerebral Contusion">Cerebral Contusion</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">Cerebral contusions and lacerations are among the most common types of parenchymal injury, second only to diffuse axonal injuries (DAI).</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Cerebral contusions are also called gyral "crest" injuries. Cerebral contusions are basically "brain bruises" that evolve with time and often are more apparent on delayed scans than at the time of initial imaging. "Gliding" contusion is sometimes used to describe parasagittal contusions.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Most cerebral contusions result from non-missile or blunt head injury. Closed head injury induces abrupt changes in angular momentum and deceleration. The brain is suddenly and forcibly impacted against an osseous ridge or the hard, knife-like edge of the falx cerebri and tentorium cerebelli. Less commonly, a depressed skull fracture directly damages the underlying brain.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">Contusions are injuries of the brain surface that involve the gray matter and contiguous subcortical white matter. Contusions range in appearance from small petechial hemorrhages to confluent hematomas. Cortical contusions are often associated with traumatic subarachnoid hemorrhage in the adjacent sulci. Frank brain lacerations with injury to the subcortical white matter is common in moderate to severe trauma. In very severe cases a "burst" lobe is present.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Microscopic Features.</fo:inline>
        <fo:inline font-weight="normal">Perivascular microhemorrhages rapidly form and coalesce over time into more confluent hematomas. Edema surrounding the hemorrhages develops. Activation and proliferation of astrocytes together with macrophage infiltration ensues. Necrosis with neuronal loss and astrogliosis and hemosiderin-laden macrophages are present in subacute and chronic lesions.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">Cerebral contusions account for approximately 45% of all traumatic parenchymal lesions. The vast majority are multiple and bilateral.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">Cerebral contusions can be found at any age, from infants to the elderly. The peak age is from 15-24 years. The male:female ratio is 3:1.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Compared to DAI, cerebral contusions are less frequently associated with immediate loss of consciousness unless they are extensive or occur with other traumatic brain lesions such as brainstem trauma or axonal injury. Initial symptoms vary from none to confusion, seizure, or obtundation.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">Radiologic progression is typical, with nearly half of all patients showing increase in lesion size and number over the first 24-48 hours. Progression is more common in older patients as well as patients with large contusions, initial low Glasgow Coma Scores (GCS), and presence of a co-existing subdural hematoma. Hematoma expansion requiring surgical intervention occurs in approximately 20% of patients initially managed conservatively.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">The clinical relevance of radiologic progression is poorly understood, with some patients receiving several CT scans per day and others few to none after initial imaging. Patients with small contusions, good initial GCS score, and absence of clinical deterioration in the first 48 hours are unlikely to progress sufficiently to require surgery. Patients with unexplained clinical deterioration should have repeat imaging.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">Treatment options vary from conservative (observation with repeat imaging if the patient deteriorates) to surgical evacuation of large focal hematomas. Craniectomy is performed in cases with severe brain swelling to prevent fatal brain herniation.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">Petechial hemorrhages along gyral crests immediately adjacent to the calvarium are the classic finding. Contusions occur in very characteristic, highly predictable locations. Nearly half involve the temporal lobes. The temporal tips as well as the lateral and inferior surfaces and the perisylvian gyri are most commonly affected. The inferior (orbital) surfaces of the frontal lobes are also frequently affected.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Convexity gyri, the superior surface of the corpus callosum body, dorsolateral midbrain, and cerebellum are less common site of cerebral contusions. The occipital poles are rarely involved, even with relatively severe closed head injury.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal">Imaging findings vary both with time and injury severity. Initial NECT scans obtained soon after CHI may be normal. A mixture of petechial hemorrhages surrounded by patchy, ill-defined hypodense areas of edema may be present.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Radiologic progression is typical with cortical contusions. Lesion "blooming" occurs with progressive increase in hemorrhage, edema, and mass effect over time. Small lesions may coalesce, forming larger focal hematomas. Development of new lesions that were not present on initial imaging is also common.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">MRI is much more sensitive than CT in detecting cerebral contusions but is rarely obtained in the acute stage of traumatic brain injury. T1WIs may show only mild inhomogeneous isointensities and mass effect. T2WIs show patchy hyperintense areas (edema) surrounding hypointense foci of hemorrhage.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">FLAIR scans are most sensitive for detecting cortical edema and associated traumatic subarachnoid hemorrhage. Both appear as hyperintense foci on FLAIR. T2* GRE or SWI are the most sensitive sequences for imaging parenchymal hemorrhages. Significant "blooming" is typical in acute lesions.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Hemorrhagic contusions follow the expected evolution of parenchymal hematomas, with T1 shortening developing over time. Atrophy, demyelination and microglial scarring are seen on FLAIR and T2WI. Parenchymal volume loss with ventricular enlargement and sulcal prominence are common.</fo:block>
       <fo:block text-align="justify" space-before="6pt">DWI in cortical contusion shows diffusion restriction in areas of cell death. DTI may disclose co-existing white matter damage in minor head trauma when both CT and standard MRI are normal.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        The major differential diagnosis is
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">diffuse axonal injury</inline>
        . Both cerebral contusions and DAI are often present in patients sustaining moderate to severe head injury. Contusions tend to be superficial, located along gyral crests. DAI is most commonly found in the subcortical white matter and compact white matter tracts such as the internal capsule and corpus callosum.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">Brain laceration</inline>
        develops when trauma is sufficiently severe to tear the pia. A "burst lobe" is the most severe manifestation of frank brain laceration. Here the affected lobe is grossly disrupted, with large hematoma formation and adjacent traumatic subarachnoid hemorrhage. In some cases, especially those with depressed skull fracture, the arachnoid is also lacerated and extension of hemorrhage from the burst lobe communicates directly with the subdural space, forming a co-existing subdural hematoma.
