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Wednesday, June 28, 2017

Low-Dose Naltrexone & Nerve Decompression Surgery

When I posted a few weeks ago, I didn't imagined I'd have such a (potentially) big update to share so soon. But things are a happenin.'

To start: I started on a new medication called Low-Dose Naltrexone (LDN) about 10 days ago. I really wasn't looking for new meds to try, but this sort of fell into my lap.

It's not that I'm at all opposed to taking medication (no one in this much pain can be, regardless of how "natural" you like to keep things); it's just that I've had so little success with everything I've tried to tackle my headache over the last six years. From various anti-inflammatories, anti-seizure meds, muscle relaxants, narcotics, anti-depressants, anesthetics, psycho actives, hallucinogens, opioids...in the form of countless pills, infusions, injections, literally nothing has touched my pain. And several have caused some unwanted side-effects to keep my headache company (drowsiness, foggy-headed, and oh yea...kidney stones!) Even my neurologist has agreed that at this point, it's clear that medication is clearly not the answer for me.

BUT (there's always a but, right?), my naturopath, Dr. Popiel, brought LDN up to Craig and I as something that still might be worth exploring. And after learning more about its therapeutic potential, along with its safety profile and minimal to nonexistent side effects, we agreed it was definitely worth a shot.

(If you don't care about reading about how LDN works, just scroll down to the section that begins with "back to this week's developments.") 

So what is Low-Dose Naltrexone?
(Source: The Promise of Low Dose Naltrexone Therapy

Naltrexone is an opiate antagonist drug developed in the 1970s and approved by the FDA in 1984 as a safe and effective treatment for opiate and alcohol abuse. Used at much lower doses in a protocol referred to as Low-Dose Naltrexone, naltrexone is reported to offer benefits in a wide range of diverse conditions including Parkinson's disease, autism, multiple sclerosis (MS), Alzheimer's disease, HIV infection and other viral illnesses, as well as several types of cancer and various autoimmune disorders.

And how does it work?
As an opiate antagonist, naltrexone blocks the opiate receptor, a protein molecule found on various cells, including immune-system cells. The opiate receptor can be compared to a lock that is opened by a key. As the only substances that can activate the opiate receptor, opiates and opiate antagonists are the keys. Naltrexone closes the opiate receptor lock and blocks other chemicals, including endogenous opioid peptides, from opening the lock. In low doses, naltrexone blocks the receptor for four to six hours.

And how does that apply to pain?
Source: Low Dose Naltrexone and chronic pain - Pradeep Chapra, MD, LDN Research Trust

Current literature in pain medicine supports the view that chronic pain, especially chronic nerve pain conditions such as Complex Regional Pain Syndrome, Reflex Sympathetic Dystrophy, Diabetic Peripheral Neuropathy are autoimmune based. A study done on treating Fibromyalgia pain with LDN showed a 30% reduction in symptoms. Below is a short description of the mechanism behind chronic nerve pain. 

The Central Nervous system (CNS) is made up of nerves and cells called glia.  The glias make up about 80% of the CNS while the nerves make up about 20%. The function of the glia is to provide immune protection and host defense to the CNS. Under normal conditions the glia remain in an inactive state. They become activated readily in response to infection or injury. The most important change that happens during inflammation of the brain and spinal cord (Central Nervous System) is activation of glia cells. 
When glia cells are activated they trigger the release of certain chemicals known as pro-inflammatory and neurotoxic factors. These factors include several cytokines such as tumor necrosis factor alpha (TNF-α) and interleukin one beta (IL1-β), fatty acid metabolites and free radicals such as nitric oxide and superoxide. In painful conditions such as Complex regional pain) and neuropathic pain, damage to the peripheral nerves shifts the glia to an activated state within the spinal cord. 
The family of glia cells are made up of microglia and astrocytes. Each of these family members have a specific role. The microglia guard and protect the immune system and the astrocytes help maintain cell fluid balance which is important for the action of chemicals in the cells called neurotransmitters (needed to control nerve function). Glia are activated by trauma, injury, infection, opioids. When activated, glia release pro-inflammatory and neurotoxic factors (cytokines). 
Drugs that block the effect of opioids (morphine) may help prevent activation of glia. Such drugs are naltrexone and naloxone.  Low dose naltrexone (hence, LDN) may inhibit the activation of glia. 
Cells use chemicals called neurotransmitters to communicate with each other. Like most drugs, neurotransmitters work by attaching to specific receptors on cells. When neurotransmitters attach to receptors on cells, it allows for the passage of other substances into the cell (such as sodium, calcium). When these substances enter the cells they trigger the cells to fire and transmit signals along the nerve fiber. 
Glutamate is the most abundant neurotransmitter found in the central nervous system. It is an excitatory neurotransmitter. Glutamate binds to a receptor called NMDA (N-methyl D-aspartate).
The NMDA receptor is the most common receptor found in the Central Nervous System. When the NMDA receptor is activated by glutamate it opens up calcium channels which cause the nerves to fire. 
To summarize, when glial cells are activated they release chemicals and neurotransmitters that cause NMDA receptors to be activated which cause nerves to fire. LDN (Low Dose Naltrexone), by its ability to inhibit microglial activation, suppresses activation of NMDA receptors by decreasing the release of glutamate neurotransmitter.

