Use of stimulants for cfs

Something I recall from the mid 90's was when a women I met told me that she felt 'better' taking Amphetamines, she was in the process of getting a diagnosis and went to see my ME doctor, he told her that if she felt better on stimulants then he had questions regarding her diagnosis. In the end he did not give her an ME diagnosis and said that long term stimulants make ME symptoms worse.
 
So @Mij your doctor said if you fell better with stimulants than you dont have m.e.? If i dont understand it wrong, this makes no sense to me. Of course stimulants dont take away all symptoms but have impact on some. Of course if you take to much and push your body over the edge you will crash, but thats a symptom of me or not? Which diagnose did she get in the end?
 
Hi @Spun, he didn't feel she had ME based on her onset and history. But feeling 'better' on stimulants after being ill for 8 years most likely didn't fit his experience (20 years of seeing ME pts)? He sent her to see another specialist and I don't know if or what diagnosis he received (if any).

He didn't feel I had ME either and sent me to see a neurologist to r/o MS. I was diagnosed with 'atypical ME PVFS'. So his criteria was very specific.
 
I was prescribed 50 mg of modafinil but I take this as a joke. I need to take at least 10 pills (1000 mg) to get me active. And it does work, however I don't know what the long term consequences will be. Addiction, withdrawal, crashing and so on. Besides, it will cost me cheaper to get amphetamines from a local dealer instead. Never tried ritalin. I have two more packs of modafinil and intend to stop it after that (though I'll miss it , I was able to play federball with it without crashing afterwords).

eta: Forgot to mention I take it together with high doses of diazepam and bromazepam, which may have a role in being active without crashing.
 
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OK on the second thought modafinil doesn't help for my fatigue, neither boosts my energy. It clears my brain fog though, which is wonderful, and I "live in the moment", and become very concentrated and chatty. However, this happens only if I take a dose of about 600-800 mg, which is double of the maximum 400 mg dose. And it's very expensive. The recommended dose is 200 mg. I took 300 mg today and it's as if I have taken nothing - just wasted the pills. When I take high doses I suffer insomnia, but maybe that's because I take part of the pills at noon. Tomorrow morning I will try taking a whole 600 mg dose and see what happens.
 
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Merged thread
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I recently discovered this resources list in the Bateman Horne Center resources website.

https://batemanhornecenter.org/education/me-cfs/

Have any of you tried any of the following? What was your experience?

Cognitive impairment and fatigue medications:

Methylphenidate (Ritalin)
Modafinil
Armodafinil
amantadine

I guess I was intrigued to find something I hadn't tried yet.
 
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Not Ritalin but dexamphetamine. I copied most of this from a post from 2020 -
A Trial of Solriamfetol in the Treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, Joel L Young, 2020

... my experience with 5 mg of dexamphetamine (family member's ADD medication) taken quite often over ten years or so. The alternative medicine doctor I was seeing in the 1990s would have been happy to prescribe it too.

I was able to think fast and get long periods of physically demanding outdoor work done with no effort, but of course paid for it afterwards for days. Another downside was that I ignored joint and muscle pain and ended up with injuries.

The last time I took it the immediate effect was the exact opposite: severe lack of energy and spaced-out feeling. That really frightened me off it for good.
 
oldtimer said:
Not Ritalin but dexamphetamine. I copied most of this from a post from 2020 -
A Trial of Solriamfetol in the Treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, Joel L Young, 2020

... my experience with 5 mg of dexamphetamine (family member's ADD medication) taken quite often over ten years or so. The alternative medicine doctor I was seeing in the 1990s would have been happy to prescribe it too.

I was able to think fast and get long periods of physically demanding outdoor work done with no effort, but of course paid for it afterwards for days. Another downside was that I ignored joint and muscle pain and ended up with injuries.

The last time I took it the immediate effect was the exact opposite: severe lack of energy and spaced-out feeling. That really frightened me off it for good.
Click to expand...

Thanks @oldtimer !

I was wondering if stimulants would ultimately be a bad idea. I get revved up and do too much then crash if I even have a cup of coffee.

