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124 - Subacute Infarct

from Section 4 - Abnormalities Without Significant Mass Effect

Published online by Cambridge University Press:  05 August 2013

Benjamin Huang
Affiliation:
University of North Carolina, Chapel Hill
Zoran Rumboldt
Affiliation:
Medical University of South Carolina
Zoran Rumboldt
Affiliation:
Medical University of South Carolina
Mauricio Castillo
Affiliation:
University of North Carolina, Chapel Hill
Benjamin Huang
Affiliation:
University of North Carolina, Chapel Hill
Andrea Rossi
Affiliation:
G. Gaslini Children's Research Hospital
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Summary

Specific Imaging Findings

The subacute period of ischemic infarcts lasts from 24 h to approximately 2 weeks. Infarcts become better defined as well-demarcated wedge-shaped areas of low density involving both gray and white matter. Mass effect with gyral swelling, compression of the adjacent ventricles, and possible herniations may initially increase but subsequently begin diminishing after approximately 1 week and usually resolve by 3 weeks. Hemorrhage is evident in up to 20% of ischemic infarcts. Between the second and third weeks, the infarct may become isodense, a phenomenon known as “fogging”.

On MRI, ADC values continue to decrease during the hyperacute and acute periods reaching the nadir at around 4 days, and then begin to rise, returning to baseline at 1–2 weeks. Thereafter, the diffusion becomes elevated. The T2 signal intensity increases over the first 4 days and remains relatively stable, while T1 signal decreases and becomes similar to the CSF in the chronic period due to encephalomalacia. Some infarcts develop gyriform cortical T1 hyperintensity in the late subacute period (approximately 2 weeks), which peaks at 1–2 months and may resolve several months later. Patchy gyriform contrast enhancement is common, appearing at 2–6 days and persisting for up to 5 months. Sometimes cortical enhancement may be the only finding in subacute infarcts.

Pertinent Clinical Information

Patients with malignant supratentorial infarctions (typically involving > 2/3 of the MCA territory) show progressive deterioration of consciousness within 24–48 h as a result of increasing edema, commonly causing subfalcine and uncal herniation. The predisposing factors include abnormalities of the ipsilateral circle of Willis and insufficient leptomeningeal collateral vessels. Conservative treatment includes pharmacologic strategies and hypothermia. Patients who fail to respond to conservative management may require decompressive hemicraniectomies. Hemorrhagic transformation is seen in 6% of ischemic strokes within 3 days, in 17–26% within 5–7 days, and in 43% by 4 weeks, but in most cases it remains asymptomatic. Symptomatic hemorrhagic transformation occurs in up to 6.8% of untreated patients and in up to 11% of cases following intra-arterial thombolytic treatment.

Type
Chapter
Information
Brain Imaging with MRI and CT
An Image Pattern Approach
, pp. 255 - 256
Publisher: Cambridge University Press
Print publication year: 2012

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References

1. Lansberg, MG, Thijs, VN, O'Brien, MW, et al. Evolution of apparent diffusion coefficient, diffusion-weighted, and T2-weighted signal intensity of acute stroke. AJNR 2001;22:637–44.Google ScholarPubMed
2. Shaefer, PW, Copen, WA, Lev, MH, et al. Diffusion-weighted imaging in acute stroke. Neuroimag Clin N Am 2005;15:503–30.CrossRefGoogle Scholar
3. Siskas, N, Lefkopoulos, A, Ioannidis, I, et al. Cortical laminar necrosis in brain infarcts: serial MRI. Neuroradiology 2003;45:283–8.CrossRefGoogle ScholarPubMed
4. Huttner, HB, Schwab, S. Malignant cerebral artery infarction: clinical characteristics, treatment strategies, and future perspectives. Lancet Neurol 2009;8:949–58.CrossRefGoogle ScholarPubMed
5. Khatri, P, Wechsler, LR, Broderic, JP. Intracranial hemorrhage associated with revascularization therapies. Stroke 2007;38:431–40.CrossRefGoogle ScholarPubMed

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