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Psychosomatic Medicine 63:579-584 (2001)
© 2001 American Psychosomatic Society

ORIGINAL ARTICLES

Neuropsychological Effects of One-Week Continuous Positive Airway Pressure Treatment in Patients With Obstructive Sleep Apnea: A Placebo-Controlled Study

Wayne A. Bardwell, PhD, Sonia Ancoli-Israel, PhD, Charles C. Berry, PhD and Joel E. Dimsdale, MD

From the University of California, San Diego, Departments of Psychiatry (W.A.B., S.A.-I., J.E.D.) and Family and Preventive Medicine (C.C.B.); and Veterans Affairs San Diego Healthcare System (W.A.B., S.A.-I.), San Diego, California.

Address reprint requests to: Wayne A. Bardwell, PhD, University of California, San Diego, Department of Psychiatry-0804, 9500 Gilman Drive, La Jolla, CA 92093-0804. Email: wabardwell{at}ucsd.edu


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
OBJECTIVE: To determine whether 1-week continuous positive airway pressure (CPAP) treatment, compared with placebo CPAP, improves cognitive functioning in patients with obstructive sleep apnea (OSA).

METHODS: 36 OSA patients (aged 32–60 years, respiratory disturbance index [RDI] > 15) were monitored 2 nights with polysomnography, then randomized for 1-week treatment to CPAP or placebo (CPAP at 2 cm H2O with holes in mask). Participants completed Wechsler Adult Intelligence Scale—Revised Digit Symbol and Digit Span, Trailmaking A/B, Digit Vigilance, Stroop Color-Word, Digit Ordering, and Word Fluency tests pre- and posttreatment. These produced 22 scores per participant, which were analyzed by use of repeated-measures analysis of variance (ANOVA) and a rank-sum test.

RESULTS: In ANOVA, only 1 of the 22 scores showed significant changes specific to CPAP treatment, a number that could be expected by chance alone: Digit Vigilance-Time (p = .035). The CPAP group improved their time (from 7.5 to 6.9 minutes, p = .013). The rank-sum test revealed that the CPAP group had significantly better overall cognitive functioning posttreatment than the placebo group (mean ranks of 17.8 vs. 20.2, respectively; p = .022).

CONCLUSIONS: Although results suggest overall cognitive improvement due to CPAP, no beneficial effects in any specific cognitive domain were found. Future studies of neuropsychological effects of CPAP treatment should include a placebo CPAP control group. Placebo studies that use longer-term treatment might demonstrate additional effects. It is also possible that, even at 2 cm H2O, CPAP conveys some beneficial neuropsychological effects.

Key Words: apnea • CPAP • neuropsychological functioning • cognitive deficits

Abbreviations: AHI = apnea/hypopnea index; ANOVA = analysis of variance; BMI = body mass index; BP = blood pressure; CABG = coronary artery bypass graft; COPD = chronic obstructive pulmonary disease; CPAP = continuous positive airway pressure; O2 = oxygen; PSG = polysomnography; RDI = respiratory disturbance index; REM = rapid eye movement; SD = standard deviation; WAIS = Wechsler Adult Intelligence Scale.


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Obstructive sleep apnea (OSA) can be a devastating illness, leaving patients exhausted from sleep deprivation and sometimes cognitively impaired (1). Research results are mixed, however, regarding the nature and cause of cognitive deficits in these patients. In 18 studies of cognitive functioning in patients with OSA, all found some impairment (2–17), although the type of impairment observed varied greatly. Most commonly reported were deficits in global cognitive functioning (2–5), memory (6–11, 17), attention (2, 3, 12, 13), and concentration (2, 7, 17). Six studies compared OSA with other disorders that have a breathing or sleep component (eg, chronic obstructive pulmonary disease or narcolepsy), with four reporting greater cognitive impairment in patients having OSA (7, 8, 11, 13) and two finding no differences between conditions (14, 18). Among studies examining the impact of OSA treatment (mainly CPAP) on cognitive functioning, most have reported at least some improvement (9, 16, 19–21), although one did not (22). Again, the specific areas of cognitive improvement varied greatly.

In summary, most but not all of the cited studies found cognitive impairment in OSA. However, tests used to assess cognitive functioning varied greatly. This impairment seems to be exacerbated by the level of hypoxemia (2–4, 6, 9, 12, 23), RDI (6, 7, 9, 23), and arousals (6). Most research that has examined cognitive functioning pre– and post–CPAP treatment has reported significant but inconsistent improvements. Some authors have speculated that neuropsychological functions that have not shown improvement may be due to cerebral damage from hypoxemia. Therefore, instrument selection and differences between patient groups regarding the presence of hypoxemia and degree of OSA severity may contribute to disparities in the literature.

