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“Visual P300” refers to a Visual Evoked Response Potential (see Glossary) or typical change in brain waves occuring 300 msec after a flash of light. The potential appears as a waveform. A waveform normal in its amplitude (strength) and latency (delay after the light) is taken as one sign of normal mental processing. The latency especially is related to attention. It is prolonged (delayed) in conditions of mental deterioration due to brain disease, like dementia (such as in Alzheimer’s Disease), in disorders of metabolism that affect the brain such as liver or kidney failure, with inborn inability to read properly, and mental impairment after head injury.
P300 latency is also prolonged with obstructive sleep apnea, whether or not the person feels sleepy.
This study asked the question whether CPAP would correct this abnormality.
Forty consecutive patients with severe OSA (RDI greater than 40/hour) were studied for auditory and visual evoked responses the morning after a night of polysomnography before starting CPAP. The same day they underwent MSLT (see Glossary). Two to four months after starting CPAP they were retested the same way. For comparison, 40 normal control subjects of similar age were also tested, for evoked responses only.
With treatment, the OSA patients experienced significant improvement in their sleep: RDI decreased from a very high but variable initial average of 77.4/hr (SD=+/-27.5) to a normal mean and less variable average on treatment of 4.5/hr (SD=+/-7.7); Desaturation Index decreased dramatically from 31.2 (SD=+/-31.0) to 0.4 (SD=+/-1.2); percentage of stage 1 (light) sleep dropped from 40.1% (SD=+/-20.2) to 12.5% (SD=+/-9.2); Sleep Efficiency improved from 76.3% (SD=+/-14.4) to 83.9% (SD=+/-9.3); and sleep latency on the MSLT naps increased modestly from 4.1 minutes (SD=+/-2.4) to 6.2 minutes (SD=+/-3.6).
All of these changes in measures of sleep from before treatment to after treatment were statistically significant, and most repesented a change of the average from markedly abnormal to within the normal range. However, note that (a) improvement is the MSLT was not as substantial; and (b) variability in most measures even after treatment was considerable, so that some subjects on CPAP would still fall in the abnormal range of each measure.
Normals and OSA patients (both before and on treatment) did not differ on auditory evoked responses, nor did they differ on the amplitude of visual evoked responses. However, OSA patients had significantly longer latencies of visual responses both before treatment (average visual latency=408.1, SD=+/-34.9) and during treatment (average VL=407.7 SD=+/-29.9) than normals (ave. VL=385.6 SD=+/-31.6). Furthermore, it is apparent that the VL of OSA patients did not improve with treatment. Neither did it correlate with any of the sleep measures before or after treatment.
The authors acknowledged that, even after treatment, at least some of their OSA patients were still pathologically sleepy. However, they mentioned prior research showing that the prolonged VL is OSA is not a simple result of sleepiness. In fact, in this study VL showed no correlation with any of the sleep measures, suggesting that it was measuring something distinct from current sleep.
They believe that the VL prolongation may be an index of mental/cognitive processing abnormalities associated with OSA> Its lack of improvement after a few months of CPAP raises concern that it may be a sign of irreversible brain damage resulting from OSA causing lack of oxygen to the brain, though it is also a possibility that lengthier treatment may be required to show improvement in VL than in sleep measures.
Let us hope that the authors’ suggested conclusions are premature. As they admit, their patients’ MSLT sleep latencies remained abnormal. As I note, some patients must have had abnormal levels of each or all of the sleep measures. In other words, their sleep abnormalities had not been fully corrected, so that their CPAP treatment either had not had sufficient time to exert its full effect or, quite possibly, the treatment itself had yet to be optimized for individual patients.
Not only would I like to see these patients followed up after a longer period of CPAP treatment, I would like assurance that the most vigorous efforts had been made in the meantime to optimize pressures, compliance, mask fit, etc., and to rule out other possible causes of sleep disruption such as periodic leg movements or coexisting conditions such as narcolepsy. Then I would like to see the subgroup of patients where the treaters had been entirely successful in normalizing all aspects of their sleep, compared both to normals and to OSA patients where sleep abnormalities persisted. The failure to see correlations of VL with sleep parameters does not convince me that there is no relationship between the sleep disturbance and the electrophysiological measure. For one thing, the absolute magnitude of the difference between normals and OSA patients, while statistically significant, was relatively small in size (about 22 msecs) compared to the standard deviations (30-35 msecs) of this measure. Therefore, it seems to me that the VL latency prolongation does not offer a robust range of abnormal values to correlate effectively with the wide ranges of sleep measure values.Furthermore, the fact that sleep measures often remained abnormal indicates to me that the disease process was still active despite CPAP, and only once the disease had been completely controlled might one see improvement in corollary consequences of the disease such as prolonged VL.
Also, while the authors make clear that theirs is an unusually sensitive measure of cerebral dysfunction, I would like to see it studies concurrently with other measures more pertinent to functional impairment, such as neuropsychological testing.
Nevertheless, I admit that this study adds to a mounting body of evidence from various perspectives—including neuropsychological testing and structural imaging-that concur in finding some evidence of organic brain dysfunction associated with OSA, so that we must add this to the lengthening list of potential complications of OSA.
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