Brain, Vol. 119, No. 1, 239-248, 1996
© 1996 Oxford University Press
research-article |
In vivo MRI and its histological correlates in acute adoptive transfer experimental allergic encephalomyelitis
Quantification of inflammation and oedema
1Departments of Neurology Würzburg, Germany 2Departments of Physics, Julius-Maximilians-University Würzburg, Germany 3Institute of Brain Research Vienna, Austria
Correspondence to:
Sean P. Morrissey, Neurologische Universitätsklinik und Poliklinik, Josef-Schneider Straße 11, D-97080 Würzburg, Germany
In vivo proton MRI was carried out on a 7 Tesla system at 23 day intervals over 10 days in rats with adoptive transfer experimental allergic encephalomyelitis (AT-EAE), an animal model of some aspects of multiple sclerosis. In order to assess the integrity of the blood-brain barrier (BBB), MRI was performed by acquiring quantitative MR-relaxation time T1 images of the AT-EAE rat brain before and after i.v. injection of gadolinium-diethylene triaminepentaacetic acid (Gd-DTPA) using an ultrafast MRI technique. The MRI findings were compared with the immunohistochemical stain of T cells, macrophages and albumin and, in addition, apoptosis of T cells was assessed using in situ nick translation (ISNT). Prior to injection of Gd-DTPA, an increase of T1 times in the brain of the AT-EAE rats was observed, which paralleled the time course of albumin in histological sections. These were MRI findings observed well before the onset of major cellular infiltration and before the onset of clinical signs. After i.v. injection of Gd-DTPA the observed decrease of T1 times paralleled macrophage activation, and less closely T-cell infiltration. Our results provide evidence that using MRI, it is possible to assess quantitatively the breach of the BBB and to distinguish in vivo between two components of the early phase of the lesion, inflammatory infiltrates and vasogenic oedema.
multiple sclerosis; experimental allergic encephalomyelitis; MRI; Gd-DTPA; blood-brain barrier
Received January 24, 1995. Revised July 5, 1995. Accepted September 7, 1995.
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