The purpose of the present study was to evaluate the effectiveness of CPAP treatment vs. placebo CPAP (at insufficient pressure) on cognitive functioning in patients with OSA. CPAP, by nature, is an obvious intervention, and controlled studies are rare. Some have compared CPAP against nontreatment or medication controls, and, recently, two other groups, like ours, used some form of placebo CPAP (24, 25). However, we are unaware of any studies that have used a credible CPAP placebo in an analysis of cognitive functioning. Placebo CPAP has the advantage of duplicating the mask, airflow, and equipment presence and sounds without having a major impact on RDI.


   METHODS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
Subjects (29 men and 7 women with OSA, defined as RDI >=15) ranged in age from 32 to 60 years (Table 1). Subjects with a history suggestive of OSA were recruited by advertising and word of mouth. To qualify, subjects had to be 100% to 150% of ideal body weight as determined by Metropolitan Life Insurance tables (26). Although OSA is more common among the obese, subjects >150% of ideal body weight were excluded because of the possibility of confounding by other conditions associated with obesity. Subjects were also excluded if they had other major illness. Subjects with hypertension were tapered from their medication before participation. All subjects gave written consent for the study, which was approved by the University of California, San Diego, Institutional Review Board.


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  		Table 1. Demographic and Polysomnographic Data (Mean ± SEM)
 
Subjects were monitored for 2 nights in the Clinical Research Center by use of standard PSG (27). Subjects with a 2-night average RDI >15 were classified as having OSA (range: 17–111) and were randomized to a CPAP (N = 20) or placebo group (N = 16). Group sizes differ because of randomization and dropouts. The placebo group received CPAP at 2 cm of H20; holes were drilled in the mask to increase its ineffectiveness. After discharge, subjects were instructed to use the nasal CPAP unit (DeVilbiss Horizon; Somerset, PA) at home during sleep for 1 week. Objective CPAP use was monitored with a hidden clock in each CPAP unit that measured the total time the CPAP unit was turned on and providing the prescribed pressure. The timer would indicate any large leak or whether subjects failed to wear the mask. After 7 days of CPAP use at home, participants returned for another night of PSG.

Optimal effective CPAP pressure to minimize OSA was determined by conventional manual overnight CPAP titration during PSG (27). Briefly, a CPAP mask was placed, and slowly increasing amounts of air pressure were applied to obliterate respiratory disturbances through the night of sleep monitoring. The placebo CPAP group had the same procedures as the CPAP treatment group, except that their CPAP pressure was maintained at 2 cm of H2O.

We selected a set of commonly used neuropsychological tests that require little special equipment, are brief, and span several important areas of neuropsychology. Subjects were given the following battery at baseline and after treatment: WAIS–Revised Digit Symbol, Digit Span (28); Trailmaking A/B (29); Stroop Color-Word (30); Digit Vigilance; Digit Ordering; and Word Fluency (31). An alternate form was used for Word Fluency posttreatment, because it was the most likely test to show a learning effect. These tests produced 22 scores per subject.

Scores were analyzed with repeated-measures ANOVA and a rank-sum test. Subjects were ranked for each of the 22 pretreatment neuropsychological scores (the best performance received a rank of 1). Ranks for each subject were then averaged across the 22 scores to yield a single pretreatment rank. The process was repeated to yield a single posttreatment rank per subject. These pre- and posttreatment ranks were then analyzed by use of repeated-measures ANOVA (32). Secondary analyses were performed to determine whether the effect of CPAP was different in cognitively impaired vs. unimpaired subjects. Published norms (available for Digit Symbol, Digit Span, Trailmaking A/B, Digit Vigilance, and Stroop) were used to identify cognitively impaired individuals (>1 SD below mean) (33–36).


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 
The groups did not differ demographically (Table 1). The CPAP group had significantly lower O2 saturations than the placebo group pretreatment (p = .018); therefore, analyses were run controlling for O2 saturations. Significant Time x Treatment interactions emerged for percentage of REM (p = .036), RDI (p < .001), number of apneas (p = .018), number of hypopneas (p = .002), and mean O2 saturations (p = .001). Post hoc analyses revealed that, as expected, the CPAP group significantly improved on all of these sleep variables (p < .001).

