Nerd Alert! I have put together this research-based post on Central Sensitization because there is some misinformation about the ‘what, the how, the why’ and what to do about it…
PAIN!! … & Anatomical Structures involved:
The most popular and frequently used definition of pain is “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”(1) However, Australian pain researcher Lorimer Moseley(10) defines pain as more multi-dimensional with all aspects of pain including context, competing stimuli, company, meaning, previous experience, etc. Regardless pain is an overpowering stimuli for the brain, taking cortical presence, causing us to forget information, decrease decision making, reducing our attention span etc.
All the above can be seen as a pattern in fMRI images in patients experiencing chronic pain. Known as the ‘Pain Matrix’ this area consists of the Anterior Cingulate Gyrus, Insular Cortex, Thalamus, and the Sensorimotor cortex. (10) The Neuromatrix is areas in the brain that tend to activate together, these areas can include motor, limbic, or sensory and they tend to demonstrate highly coordinated responses. For example: picture yourself stopped at a stop light next to a car and the car next to you starts to move… Even though you didn’t move you felt like you were moving and so you respond with the appropriate reaction as though you were experiencing the movement yourself. This is a neuromatrix example of sensory neurons (vision) working with motor neurons in your brain. The pain matrix is linked-up and can work just like that!
Central Sensitization (CS):
Central Sensitization is amplification within the central nervous system (CNS) resulting in more intense perception of pain thereby acting in the maintenance of chronic pain. (7,8) In other words you could say central sensitization puts the word ‘chronic’ in chronic pain. There are 3 main phenomenon central sensitization result by (8)… .
- CNS synapse “activity-dependent” plasticity: Simply put neuronal connections change based on their use. One could use the phrase “fire together wire together”, therefore; as certain patterns of input are used the stronger those connections become.
- Dorsal Horn wind-up: This is considered tetanus of the CNS. As C-fibers experience a longer and longer stimulus the pain fibers within the dorsal horn of the spinal cord begin to increase their frequency of depolarization. Therefore, the longer you feel the same intensity of pain the more intense that pain feels “sensitizing you”.
- Long-term potentiation (LTP): Is the basis behind cellular changes for learning and memory, but has been found to play a role in chronic pain. It has been found that a strong enough stimuli that occurs synchronously between two neurons enhances the strength of the connection between those two neurons.
These changes seem to be possible based on cellular alterations and changes in gene expression. Research(8,12,13) has found changes in microglia, astrocytes, and the gap junctions associated with central sensitization. If one thinks about the role microglial and astrocyte cells, which is to insulate, nourish, support, modulate conduction velocity, and guide growth of neurons then changes in chemical secretion of these cells seems likely it could be the source of sensitization of the CNS.
These 3 phenomena have been found to increase synaptic strength, increase neuronal membrane excitability, allow for normal subthreshold pain stimuli to now become suprathreshold stimuli, and decrease descending inhibitory input. These changes are what result in a “sensitized” CNS and allow for normally non-painful stimuli to now be painful. Depicted below is an example of changes that could occur resulting in allodynia and hyperalgesia, which are both common in central sensitization.
Summary of Central Sensitization (3)
- CNS is distorted, amplifying pain by increasing intensity and duration.
This now uncouples the natural stimulus response because what the patient feels is “centrally” driven, not peripherally driven.
- There is no injured tissue, healing times have surpassed. These patients tend to have pain lasting longer than 3-6 months that can last years.
- There is no dangerous threat, to the patient. The pain they feel is due to “sensitized nerves in the CNS” not from a harmful threat. (i.e. The patient may report increased pain after warming up on a stationary bike which they could view as dangerous due to the pain they feel, however it is from easily activated pain pathways in the CNS “tricking” them)
- There is no true noxious stimuli, therefore no true nociceptive input.
Nociceptive pain reflects a noxious stimulus, and without a noxious stimuli (an actual or potential damaging threat) there is no nociceptive pain.
- However, there is real pain. Your patient with CS actual feels pain and is not lying, it simply is from changes within and not a peripheral threat. We all know leg pain can come from the back… now arm pain may come from the CNS, etc.
Who has Central Sensitization, and how does a physical therapist differentiate with our patients? (4,5)
Nijs, 2010 describes there are specific medical diagnoses that a patient maybe referred to physical therapy with that should put the question of CS in a clinicians mind.
This figure shows a column of medical dx that then are checked if you can absolutely assume central sensitization plays a role in, and then ones that are check that might raise suspicion and further evaluation should be used. Chronic whiplash disorders, fibromyalgia, chronic fatigue syndrome, and IBS are all diagnoses that should be considered (if dx correctly of course) involving CS. The other disorders i.e. chronic low back pain central sensitization has shown up in a subgroup of that diagnosis and not in all cases.
