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Keep Calm and Carry On: Now Panic and Freak Out Expected vs. Actual Inputs and the Perception of Pain

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       The intricacies of human pain perception have long been a topic of interest in neurobiology. Pain was at one point thought to be caused by overstimulation of tactile sensory neurons, but there is more to the story than that. Special receptors, called nociceptors, are the primary pain receptors. When stimulated, they send a signal to the spinal cord where it crosses over to the opposite side of the body as the stimulation. This is different from tactile signals, which travel up the spinal cord on the same side of the body as the stimulation and cross to the opposite side once they reach the medulla. This difference in crossover location explains why, depending on the location of a spinal cord injury, a person could be able to feel pain but no other sensation from a particular point on their body[1]. 

       The perception of pain can be regulated by the body in several ways. Specialized neuronal cells in the spinal cord act as gates, regulating the speed of the pain signal. These gate cells can restrict the transmission of signals if the tactile neurons adjacent to the area that is in pain are stimulated. That is why rubbing a stubbed toe soothes the ache and why running a mosquito bite under hot water makes it itch less. The pain signals can also trigger the release of natural painkiller molecules such as endorphins. Factors such as age, sex, mental and emotional state, attitude and expectation can also affect how strongly pain is perceived[2].

       This generalized explanation, however, only scratches the surface of how pain is perceived and how that perception varies between people as well as in a single person at different times. It explains what happens between the moment your hand touches a hot stove and the moment you swear and pull your hand away, but it does not explain why sometimes you feel little to no pain when touching that same hot stove. It also does not explain pain or discomfort that is not physically inflicted, such as motion sickness or withdrawal symptoms. An explanation for these phenomena could be revealed through a closer look at the difference between the inputs that the nervous system expects to receive and the inputs it actually receives.

       The behavior of the nervous system relies heavily on patterns both genetically hardwired and built by practice or observation. A large portion of the information our brains receive does not come from direct sensory input but instead is supplied by the patterns our brains are used to. Our nervous systems combine sensory input and expected input to create our experiences. Usually, the actual input and the expected input complement one another and we are not aware of this process. However, when the actual input and the expected input clash, our nervous systems can produce outputs that we perceive as pain or discomfort. In other words, if the nervous system expects input A and experiences input A, the resulted output is "keep calm and carry on." If the nervous system expects input A and experiences input B, the resulted output is "panic and freak out." In this way, a person can experience pain without the stimulation of their nociceptors or any of their physically induced pain pathways. 

       It has already been noted that expectation can heavily influence a person's perception of pain. Expectations can be thought of as the influence the I-function has over sensory input in certain situations. For instance, if a young child has never been to see a dentist and knows nothing about going to see a dentist, the scrapes and pokes from the procedure are less likely to be painful to that child. On the other hand, if a child has never been to see a dentist and all he has ever heard are horror stories about dentists, those same scrapes and pokes might seem excruciatingly painful. This difference in response can be explained by the physiological model of pain perception. However, the opposite phenomenon is also common: a person expects a procedure to be painful before it happens, but when it actually happens, that person does not experience pain. This sometimes is the case when people get a part of their body pierced. Industrial piercings consist of two holes on the outer cartilage of the ear connected by a single piece of jewelry. When I got this kind of piercing done, I expected the experience to be painful. I was surprised when I experienced no pain associated with the first of the two piercings. While the piercer prepared to do the second piercing, a process that lasted less than a minute, I was not concerned that it might hurt. However, the second piercing was painful enough to make my head swim. 

       This can be explained in part by the first pain perception model. Before the first piercing, my nervousness about the impending procedure could have triggered the release of epinephrine or other pain-altering chemicals[3]. After the first piercing, I calmed down and no longer benefitted from the epinephrine. What this explanation doesn’t account for is the dramatic difference in the amount of pain I felt over such a short period of time. The half-life of epinephrine is about 2 minutes[4], but the time between piercings was less than a minute. Surely I would have still been affected by epinephrine at the time of the second piercing.