       </fo:block>
      </fo:block-container>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Diffuse Axonal Injury">Diffuse Axonal Injury</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">Diffuse axonal injury (DAI) is the second most common parenchymal lesion seen in traumatic brain injury (TBI), exceeded only by cortical contusions. Patients with DAI often exhibit an apparent discrepancy between their clinical status (often moderately to severely impaired) and initial imaging findings (initially often normal or minimally abnormal).</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Diffuse axonal injury (DAI) is also known as traumatic axonal stretch injury. As most DAIs are stretch--not frank shearing--lesions, the term "shearing lesion" should be avoided. True "shearing" injury with frank axonal disconnection is uncommon and typically occurs only with very severe trauma.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Direct head impact is not required to produce DAI. Most DAIs are not associated with skull fracture.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Most DAIs are caused by high-velocity auto accidents and are nonimpact injuries, resulting from the inertial forces of rotation generated by sudden changes in acceleration/deceleration. The cortex moves at different speed in relationship to underlying deep brain structures (white matter, deep gray nuclei). This results in axonal stretching, especially where brain tissues of different density intersect, i.e., the gray matter-white matter interface.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Traumatic axonal stretching causes impaired axoplasmic transport, depolarization, ion fluxes, spreading depression, and release of excitatory amino acids. Cellular swelling with cytotoxic edema ensues, altering anisotropy of the brain. Significant and widespread alterations of brain metabolites occur as a result of TBI.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt">DAI occurs in highly predictable locations. The cortex is typically spared; it is the subcortical white matter that is most commonly affected. Lesions in deep compact white matter tracts such as the corpus callosum--especially the genu and splenium--and internal capsule are frequent. The midbrain and pons are less common sites of DAI.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">The vast majority of DAIs are microscopic and nonhemorrhagic. Tearing of penetrating vessels may cause small round to ovoid or linear hemorrhages that sometimes are the only gross indications of underlying axonal injury. These visible lesions are just the "tip of the iceberg."</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Microscopic Features.</fo:inline>
        <fo:inline font-weight="normal">Axonal swellings or "retraction balls" form, leaving microscopic gaps in the white matter. Neuronal apoptosis and microglial reaction ensue. Chronic upregulation of activated microglia immunoreactive for galectin-3/ Mac-2 and nerve growth factor have been demonstrated following DAI.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Staging, Grading, &amp; Classification.</fo:inline>
        <fo:inline font-weight="normal">The Adams and Gennarelli staging defines mild, moderate, and severe traumatic brain injury. At least half of all TBI cases are moderate to severe.</fo:inline>
       </fo:block>
       <fo:block text-align="left" font-size="10pt" font-family="GillSansMTPro" hyphenate="false" space-before="6pt" keep-together.within-page="always" border="0.6pt solid black" background-color="#E6FAF5">
        <fo:block space-before="5pt" keep-with-next="always" display-align="center" font-size="10pt" font-weight="bold" font-family="GillSansMTPro" background-color="#E6FAF5">
          <fo:block line-height="1.0" text-align="center" padding-before="2.5pt" margin-right="0.0pt">GRADING OF TRAUMATIC BRAIN INJURY</fo:block>
        </fo:block>
        <fo:block margin-right="10pt">
          <fo:list-block line-height="1.0" padding-after="5pt" provisional-label-separation="3pt" provisional-distance-between-starts="8pt">
           <fo:list-item space-after="2pt" space-before="3pt" font-size="10pt" font-family="GillSansMTPro">
            <fo:list-item-label end-indent="label-end()">
              <fo:block />
            </fo:list-item-label>
            <fo:list-item-body start-indent="body-start()">
              <fo:block line-stacking-strategy="font-height" line-height="1.0">Mild TBI: Lesions at frontal, temporal lobe gray/white matter interfaces</fo:block>
            </fo:list-item-body>
           </fo:list-item>
           <fo:list-item space-after="2pt" space-before="3pt" font-size="10pt" font-family="GillSansMTPro">
            <fo:list-item-label end-indent="label-end()">
              <fo:block />
            </fo:list-item-label>
            <fo:list-item-body start-indent="body-start()">
              <fo:block line-stacking-strategy="font-height" line-height="1.0">Moderate TBI: Lobar white matter, corpus callosum lesions seen</fo:block>
            </fo:list-item-body>
           </fo:list-item>
           <fo:list-item space-after="2pt" space-before="3pt" font-size="10pt" font-family="GillSansMTPro">
            <fo:list-item-label end-indent="label-end()">
              <fo:block />
            </fo:list-item-label>
            <fo:list-item-body start-indent="body-start()">
              <fo:block line-stacking-strategy="font-height" line-height="1.0">Severe TBI: Lesions in dorsolateral midbrain, upper pons</fo:block>
            </fo:list-item-body>
           </fo:list-item>
          </fo:list-block>
        </fo:block>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">There are more than two million cases of TBI annually in the USA. TBI is the leading cause of death and disability in children and young adults. DAI is present in virtually all fatal TBI and is found in almost three-quarters of patients with moderate and severe head injury who survive the acute stage.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">DAI may occur at any age. The peak is found in young adults (15-24 years old). Males are at least twice as often afflicted with TBI compared to females.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Relatively speaking, DAI typically causes much more significant impairment than extracerebral hematomas and cortical contusion. DAI often causes immediate loss of consciousness (LOC). LOC may be transient (in the case of mild TBI) or progress to coma (with moderate to severe injury).</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">Mild TBI may result in persisting headaches, mild neurocognitive impairment, and memory difficulties. DAI is more common in moderate to severely-injured patients. While DAI itself rarely causes death, severe DAI may result in persistent vegetative state. Prognosis correlates with the number and severity of lesions as well as the presence of other abnormalities such as cortical contusions and herniation syndromes.