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Help for dystonia

Middleway

Middleway

Ex-Bluelighter
Joined
Apr 10, 2007
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Melbourne
I am dealing with a problem I have had for years, jaw clenching and agitation. I find my jaw clenching so tight and sometimes my abdominals also clenching and spasonming when its really bad. This is accomonyed by agitation and anxiety.
Benzos relive it somewhat but I can't help but think this is something different to a general anxiety disorder.
SSRI's give me acute dystonic reactions, the whole deal, jaw protruding, sometimes putting my tounge out if its really bad.
Fucking psychietrist's have been nothing but useless

I wonder if ssri's have caused it...

I can't help but think it is related to catecholamines as stimulants whilst providing a big relief initially, cause it to worsen dramatically. Even tea and especially coffee. Alcohol too. But the question is. Do I have too much or too little?
Too little I would think. Don't stimulants cause a release of catecholamines? And then what? What happens when you come down?

Whats going on? I am ok at the moment, better than ever since I got off the dexies. I use lamictal and benzo's now to control it and my anxiety. But I hate benzo's. I need something to clear my head not fog it up.
Would a neurologist be worth seeing?
Thanks
 
some stimulants cause a release of catecholamines. Amphetamine-type stimulants do. Most stimulants prevent the reuptake of dopamine, though.

AFAIK, caffeine does not cause the release of catecholamines at all. Neither does alcohol. Alcohol isn't a stimulant, either. It's a very simple depressant.

It sounds to me like you just have an anxiety disorder. You might want to try gabapentin or pregabalin. They're a good anti-anxiety agents.
 
I'm pretty sure caffeine causes DA modulation and indirect NE release as a result of it's adenosine antagonist effect.
 
Effect of chronic caffeine administration on monoamine and monoamine metabolite concentrations in rat brain.
Kirch DG, Taylor TR, Gerhardt GA, Benowitz NL, Stephen C, Wyatt RJ.

Neuropsychiatry Branch, National Institute of Mental Health, Neuroscience Center, Saint Elizabeths, Washington, D.C. 20032.

Caffeine was chronically administered in four doses (0, 10, 25, and 50 mg/kg/day) to rats via twice-daily intraperitoneal injections for 30 days. Concentrations of brain tissue monoamines, dopamine (DA), norepinephrine (NE), and serotonin (5HT), and monoamine metabolites, dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-methoxy-4-hydroxyphenylglycol (MHPG), and 5-hydroxyindoleacetic acid (5HIAA), were determined. At the 10 mg/kg/day dose, no significant changes were found compared with controls. At 25 mg/kg/day and 50 mg/kg/day significant changes were observed within each monoamine system. In striatum, DA and 5HT were increased, while DOPAC was decreased. In frontal cortex, NE was increased. In cerebellum, 5HT and MHPG were increased.

http://www.ncbi.nlm.nih.gov/sites/e...ez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVDocSum
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So, sort of, but doubtfully in the doses humans use (5mg/kg IP is probably equal to 500mg or 6 or 7 cups of coffee in humans).

I've dealt with a few people with dystonia before, and gabapentin and pregabalin were said to be not of much help (but your mileage may vary). For me, it's mostly serotonergic system agonism (especially 2A) that can cause excessive jaw clenching. You may want to try risperidone, a 5HT2A receptor antagonist, or buspirone, a 5HT1A agonist (5HT1 agonists tend to be anxiolytic and inhibit tardive dyskinesias produced by antipsychotics). However, both these have effects on dopamine that may progressively cause movement disorders.

Which stimulants make it better, and for how long?
 
N-(2-methoxy)benzyl-5-methoxy-tryptamine is a 5-HT2A antagonist afaik. (It looked like it would be a great superpotent agonist, but it wasn't...)
That could be a better choice than Risperidone if you don't want any DA anatagonist effects.
No doubt there;s others - are there any existing pharmaceutical medications that are selective 5-HT2A antagonists?
 
^By selective you mean one that is purely a 5HT2a antagonist alone, without any effects on other neurotransmitters? If that's what you mean I never heard of such drug. Like you said resperidone is a potent 5HT2a antagonist but it is also a potent DA antagonist which probably will bring unwanted effects to the op.

I'm not sure risperidone would be a good call since it affects DA drastically just like any other neuroleptic. From personal experience I had with risperidone it made me totally disphoric, unproductive, lazy (not because I lacked will, I simply couldn't do anything), not to mention I had neuroleptic malignant syndrome when I was on chlorpromazine; so I'm not a real anti-psychotic fan.
I'm a bit benzoed up right now I can't ratiotinate very clearly I'm sorry; tardive dyskinesias are resultant of prolonged DA antagonism AFAIK, how does 5HT1a agonists inhibit tardive dyskinesias? Am I missing something obvious here? Did you mean for him to take risperidone along with buspirone so to some extent prevent tardive dyskinesias from developing?
 