I do wonder if a little finesse with the right dose might be helpful for times when I truly have to do something... although it might not be any different than caffeine if I just crash in the end.
 
I was prescribed Modafinil and took it every day for quite a long time (can’t remember exactly but at least a year).
It was great and seemed like a miracle. I didn’t have to keep sleeping and the brain fog went away.

But then the side effects took hold - heart palpitations, diarrhoea, sweats. Basically what you would expect if you were taking speed.

I hadn’t really thought about it at the time as I wasn’t as knowledgable about how ME works, but you are forcing your body into overdrive the whole time so it is making your condition worse .

In the end I stopped and it was a huge come down but the right thing for my body.

however I did still take small doses if I had to do something where I needed or wanted to stay alert, such as if I had to drive anywhere further than I normally would, or if I wanted to meet someone for coffee and have a nice chat. In these instances I was happy to take the short term hit.
 
MountainRose said:
I recently discovered this resources list in the Bateman Horne Center resources website.

https://batemanhornecenter.org/education/me-cfs/

Have any of you tried any of the following? What was your experience?

Cognitive impairment and fatigue medications:

Methylphenidate (Ritalin)
Modafinil
Armodafinil
amantadine

I guess I was intrigued to find something I hadn't tried yet.
Click to expand...
I think stimulants are primarily if you don't need to rest much during the day , if you need to you can't as the on switch is on so I think in MS for example they used to help people in work feel more with it , which is completely different to helping people who are resting a lot get some mental function. My experience was total non-tolerance as a very severe-person
 
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Here's a patent application talking about using a medication similar to Modafinil, Lauflumide (aka Flmodafinil), for Long COVID and ME/CFS.
The US version has been published this year, so it looks like they are actively seeking approval.

