Distinciones esenciales entre indignidad y

Further to decomposing pain mechanisms, it is essential to recompose them in order to show how they operate in context. This involves unifying reductionistic pain research with pain research at higher explanatory levels (e.g., pain psychology, pain psychophysics,

philosophy of pain). Some philosophers of science who endorse mechanistic explanation often appeal to top-down causation to understand how operations at high levels influence those at lower levels (e.g., Bechtel, 2011; Bechtel & Hamilton, 2007; Craver & Bechtel, 2007; Powell & Dupré, 2009). These philosophers have focused on describing variations between causal relations and interlevel relations. A regular feature of the world appears to be that in all instances of causation, the cause and the effect are independently placed in time so that the cause precedes its effect temporally by some action. According to Craver and Bechtel (2007), this apparent feature of causation does not hold of interlevel relations. If a component part of a mechanism is changed, the entire mechanism is changed, and a mechanism cannot be changed without some component part of it being changed. That is, the part and the mechanism alter concurrently: the two effects co-occur; they are not independent in time. Thus, when a causal variable alters a mechanism and thereby alters a component part, a host of other changes may occur in the mechanism, with the result that the mechanism is further changed and thereafter functions differently. For example, the three specific nonsense

mutations S459X, I767X and W897X change the function of Nav1.7 in the gene SCN9A with

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According to Craver and Bechtel (2007), there is no „top-down‟ or „bottom-up‟ causation; there is only interlevel causation. The point they stress is the level at which the causation occurred, not the temporal sequence. If this view is correct, then both interlevel relations and type identity relations cannot be explained causally.

Thus, mechanistic explanation involves building understanding of levels (Bechtel, 2011; Bechtel & Hamilton, 2007; Craver & Bechtel, 2007; Powell & Dupré, 2009). Pain phenomena at the initial „macro‟ level (e.g., pain facial expression) are decomposed into finer operations (e.g., upper-face expression, lower-face expression), which are subsequently type identified with operations within specific neural regions or structures (e.g., M3 control of orbicularis-oculi, M4 control of zygomaticus). Neurophysiological mechanisms at the molecular or cellular level, such as coordination of neural network oscillations, are

concurrently delineated to explain their involvement in operations in specific contexts (e.g., M3 subunit activation of orbicularis-oculi in high empathy pain observers) (Lamm et al. 2008; Shackman, 2011). Type identity statements that successfully emerge from mechanistic pain explanation are therefore between different delineations of pain phenomena at the same

explanatory level; that is, they are intralevel. And through the continued explanatory tasks of decomposition, localization and recomposition, pain scientists and theorists may gradually increase their understanding to levels such that delineations of experience and mechanism (or behaviour and mechanism), are seen to have exactly the same type identity conditions

(Churchland, 2002; Craver & Bechtel, 2007; Sidelle, 2008). The success of such tasks implies that what might initially escape mechanistic explanation gradually contracts towards nothing (Sidelle, 2008). Thus, at the conclusion of successful pain research, the explanatory relation between the delineations on either side of the type identity sign is no longer puzzling: the explanatory gap has been bridged.

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6 Conclusions

The explanatory gap puzzle correctly reveals our inadequate understanding of how pain might be explained in terms of the NEIM. Indeed, there is a gap in the naturalistic pain explanations currently on offer. However, the existence of the gap merely represents a pragmaticlimit on our currentexplanatory successes. As described in Chapter One, some philosophers believe on a priori metaphysical grounds that pain cannot ever be explained in terms of neurophysiological mechanisms. Some of these philosophers further claim that pain is not explained by mechanism, as a matter of fact. However, since this metaphysical view was challenged in Chapters One and Two, the impossibility of bridging the gap as a matter of

principle might be false. I attempted to bridge the explanatory gap in two ways: first, based on a novel polyvagal-type identity theory of pain facial expression situated in the broad theoretical framework developed in Chapter Two; second, I reasoned that supporters of the in principle a priori gap believe that type identity theory must build type pain identities as formal logical derivations from laws. I tried to show that this belief is false, based on actual scientific explanatory practices and philosophical considerations concerning explanatory levels. The explanatory relation between the descriptions on either side of the type identity sign is, at the end of successful pain research, no longer vexing: the explanatory gap has been bridged. In the next chapter of the project, I will consider a final challenge to type identity theory of pain. This is the radical view that successful pain research will show that pain is not

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