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MR evaluation of brain iron in children with cerebral infarction
P A Cross1, S W Atlas, R I Grossman
1Department of Radiology, Hospital of the University of Pennsylvania, Philadelphia 19104.
Insights
Infants and young children with cerebral infarction often show increased brain iron. This finding is nonspecific and may have implications for understanding and treating ischemic brain injury.
Area of Science:
- Neurology
- Pediatric Neurology
- Neuroimaging
Background:
- Young children and infants typically have minimal detectable brain iron.
- Increased iron deposition is observed in various neurological conditions.
Purpose of the Study:
- To evaluate brain iron patterns in young patients with cerebral infarctions.
- To understand the neuropathology of increased iron deposition post-infarction.
Main Methods:
- Analyzed 23 MRI scans from 20 patients under 6 years old with cerebral infarctions.
- Assessed infarct characteristics and nonheme iron deposition in specific brain regions.
- Utilized spin-echo sequences at 1.5 T, 1 day to 4 years post-infarction.
Main Results:
- Sixteen of 20 (80%) infarctions were associated with increased brain iron.
- Unilateral iron deposition correlated with ipsilateral infarctions in 6 of 7 cases.
- Infarct location (deep vs. cortical) and age did not significantly influence iron patterns.
Conclusions:
- Increased brain iron is a common, nonspecific finding associated with cerebral infarction in young children.
- This iron deposition is not indicative of movement disorders.
- Iron accumulation may result from interrupted transport or direct cell injury, potentially exacerbating ischemic brain injury.
Abstract:
Young children and infants normally have essentially no detectable brain iron. We evaluated brain iron patterns on 23 MR scans in 20 patients under 6 years of age with clinical and MR-documented cerebral infarctions in an attempt to further understand the neuropathologic phenomenon of increased iron deposition, which has been observed in other disease states. MR was performed at 1.5 T with spin-echo sequences from 1 day to 4 years after infarction. MR scans were interpreted without knowledge of clinical information and were assessed for (1) location and character (i.e., bland or hemorrhagic) of infarct, and (2) nonheme iron (i.e., marked hypointensity on long TR/TE images) in the basal ganglia, red nuclei, substantia nigra, thalami, dentate nuclei, and deep white matter. Sixteen of 20 infarctions were associated with increased iron. Six of seven cases with unilateral iron deposition had ipsilateral infarctions. The location (deep versus cortical) and age of the infarction had no apparent bearing on iron patterns. We conclude that increased brain iron is commonly associated with cerebral infarction and is nonspecific, rather than a marker of movement disorders. Since iron may arise from either interruption of transport pathways or directly from cell injury and, in fact, iron itself may propagate the tissue injury, this finding may have important clinical and pathophysiologic implications in ischemic brain injury.