Their background provided in the application, some highlights and comments from me:
  • Fatigue, cognitive impairment and sleep disorders have been consistently reported to be some of the most common and debilitating features of PCS and constituting a significant global economic burden, respectively7,8,10,11. Unlike other common symptoms of PCS including dyspnea and depression, there are no established and effective treatments for post-viral fatigue and cognitive impairment, as well as related conditions such as Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)12.
  • [0007]
    ME/CFS has been identified in the 1980s. This syndrome is characterized by an extreme fatigue and a pain felt in routine activities, post-exertional malaise and unrefreshing sleep. Other secondary symptoms may also occur such as impaired memory or ability to concentrate and orthostatic intolerance.
  • [0008]
    According to Fukuda's criteria13, as modified according to Reeves, et al14, chronic fatigue syndrome (CFS) is an illness characterized by 1) the presence of persisting, debilitating fatigue that does not resolve with bed rest, and lasts for at least six months resulting in severe impairment in daily function; 2) by symptoms and disability that cannot be ascribed to any other medical and psychiatric conditions. Diagnosis relies in large part on behavioural markers, either patients' self-reported symptoms or observations by clinicians. Laboratory diagnostic and screening tests are not widely available.
  • [0009]
    CFS is responsible for significant morbidity and occurs in an estimated 0.42% of people, predominately female, in the United States and worldwide. Prior work strongly suggests this complex, multi-symptom illness has a multi-system pathogenesis that involves the nervous, endocrine and immune systems. Abnormalities in stress responses have been identified as potential triggers or mediators of CFS symptoms.
  • [0010]
    Between 836,000 and 2.5 M Americans suffer from ME/CFS. Direct and indirect economic costs to society are estimated between $17 and $24 billion each year15.
  • [0011]
    The etiology of ME/CFS is principally post-viral. Acute viral infections and subsequent overlapping immune responses are established triggers for the onset of ME/CFS symptoms. It has been shown that prior viral epidemics (SARS virus, MERS virus) led to increased ME/CFS occurrence as long-term consequences12,16,17.
  • [0012]
    There are still no effective and safe therapies up to now; no FDA approved drugs for post-COVD or Long COVID sequelae (e.g. fatigue, cognitive impairment, circadian rhythm disorders)18,19.
  • [0013]
    The only double-blind RCT of a CNS drug to provide statistically significant improvement in fatigue score and concentration was using methylphenidate. However, given the significant adverse effects and potential for dependence associated with this drug, it is not an ideal choice for the treatment of ME/CFS
  • [0014]
    Xyrem (sodium oxybate, SXB) as well shows severe side effects while not being particularly effective. The FDA declared that a dangerous drug such as SXB cannot be approved for indications involving large populations (such as ME/CFS or fibromyalgia), as this would favour illicit use as a rape drug and recreational substance20.
  • [0015]
    Jazz Pharmaceuticals is exploring the field of ME/CFS: as post-marketing data and patients reports for Sunosi® (solriamfetol) showed poor efficacy on Narcolepsy, Jazz is now looking at ME/CFS as a new indication: an 8-week single center, randomized, double-blind, placebo-controlled, flexible titration Phase 4 clinical trial with solriamfetol started on April 1st, involving 44 adult subjects21. [discussed in this link]
  • [0016]
    Neuropeptide Y (NPY) is found in both the central and peripheral nervous systems. In the peripheral nervous system, NPY is concentrated in and released from sympathetic nerve endings, either alone or with catecholamines. NPY release follows stress such as strenuous exercise, panic disorders, and cold exposure. In the periphery, NPY is activating and stimulates the stress response, but in the brain, NPY is anxiolytic, inhibitory of sympathetic activity and causes lowering of blood pressure and heart rate. Concentrations of NPY in the brain are higher than other neuropeptides, particularly in the limbic system, including the amygdala and the hypothalamus, all areas of the brain involved with emotion.
  • [0017]
    NPY has been found to be a useful biomarker for CFS22 [discussed here]. Plasma NPY was elevated in CFS subjects, compared to controls (p=0.000) and to GWI (Gulf War Illness) cases (p=0.000). Receiver operating characteristics (ROC) curve analyses indicated that the predictive ability of plasma NPY to distinguish CFS patients from healthy controls and from GWI was significantly better than chance alone. In 42 patients with CFS, plasma NPY had significant correlations (<0.05) with perceived stress, depression, anger/hostility, confusion, negative thoughts, positive thoughts, general health, and cognitive status. In each case the correlation (+ or −) was in the anticipated direction. This study reports that plasma NPY is elevated compared to healthy controls and to a fatigued comparison group, GWI patients. The significant correlations of NPY with stress, negative mood, general health, depression and cognitive function strongly suggest that this peptide be considered as a biomarker to distinguish subsets of CFS.
  • [0018]
    Even mild agonist reverse inhibitor effect on NPY1 may be of relevance in mood disorders treatment23 and histamine H2 receptor stimulation improved retention of the memory associated with a contextual fear conditioning procedure in rats24 as enhanced memory consolidation of inhibitory avoidance learning in mice25,26.
  • [0019]