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">Management of intracranial pressure is the most serious issue. In some cases with impending herniation, craniectomy may be a last resort.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">One of the most striking features of DAI is the discrepancy between clinical symptoms and imaging findings. NECT scans are almost always the initial imaging study obtained in TBI although MR is much more sensitive in detecting changes of DAI. CT is very useful in detecting co-morbid injuries such as extracerebral hemorrhage and parenchymal hematomas.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">DAI typically evolves with time. Between 10-20% of lesions evolve to gross hemorrhages with edema and mass effect</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal">Initial imaging, typically NECT scan, is often normal or minimally abnormal. Mild diffuse brain swelling with sulcal effacement may be present. Gross hemorrhages are uncommon. A few small round or ovoid subcortical hemorrhages may be visible but the underlying damage is typically much more diffuse and much more severe than these relatively modest abnormalities would indicate.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">DAI is often more apparent on follow-up scans, with more hemorrhages and edema developing.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">As most DAIs are nonhemorrhagic, T1WIs are often normal, especially in the early stages of TBI. T2WIs and FLAIR may show hyperintense foci in the subcortical white matter and corpus callosum. Multiple lesions are the rule and a combination of DAI and contusions or hematomas is very common.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">T2* scans are very sensitive to the microbleeds of DAI and typically show multifocal ovoid and linear hypointensities. SWI sequences typically demonstrate more lesions than GRE. Residua from DAI may persist for years following the traumatic episode.</fo:block>
       <fo:block text-align="justify" space-before="6pt">DWI may show restricted diffusion, particularly within the corpus callosum. DTI "tractograms" may be useful in depicting white matter disruption. MRS shows widespread decrease of NAA with increased Cho.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">Cortical contusions</inline>
        often co-exist with DAI in moderate to severe TBI. Cortical contusions are typically superficial lesions, usually located along gyral crests.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">
        Multifocal hemorrhages with "blooming" on T2* (GRE or SWI) scans can be seen in numerous pathologies, including DAI.
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">Diffuse vascular injury</inline>
        (see below) appears as multifocal parenchymal "black dots." Pneumocephalus may cause multifocal "blooming" lesions in the subarachnoid spaces. Parenchymal lesions are rare.
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Several nontraumatic lesions also appear as multifocal T2* parenchymal hypointensities. Cerebral amyloid angiopathy and chronic hypertensive encephalopathy are common in older patients. Zabramski Type IV cavernous malformations are also seen as "black dots" on T2* MR scans.</fo:block>
      </fo:block-container>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Diffuse Vascular Injury">Diffuse Vascular Injury</fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Diffuse vascular injury (DVI) probably exists as the extreme end of the diffuse axonal injury (DAI) spectrum.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">DVI is caused by the extreme acceleration/rotational forces that are incurred in high-velocity motor vehicle accidents (MVAs). The brain microvasculature is disrupted by high tensile forces, resulting in numerous small parenchymal hemorrhages.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">Autopsied brains in patients with DVI show numerous small hemorrhages in the subcortical and deep white matter as well as the deep gray nuclei.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Microscopic Features.</fo:inline>
        <fo:inline font-weight="normal">Compared to the gross appearance of the brain, many more hemorrhages are detected on microscopic examination. Blood is identified along periarterial, perivenous, and pericapillary spaces with focal hemorrhages in the adjacent parenchyma.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">Autopsy series suggest DVI is present in 1-2% of fatal MVAs and 15% of cases with diffuse brain injury.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">While DVI can occur at any age, most occur in adults.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Immediate coma from the moment of impact is typical. A very low GCS, often less than 6-8, is typical in patients who survive the initial impact.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">Death within minutes or a few hours following injury is typical although some long-term survivors have been reported.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">Many patients with DVI do not survive long enough for imaging. In those that do, the most striking feature is the dissociation between clinical severity and imaging findings. Skull fractures are absent in approximately one-third of cases.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal">NECT scans may show only diffuse brain swelling with effaced superficial sulci and small ventricles. A few small foci of hemorrhage in the white matter and basal ganglia can sometimes be identified.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">T1WIs show only mild brain swelling. T2WIs and FLAIR scans may demonstrate a few foci of hyperintensity in the white matter. Occasionally scattered hypointensities can be identified within the hyperintensities, suggesting the presence of hemorrhage.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">T2* scans, especially susceptibility-weighted sequences, are striking. Punctate and linear blooming hypointensities oriented perpendicularly to the ventricles are seen, predominately in the subcortical and deep white matter, especially the corpus callosum. Additional lesions in the basal ganglia, thalami, brainstem and cerebellum are often present.</fo:block>
       <fo:block text-align="justify" space-before="6pt">DWI may demonstrate a few foci of restricted diffusion consistent with vascular-type injury.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">
        The major differential diagnosis is
        <inline xmlns="http://www.w3.org/1999/XSL/Format" font-weight="bold">diffuse axonal injury</inline>
        (DAI). Most lesions in DAI are nonhemorrhagic whereas DVI is characterized by the presence of innumerable petechial hemorrhages on T2* imaging. Some investigators believe DAI and DVI are part of the same spectrum of lesions that occurs in diffuse brain injury.
