Fact or artifact? reply to Lobstein, Turpin and Siddle

Fact or artifact? reply to Lobstein, Turpin and Siddle

Biological Psychology 9 (1979) 225-226 © North Holland Publishing Company FACT OR ARTIFACT?. REPLY TO LOBSTEIN, TURPIN AND SIDDLE * ROBERT J. BARRY ...

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Biological Psychology 9 (1979) 225-226

© North Holland Publishing Company

FACT OR ARTIFACT?. REPLY TO LOBSTEIN, TURPIN AND SIDDLE * ROBERT J. BARRY University o f New South Wales, Kensington, NSW 2033, Australia

Accepted for publication 16 October 1979

In their comment on Barry (1979), Lobstein, Turpin and Siddle (1979) asserted that I failed to understand the bases of their sinus arrhythmia (SA) correction techniques (Lobstein, Webb and Cort, 1978; Turpin and Siddle, 1978) and that my solution to the problem of cardiac variability is inadequate. The problem of 'understanding' involves the definition of an evoked cardiac response (ECR) as the difference between extrapolated pre-stimulus heart rate (HR) and post-stimulus activity. For example, Turpin and Siddle (1978) used actua actual pre-stimulus HR values as the 'extrapolated' basal activity in the post-stimulus period, and it is the notion underlying this usage which is the kernel of the disagreement between us. My paper urged a more realistic approach using observed respiratory frequency in the post-stimulus period as the time-base for SA extrapolation. In support, I presented simulated ECRs (generated by a decrease in respiratory frequency underlying respiratory SA of a fixed amplitude) obtained using the procedure of Turpin and Siddle (1978), and noted that these spurious ECRs would not be obtained if the proposed modification in procedure was used. My labelling of these stimulated ECRs as 'spurious' was taken by Lobstein et al. (1979) as an indication of my lack of understanding of their response definition. Rather than failing to understand this definition, my rejection of its literal interpretation was on the basis of its logical implications. These implications have led to the query as to whether my simulated ECRs should be regarded as fact or artifact, serving to highlight the problem with the original response definition. Let us consider the nature of this simulation within the context of the 'traditional' averaging approach to the ECR (Barry, 1979). The change in HR across 'stimulus onset' involved only an increase in the period of respiratory SA. The expected limiting value of the averaged sinusoidal activity before and after 'stimulus onset', as the number of averaged protocols increases, is obviously the same: the mean HR level underlying the SA. Thus the traditional averaging approach to the ECR would be expected to yield zero ECRs in this simulation. To reject this conclusion is to reject the whole field of averaged evoked responses and the concept of signal to noise * Address requests for reprints to Dr. R.J. Barry, School of Education, University of New South Wales, Kensington 2033, Australia. 225

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ratio upon which it is based. The obtained ECRs were thus labelled as 'spurious'. The willingness of Lobstein et al. (1979) to accept these spurious ECRs is a logical outcome of their response definition, and as such, reflects upon the validity of that definition. There are other aspects of validity raised in defence of their response definition which deserve comment. The most obvious of these is the claim that 'the fact that differential stimulus effects can be shown (Lobstein et al., 1978) indicates that the time series method is valid' (Lobstein et al., 1979, p. 222). The simple demonstration of a new effect using a new procedure is no guarantee of the validity of the procedure. The claim that my 'solution' to the problem of cardiac variability is inadequate is supported by several arguments, the first of which is that correction for respiratory activity alone neglects blood-pressure and temperature regulating systems involved in SA. While this is obviously correct, Turpin and Siddle (1978), in discussing the relative contributions of these variables to SA, have themselves noted that 'respiratory SA is considered to be the most important' (p. 128). It is surely preferable to attempt to control for the most important potential sourse of artifact rather than to ignore the problem entirely. Additional grounds relating to amplitude and phase changes of respiration at stimulus onset and their effects upon SA were also advanced. These seem to indicate a misconception about the scope of the Barry (1979) paper which should be dispelled. My paper was concerned only with artifactual ECRs associated with changes in the frequency of respiration across stimulus onset. To avoid such artifacts, it advocated the adoption of the respiratory cycle as the timebase for use with the prcedures of Lobstein et al. (1978) or Turpin and Siddle (1978). To construe this as claiming a 'solution to the problem created by cardiac variability' (Lobstein et al., 1979, p. 221) is an unwarranted generalisation. Criticisms based upon such a generalisation can achieve little more than a clouding of the issue.

References Barry, R.J. (1979). Correction for sinus arrhythmia in the evoked cardiac response: A timebase problem. Biological Psychology, 9 (this issue), 215-220. Lobstein, T., Turpin, G. and Siddle, D.A.T. (1979). Comment on correction for sinus arrhythmia in the evoked cardiac response: A timebase problem. Biological Psychology, 9 (this issue), 221-223. Lobstein, T., Webb, B. and Cort, J. (1978). Background noise levels and heart rate orienting: response detection using time series analysis. Psychophysiology, 15, 316-319. Turpin, G. and Siddle, D.A.T. (1978) Measurement of the evoked cardiac response: The problem of pre-stimulus variability. Biological Psychology, 6, 127-138.