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“Sick” MRI syndrome
  1. M J Kushner
  1. Eastern Carolina University School of Medicine and the Wilson Neurology Center, Wilson, North Carolina, USA

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    At this time, MRI is a better indicator of tissue outcome rather than clinical destiny

    The report by Marx et al (this issue, pp572–575)1 joins the ever growing literature dealing with multiparametric MRI studies of tissue characteristics in stroke. Markers of ischaemic perturbations of cell homoeostasis and perfusion, including changes in diffusion and perfusion weighted imaging (DWI and PWI), seem now to allow human stroke studies more analogous to animal models. Although debate rages, current optimism maintains that MRI delineates the three main tissue compartments in ischaemia. Conceptually these compartments are (a) irreversibly damaged tissue, (b) minimally disrupted tissue destined for eventual recovery, and (c) the “penumbra” or “borderzone” or “at-risk” region where outcome hangs in the balance between irrevocable damage and some degree of recovery, and which may be amenable to treatment.2

    Recent human data suggest that DWI and DWI-PWI mismatches strongly predict tissue outcome after ischaemia.3 Despite this progress in neuroimaging, clinical and clinicopathological MRI correlation has lagged behind. Reconciling recent MRI studies of stroke with each other is not straightforward, and it is also daunting to relate them to previous investigations of stroke using other reliable structural and haemometabolic techniques.4,5 To date, human MRI studies have used many different paradigms, and this situation stands in contrast with standardised models found in the animal stroke literature. Variations in clinical criteria, imaging protocols, and myriad other factors introduce obvious confounding influences in these studies, and it should be assumed that lack of standardised approaches can only increase exposure to not so obvious bias.

    Marx et al1 report a relatively high incidence of DWI changes following posterior circulation ischaemia where the clinical syndrome actually was transient or reversible. DWI alterations tended to be more prominent with longer lasting ischaemic symptoms yet were detected despite ultimate clinical recovery. This bears mention, indeed, for one would expect the observed DWI changes to bode ill when in actuality full recovery was the case. This represents a potential quandary: how should one reconcile a “sick” MRI with a healthy patient? A simple explanation may be that, at this time, MRI is a better indicator of tissue outcome rather than clinical destiny. If future reports invoke MRI as an indicator of clinical outcome, or as a marker of the impact of therapeutic intervention, then data will be needed across the full spectrum of stroke severity from fixed deficits to transient syndromes. Standardised study designs are needed so that the true utility of functional MRI is established in both natural history and interventional studies of stroke. Consensus on this score would be useful now, for the widespread availability of MRI, in contrast with other techniques such as PET or SPECT, suggests that this literature will continue to proliferate.

    While this field remains in flux, clinical neurology should take note. At a minimum, these MRI markers of ischaemia must be regarded as new harbingers in the menagerie threatening haemometabolic risk, and attention must be paid. Their appearance should spur the clinician to redouble efforts to apply available medical and surgical treatments, whether they be acute, or pre-emptive and prophylactic, to address treatable haemorheological and haemodynamic abnormalities.

    At this time, MRI is a better indicator of tissue outcome rather than clinical destiny