Prof Amy Brodtmann

Two Australian-led studies have shed new light on brain atrophy and cognitive decline in people who have had an ischaemic stroke.

Professor Amy Brodtmann and colleagues at the Florey Institute of Neuroscience and Mental Health, Melbourne, have shown that stroke survivors had significant total brain volume (TBV) loss associated with cognitive decline in the three years following a stroke.

In a study using MRI and cognitive assessments in 93 ischaemic stroke patients they found that TBV loss in stroke patients was greater than in a control group of 39 matched individuals without stroke. (mean 20.3 cm3 vs 14.2 cm3  [adjusted mean difference 7.88].

They also noted that TBV decline was greater in those stroke participants who had early cognitive impairment at three months (adjusted mean difference 10.42).

No statistically significant differences in hippocampal volume (HV) change were observed.

“Early cognitive impairment was associated greater subsequent atrophy, reflecting the combined impacts of stroke and vascular brain burden,” they reported in Frontiers in Neurology.

“ Atrophy rates could serve as a useful biomarker for trials testing interventions to reduce post-stroke secondary neurodegeneration,” they suggested.

Meanwhile, in a separate study, researchers at the Centre for Healthy Brain Ageing (CHeBA), UNSW Sydney, have characterised the trajectory and magnitude of cognitive decline after ischaemic stroke based on neuropsychological test scores obtained from nine international cohorts involving 1488  patients.

Their findings, published in Stroke, show that patients experienced a faster cognitive decline at one-three years after a stroke compared to stroke free controls. After an initial period of improvement through up to one year poststroke, decline was seen in global cognition and all cognitive domains except executive function after adjusting for age, sex, education, vascular risk factors, and stroke characteristics (−0.053 SD/year [95% CI, −0.073 to −0.033]; P<0.001 for global cognition).

An increased rate of cognitive decline was associated with recurrent stroke and older age.

The researchers said the initial period of improvement was likely to have been the result of a combination of genuine recovery as well as practice effects. The longer term decline may have been due to factors such as clinically “silent” progression of cerebrovascular disease, or the initial burden of cerebrovascular disease.

Cognitive decline may also have been related to comorbid medical conditions such as those that might be associated with cerebral hypoxia or ischemia, they suggested.

They concluded their study in stroke patients “has implications for the design of clinical trials of therapies to prevent or slow poststroke cognitive decline, which should take into consideration the trajectory of initial improvement and subsequent decline in cognition after stroke.”

“Our results could also help clinicians better understand and plan for the long-term needs of patients with stroke,” they added.