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This paper paper brings about many thought provoking ideas especially issues concerning consciousness and pain. The study revealed that there exists a reduced peak B endorphin concentration in the Cerebrospinal fluid (CSF) of patients having a chronic pain state. Also peak B endorphin levels were shown to increase when placebo administered patients reported pain relief. Reversely for patients who didn't experience any pain relief, no such change in B endorphin concentrions were detected.
What first came to mind upon reading this paper was the biological process of pain perception and that this system must be closely related to consciousness. This article suggests to me that Pain is a very subjective experience, and biology doesn't seem to offer much room for subjectivity. I assert that pain is a subjective experience because in this paper, when chronic pain patients were given a placebo, of saline, they reported an allievation of their pain. Why is it that this happened??? The most plausible reason is that it is pyschological; the patients thought that they were being given a drug to reduce their pain, and this caused them to actually feel better, thus causing a elevation in B endorphine levels. But what exactly caused this rise in B endorphin concentration in Cerebrospinal fluid - not something that can be explained biologically. So in this sense, I feel that the article doesn't address why B endorphin concentration rises, and for obvious reasons, avoids any discussion on consciousness, making it seem as though this whole process is biological.
The fact that there exists a neurotransmitter in the brian which affect mood, perception of pain by behave as pain regulators, and contribute to an euphoric feeling definately needs to be further addressed with respect to consciousness. The paper definately supported its findings, but at the same time, very well avoided the idea of consciousness. It makes sense that B endorphin levels of chronic pain patients are lower than those of pain free patients - according to the definition of endorphins. Something I would like to know about the study was if there was a correlation the patients who did not respond to any affect of the placebo with their report on how much pain they experience (the 1-to 10 scale question). Did these patients have a higher or lower pain threshold with respect to the patients who did experience less pain due to the placebo. These, and similar questions would bring the topic of consciousness more into the paper.
Statistical analysis of enorphin levels in both sets of CSF samples took place. There was a significant level of B-endorphin increase between initial sampling and placebo administration in the responder group while there was no significant data from the non-responder group.
In addition to what this experiment had to say in terms of endorphin levels being the biochemical mediator of human autoanalgesic responses, it implicitly said a lot about consciousness and its role in pain reduction and sensation. As stated, "the peak B-endorphin level is controlled by psychogenic processes." Since the drug administered was a placebo, it is assumed that any pain alleviation was due to some mental release of the endogenous opioid. However, is this conclusion too assuming? That is to say, could there have been some other reason for which pain alleviation occurred? Though I think it's difficult to come up with alternative explanations, one might consider the differences in the chronic pain type in the patients. It seems that patients were lumped together in terms of chronic pain but not really separated into different divisions. I question whether the same data would arise if the initial pain of teh patients was categorized into those with EXTREME pain versus less severe, etc. Perhaps only those with the most severe of pains can be aided by the work of endogenous opioids whereas those with less severe (though still very high) pain might not be helped in such a way. This would place limitation on the idea of consciousness alleviating pain. One would therefore be forced to ask why only one type of pain can be helped this way and not others.
One thing that I was unsure of was the authors’ conclusion that B endorphin is "the biomechanical mediator of human autoanalgesic response". It seems too easy to be able to attribute one compound to the placebo effect, when science has not been able to understand the matter in the past. They did test a series of other endorphins, none of which showed a correlation with the chronic pain. But I still find it hard to believe that the body only uses one chemical compound to respond to an expected effect. One would think that something so complex as having the body react to what the mind perceives as effective could not be reduced so easily down to the concentration of one chemical in the cerebral spinal fluid. It’s possible that the complexity of this problem lies in the triggering mechanism of this reaction, which the paper does not really address, but it still seems odd that the problem can be so reducible. But since the body is just made up of a series of these reactions it is feasible that these findings are more comprehensive than they seem at first glance.
While Weiskrantz's article did not provide much in the way of empirical methods for one to critique, it offered an interesting perspective with which to approach consciousness, that of diverging from the neurological discipline.