    Lauflumide [2-((bis(4-fluorophenyl)methyl)sulfinyl)acetamide] is a next-generation of selective dopamine (DA) reuptake inhibitor, an enantiomeric form (R) optically pure with an enantiomeric excess of more than 95% of bis (p-fluoro)phenyl ring-substituted derivative of modafinil (USPTO Patent Application 20130295196, Lauflumide and the enantiomers thereof, method for preparing same and therapeutic uses thereof, issued).
  • [0020]
    Lauflumide is a highly potent wake-promoting agent with no sign of hypersomnia rebound, a potent stimulant with different effects than primary modafinil parent analogues investigated so far27 and most other stimulants in terms of potency and effects on effectiveness sleep rebound and the sleep spectral analysis28. As compared to modafinil, recovery sleep after Lauflumide treatment is characterized by fewer non-rapid eye movement (NREM) amount and delta activity, suggesting a lower need for recovery despite longer drug-induced wakefulness28. [Is this true?]
  • [0021]
    Lauflumide as a wake-promoting agent with a potential cognitive benefit and anti-impulsive effects, shows a lower risk of side effects such as arterial hypertension, or sleep rebound, and could be useful in the treatment of ADHD and arousal-related disorders (e.g. narcolepsy with or without cataplexy and idiopathic hypersomnia)28.
  • [0022]
    As opposed to modafinil and most of wakefulness agents, Lauflumide fails to stimulate the norepinephrine (NE) sympathetic nervous system leading to deleterious effects on cardiovascular system with a potent arterial hypertension at long-term processing.
  • [0023]
    Modafinil is weakly DAT inhibitor compared to Lauflumide. Above all, modafinil is thought to be dependent on catecholaminergic (DA and NE) signalling for its wake-promoting effects27,29,30.
  • [0024]
    Past and recent studies of modafinil analogues demonstrated that DAT inhibition did not correlate with wakefulness-promoting effects in animals, and a number of analogues without any significant inhibition of the DAT still produced wakefulness-promoting effects31,32.
  • [0025]
    Another study found that modafinil has a long duration of action, with its wake promoting properties largely arising from dopaminergic activity33.
  • [0026]
    Other possible mechanisms for the wakefulness effect besides the DAT inhibitor include the indirect activation of orexin systems34,36.
  • [0027]
    Concerning behavioural data, it has been reported that modafinil (128 mg/kg) strongly reinstated cocaine conditioned place preference following extinction in rats, suggesting that modafinil may induce relapse or increase the vulnerability of addicts to the reinforcing effects of environmental triggers37,38, when the benefit on impulsivity has not been demonstrated. Impulsive choices on a decision-making task in ambiguous situation in patients with narcolepsy, when psychostimulants fail to have an effect on that, remain troublesome39.
  • [0028]
    Surprisingly, the inventors observed that Lauflumide is a reverse agonist inhibitor of NPY1.
  • [0029]
    Indeed, Lauflumide is found to weakly bind with neuropeptide Y1 (NPY1), as a reverse agonist inhibitor (27.3%), and possibly exert some of a histaminergic H2 receptor-mediated inducer (>40%) when it was tested at 1.0×10-05 M and that its binding property was calculated as a percent inhibition of the binding of a radioactively labelled ligand specific for each target in accordance with Eurofins validation Standard Operating Procedure (Study 100014859 Eurofins CEREP 20/03/14, unpublished data).
  • [0030]
    Previous findings have implicated the relaxin-3/RXFP3 system in control of pain transmission, providing new opportunities for the development of therapeutic tools for pain management, by targeting a neuropeptide system that impacts several behaviours that are altered in chronic pain conditions (e.g. fibromyalgia).
  • [0031]
    Other findings have suggested relaxin-3/RXFP3 signaling in key hypothalamic and limbic circuits is capable of integrating stress-related external and internal information, by regulating the networks responsible for orexigenic and goal-directed (motivated) behaviors40.
  • [0032]
    On circadian rhythm and arousal, the relaxin-3/RXFP3 signaling promote a range of consummatory behaviors is in line with its likely primary role in driving arousal and motivated behavior more broadly41,42.
  • [0033]
    The inventors postulate that Relaxin-3/RXFP3 signaling was involved in ME/CFS circuit via DAT inhibition.
  • [0034]
    RXFP3 influencing neuroendocrine control of metabolism, it is highlighted that Lauflumide targeting on RXFP3 receptors may potentially treated feeding-related disorders43.
  • [0035]
    Lauflumide is a strong DAT inhibitor, and improved impulsivity at the three doses tested with a better significant response than modafinil.
  • [0036]
    Lauflumide acting on RXFP3 receptors (23.9%) and as a DAT reuptake inhibitor (84.4%) [at 10 µM] may explain why Lauflumide do not lead to hypersomnolence rebound compared to modafinil in same experimental conditions28.
  • [0037]
    As an agonist reverse inhibitor effect based on NPY1 receptors, Lauflumide may be of relevance in mood disorders treatment and also acting on histamine H2 receptor may improve retention of the memory associated with a contextual fear and also acting on RXFP3 receptor and DAT inhibition may improve arousal and motivated behavior as impulsivity.
  • [0038]
    Lauflumide is considered as a potential candidate for post-COVID-19 fatigue pharmacotherapy.
  • [0039]
    Lauflumide as a wake-promoting agent with a potential cognitive benefit and anti-impulsive effects, shows a lower risk of side effects such as arterial hypertension, or sleep rebound, and could be useful in those with an arousal-related disorders and CFS subsequent to COVID-19 infection (post-COVID syndrome, long COVID).
Click to expand...

