D:
–0.021 to 0.019
–0.028 to 0.014
–0.005
–0.007
–0.002
0.316
–0.042 to 0.004
p-value
Physical activity post-stroke to prevent cognitive impairment
649
ment in cognitive function may follow a similar pattern
(20), suggesting that earlier initiation, and perhaps
more specific and intensive, future interventions would
be beneficial. In addition, the intervention was based
on patient’s preferences more than the type of training
aiming at cognitive gain. Combining aerobic exercise
with other training programmes seems to achieve bet-
ter cognitive function and might be applied in future
trials (7, 21).
The lack of effect on cognition might be explained
by lack of adherence to the intervention. However,
another possible explanation for no effect on cogni-
tion is the heterogeneity of the stroke population and,
probably also, the underlying brain pathology (22).
Theoretically, the effect of physical activity on brain
function includes neurogenesis, building brain reserve,
angiogenesis and prevention of progressive small ves-
sel disease (23). Light-to-moderate physical activity
may represent a treatment strategy less likely to affect
the underlying pathology in the chronic phase. How
ever, it might halt or slow decline through building
brain reserve and thereby delay symptom onset. A po-
tential benefit on vascular pathology, to prevent cogni-
tive dysfunction due to chronic cerebral hypoperfusion
may need longer follow-up. Physical activity could
have a beneficial effect on cognitive flexibility and
brain reserve, but an effect through neurogenesis and
angiogenesis may be achieved through interventions
with higher intensities (22). Secondary prevention after
cerebrovascular disease involves both pharmacological
treatment and interventions for behaviourally modi-
fiable risk factors (24). A multimodal individualized
intervention including optimal medication, dietary,
social and cognitive stimulation in addition to physical
activity might also be needed to improve cognition
after stroke, perhaps with longer follow-up (25–27).
Post-stroke, there is also a wide spectrum of
neuropsychological manifestations. Apparent brain
damage gives rise to different cognitive deficits, es-
pecially executive function, attention and processing
speed and working memory (28, 29). It is a limitation
that HADS, MMSE and the Trail Making Tests are
primarily designed as screening tools and might not be
sensitive to detect changes that occur during follow-up
after stroke. Hence, future research should investigate
the psychometric properties of these measures in the
stroke population. Furthermore, the study population
may, due to the rather high mean age, have been too
heterogeneous regarding both underlying additional
degeneration and comorbidities. In addition, the study
was designed or powered for a potential effect on
functional outcome, and length of education was not
registered. Furthermore, functional impairments in
the dominant arm/hand may have affected the results
J Rehabil Med 51, 2019