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Dr. Bob is Robert Hsiung, MD,
bob@dr-bob.orgShown: posts 1 to 23 of 23. This is the beginning of the thread.
Posted by g_g_g_unit on July 20, 2014, at 8:12:25
I haven't posted here for a while, mostly because I haven't seen the point in much anymore, but for the past 6 months I've been suffering from this inner restlessness that starts from when I wake up, and then persists for the rest of the day. It literally feels like I'm being tortured and is accompanied by severe concentration difficulties, plus this abstract terror/feeling of being completely overwhelmed/inability to do any kind of purposeful activity etc. It's really hard to describe accurately, but just basic activities like needing to go in a car or shower provoke the utmost fear.. and lying down or relaxing or getting a break from the relentless unrest is impossible. The only thing that alleviates the feeling is being in motion .. but I can't commit to any single activity for very long at all ..
Unfortunately, I can't tolerate anything anymore either. Even supplements. Benzos agitate me, so did clonidine, so did Guanfacine. What's probably saved my life has been melatonin, which lets me lie still enough after I ingest it to fall asleep. I don't want to precisely label what I have as akathisia, because strangely it appeared after stopping a low dose of Mirtazapine .. but it feels precisely how akathisia felt on the various meds I experienced it on. It isn't just a normal restlessness or dissatisfaction or overstimulation .. it's an inner *discomfort* or pressure or something. I also have leg jerking when I lie down at night, toe curling, plus bruxism/jaw clenching.
I saw a neurologist who said the only treatment was Propanolol, which doesn't really help, and he wouldn't prescribe it anyway because it exacerbates depression .. so I had to see a neuropsychiatrist first, who spent 45 minutes quizzing me on my relationships/life, was mostly incensed about the various benzos I'd been permitted to try, then told me nothing was wrong with me. The problem is that Propanolol and Nicotine control the symptoms enough that I can go out and sit in a doctor's room for 50 minutes, but it's not normality, or anywhere near .. and I ran out of money after that, so couldn't afford to go back to the neurologist or run any tests ..
So I don't really know what to do. I don't trust medical professionals anymore, feel profoundly trapped and quite literally backed into a corner because being taken out of this very small zone where I'm existing now seems nightmarish. I'm going to try see a mental health GP who had positive reviews on ratemd tomorrow, but I just can't bear to try and explain this all to him coherently or not make it sound like just anxiety or something.
Some supplements helped at first (theanine, Nicotine, magnesium ..) which is how I've kept going .. but it's not getting any better. I even tried buprenorphine very briefly, but was too nauseous to persist. I have a script for Requip, which my old GP was pushing on me, but I'm scared it might not be a sustainable solution, or whether it might make things worse in the long-run (receptor downregulation etc.)? He didn't seem to have any idea, and had never used it to treat akathisia, which didn't really make me feel at ease.
Anyway, I guess I just wanted to rant. And I hate to do this, but I saw poser98 add a disclaimer to phiddipus about not replying to his stuff once .. if all you want to add is how what I'm experiencing is anxiety, or need an SSRI, or that med sensitivities don't exist .. then please don't, that stuff just triggers me and makes me feel worse.
Posted by Phillipa on July 20, 2014, at 9:51:11
In reply to ongoing akathisia, posted by g_g_g_unit on July 20, 2014, at 8:12:25
Personally I also don't trust the medical profession. But I was given a beta blocked initially years ago before my first antidepressant. Doc said to prepare my body for the med. It made me very tired it was 25mg of Lopressor. Didn't take that long. But this leg stuff and all sounds medical to me. Just my thoughts. Phillipa
Posted by Christ_empowered on July 20, 2014, at 15:53:03
In reply to ongoing akathisia, posted by g_g_g_unit on July 20, 2014, at 8:12:25
Akathisia is terrible. I think its one of those things that many docs deny, unless its obvious. Kind of like TD, before all the lawsuits (and even now, in the age of the atypicals, to some extent).I was gonna say opiates but that didn't work out :-(
Maybe high doses of niacinamide? Coupled with C, B-complex, maybe some taurine in there? I'm prone to akathisia and that's some of what I take (modified Orthomolecular) and it seems to keep akathisia and TD (to which I am also prone) at bay, despite ongoing Abilify use.
