Cortical laminar necrosis

Case contributed by Dr T Fassaert

Presentation

Patient with a prior history of infarction of left frontal lobe and a known obstruction of internal carotid artery on both sides with an intact circle of Willis. Now the patient presents with semi-acute swallowing disorder and hoarseness.

Patient Data

Age: 65
Gender: Male
Modality: CT

Axial slice shows a large tissue defect left frontal, due to an infarction. Retrospectively there is subtle swelling of the right occipital lobe with diminished grey-white matter differentiation.

MRI was obtained 7 weeks later

Modality: MRI

A large defect of left frontal lobe and some small defects in cerebellum are preexistent. 

In right occipital lobe a new abnormality is present:

  • Enlarged arachnoidal spaces indicating tissue loss
  • Cortical thinning an loss of subcortical white matter
  • Typical guirlande T1 hyperintensity of cortex and subcortical T2 and FLAIR hyperintensity
  • No Diffusion Restriction

Imaging findings are with subrecent infarction. The T1 shortening of the (sub)cortical tissues are typical for Cortical Laminar Necrosis.

Case Discussion

Cortical laminar necrosis is a form of ischemic brain damage. The patient profile of patients with cortical laminar necrosis is consistent with patients at risk for vascular events: elder patients, male > female, history of vascular disease of risk factors (e.g. diabetes, hypertension, hypercholesterolemia, smoking etc.). It is also reported to occur in cases with prolonged anoxia, hypoglycaemia or after status epilepticus.

The typical signal changes occur in the early and late subacute phase (e.g. weeks) and change over time: Typical imaging findings are:

  • watershed area or lobar distribution
  • tissue loss
  • subcortical hyperintensity on T2 and FLAIR with hypointensity on T1 from day 6 onwards
  • cortical hyperintensity on T1; the signal intensity peaks after 4-8 weeks and slowly diminishes (months-1.5 year)
  • cortical hyperintensity on FLAIR. Intensity increases first month and gradually decreases in the following months to a year
  • GRE/ T2*: no low signal is reported (without haemorrhage)
  • in relevant literature there is no report about DWI. In acute and early subacute phase Diffusion restriction may be expected. In our case after 7 weeks no restricted diffusion was visible suggesting the expected signal changes known with cytotoxic oedema
  • T1 imaging post Gadolinium -when obtained- may show some degree of (subcortical enhancement in the early and late subacute phase (2 weeks-6 months)

In the literature there is some debate about the pathophysiology leading to the signal changes; some authors suggest the T1-shortening might be due to haemorrhagic components or calcifications. Other case series report however no signs of haemorrhage or calcifications on imaging. Some case series include autopsy and in these no signs of haemorrhage were found as well. Based on in vivo and postmortem evaluation the T1 and FLAIR hyperintensity is thought to result from the deposition of  lipid-laden macrophages in the area of subcortical necrosis. Signal chances occur in the cortical and subcortical area, because grey matter is most vulnerable to ischaemia and hypoperfusion. Why this tissue chances occur and why in some but not all patients remains to be resolved.

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Case Information

rID: 26502
Case created: 24th Dec 2013
Last edited: 14th Sep 2015
Inclusion in quiz mode: Included

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