       </fo:block>
      </fo:block-container>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Subcortical Injury">Subcortical Injury</fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Subcortical injuries (SCIs) are traumatic lesions of deep brain structures such as the brainstem, basal ganglia, thalami and ventricles. SCIs are typically manifestations of moderate to severe closed head injury (CHI).</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Most SCIs are actually just deep axonal injuries and cerebral contusions. They represent shear-strain injuries that disrupt axons, tear penetrating blood vessels, and damage the choroid plexus of the lateral ventricles. Most SCIs are caused by the violent acceleration/ deceleration and brain rotation that occurs with severe, often fatal, motor vehicle accidents. Sudden craniocaudal displacement or lateral impaction of the midbrain against the tentorial incisura is common with these injuries.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">Hemorrhagic contusions, nonhemorrhagic lacerations, intraventricular bleeds and traumatic subarachnoid hemorrhage (tSAH) are typical and often coexist with other severe traumatic injuries. SCIs rarely occur in the absence of other traumatic lesions.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">Between 5-10% of patients with TBI sustain subcortical injuries. SCIs are the third most common parenchymal brain injury, after cortical contusion and DAI.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">As with most traumatic brain injuries, SCIs are most common in males between the ages of 15 and 25.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Immediate loss of consciousness with profound neurologic deficits is typical. Obtundation is the rule, not the exception. Gross discrepancy between immediate imaging findings (often minimal) and GCS (low).</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">Prognosis is poor in these severely injured patients. Many do not survive and those that do typically have profound neurologic impairment with severe long-term disability.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">Control of intracranial pressure is the goal. Craniectomy may be an option in exceptionally severe cases of uncontrollable brain swelling.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">As SCI typically exists with other co-morbid injuries, imaging findings are very abnormal with a spectrum of lesions that ranges from subtle tSAH to gross parenchymal hemorrhages. Mass effect with cerebral herniation and gross disturbances in regional blood flow are common. Minimal abnormalities may be present on initial imaging and show dramatic increase on follow-up scans.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal">NECT scans often show diffuse brain swelling with punctate and/or gross hemorrhage in the deep gray nuclei and midbrain. Intraventricular (IVH) and choroid plexus hemorrhages (CPHs) are common and may form a "cast" of the lateral ventricles. Blood-fluid levels are common.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">MR is much more sensitive than CT even though acute hemorrhage is isointense with brain on T1WIs. FLAIR and T2* are the most sensitive sequences. DWI may show foci of restricted diffusion. DTI mapping delineates the pattern of white matter tract disruption.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">Secondary midbrain ("Duret") hemorrhage may occur with severe descending transtentorial herniation. These hemorrhages are typically centrally located within the midbrain whereas contusional SCIs are dorsolateral.</fo:block>
      </fo:block-container>
    </fo:block-container>
   </fo:block-container>
   <fo:block keep-with-next="auto">
    <fo:block space-before="12pt" keep-with-next="always" margin-left="-15pt">
      <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
    </fo:block>
    <fo:block language="en" hyphenate="false" margin-left="-15pt" keep-with-next="always" space-before="12pt" font-size="18pt">Miscellaneous Injuries</fo:block>
    <fo:block space-before="12pt" keep-with-next="auto" margin-left="-15pt">
      <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
    </fo:block>
   </fo:block>
   <fo:block-container language="en" hyphenate="true" font-family="TimesNewRomanPSMT" font-size="10.5pt" id="group-Miscellaneous Injuries">
    <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
      <fo:block text-align="justify" space-before="6pt">A broad spectrum of miscellaneous primary injuries occur in head trauma. Some--such as pneumocephalus--are relatively common. Other lesions--like pituitary stalk transection with hypopituitarism--are rare. In this section we consider these miscellaneous lesions and also consider the topics of child abuse and gunshot wounds.</fo:block>
    </fo:block>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Pneumocephalus">Pneumocephalus</fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Pneumocephalus simply means the presence of gas or air within the skull. In pneumocephalus, air can be found anywhere within the cranium, including blood vessels, and within any compartment. Intracranial air does not exist under normal conditions. While it is pathologic, it is also often normal and expected (e.g., after surgery). "Tension pneumocephalus" is a collection of intracranial air that is under pressure and causes mass effect on the brain. Pneumatocele is a less-commonly used term and refers to a focal air collection.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Intracranial air is most often associated with trauma and surgery. Infection with gas-forming organism is a rare cause of pneumocephalus.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Iatrogenic causes (e.g., surgery) or blunt trauma breaches the integrity of the calvarium, central skull base, mastoid, or paranasal sinuses. If the dura and arachnoid are also transgressed air can enter the cranium. A ball-valve mechanism may trap the air and can be exacerbated with sneezing, coughing, straining, and Valsalva maneuver.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Intravascular air is usually secondary to intravenous catheterization, is most commonly found in the cavernous sinus, and is of no clinical importance. Intraarterial air is seen only with air embolism (transient) or brain death.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">Trauma is the most common cause of pneumocephalus. It is present in 3% of all skull fractures and 8% of paranasal sinus fractures. Virtually all patients who have supratentorial surgery have some degree of pneumocephalus within the first 24-28 hours as a normal finding. Tension pneumocephalus is a relatively uncommon complication of surgery, usually after subdural hematoma evacuation. Rarely, spontaneous pneumocephalus can occur with idiopathic sphenoidal defects or rupture of an enlarged paranasal sinus air cell ("pneumosinus dilatans").</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">The most common presentation is nonspecific headache. Less commonly, neurologic deficit and disturbances of consciousness are observed.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">Unless it is under tension, most intracranial air resolves spontaneously with a few days after trauma or surgery. Occasionally, air collections will increase with sneezing, coughing, etc. and may require surgical intervention.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">Tension pneumocephalus may require evacuation and repair of dural defects.