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  • 1
    ISSN: 1432-1920
    Keywords: Magnetic resonance imaging ; Spinal cord infarction ; Gadolinium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Spinal cord infarcts are rare. We report serial MRI studies of a patient with a clinically diagnosed spontaneous spinal cord infarct. The usefulness of gadolinium diethylenetriaminepentaacetic acid-dimeglumine (Gd-DTPA) enhancement is also discussed. Serial MRI with Gd-DTPA is useful to diagnose the spinal cord infarction.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1920
    Keywords: Key words Infarcts ; brain ; Basal ganglia ; Cerebellum ; Magnetic resonance imaging ; T1 shortening
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Our purpose was to investigate nonhaemorrhagic infarcts with a short T1 in the cerebellum and basal ganglia. We carried out repeat MRI on 12 patients with infarcts in the cerebellum or basal ganglia with a short T1. Cerebellar cortical lesions showed high signal on T1-weighted spin-echo images beginning at 2 weeks, which became prominent from 3 weeks to 2 months, and persisted for as long as 14 months after the ictus. The basal ganglia lesions demonstrated slightly high signal from a week after the ictus, which became more intense thereafter. Signal intensity began to fade gradually after 2 months. High signal could be seen at the periphery until 5 months, and then disappeared, while low or isointense signal, seen in the central portion from day 20, persisted thereafter.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Neuroradiology 39 (1997), S. 474-479 
    ISSN: 1432-1920
    Keywords: Key words Brain infarcts ; Cortical laminar necrosis ; Magnetic resonance imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We studied the MRI characteristics of cortical laminar necrosis in ischaemic stroke. We reviewed 13 patients with cortical laminar high signal on T1-weighted images to analyse the chronological changes in signal intensity and contrast enhancement. High-density cortical lesions began to appear on T1-weighted images about 2 weeks after the ictus. At 1–2 months they were prominent. They began to fade from 3 months but could be seen up to 11 months. These cortical lesions showed isointensity or high intensity on T2-weighted images and did not show low intensity at any stage. Contrast enhancement of the laminar lesions was prominent at 1–2 months and became less apparent from 3 months, but could be seen up to 8 months.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Neuroradiology 40 (1998), S. 771-777 
    ISSN: 1432-1920
    Keywords: Key words Brain infarction ; Contrast enhancement ; Cortical laminar necrosis ; FLAIR images ; Magnetic resonance imaging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract To examine the chronological changes characteristic of cortical laminar necrosis caused by brain infarction, 16 patients were repeatedly examined using T1-, T2-weighted spin-echo, T2*-weighted gradient echo, fluid attenuated inversion recovery (FLAIR) images, and contrast enhanced T1-weighted images at 1.0 or 1.5 T. High intensity cortical lesions were visible on the T1-weighted images from 2 weeks after ictus and became prominent at 1 to 3 months, then became less apparent, but occasionally remained at high intensity for 2 years. High intensity cortical lesions on FLAIR images became prominent from 1 month, and then became less prominent from 1 year, but occasionally remained at high intensity for 2 years. Subcortical lesions did not display high intensity on T1-weighted images at any stage. On FLAIR images, subcortical lesions initially showed slightly high intensity and then low intensity from 6 months due to encephalomalacia. Cortical lesions showed prominent contrast enhancement from 2 weeks to 3 months, but subcortical lesions were prominent from 2 weeks only up to 1 month. T2*-weighted images disclosed haemosiderin in 3 of 7 patients, but there was no correlation with cortical short T1 lesions. Cortical laminar necrosis showed characteristic chronological signal changes on T1-weighted images and FLAIR images. Cortical short T1 lesions were found not to be caused by haemorrhagic infarction.
    Type of Medium: Electronic Resource
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