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  • Brain oedema  (2)
  • intracranial pressure rebound  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Acta neurochirurgica 104 (1990), S. 126-135 
    ISSN: 0942-0940
    Keywords: Magnetic resonance imaging ; intracranial mass lesion ; intracranial pressure rebound ; brain oedema
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The rebound of intracranial pressure (ICP) occurring after decompression of an intracranial mass lesion was studied in an epidural balloon compression model. Intracranial morphology and brain tissue water content were assessed with magnetic resonance imaging (MRI). Fast and slow components of the transverse relaxation time (T2) were used as indicators of brain oedema development. During balloon compression a progressive prolongation of both the fast and the slow T2 components took place. Following deflation of the balloon both components increased rapidly, particularly the slow-T2. The MR scans displayed progressive occlusion of the aqueduct, and obliteration of the ambient and pontine cisterns. The changes in morphology and in water content after decompression had largely the same time course as the development of the rebound of ICP. In contrast, no changes in morphology and tissue water content occurred after hydrostatic brain compression achieved by subarachnoid fluid infusion. The findings suggest that the intracranial pressure rebound is caused by cerebral oedema accumulated during and particularly in the recirculation phase after an ischaemic injury of adequate intensity and adequate duration.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1084
    Keywords: Magnetic resonance imaging ; Middle cerebral occlusion ; Brain oedema ; Cerebral infarct ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The development of ischaemic brain oedema caused by middle cerebral artery (MCA) occlusion was studied by serial magnetic resonance imaging (MRI) in rats. Multiple spin echo sequences were used with TR = 1500 ms and TE = 30–240 ms (8 echos). Subtraction images were obtained by subtracting the last three echos from the first echo. Fourteen rats were studied 3, 6, and 12 h and 1, 1.5, 3, 4, 6, and 8 days after MCA occlusion, and 2 of them also 3 and 6 weeks later. Two T2 components could be separated, a fast one representing bound water and a slow one representing free bulk water. MR showed T2 prolongation even on the first examination, and the highest values were observed 24h after occlusion. The subsequent examinations showed a slow reduction in oedema. MR studies 3 and 6 weeks after occlusion revealed an area of very long T2, which correlated well with infarction shown by histology. The subtraction images demonstrated both the infarct location and the oedematous changes in the surrounding uninfarcted tissue. MRI imaging employing T2 components and subtraction images appears to be a valuable method for observing the time course of the development and resolution of oedema in cerebral infarction.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1084
    Keywords: Brain oedema ; Dehydration ; Magnetic resonance imaging ; Middle cerebral artery occlusion ; Rat
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Mannitol and furosemide treatment of ischaemic brain oedema caused by middle cerebral artery occlusion (MCAO) was studied by MRI in 87 rats. MRI was performed in all rats before and 30–360 min after drug infusion. The examinations were performed in the presence of an intact blood-brain barrier (BBB) 6 h after MCAO, and 3 days after MCAO at the time of maximal disruption of the BBB. Spin echo (SE) sequences were used for imaging and for determination of the relaxation times T1 and T2. Subtraction images were constructed. Furosemide dehydrated healthy and ischaemic brain. Mannitol had no dehydrating effect on healthy brain tissue. However, when the BBB was disrupted in severe oedema mannitol produced a decrease in water content, a shortening of T1 and T2, and a decrease in intracranial pressure (ICP), while in less severe oedema mannitol could increase brain water content, thus aggravating ICP. The subtraction technique allowed visualisation of the transient change in bulk in water animals with disruption of the BBB after mannitol treatment.
    Type of Medium: Electronic Resource
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