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">Intracranial air can exist in any compartment and confirms to the shape of that compartment or potential compartment. Epidural air is typically unilateral, solitary, biconvex in configuration, and does not move with changes in head position. Subdural air is confluent, crescentic, often bilateral, frequently contains air-fluid levels, moves with changes in head position, and surrounds cortical veins that cross the subdural space.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Subarachnoid air is typically seen as multifocal small "dots" or "droplets" of air within and around cerebral sulci. Intraventricular air forms air-fluid levels, most often in the frontal horns of the lateral ventricles.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal">Air is extremely hypodense on CT, measuring approximately -1000 Hounsfield units. The "Mount Fuji sign" of tension pneumocephalus is seen as bilateral subdural air collections that separate and compress the frontal lobes. The frontal lobes are displaced posteriorly by air under pressure and are typically pointed where they are tethered to the dura-arachnoid by cortical veins, mimicking the silhouette of Mount Fuji.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Distinguishing air from fat on CT is extremely important. With typical narrow soft tissue windows, both appear similarly hypodense. Increasing window width or simply looking at bone CT algorithms (where air is clearly distinct from the less hypodense fat) helps differentiate fat from air.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">Air is seen as areas of completely absent signal intensity on all sequences. On T2* GRE, intracranial air "blooms" and appears as multifocal "black dots."</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">Air is air and shouldn't be mistaken for anything else. If wide windows are not used, a ruptured dermoid cyst with fat droplets in the CSF cisterns can mimic subarachnoid air.</fo:block>
      </fo:block-container>
      <fo:block margin-left="-15pt" space-before="5pt" keep-with-next="always" font-weight="normal" font-size="14pt">Reminder!</fo:block>
      <fo:block text-align="justify" space-before="6pt">Pneumocephalus itself generally isn't the problem; figure out what's causing it!</fo:block>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Child Abuse">Child Abuse</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">Radiologists play a key role in the early diagnosis and imaging of suspected inflicted injury. Imaging must be performed with care, interpreted with rigor, and precisely described.</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Child abuse or nonaccidental trauma (NAT), also known as nonaccidental injury (NAI) or shaken-baby syndrome (SBS), are terms for intentionally-inflicted injury. Abusive head trauma (AHT) and acute inflicted head injury are more specific terms applied to brain injuries.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">NAT injuries can be divided into two major groups: Direct impact injuries and shaking injuries.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Direct injuries are inflicted blows to the head or direct impact of the cranium on an object. These generally result in skull fractures with injury to the immediate subjacent brain.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Indirect injuries are typically shaking injuries that result in violent "to and fro" motions. The head of an infant or young child is relatively large compared to its body and the cervical musculature is comparatively. Shaking results in a form of whiplash injury, causing rapid rotation of the head relative to the neck. The most common result is diffusely-distributed subdural hematomas.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Gross Pathology.</fo:inline>
        <fo:inline font-weight="normal">Subdural hematomas of differing ages are the hallmark of inflicted brain injury.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Epidemiology.</fo:inline>
        <fo:inline font-weight="normal">The annual incidence of child abuse is estimated at 15-25:100,000.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">NAT is the most common cause of traumatic death in infants. Most abused children are under two years old. The peak age is between two and five months. While the majority of victims are males, in some cultures female infants are more common victims of NAT.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">No nationality or demographic group is exempt. NAT can be found in all socioeconomic groups although some predisposing factors such young age of the parents, domestic conflict, financial or emotional stress, drug and alcohol abuse are common.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Discordance between stated history and severity of injury is common. "Falling off a couch" typically does not induce enough force to cause the types of brain injuries observed in NAT. Apneic episodes and unarousability are common. Unusual bruises, patches of torn hair, lip lacerations and retinal hemorrhages should raise the suspicion of NAT and prompt appropriate imaging.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">Finding evidence for repetitive violence indicates a high risk for further injury and death. Mortality in NAT ranges from 15-60% and morbidity is high. Post-traumatic brain damage with seizures and retardation are common.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Treatment Options.</fo:inline>
        <fo:inline font-weight="normal">The medical imperative is to protect the child. Radiologists must clearly communicate any suspicion of abuse and the degree of certainty to appropriate clinicians. Notifying Child Protective Services of any suspected case of child abuse is legally mandated in many countries.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">The Section on Radiology of the American Academy of Pediatrics recently updated their recommendations on diagnostic imaging of child abuse.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Initial imaging in cases of suspected child abuse should include a complete skeletal survey and brain CT and/or MR. Many experts emphasize that while dating of both brain and skeletal injuries is imprecise, the most important goal is to determine if the pattern is of "age-different" lesions.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal" />
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">NECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">NECT using both soft tissue and bone algorithm with multiplanar reformatting is the primary tool in the initial evaluation of abusive head trauma. Skull fractures and scalp hematomas can be readily detected.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">The identification and characterization of intracranial hemorrhages, especially "differing age" subdural hematomas, is critical. EDHs are rare in NAT but SDHs are seen in over half of all cases and are the dominant feature in shaking-type NAT. Bifrontal, interhemispheric and peritentorial subdural hematomas of differing ages strongly suggest inflicted injury. Traumatic subarachnoid hemorrhage, cortical contusions, and occasionally diffuse axonal injuries are common. Ischemic injury may also be present and varies from territorial infarcts to global hypoxic brain injury.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">MR Findings.</fo:inline>
