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Neuroradiology Case of the Week

Case 57

Ravinder Sidhu MD, Ramon DeGuzman MD,
and P-L Westesson MD, PhD, DDS

Clinical Presentation: A 58-year-old male with history of diabetes and renal failure presented with mental status changes.

Radiological Findings: Non-contrast enhanced CT head did not reveal any abnormality. T2-weighted MR and FLAIR images showed patchy hyperintensities in the right posterior temporal and parietal region (Fig. 1A&B). On T1-weighted MR images, these hyperintensities were isointense to gray matter. Post-contrast MR images did not show significant enhancement (Fig. 2A&B). Three month follow-up MR revealed gyriform increased T1 signal areas in the right temporal and parietal region. Corresponding areas were dark on T2-weighted MR and FLAIR images (Fig. 3A-C).

Diagnosis: Cortical laminar necrosis

Discussion:  Chronic brain infarcts are typically seen as low-intensity lesions on T1-weighted and high-intensity lesions on T2-weighted MR images due to prolonged T1 and T2 values [1,2]. In some infarcts, high-intensity lesions may be seen on T1-weighted images. High intensity lesions on T1-weighted MR images can be due to methaemoglobin, mucin, high protein concentration, lipid or cholesterol, calcification and cortical laminar necrosis. In ischemic stroke, high intensity laminar lesions can be cortical laminar necrosis, hemorrhagic infarcts, or a combination of the two. Initially thought to be caused by hemorrhagic infarction, histopathological examination has demonstrated these cortical short T1 lesions to be cortical laminar necrosis without hemorrhage or calcification. Although, the mechanism of T1 shortening in cortical laminar necrosis remains unclear, high cortical intensity on a T1-weighted image is believed to occur by neuronal damage and reactive tissue change of glia and deposition of fat-laden macrophages [3].
   The gray matter has six layers. The third layer is the most vulnerable to depletion of oxygen and glucose. Cortical laminar necrosis is a specific type of cortical infarction, which usually develops as a result of generalized hypoxia rather than a local vascular abnormality. Depletion of oxygen or glucose as in anoxia, hypoglycemia, status epilepticus, and ischemic stroke has been attributed as an underlying cause of cortical laminar necrosis. Immunosuppressive therapy (cyclosporin A and FK506), and polychemotherapy (vincristine and methotrexate) have been observed to cause laminar necrosis due to hypoxic-ischemic-insult. Hypoxic insult leads to death of neurons, glia and blood vessels along with degradation of proteins [4].
   The cortical laminar necrosis, seen as a laminar high-signal lesion on T1-weighted MR images, was first described by Swada et al. in a patient of anoxic encephalopathy [5]. Early cortical changes usually show low signal intensity on T1-weighted, which could be due to acute ischemic changes (tissue edema). Usually, cortical high intensity lesions on both T1-weighted and FLAIR images appear 2 weeks after the ictus indicating short T1 and long T2 lesions. Proton-density images are more sensitive than T1-weighted MR images. On proton-density images, cortical laminar necrosis may be seen as high intensity due to increased mobile protons in the reactive tissue [6].
   To conclude, cortical laminar necrosis shows characteristic chronological signal intensity changes, and T1-weighted, FLAIR and proton-density MR images are especially helpful in depicting these changes.

References:

1. Sipponen JT. Visualization of brain infarction with nuclear magnetic resonance imaging. Neuroradiology 1984; 26:387-391.
2. Brant-Zawadzki M, Weinstein P, Bartkowski H, Moseley M. MR imaging and spectroscopy in clinical and experimental cerebral ischemia: a review. AJNR Am J Neuroradiol 1987; 8:39-48.
3. Boyko OB, Burger PC, Shelburne JD, Ingram P. Non-heme mechanisms for T1 shortening: pathologic, CT, and MR elucidation. AJNR Am J Neuroradiol 1992; 13:1439-1445.
4. Bargallo N, Burrel M, Berenguer J, Cofan F, Bunesch L, Mercader M. Cortical laminar necrosis caused by immunosuppresive therapy and chemotherapy. AJNR Am J Neuroradiol 2000; 21:479-484.
5. Sawada H, Udaka F, Seriu N, Shindou K, Kameyama M, Tsujimura M. MRI demonstration of cortical laminar necrosis and delayed white matter injury in anoxic encephalopathy. Neuroradiology 1990; 32:319-321.
6. Komiyama M, Nishikawa M, Yasui T. Cortical laminar necrosis in brain infarcts: chronological changes on MRI. Neuroradiology 1997; 39:474-479.