Table 2 shows pre- and posttreatment means for the 22 neuropsychological test scores by placebo and CPAP groups. The scoring column specifies whether a lower (minus) or a higher score (plus) indicates better performance. When repeated measures ANOVA was used, significant changes over time, regardless of treatment, were not observed for any neuropsychological test. Of the 22 scores from the assessment battery, one showed a significant Time x Treatment interaction (Table 2): Digit Vigilance-Time (minutes to mark each occurrence of number "6" in a page of numbers; p = .035). The placebo group showed a slight worsening pre- to posttreatment (from 6.4 to 6.6 minutes), whereas the CPAP group improved (from 7.5 to 6.9 minutes). Because there were differences between the placebo and CPAP groups on pretreatment test scores on Digit Vigilance-Errors (p = .049), we conducted an analysis of covariance using change scores while simultaneously controlling for pretreatment scores. There were no differences between groups over time, after controlling for initial differences.


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  		Table 2. Neuropsychological Test Scores (Mean ± SEM)
 
For the rank-sum test, a significant Time x Treatment interaction emerged: the CPAP group had significantly better posttreatment performance across the neuropsychological battery than the placebo group (rank of 17.8 vs. 20.2, respectively; p = .028). Post hoc analyses failed to reveal significant differences for any individual test.

We also examined whether CPAP had a different specific effect on cognitively impaired individuals. Three individuals were impaired (>1 SD below the mean) on Digit Symbol, 11 on Digit Span, 11 on Trailmaking A, 9 on Trailmaking B, 12 on Digit Vigilance-Time, 11 on Digit Vigilance-Errors, and 2 on Stroop. We again used a repeated-measures ANOVA, adding impaired/nonimpaired as a new factor. No significant Time X Treatment or Time x Treatment x Impairment interactions emerged. However, we did find significant Time x Impairment interactions for Trailmaking A (p = .021) and B (p = .011), and Digit Vigilance-Errors (p = .014). The impaired group improved regardless of treatment received.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
ACKNOWLEDGMENTS
 REFERENCES
 
Most studies of cognitive dysfunction in OSA have described significant neuropsychological sequelae, particularly diminished attention, concentration, memory, and vigilance. Clinical interventions have often shown significant improvement in cognitive functioning, particularly with CPAP treatment, but findings have not been consistent. In addition, there have been few placebo-controlled studies that duplicate the conditions of CPAP intervention while studying cognitive changes. In the current study, we used CPAP at a pressure of 2 cm of H2O, with holes in the mask to further limit its effectiveness. This allowed duplication of the obvious aspects of the intervention yet without the benefit that results from fully effective treatment. We wondered whether cognitive improvements specific to CPAP treatment would also emerge from this placebo-controlled design.

When the 22 neuropsychological scores were analyzed individually, only one showed a significant Time x Treatment interaction—a number that could be due to chance alone. When performance across the neuropsychological assessment battery was analyzed by use of the rank-sum test, the CPAP group scored significantly better than the placebo group posttreatment. This suggests improvement in general cognitive performance; however, statistically significant changes for any specific test score could not be demonstrated with these data, perhaps because of the short treatment time of only 1 week. Previous studies had treatment durations that ranged from 2 days to 10 months. Longer treatment may be required for specific cognitive changes to take effect. However, others found cognitive improvement after 2 (37), 3 (38), and 7 (21) days. Whether length of treatment explains our divergent results remains to be determined.

CPAP was clearly more effective than placebo for reducing RDI. A significant Time x Treatment interaction emerged for RDI, with the CPAP group normalizing pre- to posttreatment (from 57 to 3). The placebo group, although still having substantial respiratory disturbance post-treatment, also showed a nonsignificant improvement (from 44 to 28). The 2-cm H2O pressure used in our placebo may have had a partial therapeutic effect, which suggests a dose-response nature of CPAP treatment. However, this level of pressure is much lower than what would be expected to significantly reduce the RDI. Previous reports showed that a minimum CPAP pressure of 4 to 6 cm of H2O was needed to control RDI (39) and 4 cm H2O just to prevent snoring in nonapneics (40). The average CPAP required to control OSA in our CPAP-treated group was 10 cm of H2O. Although the possibility must be considered that CPAP at 2 cm of H20 pressure might not be a true placebo, previous reports do not support this interpretation of our results.

