Central Sensitization from Endometriosis

There is a process that happens in the body overtime when a threat is persistent. Ideally, something causing a threat to the body would be temporary, and the body is equipped to send pain signals and therefore protect the body from whatever is causing the pain. Think about how quickly your brain tells you to remove your hand from a hot element. That is a perfect example of a short lasting threat, and a quick neural response from the brain to your hand. But what if that threat doesn’t go away? How does your brain make up for the long lasting stimulus in order to protect you?

Think about endometriosis. You have foreign lesions growing within the body, that cause pain and relay this pain to the brain. In some cases – say over several years of menstrual cramps – your body gets used to the same intensity of pain over and over again, such that your body stops reacting to it (or rather, becomes tolerant of it). Whatever doesn’t kill you will make you stronger, right? But in some cases, the pain signal occurring over and over again can send a different message to your brain; one that says this is a very dangerous threat and we need to up our anti. This in turn worsens the pain. Research has shown that as these signals remain turned on, the pain system remains wound up. In parallel when the body detects a threat it recruits what are known as inflammatory factors, biological elements that physically create inflammation as a protective barrier from the threat. This can be seen as the cause of the pain but is yet another way the body is protecting itself. Taking anti-inflammatory medications usually will cause more pain as the swelling decreases and the pain becomes more prevalent. A bit of a catch 22, I know.

We as patients should be offered excision surgery from an expert surgeon as a first line of defence. It truly is the only way to officially diagnose, and thoroughly remove the disease, aka the threat. So why is it that pain can persist long after the threat has been removed, and in many cases, in areas that were never affected by the disease? There are two things at play here. Areas that are diseased may press on nerves to cause referred pain signals to different parts of the body. A great example is when abdominal endometriosis causes right shoulder tip pain. This is how other parts of the body can seem like they are affected but are simply a byproduct of the pain pathways. The persistent pain though, is a mechanism that is worth spending some time on as it may never get corrected without the right attention to it. This process – persistent pain long after the threat has been removed – is part of a mechanism called Central Sensitization.

Ongoing nociceptor activation generates an afferent bombardment of noxious information into the dorsal horn of the spinal cord. This process, in turn, induces structural and functional changes throughout the spinal cord and more rostral structures, which ultimately lead to central sensitization and evoked exaggerated repossess to peripheral stimuli.

In order to continue to protect you from endometriosis for all these years, the brain and the spinal cord have built more adrenaline sensors to detect threatening circumstances. Adrenaline production is often a sign that the body is in danger. And through persistence, more of the neurons in the brain started paying more attention to the threat. So now you have more neurons paying attention, and more sensors listening and reacting to the pain. What this means is that pain message from the stimulus to the brain have overreacted because they are overly sensitive to this chronic disease, and now the protective mechanisms from the brain to the stimulus are now overcharged. As a double whammy, your muscles have also learned over the years – as a product of these pain signals – to remain turned on or clenched in order to again, protect you from the pain. All of those changes that the body has made in order to keep you safe are now numb (or dumb) to the fact that the threat has been removed during surgery and continue to do what they have done for years.

Remember we talked about referred pain as well. The inflammation and the visceral pain also lead to muscle tightening in these referred areas, one of which is the pelvic floor. Through persistence of ongoing clenching of the pelvis, the pelvic floor continues this hyperactivity even after the endometriosis is removed and could result in pelvic floor dysfunction.

Going into the weeds a little bit for those of you who are science crazy: the mechanism I talk about above with the pelvic floor is the perfect environments to generate or activate what are called myoafascial trigger points (MTrPs). These trigger points can generate all over the body but are commonly found on the pelvic floor where they may refer pain to other sensitive areas such as the the vagina, urethra, and all the way up to the lower back. We now know that MTrPs are common in those with endometriosis and interstitial cystitis among other gynecological, genitourinary and gastrointestinal conditions. While still very understudied, more research is showing that these MTrPs exacerbate the pain inherent to these conditions making the pain that much worse.

Ok lets come back out of the weeds. So you have just had your excision surgery and within a few short weeks you start feeling certain kinds of tension and pain; some you had before and others seem to be a reaction to the surgery but you know the endo and adhesions are gone. With the right doctor, you should be cognizant of this pain and willing to work on a few different therapeutic mechanisms to see if you can reverse them.

One line of treatment is through myofascial release, working directly with those myofascial trigger points through gentle massage, deep pressure massage, stretching, and breathing techniques to focus on subtle but important movements of the body. This may seem familiar to any of you seeing a pelvic floor therapist or an osteopathic doctor. Simply being attuned to how your pelvic floor moves with your ribs and your breath can make a drastic difference in calming the nerves. And giving your body the opportunity to be calm also gives it the opportunity to start replacing those highly sensitive sensors with more normal (low sensitivity; high threshold) sensors.

