Radiological pathology of cortical laminar necrosis

Professor Yasser Metwally
www.yassermetwally.com



INTRODUCTION

INTRODUCTION
Cortical laminar necrosis occurs as a consequence of oxygen or glucose depletion in the
watershed intracortical area in the third cortical layer, as in anoxia, hypoglycaemia, status
epilepticus, ischaemic stroke CNS vasculitis, neuro-lupus and drugs [1]. Cortical
pseudolaminar necrosis, also known as cortical laminar necrosis and simply laminar
necrosis, is the (uncontrolled) death of cells in the (cerebral) cortex of the brain in a bandlike pattern,[1] with a relative preservation of cells immediately adjacent to the meninges.
Pathologically Cortical laminar necrosis represents cytotoxic oedema affecting a particular
layer of cerebral cortex (third grey matter layer) at the acute stage and is
neuropathologically characterized by delayed selective neuronal necrosis at the acute stage
followed by reactive change of glia and deposition of fat-laden macrophages. In particular
the characteristic high intensity on precontrast Tl-weighted images in Cortical laminar



necrosis, which generally begins to appear about 2 weeks after the ictus, becomes
prominent at 1-2 months and began to fade at 3-11 months, is due to the deposition of fatladen macrophages or methemoglobin representing intracortical microhemorrhages.
Chronic brain infarcts are typically seen as low-intensity lesions on T1-weighted and highintensity lesions on T2- weighted images due to prolonged T1 and T2 values [3, 4]. In some
infarcts, high-intensity lesions are observed on precontrast T1-weighted images.
Haemorrhagic infarcts show characteristic changes of the signal intensity, similar to those
of haemorrhage, due to deoxyhaemoglobin, methohaemoglobin, and haemosiderin [7, 8].
Petechial haemorrhage may occur in cortical infarcts (cortical laminar necrosis) but cannot
explain the high-intensity laminar lesions in all patients on precontrast TI images [9]. In
general high intensity on precontrast Tl-weighted images (T1 shortening) can be due to
methaemoglobin, mucin, high protein concentration, lipid or cholesterol, calcification and
cortical laminar necrosis [6]. In ischaemic stroke, high intensity laminar lesions can be
cortical laminar necrosis, haemorrhagic infarcts (microhaemorrhage), or a combination of
the two.
The grey matter has six layers. The third is the most vulnerable to depletion of oxygen and
glucose (watershed intracortical zone). When a relatively mild ischaemic or hypoglycaemic
insult occurs, the vulnerable layers are selectively injured (selective neuronal vulnerability)
[1].
Because the third grey matter layer is the most vulnerable to anoxia and hypoglycemia,
Cortical laminar necrosis is a specific type of cortical infarction, usually seen in the setting
of anoxic encephalopathy. Other etiologies like hypoglycemia, status epilepticus and
immunosuppressive chemotherapy have been implicated.[11,12] The appearance of the MR
images in the setting of diffuse cortical laminar necrosis can be deceptive. Properly
windowed diffusion weighted imaging can be very helpful in detecting cortical laminar
necrosis, especially in the setting of anoxic-hypoxic encephalopathy in the early subacute
phase.[13] Cortical laminar necrosis in the setting of anoxic encephalopathy has a
universally poor prognosis, with most patients either progressing to brain death or
remaining in a persistent vegetative state.[12].
Boyko et al. [6] described cortical laminar necrosis in brain infarcts as linear high on
precontrast TI imags signal based on the cortical surface and becoming less intense over
time (months). In hypoxic brain damage, Precontrast Tl-weighted images revealed a
laminar hyperintensity lesion in the cortex in the late subacute stage (21-28 days) which
tended to fade after 2 months but persisted up to 11 months [9]. In laminar cortical
necrosis, cortical high intensity on precontrast Tl-weighted images generally begins to
appear about 2 weeks after the ictus, became prominent at 1-2 months and began to fade at
3 months, although it could persist up to 11 months. FLAIR images are more sensitive than
Tl weighted images to the cortical laminar lesions. Early cortical changes on day 1 showed
high intensity on T2- weighted images and low intensity on Tl-weighted images, which later
became high intensity on precontrast T1 images. This early change is due to prolonged Tl
and T2 values caused by acute ischaemic change (tissue oedema).



