What Is A Trigger Point?

The term ‘Trigger Point’ (TrP) may mean different things to different doctors, pain practitioners and patients. I am going to use the term in its true form, albeit with my own thoughts on the mechanism’s fine print.

The basic question – what is happening in these blobs of painful muscle?

I consider myself a “myofascist” – someone who understands and believes in muscle pain, respecting the ability of muscles to cause excruciating pain. Myofascists accept the research that suggests that up to 95% of all patients with chronic pain having muscle trigger points as a sole, major or contributing cause of their pain. If I were a betting man and could place bets on my ability to improve someone’s pain in a few minutes, I would win 95% of the time – not bad odds!

Before launching into a detailed description of TrPs, I would like to give recognition to Dr. Janet Travell, Dr. David Simons and Lois Simons for their excellent life’s work in this field, bequeathing us with their valuable two-volume Trigger Point Manual (1983) that provides an incredibly rich and accurate account of TrPs. The second edition (1999) has been updated by equally committed and talented clinician researchers, led by Dr. Robert Gerwin. 

What Is A Trigger Point?

A trigger point is a segment of a muscle that has locked up – in a rigor or latched state – and is no longer able to relax. This latched state represents catastrophic muscle failure. It happens predictably after death, when blood flow stops and hours later the muscle cells run out of energy. The muscle cells latch and the whole muscle becomes rigid, something we all know about and call 'rigor mortis' – latched state of death.

Latching also happens after a heart attack where a coronary artery is blocked and blood flow stops to a segment of heart muscle. Some of the heart muscle dies (myocardial infarction) while an area of muscle around the infarcted segment can become latched and unable to contract and relax. This creates a dormant zone around the infarct that eventually dies. Researchers in this field are trying to find ways to rejuvenate this muscle and get it back to a healthy functioning state.

Once we understand that muscle switching (contracting and relaxing) is provided by changing relative calcium and magnesium levels in the cell, things get easier to grasp. Calcium is the ON switch. Calcium is packed tightly in storage in all muscle cells, kept there against its natural will to disperse by calcium pumps. Calcium pumps are vital for life and run on energy produced by our cellular batteries, the mitochondria.

While calcium is kept at bay, magnesium - calcium’s biological opposite and the OFF switch in muscle - has free reign and is found in concentrations in muscle cells up to ten thousand times higher than calcium. This is the healthy state in a resting muscle cell with the protein rods slid apart and relaxed and the calcium pumps ticking over, keeping calcium in check.

When muscles fail, both after death and in everyday life, this delicate and energy-intensive OFF-switch fails and the muscle cells latch. The cell is not dead, but it is stuck contracted. That is why we feel our muscles stiffen up as we tire when performing muscle activity. We don’t get weak and collapse in a jelly state, we tighten up and get stiff. After a brief period of rest, the tired muscle is usually able to relax normally. When muscles fail in everyday life, it is usually not the whole muscle, but rather a segment of it.

I am unable to find any published research that helps me understand what the common characteristic of that segment is. Does it have a common nerve supply, blood supply or is it the physical segment of the muscle subject to the most stress?

I suspect it is one or all of these three features and hope that one day some bright researcher(s) figures it out. Until then, we do know that these failed segments are very common and highly predictable. They also occur in increasingly recognizable patterns, which we’ll get into in more depth in future posts.

We do know that trigger points are visible on ultrasound, showing up as hypoechoic nodules (black blobs) within the muscle that represent a stiff, contracted segment of muscle with less or no blood flow passing through it.

So, while it is possible to ultrasound muscles to diagnose myofascial pain, this technique has only been reported by one research team from George Mason University in Fairfax, Virginia, USA. I predict that ultrasound diagnosis of trigger points will become standard practice in the not-too-distant future.

Not all trigger points cause pain, but all trigger points are painful when squeezed. At any given time, roughly one-third of people do not have trigger points (the lucky ones!),  and one third have trigger points that are not causing pain. The last one third have trigger points with pain. It is my opinion that it’s the one-third of us with painful trigger points that have chronic pain. Interestingly, this rule of thirds is quite common in medicine.

What is the difference between the painful and non-painful trigger points?

Another team of researchers in Baltimore, Maryland led by Dr. Jay Shah used tiny micro-needles to sample fluid from both types of trigger points and normal muscle. They found that only pain-causing TrPs had a low pH (less than 6), while non-pain causing TrPs and normal muscle both had a pH above 6. 

Let’s examine this pH issue in a bit more detail and try to make sense of it.

All muscles are equipped with crucial acid-sensing sensors (acid-sensing ion channels – ASICs) on nociceptive nerves that monitor the pH of muscle. This pain-causing system is used to ensure that the muscle gets sufficient blood flow by telling us when the pH drops. A drop in pH usually means that there is not enough blood flow to remove the acid ions produced by the muscle as it produces energy to perform its tasks of movement – contraction and relaxation. When the pH drops below 6, the muscle is flirting with metabolic danger and needs its blood supply re-established and soon.