If melatonin works, I wonder if other antioxidants may help, too? Natural form E with mixed tocopherols (with c, of course) comes to mind, as does high dose tocotrienols.
b6 in high doses helps acute akathisia. I don't know if your akathisia will respond, but it may well be worth a shot.
Posted by g_g_g_unit on July 21, 2014, at 4:06:26
In reply to Re: ongoing akathisia, posted by Christ_empowered on July 20, 2014, at 15:53:03
Thanks for replying CP ..
> Akathisia is terrible. I think its one of those things that many docs deny, unless its obvious. Kind of like TD, before all the lawsuits (and even now, in the age of the atypicals, to some extent).
Yeah, it sucks big time .. not just the restlessness, but the complete inability to organize myself, concentrate, make decisions etc. The paradox is that if I allowed it to be obvious, I wouldn't make it the doctor's office, but then how do you convey it's real?
>
> I was gonna say opiates but that didn't work out :-(I'm not ruling buprenorphine out, since I could care less about an addiction at this point. I have a whole stash of strips, though they're a few month's expired. I took a low dose once and felt horribly nauseous for about 10 hours, though I was wondering if you acclimate to that nausea.
>
> Maybe high doses of niacinamide? Coupled with C, B-complex, maybe some taurine in there? I'm prone to akathisia and that's some of what I take (modified Orthomolecular) and it seems to keep akathisia and TD (to which I am also prone) at bay, despite ongoing Abilify use.Niacinamide worked for a day, then the GABAergic effect agitates me (same with benzos). Vitamin C is involved in norepinephrine synthesis and makes it worse, unfortunately.
>
> If melatonin works, I wonder if other antioxidants may help, too? Natural form E with mixed tocopherols (with c, of course) comes to mind, as does high dose tocotrienols.I take Vitamin E, which helps a little .. and Vitamin A too.
>
> b6 in high doses helps acute akathisia. I don't know if your akathisia will respond, but it may well be worth a shot.Tried B6, but it seemed stimulating. I'm thinking about just taking the Propanolol more regularly (it depresses and fatigues me) and seeing if it allows me to tolerate the supplements that might help. Uridine was quite good, but overstimulating .. however, it seems to have powerful effects on restoring normal dopaminergic tone.
Someone recommended Galantamine or possibly a low dose of Deprenyl, though I guess that would be quite experimental.
I didn't make it to the doctor today ..
Posted by rjlockhart37 on July 23, 2014, at 23:16:29
In reply to ongoing akathisia, posted by g_g_g_unit on July 20, 2014, at 8:12:25
did stimulants help with the motion control? the reason im asking is, i know akathisia is totally different from hyperactivity from ADHD, but that could do a good trial to try ritilin, methyphenidate, dexedrine and adderall should be waited on becuase amphetamine can induce speedy movements....it's all i think with a dopamine dyregulation i think with movement agitation, if you look at it, parkisons's disease is a severe form of lack dopamine inducing movement disorder, but still that could be totally diffrent...
i really would warn against using zyprexa and all the other antipsychotic medinces because those can vary much create what your having with, i took zyprexa in a psych hospital at 30mg, i went to sleeo and sleot like a baby and was phenobarbital like sedation, but during a psych class lesson on managing emotions, i started slowly jerk inside, i would sit down and get reflex movements, sit and my back would twitch... and then when i spoke i had hiccuplike reflexes and effectted the speech, they can block dopamine and induce movement disorder TD, where dopamine is lowered... makee things slow and start to effect cognitive aspects to deteriorate, so if your taking anything in that class that can be an indicator....but if not....
maybe go workout, or jog for a hour and try to get all that stillness that makes you wanna move....work out like really hard, do running intervalsare you doing ok now?
Posted by phidippus on July 26, 2014, at 18:01:27
In reply to ongoing akathisia, posted by g_g_g_unit on July 20, 2014, at 8:12:25
Those with tardive akathisia often have difficulty sitting at all. The disease was first noted in 1903, 50 years before antipsychotic medications were introduced. A doctor named Hasovec observed a pair of patients who exhibited symptoms of psychoneurosis.
