Cortical laminar necrosis
Updates to Article Attributes
Cortical laminar necrosis (aka(also known as pseudolaminar necrosis) is characterised by the cortex cell death, mainly in 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 occur as a result of glucose depletion. A pan-necrosis results as neurons as well as glial cells are damaged.
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 these cortical changes 6.
CT
Appearances of cortical laminar necrosis on CT can be subtle, appearing as gyriform changes in attenuation, both hypodense and hyperdense depending on timing. No haemorrhage or calcification is evident acutely. After a few days, gyral enhancement will be seen which typically persists for up to 3 months.
MRI
Although early cytotoxic oedema causes high signal seen on DWI with corresponding low apparent diffusion coefficient (ADC) values in the affected cortex, and cortical enhancement may be seen later, typically after 2 weeks, intrinsic T1 signal increase is the most specific imaging feature.
T1 curvilinear hyperintensities signalling laminar necrosis become evident as early as 3 to 5 days after stroke, but typically after 2 weeks, with a peak of intensity around 1month, and then slowly fades usually over 3 or so months 6-8. Occasionally it can remain visible for over a year after the insult 7,8. This T1 high signal is believed to be caused by the accumulation of denatured proteins in dying cells and/or lipid laden macrophages. Importantly it does not represent the presence of haemorrhage or calcium 6,7.
T2 wieghted images demonstrate either increased signal or iso-intensity to unaffected cortex 8.
See also
-<p><strong>Cortical laminar necrosis</strong> (aka <strong>pseudolaminar 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>- +<p><strong>Cortical laminar necrosis</strong> (also known as <strong>pseudolaminar 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>
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