The cortical laminar necrosis, seen as a laminar high signal lesion on precontrast T1weighted images, was first described by Sawada et al. [10] in a patient with anoxic
encephalopathy. The cortical lesion is usually in the watershed region (watershed
intracortical zone) in this condition [9]. Cortical laminar necrosis is also reported in
ischaemic stroke [5,6]. Although Nabatame et al. [5] thought the high intensity on
precontrast T1-weighted images was due to methohaemoglobin in haemorrhagic tissue,
pathological studies revealed no haemorrhage [6, 11]. Takahashi et al. [9] reported a
patient with a cortical laminar lesion showing low intensity on T2-weighted images in the
chronic stage, which they thought due to haemosiderin.

Figure 1. Cortical laminar necrosis.



Figure 2. Cortical laminar necrosis. Early in
the disease, gross findings will be characterized
by edema and swelling. Note the swollen
glistening appearance of the cerebral cortex.
Note the vague line between cortex and
subcortical
white
matter
(arrows).
Histologically this line would correspond to an
early (laminar) band of cortical necrosis.

Figure 3. A 60-year-old woman with an anti phospholipid antibody syndrome. All images 1
month after ictus. a A Tl weighted image shows a high-intensity right occipital laminar
lesion, with low intensity in white matter. b There is intense contrast enhancement of the
grey matter, none of the white matter. c A T2-weighted image demonstrates an isointense
laminar lesion, while the white matter shows very high intensity. d A proton-density image
demonstrates the high-intensity laminar cortical lesion.



Figure 4. A 73-year-old man with speech disturbance. a At 1.5 months after
the ictus, a precontrast T1-weighted image demonstrates a high-intensity left
parietal laminar lesion (arrow). B, At 6 months, there is no high intensity and
no contrast enhancement (C), but a FLAIR image (D) still shows a highintensity laminar lesion.



Figure 5. Precontrast T1 image showing cortical laminar necrosis
demonstrated as a laminar linear cortical hyperintensity.
In cortical laminar necrosis, CT does not demonstrate haemorrhage or
calcification, and MRI also fails to demonstrate haemorrhage. Although the
mechanism of Tl shortening (precontrast T1 hyperintensity) in the cortical
laminar necrosis remains unclear, high cortical intensity on precontrast Tlweighted image (generally begins to appear about 2 weeks after the ictus,
becomes prominent at 1-2 months and began to fade at 3 months) is believed to
occur by neuronal damage and reactive tissue change, (reactive change of glia
and deposition of fat-laden macrophages) [9, 10] . On FLAIR images, cortical
laminar necrosis is demonstrated as linear cortical hyperintensity due to
increased mobile protons in the reactive tissue. A less likely explanation is that
microhaemorrhage in the cortical laminar lesion can occur in some patients,
which may contribute to Tl shortening.
On CT cortical laminar necrosis shows contrast enhancement due to
disruption of the blood-brain barrier, where loss of neurons and vascular
proliferation occur [11]. On MRI contrast enhancement occurs in the cortical
lesion with disruption of the blood-brain barrier. Parenchymal enhancement
in brain infarcts is common and is generally maximal between 3 days and 3
weeks; it disappears by 3 months [13-15]. The greater sensitivity of MRI to
changes in the blood-brain barrier results in prolonged detection of blood-



brain barrier disruption in the cortical lesion, at up to 8 months in our series.

Figure 6. MR (diffusion weighted imaging) showing gyriform increased signal
suggestive of cortical laminar necrosis


Epilepsy, metabolic disorders and Neuro-lupus

Transient radiological changes, such as hyperintense cortical lesions in T2,
FLAIR, and diffusion weighted images, have been reported in patients with
focal Neuro-lupus.2,3,4. Radiologically, Cortical laminar necrosis is
characterised by high intensity cortical lesions on T1 weighted and FLAIR
images following a gyral distribution, associated with volume loss over the
underlying cortex. Cortical laminar necrosis has been described associated
with hypoxia, metabolic disturbances, drugs, infections, and Neuro-lupus.
Cortical laminar necrosis associated with Neuro-lupus is mostly due to severe
hypoglycaemia or hypoxia or significant decreases in blood pressure during
the episodes of focal Neuro-lupus. The hypothesis that the necrosis observed in
these patients is primarily a consequence of repeated seizures is further
supported by the fact that Cortical laminar necrosis is seen in the same areas
as those displaying acute cortical oedema and hyperperfusion during the acute
phase of Neuro-lupus. Furthermore, these hyperintense lesions did not involve
separate vascular territories and occurred at a distance from the structural
lesions. The location of Cortical laminar necrosis is also concordant with the
location of continuous epileptic activity shown by surface EEG during Neurolupus.





