Author: hatmaker510
Posted: Fri Dec 30, 2011 1:54 pm
When I was in active addiction myself, I’m pretty damn sure my usage led to hyperalgesia. A large amount of my pain went away when I started on suboxone. Since then (over 3 years ago), my pain is of course still present, but for the most part manageable. I’m still disabled and I still have good days and still have hellish days. But I’m not as miserable as when I was in active addiction – I always thought my pain was going to kill me back then.
I know we’ve talked about opiate-induced hyperalgesia before on this site. Lately we’ve touched on whether or not suboxone also can induce hyperalgesia. I found myself curious so I did a cursory search and this is something I found:
http://www.ncbi.nlm.nih.gov/pubmed/21114985
It’s just the abstract, so I’ll just paste it here:
| Quote: |
| In addition to analgesia opioids may also enhance pain sensitivity. Opioid-induced hyperalgesia, typically associated with potent mu-opioid agonists (e.g. fentanyl, morphine, and heroin), may be of clinical importance due to the possible counteraction of analgesia and/or paradoxical enhancement of a pre-existing pain condition during opioid therapy. Buprenorphine, a potent opioid analgesic, has a complex pharmacology on mu and kappa receptors. Buprenorphine has a better analgesia/toxicity profile (a ceiling effect for respiratory depression, less potential for abuse) compared to typical mu-opioids. Little is known about buprenorphine-induced hyperalgesia. Potentially, a lack of hyperalgesia with these other characteristics could make buprenorphine a more desirable opioid for management of chronic pain. Responsiveness to high and ultra-low doses of buprenorphine was examined following acute and repeated administration in a rat model of thermal nociception (the tail-flick test). Buprenorphine produced a dose-related antinociception. Loss of efficacy (tolerance) followed by enhanced pain sensitivity occurred with repeated dosing of buprenorphine. Delayed hyperalgesia, seen in association with antinociceptive tolerance, was blocked by the NMDA receptor antagonist, ketamine. Buprenorphine (ultra-low dose) resulted in immediate hyperalgesia, which was also reversed by ketamine, in a dose-related fashion. No tolerance to hyperalgesia was seen with repeated dosing of low-dose buprenorphine. The antinociceptive effect of buprenorphine was diminished in rats, which previously exhibited hyperalgesia with buprenorphine. In summary, bimodal properties of buprenoprhine were separately demonstrated: pronociceptive at ultra-low dose and antinociceptive at higher doses. An NMDA-receptor mechanism was involved in hyperalgesia with buprenorphine. |
Obviously, low vs high dose bupe is part of the equation and we’re all on high dose bupe – that’s clear to me, as was the first part of the abstract. But considering I’ve had 5 hours of sleep in the last 50+ hours, I’m not all that clear right now and the abstract lost me at the end.
Thoughts on the meaning of this? It’s pretty clear that there are little to no studies on this. The article itself said, "Little is known about buprenorphine-induced hyperalgesia." And this study was conducted with rats and "ultra-low" doses, which BTW, wasn’t even defined in the abstract, so we don’t even know how they define "ultra low". Also, I’ve searched high and low to find access to the whole study and it’s methods, but only the abstract is available.
I’d really be interested to hear others’ take on this – maybe from someone who can translate some of this into layman’s terms for us non-genius folks?