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Pain is one of the most basic primitive mechanisms of survival and biological enhancement. Almost all basic biological organisms contain inherent mechanisms that allow them to react to certain stimuli that may affect its normal function. These basic mechanisms have evolved to allow survival and progression of all organisms which in turn has created more complex means of survival and evolution. The experience of pain is a fundamental human sense.

Why do we experience pain?
We all need to experience pain to allow the optimum chance of survival. Without the feeling of pain we will not have the motivation to do something to escape it. Pain allows us to recognise a feeling of unpleasantness and it creates a focus on the area of the body the stimulus is coming from. Pain signals aim to create a change in behavioral patterns through conscious intervention. Pain will stimulate us to reduce the noxious stimuli, protect us from further damage, create an environment for tissue repair, and store memory for future protection.

It is important to recognise that pain does not necessarily represent the amount of tissue damage. Pain is essentially a signal to alert us to that fact that something is not functioning optimally and is not just restricted to representing areas of the body. There  may be simple specific tissue damage (e.g. a sprained ankle) and there may also be complex and non specific signals (e.g. pain down the arm as a result of a heart attack).

The physiology of pain signals: Nociceptors (Danger Receptors)
A stimulus that is potentially or actually damaging is known as a noxious stimuli. Nociceptors are neurons found in all tissues (except the brain) that detect a noxious stimuli. When the stimuli passes a threshold (usually when there is tissue damage occurring) signals are sent back through our central nervous system.Nociceptors respond to thermal, chemical or mechanical changes within a tissue and can either send signals to the spinal cord for immediate response (e.g. sudden taking away of hand after touching a hot plate) or signals can reach the brain for higher processes and conscious intervention.

Nociceptor Sensitisation
Some nociceptors become sensitive to certain irritants (e.g. inflammation) which can cause them to become hypersensitive and hyper-excitable. This can cause certain areas of the body to react to stimuli that would not normally cause pain. Interestingly, this hypersensitivity may also develop in the spinal cord and has been theorised to have implications for the biopsychosocial model of pain perception.

Ultimately pain does not follow a simple path of noxious stimuli to signaling through nociception through to messaging of pain to the brain. It is much more complex than this.....

Pain in the brain
The brain ultimately is the ultimate communicator of pain. Without the brain there is no pain. Pain is represented in the brain by a distribution of brain cells called "neurotags" that represent areas of the body. Interestingly these neurotags are inter-connected with many constituents of many neurons within the brain displaying the complexity to the neurophysiology of pain which we are yet to fully comprehend. Pain perception is regulated in the brain stem (the primitive part of the brain). Pain signals from the body meets pain perception from the brain at the brain stem and this results in the overall feeling of pain.

Neurotags are theorised to be inter-connected with our consciousness creating a connection between between thought processes and pain. Essentially it is this framework that reveals the complex relationship between pain perception and the actual feeling of pain. Furthermore the development of sensitivity through a mechanical,chemical, or thermal means along with conscious sensitivity and the relationship between these factors assists in revealing why pain is not a very good marker of where and what the problem is.

Brain Sensitisation
Much like nocicepters can become sensitised so can areas of the brain. Constant stimulus of a neurotag may cause it to become active further than it should. This may result in a phenomenon called "over-generalisation" in which pain begins to be felt for reasons that become more unpredictable and less related to problematic tissues (this is not yet well understood).

