by XXXXX XXXXXXXX
Sensation and Perception Literature Review
Psychology 325
18 April 2004
Fear and pain constitute two of the most commonly misinterpreted concepts in human perception. When we are in a state of fear can we sense pain more or less acutely? It is commonly believed that amygdalitic coherence channels pain from the so-called 'fear centers' via the relatively well understood epineuronic and pseudoneuronic mechanisms. Yet, there is little understanding of how the sensory homunculus finally integrates both types of information (Irvine 2003; Podgorny & Laslo 1992; Anselmo et al. 1998) especially in light of the supposed modulating capabilities of fear. In this paper we will discuss the various hypothesized …show more content…
mechanisms for the eventual integrations of this information and attempt to reconcile the two positions set forth by Gibson (1952) and Irvine (2003) with respect to both fear and pain.
What are the 'quanta' of pain?
More importantly, how are the feelings of 'pain' encoded when we feel the very different sensations of, say, the sting of a bee or the heartburn of indigestion? How does fear enhance or detract from the eventual sensation of pain? Anselmo (1998) posits a quantum mechanism that encodes pain in discrete neural chunks, modulated by the source of the pain and its locus in the body. Pleanty of evidence supports this position, the process being most recently demonstrated by Rosetta (2004) and expanded and enhanced by the fMRI work of Irvine and colleagues (2003). The former investigators began the process of re-introducing fear to the experimental paradigm. Subsequently, Siraigal and colleagues (2004) used functional imaging to investigate the directionality of this fear-pain connection. They found that fear _preceeding_ pain lessens the sensation of the eventua pain event while events in the opposite order (pain followed by fear-inducing stimuli) enhances the pain. (See also Edding and DeSimone, …show more content…
2004).
On the other side of the debate, Thompson & Huges (2003) find that fear has no modulating effects at all with respect to pain, regardless of its origins.
This work was replicated, again, via functional imaging (fMRI and PET) by Irvine and Sisiht (2004), totally discounting Gibson's position that the pseudoneuronic system, paired with the hypothalamic fight-or-flight system are key in modulating this behavior. This further means that any attempt to modify human response to pain via perceptual mechanisms (especially those thalamic and hypothalamic) are destined to fail. It is also interesting to note that there were some modulating effects of caffeine and methamphetimine, substances frequently used by those in combat and military situations. It would not be surprising to find that illicit consumption of these substances by troops in Iraq, Afghanastan or other Persian Gulf locations. Voshell & Oomes (2004) suggest a potential interaction of visual stimulation with the consumption of thes dopagenetic systems and drugs, along with some substantial psychophysical evidence of fear-pain interaction when under the influence of these
drugs.
How can this evidence be used to support the positions of either Gibson or Irvine? There is a clear division between the two camps, one saying that pain and fear are related and the other that there is no relationship at all.
A clever experiment by Diaz and Roshia (2004) may just demonstrate a technique to finally resolve this question. In this experiment, subjects were shown images consisting of synchronous or asynchronous texture gradients, both scaled according to Weber's law. A small electric shock was delivered to their wrist area each time the stimulus was about to desynchronize. A transcranial magnetic stimulator then was used to stimulate the amygdyla either before or after the shock. In the prior presentation condition, subjects reported no desynchrony of the texture patterns while in the post presentation condition a clear break of perceptual experience occurred (p