Response to Professor Kawada

Sirs, We thank Professor Kawada [1] for his interest in our study regarding ongoing impairments following transient ischaemic attack (TIA) [2]. We are particularly encouraged that he recognized the need to improve care for TIA patients presenting with signs of fatigue, psychological impairment or cognitive impairment. The study of impairments post-TIA is currently under-researched. Indeed, the findings of our systematic review [3], which aimed to establish the prevalence of impairments post-TIA/minor stroke, were inconclusive because the quality of the included studies was not high. Our review identified the limitations of existing research and our current study was conducted in response to this gap in the literature. We addressed these limitations through subsequently conducting a retrospective cohort study which has a large sample size, included matched controls and adjusted for confounding variables and the presence of impairments preTIA. We believe this robust study design provides reliable estimates to measure the association between TIA and subsequent impairments. However, future research is required to determine the incidence, prevalence and natural history of impairments post-TIA. In response to Professor Kawada’s second comment regarding the possibility of impaired cognitive function being present prior to TIA, for this reason we purposefully adjusted for the presence of cognitive impairment prior to TIA in our main analysis. Furthermore, we conducted an exploratory analysis which excluded people with cognitive impairment recorded prior to TIA. In this exploratory analysis the association between TIA and cognitive impairment remained; indeed, the adjusted hazard ratio actually increased from 1.45 (95% confidence interval 1.28–1.65) to 1.54 (95% confidence interval 1.35–1.77). However, as we discussed in the limitations, it is possible that cognitive impairment prior to TIA may have been undetected or not recorded. We agree that caution should also be paid regarding the inclusion of patients with dementia; however, only 4% and 3.4% of TIA patients and controls, respectively, had dementia recorded. The mechanism of residual impairments post-TIA is unknown and in our discussion we hypothesized three potential explanations: (i) the presence of cerebral infarction, i.e. minor stroke misdiagnosed; (ii) undetected microinfarcts; and (iii) psychological impact of the event. An alternative hypothesis could be that cognitive impairment is caused by vascular risk factors which predispose to TIA. However, a systematic review by Blom et al. [4] found inconsistent results for the association between vascular risk factors and cognitive decline in patients with dementia. We agree that the mechanism of cognitive impairment necessitates further research and this information may facilitate the development of an intervention to improve cognition in TIA patients.