       The second model of pain perception can help account for this discrepancy. Before the first piercing, I expected input A: getting a piercing hurts. During the first piercing, my nervous system experienced input A: getting a piercing hurts. Because the actual input matched the expected input, I did not experience the pain. Before the second piercing, I expected input B (getting a piercing does not hurt) based on my previous experience. During the second piercing, my nervous system experienced input A: getting a piercing hurts. Because the actual input did not match the expected input, I experienced pain.     

       Perhaps a more familiar example of the second pain perception model at work is motion sickness. Motion sickness occurs because signals from the inner ear report to the nervous system that your body is moving or accelerating while signals from your muscles report that you are not actively moving your body. In some cases, such as seasickness or motion sickness while riding in the back seat of a car, your eyes are also reporting that your body is not moving in relation to your surroundings[5]. The nervous system is expecting to receive complimentary signals: I am not moving my body, my body appears not to be in motion, and I do not feel like I am in motion. If it were indeed the case that all of the inputs compliment one another, the nervous system would generate the “keep calm and carry on” response that would go unnoticed. Instead, the nervous system is receiving conflicting signals: I am not moving my body, my body appears not to be in motion, but I feel like I am in motion. Because of this discrepancy, the nervous system generates the “panic and freak out” response that we perceive as motion sickness.

       This second pain perception model can also help explain the placebo effect, in the case of caffeine dependence for example. A person becomes dependent on caffeine if they consume enough of it regularly over a long period of time. The nervous system adjusts to the persistently high levels of caffeine and over time more caffeine is needed to produce the same effect. If a person who is dependent on caffeine reduces or ceases their caffeine intake, their blood pressure drops, causing a headache which can be alleviated with the use of analgesics, many of which also contain caffeine[6]. It is sometimes the case that a caffeine dependent’s headache can be alleviated through the placebo effect[7]. If they are given decaffeinated coffee but they believe they are drinking caffeinated coffee, the negative effects of caffeine reduction can disappear. In these cases, their nervous system expects the coffee to be caffeinated and that the caffeine in the coffee will alleviate the headache. Their nervous system experiences drinking caffeinated coffee and, since they receive no input to the contrary, the pain of the headache ceases to register. 

       These are only a few examples of phenomena that can be explained by the “Keep Calm and Carry On: Now Panic and Freak Out” model of pain perception. This model can most likely be improved and fleshed out by studying its interaction with the nociception model of pain perception. It is possible that a similar model can be applied to better understand the intricacies in the perception of any of the types of inputs the nervous system receives.



Works Cited

1. Luttrell, Andy. “The Neurology of Pain Perception: How the Brain Feels Pain with Nociception” Oct. 28, 2009.



2. “How You Feel Pain” Feb. 13, 2009.



3. Ranney, Don. “Anatomy of Pain” University of Waterloo Nov. 29, 1996



4. Voet D, Voet J (2004). Biochemistry (3rd ed.). USA: Wiley


5. Marks, Jay W. “Motion Sickness” Accessed Apr. 5, 2010.



6. “Caffeine Addiction” Accessed Apr. 5, 2010.



7. Flaten, M.A., Aasli, O., & Blumenthal T. D. “Expectations and placebo responses to caffeine-associated stimuli.” Psychopharmacology 169.2 (2003) pg 198-204.

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Serendip Visitor's picture

Keep Calm vs. Freak Out

I enjoyed reading your blog -- interesting!

Paul Grobstein's picture

alternatives to thinking of pain (and ... ), as "localized"

A very useful way to think about the relation between "classical" and ... more current ways of thinking about pain, and perhaps, as you suggest, about other phenomena as well.  Thanks, will use it in the future.  What it also does is to make me think about what the appeal, here and elsewhere, is of stories that make sense of things in terms of particular receptors, ie of nervous system "localization," and what general lessons there are to learn from the inadequacies of such stories in a variety of contexts.