        <fo:inline font-weight="normal">"Differing age" SDHs on T1WIs with mixed hyper- and isointense components is highly suggestive of NAT. FLAIR is helpful in detecting small extra-axial collections and white matter injury. T2* (GRE or SWI) scans are very sensitive for chronic blood products, particularly subtle petechial cortical contusions and hemorrhagic axonal injuries. DWI is essential for evaluating foci of ischemic injury.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="4pt" font-weight="normal" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">PET Findings.</fo:inline>
        <fo:inline font-weight="normal">PET in conjunction with high-detail skeletal survey is helpful the assessment of skeletal trauma but of limited utility in evaluating brain injury.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Differential Diagnosis</fo:block>
       <fo:block text-align="justify" space-before="6pt">Rarely, an inborn error of metabolism (such as glutaric aciduria and Menkes' kinky hair syndrome) can mimic NAT. Bleeding dyscrasias can cause recurrent subdural hematomas. Metastatic neuroblastoma with "raccoon eyes" can mimic NAT.</fo:block>
      </fo:block-container>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Missile and Penetrating Injuries">Missile and Penetrating Injuries</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">The extent of tissue damage from a projectile is influenced by the type of bullet, its velocity and mass, and the physical characteristics of the affected tissues. Projectile craniocerebral injuries are qualitatively different from other traumatic brain injuries and from injuries in unconfined soft tissues with similar impact.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Penetrating injuries are influenced by the physical properties of the projectile as well as its ballistics. While a detailed discussion of projectiles and their ballistics is beyond the scope of this text, we will briefly consider the ballistics of projectile injury and their craniocerebral consequences.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Readers interested in greater detail are referred to the definitive article by Jandial et al., Ballistics for the Neurosurgeon, Neurosurgery 62: 472-80, 2008. Much of the information on ballistics and tissue injury summarized below is derived from this excellent source.</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Terminology</fo:block>
       <fo:block text-align="justify" space-before="6pt">The high-velocity projectile brain injuries seen in civilian populations are predominately gunshot wounds (GSWs). Stabbing injuries with sharp objects such as a knife, screwdriver, or icepick may also penetrate the calvarium and damage the underlying brain.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Injuries caused by blunt impact of a large projectile moving at low speed typically cause tissue damage immediately below the impact with limited penetration of the brain.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">The major factors that determine whether a projectile will penetrate the cranium are (1) its energy at impact on bone, (2) the contact area, and (3) the thickness of bone at the point of impact. Bone penetration by a ballistic projectile is a fracture event. Penetration punches out bone, cratering it inwards toward the dura and brain.</fo:block>
       <fo:block text-align="justify" space-before="6pt">The severity of tissue damage is proportional to the kinetic energy deposited in the tissue by the penetrating projectile PLUS a "rate effect" that is dependent on projectile size.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Pressure is very high at the tip of an advancing projectile. As a projectile penetrates brain, it leaves a temporary cavity in its wake. It also causes outward radial stretching of adjacent tissue, depositing energy at very high strain rates.</fo:block>
       <fo:block text-align="justify" space-before="6pt">As a bullet penetrates the brain, it yaws (not tumbles). This explains why the entry wound is typically small and tissue damage expands as the bullet slows. The exit wound may be quite large.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Projectiles with high kinetic energy may transfer enough energy to the skull to transform the bone fragments themselves into tiny secondary missiles, which in the aggregate can be just as lethal as through-and-through hits by the projectile.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Pathology</fo:block>
       <fo:block text-align="justify" space-before="6pt">The pathology of GSWs depends not only on the physical properties of the projectile (size, caliber), but on its ballistics. The behavior of a projectile acting on tissue (i.e., brain) that is anatomically constrained within a closed space (i.e., the skull) is different from injuries in unconfined soft tissue with similar impact.</fo:block>
       <fo:block text-align="justify" space-before="6pt">Bullets take a slightly curved path between the entry point and final location. The path is marked by macerated tissue, torn vessels, and disrupted axons.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Clinical Issues</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Demographics.</fo:inline>
        <fo:inline font-weight="normal">While patients at virtually any age can be affected, GSW patients tend to be overwhelmingly male and young.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Presentation.</fo:inline>
        <fo:inline font-weight="normal">Patients with GSWs to the brain typically present with signs and symptoms of brain swelling and herniation, including apnea and bradycardia. The sudden increase in intracranial pressure caused by the cavitation and expansion of brain can cause coma or death, even if eloquent structures are not directly affected.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">Patients with tangential gunshot wounds(TGSW) commonly present with a relatively good GCS and no loss of consciousness. In these cases, the bullet typically does not breach the skull although the TGSW may transfer considerable force to the brain and result in an extra-axial hematoma, cortical contusion, and traumatic subarachnoid hemorrhage.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Natural History.</fo:inline>
        <fo:inline font-weight="normal">Prognosis is highly variable and ranges from death to full recovery. GSWs that have a central trajectory and are transventricular or bihemispheric have a high morbidity/ mortality. Most fatalities occur within the first 24 hours after injury. Tangential GSWs with smaller caliber, low-velocity bullets may have a better outcome.</fo:inline>
       </fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt">The morphology of GSWs is extremely variable. GSW injuries are most severe with large-caliber missiles traveling at high velocity that fragment early on entry into the cranium.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">General Features.</fo:inline>
        <fo:inline font-weight="normal">CT with both bone and soft tissue reconstruction is the diagnostic procedure of choice. The radiology report should include determination of the entry site, describe the missile path including bone fragmentation and ricochet paths, and evaluate for exit wound. Possible damage to critical blood vessels should be noted along with secondary effects such as ischemia and herniation syndromes.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt">In general, a small caliber, low velocity projectile will have a relatively small linear track through the brain. The track is larger with large caliber, high-velocity bullets.</fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">CT Findings.</fo:inline>