Yea, by selective I mean without affinity to other neurotransmitter receptors. Well as far as i'm aware it doesn't have any appreciable afinity for DA, i'd expect it to have appreciable affinity for some other 5-HT receptor isoforms though, most noteably 2C... 2A and 2C affinity seem to go hand in hand.
 
^Yeah, exactly. I don't think there's such thing as a selective 5HT2a only drug out there, unfortunatly I guess... :\
 
I am on a 1mg bd dose of Stellazine as well and I find that helps. Dexies make me feel fucking fantastic at first but screw me up big time. I just flushed the last of a supply I had at my parents place and feel very proud of doing so considering the voice inside me that was screaming for them.
I have just started selegiline at 5mg bd. Not sure what the implications of mixing it with the stelazine is as they both exert an action in the striatum. Also don't you need to take selegiline with some kind of antioxident?
 
Selegiline is an indirect antioxidant by means of MAO-B inhibition so there's no real need to take an antioxidant with it.

Trifluoperazine (Stelazine) is sort of nasty stuff, and is more likely to cause malignant movement disorders than the above mentioned anxiolytics/antipsychotics. I would recommend switching to a never antipsychotic. Are you schizophrenic? Selegiline can exacerbate psychotic symptoms. Very weird for you to be scripted trifluoperazine and selegiline together, as they're sort of contradictory. Clozapine is another option that is low on movement side effects.

They're not sure how 5HT1A agonists alleviate EPS, but they seem to do so in rats. It does not seem to be moderated by the dopaminergic system:

The effect of a 5-HT1A receptor agonist on striatal dopamine release.
Bantick RA, De Vries MH, Grasby PM.

Cyclotron Unit, CSC, The Hammersmith Hospital, Imperial College London, London W12 0NN, United Kingdom. [email protected]

5-HT1A receptor agonists consistently reduce neuroleptic induced catalepsy in rats. A serotonin-dopamine interaction has been proposed to underlie this effect. Specifically, 5-HT1A receptor agonists may reduce the activity of serotonergic projections that inhibit dopaminergic nigrostriatal neurones, therefore increasing dorsal striatal dopamine levels and partially overcoming the neuroleptic blockade of D2 receptors. We tested the hypothesis that 5-HT1A receptor agonists increase striatal dopamine release in man using PET scanning with the selective D2 receptor radioligand [11C]raclopride, which is sensitive to endogenous dopamine levels. Six healthy volunteers received two PET scans, one after placebo, the other after 1 mg flesinoxan, a selective 5-HT1A receptor agonist. Binding potential values for striatal subdivisions were determined using a simplified reference tissue model. We did not find any difference in striatal [11C]raclopride binding between conditions, even though flesinoxan lead to typical 5-HT1A receptor agonist side effects and produced elevation of growth hormone in five of the six subjects. Our results suggest that the anticataleptic effect of 5-HT1A receptor agonists is not mediated by striatal dopamine release, and indicates a need for further research with other suitable 5-HT1A receptor agonists. Copyright (c) 2005 Wiley-Liss, Inc.
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http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&uid=15906386&cmd=showdetailview&indexed=google

Hmm, growth hormone elevations, maybe the steroids forum would be interested in this compound...

I'm not sure that a neurologist would be especially worth going to unless you're showing some other symptoms of common movement disorders.. Many of the more common movement disorders are difficult to detect on MRI (Parkinson's), though they may be able to eliminate other more worrysome causes of your dystonia. If your symptoms are becoming progressively worse and more disabling, you should probably see a neurologist, but it's hard to say if they've been stable for a long time.
 
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Very weird for you to be scripted trifluoperazine and selegiline together, as they're sort of contradictory.
Click to expand...

Called, self medication, all the cool kids are doing it 8o

So what is that study saying? Stellazine is a 5-HT1A receptor agonist yeah?
In any case I have dropped off the stellazine now. It was perscribed for anxiety and compulsive type thinking but I have got that under control with clonazapam and lamictal I think. The selegiline definetly helps my concentration and energy levels. The stellazine does the oppisate, even at low doses like I was taking.

So yeah, is that study refering to selegiline or stellazine type drugs?
 
Stellazine is a 5ht2a, dopamine, and adrenergic antagonist. I don't think it's even been evaluated as a 5HT1A agonist, or it was inactive there (like most of the typical antipsychotics).

The study is referring to 5HT1A agonists eg buspirone (partial), clozapine (full), flesinoxan (full if the s-enantiomer), ipsapirone (partial), naratriptan(full), olanzapine (full), piribedil (partial), quetiapine (full), rizatriptan (full), roxindole (partial), sumatriptan (full), terguride (partial), ziprasidone (partial)...
 
Nah, I actually got perscibed that, I added the selegiline myself to try to lift my mood and concentration a bit. Fucking hate all the other antidepressants and selegaline seems better than benign to the body, seems like the logical choice
 
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