History & subjective report from the patient (4,5)
It is crucial to listen to your patient and not to ignore information or rush onto your objective. There can be lots of information gathered here about their complaints. It is also important to know how to ask the right questions.
Your patient with suspected central sensitization may lead you down a path to further confirming your suspicion. Due to the changes in the central nervous system they tend to not only have hypersensitivity to tactile/mechanical stimuli. Now, they do not have to have all these complaints but it is reported that if only a few are present then that is enough.(5) Your patient may mention they have increased sensitivity to light, touch, noises, pesticides or temperature. If so that has been shown to be a strong characteristic associated with CS. The second half of the list in the figure above like sleep disturbances of poor concentration has show to be associated but not as strongly or isolated to CS.
During your evaluation that patient with CS will have a general sensitivity often in remote locations. For example a chronic whiplash patient my be experience increased sensitivity in the lower extremities. To test for these sensitivities it is recommended to use a algometer and <4kg/cm2 elicits tenderness or pain then that is a positive test. If an algometer is not present then use of clinical experience and common sense can tell you that the pressure you used on the patient should not be noxious as it has presented. To test for hypersensitivity to hot/cold the clinician can use a hot or cold pack. The patient should report it as feeling exactly that (hot or cold) but it should not be painful or disturbing. Hypersensitivity to vibration can simply be tested with a tuning fork in generalized locations. Brachial plexus provocation tests is specific in looking for CS in chronic whiplash patients and demonstrates hypersensitivity to nerves from the brachial plexus. A positive test would be the combination of upper extremity + neurodynamic tests with a bilateral loss of elbow extension >30 degrees due to pain.
Hypersensitivity to exercise can be tested with the recommended bike test.
- Using a stationary bike gradual increased resistance is used (recommended start point 10-20kW/min). Or just start on level 1 and work up from there.
- Test pressure pain threshold before the test, every 1-2 min during the test, and then after exercise. You can use your algometer or simple palpation.
- Assess for increase, decrease, or no change of pain.
- Increased pain is further suggestive of CS.
To summarize your evaluation and making your decision if CS is present or not this flow chart can be used. The flow chart incorporates the 3 previous tables above to help you make a dichotomous decision based on each one leading you to your Dx of CS or no CS.
Treatment for patients presenting with Central Sensitization
Treatment begins with the utmost important aspect when dealing with CS, that is education. Specifically Pain Neuroscience Education. Chronic pain can be pictured and described as a Vicious physical and psychological cycle as depicted below.
Image From: http://www.backexperts.co.uk/
This cycle has been found to be broken with Pain neuroscience education. (4,6,9) The goal of this education is convincing patients pain is not a result of tissue damage or a threat of one or “its all in your head” as some might say. The result often seen is increased motivation and compliance to graded exercise and allowing for a better outcome with physical therapy.Break the Cycle!
Depicted below is the result after a good response to education allowing recovery.
As described above, much of the pain matrix (networks of neurons in the brain that activate with pain) are also the areas in the brain that control learning, attention, mood, goal-orientation, and decision making. When these areas are consumed by pain it makes it difficult to function. This is why patient education can be so challenging with this patient population. Nijs, 2011 describes a specific sequence of education and what material should be included when informing your patient for the best result.
First education session with your patient(4,6,9)
- It is first recommended to cover basic operation of the nerves and how we experience pain. Don’t be afraid of too much detail like axons, depolarization, etc.
- Next describe Acute Pain (i.e. tissue damage causing pain)
- Then dive into central sensitization and clarify how it differs from acute pain (i.e. No tissue damage!)
- Lastly, describe your treatment rationale for central sensitization and how pain should not be the limiting factor.
- The goal: Changing the patients thoughts about pain
- Before the patient leaves this recommended 30min pain neuroscience education they should be given a test on what was covered.
Homework after session one (4,6,9)
- Resources and the neurophysiology pain test is given to reinforce information at home.
- The patient is to write down any questions they have and complete the test
Second education session with your patient (4,6,9)
- Let the homework guide this session. The therapist should go over the patients homework with them covering areas of misconceptions and summarizing the material.
- After the knowledge has been transferred to the patient it is of critical importance to discuss how this new knowledge will change the patients everyday activities and their willingness to change. For example will they be willing to put effort into decreasing ruminating thoughts of pain, increasing their activity levels, develop relaxation methods and find ways to lower stress their levels.
Ascertain the patient’s reconceptualization on pain
How about an objective measure?
