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The authors note that "previous studies have suggested that severe SDB [sleep disordered breathing], associated with a respiratory disturbance index (RDI) [greater than] 40, is associated with a broad range of neuropsychological deficits, some [italics mine] of which may be reversed with treatment. On the other hand, simple snorers showed no differences from non-snorers on such tests, nor did older subjects with RDIs less than 15 show any relationship between RDI and impairment of attention. In this study, the authors planned to examine patients with intermediate levels of SDB (RDIs between 10 and 30) and attempt to relate any impairment to degree of sleepiness. Patients were volunteers, ages 40-65, told they would participate in a study of "snorers and nonsnorers." They were separated into "cases" with RDIs between 10 and 30, or "controls" with RDI's less than 5 and without any history of frequent snoring or observed apneas. Extensive exclusion criteria attempted to eliminate subjects with other possible causes of neuropsychological deficits, including a history of neurological disease or head trauma, substance abuse, current medications, low education, etc. Neuropsychological tests were given between naps in the course of a Multiple Sleep Latency Test (MSLT). These included four subtests of a standard IQ test, and included measure of attention, memory, general information processing efficiency, and executive functions--all shown impaired in previous studies of more severe SDB. Subjects were initially screened for eligibility with in-home sleep monitoring of nasal and oral thermistry (i.e., air flow), chest wall musculature, finger oximetry (measurement of oxygen saturation), body position, and heart rate. A standard lab polysomnogram was later done on subjects with RDIs estimated at more than 5, followed by the MSLT. The MSLT was used to measure sleepiness, as was the Epworth sleepiness scale (ESS) completed the same day as the other testing, which took place betweeen naps. Another questionnaire assessed self-reported symptoms of SDB such as gasping, apneas, and excessive daytime sleepiness. There were 32 subjects with SDB and 20 controls, similar in average age (49-51), proportion of males (half), average education past high school, estimated IQ 100-102. The two groups differed in body mass indices (28 for controls vs. 35 for cases) and in proportion of blacks, who were more frequent among the controls. Average RDI among cases was 17, with little hypoxia observed and less severe sleep fragmentation than that reported in more severe apnea. Cases reported more snoring, breathing pauses, and sleepiness than controls, but didn't differ from controls on MSLT or ESS scores. The two groups differed in one of four attention measures. On a vigilance test, cases did worse with the passage of time (a couple of minutes) whereas controls improved. Cases also were less able to recall digits in reverse order (a test of short term memory), and made more "perseverative" errors (indicating difficulty changing approach to a problem) on the Wisconsin Card Sort test. Results on this test correlated with sleepiness measured on the MSLT and with sleep fragmentation. In summary, the authors concluded that mildly breathing disordered subjects without much hypoxemia or pathological sleepiness still showed neuropsychological deficits, similar in nature (but milder in severity) to those of patients with more severe sleep apnea. The relative lack of symptoms among the cases led the authors to caution against extending their results to patient populations. The key deficits seemed to be in attention, memory, and executive cognitive functions--but it was unclear whether these were sufficient to impair daily functioning.

Few of us who have been diagnosed with sleep apnea would fall within the category of relatively symptom-free, mildly breathing-disordered "cases" the authors studied here. However, we may be interested to learn that even such mildly ill people show impairments of mental functioning. The kind of mental impairment being studied here is typical of that seen in patients with “organic brain disease" from numerous different causes. In the “cases” studied here, there did not seem to be significant hypoxia to represent a plausible cause, but the impairments did seem related to sleep fragmentation and daytime sleepiness. It should come as no surprise that people who have had a poor night’s sleep and are as a result sleepy the next day would have trouble concentrating on mental tasks. Bear in mind that these people were untreated. There is nothing in this study to suggest that some sort of irreversible brain damage has occurred, or anything that a few nights’ good sleep with CPAP wouldn’t remedy. However, we should be aware that other evidence exists to suggest that some deficits may persist even with treatment. In my own experience, neuropsychological testing I had done six years ago (when I had already had untreated sleep apnea for many years) showed no such deficits. Later, when I noticed problems sustaining concentration, such as difficulty reading books, I requested reevaluation. The final results aren’t in, but I left reassured that neither my performance on Digit Span Reversals or the Wisconsin Card Sort Test was any worse than it had been six years ago.

"To achieve the impossible dream, try going to sleep." Joan Klempner

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