Cortical laminar necrosis
Updates to Article Attributes
Cortical laminar necrosis is characterised by the cortex cell death, mainly onin the third layer, in situations of reduced energy supply to the brain.
Pathology
Cortical laminar necrosis occurs as a consequence of selective vulnerability of watershed intracortical area (cortical layers 3, 4, and 5) to anoxia and ischaemia. This can also could occur as a result of glucose depletion. Not only A pan-necrosis results as neurons, but as well as glial cells and blood are also damaged, resulting in a pan-necrosis.
The selective vulnerability of gray matter may be due to higher metabolic demand and denser concentration of receptors for excitatory amino acids that are released after an anoxic-ischaemic event. This can be seen in:
- cerebral hypoperfusion secondary to cardiac arrest or hypotension
- hypoxia
- status epilepticus (as the brain demands more glucose and oxygen)
- hypoglycemia
- blood diseases such as severe anaemia
Radiographic features
Laminar necrosis may be identified within hours of the anoxic-ischaemic event. In the acute phase DWI is superior to conventional MRI sequences to distinguish thisthese cortical changes 6.
CT
It is seen on imaging as a curvilinearCurvilinear gyriform hyperdensities that follow the gyral anatomy on CT. MayIt may also be seen also as areas of cortical hypoattenuation.
MRI
Early cytotoxic oedema causes the bright signalssignal seen on DWI and the corresponding low apparent diffusion coefficient (ADC) values.
T1 curvilinear hyperintensities signalling laminar necrosis become evident after 2 weeks, peak at 1 to 3 months, and then fade slowly but can still be visible for a late period after the insult. This T1 high signal is believed to be caused by the accumulation of denatured proteins in dying cells and does not represent the presence of haemorrhage 6.
Cortical enhancement may be present after 2 weeks, with peaks after 1 to 2 months.
See also
-<p><strong>Cortical laminar necrosis</strong> is characterised by the cortex cell death, mainly on the <a href="/articles/cortex-layers">third layer</a>, in situations of reduced energy supply to the brain.</p><h4>Pathology</h4><p>Cortical laminar necrosis occurs as a consequence of selective vulnerability of watershed intracortical area (cortical layers 3, 4, and 5) to anoxia and <a href="/articles/ischaemic-stroke">ischaemia</a>. This also could occur as a result of glucose depletion. Not only neurons, but glial cells and blood are also damaged, resulting in a pan-necrosis.</p><p>The selective vulnerability of gray matter may be due to higher metabolic demand and denser concentration of receptors for excitatory amino acids that are released after an anoxic-ischaemic event. This can be seen in:</p><ul>- +<p><strong>Cortical laminar necrosis</strong> is characterised by the cortex cell death, mainly in the <a href="/articles/cortex-layers">third layer</a>, in situations of reduced energy supply to the brain.</p><h4>Pathology</h4><p>Cortical laminar necrosis occurs as a consequence of selective vulnerability of watershed intracortical area (cortical layers 3, 4, and 5) to anoxia and <a href="/articles/ischaemic-stroke">ischaemia</a>. This can also occur as a result of glucose depletion. A pan-necrosis results as neurons as well as glial cells are damaged.</p><p>The selective vulnerability of gray matter may be due to higher metabolic demand and denser concentration of receptors for excitatory amino acids that are released after an anoxic-ischaemic event. This can be seen in:</p><ul>
-<a title="Status epilepticus" href="/articles/status-epilepticus">status epilepticus</a> (as the brain demands more glucose and oxygen)</li>- +<a href="/articles/status-epilepticus">status epilepticus</a> (as the brain demands more glucose and oxygen)</li>
-</ul><h4>Radiographic features</h4><p>Laminar necrosis may be identified within hours of the anoxic-ischaemic event. In the acute phase DWI is superior to conventional MRI sequences to distinguish this cortical changes <sup>6</sup>.</p><h5>CT</h5><p>It is seen on imaging as a curvilinear hyperdensities that follow the gyral anatomy on CT. May be seen also as areas of cortical hypoattenuation.</p><h5>MRI</h5><p>Early cytotoxic oedema causes the bright signals seen on DWI and the corresponding low apparent diffusion coefficient (ADC) values.</p><p>T1 curvilinear hyperintensities signalling laminar necrosis become evident after 2 weeks, peak at 1 to 3 months, and then fade slowly but can still be visible for a late period after the insult. This T1 high signal is believed to be caused by the accumulation of denatured proteins in dying cells and does not represent presence of haemorrhage <sup>6</sup>.</p><p>Cortical enhancement may be present after 2 weeks, with peaks after 1 to 2 months.</p><h4>See also</h4><ul><li><a href="/articles/hypoxic-ischaemic-brain-injury-1">hypoxic-ischaemic brain injury</a></li></ul>- +</ul><h4>Radiographic features</h4><p>Laminar necrosis may be identified within hours of the anoxic-ischaemic event. In the acute phase DWI is superior to conventional MRI sequences to distinguish these cortical changes <sup>6</sup>.</p><h5>CT</h5><p>Curvilinear gyriform hyperdensities that follow the gyral anatomy on CT. It may also be seen as areas of cortical hypoattenuation.</p><h5>MRI</h5><p>Early cytotoxic oedema causes the bright signal seen on DWI and the corresponding low apparent diffusion coefficient (ADC) values.</p><p>T1 curvilinear hyperintensities signalling laminar necrosis become evident after 2 weeks, peak at 1 to 3 months, and then fade slowly but can still be visible for a late period after the insult. This T1 high signal is believed to be caused by the accumulation of denatured proteins in dying cells and does not represent the presence of haemorrhage <sup>6</sup>.</p><p>Cortical enhancement may be present after 2 weeks, with peaks after 1 to 2 months.</p><h4>See also</h4><ul><li><a href="/articles/hypoxic-ischaemic-brain-injury-1">hypoxic-ischaemic brain injury</a></li></ul>
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