Abnormalities of cerebral perfusion in multiple sclerosis

W Rashid, L M Parkes, G T Ingle, D T Chard, A T Toosy, D R Altmann, M R Symms, P S Tofts, A J Thompson, D H Miller, W Rashid, L M Parkes, G T Ingle, D T Chard, A T Toosy, D R Altmann, M R Symms, P S Tofts, A J Thompson, D H Miller

Abstract

Background: Measuring perfusion provides a potential indication of metabolic activity in brain tissue. Studies in multiple sclerosis (MS) have identified areas of decreased perfusion in grey matter (GM) and white matter (WM), but the pattern in clinical subgroups is unclear.

Objectives: This study investigated perfusion changes in differing MS clinical subgroups on or off beta-interferon therapy using a non-invasive MRI technique (continuous arterial spin labelling) to investigate whether different clinical MS subtypes displayed perfusion changes and whether this could give a further insight into the pathological mechanisms involved.

Methods: Sixty patients (21 relapsing remitting, 14 secondary progressive, 12 primary progressive, 13 benign) and 34 healthy controls were compared. Statistical parametric mapping (SPM '99) was used to investigate regional variations in perfusion in both GM and WM. Global WM perfusion was derived by segmenting WM from images using T(1) relaxation times.

Results: Regions of lower perfusion in predominantly GM were observed in the primary and secondary progressive cohorts, particularly in the thalamus. Increased WM perfusion was seen in relapsing remitting and secondary progressive cohorts.

Conclusions: Low GM perfusion could reflect decreased metabolism secondary to neuronal and axonal loss or dysfunction with a predilection for progressive forms of MS. Increased WM perfusion may indicate increased metabolic activity possibly due to increased cellularity and inflammation. Improved methodology and longitudinal studies may enable further investigation of regional and temporal changes, and their relationship with physical and cognitive impairment.

References

    1. N Engl J Med. 1998 Jan 29;338(5):278-85
    1. Magn Reson Med. 1990 Apr;14(1):154-9
    1. Brain. 1998 Jan;121 ( Pt 1):103-13
    1. Mult Scler. 1998 Jun;4(3):93-8
    1. Radiology. 1999 May;211(2):489-95
    1. Ann Neurol. 1999 Aug;46(2):197-206
    1. Curr Opin Neurol. 1999 Jun;12(3):295-302
    1. Neurology. 2000 Feb 8;54(3):558-64
    1. Ann Neurol. 2000 Mar;47(3):391-5
    1. J Magn Reson Imaging. 2000 May;11(5):495-505
    1. Brain. 2000 Nov;123 ( Pt 11):2321-37
    1. Stroke. 2000 Nov;31(11):2723-31
    1. Mult Scler. 2002 Apr;8(2):93-7
    1. Magn Reson Med. 2002 Jul;48(1):27-41
    1. J Neurol. 2002 Aug;249(8):1072-7
    1. Eur J Nucl Med Mol Imaging. 2002 Oct;29(10):1342-8
    1. Ann Neurol. 1991 Jan;29(1):53-62
    1. J Neurol Neurosurg Psychiatry. 1991 Feb;54(2):110-5
    1. Magn Reson Med. 1992 Jan;23(1):37-45
    1. Neurology. 1992 Jan;42(1):60-3
    1. Eur Neurol. 1993;33(2):163-7
    1. J Magn Reson Imaging. 1994 Sep-Oct;4(5):681-91
    1. Brain. 1996 Jun;119 ( Pt 3):715-22
    1. Neurology. 1996 Apr;46(4):907-11
    1. J Cereb Blood Flow Metab. 1996 Nov;16(6):1236-49
    1. Brain. 1996 Dec;119 ( Pt 6):2009-19
    1. Neuroimage. 1996 Oct;4(2):87-96
    1. Eur J Nucl Med Mol Imaging. 2002 Nov;29(11):1447-54
    1. Ann Neurol. 2002 Nov;52(5):650-3
    1. J Neurol Sci. 2002 Nov 15;203-204:215-9
    1. Mult Scler. 2003 Feb;9(1):102-7
    1. Eur J Neurol. 2003 May;10(3):257-64
    1. Acta Neuropathol Suppl. 1981;7:176-8
    1. Ann Neurol. 1983 Mar;13(3):227-31
    1. Neurology. 1983 Nov;33(11):1444-52
    1. J Neurol Neurosurg Psychiatry. 1984 Nov;47(11):1182-91
    1. Magn Reson Med. 1989 Sep;11(3):331-6
    1. J Neurol Neurosurg Psychiatry. 1989 Aug;52(8):1019-20
    1. Brain. 1990 Feb;113 ( Pt 1):27-47
    1. Neurology. 1998 Jan;50(1):238-44

Source: PubMed

Подписаться