Odd reactions to stimulants post-illness

[Iritu1021]

Just out of mere curiosity did anyone else an here also have an adhd diagnoses before coming down with this illness? Wondering if there are preexisting conditions that may distinguish those that will now have a bad reaction. I know @debored13 you mentioned you use to take stimulants before this illness so I though you might of had that diagnoses as well.

I was initially diagnosed with ADD and depression.

 

[frozenborderline]

Just out of mere curiosity did anyone else an here also have an adhd diagnoses before coming down with this illness? Wondering if there are preexisting conditions that may distinguish those that will now have a bad reaction. I know @debored13 you mentioned you use to take stimulants before this illness so I though you might of had that diagnoses as well.

yes, ADD diagnosis pre-illness

 

[S-VV]

@debored13 how are you doing? Is the T3/T4 still proving to be somewhat helpful?

 

[Jackb23]

Did some thinking today which led to a complete shot in the dark "perhaps." The caudate nucleus in individuals with ADHD is said to be awry and this can even predict severity in some cases. Its hypodopaminergic actions in ADHD have been a well known hallmark of the disorder for a long time. Not only this, but in lesion studies, individuals with caudate lesions/injuries often report agitation, hyperactivity, etc. What I am wondering is if individuals with ADHD prior to their me/cfs are more vulnerable to agitation, restlessness, etc. and paradoxical reactions to things due to the fact that their neural anatomy leaves them predisposed. More interestingly, I find SSRI's to be the thing that I react the worst to so I did a little research. It turns out that serotonin inhibits the caudate nucleus in some instances. If this is the case (who knows), this would turn a hypoactive caudate into an extremely hypoactive caudate (exacerbating symptoms and reactions)- especially if this illness perturbs and underwhelms this brain region by its own manner. If you want to post substances that you now react poorly to (in regards to agitation, restlessness, etc), I will happily research them and how they might tie into Caudate activity.

Caudate nucleus volume asymmetry predicts attention-deficit hyperactivity disorder (ADHD) symptomatology in children.
https://www.ncbi.nlm.nih.gov/pubmed/12593459

Caudate asymmetry is related to attentional impulsivity and an objective measure of ADHD-like attentional problems in healthy adults

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4433431/


Acute Caudate Vascular Lesions
https://www.ahajournals.org/doi/pdf/10.1161/01.STR.30.1.100

Delirium: a neurologist's view--the neurology of agitation and overactivity
https://www.ncbi.nlm.nih.gov/pubmed/21206426
" In many patients, agitation and overactivity are explained by toxic and metabolic factors and infections. Lesions, especially strokes, in some brain regions have been reported to cause sudden agitation and a hyperactive state, often with an increased amount of speech output, the topics of which flit from one subject to another. Strokes and other lesions that involve the temporal lobes, fusiform and lingual gyri, caudate nucleus, and anterior cingulum have been reported to cause an acute hyperactive state similar to that found in patients with delirium tremens related to alcohol withdrawal."

Effect of the serotonergic system on the caudate nucleus.
https://www.ncbi.nlm.nih.gov/pubmed/6967608

"The inhibitory effect of L-5HTP on the caudate spindle was stronger than that on the VA spindle. These inhibitory effects of L-5HTP were observed when L-5HTP showed synchronization on spontaneous EEG and no effect on the duration of the cortical after discharge. In the evoked potential study, both electrical stimulation of the dorsal raphe nucleus and exogenous L-5HTP inhibited the activity of the potentials in the caudate nucleus induced by electrical stimulation of the radial nerve. These results suggest that the neuronal activity of the caudate nucleus is inhibited by the serotonergic system."


In vivo presynaptic control of dopamine release in the cat caudate nucleus—II. Facilitatory or inhibitory influence ofl-glutamate


"Therefore, high concentrations ofl-glutamate exerted an inhibitory presynaptic control on [3H]dopamine release which seemed to be indirect and mediated partly by GABAergic neurons"

 

[Fogbuster]

I can't tolerate any stimulant herbal supplements, pharmaceutical drugs or caffeinated drinks. Surely this has to be a major sign of HPA dysfunction?