So I started on LDN at a very low dose (1 mg) and have increased it by 1 mg every week with the plan of working my way up to 4-5 mg. Dr. Popiel suggested I give it at least a month before I decide if it's worth staying on. I haven't felt any changes yet (two weeks in) but actually need to stop it this week (more on that below).

Resources to check out if you're interested in LDN for chronic pain or some other health issue mentioned above:


 LDN Research Trust

www.facebook.com/groups/GotEndorphins/ (this is a private FB group that you just have to send a request to join - I've found it to be a been a super helpful resource)

Okay, back to this week's developments.

Yesterday, Craig and I spent about an hour on Skype with a San Francisco-based plastic surgeon, Dr. Peled of Peled Migraine Surgery, who is a world-renowned surgeon known for successfully treating chronic headache patients suffering from nerve compression with his peripheral nerve surgery.

I found out about Dr. Peled in what now feels like a bit of a whirlwind of events. A few weeks ago, I was trying to make it through another frustrating and discouraging physical therapy session when the therapist pointed out that the tender "spots" I kept pointing to on the top of my neck (which I've always felt to be pain sources) could very well have to do with my occipital nerve. 


In case you've been reading this blog from the very beginning, you may remember (but probably not because I can hardly remember all of the procedures) that about 3.5 years ago, Craig and I traveled to Baltimore for a series of occipital nerve blocks with neurologist Dr. Crutchfield. He injected me with Lidocaine (a local anesthetic) and Kenalog (an anti-inflammatory corticosteroid). At that time, Dr Crutchfield has suspected that my headache may have been due to inflammation around my occipital nerve (also known as "occipital neuralgia.") 

By definition, occipital neuralgia is caused by the occipital nerve being trapped and irritated by the tendons of the back of the neck. Every time my head moves (which, let's face it...is pretty much all of the time, even when my activity level is modified) the nerve will be irritated and can cause a headache that extends over the top of the head to the temples and behind the eyes, which is exactly where I feel my pain. 

If I had had a positive response from the blocks (i.e. immediate and temporary pain reduction), he would have referred me to a plastic surgeon, Dr. Ducic, who performs a similar nerve decompression surgery as Dr. Peled. BUT, I didn't have the response we were hoping for and so that theory was sidelined. 

But after talking to Dr. Peled, Craig and I are convinced that there are multiple variables that could have prevented the blocks from working back in 2014 (if the needles weren't injected in exactly the right spots, the right nerves may have never been hit), and it's 100% worth trying again.

There's some very helpful information on his website explaining why treating headaches under the assumption they are coming from the central nervous system doesn't always work (sure as hell hasn't for me) and how peripheral nerve irritation can actually be the root cause.

