How brain imaging technology is placing emphasis on the potential for the mind to influence our physiology, and how this influence should not be underestimated.
What really determines how we feel pain? Scientists are now suggesting that the complex emotional state of the brain may in fact bias how we process and thus experience this highly protective sensation. What’s more is that this may explain how there is such variation in our pain thresholds and how some individuals can be susceptible to conditions of chronic, prolonged pain.
Our ability to detect pain acts as an alarm system, protecting and guarding our bodies against potentially damaging aspects of our environment. This imperative awareness is mediated by ‘nociceptive’ nerve fibres that innervate our skin and organs, and feed into the pain processing pathways of the central nervous system. These fibres feed via the spinal cord to the brain stem, to the pain generating centres of the brain, most commonly the somatosensory cortex.
The complexity of the relationship between peripheral pain input, the actual painful experience, and subsequent report of the sensation makes documenting pain in clinical research particularly problematic. Over the past decade, scientists have been addressing the inherent flaws that exist in pain research, and how this limits our understanding and progress in anaesthetic therapeutics. Experimental neuroimaging is emerging as a highly efficient method in mainstream pain research to accurately identify the key areas of the brain responsible for mediating these protective and highly important sensations. By allowing access to the brain activity where these sensations originate, experimental brain imaging allows for a more accurate and objective measure of the pain experience.
The multidimensionality of pain may be explained by the variety of sensory and cognitive aspects that may ‘tune’ our individual pain thresholds. In anaesthetic research, much emphasis is now being placed on the emotional factors and thought processes that impact how we experience pain. Consider first the manner in which we can allocate our attention to different aspects of our environment. Our ability to focus on relevant events and attenuate our responses to irrelevant events is an integral component of higher cognitive functioning. So much so, that these attentional influences may have an impending impact on the intensity of our peripheral sensations. In 2003, researchers tested the power of distraction by presenting a series of unpleasant odours to subjects whilst they were subjected to thermal pain. They found, like many other psychophysical studies, that when the subject’s attention was focused on the pain, they described the sensation as more intense and unpleasant.
Then consider, how our subjective experience of pain could be impacted by our expectations and that these expectations of pain can be attributed in part to individual trait differences: fear and anxiety may play a prominent role in the activation of pain pathways. Our cognitive predictions can be impacted by false and unequivocal beliefs stemming from inaccurate memories or inappropriate anxiety that distorts our interaction with the situation in the future. In a neuroimaging investigation in 2006, researchers identified that those individuals that were more anxious about pain (as determined by the Fear of Pain Questionnaire) showed a heightened response in brain areas that encode the emotional aspects of pain, showing their anticipatory fear could actually physically heighten their sensitivity to the painful sensation.
To the ‘normal person’, pain is a mostly acute and infrequent sensation such as a headache, bruise, or the occasional back twinge. For some people however, pain can persist for months at a time, and is often completely unexplainable. Chronic pain states include migraines, neuropathic pain and arthritis. Chronic pain is one of the largest medical health problems in the developed world because it cannot often be efficiently managed or treated. This is however, not for a lack of trying. Currently, there is little research that focuses on understanding the biology of chronic pain, but the development of neuroimaging techniques may be opening the first window of insight into the neurological framework for such conditions.
The problem with chronic pain states are that ‘secondary pain’ often develop as a consequence of the negative impact of unsuccessful treatments. Prolonged worry and emotional turmoil about chronic pain diagnosis leads to the secondary development of mood disorders and depression. The majority of this area of research has identified that a positive mood has a significant pain-attenuating effect and negative mood increases sensitivity to experimentally induced pain. Furthermore, population-based longitudinal investigations have observed that depressed individuals are at an increased risk of developing chronic pain conditions, than those without mood disorders. This evidence establishes a role for emotion-based tuning of pain modulatory systems and provides a basis for novel strategies in chronic pain management by addressing the negative lifestyle impacts associated with such conditions.
