Day 28: Why This Funky Drug Works on Lupus

The weird and funky mechanism of the new medication I was put on this week, and why it’s starting to work (at least on some of my symptoms):

OK, I’m getting science-y again, and I’m the first to say I don’t really understand this. In fact, I’m pretty sure the scientists don’t fully understand this either.

So, I have two different types of pain going on, not uncommon for someone with Lupus. The first is due to inflammation, and was either visually observed or felt through physical examination by the rheumatologist. The NSAIDs (non-steroid anti-inflammatory drugs) I’m on should be taking care of that; however, since they aren’t sufficient, we have to wait to figure out what’s wrong with the lungs before jumping to the next level of treatment.

The other sort of pain I have is neuropathic pain, which doesn’t really respond to NSAIDs or opioid analgesics (e.g. codeine). Neuropathic pain is due to interruption in the connections of nerve cells in my peripheral nervous system, and manifests as pain in response to stimuli that normally wouldn’t cause pain (e.g. a light touch), and increased pain in response to normally painful stimuli (e.g. a punch on the affected arm could be excruciating). 

In order to manage the pain, I have been placed on an extremely low dose of a tricyclic antidepressant, amitriptyline. In use for depression, the normal dose of amitriptyline would be between 100-300 mg. However, I take 10 mg, a few hours before bed.

It is believed that the mechanism for the drug to work is through its ability to inhibit the re-uptake of serotonin and norepinephrine within the dorsal horn. Though not fully understood, scientists think that the main cause of neuropathic peripheral pain is due to imbalance of serotonin and norepinephrine in endogenous pain inhibitory pathways (totally copied that from the article I read). Basically, by using low-levels of anti-depressants, the pain messages in nervous system are returned to normal through regulation of serotonin and norepinephrine.

The mechanism is most effective when the brain is asleep– and that is what I plan to do now! (Friends, feel free to chip in, I don’t really get this stuff!)

When you need it for pain, 10mg amitriptyline is a miracle. However, I hate being on it long term, because it makes you extra groggy in the morning, and mornings are already hard with Lupus. I’ve wanted to get off it for the last two years, but my doctor was hesitant because I’ve had a lot on, and she didn’t want me to risk my pain coming back in the middle of fieldwork, conferencing, etc. However, once the initial stress of self-isolation was over, I realised now was the perfect time to stop amitriptyline. With my doctor’s blessing, I am now six weeks free of it, and my mornings are transformed. Plus, I don’t have any recurring nerve pain. Life is good!

Wondering what’s going on with these posts? Check out my explanation HERE!

Leave a comment