In this issue of the AJNR, Rovira and colleagues (page 77) present diffusion-weighted MR findings from a series of patients after transient ischemic attacks (TIAs). Data were collected on lesions detected with diffusion-weighted MR imaging within 10 days of symptom onset in a group of 58 patients. In this study, TIA was defined as stroke symptoms that completely resolved within 24 hours. Most patients manifested lesions, either in deep parenchymal foci or involving the cortex, despite the symptom resolution. The percentage of that majority exceeds previously defined percentages in other reports.
A TIA has generally referred to a patient with clinical stroke that then resolves within the first day after onset. Colloquially this has varied greatly. For some, the time period for recovery shortens, even down to a 1-hour increment for return to a normal baseline of neurologic function. Of greater concern have been variations of definition regarding the symptoms, where for some any deficit that resolves may suffice, but for others only specific dysfunction registers. Then of course we are all faced with great variation among specialists who evaluate not only the initial set of symptoms but also the effectiveness of the recovery. Surely the neurologic examination by a neurologist will differ from that of a primary care provider or a busy emergency room doctor.
Investigation of patients with TIA with diffusion-weighted MR imaging has varied widely in the timing of image acquisition relative to the onset of symptoms. Even in Rovira et al’s study, the imaging occurred any time within the first 10 days after the neurologic event. Indeed, only a small minority of patients underwent imaging examination in the first 2 days after onset. In a previous report, the imaging occurred in the first 3 days after TIA (1). Range of timing limits the study of the precise cause of infarct and does not yet answer to the sensitivity of the technique in the first hours after onset when therapeutic interventions are under consideration. Sensitivity at early onset remains a concern, as data from our series of MR imaging in hyperacute stroke patients and from others investigators show us that a substantially low number of patients imaged very acutely will have false-negative diffusion-weighted imaging findings (2).
The duration of the transient symptoms in patients with TIA seems to correlate directly with the likelihood of positive findings on diffusion-weighted images. The current study reports average symptom duration of 1 hour for those patients without any imaging evidence of ischemia compared with 7 hours for those with a lesion on diffusion-weighted images. This reinforces the intuitive conclusion that longer standing deficits, even when they resolve, do represent more substantial insults. The current investigation should also pique our interest, because many of the lesions identified had cortical involvement. Thus, we should not consider a TIA as limited to deep perforating artery territories.
The TIA remains an important and timely health issue for us all, as it represents a leading diagnosis for emergency room visits and admissions to hospitals. Of greater concern, patients evaluated for TIA often “bounce back” with either repeat transient events, delayed permanent cerebral infarcts, or even fatalities (3). Therefore, TIA represents a prevalent, high-risk diagnosis for our patient population. However, TIA remains a diagnosis based on symptoms and their resolution, and until recently, lacking in objective findings so useful for classification, characterization, and comprehension of the underlying disease processes.
The advance of diffusion-weighted MR imaging has provided exactly this objectivity, and not surprisingly we have encountered a wide range of variations beneath the catchall term of TIA. The imaging data add needed specificity to the evaluation, for now we can distinguish those who have undergone a true transient phenomena, even when lacking image-based sequelae, from those who have had infarction, although the natural redundant neurologic pathways have quickly compensated for the loss. We must continue to pursue the application of advanced imaging of patients with TIA, perhaps for example, with evaluation of the perfusion parameters in affected regions. We must strive to define those who have ischemia that may produce infarct, and further define those lesions that will produce permanent debilitation in order to justify intervention to attempt repair. Our imperative should remain to better understand the pathologic behavior of TIAs, and importantly, to more strongly lead our clinical colleagues to the best care that can be offered to our collective patients.
References
- American Society of Neuroradiology