Sure reads like "just another stimulant" and they don't mention PEM once.
Still interesting that people are working on ME/CFS drug development.
Also wondering whether NPY, H2 or RXFP3 they mentioned are of any use to look into further.

WO LINK and PDF
US LINK and PDF
 
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rapidboson said:
Here's a patent application talking about using a medication similar to Modafinil, Lauflumide (aka Flmodafinil), for Long COVID and ME/CFS.
The US version has been published this year, so it looks like they are actively seeking approval.

Their background provided in the application, some highlights and comments from me:


Sure reads like "just another stimulant" and they don't mention PEM once.
Still interesting that people are working on ME/CFS drug development.
Also wondering whether NPY, H2 or RXFP3 they mentioned are of any use to look into further.

WO LINK and PDF
US LINK and PDF
Click to expand...
I wonder what research there is on the consequences of using stimulants like (Go) modafinil for ME/CFS and/or long COVID.

I wonder if it will push people over their limits and trigger PEM? A little bit like using painkillers when you have an injury so that you can play that important match, but you're doing more damage to your injury.

I have tried Modafinil and found it awful. I could feel my symptoms increasing under the layer of stimulants and couldn't stop because of them. Very hard to explain, but just awful.

I should of course first search for research on this on the existing threads. I will later, when I have more energy.
 
MinIreland said:
I wonder what research there is on the consequences of using stimulants like (Go) modafinil for ME/CFS and/or long COVID.

I wonder if it will push people over their limits and trigger PEM? A little bit like using painkillers when you have an injury so that you can play that important match, but you're doing more damage to your injury.
Click to expand...
My consultant got permission for me to try it years ago when he was running a trial to use it to treat a different chronic condition. It's kind of workedto give me more to give me more energy. It also ended up in a relapse for obvious reasons.

A couple of years later, when I was doing better overall, I asked him if I could try it again. And he said no because my experience wasn't so unusual (I'm not sure if he tried it for other people with ME/CFS , or he was referring to the condition he had trialled it on.)
 
Also, and this might show my lack of knowledge, but that's ok... How can researchers work on a medicine for ME/CFS if they don't understand the underlying mechanisms (not sure if that's the right term). Wouldn't you need to know what you're targeting when you use medication? @Jonathan Edwards - tagging you because you're the only doctor I know on this forum.
 
MinIreland said:
I have tried Modafinil and found it awful. I could feel my symptoms increasing under the layer of stimulants and couldn't stop because of them. Very hard to explain, but just awful.

I should of course first search for research on this on the existing threads. I will later, when I have more energy.
Click to expand...
I had it in about 2010 and all it did was make me feel sick. It had no effect on any ME/CFS symptoms. It doesn’t really feel like a stimulant to me. It is a bit questionable what in the brain it actually does. When it was released it was supposed to act on histamine but I think that theory has been a bit debunked.
 
MinIreland said:
How can researchers work on a medicine for ME/CFS if they don't understand the underlying mechanisms (not sure if that's the right term). Wouldn't you need to know what you're targeting when you use medication?
Click to expand...
You could just see that it works when patients take it for an unrelated reason. That appears to be the basis of all the B cell depletion drug trials in Norway. Cancer patients took chemo drugs and their ME/CFS got better.

Wikipedia says the tree that contains a similar chemical to Aspirin was used in Ancient Egypt for pain relief. I doubt they knew the molecular mechanisms of pain or how it helped. Someone probably just tried and noticed it relieved pain.
 
forestglip said:
You could just see that it works when patients take it for an unrelated reason. That appears to be the basis of all the B cell depletion drug trials in Norway. Cancer patients took chemo drugs and their ME/CFS got better.

Wikipedia says the tree that contains a similar chemical to Aspirin was used in Ancient Egypt for pain relief. I doubt they knew the molecular mechanisms of pain or how it helped. Someone probably just tried and noticed it relieved pain.
Click to expand...
Ok. So some meds fall into the category 'they work but we don't know how or why'?
 
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