Explaining a difference requires a difference, but how much difference is enough, and when do you know if you have the right kind of difference?
The most fundamental fact about sensory experiences, aside from the fact that we have them, is that they are all qualitatively different. Hearing the violin is nothing at all like seeing it which is nothing at all like touching it or smelling the varnish on it. Sensory modalities are fundamentally different experientially, yet this is hard to explain on the neurological level. Let us call these differences: Inter- Modal Phenomenal Differences, or IMPD. It is easy to explain IMPD if you don’t know much- e.g., seeing is different from hearing because eyes are different from ears; easy and obvious.
This “explanation” becomes a little less obvious if we learn some physiology however and even more difficult to hold if we adopt a theory of the brain as an information system.. (Scientific developments produce new philosophical problems? Not unheard of- quantum mechanics.) Neurological activity is all basically ionic flow through semi- permeable membranes. The patterns may change, but so what? Is this suppose to account for IMPD? Why, if IMPD is basically a cortical phenomenon, is a pattern of activity in the auditory cortex so different at the experiential level from a pattern of activity in the visual cortex? The sensory organs are different off course, but we are not aware of the states of our sensory organs without higher level neurological activity. Further, from brain stimulation experiments, it looks like we can have sensory experience without sensory organ simulation. (Is there retrograde activity out this far –to the sense organs- with direct electrical simulation of the brain?) So there is a suggestion here that experience is a cortical phenomenon.
“ Cortical only” theories are a problem since they fail the “difference tests”. “Transducer/sense organ only” theories fail also perhaps because, at least, I can’t know what’s going on without cortical operations. But it is not at all obvious that this counts. Having a sensation and being aware of it or being able to respond to it are two different things. But other problems with transducer theory abound. First of all, moving the experiential level out to the sensors does no good. Its still the same sort of neuro- biochemistry out there; this too fails the difference test. Combining the two, holding that sensation involves both transducer and cortical neurological activity doesn’t help if their both basically the same thing.
Am I directly aware of the state of my sensory organs? This would seem hard to maintain-who is this “I”?. Our operating hypothesis is this: I am the sensation in that having the sensation is a state that I’m in, I am the sensing thing and the sensation. The total state of the organism is that of having or being aware of the sensation. If –sense organ and central neurological activity apart, each separately, or together are not enough for experience, which seems likely. So the sensation is a totals state of the system which involves the transducers which are different from one another, e.g. organ of corti, cones in retina, and the required difference now lies at the sense organ or transduction level.. (This is a great philosophical position since it is confusing, and explains nothing and with luck is irrefutable!)
. Including the interface level would seem to be required. Right now I’d say that the interface is were its happening, where the sensation is, or what it is but I find this close to incomprehensible. One problem is that sensation involves more than commutable aspects, more than information type operations and I seem to be aware of non-informational aspects of the process in sensing. At the sense organs, at the interface with the external world information is converted and phenomenological aspects of sensation are eliminated. (An important question here is : Is the cortex , or the nervous system in total, an information (only) system or not.)
((Note that we think that are visual world perceptions or experiences mirror or reflect in some sense optical reality or that they reflect actual aspects of it, e.g., spatial relations, colors, depth of field. Are their analogous views for the other modality? ))
Can brain stimulated people know that their current experience is different from that which occurs due to external stimulation? They can figure it out by consideration of their total situation –“I’m in an operating room now, not out in the woods listening to a bubbling brook”, but can they sense the difference?.
This is the best argument yet for the ghost in the machine, but the ghost has to have a really great home entertainment system for presenting the external world show. Introducing the ghost here really only ends the explanation; metaphysics as the terminator of enquiry rather than as an initiator- a god of the gaps introduced at some electro-physiological level.
The problem again is that it is not clear what sort of account of the variations in neurological activity, and especially in neural network activity could be seen as sufficient explanation for IMPD. IMPDs are as different as different gets, comparisons are impossible, yet the underlying physiology does not seem to admit to this order of qualitative difference.
Sense Data
A casual inspection of sense data theory suggests that the IMPD problem is not central, nor perhaps even considered. Does any one ask why sense datum have the secondary properties they do?
Dualism will not survive on quantum-mechanical tricks (Popper –Eccles), little miracles going on inside our heads against an informative theory of network function. Network operation is the key problem, especially the problem of syntactic (timed, structured, sequenced, controlled) behavior. The problem with the single photon response example is that in order to get this sensitivity, a whole lot of other things have to be going on, everything else has to be shut down or inhibited. Banging on a single receptor on a single neuron won’t do it, this selectivity, concentration, focus, whatever has to be generated by a whole lot of other activity. Focus or sensitivity has to be dialed in, that’s the problem, the system is too sensitive and has to be globally inhibited, that’s why we have GABA all over the place.
( The theory ((a theory?)) of IMPD is important because this will be the last refuge of serious mentalism (dualism). But the theory –I am the sensation; not I have the sensation- must accommodate other aspects of our mental life.)
Information and Qualia
Information has no qualia, no phenomenal properties, it is pure causation. More specifically, in the case of the aptly named action potential, it is a causation vector, a potential cause of a particular origin. This is another aspect of the problem of IMPD, since the information stream in the brain has no phenomenal characteristics, it cannot explain how variations in them can arise. It can have no phenomenal characteristics as a matter of empirical fact because action potentials of different sorts, say visual and auditory can impinge on single cell and we don’t have a see/hear sensation, we see and hear at the same time, but we don’t see/hear. Seeing is because of visual tract activity, but it is not that activity, this because seeing is more than having the information associated with seeing, it is an experience.
Not only can’t information theory explain IMPD, it can’t explain why qualia very within the modality. It can’t explain why orange is different from red, much less why red is different from loud or sweet. The problem is not that we know their different, the problem is that they look or are experienced as different. The problem isn’t that we can know, say or think they’re different; the problem is the difference in the qualia. Saying, knowing, realizing, acting as though, being aware of…these are cognitive, information based, cortical.
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