Cortical laminar necrosis

Cortical laminar necrosis, also known as pseudolaminar necrosis, is necrosis of neurones 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 hypoglycaemia. 

It should not be confused with intrinsic T1 signal within the cortex frequently encountered following cerebral infarction ¹³. 

Terminology

Cortical laminar necrosis and pseudolaminar necrosis, are often used interchangeably, although some publications claim a distinction ^9,10.Whether on not this is a meaningful distinction to make is probably debatable, but unfortunately, both terms are often used inappropriately for a broader range of ischaemic events which result in areas of cortical T1 intrinsic hyperintensity, or cortical enhancement, or eventual cortical dystrophic calcification in the weeks following a run of the mill "full-thickness" cerebral infarct; this is simply incorrect makes the term meaningless ¹³. 

Although the underlying reason for changes at a cellular level is presumably the same (i.e. liquefactive necrosis involving 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 ischaemic 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 rather reserved for when there is isolated involvement of the correctcortex. 

Clinical presentation

Cortical laminar or pseudolaminar necrosis tend to be seen in patient who have had events that impair the ability to provide the brain with sufficient nutrients for its required function. This can be due to either reduced supply (e.g. hypoxia, ischaemia, and sometimes hypoglycaemia) or increased demand (e.g. status epilepticus) ¹¹.  

More specifically it is encountered in:

• cerebral hypoperfusion
  • generalised secondary to cardiac arrest or hypotension
  • watershed (borderzone) distribution due to hypotension and stenosis of relevant vessel (typically internal carotid artery)
• hypoxia
• hypoglycaemia 
• haematological diseases such as severe anaemia
• status epilepticus (as the brain demands more glucose and oxygen)
• cyanide poisoning¹²

Pathology

Cortical laminar necrosis occurs as a consequence of the neurones within the cortex being far more metabolically active than glial cells or adjacent white matter. Additionally, there is selective vulnerability of certain layers of the cerebral neocortex to metabolic stress, as well as certain regions of the brain (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 ischaemia/hypoxia, with the first and sixth being of intermediate vulnerability ¹³. 

The distribution of involvement tends to favour the banks (sides) and base of sulci rather than the gyral crests ¹³. 

In the chronic phase, there is limited subcortical white matter involvement characterised by iron deposition rather than encephalomalacia as is seen in cerebral infarcts ¹³. 

The selective vulnerability of grey 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.

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 one month, 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 ^6,7,13.

T2 weighted images demonstrate either increased signal or iso-intensity to unaffected cortex ⁸.

See also

• hypoxic-ischaemic brain injury