Hypoglycemia

First described in a patient with anoxic encephalopathy, it was found later that
laminar cortical necrosis represented cytotoxic oedema affecting a particular
layer of cerebral cortex neuropathologically characterised by delayed selective
neuronal necrosis and is a consequence of hypoxic-ischaemic encephalopathy,
hypoglycaemic encephalopathy, status epilepticus and ischaemic stroke.
Mechanisms of laminar cortical necrosis are not well elucidated.

Figure 7. Cortical laminar necrosis in a patient with hypoglycemia. (A)
Diffusion- weighted MRI shows linear hyperintensities in a gyral pattern in
right parietal and insular cortices (white arrow). (B) MRI Apparent diffusion
coefficient image showing hypo intensities in these areas suggestive of
restriction of diffusion.(C) Susceptibility weighted image shows hyper
intensities within the right parietal and insular cortices without blooming
artifacts.

Figure 8. Cortical laminar necrosis in a patient with hypoglycemia (A) MRI
coronal T2-weighted image of brain showing hyperintense signals from medial
temporal lobe (thick white arrow) of right side sparing cerebellar hemispheres.
(B) MRI FLAIR images showing hyperintensities in the hippocampal region
and parahippocampal gyrus right more than the left. (C) MRI brain coronal



section T2-weighted images showing hyperintensities bilaterally in the
hippocampal region.

References
1. Graham DI (1992) Hypoxia and vascular disorders. In: Adams JH, Corsellis
JAN, Duchen LW (eds) Greenfield's neuropathology. 5 th edn. Arnold,
London, pp 153-268
2. Bryan RN, Willcott MR, Schneiders NJ, Ford 11,Derman HS (1983) Nuclear
magnetic resonance evaluation of stroke. A preliminary report. Radiology 149:
189-192
3. Sipponen JT (1984) Visualization of brain infarction with nuclear magnetic
resonance imaging. Neuroradiology 26: 387-391
4. Brant-Zawadzki M, Weinstein P, Bartkowski H, Moseley M (1987) MR
imaging and spectroscopy in clinical and experimental cerebral ischemia: a
review. AJNR 8: 39-48
5. Nabatame H, Fujimoto N, Nakamura K et al. (1990) High intensity areas on
noncontrast T'l-weighted MR images in cerebral infarction. J Comput Assist
Tomogr 14: 521-526
6. Boyko DB, Burger PC, Shelburne JD, Ingram P (1992) Non-heme
mechanisms for T1 shortening: pathologic, CT, and MR elucidation. AJNR
13: 1439-1445
7. Hecht-Leavitt C, Gomori JM, Gross man RI et al. (1986) High-field MRI of
hemorrhagic cortical infarction. AJNR 7: 581-585
8. Hesselink JR, Healy ME, Dunn WM, Rothrock JF, McCreight PHB,
Brahme F (1986) Magnetic resonance imaging of hemorrhagic cerebral
infarction. Acta Radiol [Suppl] 369: 46-48
9. Takahashi S, Higano S, Ishii K et al. (1993) Hypoxic brain damage: cortical
laminar necrosis and delayed changes in white matter at sequential MR
imaging. Radiology 189: 449-456
10. Sawada H, Udaka F, Seriu N, Shindou K, Kameyama M, Tsujimura M
(1990) MRI demonstration of cortical laminar necrosis and delayed white
matter in jury in anoxic encephalopathy. Neuro radiology 32: 319-321
11. Donaire A, Carreno M, Gomez B, Fossas P, Bargallo N, Agudo R, et al.



Cortical laminar necrosis related to prolonged focal status epilepticus. J
Neurol Neurosurg Psychiatr 2006;77:104-6.
12. Yoneda Y, Yamamoto S. Cerebral cortical laminar necrosis on diffusionweighted MRI in hypoglycaemic encephalopathy. Diab Med 2005;22:1098-100.
13. McKinney AM, Teksam M, Felice R, Casey SO, Cranford R, Truwit CL, et
al. Diffusion-weighted imaging in the setting of diffuse cortical laminar
necrosis and hypoxic-ischemic encephalopathy. AJNR Am J Neuroradiol
2004;25:1659-65.


Radiological pathology of cortical laminar necrosis

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