It is a common fallacy that placebo effects lack credibility or significance in modern healthcare systems. In fact, since the post-World War II introduction of placebo effects into mainstream medicine, scientists have used the impact of placebos in controlled drug trials to gather information on the qualitative nature of pain. A placebo describes an ineffectual treatment (often in the form of a sugar pill) that is intended to deceive the recipient to believe they are taking a pharmacotherapy to treat their condition. Placebo research has implicated prefrontal pathways in the brain as a source of cognitive pain modulation, because studies have consistently observed that activation of this area correlates with ‘emotional detachment’ from the pain, and thus a higher ability to cope with it. With its extensive connections to the emotion and pain processing centres, this area acts as a powerful modulator in expectation and reappraisal of the placebo effect, by dampening fear by suppressing amygdala (the emotion centre) activation. Remarkably, other personality traits like dispositional optimism can seriously enhance placebo analgesia. This research reinforces the importance of positive expectations about the efficiency of a drug and may provide an explanation for why many analgesic treatments in chronic pain are unsuccessful at a population level.
“To consider only the sensory features of pain, and ignore its motivational and affective properties, is to look at only part of the problem, not even the most important part at that” are words from the pain researchers R. Melzack and K.L. Casey who even 50 years ago, placed emphasis on the multidimensionality of pain perception. The rapid development of neuroimaging techniques means the next 20 years are predicted to be particularly prosperous for identifying new targets in surgical and pharmacological pain relief tools. In the mean time, it seems a ‘mind over matter’ attitude could be more beneficial than we would ever have expected.
Post by Isabelle Abbey-Vital
Neuroimmaging is changing the way we look at pain. Catastrophic thinking certainly affects the emotional aspect of pain perception/nociception. As an RN, fibromyalgia expert, author and pain advocate, I believe caution should be used with the term “mood disorders.” Mood disorders are very serious mental illnesses, such as bi-polar, clinical depression, and any other group of psychiatric conditions that have a biological chemical abnormality. This is not to be confused with the situational anxiety and depression we see in response to the pain experience and experience during the grieving process, something everyone has experienced at one time or another. We can’t think pain away, but I do agree we can change the way our brain perceives it by changing our reaction to a certain extent.
I take offense to the term “normal person.” Who would that be, and what parameters are you using to determine normal? A better analogy might be, “the otherwise healthy person.” To say otherwise is to say that the patient in pain is not normal, and that simply is not true. A person in the throes of a migraine, vomiting to the point of exploding blood vessels in their face, can hardly get a grip on positive thinking.
While the research is exciting, and I write a great deal on healthy coping and ways to defer pain thoughts, I do believe that the human brain plasticity is part of human evolution. Over time, possibly decades or centuries, we can transform this phenomenon, but great care must be extended to the patient in pain when explaining how their “mood” can improve or compound their pain. We must tread very lightly. Pain is very real to the person experiencing it. I suggest we use care not to become part of the emotional conundrum patients in pain experience. A simple validation of pain can often be all a patient needs.
It is also important that the research does not get caught up in only studying emotional responses to pain. Even chronic pain can be a warning sign that something is physically wrong. Something that was not diagnosed property, say 7 months to 5 years ago can cause chronic pain. It is possible to relieve chronic pain by getting the physical root cause and it also possible that the causative physical problem is too extensively to obtain pain relief.
The brain is in pain, physical and emotional pain has an effect on the brain. We will not have clear iron clad answers until we can understand how the brain thinks.
This article represents the failure of medicine to understand and treat pain effectively. This stems from longstanding prejudice of doctors toward people in pain which continues today. Undoubtedly doctors find fault with peoples minds and emotions as they have proven themselves incapable of finding the the physical causes of pain.
There is more added to pain than just emotions. There is memory and cognitions added, as well as motor components. In the limbic system memory, emotions and cognitions are processed, and along with contributions to pain signals, the output goes to the motor cortex via the basal ganglia. So changes in any of these components can have an effect on each other. We reported on this in 2001 in Tollison’s Practical Pain Management and in further updated detail in the American Academy of Pain Medicine new (2013) textbook entitled Comprehensive Treatment of Chronic Pain by Medical, Interventional, and Integrative Approaches. Check out Chapter 70: “Pain as a Perceptual Experience” and Chapter 71: “Neuroplasticity, Sensitization, and Pain.” They may help and include references.
Also, be cautious about f-MRIs, as the brain can be turned on by imagining something from the past, and look like it is happening currently. So the brain, which has no time perception, can only tell you if something has ever been, not necessarily if it is current.