The Willis lecture: transient ischemic attacks, scientific method, and new realities.

Abstract

First described by Thomas Willis in 1679 and defined in the 1950s, transient ischemic attack is universally agreed to be an episode of focal neurologic deficit in a vascular distribution, sudden in onset and resolving without residual deficit in < 2 4 hours. Transient ischemic attack is diagnosed by characteristic history and absence of residua on neurologic examination. After these criteria had been accepted, regional cerebral blood flow and computed cranial tomography in the 1970s, later positron emission tomography, and even more recently, magnetic resonance imaging reveal prolonged pathophysiologic and metabolic disturbances even in persons with all the definitional characteristics of transient ischemic attack. These persistent abnormalities necessitate reexamination of the validity of the concept of transient ischemic attack. Furthermore, our group suspects that transient ischemic attack is probably only a marker, and not itself the risk factor, for the cerebral infarction which frequently follows transient ischemic attack. Additionally, the surprising frequency with which cerebral infarction, unrecognized by patient or physician, is revealed using neuroimaging techniques has created a need to redefine the categories heretofore used for diagnosis and assessment of therapy and prognosis for transient ischemic attack and cerebral infarction. (Stroke 1991;22:99-104).

Diffusion MRI in Patients With Transient Ischemic Attacks

“…28 In the Dutch TIA trial, 29,30 evidence of any cerebral infarct on CT was an independent risk factor for subsequent stroke, myocardial infarction, or vascular death. Evans and colleagues 7 reported that in TIA patients, CT-verified infarction increased the risk of death by 109% over a 10-year period following the TIA.…”

Prevalence and Associations of MRI-Demonstrated Brain Infarcts in Elderly Subjects With a History of Transient Ischemic Attack

“…It is possible that the cortical infarcts observed in our study represent the lesions in the regions related to a TIA event. However, since the determination of the duration and side of TIA may be less reliable several months or perhaps years after the initial event, 3 we did not attempt to classify the MRI infarcts as related or unrelated to TIA event. Furthermore, the clinical significance of both of these types of infarcts may be similar, 13 and therefore we evaluated all infarcts observed on MRI scans regardless of their location.…”

“…Plausible explanation for this finding include morphological changes secondary to prolonged hemodynamic disturbances resulting from TIA. 3,43 TIAs can be mimicked by migraine, arthritis, and other nonspecific symptoms. 3 It is possible that results obtained entirely from self-reports may inadvertently misclassify these nonspecific symptoms as TIA.…”

“…3,43 TIAs can be mimicked by migraine, arthritis, and other nonspecific symptoms. 3 It is possible that results obtained entirely from self-reports may inadvertently misclassify these nonspecific symptoms as TIA. 44 Our results show that the subjects with TIA were clearly different from those not reporting TIA with regard to many cerebrovascular risk factors and measures of CVD.…”

Untitled

“…In 200 consecutive patients admitted to our Acute Stroke Unit, the interval from onset to admission was exact in only 57% of cases, but by including known details of when the patient was last well, we were able to define onset to presentation as under 6 h in 50% of cases, and under 12 h in 70% of cases Group, 1990). The preliminary successes of Brott, Barsan and colleagues (Barsan et al, 1988(Barsan et al, , 1989 Toole (1991) has emphasised that the deficit may be transient but that there may be persistent metabolic and structural damage.…”