Fifty-one years later, another doctor named Steck observed similar symptoms in patients who had been treated with the new antipsychotic medications that a corporation called Smith, Kline and French had just introduced. In the most extreme cases, these patients must pace around, remaining in an agitated state of motion at all times. This compulsion is largely due to feelings of intense paranoia and undefined anxiety. For this reason, it has often been misdiagnosed as a mental state, for which additional drugs are prescribed, making the problem even worse. Violent and even suicidal tendencies have been reported among these patients.
There have been indications that the use of the hormone melatonin and vitamin B6 may help to alleviate symptoms. As far as drugs go beta blockers are the first choice. amantadine or clonidine can be tried. Other agents that have been investigated include ritanserin, piracetam, valproic acid (sodium valproate) and tricyclic antidepressants. Ropinorole may be of use. Also, artane and cogentin may .be given. Evidence on the treatment of tardive akathisia is unsatisfactory.
Eric
Posted by g_g_g_unit on July 27, 2014, at 9:48:28
In reply to Re: ongoing akathisia, posted by rjlockhart37 on July 23, 2014, at 23:16:29
> did stimulants help with the motion control? the reason im asking is, i know akathisia is totally different from hyperactivity from ADHD, but that could do a good trial to try ritilin, methyphenidate, dexedrine and adderall should be waited on becuase amphetamine can induce speedy movements....it's all i think with a dopamine dyregulation i think with movement agitation, if you look at it, parkisons's disease is a severe form of lack dopamine inducing movement disorder, but still that could be totally diffrent...
I can barely get stimulants prescribed for my ADD, so I don't see a doctor giving me one for akathisia. Dexedrine wasn't all that helpful in the past, and I've never really tried the others. Nicotine works partially.
>
> i really would warn against using zyprexa and all the other antipsychotic medinces because those can vary much create what your having with, i took zyprexa in a psych hospital at 30mg, i went to sleeo and sleot like a baby and was phenobarbital like sedation, but during a psych class lesson on managing emotions, i started slowly jerk inside, i would sit down and get reflex movements, sit and my back would twitch... and then when i spoke i had hiccuplike reflexes and effectted the speech, they can block dopamine and induce movement disorder TD, where dopamine is lowered... makee things slow and start to effect cognitive aspects to deteriorate, so if your taking anything in that class that can be an indicator....but if not....
> maybe go workout, or jog for a hour and try to get all that stillness that makes you wanna move....work out like really hard, do running intervalsThanks for the suggestions. I do make sure I go for a walk daily, and spend a lot of time on my feet whenever possible. I'm not on an antipsychotic right now ..
>
> are you doing ok now?
>Thanks for asking. I'm doing okay. I mean, the things that I've found that help (Melatonin, Magnesium, Vitamin E, ibuprofen etc.) allow me to get through the day, but I couldn't see surviving like this indefinitely. I'm going to try get to a doctor soon ..
Posted by SLS on July 27, 2014, at 10:05:03
In reply to Re: ongoing akathisia » g_g_g_unit, posted by phidippus on July 26, 2014, at 18:01:27
Hi Eric.
What is it about ritanserin that is credited for mitigating akathisia? Would any 5-HT2 receptor antagonist help? Since ritanserin is not available, it might be worth researching the use of low-dose Remeron, or cyproheptadine.
- Scott
Posted by phidippus on July 27, 2014, at 13:12:56
In reply to Re: ongoing akathisia » phidippus, posted by SLS on July 27, 2014, at 10:05:03
http://www.ncbi.nlm.nih.gov/pubmed/1980375
Eric
Posted by SLS on July 27, 2014, at 13:44:46
In reply to Re: ongoing akathisia » SLS, posted by phidippus on July 27, 2014, at 13:12:56
> http://www.ncbi.nlm.nih.gov/pubmed/1980375
>
> EricI understand that ritanserin has been found effective for treating akathisia. That was not my question. Unfortunately, ritanserin is not available for human consumption. The patent expired long ago, and it is used only for lab experiments. Therefore, other agents must be considered. Cyproheptadine and low-dose mirtazapine seem to be good alternatives.
- Scott
Posted by phidippus on July 27, 2014, at 16:01:45
In reply to Re: ongoing akathisia » phidippus, posted by SLS on July 27, 2014, at 13:44:46
g g g unit contends the tardive akathisia started when he was taking mirtazapine.