Factors Influencing Pain
The following factors can Influence pain:
  • Exercise: Exercise can be both a treatment and a stimulus of pain, so that too much exercise increases pain, while too little exercise may worsen pain through multiple mechanisms (e.g., pain posturing, deconditioned muscle microtrauma, and neuroendocrine responses. (1)(2) Exercise activates endogenous analgesia (in healthy individuals and clinical patients) via triggering the release of beta-endorphins from the pituitary (peripherally) and the hypothalamus (centrally), which in turn enables analgesic effects by activating μ-opioid receptors peripherally and centrally, respectively (3)
  • Lifestyle (e.g.smoking/alcohol): whilst nicotine and alcohol have properties that provide analgesia, multiple clinical pain studies evidenced that smokers and drinkers are at increased risk of developing back pain and other chronic pain disorders. (4)(5)
  • Age: Pain sensitivity may diminish in adults of advanced age (6) pain frequency increases with each decade. (7)
  • Pain “catastrophizing”: an inability to stop thinking about one’s pain and to characterize pain as unbearable, which increases activity in areas of the brain related to anticipation of pain, according to several studies. Catastrophizing alters pain modulation in patients with persistent clinical pain (8)
  • Anxiety, Fear, Boredom, Anticipation of more pain: “bad mood” and somatization (e.g., behavior characterized by recurring multiple clinically significant complaints about different physical symptoms and extensive health care seeking). Indeed, somatization as well as increased, intense, or persistent depression and anxiety are the most important predictors of adverse outcomes of invasive interventions for chronic pain [9], and evidence indicated a correlation between pain intensity and presence of somatization (10)
  • Depression: Depressed mood is a common and powerful emotional state that affects the pain experience. Depression is defined as a psychological problem characterized by negative mood, hopelessness, and despair, and an average of 52% of patients with pain fulfill the criteria for depression (34). Even more people have a depressed mood but do not fulfill the diagnostic criteria for major depression (35). The presence of depression in a pain condition is associated with higher levels of pain intensity and is a potent risk factor for disability (35) (36). Furthermore, people who have musculoskeletal pain and are depressed have been found to have twice the sick leave duration as those who have pain but are not depressed (37)(38)
  • Sleep Disturbance: Studies in clinical populations, as well as experimental studies in healthy adults, suggest that pain experience and sleep are bidirectionally connected so that severe or persistent pain may disturb the sleep, while sleep disturbance enhances pain [11]. Hours of reported sleep on the previous night highly significantly predict the current day’s pain frequency, and less hours of sleep correlate with greater next-day pain in general population [12]. Alterations in sleep may also mediate the effects of pain catastrophizing on clinical pain [13].
  • Stress (current and previous episodes): Stressful experiences, depending on the type, intensity, and duration of stressor can alter human pain sensitivity by either reducing pain (“stress-induced analgesia”) or exacerbating pain (“stress-induced hyperalgesia”), and the mechanisms of both phenomena are not fully understood. Generally, acute stress induces analgesia (found, e.g., among athletes injured in games and soldiers injured in battle), while the effects of chronic stress in nociception are less predictable [14]. Epidemiological studies have implicated stress (psychosocial and physical) as a trigger of first onset or exacerbation of many painful disorders such as irritable bowel syndrome [15] and low back pain [16]. An individual’s response to stress, either physical or emotional, includes activation of the hypothalamic-pituitary-adrenal (HPA) axis, which is accomplished by the secretion of corticotrophin-releasing hormone and arginine vasopressin from the paraventricular nucleus of the hypothalamus [17]. There is evidence that the HPA axis is involved in acute pain and chronic pain.
  • Personality-related factors: for example previous pain experiences, emotionality and cognition.
  • Fear of Pain: can lead to a patient not moving, especially when a certain movement caused pain in the past
  • Negative affect (neuroticism): a more irritable or anxious personality, which may be a precursor to pain-related fear or catastrophizing
  • Socioeconomic factors: social support, acceptance, incentives, education, financial stress, occupation, quality of life
  • Clinical Conditions and health status
  • Gender, Genetics, Ethnicity: current studies in genetics and genetic coding are revealing genetic components of our experience of pain.
A Model of the Psychological Process of Pain and Pain Perception (a)
As a sequence of processes, starting with initial awareness of the noxious stimulus (pain site), then processing the pain in the brain (cognitive processing), evaluating (appraisal), and interpretation that leads people to act on their pain (ie, their pain behavior) (18):
  • Attention: One function of pain is to demand attention (19). Viewed as a warning signal, pain is helpful because this attention should lead to appropriate responses in dealing with the injury (20). If pain is considered a “threat,” then the threat value of the (noxious) stimulus helps to steer awareness: the greater the threat, the more attention given. Attention to pain then may be linked to fear and anxiety and the need to take action (eg, escaping or avoiding it). Vigilance refers to an abnormal focus on possible signals of pain or injury that might help explain why a seemingly small injury results in intense pain. This mechanism also underscores the close link between emotional and cognitive processes and attention (19)(21).
  • Interpretation: Cognitive processes are highly intertwined with emotional processes, and it sets the stage for behaving (19). How we think about a noxious stimulus is shaped by our previous experiences, which explains why the simple directive “think about something else” often is impossible to accomplish. Indeed, the paradox is that attempting to suppress thoughts about pain actually increases the pain experience (22). Cognitive processes are central in explaining why we sometimes may experience an insignificant stimulus, such as light pressure, as severe pain, or a serious injury as little or no pain. Several basic cognitive and emotional aspects are involved in the interpretation of pain
  • Beliefs and Attitudes: Beliefs provide cognitive pathways to serve the useful purpose of aiding in rapid interpretation of stimuli. They are like shortcuts that help our brain process the enormous amount of information flowing in. They provide a sort of automatic interpretation of the stimuli; thus, these stimuli do not need lengthy processing in the brain. Yet, this very propensity can lead to responses that may be detrimental. Many factors affect beliefs and attitudes to pain (e.g. socioeconomic status, current health status, psychological status, social representation etc.) Several attitudes and beliefs have been found to be related to the development of persistent pain and disability (23)(24).
  • Expectations: The ideas or perceptions we have about our pain also are mirrored in our expectations and may have considerable impact on our experience of the pain (23). Normally, we have ideas about the cause of the pain, its management, and how long it should take for recovery (25)(26). These expectations appear to drive coping behavior, even in the seeming absence of actual feedback. Furthermore, such expectations or health perceptions are a good predictor of outcome in a host of medical conditions (25)(26). One significant determinant of our experience of pain is whether our expectations are fulfilled. We may expect, for instance, that we will fully recover from a bout of neck pain in 3 or 4 days. Epidemiology tells us that this is a very optimistic expectation, and when the expectation is not fulfilled, it may generate further negative cognitions and motivate behaviors that may not be particularly helpful (27)(28) .
  • Cognitive sets: In the process of making sense out of incoming signals, we use various “ways of thinking” to help provide a framework. This is a normal and helpful process, but in some cases cognitive patterns misrepresent actual events or probable future events causing interpretation to be tantalizing and well connected with the emotional state  where a consistent “error” in interpreting reality is made (18). This pattern of interpretation is like a lens that distorts one's view of the world and appears to function as a part of our response to stress (28). An example of such a thought process is pain catastrophizing (E.g. the person imagines the worst possible result that could happen, but accepts it as the given result). Catastrophic thoughts usually are stated as assumptions (eg, “If the pain does not get better, I will end up in a wheelchair” or “The pain will never stop, it will only get worse and worse”). Catastrophizing is associated with a variety of problems that hinder recovery, making treatment more difficult and increasing the risk of developing persistent pain and disability (24)(29)(30).
  • Emotions and their regulation: The typical emotional reaction to pain includes anxiety, fear, anger, guilt, frustration, and depression. How these emotions are regulated by the patient has implications for their impact on pain. Indeed, emotions are powerful drivers of behavior and shape our experience of the pain via direct neural connections. Negative affect is a key reason we associate pain with suffering. Thus, pain activates negative emotions that vary from tolerable to miserable (31). Anxiety and worry are prevalent emotions, as pain represents an imminent threat to our welfare (32). People with persistent pain typically have significantly higher rates of anxiety disorders than do those without persistent pain (32). Fear, which is characterized by an extreme reaction that prepares us for “fight or flight,” is one form of anxiety that has powerful consequences (eg, for our cognitions, attention, and behavior). Fear, however, is time limited. More common is worry, which is distinguished by frequent cognitive intrusions where the person considers “what if” possibilities (28) that are quite negative and aversive (33). Because of this
    nature, worry drives behavior, attention, and cognitions.
  • Coping Strategies: When a painful stimulus has been attended to and interpreted as being a threat, strategies for dealing with this threat are activated (36). These strategies first may be activated cognitively and involve a host of cognitive techniques (eg, ignoring, visualizing) and overt behavioral techniques (eg, relaxation, self-statements) believed to reduce the threat of the pain. Coping strategies are learned and involve an integration of emotional, cognitive, and behavioral systems. The learning experiences help to fine-tune these strategies by providing feedback as to whether they work or not. Although some situations offer the opportunity to ponder which strategy might be best, such as a relapse or flare-up, the choice of coping strategy may occur quickly without conscious thinking in acute situations, such as an acute injury (eg, cut yourself with a knife, smashed finger with a hammer). Once the strategy is activated, it is likely that this process will be reflected in actual behavioral attempts to cope with the pain.

