Figure 1: Masslike, cortical FLAIR hyperintense signal (top row left) with heterogeneous enhancement (top row right) in the anterior left temporal lobe and right occipital lobe. No evidence of reduced diffusivity on DWI (bottom row left). This presentation is often challenging and requires an appropriate history to make the correct diagnosis as a subacute infarction can commonly be mistaken for a neoplasm. The faint T1 hyperintensity in the cortex (bottom row right) can be a clue to cortical laminar necrosis of subacute infarct.
- Interrupted flow to brain resulting in cerebral ischemia or infarction with variable neurologic deficits
- Critical disturbance in cerebral blood flow (CBF)
- Severely ischemic core
- CBF < (6-8 mL)/(100 g/min)
- Oxygen depletion, energy failure, terminal depolarization, ion homeostasis failure
- Evolution from ischemia to infarct
- Ischemic penumbra is theoretically salvageable tissue
- Focal acute neurologic deficit
- Paresis, aphasia, altered mental status
- Slightly more common in men
- 2nd most common cause of death worldwide
- Abnormalities within particular arterial distributions
- Rarely, an acute ischemic stroke may demonstrate an ill-defined cerebral lesion with mass effect, with or without parenchymal enhancement
- Subacute infarction is more likely to mimic a brain tumor.
- Often demonstrates contrast enhancement, particularly in involved areas of gray matter
- DWI may be falsely negative at the point of ADC sequence pseudonormalization
- Modality specific
- Loss of gray-white differentiation
- Hyperdense thrombosed vessel sign (commonly MCA)
- Insular ribbon sign – blurring of the insular gray-white junction with hypoattenuation
- Gyral swelling and sulcal effacement
- Hemorrhagic transformation (15-45%)
- Perfusion CT
- Infarcted tissue: prolonged mean transit time, decreased cerebral blood flow and cerebral blood volume
- Ischemic penumbra: similar to infarcted tissue but will have near normal or even increased cerebral blood volume
- CT Angiogram (CTA)
- Confirm occlusions, stenoses and collateral flow
- T1WI and T2WI
- Variable with phase and hemorrhagic transformation
- Restricted diffusion lasting 7-10 days
- Variable enhancement
- Hyperacute: intravascular enhancement
- Acute: meningeal enhancement
- Subacute: parenchymal enhancement, particularly in the involved gray matter (either cortex or basal ganglia)
- MR Angiogram (MRA)
- Identify occlusions, stenoses, and status of collateral flow
- MR Spectroscopy
- Elevated lactate and decreased NAA
- Imaging Recommendations
- Nonenhanced CT as initial study to exclude hemorrhage or focal mass
- If available get a perfusion CT and CT Angiogram for potential intravascular treatment
- If uncertain or need confirmation, obtain an MR with contrast (including DWI, GRE and possibly PWI)
- When in the subacute phase, demonstrating ring enhancement, infarction can be difficult to distinguish from tumor on imaging. Subacute lacunar infarcts, in particular, often have the appearance of small metastases. Diffusion abnormalities of subacute infarct, vascular territory of involvement, or sequelae of other prior infarcts may help to indicate infarct over tumor, but sometimes a followup MRI is the best next step in evaluation.
Contributor: Sean Dodson, MD
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Copen WA, et al. MR Perfusion Imaging in Acute Ischemic Stroke. Neuroimaging Clin N Am. 2011; 21(2):259-83.
Cunliffe CH, et al. Intracranial Lesions Mimicking Neoplasms. Arch Pathol Lab Med. 2009; 133:101-123.
Kamalian S, et al. Stroke differential diagnosis and mimics: Part 1. Applied Radiology. 2015; 44(11):26-39.
Huisman T. Tumor-like lesions of the brain. Cancer Imaging. 2009; 9(Special Issue A): S10-S13.
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