Cortical laminar necrosis
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Cortical laminar necrosis, also known as pseudolaminar necrosis, is necrosis of neurons in the cortex of the brain in situations when the supply of oxygen and glucose is inadequate to meet regional demands. This is often encountered in cardiac arrest, global hypoxia and hypoglycemia.
It should not be confused with intrinsic T1 signal within the cortex frequently encountered following cerebral infarction 13.
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Cortical laminar necrosis and pseudolaminar necrosis are often used interchangeably, although some publications claim a distinction 9,10. Whether or not this is a meaningful distinction to make is probably debatable. Still, unfortunately, both terms are often misused for a broader range of ischemic events which result in areas of cortical T1 intrinsic hyperintensity, cortical enhancement, or eventual cortical dystrophic calcification in the weeks following a run-of-the-mill "full-thickness" cerebral infarct; this is incorrect and makes the term meaningless 13.
Although the underlying reason for changes at a cellular level is presumably the same (i.e. liquefactive necrosis involving the cortex with an influx of monocytes and phagocytosis of cellular debris), it is the overall pattern of cellular damage (i.e. restricted to the cortex) that distinguishes cortical laminar and pseudolaminar necrosis from other more regional forms of ischemic damage (e.g. thromboembolic cerebral infarction) 10.
These terms should, therefore, not be used in the setting of an infarct, even though similar pathological changes are seen at the margins of an infarct 13, but somewhat reserved for when there is isolated involvement of the cortex.
Cortical laminar or pseudolaminar necrosis tends to be seen in a patient who has had events that impair the brain's ability to provide sufficient nutrients for its required function. This can be due to either reduced supply (e.g. hypoxia, ischemia, and sometimes hypoglycemia) or increased demand (e.g. status epilepticus) 11.
More specifically, it is encountered in:
- cerebral hypoperfusion
- generalized secondary to cardiac arrest or hypotension
- watershed (border zone) distribution due to hypotension and stenosis of the relevant vessel (typically internal carotid artery)
- hematological diseases such as severe anemia
- status epilepticus (as the brain demands more glucose and oxygen)
- cyanide poisoning12
Cortical laminar necrosis occurs due to the neurons within the cortex being far more metabolically active than glial cells or adjacent white matter. Additionally, there is the selective vulnerability of specific layers of the cerebral neocortex to metabolic stress and certain brain regions (e.g. primary visual cortex and perirolandic cortex). The third layer is most vulnerable, whereas the second and fourth layers are far more resilient to ischemia/hypoxia, with the first and sixth being of intermediate vulnerability 13.
The distribution of involvement tends to favor the banks (sides) and base of sulci rather than the gyral crests 13.
In the chronic phase, there is limited subcortical white matter involvement characterized by iron deposition rather than encephalomalacia, as seen in cerebral infarcts 13.
The selective vulnerability of grey matter may be due to higher metabolic demand and denser concentrations of receptors for excitatory amino acids released after an anoxic-ischemic event.
Laminar necrosis may be identified within hours of the anoxic-ischemic event. DWI is superior to conventional MRI sequences in the acute phase to distinguish these cortical changes 6.
Appearances of cortical laminar necrosis on CT can be subtle, appearing as gyriform changes in attenuation, both hypodense and hyperdense depending on timing. No hemorrhage or calcification is evident acutely. After a few days, gyral enhancement will be seen, which typically persists for up to 3 months.
Although early cytotoxic edema causes a high signal on DWI with corresponding low apparent diffusion coefficient (ADC) values in the affected cortex, and cortical enhancement may be seen later, typically after two weeks, intrinsic T1 signal increase is the most specific imaging feature.
T1 curvilinear hyperintensities signaling laminar necrosis become evident as early as 3 to 5 days after stroke, but typically after two weeks, with a peak of intensity around one month, and then slowly fades, usually over three 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 hemorrhage or calcium 6,7,13.
T2 weighted images demonstrate either increased signal or iso-intensity to unaffected cortex 8.
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