Management of Pain
The management of pain falls under these broad categories:
  • Pharmacological: One of the more common methods of pain management. Pharmacological drugs are generally over the counter or prescription medication. The most common pharmacological option is analgesic medication the most powerful of which are morphine and codeine which act on the opiate receptors of the brain. Overall, growing evidence suggests that multiple genetic factors influence pharmacokinetics and pharmacodynamics of analgesic drugs, and many common functional polymorphisms may affect analgesic response independently and through interaction [39]
  • Endogenous Opiates (enkephalins and endorphins): Opiates that are derived from the body that have properties similar to pharmaceutical opiates. Human activities such as eating certain foods, laughing, and exercising all have an influence on endogenous opiates.
  • Alternative Therapies: therapies such as osteopathy and acupuncture are theorised to have an effect of endogenous opiates and assist in augmenting the bodies natural healing mechanisms.
  • Placebo Effect: research suggests that placebo can have a considerable effect on pain perception.

Osteopathy and the treatment of Pain
It is clear by this summary that pain involves complex processes throughout the whole body and mind. The osteopathic model of treating the body as a functioning unit respects the complexity of pain. Osteopaths pride themselves on their understanding of the anatomy and physiology of the body and use this knowledge to treat the individual according to their systemic needs. An understanding of this complexity allows osteopaths to evaluate and treat the many different elements that make up an individuals pain presentation.

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Other Sources

  • (a) Journal of the American Physical Therapy Association:
  • Today in PT Website:
  • University of Calgary Website:
  • Scientifica Volume 2013 (2013), Article ID 415279, 19 pages: