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Psychedelic jitters: Fevered rigor, motor psychedelia, or dopamine antagonism?

I

invert

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I have experienced 'jitters' or excessive motor activity (most notably uncontrollable shaking in legs) during the coming-up phases of various psychedelics, and most especially DiPT (several occasions) and 2C-C (one occasion). I understand that such jitters are a not uncommon experience among psychedelics-users generally.

I would very much like to know why they arise, or at least what's going on in the brain when they arise. I have a couple of vague hypotheses, which I'll give below, but my knowledge of neurochemistry is very slight, so I'd appreciate it very much if any of you with more knowledge of this area can comment on the plausibility of the hypotheses, or offer alternatives...

1) Fevered rigor: The jitters are due to actual temperature changes, with the jitters being a case of rigor.

2) Motor psychedelia: The jitters are due to serotonergic partial agonism in the motor cortex, causing neurons there to behave oddly much as neurons in, say, the visual cortex respond oddly to psychedelics' partial agonism.

3) Dopamine antagonism: The jitters are due to a reduction in the availability of dopamine (whether directly or indirectly caused by the psychedelic), with the jitters being a temporary parkinson's-like movement disorder.

The fevered rigor hypothesis could be quite easily checked by measuring objective temperature to see if it correlates with the experience of jitters. Perceived temperature changes (which are reported under psychedelics) could either be due to real changes or due to thermoreceptor psychedelia, I guess. From my personal experience, my symptoms during jitters were not consistent with high fever.

The motor psychedelia hypothesis seems quite plausible to me, just because it assumes only an extension of the main serotonergic activity of psychedelics to the motor cortex, without speculating about the involvement of other neurotransmitter systems.

The dopamine antagonism hypothesis (I'm not sure if antagonism is the right thing to suggest - maybe inverse agonism?) seems to have quite a few (anecdotal) things to support it:

  • Predosing with MDMA is reported to prevent the jitters with 2C-C at least.
  • I have sometimes found that, with milder jitters, orgasm appears to bring the jitters to an end (though this may be coincidental - have others experienced this?)
  • The main thing that MDMA and orgasms have in common, in terms of their receptor activity, is - I believe - dopamine release
  • Movement disorders such as the jitteriness in Parkinson's disease are associated with lack of dopamine. I also note, from personal experience, that the jitters are most prominent when resting, which is consistent with parkinsonism.
  • Psychedelics are - on the whole - not liable to habit-forming, and some have been considered useful in breaking addiction. Addiction is mediated by dopamine activity, and I would imagine dopamine antagonism (or some such mechanism) might be consistent with addiction-breaking

I guess this dopamine hypothesis could best be tested by comparing the experience of jitters on psychedelics alone versus psychedelics combined with a selective dopamine releaser (is there such a drug?)

I reiterate, and apologize for the fact, that, as a result of my general ignorance of neurochemistry, the above is all appallingly speculative and may be nonsense. If any research already exists that could speak to the above, I'll be most interested to read about it. :)
 
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Personally, I experience slight (but controllable) chattering of teeth on LSD. Looks like it would fit your description of 'jitters' to a degree...

I would exclude the 'fever'-explanation, as I never noticed significant rise in body temperature during this experiences.

The dopaminergic thing sounds reasonable to me, but it's just a gut feeling this time. This would be in good agreement with LSDs affinity to D-receptors.

Just my 2 cent...

Murphy
 
I doubt it's dopamine antagonism. Unless you're in opiate withdrawal, it's unlikely you're ever going to notice those sorts of side effects from such small doses.
 
How could it be DA antagonism? I thought most 5-ht psychs release large amounts of dopamine, thus the use of DA antagonist antipsychotics to aborts trips.

At least I know for sure LSD and Mescaline result in strong dopaminergic stimulation.
 
theWorldWithin said:
How could it be DA antagonism? I thought most 5-ht psychs release large amounts of dopamine, thus the use of DA antagonist antipsychotics to aborts trips.

At least I know for sure LSD and Mescaline result in strong dopaminergic stimulation.
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Ah, okay... thank you! Is there no possibility that DA antagonism might be present (directly, or indirectly via its serotonergic effects effecting other systems) in early stages, followed by DA stimulation? Or alternatively, is there any way that DA agonism could paradoxically produce the jittery symptoms typical of dopamine depletion under certain circumstances? Could competitive agonism of some sort be relevant here?

