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Different Signals of Magnetic Resonance Imaging and Ultrasound from Substantia Nigra in Parkinson's Disease and Control - Is Iron the Cause?

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Szlachta K., Sadowski K., Kuliński R., Gałązka-Friedman J., Friedman A.
Acta Physica Polonica A
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2012
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vol. 121
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issue 2
454-456
EN
Motor symptoms of Parkinson's disease are caused by a progressive degeneration of substantia nigra, a small structure located deep in the brain. The cause of this process is unknown but may be related to iron mediated oxidative stress. The aim of this study was to understand the mechanism of the change of magnetic resonance and ultrasound signals found in patients with Parkinson's disease, which were attributed by several authors to an important increase of the concentration of iron in substantia nigra. USG and MRI measurements were performed on phantoms simulating human brain to which high amounts of iron were introduced. The USG signal was unaffected by insertion of iron-loaded ferritin, while it was by insertion of glial tissue. Injections of iron-loaded ferritin and iron ions to the phantoms decreased T_2 relaxation time. Our results suggest that the observed change of the signal from Parkinsonian brains is probably due to a proliferation of glia and not to an increase of the concentration of iron.
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T1 and T2 Relaxation Times from Substantia Nigra in Parkinson's Disease and Control

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Kuliński R., Szlachta K., Gałązka-Friedman J., Friedman A.
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vol. 125
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issue 4
869-871
EN
The diagnosis of Parkinson's disease, and also other neurodegenerative disorders, is based on clinical examination. Many attempts are undertaken to find a test that could confirm this clinical diagnosis. Many hopes were attributed to magnetic resonance imaging but its importance remains obscure. The aim of this study was to compare T1 and T2 relaxation times from substantia nigra of patients with clinical diagnosis of Parkinson's disease and age-matched controls. A decrease of T2 (54.5 ± 1.4 ms vs. 58.0 ± 1.5 ms) in Parkinson's disease vs. control was found with confidence level of 5%. T1 did not differ significantly between Parkinson's disease and control (624 ± 17 ms vs. 614 ± 21 ms).
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