Everything we have thus far read has relied very heavily on what is typically considered science to explain consciousness at the cost of being eluded by the truth; even Searle, despite his background in philosophy, refused to admit there was even a possibility that something else in the mind could exist without being detected by traditional biology. This is not to say that Weiskrantz's article was in any way related to the "metaphysical" as he was criticized for; he did provide enough scientific evidence to allow his studies to remain within the realm of science and not be "inadmissible to science." What made the article interesting to me, however, was his refusal to abandon a topic such as this that could easily be attacked as a result of its lack of adherence to what is currently perceived as scientific grounding.
Though he was criticized for exploring a phenomenon that others apparently found to be too vague or ill-defined or philosophical, Weiskrantz continued his investigation and was able to approach an explanation of sorts. What this means for me is a reinforcement of my belief that science needs to begin to allow the possibility that not everything can be explained by science, or at least by present-day, conventional methods and theories. I am not necessarily saying that science cannot explain everything; I am saying that there are many things that cannot be explained in the way modern science permits. There are many issues and phenomena that have yet to be studied simply because current thinking does not allow the possibility of their existence, despite overwhelming evidence to support their existence. Science needs to become more open-minded and acknowledge that there are phenomena beyond our current understanding that cannot be explained, not because of a lack of proof of the reality of these phenomena, but because science is unwilling to admit that something could exist outside the realm of its current understanding.
After he discussed blindsight in monkeys, Weiskrantz addressed a difficulty with neurological research which had previously led to there being misconceptions about blindsight in humans. Due to human error, it is often difficult to isolate brain areas; often surrounding tissue is damaged in the process. Research with Daniel was so informative because he was known to have only visual cortex damage and because the scientists used a new method. This novel procedure involved directing patients to move their eyes towards the light in their blind fields and then asking them to make guesses.
One of the interesting findings with Daniel was that he could say whether a light was present with remarkable accuracy. He actually performed the best when he said he was merely guessing. Other patients have been shown to retain even some semantic ability when words are flashed in their blind fields.
The subjective experiences of patients are varied. Many report randomly guessing at times and at other times feeling different ways depending on the objects in their blind fields.
It is good to see that researchers have been fairly thorough in their study of blindsight. They have been able to determine through extensive studies that blindsight is not simply a byproduct of processing in the fully functional part of the visual field. I was convinced of this finding by the study which proved the existence of blindsight in a person who was missing both visual cortexes and by evidence from tests done on the natural blind spot. I am skeptical, however, of whether the study by Rafal et al. lends support. These researchers have noticed that people with blindsight are much slower to move their eyes towards a light in the good part of the visual field when there is a light present in their blind field (Weiskrantz 1992). Perhaps their argument would be more clear if the author would have specified whether the light in their "good field" was on at the same time or after the light went on in their blind field. If both lights went on simultaneously then the "slow eye movement effect" could still be due to processing in the sighted field which would have occurred when the light was detected by the peripheral vision.
Moving on...I found that the author presented convincing evidence for the midbrain area known as the superior colliculus being a "backup for the visual cortex" (Weiskrantz 1992). I also found it interesting what the author says about blindsight and normal vision being controlled by different brain regions. This reminded me of the "off-line" and "on-line" systems which Crick and Koch mentioned in their paper. It is wild to me that a bias could come into the guessing process of which a patient is completely unaware. It almost seems like magic.
It Is also interesting to me that "learning" seems to take place in the brains of people with blindsight. The author suggests that blindsight fields are reduced, for example, because the brain utilizes intact pathways in the cortex and/or the midbrain (Weiskrantz 1992). The author also mentioned earlier in the paper that residual vision in monkeys is increased when the visual cortex is removed from only one occipital lobe. It seems likely that the pathways in the fully functional visual cortex are recruited.
This paper definitely captured my interest and inspired me to learn more about the topic, especially with regards to the mechanism involved in the improvement over time observed in blindsight patients who were given testing.
