Radiological pathology of cortical laminar necrosis


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Radiological pathology of cortical laminar necrosis

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Radiological pathology of cortical laminar necrosis

  1. 1. Professor Yasser Metwally  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
  2. 2. Professor Yasser Metwally 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).
  3. 3. Professor Yasser Metwally 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.
  4. 4. Professor Yasser Metwally 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.
  5. 5. Professor Yasser Metwally 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.
  6. 6. Professor Yasser Metwally 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-
  7. 7. Professor Yasser Metwally 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.
  8. 8. Professor Yasser Metwally  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
  9. 9. Professor Yasser Metwally 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.
  10. 10. Professor Yasser Metwally 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.