Authors' reply.

Sir,

The authors highly appreciate the keen interest and the knowledge of the commentators[1] over the subject covered in the present study. Cognitive functions evoke significant interest in medical fraternity as evident by huge data existing in the medical literature to identify various factors linked with cognitive decline in human beings. A search over PUBMED, URL >http://www.ncbi.nlm.nih.gov/pubmed< with key word ′cognitive decline′ and a filter ′human studies′ provides around 10,596 articles related to cognitive decline. The factors vary widely and include traumatic brain injury,[2] concussive and subconcussive head impacts,[3] hormonal changes,[4] asymptomatic cerebral emboli leading to silent brain infarct,[5] rheumatoid arthritis linked physical inactivity,[6] chronic renal diseases,[7] and vitamin D deficiency[8] just to enumerate a few. The well-established and more widely known factors linked with cognitive dysfunctions are diabetes, smoking, depression, hypertension, congestive heart failure, elevated cholesterol, alcohol abuse, drug abuse, vitamin deficiencies, liver disease, brain tumor, encephalitis, meningitis, chromosomal abnormalities such as down syndrome, genetic abnormalities such as phenylketonuria, metabolic conditions, heat stroke, profound dehydration, lack of physical exercise, and infrequent participation in mentally or socially stimulating activities. Therefore, smoking indeed is also linked with cognitive decline.

While conducting a study, the researchers are often inclined to provide necessary statistical power to analysis of their objective in the best possible and practically feasible manner. Our aim in the mentioned study[9] was to assess subclinical cognitive dysfunctions in stable COPD patients having no hypoxemia vs. age-matched healthy volunteers using two tools: An electrophysiological test (auditory event-related potential, P300 test) and a questionnaire tool [mini mental state examination (MMSE) questionnaire]. These two tools have been used separately in prior studies, however, we assessed cognitive functions using both these tools simultaneously to see their relative relevance in clinical setup and under electrophysiological setup. Our study highlighted the relative importance of using MMSE and P300. Cognitive dysfunctions were detected both by MMSE and P300; however, MMSE abnormalities were more frequent as compared to P300 abnormalities (27/40 vs. 10/40) in COPD patients. The study methodology provides full justification to the hypothesis under scrutiny and there are no flaws as suggested by the commentators without considering the concept of the study. It was not the aim of present study to analyze the numerous causes of the cognitive decline in COPD patients. It has not been mentioned anywhere in the study that smoking is not a risk factor for cognitive decline.

Moreover, it is perhaps erroneous to suggest a study including COPD patients against controls without COPD (but all smokers). As we know, smoking is the most powerful factor causing COPD; it is not frequent to find a volunteer for study with 56.9 ± 9.21 years of age and with a smoking history of 39.95 ± 20.94 pack years (as it was for COPD patients in the study under discussion) and yet without COPD. Even if we have found few, many of these might have been on course to develop COPD in the coming years, negating the concept of healthy volunteers.

We understand that the study of this kind and on such a hot subject shall generate more questions than the answers it may provide. This is exactly what medical science is all about. We have mentioned the limitations of the study and that the study is the end-of-beginning and not the beginning-of-end of research over this subject.

Thanks for the opportunity to let us share our view point.