I think that many folks, including the more knowledgeable like you and I and some of these other thread participants, tend to make the mistake of assuming that because the JWH, CP, etc. class cannabinoids act on the same receptors (CB1/CB2 primarily....though there are plenty of other receptors such as vanilloid, terpenoid, and so on which are also potential targets) as natural and FDA-approved synthetic cannabinoids, that they will have the same effects.
I can't posit an exact method of action -- if I could, we'd be far closer to understanding what is happening to Morrow and others who've reported these neuropathy-like effects -- but I don't think this is a matter of "simple overdose." In fact I suspect that 'normal' recreational dosages could affect some people quite badly the very first time, while for others it could take long-term use at high doses to bring on these effects....or they may not be susceptible to them at all without some kind of external trigger or "drug interaction" (even if the "drug" is actually a unique personal biochemistry rather than an external substance).
The natural (THC, CBD, CBN, THCV, et al) and well-known synthetic (Nabilone, for example) cannabinoids have very unique neuroprotective, neural-plasticity-inducing,
immune modulating and inflammation-fighting properties.
Imagine that all other traits are preserved, but that these benefits are absent from JWH-class molecules (I'm not saying this is the case....it's just the simplest possibility that I can think of off of the top of my head). It's possible that these beneficial effects are preventing cannabis itself from being harmful....and without them, one or more other cannabinoid effects are coming to the fore which have almost the exact reverse effect versus what we'd expect out of cannabis itself.
After all, just look at opiates.....pure agonists, mixed ag/antag, and pure antagonist opioids have dramatically different, and often dead opposite, effects. But even within those individual categories, there can be wide variations in effects as well as tolerance, dependence and withdrawal profiles. Yet they're all acting primarily on the same opiate receptors, right?
So, if cannabis and low-dose naltrexone have similar immune modulating properties that help reduce auto-immune disease symptoms at the source, prevent infections, slow/reverse cancer progression, cause neuropathies including MS to go into remission, etc.....then I would expect that if one tried enough different opioid-class molecules, one could induce the precise opposite effects. Cause neuropathies, make a wide range of immune-related diseases worse or even cause them in the first place, make the patient prone to infection or cancer, etc....
Thusly, while I am wishing I could posit a more specific mechanism of action (excessive over-amping of neural signaling by direct p-glycoprotein induction? reduction in levels of inhibitory neurotransmitters like GABA and endorphins?)....I think that the general method by which this happened to Morrow and other unfortunate "crash test dummies" can be sketched out in at least the broad strokes.
One interesting conclusion that could be drawn from the above-mentioned vague theory is the notion that cannabis could potentially reverse or moderate these symptoms.
Some commenters scoffed at the notion that "more drugs" could do anything but make Morrow Syndrome sufferers worse....but if it's as relatively simple as what I've described, then it's very possible that some treatments -- despite the unlikelihood of an actual cure -- could be derived from what are normally considered recreational substances, or "supplements" that are of limited use to healthy people.
As unpleasant as it is to experiment on oneself with a high likelihood that one will make oneself worse several times before finding anything that actually helps....it's possible that trying out a few things like cannabis use, GABA/other neurochemical precursor supplementation, etc may be one of the best ways of both diagnosing this strange syndrome and of developing avenues of relief.
We should! I'm coming down offa some 4-methoxy-PCP, about to drive from Austin to Cali!
I didn't expect to see a post telling a story like yours here; I offered my standpoint based on the fact that an acute CB1/CB2 agonist overdose, or hell any psychedelic, cannabinoid, or dissociative drug overdose, probably couldn't cause any nerve damage of the type you suffer from.
I'm not trying to tell everyone in the world to meditate their pain away; just that someone who has suffered a textbook 'panic attack' and now suffers from textbook 'Post-Traumatic Stress Disorder' should realize that in a healthy and normally functioning nervous system, most pain is psychosomatic.
JWH-018 gets me stoned as fuckkkkkk.
