Obstructive sleep apnoea may cause early cognitive decline: Research

Researchers from the UK, Germany, and Australia have said that obstructive sleep apnoea (OSA) can cause early cognitive decline in middle-aged men, including those who are otherwise healthy and not obese.
 
The findings stem from a study published in Frontiers in Sleep, which involved a group of 27 men aged 35–70 with a new diagnosis of mild-to-severe OSA but without any co-morbidities and seven matched ‘control’ subjects.
 
Having confirmed the OSA via a so-called WatchPAT test of their respiratory function during sleep at home and also by video-polysomnography at King’s College sleep centre, the researchers tested the subjects’ cognitive function with the Cambridge Neuropsychological Test Automated Battery (CANTAB) of tests.
 
Patients with severe OSA reportedly had poorer vigilance, executive functioning, short-term visual recognition memory, and social and emotion recognition than the matched controls. Patients with mild OSA also performed better in these areas than patients with severe OSA, but worse than the controls.
 
Dr Ivana Rosenzweig, a neuropsychiatrist at King’s College London and the lead author of the study, said the research is important as ‘most of these deficits’ had previously been ascribed to co-morbidities.
 
‘The most significant deficits … were demonstrated in the tests that assess both simultaneous visual matching ability and short-term visual recognition memory for non-verbalisable patterns, tests of executive functioning and cued attentional set shifting, in vigilance and psychomotor functioning, and lastly, in social cognition and emotion recognition,’ the authors wrote.
 
However, while leading sleep health researcher and Bond University Executive Dean Professor Nick Zwar told newsGP the research is ‘interesting’, he believes more work is required for it to impact clinical practice due to its small sample size and the need for follow up study.
 
‘The experience that we have as practitioners is that people with OSA, particularly if it’s mild to moderate, do seem to be affected by it cognitively,’ he said.
 
‘It’s hard to know, as the study points out, whether that’s due to the obstructive sleep apnoea. It may be associated with desaturation of oxygen overnight or poor sleep, or a combination of all those things, or even from age or other co-morbidities.
 
‘The study is trying to kind of sort that out. But I think it’s a long way to go because it is small and it’s only in men – and they recognise that in the limitations section.’
 
Professor Zwar also said another crucial question not answered in the study is whether or not treating OSA would have an effect on reducing cognitive impairment.
 
‘People can have quite marked OSA on their sleep study in terms of the [apnoea hypopnea index] measure but have very little symptoms,’ he said.
 
‘We know that there’s an association with OSA and difficult to control hypertension … and developing type 2 diabetes. We also know there’s an association with dementia and perhaps earlier onset dementia, but whether it’s causal and whether treating OSA has an impact on the progress of those conditions is less clear.
 
‘That’s part of challenge of obstructive sleep apnoea – which patients do you decide to treat? And it isn’t just based on how bad the sleep study measure is.’
 
Another question left unanswered by the study is the mechanism by which OSA causes premature cognitive decline.
 
However, the authors speculate that the deficits are due to intermittent low oxygen and high carbon dioxide in the blood, changes in blood flow to the brain, sleep fragmentation, and neuroinflammation in OSA patients.
 
‘This complex interplay is still poorly understood,’ Dr Rosenzweig said. ‘But it’s likely that these lead to widespread neuroanatomical and structural changes in the brain and associated functional cognitive and emotional deficits.’
 
Likewise, it is not known whether co-morbidities have similar negative effects on cognition above and beyond those caused directly by OSA.
 
‘Our study is a proof of concept. However, our findings suggest that co-morbidities likely worsen and perpetuate any cognitive deficits caused directly by OSA itself,’ Dr Rosenzweig said.
 
‘What remains to be clarified in future studies is whether co-morbidities have an additive or synergistic effect on the latter deficits, and whether there is a difference in brain circuitry in OSA patients with or without co-morbidities.’
 
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