Poststroke cognition and the fight against the hard problem: vascular neurologists, enter the arena!

See related article, pages 198–203 In this issue of Stroke, Snaphaan and de Leeuw report on their results obtained from a systematic review on poststroke memory dysfunction.1 Of the 798 articles their search strategy identified, only 5 mentioned memory testing at different poststroke intervals, only 3 studies followed patients for at least 1 year, whereas the largest study contained only 196 patients. The results of the review allow at least 2 conclusions. One is drawn by the authors, in that memory dysfunction, a key element in the “diagnosis” of poststroke dementia, does not follow a linear time course after stroke. Leys et al came to a similar conclusion with regard to poststroke dementia, which was defined as any dementia after stroke.2 Short-term studies overdiagnose cognitive poststroke dysfunction. The finding warns us against making simple models of reality when it comes to poststroke cognitive impairment, and makes us aware that we should save our patients the embarrassment of early, falsepositive predictions in this respect. The second conclusion the review allows is that our current knowledge of poststroke cognitive impairment and its longterm development is rather poor, as illustrated by the review’s data on memory dysfunction, a key element in the diagnostic criteria for dementia. The poststroke dementia studies reviewed by Leys et al, although larger and with longer follow-up by some, did not provide any detail either except for the criteria that they used for the diagnosis.2 One may question the value of studying any cognitive details when we can already make diagnoses such as vascular dementia to characterize the condition. We, physicians, are keen on making a diagnosis because it will tell us something about disease cause, spectrum of clinical manifestation, progression, and hopefully also about treatment. Exactly for those reasons we should not be misled by the concepts of “vascular dementia” (VaD) or “poststroke dementia”; these are not diagnoses but concepts that have resulted from the procedure of medical consensus. The word diagnosis implies the “identification of the nature or cause of some phenomena”; it stems from the Greek dia, meaning “through”, and gnosis, meaning “knowledge”.3 It is obvious that our “gnosis” about the relationship between the clinical syndrome defined as “dementia” and manifestations of cerebrovascular disease suffers too badly to allow the definition of a diagnosis. How can we reliably estimate a specific cause of a symptom complex if we don’t know the (time contingent?) spectrum of symptoms that follows from that specific cause? One might oppose that at least the syndrome of “subcortical ischemic vascular dementia” appears to be a homogeneous concept if not a diagnosis: cerebral small vessel disease causes lacunar infarcts and white matter hyperintensities, which are strongly associated with a homogeneous pattern of cognitive impairment.4 However, such brain lesions are also associated with the syndrome of Alzheimer disease, and the severity of dementia in subcortical ischemic vascular dementia is more strongly associated with the degree of hippocampal and cerebral atrophy than with the severity of white matter hyperintensities.4,5 So, even for this “specific” vascular type of dementia the difference between the sets of neuroimaging characteristics in use to differentiate between types of dementia is rather one of degree than of category. The same holds true for cardiovascular risk factors with respect to VaD and Alzheimer disease in general.5 Snaphaan and de Leeuw found prestroke medial temporal lobe atrophy, a predictor of Alzheimer disease, related to poststroke memory function. The “diagnostic criteria” for VaD as defined in 1992 were “intended as a guide for case definition in neuroepidemiological studies. . . . ”, but had not been validated.6 Now, almost 15 years on, they are still not validated, and the criteria were never revised. The need for uniform criteria at that time probably arose from the increasing number of studies in subjects with memory complaints, who visited an ever growing number of so-called memory clinics, and easy accessibility to CT scanning which allowed for specific causes of memory problems to be ruled out. Because most patients were older, vascular lesions were detected in varying kinds and degrees. This further increased after the wide introduction of MRI, and their strength as “independent risk factors” identified by statistical modeling. However, such procedures do not falsify the inappropriate a priori assumption about causality between these factors and cognitive impairment. Apart from the fact that we do not know the exact contribution of vascular lesions on CT or MRI to cognitive defects, we should be aware of possible relevant vascular factors causing functional rather than structural impairment, such as inadequate local cerebral blood flow, impaired cerebral autoregulation, metabolic disturbances, dysfunction on a cellular or molecular level, which may also influence cognition. Insight into the role of such factors in cognitive impairment The opinions in this editorial are not necessarily those of the editors or of the American Heart Association. From the Department of Neurology, University Hospital Maastricht, The Netherlands. Correspondence to Dr Jan Lodder, Professor of Vascular Neurology, Department of Neurology, University Hospital Maastricht, PO Box 5800 6202 AZ, Maastricht, The Netherlands. E-mail [email protected] (Stroke. 2007;38:7-8.) © 2006 American Heart Association, Inc.