Personally, I'd be delighted if the 'motor psychedelia' explanation turned out most plausible, as it seems the most innocuous of the available explanations for the jitters; so if the DA hypothesis can be ruled out as highly implausible, that'd be cool. :)

irobeth said:
I experience this and am very interested in this as well.
Can I ask what the relative frequency (as in Hz) of your jitters are?
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I haven't taken care to note the frequency at the time, but in retrospect I'd say about 3 or 4 Hz.
 
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^^^I believe the DA antagonism hypothesis is not supported by the known neuropharmacology of psychedelics, but indirect DA agonism could account for these effects. However, I think that NE is a far more likely candidate for causing these jitters, as there is far more evidence for psychedelic-induced release of this neurotransmitter.
 
Especially the ergoloids have direct affinity for DA receptors; I don't remember if LSD has any agonistic or antagonistic effects.
 
Many thanks for replies, O knowledgeable people of ADD. :)

5-HT2 said:
^^^I believe the DA antagonism hypothesis is not supported by the known neuropharmacology of psychedelics, but indirect DA agonism could account for these effects. However, I think that NE is a far more likely candidate for causing these jitters, as there is far more evidence for psychedelic-induced release of this neurotransmitter.
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Ah! I'm jolly glad I asked about this here... I had no idea about anything other than the serotonergic activity of psychedelics. Would I be right in thinking that, if the jitters are NE-induced, the motor activity component of the jitters should also be accompanied by increased pulse and b.p.?

Hammilton said:
Especially the ergoloids have direct affinity for DA receptors; I don't remember if LSD has any agonistic or antagonistic effects.
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Do any chemicals have agonism at one subtype of a given receptor and antagonism at another subtype of the same receptor? (Just a general curiosity question, this. I don't know that it's relevant to my original question, although I suppose it might be.)
 
invert said:
I haven't taken care to note the frequency at the time, but in retrospect I'd say about 3 or 4 Hz.
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Same here, I'm leaning towards the motor cortex theory because this coincides with the low border of theta rhythm, which is known to be involved with integrating sensory information with motor output.
 
i think that theres another possible reason that you didn't bring up, it's psychosomatic. perhaps the jitters are just a result of some kind of underlying anxiety or tension? i think this is supported by your claim that predosing with MDMA can prevent these jitters, it is a pretty strong anxiolytic.
 
stirfry said:
i think that theres another possible reason that you didn't bring up, it's psychosomatic. perhaps the jitters are just a result of some kind of underlying anxiety or tension? i think this is supported by your claim that predosing with MDMA can prevent these jitters, it is a pretty strong anxiolytic.
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Oh good point, that's a very interesting idea. The jitters do seem to precede the moment where the trip is fully accepted and engaged with (for me, anyway), but then - their position in the trajectory of the trip is such that that contiguity may be coincidental. I'm inclined against that idea, plausible though it is on the face of it, because I'm not sure psychosomasis could generate jitters of such unavoidability and amplitude. It was on a par with fairly bad rigor (which I've had once during high fever) in terms of the severity of the symptoms, but without corresponding fever (I think - although their were perceived temperature changes)).

... But quite possibly I underestimate psychosomasis...

ETA: By the way, the thing about MDMA predosing isn't my claim from personal experience, but someone else's report of this effect (in this post) in the B&D 2C-C thread in PD.
 
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I really dont think its DA antagonism...I've never seen any physedelic that had a known DA antagonist effect. (but IIRC...the reason AP abort a trip is they are also 5ht2a antagonists...)

I'm thinkings its probably NE related, either directly from the action of the drug, or from your own anxiety and nervousness, and perhaps regular old epinepherine having a PNS effect from the same anxiety....try a strong PNS stimulant in a high dose (epinepherine, phenylpropanolamine, ephedrine) and you'll notice a good amount of shake/quiver in your muscles.

I would imagine a phenylethylamine, what with its closeness to amphetamine in general would release a good bit of NE and probably DA as well, not antagonist DA.

perhaps a beta blocker would help?
 
But aren't the PEA psychedelics even more selective for 5HT2a receptors than even the tryptamines?
 
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