Migraine headaches have traditionally been thought to begin within the central nervous system (i.e. the brain and/or spinal cord) and then produce symptoms elsewhere such as throbbing in the back of the head, forehead or temples. There are many theories as to what exactly within the central nervous system is causing these chronic and often debilitating headaches. Some of these theories include pathologic blood vessel dilatation and constriction (loosening and tightening), abnormal firing of neurons within the brain, and abnormalities of various biologic substances (e.g. serotonin, calcitonin gene-related peptide). The fact that no one theory has been proven correct is likely one of the many reasons that there are so many different methods for the treatment of chronic headaches like migraines. In fact, from a medication standpoint alone, there are not only dozens of medications used to treat migraines, but dozens of classes of medications such as triptans, anti-depressants, muscle relaxants, blood pressure medications, narcotics, anesthetics, ergotamines, and so on. Fortunately, a different perspective on chronic headaches has produced remarkable results that have been previously unheard of.

This different school of thought suggests that peripheral nerve irritation (i.e. irritation of nerves outside of the brain and spinal cord such as those within the scalp or forehead) can cause irritation within the central nervous system thus leading to the perception of and symptoms of a headache. If this mechanism were in fact the culprit, then identifying and correcting the cause of such irritation could produce relief from the headache symptoms. Plastic surgeons have been doing exactly that with a common nerve irritation problem known as carpal tunnel syndrome. In this syndrome, a nerve within the wrist is compressed (i.e. pinched) and surgeons decompress (i.e. un-pinch) it thereby relieving the symptoms of pain with a greater than 90% success rate. Recent research has demonstrated that just like at the wrist, there are nerves within the head and neck that are compressed and that decompressing them, can produce significant or even complete relief that is permanent.

What kind of results can be expected from decompression surgery?
The results with these types of procedures have been quite dramatic. In one study out of Georgetown University, data from 190 patients with pain/headaches in the back of the head who underwent surgical decompression were analyzed. Over 80% of patients experienced at least 50% pain relief and over 43% of patients experienced complete relief of their headaches! In February 2011, the five-year results of such procedures were published in the medical journal, Plastic and Reconstructive Surgery. These results demonstrated five years following their operation, 88% of patients still reported greater than 50% improvement in their headache symptoms and 29% were completely headache-free!
So, am I a candidate?
Maybe. Hopefully. Please, please please let me be.
There's a very good chance I am a prime candidate for nerve decompression - based on my symptoms (including the nature and location of pain) and extensive history (including every traditional and non-traiditoinal treatment option that's been exhausted), but we won't know FOR SURE until Dr. Peled performs the diagnostic blocks. 
It would have taken some time to get on his schedule (definitely post-wedding, which is in September), but he just so happened to have a last minute opening for next week, so Craig and I will fly to San Francisco for the nerve blocks on Thursday. The plan is that if they work (which I'll know right away), we'll stay in town for a pre-op appointment on Friday, and I'll go into surgery on Monday. Woah, right? (This fast timeline is also the reason I need to go off the LDN.) 
If I have the surgery, recovery will totally depend on how many nerves need to be decompressed, and which nerves they are (which the blocks will tell us), and just what kind of state those nerves are in (which he won't really know until he gets in there). Some patients experience pretty immediate relief, while others take more time. Post-surgical pain is unavoidable, but that doesn't scare me in the least. 
There aren't words to express just how desperate I am to be a candidate for this surgery. I know better than to expect miracles, but the more I learn about occipital neuralgia, the more patient testimonials I see and the more I connect with current and past patients of his on an occipital neuralgia Facebook group, the more hopeful I feel that this truly could change my life. Just typing that fills my eyes with tears. But for now, I'm trying to really just take things one step at a time. Cautiously optimistic, as Craig likes to say. A week from tomorrow, I'll have a much better idea of what the next step will be. Fingers crossed that I have another buzz cut in my very near future. Stay tuned! 


  1. Hello Katie did you have an injury to have C1/C2 fusion ? Just wondering because I had the same surgery in 2014 due to a skiing accident..I don't know of anyone else who has had this done and I can't find anyone to talk to about pain management..any response would be greatly appreciated..Thanks,Ed

    1. Hi Ed - Yes, the incident that set this whole thing off for me was a mountain bike accident in 2011. If you scroll back through to that year on my blog there's a lot more information about it. I am still suffering from my head pain and most recently, recovering from occipital nerve decompression and excision surgeries. I know what you mean - there aren't many people with C1/C2 fusions out there! Please free to also email me directly kathrynLdalton@gmail.com.