        <fo:inline font-weight="normal" />
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">NECT.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">Entrance wounds are typically "punched-in" cones of bone. The bullet path is hyperdense and tends to curve slightly, broadening as the bullet yaws and slows. Bullet and bone fragments should be noted. The exit wound is typically either a ledge-shaped fracture or "punched-out" bone. Pneumocephalus may be present.</fo:inline>
       </fo:block>
       <fo:block text-align="justify" space-before="6pt" font-family="TimesNewRomanPSMT" font-size="10.5pt">
        <fo:inline font-family="Times-BoldSC">Angiography.</fo:inline>
        <fo:inline font-weight="normal" />
       </fo:block>
       <fo:block text-align="justify" font-weight="normal" font-size="10.5pt" space-before="6pt" text-indent="18pt">
        <fo:inline font-style="italic" font-weight="normal">CTA.</fo:inline>
        <fo:inline margin-left="4pt" font-weight="normal">CTA with multiplanar reconstruction and MIP images is helpful in evaluating vascular injuries such as pseudoaneurysm, dissection, traumatic dAVF, and venous injury or thrombosis.</fo:inline>
       </fo:block>
      </fo:block-container>
    </fo:block-container>
    <fo:block-container>
      <fo:block hyphenate="false" color="#2254D1" space-before="9pt" keep-with-next="always" font-family="TimesNewRomanPSMT" font-style="italic" font-weight="bold" font-size="16pt" margin-left="-15pt" id="Post-Traumatic Hypopituitarism">Post-Traumatic Hypopituitarism</fo:block>
      <fo:block font-weight="normal" font-size="10.5pt" font-family="TimesNewRomanPSMT">
       <fo:block text-align="justify" space-before="6pt">Post-traumatic hypopituitarism is an underrercognized consequence of traumatic brain injury (TBI). Minor hormonal deficiencies occur in 30-40% of long-term TBI survivors. Approximately 20% of patients develop major pituitary hormonal deficiencies. Most are associated with relatively severe initial injury (mean GCS of 7) and are usually identified 6-9 months after injury.</fo:block>
      </fo:block>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Etiology</fo:block>
       <fo:block text-align="justify" space-before="6pt">Many cases of post-traumatic hypopituitarism are associated with complex skull base fractures. In others, torsion of the pituitary stalk during closed head injury may be the primary etiology.</fo:block>
      </fo:block-container>
      <fo:block-container>
       <fo:block keep-with-next="always" space-before="7pt" margin-left="-15pt" font-weight="normal" font-family="TimesNewRomanPSMT" font-size="14pt">Imaging Findings</fo:block>
       <fo:block text-align="justify" space-before="6pt">While changes in the pituitary gland following acute TBI are common, they mostly consist of nonspecific pituitary gland enlargement and heterogeneity on MR. In these patients, the diagnosis is usually established with endocrine profiling</fo:block>
      </fo:block-container>
    </fo:block-container>
   </fo:block-container>
   <fo:block break-before="page" font-size="9pt">
    <fo:block keep-with-next="auto">
      <fo:block space-before="12pt" keep-with-next="always" margin-left="-15pt">
       <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
      </fo:block>
      <fo:block language="en" hyphenate="false" margin-left="-15pt" keep-with-next="always" space-before="12pt" font-size="18pt">Selected References</fo:block>
      <fo:block space-before="12pt" keep-with-next="auto" margin-left="-15pt">
       <fo:leader leader-length="100%" rule-thickness="4pt" alignment-baseline="before-edge" color="#2254D1" leader-pattern="rule" />
      </fo:block>
    </fo:block>
    <fo:block language="en" hyphenate="false" color="#2254D1" margin-left="-15pt" keep-with-next="always" space-before="12pt" font-style="italic" font-size="16pt">Skull and Scalp Injuries</fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Scalp Injuries</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Hymel KP et al: Head injury depth as an indicator of causes and mechanisms. Pediatrics. 125(4):712-20, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Holmgren EP et al: Facial soft tissue injuries as an aid to ordering a combination head and facial computed tomography in trauma patients. J Oral Maxillofac Surg. 63(5):651-4, 2005</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Skull Fractures</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Ringl H et al: The skull unfolded: a cranial CT visualization algorithm for fast and easy detection of skull fractures. Radiology. 255(2):553-62, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block language="en" hyphenate="false" color="#2254D1" margin-left="-15pt" keep-with-next="always" space-before="12pt" font-style="italic" font-size="16pt">Extraaxial Hemorrhage</fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Acute Epidural Hematoma</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Huisman TA et al: Epidural hematoma in children: do cranial sutures act as a barrier? J Neuroradiol. 36(2):93-7, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Le TH et al: Neuroimaging of traumatic brain injury. Mt Sinai J Med. 76(2):145-62, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Pruthi N et al: Mixed-density extradural hematomas on computed tomography-prognostic significance. Surg Neurol. 71(2):202-6, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Acute Subdural Hematoma</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Cantu RC et al: Second-impact syndrome and a small subdural hematoma: an uncommon catastrophic result of repetitive head injury with a characteristic imaging appearance. J Neurotrauma. 27(9):1557-64, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Dalfino JC et al: Visualization of an actively bleeding cortical vessel into the subdural space by CT angiography. Clin Neurol Neurosurg. 112(8):737-9, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Chieregato A et al: Hyperemia beneath evacuated acute subdural hematoma is frequent and prolonged in patients with an unfavorable outcome: a xe-computed tomographic study. Neurosurgery. 64(4):705-17; discussion 717-8, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Naama O et al: Acute spontaneous subdural hematoma: an unusual form of cerebrovacular accident. J Neurosurg Sci. 53(4):157-9, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Westermaier T et al: Clinical features, treatment, and prognosis of patients with acute subdural hematomas presenting in critical condition. Neurosurgery. 61(3):482-7; discussion 487-8, 2007</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Subacute Subdural Hematoma</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Wind JJ et al: Images in clinical medicine. Bilateral subacute subdural hematomas. N Engl J Med. 360(17):e23, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Kuwahara S et al: Diffusion-weighted imaging of traumatic subdural hematoma in the subacute stage. Neurol Med Chir (Tokyo). 45(9):464-9, 2005</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Chronic/Mixed Subdural Hematoma</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Kakeda S et al: Superficial siderosis associated with a chronic subdural hematoma: T2-weighted MR imaging at 3T. Acad Radiol. 