 

[Iritu1021]

I am now able to tolerate stimulants again thanks to lithium orotate stabilizing my neural receptors (my guess is primarily some type(s) of 5HT receptor. If anything my response to them is now rather muted while in the past it was over-exaggerated.

 

[Wolfcub]

Sometimes for no reason I can work out I cannot tolerate coffee, even one weak cupful. The next day I can and enjoy it. The same with chocolate especially dark chocolate even though I adore all chocolate! I know it has to be the caffeine content which makes me extremely shaky. This happens randomly and many times it doesn't happen at all!

The same with alcohol (though alcohol I think is not a stimulant as some believe, but a depressant...that is has sedative/depressive effects on the nervous system.)
I have never had ADHD symptoms throughout my life though or ever been diagnosed with ADHD.

 

[hailkaine]

I used to do pretty well on Ritalin before I got sick, and after I got sick (my trigger was lyme) there was a change in how I reacted to it, not overnight, but it eventually reached a state of intolerance that was a stark difference to how I used to react to it.

I was originally prescribed ritalin for ADD, and I got the characteristic "paradoxical relaxation" at the right dose with it, where I felt calmer, but also more organized cognition. Sometimes I would get overstimulated if I mixed it with coffee and tried to chase the effect (which really was more of a consequence of workload than anything), but overall it was very tolerable and I still slept decently.


After I got sick I started not being able to tolerate /get benefit from Ritalin in general. You would think stimulants would help fatigue but not in this case. I was at school during the first year I was sick (I was more mildly sick, gradually getting worse at the time), and I would still try and push through the side effects of ritalin for the more cognitively demanding tasks, like coding and writing my final paper.

The effects started to be extreme adrenergic reactions. I know this seems consistent with stimulant usage in general, but this was way more extreme. Like the dopamine/norepinephrine ratio had shifted unfavorably. I would be able to tolerate this barely at first, and it would mean things like decreased sleep and feeling on edge all the time, but gradually this became more extreme, and I would not be able to sleep for 24 hours after a dose of ritalin that barely even helped me concentrate. Several times that I took ritalin I would become so adrenaline soaked that I was literally shivering--people I was studying with asked me if I was alright. But even at these doses I didn't experience the same cognitive benefits I used to.
This is why I bring up the dopamine/norepinephrine ratio.

Based on my experience with medication, I think that contrary to a classic, simplified view of stimulation and alertness being excitation that is opposite to inhibition, a lot of stimulants can be inhibitory, and this may mean at an ideal dose range they don't release excessive norepinephrine (also this has to do with the entianomers but also must have to do with a number of conditions).

I started speculating this based on finding @Iritu1021 's blog post on histamine (http://www.chronicfatiguediagnosis.com/2018/02/24/histamine-the-song-of-ice-and-fire/), in which she mentions sort of similar reactions to methylphenidate. However, I'm not sure if she had the similar experience I did of favorable experiences pre-illness and unfavorable after.

Anyway, the only way I could use ritalin was with also taking trazodone to sleep. this is unsurprisng as trazodone is a powerful sleeping medication, but, like a lot of older gen antidepressants, has antihistaminic effects too, so I speculate about its role in inhibition.



I could go on and on about drug sensitivities induced by CFS, and I think that could possibly reveal something with enough theory and speculation, but I'll stick with ritalin for now.

I’ve been on stimulant medication for the vast majority of my life and after contracting morgellons stimulants stopped having any psychological effect on me. They also began making the tremors I developed with it far worse. It feels like stimulants suck the dopamine out of
my brain instead of raising it. After taking some concerta i developed what i can only describe as a dystonic reaction and could barely move my legs, hands were stuck curled inwards, and my back was extremely rigid. For me the neurological effects have been vastly more devastating than the physical.

 

[hailkaine]

I used to do pretty well on Ritalin before I got sick, and after I got sick (my trigger was lyme) there was a change in how I reacted to it, not overnight, but it eventually reached a state of intolerance that was a stark difference to how I used to react to it.

