Supplemental material for yearlong course
In addition to in-class instruction and the lab manual, we provide supplemental material for the yearlong course in the form of technique videos, theory lecture videos and online blog posts related to evidence-based practice. Below are just a few examples from our online content library
Technique Video: Lumbar localized rotation
Theory Lecture: Manual Therapy Contraindications and Precautions
Blog Post on Pain Hypersensitity
To me, it seems that in the 1950's and 1960's Physical Therapists expanded their practice from restoration of movement dysfunction secondary to neuromuscular disease, stroke or amputation to include the treatment of musculoskeletal pain. At that time, our approach to treating musculoskeletal pain revolved around two primary strategies: 1) improving posture and movement (eg training scapula retractors to decrease postural loads on the cervical spine), and 2) treating the musucloskeletal pathology (eg mechanical traction to decrease cervical nerve root irritation). Our profession mostly considered pain to be purely a communication mechanism: pain informed the individual of injury or damage in the musculoskeletal system. However, it was clear that some patients were having pain in excess of their apparent tissue pathology.
The 1990's brought us the pain science revolution. David Butler and Louis Gifford translated scientific breakthroughs in the understanding of the role of the central nervous system in the modulation of pain. In particular, they presented the concept of central sensitization as one of the primary mechanisms behind ongoing pain. With this new understanding, our profession adapted our practice to address "central sensitization". In the late 1990's Lorimer Mosely, a Physiotherapist that I trained with, started to focus his research on the role of the brain in chronic pain and currently, he is a world renowned clinical neuroscientist. This post focuses on the history of pain hypersensitivity and new hypotheses to explain ongoing pain.
CAUSALGIA AND HYPERALGESIA
Much of the discussion of pain hypersensitivity can be traced back to Silas Weir Mitchell's publications on nerve injuries suffered by soldiers during the American Civil War (Tahmoush - 1981). Mitchel proposed the term Causalgia to describe the clinical presentation of ongoing pain secondary to peripheral nerve injury. Later, it was concluded that Reflex Sympathetic Dystrophy (RSD) was a separate entity and should not be included under the term Causalgia (Walters -1959). More recently, the terms Causalgia and RSD were replaced with the term Complex Regional Pain Syndrome (CRPS). With RSD being classified as CRPS Type I (no obvious peripheral nerve damage) and Causalgia being classified as CRPS Type II (evidence of obvious nerve damage). This review of early writings is relevant to this discussion as hyperalgesia is a frequent symptom of Causalgia (CRPS Type II).
Mitchell (1872) used the term hyperaesthesia to describe the elevated pain responses to mechanical stimuli seen in those suffering peripheral nerve injuries. Since, there has been discussion on the most appropriate term to describe pain responses in excess of the apparent stimulus. The term hyperaesthesia was eventually replaced with the term hyperalgesia.
Hardy et al (1949) defined hyperalgesia "as a state of increased intensity of pain sensation induced by either noxious or ordinary non-noxious stimulation of peripheral tissue." Walters (1959) felt that hyperaesthesia and hyperalgesia were inappropriate as it "would really imply increased sensation". He proposed the term hyperpathia to describe "excessive painfulness". It is important to note that Walters also included excessive pain due to "unpleasant stimuli and some pleasant" stimuli.
From Walters - 1959
Although reasonable in argument the term hyperpathia did not become popular and hyperaglesia remained the most commonly used term to describe pain in excess of stimulus. Technically, hyperpathia and hyperesthesia are still defined by the International Society for the Study of Pain but they do not seem have significant clinical relevance.
THE INTRODUCTION OF ALLODYNIA: PAIN DUE TO NON-NOXIOUS STIMULI
As mentioned above, hyperalgesia was used to describe excessive painfulness to both noxious and non-noxious stimuli, but sometime between 1960 and the 1990's the term hyperalgesia was restricted to only describe excessive pain due to noxious stimuli and another term was introduced to describe pain due to non-noxious stimuli: allodynia.
From the International Association for the Study of Pain (IASP):
The term allodynia was originally introduced to separate from hyperalgesia and hyperesthesia, the conditions seen in patients with lesions of the nervous system where touch, light pressure, or moderate cold or warmth evoke pain when applied to apparently normal skin. Allo means "other" in Greek and is a common prex for medical conditions that diverge from the expected. Odynia is derived from the Greek word "odune" or "odyne," which is used in "pleurodynia" and "coccydynia" and is similar in meaning to the root from which we derive words with -algia or -algesia in them. Allodynia was suggested following discussions with Professor Paul Potter of the Department of the History of Medicine and Science at The University of Western Ontario. (www.iasppain.org/taxonomy-2016)
Sandkuhler (2009) reports that the IASP introduced the term allodynia in 1994. However, Tahmoush mentions allodynia -- "allodynia (pain due to non-noxious stimuli)" -- in his paper on causalgia in 1981, so the term allodynia was probably in use prior to IASP adopting the term in 1994.