Eric
Posted by SLS on July 27, 2014, at 22:14:30
In reply to Re: ongoing akathisia » SLS, posted by phidippus on July 27, 2014, at 16:01:45
> g g g unit contends the tardive akathisia started when he was taking mirtazapine.
>
> EricMirtazapine can cause or exacerbate akathisia at higher dosages due to the induction of NE alpha-2 antagonism. At low dosages, mirtazapine reduces akathisia.
http://www.cnsspectrums.com/aspx/articledetail.aspx?articleid=3578
http://www.ncbi.nlm.nih.gov/pubmed/12826992
- Scott
Posted by g_g_g_unit on July 27, 2014, at 22:58:57
In reply to Re: ongoing akathisia » SLS, posted by phidippus on July 27, 2014, at 16:01:45
> g g g unit contends the tardive akathisia started when he was taking mirtazapine.
>
> EricNo, it was after I withdrew. Upregulation of 5-HT2 receptors is one plausible explanation.
Posted by SLS on July 28, 2014, at 8:48:33
In reply to Re: ongoing akathisia » phidippus, posted by g_g_g_unit on July 27, 2014, at 22:58:57
> > g g g unit contends the tardive akathisia started when he was taking mirtazapine.
> >
> > Eric
>
> No, it was after I withdrew. Upregulation of 5-HT2 receptors is one plausible explanation.
>That makes a great deal of sense.
- Scott
Posted by phidippus on July 28, 2014, at 16:21:21
In reply to Re: ongoing akathisia » phidippus, posted by SLS on July 27, 2014, at 22:14:30
How exactly does Mirtazapine treat akathisia?
Eric
Posted by phidippus on July 28, 2014, at 16:28:22
In reply to Re: ongoing akathisia » phidippus, posted by g_g_g_unit on July 27, 2014, at 22:58:57
Nobody knows what causes akathisia, especially tardive akathisia.
Have you tried Cogentin or Artane? Amantadine, Clonidine or Ropinirole? What beta blockers have you tried?
How much anxiety is tied into your disposition?
Eric
Posted by phidippus on July 28, 2014, at 16:47:03
In reply to Re: ongoing akathisia » g_g_g_unit, posted by SLS on July 28, 2014, at 8:48:33
Although akathisia is commonly attributed to antipsychotic medication and considered as an extrapyramidal symptom, the reports in the literature suggest varying underlying pathways. Deficiency of dopamine in the nigrostriatal pathway is considered to be responsible for extrapyramidal symptoms; however, serotonergic-induced inhibition of dopamine in the mesocorticolimbic pathway projecting from the ventral tegmental area (VTA) of the brain to the prefrontal cortex is thought to be responsible for the arising of akathisia. Like serotonin, norepinephrine acts similarly to inhibit dopamine in the VTA. Consequently, drugs that increase the stimulation of serotonergic or noradrenergic receptors in the mesocorticolimbic pathway theoretically could be responsible for inducing akathisia.
Eric
Posted by phidippus on July 28, 2014, at 16:58:05
In reply to ongoing akathisia, posted by g_g_g_unit on July 20, 2014, at 8:12:25
Although there are many possible hypotheses for the pathophysiology of acute akathisia, all are insufficient and incompletely satisfactory, but it is unlikely that a single neurotransmitter hypothesis will explain all the complex features of the disorder, and the interaction of several neurotransmitters is undoubted involved.
Research seems to indicate that akathisia likely arises from complex interactions of the dopamine/norepinephrine systems in the subcortical area of the brain and possibly spinal cord. Historically, the most attractive hypothesis explaining akathisia the so-called Dopamine hypothesis predicts that akathisia will result from blocking dopamine receptors on nerves in the mesocortical and mesolimbic regions (areas of the brain involved in regulation of motivation, attention and reward).
I would focus on drugs that agonize dopamine. Requip, Mirapex and Cogentin are all options.
Eric
Posted by jono_in_adelaide on July 29, 2014, at 2:02:37
In reply to ongoing akathisia, posted by g_g_g_unit on July 20, 2014, at 8:12:25
Have you considered treatment in a specialised institution sich as the Black Dog Institute or the Westmead Hospital ggg?
I have no doubt med sensetivities exist, but I do doubt that one person can be sensetive to every med from a dozen different chemical classes without somthing deeper going on.
