Cerebral amyloid angiopathy-associated lobar intracerebral hemorrhage

Case contributed by Mark Rodrigues , 22 Feb 2018
Diagnosis certain
Changed by Mark Rodrigues, 22 Feb 2018

Updates to Case Attributes

Body was changed:

Left parietal lobar haemorrhage with involvement of the cortex. There is no extension into the subarachnoid space or ventricles. Background changes of severe small vessel disease (periventricular low attenuation) and atrophy.

Lobar intracerebral haemorrhage is frequently attributed to small vessel diseases (cerebral amyloid angiopathy or arteriolosclerosis).  Differentiating lobar haemorrhage due to cerebral amyloid angiopathy and arteriolosclerosis is important due to differences in recurrent ICH and post-stroke dementia risk (higher with CAA-associated ICH).

The Edinburgh CT and genetic diagnostic criteria for lobar intracerebral haemorrhage associated with cerebral amyloid angiopathy uses CT features (presence of subarachnoid haemorrhage, finger-like projections arising from the ICH) and APOE e4 genotype (if available) to classify a patient as high, intermediate or low risk of CAA-associated ICH. The initial CT shows no subarachnoid haemorrhage or finger-like projections from the haematoma. The patient possessed at least one APOE e4 allele. Therefore they are intermediate risk for CAA-associated ICH on the Edinburgh CT and genetic diagnostic criteria for lobar intracerebral haemorrhageassociated with cerebral amyloid angiopathy.

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PATHOLOGY: Post mortem showed left parietal haematomata with extension into the subarachnoid space. There is small vessel disease throughout the white matter with enlarged perivascular spaces and rarefaction, lipohyalinosis and arteriolosclerosis. Widespread amyloid angiopathy with concentric splitting of some vessels.  There is also extensive parenchymal amyloid. 

The pathology demonstrates extensive cerebral amyloid angiopathy and arteriolosclerosis, both of which could result in the haemorrhage.  The distribution of haemorrhage is more suggestive of cerebral amyloid angiopathy

  • -<p>Left parietal <a href="/articles/lobar-haemorrhage">lobar haemorrhage</a> with involvement of the cortex. There is no extension into the subarachnoid space or ventricles. Background changes of severe <a href="/articles/leukoaraiosis">small vessel disease</a> (periventricular low attenuation) and atrophy.</p><p>Lobar intracerebral haemorrhage is frequently attributed to small vessel diseases (cerebral amyloid angiopathy or arteriolosclerosis).  Differentiating lobar haemorrhage due to <a href="/articles/cerebral-amyloid-angiopathy-1">cerebral amyloid angiopathy</a> and arteriolosclerosis is important due to differences in recurrent ICH and post-stroke dementia risk (higher with CAA-associated ICH).</p><p>The Edinburgh CT and genetic diagnostic criteria for lobar intracerebral haemorrhage associated with cerebral amyloid angiopathy uses CT features (presence of subarachnoid haemorrhage, finger-like projections arising from the ICH) and APOE e4 genotype (if available) to classify a patient as high, intermediate or low risk of CAA-associated ICH. The initial CT shows no subarachnoid haemorrhage or finger-like projections from the haematoma. The patient possessed at least one APOE e4 allele. Therefore they are intermediate risk for CAA-associated ICH on the Edinburgh CT and genetic diagnostic criteria for lobar intracerebral haemorrhage associated with cerebral amyloid angiopathy.</p><p>---</p><p><strong>PATHOLOGY:</strong> Post mortem showed left parietal haematomata with extension into the subarachnoid space. There is small vessel disease throughout the white matter with enlarged perivascular spaces and rarefaction, lipohyalinosis and arteriolosclerosis. Widespread amyloid angiopathy with concentric splitting of some vessels.  There is also extensive parenchymal amyloid. </p><p> </p><p>The pathology demonstrates extensive cerebral amyloid angiopathy and arteriolosclerosis, both of which could result in the haemorrhage.  The distribution of haemorrhage is more suggestive of cerebral amyloid angiopathy</p>
  • +<p>Left parietal <a href="/articles/lobar-haemorrhage">lobar haemorrhage</a> with involvement of the cortex. There is no extension into the subarachnoid space or ventricles. Background changes of severe <a href="/articles/leukoaraiosis">small vessel disease</a> (periventricular low attenuation) and atrophy.</p><p>Lobar intracerebral haemorrhage is frequently attributed to small vessel diseases (cerebral amyloid angiopathy or arteriolosclerosis).  Differentiating lobar haemorrhage due to <a href="/articles/cerebral-amyloid-angiopathy-1">cerebral amyloid angiopathy</a> and arteriolosclerosis is important due to differences in recurrent ICH and post-stroke dementia risk (higher with CAA-associated ICH).</p><p>The initial CT shows no subarachnoid haemorrhage or finger-like projections from the haematoma. The patient possessed at least one APOE e4 allele. Therefore they are intermediate risk for CAA-associated ICH on the <a title="The Edinburgh CT and genetic diagnostic criteria for lobar intracerebral haemorrhage associated with cerebral amyloid angiopathy" href="/articles/edinburgh-criteria-for-lobar-intracerebral-haemorrhage-associated-with-cerebral-amyloid-angiopathy">Edinburgh CT and genetic diagnostic criteria for lobar intracerebral haemorrhage</a><a href="/articles/edinburgh-ct-and-genetic-diagnostic-criteria-for-lobar-intracerebral-haemorrhage"> </a><a title="The Edinburgh CT and genetic diagnostic criteria for lobar intracerebral haemorrhage associated with cerebral amyloid angiopathy" href="/articles/edinburgh-criteria-for-lobar-intracerebral-haemorrhage-associated-with-cerebral-amyloid-angiopathy">associated with cerebral amyloid angiopathy</a>.</p><p>---</p><p><strong>PATHOLOGY:</strong> Post mortem showed left parietal haematomata with extension into the subarachnoid space. There is small vessel disease throughout the white matter with enlarged perivascular spaces and rarefaction, lipohyalinosis and arteriolosclerosis. Widespread amyloid angiopathy with concentric splitting of some vessels.  There is also extensive parenchymal amyloid. </p><p> </p><p>The pathology demonstrates extensive cerebral amyloid angiopathy and arteriolosclerosis, both of which could result in the haemorrhage.  The distribution of haemorrhage is more suggestive of cerebral amyloid angiopathy</p>

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