Allodynia Definition (IASP): Pain due to a stimulus that does not normally provoke pain.
Hyperalgesia Definition (IASP): Increased pain from a stimulus that normally provokes pain.
According to Sandkuhler there are additional restrictions to the definition of allodynia. Pain should only be referred to as allodynia if it is known to be non-noxious. Very low intensity noxious stimulus should be referred to as hyperalgesia. Please consult Sandkuhler (2009) for a more detailed explanation.
ALLODYNIA AND HYPERALGESIA ARE SYMPTOMS NOT PATHOLOGIES
Why do we care about the time of adoption of terminology? Currently, there is some conflict among the pain science community regarding the physiological basis behind chronic pain, and some scientists have proposed that allodynia and hyperalgesia should be reserved for use only when discussing spinal cord sensitization due to excessive peripheral input. However, it is clear historically that the terms allodynia and hyperalgesia were in use prior to the introduction of the concept of central sensitization by Woolf in 1989 (Woolf-2014). And most pain scientists see allodynia and hyperalgesia as a signs and symptoms in patients with chronic pain that can occur due to a variety of pathologies.
The proper function of the nociceptive system enables and enforces protective behavioral responses such as withdrawal or avoidance to acutely painful stimuli. In case of an injury, the vulnerability of the affected tissue increases. The nociceptive system adapts to this enhanced vulnerability by locally lowering the nociceptive thresholds and by facilitation of nocifensive responses, thereby adequate tissue protection is ensured. The behavioral correlates of these adaptations are allodynia and hyperalgesia. Thus neither hyperalgesia nor allodynia is per se pathological or a sign of an inadequate response but may rather be an appropriate shift in pain threshold to prevent further tissue damage. Painful syndromes are typical for a large number of diseases and pain intensity if often used by the patients and their health professionals to evaluate the progression of the disease or the success of the therapy.
From Moseley and Flor-2012
Sensitization occurs in the spinal cord and supraspinal centers.
Central sensitization is categorically different from symptoms such as allodynia or hyperalgesia, even though they may help identify its presence
Classical nomenclature such as hyperalgesia and allodynia should still be used to label the relevant clinical signs.
From Moseley and Vlaeyen-2015
importantly, associative learning and central sensitization are not necessarily mutually exclusive, but both would manifest in clinical signs such as allodynia and hyperalgesia.
CHRONIC PAIN: IS IT DUE TO CENTRAL SENSITIZATION OR BRAIN IMPRECISION?
For the past two decades the primary explanation used to explain chronic pain was ongoing central sensitization. Through experiments on animals Woolf (1983) was able to show that "the afferent activity induced by peripheral injury triggered a long-lasting increase in the excitability of spinal cord neurons, profoundly changing the gain of the somatosensory system. This central facilitation manifested as a reduction in threshold (allodynia), an increase in responsiveness and prolonged aftereffects to noxious stimuli (hyperalgesia), and a receptive ﬁeld expansion that enabled input from non-injured tissue to produce pain secondary hyperalgesia)." (woolf, 2011). This process is largely thought to occur in the dorsal horn of the spinal cord but is influenced by the higher centers.
More recently, there has been an explosion of research into the brain's role in chronic pain, and this has led some pain scientists to challenge the plausibility of central sensitization being the the underlying cause of ongoing pain.
One such example is a paper by Hansson (2014) calling for the use of the term "cognitive-emotional sensitization":
hypersensitivity may suffice as a descriptive term without a link to any underlying mechanisms. Increased attention or hypervigilance are other possibilities, that is, resulting from a patient setting new criteria for pain reporting as a result of a concomitant pain experience. These suggestions may overlap with regard to their physiology and perhaps all fit under the heading of ‘‘cognitive-emotional sensitization’’
Moseley and Vlaeyen (2015) propose their "Imprecision Hypothesis" to challenge the importance of central sensitization.
How different is the Imprecision Hypothesis from the concept of central sensitization? The key difference is that central sensitization has been attributed to entirely nonassociative mechanisms. Even regarding allodynia, where non-nociceptive input triggers pain, no import is given to the previous association between nociceptive and non-nociceptive input. Indeed, what is currently known about central sensitization attributes it to sprouting of non-nociceptive primary neurons induced by death of nociceptive neurons, for example after peripheral nerve injury, or to heterosynaptic facilitation induced by ongoing primary nociceptor input, descending facilitation, or both. That is, that nonnoxious stimuli come to trigger nociceptive input, manifest in allodynia, hyperalgesia, and spreading of receptive fields is thought to depend on sprouting of primary non-nociceptive afferents or sustained activation of the spinal nociceptor, not association between nociceptive and non-nociceptive input. Importantly, associative learning and central sensitization are not necessarily mutually exclusive, but both would manifest in clinical signs such as allodynia and hyperalgesia.