The Black Dog Institute looks good, i was seriously considering treatment therewhen i was at myworst, i would really encourage you to give them a try - not sure about costs, but it would be worth enquiring about
Posted by g_g_g_unit on July 29, 2014, at 8:52:45
In reply to Re: ongoing akathisia » g_g_g_unit, posted by phidippus on July 28, 2014, at 16:28:22
> Nobody knows what causes akathisia, especially tardive akathisia.
>
> Have you tried Cogentin or Artane? Amantadine, Clonidine or Ropinirole? What beta blockers have you tried?I tried Cogentin briefly, but didn't stay on it very long; it was at the beginning and I hoped the symptoms might fade on their own. Clonidine helps, but makes me irritable and depressed and ruins my sleep. I've tried Atenolol, which helped slightly, as well as Propanolol. I have a box of Requip sitting in my drawer, but am hesitant about how safe dopamine agonists are in the long-term .. the neurologist I saw said he doesn't use DA agonists to treat akathisia.
>
> How much anxiety is tied into your disposition?Into my current symptoms? Well, a significant amount, but anxiety is also a symptom of akathisia. I have strong suspicions it is akathisia because Prazosin helped a lot of my anxiety, but significantly worsened the restlessness (a1-agonism can worsen movement disorders). On the other hand, Guanfacine or clonidine do nothing for my anxiety, but help me sit still.
Posted by g_g_g_unit on July 29, 2014, at 8:58:24
In reply to Re: ongoing akathisia » g_g_g_unit, posted by phidippus on July 28, 2014, at 16:58:05
> Although there are many possible hypotheses for the pathophysiology of acute akathisia, all are insufficient and incompletely satisfactory, but it is unlikely that a single neurotransmitter hypothesis will explain all the complex features of the disorder, and the interaction of several neurotransmitters is undoubted involved.
>
> Research seems to indicate that akathisia likely arises from complex interactions of the dopamine/norepinephrine systems in the subcortical area of the brain and possibly spinal cord. Historically, the most attractive hypothesis explaining akathisia the so-called Dopamine hypothesis predicts that akathisia will result from blocking dopamine receptors on nerves in the mesocortical and mesolimbic regions (areas of the brain involved in regulation of motivation, attention and reward).
>
> I would focus on drugs that agonize dopamine. Requip, Mirapex and Cogentin are all options.
>
> EricNMDA antagonists also supposedly help. I've been having quite a noticeable improvement since starting Magnesium Threonate a few days ago. Once I get to a doctor, I'll discuss the other options.
Posted by SLS on July 29, 2014, at 11:24:55
In reply to Re: ongoing akathisia, posted by g_g_g_unit on July 29, 2014, at 8:58:24
> > Although there are many possible hypotheses for the pathophysiology of acute akathisia, all are insufficient and incompletely satisfactory, but it is unlikely that a single neurotransmitter hypothesis will explain all the complex features of the disorder, and the interaction of several neurotransmitters is undoubted involved.
> >
> > Research seems to indicate that akathisia likely arises from complex interactions of the dopamine/norepinephrine systems in the subcortical area of the brain and possibly spinal cord. Historically, the most attractive hypothesis explaining akathisia the so-called Dopamine hypothesis predicts that akathisia will result from blocking dopamine receptors on nerves in the mesocortical and mesolimbic regions (areas of the brain involved in regulation of motivation, attention and reward).
> >
> > I would focus on drugs that agonize dopamine. Requip, Mirapex and Cogentin are all options.
> >
> > Eric
>
> NMDA antagonists also supposedly help. I've been having quite a noticeable improvement since starting Magnesium Threonate a few days ago. Once I get to a doctor, I'll discuss the other options.
If you find other treatments inadequate, you could explore using 5-HT2 receptor antagonists like cyproheptadine or low-dose mirtazapine, perhaps in combination with propranalol.
- Scott
>
Posted by phidippus on July 29, 2014, at 16:59:59
In reply to Re: ongoing akathisia » phidippus, posted by g_g_g_unit on July 29, 2014, at 8:52:45
There's no harm in trying the Ropinirole. You're going tto have to choose between your disposition and the effects of any drug.
Eric
This is the end of the thread.
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