There is an interesting paper on symptomatic cerebral infarcts and Alzheimer’s Disease by Cho and colleagues titled ‘Importance of Symptomatic Cerebral Infarcts on Cognitive Performance in Patients with Alzheimer’s Disease’ and published under a Creative Commons Attribution Non-Commercial license here. I found this paper particularly interesting because it addresses the difficult question of how to interpret the contribution of vascular lesions on cognition in people who have Alzheimer’s Disease and comorbid vascular lesions. In the abstract, the researchers conclude that
‘Adjusting for all covariates, AD patients with symptomatic infarcts had more impairment of executive function (P < 0.05)‘
The researchers recruited subjects who were enrolled in the Alzheimer’s Disease Research Centre at Columbia University. For some of the details in the methodology, the readers are referred to other papers presumably using the same cohort. The researchers start with 1781 people diagnosed with Alzheimer’s Disease and exclude according to the presence of information about stroke (radiological or from the history) as this is the key focus for the study. They are interested in people who either have radiological evidence of infarcts, evidence from the history or both. They use these features to classify strokes as silent or symptomatic.
The included cohort with Alzheimer’s Disease had a number of characteristics including a higher prevalence of hypertension than the excluded group. A neuropsychological battery is administered in the cohort and within the study the data is used to normalise the results. They then examine a number of models incorporating the neuropsychological test results. For instance they look at the effects of silent infarcts, frontal infarcts, multiple infarcts and symptomatic infarcts after controlling for important demographic variables. The robust finding both statistically and clinically is that executive functioning is icorrelated with symptomatic infarcts. Thus there is more likely to be an impairment of executive functioning if there are symptomatic infarcts.
However looking further at the distribution of the lesions the researchers write that
‘A total of 503 infarcts were detected in the following locations: frontal 34; temporal 14; parietal 28; occipital 17; thalamus 51; basal ganglia 106; white matter 161; brainstem 27; cerebellum 32, and unclassified 33‘
A reasonable proportion of the infarcts above are in locations which can potentially interfere with the functioning of frontal-subcortical loops. What I thought this might mean was either that such lesions are more likely to occur in these regions because of a peculiarity of the neuroanatomy (vascular supply vulnerability for instance) or else these regions occupy a disproportionate volume of the brain relative to other circuits. There is one other possibility which is that executive functioning is more widely distributed through the brain than the other functions assessed meaning that it is more sensitive to injury.
One thing is clear. The researchers have used an interesting approach to a clinically important and complex question which will hopefully inform other research groups.
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