OSA is currently underdiagnosed: it may affect up to 15% of men and 10% of women, or approximately 1 billion adults worldwide, with an estimated 80% unaware that they have it. Obesity, smoking, chronic nasal blockage, high blood pressure, and being male are all major risk factors for OSA.
Researchers from the United Kingdom, Germany, and Australia have now demonstrated for the first time that OSA can cause early cognitive decline in middle-aged men, even in patients who are otherwise healthy and not obese. The findings were published in the journal
.
“We show poorer executive functioning and visuospatial memory and
deficits in vigilance sustained attention, and psychomotor and impulse
control in men with OSA. Most of these deficits had previously been
ascribed to co-morbidities,” said Dr Ivana Rosenzweig, a
neuropsychiatrist who heads the Sleep and Brain Plasticity Centre at
King’s College London, and the lead author of the study. “We also demonstrated for the first time that OSA can cause
significant deficits in social cognition.”
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Rosenzweig and colleagues examined a group of 27 men aged 35 to 70 with a new diagnosis of mild to severe OSA but no co-morbidities. Because most men and women with OSA have co-morbidities such as cardiovascular and metabolic disease, stroke, diabetes, chronic systemic inflammation, or depression, such patients are uncommon.
The men were not current smokers or alcoholics, and they were not obese (body mass index (BMI) less than 30). The researchers used a group of seven age-, BMI-, and education-matched men without OSA as a control group. A WatchPAT test of their respiratory function during sleep at home, as well as video-polysomnography at King’s College sleep centre, confirmed the OSA diagnosis. Electroencephalography (EEG) was used to measure the brain waves of sleeping subjects, while blood oxygen levels, heart rate, breathing, and eye and leg movements were tracked.
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The CANTAB, or ‘Cambridge Neuropsychological Test Automated Battery,’ tests were also used to assess the subjects’ cognitive function.
Patients with severe OSA had lower vigilance, executive functioning, short-term visual recognition memory, and social and emotional recognition than matched controls, according to the findings. Patients with mild OSA performed better than patients with severe OSA but worse than controls in these domains.
“The most significant deficits…were demonstrated in the tests that
assess both simultaneous visual matching ability and short-term visual
recognition memory for non-verbalizable patterns, tests of executive
functioning and cued attentional set-shifting, in vigilance and
psychomotor functioning, and lastly, in social cognition and emotion
recognition” wrote the authors.
The authors conclude that OSA is sufficient to cause the cognitive deficits previously attributed to OSA’s most common co-morbidities, such as systemic hypertension, cardiovascular and metabolic diseases, and type 2 diabetes.
But what is the mechanism by which OSA causes cognitive decline so early? The authors hypothesised that cognitive deficits in OSA patients are caused by intermittent low oxygen and high carbon dioxide levels in the blood, changes in blood flow to the brain, sleep fragmentation, and neuroinflammation.
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“This complex interplay is still poorly understood, but it’s likely
that these lead to widespread neuroanatomical and structural changes in
the brain and associated functional cognitive and emotional deficits,”
said Rosenzweig.
Whether co-morbidities have similar negative effects on cognition above
and beyond those caused directly by OSA is not yet clear.
“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,” said Rosenzweig.
“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.”
Source: Medindia
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