I was originally prescribed ritalin for ADD, and I got the characteristic "paradoxical relaxation" at the right dose with it, where I felt calmer, but also more organized cognition. Sometimes I would get overstimulated if I mixed it with coffee and tried to chase the effect (which really was more of a consequence of workload than anything), but overall it was very tolerable and I still slept decently.


After I got sick I started not being able to tolerate /get benefit from Ritalin in general. You would think stimulants would help fatigue but not in this case. I was at school during the first year I was sick (I was more mildly sick, gradually getting worse at the time), and I would still try and push through the side effects of ritalin for the more cognitively demanding tasks, like coding and writing my final paper.

The effects started to be extreme adrenergic reactions. I know this seems consistent with stimulant usage in general, but this was way more extreme. Like the dopamine/norepinephrine ratio had shifted unfavorably. I would be able to tolerate this barely at first, and it would mean things like decreased sleep and feeling on edge all the time, but gradually this became more extreme, and I would not be able to sleep for 24 hours after a dose of ritalin that barely even helped me concentrate. Several times that I took ritalin I would become so adrenaline soaked that I was literally shivering--people I was studying with asked me if I was alright. But even at these doses I didn't experience the same cognitive benefits I used to.
This is why I bring up the dopamine/norepinephrine ratio.

Based on my experience with medication, I think that contrary to a classic, simplified view of stimulation and alertness being excitation that is opposite to inhibition, a lot of stimulants can be inhibitory, and this may mean at an ideal dose range they don't release excessive norepinephrine (also this has to do with the entianomers but also must have to do with a number of conditions).

I started speculating this based on finding @Iritu1021 's blog post on histamine (http://www.chronicfatiguediagnosis.com/2018/02/24/histamine-the-song-of-ice-and-fire/), in which she mentions sort of similar reactions to methylphenidate. However, I'm not sure if she had the similar experience I did of favorable experiences pre-illness and unfavorable after.

Anyway, the only way I could use ritalin was with also taking trazodone to sleep. this is unsurprisng as trazodone is a powerful sleeping medication, but, like a lot of older gen antidepressants, has antihistaminic effects too, so I speculate about its role in inhibition.



I could go on and on about drug sensitivities induced by CFS, and I think that could possibly reveal something with enough theory and speculation, but I'll stick with ritalin for now.

I used to do pretty well on Ritalin before I got sick, and after I got sick (my trigger was lyme) there was a change in how I reacted to it, not overnight, but it eventually reached a state of intolerance that was a stark difference to how I used to react to it.

I was originally prescribed ritalin for ADD, and I got the characteristic "paradoxical relaxation" at the right dose with it, where I felt calmer, but also more organized cognition. Sometimes I would get overstimulated if I mixed it with coffee and tried to chase the effect (which really was more of a consequence of workload than anything), but overall it was very tolerable and I still slept decently.

Also, I developed the same issue with extreme adrenergic activity with stimulants, as well as without them. Would sweat and shake constantly and had hyperadrenergic POTS. Look into


After I got sick I started not being able to tolerate /get benefit from Ritalin in general. You would think stimulants would help fatigue but not in this case. I was at school during the first year I was sick (I was more mildly sick, gradually getting worse at the time), and I would still try and push through the side effects of ritalin for the more cognitively demanding tasks, like coding and writing my final paper.

The effects started to be extreme adrenergic reactions. I know this seems consistent with stimulant usage in general, but this was way more extreme. Like the dopamine/norepinephrine ratio had shifted unfavorably. I would be able to tolerate this barely at first, and it would mean things like decreased sleep and feeling on edge all the time, but gradually this became more extreme, and I would not be able to sleep for 24 hours after a dose of ritalin that barely even helped me concentrate. Several times that I took ritalin I would become so adrenaline soaked that I was literally shivering--people I was studying with asked me if I was alright. But even at these doses I didn't experience the same cognitive benefits I used to.
This is why I bring up the dopamine/norepinephrine ratio.

Based on my experience with medication, I think that contrary to a classic, simplified view of stimulation and alertness being excitation that is opposite to inhibition, a lot of stimulants can be inhibitory, and this may mean at an ideal dose range they don't release excessive norepinephrine (also this has to do with the entianomers but also must have to do with a number of conditions).

