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.