Ischemic (impaired blood flow) muscles are adept at sending a message of pain to the brain. This pain starts off as discomfort but can ramp up to be excruciating “shoot me now pain” as the pH drops down to 4, a sign of imminent death for the cell. Just as heat sensing nerves can report gentle warmth, high heat and life-threatening boiling water, so too the ASICs sensors are graded to report the severity of the pH drop in our muscles.

Our typical response to acid pain in muscles is to change position or relax the painful muscle. We do this many times in the course of a normal day, each time rewarded with that almost instant cessation of pain as blood flows through the muscle again.

A segment of failed muscle in a latched state forming a TrP is beyond our control to relieve. The failure is inside the muscle and does not respond to the absence of a contraction signal in the motor nerve by relaxing. Relaxation requires calcium to be pumped back into storage. To relax the segment requires energy, to get the energy it needs blood flow, to get blood flow it needs to relax. And right there is the crux of the problem of chronic pain. If the segment is large enough and cannot get enough blood flow close enough to break this catch-22 state, it is at risk for staying latched.

There are three crucial issues that are worth knowing about trigger points once they form.

1. The nociceptive nerves that are stimulated by the low pH not only cause severe and unrelenting pain that wakes us up, fights for our attention and make us depressed and tired. The nerves themselves also, in turn, produce neuropeptides (proteins) that are transported to both ends of the nerves and secreted out of the nerves into the surrounding tissue, both the monitored muscle tissue and the segment of the spinal cord that the nerves report to.

These powerful peptides sensitize the surrounding nerve ending, making them respond with pain signals to usually light and even pleasant stimulation such as stroking the skin. Those researchers who placed needles into TrPs found high levels of these pain-causing neuropeptides only in the low-pH painful TrPs. Further research found elevated levels of these peptides in other muscles in patients suffering from painful TrPs.

This is why nociceptive nerves are thought to be causing pain and why the problem is labeled neuropathic pain.If one takes this neuropathic state as a rogue source of the problem, ignoring the screaming ischemic muscle trying to get attention, then that is how we are currently approaching the problem of chronic pain today.

2. The TrP segment of muscle relies on blood flow in surrounding muscle tissue to provide some support in the form of diffused oxygen and nutrients in and acid (carbon dioxide) out. Anything that improves blood flow through the surrounding muscle will provide more relief, thereby increasing the pH of the TrP and thus decreasing pain.

Many forms of treatment for chronic pain are directed at increasing blood flow in muscle, including mindfulness and relaxation therapy, acupuncture, massage and stretching. Lying on the beach in the warm sun with a full glass of liquid close at hand usually works wonders for my patients.

Eventually, the low oxygen level in the TrP will cause an increase in the number of capillaries in the muscle surrounding the TrP. This is tantamount to forming a placenta around the TrP – trying to get as much oxygen delivery to the ischemic muscle as possible. Anything that impairs this blood vessel proliferation such as the nonsteroidal anti-inflammatory drugs (NSAID) commonly used in chronic pain, will cause an increase in pain.

That is why it is unduly painful to use, stretch or put pressure on a muscle with TrPs in it. Those patients know that there are some positions that they cannot stand at all or for very long. Some can’t sit, some can’t sleep on one side or the other. Again, our options diminish.

3. Over time, the low pH in the TrP will have severe negative effects on the mitochondria within those acidic cells. In severe situations the mitochondria may not be recoverable, may cease functioning altogether and the cell may in fact die.

The longer the TrP lasts the harder it will be to restore normal function, even when the TrP is released and normal blood flow temporarily returns.

It is well respected by all those who try to alleviate chronic pain that time is of the essence and that after many years of severe pain it may not be possible to restore a healthy state.

Don’t despair, I think that with a little ingenuity restoration is possible in most cases.

Summary

A trigger point (TrP) is a segment of failed muscle that is unable to get enough blood supply to deliver enough energy to run the calcium pumps, pump calcium back into storage in the sarcoplasmic reticulum, thereby allowing the ambient magnesium in the cell to cause relaxation. 

Pain is caused when the acid-sensing ion channels (ASICs) detect a pH (acid level) of 6 or less. This further causes the nociceptor C-fiber nerves that carry the ASICs receptors to further augment the pain by producing powerful neuropeptides, which are sent to the acidic muscle and the receiving area of the pain nerves in the spinal cord.

These neuropeptides increase the sensitivity of the nerves in both the muscle and the spinal cord, causing heightened pain and even causing mild pain and normally pleasant sensations to be felt as pain. This can become widespread. 

While anything that increases blood flow to the muscle tissue around the TrP will increase the pH of the TrP and therefore reduce pain or even stop it. However, it may not be enough to cause that TrP to unlatch and the pain will return when muscle blood flow is decreased again.

The longer a TrP is left in the latched state and causing pain, the more damage is inflicted on the pH-sensitive mitochondria (battery power packs) within the muscle cells caught within the TrP. Eventually, this damage can cause complete mitochondrial failure and cell death, making the TrP very difficult or impossible to rectify.