RESUMO
We aimed at studying the effect of the pathophysiological changes associated with chronic obstructive pulmonary disease [COPD] on the nervous system and its aetiopathogenesis using the pattern shift visual evoked potentials [PSVEPs] and the brainstem auditory evoked potentials [BAEPs]. There are still great controversies between different studies that assessed cranial nerves and central nervous system functions in COPD patients using different neurophysiological techniques. In addition, those who reported abnormalities did not find any correlation between their findings and the pulmonary functions and arterial blood gas measurements. Design and methods: Participants consisted of 35 COPD male patients. Sixteen patients diagnosed as stable at risk or mild COPD and 19 patients diagnosed as stable moderate or severe COPD were included in the study as group I and II respectively. In addition, 20 age- and sex- matched healthy individuals were included in this study as a control group [group III]. We performed pulmonary function tests, arterial blood gas analysis, audiogram, auditory brainstem evoked responses [ABR] and visual evoked potentials [VEP] for all patients and controls. All patients in group I had normal BAEPs. Conversely, all patients in group II had abnormal BAEPs studies. All of them had significantly delayed wave I, III and V absolute latencies. However, 11 [58%] patients had significantly delayed IPLs III-V and I-V. There were significant negative correlations between PaO2 and wave I peak latency [p< 0.05]. There were also significant positive correlations between PaCO2 and wave V peak latency, I-V and III-V interpeak latencies [P< 0.01]. Lastly, there was a significant correlation between the Forced Expiratory Flow [FEF25-75%] and all BAEPs abnormalities. VEP study showed that the P100 was mildly but insignificantly delayed in group II. The function of the eighth nerve and the brainstem were highly abnormal in moderate and severe COPD. We also found that the impairment of the eighth nerve is mostly due to hypoxia and the impairment of the brainstem is mostly due to hypercapnea. Finally, our results have shown that the nervous system function could also be impaired in COPD through other mechanisms rather than hypoxia and hypercapnea