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Neuroradiology Case of the Week
Case 388
March 2009
Charles Hubeny, MD
Clinical
Presentation: A 45-year-old male, post-aortic dissection repair, presented with multiple neurological deficits.
Imaging Findings: Findings consistent with subacute ring-enhancing infarcts of the right basal ganglia with areas of early cortical laminar necrosis.
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| Figure 1: Non-contrast CT shows a large low-density lesion in the right basal ganglia as well as multiple other low-density cortical lesions especially on the right.
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| Figure 2: Flair image demonstrate high signal lesion. The lesion is not well visualize on T1 but the post-contrast T1 image shows a ring-enhancing lesion.
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Figure 3: DWI image shows abnormal increased signal in the right thalamus. The lesion on ADC does not show uniformly low-signal.
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| Figure 4:
Flair images shows high-signal lesions following the gyri. Again, the lesion is not well seen on T1 but the post contrast T1 image demonstrates gyriform enhancement.
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| Figure 5: DWI image shows abnormal increased signal. The lesions on ADC do not show uniformly low-signal.
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Diagnosis: Subacute ring-enhancing infarcts in the setting of luxury perfusion with areas of early cortical laminar necrosis
Discussion: There are many causes of ring-enhancing lesions of the brain. Schwartz, et al. [1] reviewed 221 ring-enhancing brain lesions seen on MR and reported that 40% were gliomas, 30% metastases, 8% abscesses, and 6% from multiple sclerosis. The remaining 16% include infarcts, lymphoma, non-bacterial, other non-brain tumors, other brain tumors, radiation necrosis, and miscellaneous causes.
Contrast enhancement of ring-enhancing lesions results from either or both of two processes: intravascular (vascular) and extravascular (interstitial) enhancement. The breakdown of the blood-brain-barrier results in interstitial enhancement while vascular enhancement relies on increases in blood flow or blood volume.
Ring-enhancement of necrotic neoplasms from neovascularity as well as luxury perfusion from increased circulation through an area of infarcted brain are forms of vascular enhancement. Examples of interstitial enhancement include leakage of fluid into the interstitium from low-grade fluid secreting neoplasms (hemangioblastoma, ganglioglioma, pleomorphic xanthoastrocytoma) and venous perivascular inflammation in demyelation from multiple sclerosis (MS). Abscess enhancement results from both increased vascularity and abnormal permeability.
The useful pneumonic MAGICAL DR is commonly used for the differential diagnosis ring-enhancing lesions of the brain.
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Metastasis
Abscess
Glioma, Granuloma
Infarct/Infection
Contusion
AIDS
Lymphoma
Demyelinating disease
Radiation necrosis/Resolving hematoma |
Chronic infarcts are usually low-intensity on T1 and high on T2-weighted imaging. High intensity laminar lesions on T1 can be from cortical laminar necrosis, hemorrhagic infarcts, or both in ischemic stroke. In cortical laminar necrosis the high-intensity on T1 is thought to be a result of neuronal damage and reactive tissue changes of glia and deposition of lipid-laden macrophages. Depletion of glucose in status epilepticus and depletion of oxygen ischemic stroke is the usual underlying cause of cortical laminar necrosis. The third layer of gray matter is most vulnerable to these insults. Immunosuppressive and chemotherapy have also been implicated due to hypoxia of tissue.
T1-weighted images show low-signal early in cortical laminar necrosis, most likely from tissue edema, and high-signal in late imaging due to the lipid laden macrophages.High T2-signal appears after two weeks. Proton density images also show high-signal due to increased mobile protons in the affected tissue and is more sensitive than T1. Gyriform enhancement is also common.
References:
- Schwartz KM, Erickson BJ, Lucchinetti C. Pattern of T2 hypointensity associated with ring-enhancing brain lesions can help to differentiate pathology. Neuroradiology. 2006 Mar;48(3):143-9. [PubMed]
- Smirniotopoulos JG, Murphy FM, Rushing EJ, Rees JH, Schroeder JW. Patterns of contrast enhancement in the brain and meninges. Radiographics. 2007 Mar-Apr;27(2):525-51. [PubMed]
- Komiyama M, Nishikawa M, Yasui T. Cortical laminar necrosis in brain infarcts: chronological changes on MRI. Neuroradiology. 1997 Jul;39(7):474-9. [PubMed]
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