Researchers have long known that obstructive sleep apnea (OSA) is associated with cognitive deficits. Some have even speculated that the deficits arise from brain damage suffered when nighttime interruptions in breathing temporarily choke off the brain's oxygen supply.
Now, a study in the American Journal of Respiratory and Critical Care Medicine (Vol. 166, No. 10) offers new evidence to suggest that OSA patients suffer from mild brain damage. Surprisingly, the study also hints that some of the damage may actually precede the onset of OSA and contribute to its development.
Ronald Harper, PhD, Paul Macey, PhD, and their collaborators at the University of California, Los Angeles, used magnetic resonance imaging to scan the brains of 21 OSA patients and 21 healthy control participants. They found that patients had less gray matter than controls in brain regions associated with attention, memory, motor control and respiration.
Most of the reductions occurred on both sides of the brain, a typical pattern for damage caused by oxygen deprivation. But many of the OSA patients also showed one-sided reductions in certain areas, including areas associated with speech and upper airway control.
Thirty-eight percent of participants with sleep apnea also reported having problems with stuttering as children. The findings suggest that the roots of the disorder, which affects 15 percent of the population over age 65, may lie in childhood.
"What we suspect happens is that the deficits in wiring that these children who stutter have lead to a discoordination of the upper airway muscles," says Harper. Combined with obesity, a small airway or other anatomical factors, difficulty in controlling those muscles could lead to OSA, he says.
In an editorial accompanying the study, David Gozal, MD, of the University of Louisville in Kentucky, wrote that the study's findings are speculative, but that they're intriguing and warrant further research on the "chicken and egg" question of whether brain disorder or sleep apnea comes first.
"It would be very interesting to see whether individuals who do not have the disease, but who come from families where the disease is prevalent, have the defects that this study has found," says Gozal.