Chronic or persistent pain is the leading cause of disability in the Western world, with up to 49% of people suffering pain lasting for than 3months duration (Gerdle et al 2004). Around 90% of spinal pain is “non-specific” meaning that imaging like MRI or Xrays cannot find a structural cause.
If chronic pain is NOT caused by structural damage in 90% of cases, then what causes it?
The latest review of chronic pain sheds light on this complex problem by uniquely tying together all the science that has come before and for the first time presenting a clear and coherent mechanism for persistent pain (Tuckey et al 2021). What’s even more encouraging is that the concept of how pain persists and becomes chronic also illuminates how manual therapy can effectively create a positive and lasting resolution. As you read on bear in mind that chronic pain is extremely complex with literally thousands of possible contributing factors, so I’ll try to explain things as simply as possible.
Let’s say you have an injury or develop some pain from overuse. In order for your body to heal and recover, the injured region needs a properly functioning lymphatic pump mechanism and normal venous drainage in order to remove inflammatory (ie pain generating) chemicals from the region. If this mechanism does not drain the inflammatory chemicals, then the tissues remain irritated, inflamed, and painful. Inability to clear inflammation is one of the fundamental things resulting in a chronic complaint but is not the sole cause.
What is the lymphatic system and how is it involved in persistent pain?
Most of us are familiar with arteries which carry blood to the capillaries and onto the tissues to supply fuel and oxygen, and veins which take the deoxygenated blood back to the lungs. The lymphatics are a third set of vessels and perform the job of draining the tissues of any fluid that has leaked from the capillaries and return it to back into the circulation (this amounts to about 3 litres of fluid per day) (for more on the lymphatic system see my post here). Without lymphatics we develop some serious swelling! The lymphatics also have important immune functions, but for the purpose of explaining chronic pain we will focus on their ability to remove fluid and inflammatory chemicals (often called inflammatory mediators or cytokines) from around your cells. As you can imagine, if the lymphatics are prevented from draining the tissue of unwanted inflammatory chemicals around your cells, then things will remain painful!
The continued presence of inflammatory mediators in chronic pain states is well documented. The lymphatic vessels which drain the inflammatory cytokines from around the cells start as tiny vessels with thin walls to absorb fluids. The minute fragile vessels are joined to the surrounding tissues by microscopic filaments, which means that abnormal tension in the surrounding structures can affect their ability to transport fluid and wastes. As lymphatic vessels merge and become larger structures, they begin to get thicker walls, contain valves to prevent backflow and gain some smooth muscle in the vessel wall which, along with movement of your body, help to propel fluid back to the heart and into the circulation and helps to prevent them from collapsing as easily.
What prevents the lymphatic mechanism from working correctly? There are quite a few causes that have been proven in the scientific literature. Here is a list of some of them:
Specific inflammatory cytokines (chemicals) shut down or slow the lymphatic muscular pump (for the scientifically interested these include IL-1b, IL-6, TNF- α). This means that the lymphatics cannot remove fluid and inflammatory mediators as effectively, so they begin to accumulate in the tissues and cause pain.
Inflammatory cytokines are also involved in activating the sympathetic nervous system, which is that part of the “automatic” or subconscious nervous system that controls blood flow. This Sympathetic Nerve Activation (SNA) causes constriction of vessels and further reduces blood flow, slowing everything down (including healing and lymphatic-venous drainage). SNA has the added (usually unwanted) effect of amplifying the level of pain you feel (complicated neural mechanisms are involved and will be the topic of a future blog).
The same cytokines (esp. TGF-ß1) have been shown to cause fascial cells to contract sufficiently to block the delicate lymphatic vessels and trap inflammatory chemicals in the tissues, thus perpetuating pain. The fascial cells we are speaking of are fibroblasts, which in the presence of inflammation convert into myofibroblasts which are contractile, causing the collagen fibre network of the tissues to develop tension. This tension is sufficient to irritate pain receptors and further disrupt flow in the delicate lymphatic vessels which are physically joined to the surrounding fascia by microfilaments. For more on fascia and pain see my blog here.
The net result of this process is known as Interstitial Inflammatory Hypostasis (IIH):
Interstitial means between the cells (such as between your muscle cells or indeed organ cells);
Inflammatory meaning that inflammatory chemicals (cytokines) are present in the interstitial space around your cells;
and Stasis means the fluid isn’t moving terribly well, so the inflammatory chemicals remain trapped and continue to activate pain nerves and annoy cells directly.
What is fascia and how is it involved in persistent pain?
Fascia is a connective tissue made up of collagen fibres, nerve receptors and fibroblasts (more on fascia in my post here). You have most likely seen and touched it if you have a joint of roast meat to cook for dinner – that white fibrous covering outside the red meat is one type of fascia is which is tough yet flexible. Fascia surrounds every tissue including muscles, bones, nerves, vessels, and organs. It is interconnected everywhere in your body and is richly supplied with sensory nerves including pain receptors. When inflammation or mechanical stress is applied to fascia, its fibroblasts convert into myofibroblasts causing contraction of the fascia, which is a strong enough to cause a wound to close and strong enough to block / impair the lymphatic pump mechanism. This is the fascial contraction component of our IIS pathway into chronic pain.
Why is fascia and the “Interstitial Inflammatory Hypostasis” (IIH) so important in chronic pain?
The concept of IIH is absolutely critical – it explains exactly the peripheral mechanisms as to why you have chronic persistent pain!
IIH explains the peripheral (ie outside the central nervous system) components of persistent pain. If you are a practitioner treating patients with chronic non-specific pain then you need to understand IIH and be trained in skills that allow you to address the specific causes such as dysfunction in the fascial, sympathetic and lymphatic-venous systems (amongst others!). Simple treatments like massage, manipulation or mobilisation of joints or needling trigger points just won’t pass muster here! After all, the evidence is that trigger points are usually secondary to IIH not the other way around (Tuckey et al 2021).
Fascia and the contractions caused by injury, sympathetic nervous system activation, and lymphatic congestion, are very treatable using a manual therapy technique known as Fascial Counterstrain (FCS). I’ll talk more on FCS in an upcoming post! The mechanisms outlined above also indicate that simple stretching and strengthening are unlikely to be successful as the primary treatments for persistent pain as they don't specifically alter the reflex changes involved in the lymphatic, fascial or nervous systems - they are more useful interventions at restoring function after the pain mechanisms have been treated and are very useful in preventing recurrence.
References:
Gerdle B, Björk J, Henriksson C, Bengtsson A. Prevalence of current and chronic pain and their influences upon work and healthcare-seeking: a population study. J Rheumatol. (2004) 31:1399–406.
Tuckey B et al (2021): Impaired Lymphatic Drainage and Interstitial Inflammatory Stasis in Chronic Musculoskeletal and Idiopathic Pain Syndromes: Exploring a Novel Mechanism. Frontiers in Pain Research 23:2:691740.
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