I think the disagreement revolves around the relative important of spinal cord changes versus brain changes in the development of ongoing pain. Clearly, both parties (brain versus cord) concede that both areas (brain and cord can result in allodynia and hyperalgesia.
A DIFFERENCE IN DEFINITIONS?
Part of this disagreement relates to how one defines central sensitization. Does it refer to the specific spinal cord changes identified by Woolf two decades ago, or is it a category of nervous system changes (brain and spinal cord) that happens to include Woolf's discovery as well as other central nervous system mechanisms. In fact, Woolf's (2014) response said as much:
Dr. Hansson narrows the definition of central sensitization to that related to its discovery, which our group spearheaded . We also were the first to use the phrase, at least in print. The first manifestation of the phenomenon, as evoked by peripheral tissue injury or brief activation of nociceptors electrically or chemically, was certainly both activity-dependent and induced by peripheral input, and its rostrocaudal extent in the spinal cord was somewhat restricted, but this does not mean that this is the only central generator of pain hypersensitivity—it just happens to be the one first discovered, and certainly not all causes of central sensitization are single or focal.
Central Sensitization Definition (IASP): Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields.
Nijs et al (2009) include the following in their discussion of what constitutes central sensitization:
- Augmentation of neurone responsiveness to peripheral nociceptor input
- Abnormal sensory processing in the brain
- Dysfunction in descending inhibitory mechanisms
- Activation of pain facilitating pathways
- Temporal summation
- Long-term potentiation
- Release of pro-inflammatory cytokines in the periphery
CONCLUSION AND TAKE HOME MESSAGE
I am certainly not qualified to ascertain whether spinal cord changes or brain changes play the primary role in the development of ongoing pain. However, as there is considerable evidence for both, one must conclude that spinal cord central sensitization and maladaptive learned responses in the brain remain possible entities in our patients with ongoing pain. The end result of spinal cord sensitization due to peripheral nociceptor input or imprecise coding of stimuli by the brain due associative learning will be the clinical presentation of allodynia and hyperalgesia. Without evidence of significant allodynia and/or hyperalgesia it is unlikely that any central nervous system process is responsible for the majority of someones symptoms.
WHAT ABOUT THE PAIN HYPERSENSITIVITY?
Perhaps, due to disagreements about the meaning behind central sensitization, clinicians and scientists should use the term Pain Hypersensitivity in our professional discussions. However, in the clinic there are negative connotations with the term hypersensitivity that may disturb patient rapport. One of the great benefits from the pain science revolution was being able to explain to a patient, how a non-cognitive process was responsible their chronic pain. Prior to Woolf's work the only options a clinician had to explain ongoing pain were the concepts of "psychosomatic pain" and "malingering", neither of which increase patient buy-in to a long-term rehabilitation process.
- Hansson, P. (2014). Translational aspects of central sensitization induced by primary afferent activity : What it is and what it is not. Pain, 155(10), 1932–1934.
- Hardy, B. J. D., Wolff, H. G., & Goodell, H. (1949). Experimental evidence on the nature of cutaneous hyperalgesia. Journal of Clincal Investigation, (9), 115–140.
- Mitchell, S. W. (1872). Injuries of Nerves and Their Consequences. Ph: Lippincott. Retrieved from http://www.archive.org/details/injuriesof nerves00micuoft
- Moseley, G. L., & Flor, H. (2012). Targeting cortical representations in the treatment of chronic pain: a review. Neurorehabilitation and Neural Repair, 26(6), 646–52.
- Moseley, G. L., & Vlaeyen, J. W. S. (2015). Beyond nociception : the imprecision hypothesis of chronic pain. Pain, 156(1).
- Nijs, J., Houdenhove, B. Van, & Oostendorp, R. A. B. (2010). Recognition of central sensitization in patients with musculoskeletal pain : Application of pain neurophysiology in manual therapy practice. Manual Therapy, 15(2), 135–141.
- Sandkuhler, J. (2009). Models and Mechanisms of Hyperalgesia and Allodynia. Physiological Reviews, (89), 707–758.
- Tahmoush, A. J. (1981). Causalgia: redefinition as a clinical pain syndrome. Pain, 10(10), 187–197.
- Woolf, C. (1983). Evidence for a central component of post-injury pain hypersensitivity. Nature, 306(15 Dec), 686–688.
- Woolf, C. J. (2011). Central sensitization: Implications for the diagnosis and treatment of pain. Pain, 152(SUPPL.3), S2–S15.
- Woolf, C. J. (2014). What to call the amplification of nociceptive signals in the central nervous system that contribute to widespread pain ? Pain, 155(10), 1911–1912.