Jose Gutierrez, MD, MPH
Among markers of small vessel disease, lacunar infarcts have long been associated with worse cognitive performance. Several hypotheses have been invoked to explain this association and in this Stroke article, Reijmer and his group from Netherlands add on information about these questions. In a small sample of 17 subjects without dementia but with evidence or history of stroke localized to one hemisphere. Subjects underwent 3T MRI to obtain Fractional Anisotropy and Mean Diffusivity in tracts related to the infarcts compared to homonymous tracts in the non-affected hemisphere. Measures of cognition were obtained from each participant as well as WMH load (visual rating) and tract volumes.
The authors found that the affected tracts in relationship to lacunar infracts showed decreased anisotropy and increased mean diffusivity suggestive of WM loss of integrity compared to the unaffected contralateral tracts. These measures were correlated with worse cognitive performance including verbal fluency, information processing speed and word recall test. The association remained significant for all except memory after controlling for WMH load and hemisphere side with the exception of memory. Repeating the analysis in tracts not containing the infarcts did not reproduce these associations.
These are exciting results, although caution is advised due to its limited sample size. Some questions arise that might be worth exploring. What are the effects of cognition in tracts that are not known to play a role in the cognition, for example, primary motor cortex? Would these lesions be related to worse cognition? Some potential etiologies of lacunar infarcts include microatheroma, embolism or branch occlusive disease, is the etiology of a lacunar infarct important in determining the extent to which white matter is disrupted in the affected tracts? Is wallerian degeneration the explanation for the decreased fractional anisotropy and increased mean diffusivity in the surroundings of an infarct or could there be a role for perilesional inflammation? These questions seem important because understanding the pathophysiology of this cascade might offer some potential target to intervene and blunt the increasing prevalence of vascular cognitive impairment.