The therapist can measure their success level (before/after) at changing the patients thoughts about pain using the Pain Catastrophizing Scale(6,11).Image From: http://www.physio-pedia.com/Pain_Catastrophizing_Scale
Now that you finished the first step of treatment you should move into your graded exercise program.
Graded Exercise Program(10)
–First, establish working baseline
- Conversing with the patient get an estimate on how long they think it takes during specific tasks to flare-up their pain. A flare-up differs from pain in that it significantly alters all movement patterns, sleep, and lasts minutes to hours to days after exercise.
- Set easily attainable movement goals and once achieved they become the new baseline.”Progress alittle, alot.”- Moseley
An example of exercise and ADLs in a graded exercise program is below.
Lorimer Moseley(10) established a flow chart demonstrating the fine balance between progression and regression within a graded exercise program. Essentially, monitor the patient for proper movement patterns and symptoms, if they are appropriate and non-symptomatic increase the difficulty via physical means (weight, reps, speed, etc), contextual means (while completing parts or a whole task that use to be noxious like reaching overhead), or change the cognitive load (making them manipulate objects in hand while marching over cones). Now, if the patients starts to exhibit symptoms and maladaptive movement strategies, decrease the physical, contextual, and cognitive difficulty. The therapist may also add motor imagery.
Nijs, 2014(4) suggests using a “time-contingent approach” vs. “symptom-contingent approach”. With a time-contingent approach to exercise is set with repetitions or time ignoring the symptoms. This is used with the goal to desensitize the pain attempting to restore normal function. This is compared to the “symptom-contingent approach” where exercise is immediately halted with onset of symptoms that is used with acute injury.
Central Sensitization results in changes in the CNS that uncouples sensory responses… Pain is driven centrally not peripherally (opposite from what one could assume)
Educate your patient on the difference of acute vs. chronic pain to change their perception of pain.
Establish an exercise program that is constantly progressing… think “alittle progression, alot of the time” to “desensitize” the CNS.
– Stephen Henry
- International Association for the Study of Pain. Pain, IASP Pain Terminologyhttp://www.iasp-pain.org/AM/Template.cfm?Section=Pain_Definitions&Template=/CM/HTMLDisplay. cfm&ContentID=1728#Pain. 1994
- Chronic Pain. American Chronic Pain Association Web site.http://theacpa.org/condition/chronic-painUpdated June 2, 2014. Accessed June 8, 2014
- Woolf C. Central sensitization: Implications for the diagnosis and treatment of pain. March 2012; 152(3):1-31. J.Pain. doi:10.1016
- Nijs J, Meeus M, Danneels L, et al. A Modern Neuroscience Approach to Chronic Spinal Pain: Combining Pain Neuroscience Education With Cognition-Targeted Motor Control Training. Physical Therapy [serial online]. May 2014;94(5):730-738. Available from: CINAHL Plus with Full Text, Ipswich, MA. Accessed June 16, 2014.
- Nijs J, Houdenhove B. Recognition of central sensitization in patients with musculoskeletal pain: application of pain neurophysiology in manual therapy practice. Manual Therapy 2010; 15: 135-141
- Nijs, J., Wilgen, P., Oosterwijck, J., Ittersum, M., Meeus, M. How to explain central sensitization to patients with ‘unexplained’ chronic musculoskeletal pain: Practice guidelines. Manual Therapy 2011. 16: 413-418.
- McAllister M. Understanding Chronic Pain. Central Sensitization: Institute for chronic pain. http://www.instituteforchronicpain.org/understanding-chronic-pain/what-is-chronic-pain/central-sensitization. Published April 27 2012, Assessed June 9, 2014.
- Woolf, C. Central sensitization: Implications for the diagnosis and treatment of pain. Pain 2011. 152:s2-s15
- Moseley GL. Evidence for a direct relationship between cognitive and physical change during an education intervention in people with chronic low back pain. European Journal of Pain 2004;8:39e45.
- Moseley GL. A pain neuromatrix approach to patients with chronic pain. Manual Therapy 2003b;8:130e40.
- Sullivan MJL, Bishop SR, Pivik J. The pain catastrophizing scale: development and validation. Psychological Assessment 1995;7:524e32.
- Vlaeyen J, Linton S. Fear-avoidance and its consequences in chronic musculoskeletal pain: a state of the art. Pain (03043959) [serial online]. April 2000;85(3):317-332. Available from: CINAHL Plus with Full Text, Ipswich, MA. Accessed June 16, 2014.
- Tenschert S, Reinert A, Hoheisel U, Mense S. Effects of a chronic myositis on structural and functional features of spinal astrocytes in the rat. Neuroscience Letters [serial online]. May 6, 2004;361(1-3):196-199. Available from: MEDLINE, Ipswich, MA. Accessed June 17, 2014.