The second line of treatment is with injection therapy, using either wet or dry needles directly into the muscle to force them to relax. Additionally, your specialist may use the same technique using a local anesthetic to further blunt the ability to transmit pain through this neural pathway. This technique is usually only done when the pain can be localized to a nerve or pathway rather than dispersed general pain.

The third line of treatments is though neuromodulators which can also be used to dampen the pain signals associated with central sensitization. Gabapentin and Amitriptyline are two of the more common pharmaceuticals being used for this purpose.

Hopefully through one or a combination of treatments your body will allow you to get to a point where the body will act appropriately to new and threatening stimuli and will eventually register that the previous stimuli has been removed. Just remember that it took years for your body to get to this point, so patience is critical. If you have any questions as you follow me through my central sensitization reversal journey please reach out!


Understanding Pain, Live well again (rights reserved. No Link available)

New Developments in the pharmacotherapy of neuropathic chronic pelvic pain

Pharmacological Modulation of the pain-related brain activity during normal and central sensitization states in humans

Related Chronic pelvic pain and endometriosis to signs of sensitization and myofascial pain and dysfunction

The math doesn’t add up

I don’t know if anyone reads blogs anymore; certainly with Instagram and Twitter taking the main stage for social media. But, to me this is the only place I can fully capture the emotions that I endure throughout these new stages of my journey. I’m struggling with the words though because things are not adding up. Right when I think I have found an ounce of hope, something else throws me off.

When Visanne didnt work the next step was to insert the Mirena IUD. When it was inserted last March (nearly 11 months ago now), I was told that the intent was to normalize my hormones, remove a ‘cycle’ and stop the bleeding. No more ups and downs of hormones, no more intense crashes of hormone and therefore no stage for endometriosis to play on. According to Mayo clinic:

The device is a T-shaped plastic frame that’s inserted into the uterus, where it releases a type of the hormone progestin. To prevent pregnancy, Mirena: Thickens mucus in the cervix to stop sperm from reaching or fertilizing an egg. Thins the lining of the uterus and partially suppresses ovulation.”

Aside from the horrible emotional and physical setbacks I’ve experienced with my IUD, moving ahead it certainly did appear to drastically decrease (almost stop) the bleeding but I have always felt a cycle in place. So maybe it was kind of working? One thing was for sure though. The Gabapentin was NOT working. It was absolutely not doing anything for the pain (though it did seem to help with the leg spasms at night). Everything came to a head in December when Dr. Singh called and I felt like I had run out of tools. The list of treatments that I had exhausted well outrun the list of options I had yet to try. And then there it was. A plan A and a plan B. I’ll give to Singh that he never laid it out quite so plainly but this is how my brain interpreted it. Plan A: go on Orilissa for 3-6 months to determine if estrogen, and thereby the endometriosis, was impacting the pain. Plan B: VATS. It was the first time in the last three years that I’ve felt secure about Orilissa and despite the public bashing I proceed to do with Lupron I was ok to take the plunge with Orilissa. The first week was hell. The second week was hell-er and it induced a period. Weeks 3 and 4 are a blur but I an safely say the profound effects of Orilissa snuck up on me when I one day woke up on my left side – something that was impossible to do when I was in chronic pain before Orilissa – and had an a-ha moment that something was different. 4 nights of this in a row and I could safely chalk it up to Orilissa.

I did the unthinkable: I shared my success story on social media. Others who are taking Orilissa chimed in with their stories too and several women DM’ed me about their fears about trying the drug. “Its not for everyone” I told them, while secretly encouraging them to take the plunge. And then… my worst fear. I got a period. I bleeding period. A ‘run to the bathroom with diarrhea’ period. A ‘holy hell my uterus’ period. And on top of that – that, being something I havent experienced in nearly two years – my diaphragm came back. My shoulder tip pain came back. My fatigue came back. My mood swings came back.

One step forward and two steps back.

Some things are just not adding up. Mirena was intended to thin my lining and help reduce my cycle, bleeding and pain. Orilissa was intended to block estrogen and therefore reduce potential spreading and growth of new endo lesions. Together, I should be a pretty pain free, bleed free spot. So why, why 11 and 2 months in am I dealing with the most all-over-body excruciating pain I’ve had in years? The math isnt adding up.

I’m here. I’m showing up consistently. But its starting to get harder and harder to hide the anger. My therapist wants me to work through the anger. She says it impacts the way I deal with the pain and blocks the ability to face it head on. But the reality is that the anger pushes away the depression. Cus depression is a slippery slope. Once I get on that slide I may not be able to find a ladder. So tell me, how does one cope with all these let downs?