I started speculating this based on finding @Iritu1021 's blog post on histamine (http://www.chronicfatiguediagnosis.com/2018/02/24/histamine-the-song-of-ice-and-fire/), in which she mentions sort of similar reactions to methylphenidate. However, I'm not sure if she had the similar experience I did of favorable experiences pre-illness and unfavorable after.

Anyway, the only way I could use ritalin was with also taking trazodone to sleep. this is unsurprisng as trazodone is a powerful sleeping medication, but, like a lot of older gen antidepressants, has antihistaminic effects too, so I speculate about its role in inhibition.



I could go on and on about drug sensitivities induced by CFS, and I think that could possibly reveal something with enough theory and speculation, but I'll stick with ritalin for now.

Also, I developed the same issue with extreme adrenergic activity with stimulants, as well as without them. Would sweat and shake constantly and had hyperadrenergic POTS. I’d recommend guanfacine since it redcues peripheral norepinephrine. It helped me a lot.

 

[Iritu1021]

Hi, it’s been a while since I’ve been here but I saw that I got tagged so I thought I would comment some more on my stimulant misadventure nice I’m a few years wiser than last time I’ve been here and people are reporting things I recognize from my own past.

1. There is an issue of neurotransmitter “turnover” which is more than just amount of released neurotransmitter (NT). Turnover refers to flow of neurotransmitter from one neuron to another and is a net sum of synthesis, release, uptake and degradation. The synthesis and degradation are influenced by metabolic rate. This is why thyroid hormone played such a huge role both in my crash (NDT) and subsequent recovery (T4). The Vyvanse I was taking back then (not Ritalin) has in turn affected the number of receptors My hypothesis is that the range and severity of symptoms progress as more components of this turnover equation get knocked out of balance. It can feel very uncomfortable to address only one because that will disrupt already shattered balance even more. Sometimes you have to get worse to get better but you also need to be very careful with this and patient. It’s not an easy feat.

Of note, thyroid worked for me (despite normal TSH) but you may have other reasons for energy deficit. Any deficiency of vitamin or mineral involved in mitochondrial energy production (i.e. vitamins or mineral) can be involved too.

2. Dopamine is in balance with serotonin. If both are low and you only raise one at a time you once again disrupt balance.

3. The number of receptors will affect binding. Sometimes in order to genetically move the receptors in the right direction (it’s called up regulating or downregulating) you might have to take the drug that actually makes you feel worse and then after you stop it you may find yourself in a new place. But once again - be careful and use sound judgement, I can’t stress that enough. For me that drug was lithium orotate which I also documented on my blog. Again, that was me, your drug might be different. But generally things that make you feel better right away (on day 1) will shift your receptors in the wrong direction if taken long term. They are still fine for occasional symptomatic relief.

4. There might be an issue with calcium flux or with Na/K ATPase that needs to be addressed first before you can restore neurotransmitter levels.

5. Fatty acids, cholesterol and sphingolipids are also important for signaling.

6. Traditional Chinese herbal formulas can be an excellent alternative because they are milder than pharmaceuticals and often tailored to an individual’s chemistry to address many of the issues simultaneously.

There are other things too but those are my main takeaways. If anyone has any questions about all this the best way to reach is me is by commenting on my blog as I don’t log in here much. I can’t provide exact medical advice but I’m always happy to tutor people in neuroscience or TCM or whatever else I’ve written there about. I haven’t updated my blog in a long time because I keep on planning to write an e-book but due to serious family issues and with the pandemic and all couldn’t get motivated. If I see some more interest in folks interested in learning my art and craft of neurohacking then I might finally get motivated to start writing

 

[Iritu1021]

P.S. One more thing specifically about Ritalin is that it’s a 5HT1A agonist. You can read on my blog (“Breaking Through The Fog” post) that I later attributed a lot of what I thought initially “adrenergic” symptoms to serotonergic effects mediated by 5HT1A and 5HT2A receptors. Adderal and Vyvanse release serotonin directly so they are even worse offenders because they knock out multiple receptors. But there is probably some genetic supersensitivity that affects certain receptors in certain people.