One possible explanation for the lack of specific cognitive changes might be that we had insufficient statistical power. Although our sample size is 20% larger than the average of all the studies cited in the present article and is 57% larger than the CPAP studies, power remains a concern in this area of research. To determine whether our lack of significant findings was due to low power, we compared effect sizes for tests of cognitive domains that were common to the present and previous studies. The effect sizes observed in our data set were significantly smaller (p < .01). This suggests that differences between previous studies and the present study are not merely due to power—that is, we had enough power to prove that the effect sizes in our placebo-controlled study are smaller than those previously observed. Thus, we feel that the link between CPAP and improved neuropsychological functioning is only tenuously established and our findings, although not definitive, may add a valuable new perspective to this literature.

One notable aspect of sleep architecture in our sample is the relatively short total sleep time (310–337 minutes). If this were chronic, it could be that chronic sleep deprivation is affecting both groups, masking an effect for CPAP. We ran Pearson correlations between total sleep time and the neuropsychological test scores; however, none was significant. It is not unlikely that the short sleep time represents diminished sleep on the sleep unit, as is commonly reported in sleep studies

Our subjects were tested in the early afternoon. Some have suggested that morning cognitive functioning may be more likely to show improvement with CPAP than functioning at other times of the day. Although speculative, it is possible that, had our subjects been tested in the morning, additional specific effects for CPAP might have been apparent.

Referring again to Table 2, and ignoring statistical significance, 14 of the mean scores for the placebo group and 19 for the CPAP group improved over time. Because previous studies have not included a valid placebo, it may be that some of the improvements in the literature attributed to CPAP were due, in part, to regression to the mean. Alternatively, ineffective CPAP treatment may result in a placebo effect not observed when other methods of experimental control are used. Also, there may be a learning effect in response to repeated neuropsychological testing. If so, this further supports the importance of a valid placebo.

Some researchers have asked whether it is appropriate to expect a consistent effect of CPAP on cognitive functioning across a broad sampling of patients. For instance, perhaps patients with significant cognitive impairment are relatively refractory to improvement because of anoxic brain damage. If correct, one would expect beneficial effects of CPAP only in individuals with mild cognitive impairment. Conversely, one might suspect that the more impaired patients would improve most because of regression to the mean. Although our sample size was limited, we examined the possibility that cognitively impaired individuals might be more or less responsive to CPAP in terms of subsequent cognitive performance. Although we found no evidence for this, it is still possible that such a difference may exist and would require a larger sample to be perceived.

Although not statistically different, some of the observed changes might be clinically important. Cognitively impaired individuals on placebo improved on six of nine test scores for which we had norms; unimpaired subjects did not improve. Very low pressure CPAP might result in improvement in the cognitively impaired, but higher pressures may be needed to affect functioning in the unimpaired. This hypothesis needs to be tested with larger samples or longer treatment. In addition, it is possible that a different population of patients with OSA may have different neuropsychological characteristics and, thus, a different response to treatment. Our population was not a clinic sample but rather a group of volunteers. Although they had moderate to severe OSA (mean RDI =51), they may differ in some respects from clinic patients. Patients who are more cognitively impaired, who might be seen in the clinic, are less likely to volunteer for research, yet might show greater improvement. This same study should be repeated in a clinic sample.

These findings document the vital importance of including a placebo-control group in studies of the neuropsychological impact of CPAP treatment. In addition to placebo effects, learning effects can occur in repeated neuropsychological testing even when alternate forms are used. We come up with two different conclusions about the effects of CPAP on neuropsychological functioning depending on the statistical approach employed. Using the rank-sum test, we found a subtle but significant improvement in overall cognitive performance in individuals who received CPAP, compared with those who received placebo. Post hoc analyses, however, did not reveal significant differences for any particular test score. Therefore, deficits in specific cognitive domains could not be demonstrated. When we used a simpler analytic approach, examining differences test by test, we found a significant Time x Treatment effect for only 1 of 22.

We regard this as a work in progress. Further studies that include larger sample sizes, longer treatment, and an evaluation of the pressure required for a true placebo are necessary to answer questions that remain in this area of research. However, balancing these suggested design improvements is a concern about how long it is appropriate to maintain an individual on placebo CPAP.


   ACKNOWLEDGMENTS
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
REFERENCES
 
This work was supported by the National Institutes of Health Grants HL44915, RR00827, AG08415, and AG02711.

Received for publication May 3, 2000.


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 METHODS
 RESULTS
 DISCUSSION
 ACKNOWLEDGMENTS
 REFERENCES
 

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