17(7):871-6, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Kristof RA et al: Cerebrospinal fluid leakage into the subdural space: possible influence on the pathogenesis and recurrence frequency of chronic subdural hematoma and subdural hygroma. J Neurosurg. 108(2):275-80, 2008</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Zanini MA et al: Traumatic subdural hygromas: proposed pathogenesis based classification. J Trauma. 64(3):705-13, 2008</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Traumatic Subarachnoid Hemorrhage</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Beretta L et al: Post-traumatic interpeduncular cistern hemorrhage as a marker for brainstem lesions. J Neurotrauma. 27(3):509-14, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Wu Z et al: Evaluation of traumatic subarachnoid hemorrhage using susceptibility-weighted imaging. AJNR Am J Neuroradiol. 31(7):1302-10, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Lee DJ et al: Intra-arterial calcium channel blocker infusion for treatment of severe vasospasm in traumatic brain injury: case report. Neurosurgery. 63(5):E1004-6; discussion E1006, 2008</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block language="en" hyphenate="false" color="#2254D1" margin-left="-15pt" keep-with-next="always" space-before="12pt" font-style="italic" font-size="16pt">Parenchymal Injuries</fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Cerebral Contusion</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Alahmadi H et al: The natural history of brain contusion: an analysis of radiological and clinical progression. J Neurosurg. 112(5):1139-45, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Khan S et al: Evolution of traumatic intracerebral hemorrhage captured with CT imaging: report of a case and the role of serial CT scans. Emerg Radiol. 17(6):493-6, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Diffuse Axonal Injury</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Govind V et al: Whole-brain proton MR spectroscopic imaging of mild-to-moderate traumatic brain injury and correlation with neuropsychological deficits. J Neurotrauma. 27(3):483-96, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Venkatesan C et al: Chronic upregulation of activated microglia immunoreactive for galectin-3/Mac-2 and nerve growth factor following diffuse axonal injury. J Neuroinflammation. 7:32, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Li XY et al: Diffuse axonal injury: novel insights into detection and treatment. J Clin Neurosci. 16(5):614-9, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Skandsen T et al: Prevalence and impact of diffuse axonal injury in patients with moderate and severe head injury: a cohort study of early magnetic resonance imaging findings and 1-year outcome. J Neurosurg. 113(3):556-63, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Diffuse Vascular Injury</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Onaya M: Neuropathological investigation of cerebral white matter lesions caused by closed head injury. Neuropathology. 22(4):243-51, 2002</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Subcortical Injury</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Mamere AE et al: Evaluation of delayed neuronal and axonal damage secondary to moderate and severe traumatic brain injury using quantitative MR imaging techniques. AJNR Am J Neuroradiol. 30(5):947-52, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block language="en" hyphenate="false" color="#2254D1" margin-left="-15pt" keep-with-next="auto" space-before="12pt" font-style="italic" font-size="16pt">Miscellaneous Injuries</fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Pneumocephalus</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
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          <fo:block>Sinclair AG et al: Imaging of the post-operative cranium. Radiographics. 30(2):461-82, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Child Abuse</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
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        <fo:list-item-body start-indent="body-start()">
          <fo:block>Adamsbaum C et al: How to explore and report children with suspected non-accidental trauma. Pediatr Radiol. 40(6):932-8, 2010</fo:block>
        </fo:list-item-body>
       </fo:list-item>
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        <fo:list-item-label end-indent="label-end()">
          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
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        <fo:list-item-body start-indent="body-start()">
          <fo:block>Sato Y: Imaging of nonaccidental head injury. Pediatr Radiol. 39 Suppl 2:S230-5, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Section on Radiology; American Academy of Pediatrics: Diagnostic imaging of child abuse. Pediatrics. 123(5):1430-5, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Missile and Penetrating Injuries</fo:block>
    <fo:block space-before="5pt" font-size="9pt" font-style="normal">
      <fo:list-block provisional-label-separation="3pt" provisional-distance-between-starts="0.15in">
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
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          <fo:block>Farhat HI et al: A tangential gunshot wound to the head: Case report and review of the literature. J Emerg Med. Epub ahead of print, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
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        <fo:list-item-body start-indent="body-start()">
          <fo:block>Maiden N: Ballistics reviews: mechanisms of bullet wound trauma. Forensic Sci Med Pathol. 5(3):204-9, 2009</fo:block>
        </fo:list-item-body>
       </fo:list-item>
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Jandial R et al: Ballistics for the neurosurgeon. Neurosurgery. 62(2):472-80; discussion 480, 2008</fo:block>
        </fo:list-item-body>
       </fo:list-item>
       <fo:list-item space-before="3pt">
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
        <fo:list-item-body start-indent="body-start()">
          <fo:block>Oehmichen M et al: Gunshot injuries to the head and brain caused by low-velocity handguns and rifles. A review. Forensic Sci Int. 146(2-3):111-20, 2004</fo:block>
        </fo:list-item-body>
       </fo:list-item>
      </fo:list-block>
    </fo:block>
    <fo:block keep-with-next="always" space-before="6pt" font-style="normal" font-size="14pt">Post-Traumatic Hypopituitarism</fo:block>
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
        </fo:list-item-label>
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          <fo:block>Maiya B et al: Magnetic resonance imaging changes in the pituitary gland following acute traumatic brain injury. Intensive Care Med. 34(3):468-75, 2008</fo:block>
        </fo:list-item-body>
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          <fo:block font-size="9pt" font-family="TimesNewRomanPSMT">•</fo:block>
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        <fo:list-item-body start-indent="body-start()">
          <fo:block>Gasco V et al: Hypopituitarism following brain injury: when does it occur and how best to test? Pituitary. Epub ahead of print, 2010</fo:block>
        </fo:list-item-body>
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