What if ME is simply brain damage after encephalitis?

[Woolie]

If there is an issue with brain hypoxia do you think there's any benefit in using an oxygen concentrator for 30 minutes twice a day?

I can't see how that could hurt, but its a little outside what I know.

It could be worth asking others with lots of cog symptoms if there's anything they know of that eases their symptoms.

Are you sleeping okay? Many people say lack of sleep makes them much worse, and I'm one (even though I have more of the immune, and less of the cognitive symptoms). I know sleeping meds are a very personal decision, but they make everything manageable for me. I wish I'd discovered them years ago, but I had some fears that I wouldn't be able to sleep naturally if I took them, or something.

 

[silky]

@Woolie I sleep alright sometimes but not as deeply as I used to. When I don't sleep I feel absolutely dreadful. I have been looking at trazadone as a potential sleep aid because it induces stage 3 and 4 sleep, acts as an antidepressant, and calms microglia. But like you were I am a bit hestitant to put another toxin into my body

Which sleep aid has helped you? And what's your experience been like using it?

 

[alex3619]

I'm pretty sure every one of us has had periods where our symptoms have seemed to lessen, and our cognitive problems eased.

The last two weeks I have been improving after a five year decline. There appears to be a small subset who are always about the same, and a small subset who keep declining, but for most it has variability or even phases. Some even steadily improve. We need better understanding of the longtitudinal impact of ME and CFS.

 

[Woolie]

@silky, I guess you need to weigh it up. And not as a normal healthy person, but as one who is struggling with a very serious illness.

I don't know what a toxin is - its a pretty loose term - but there's nothing good to say about the effects of sleep deprivation, its really hard on your brain and body.

There's two types of sleep meds - sleep inducers and sleep sustainers. If you get to sleep okay, but wake up a lot, the sustainers may help you. This is a good place to start, as they are generally less strongly associated with tolerance effects than inducers. There's an OTC medication you can get here in my country, called phenergen, that's quite a good sustainer. 50mg an hour before bed. If you use continuously, it will be less effective with time, so best to use it for just a few days, then have a few days off. Melatonin, if its available OTC, is another good one (buy the kind with the largest dose per pill, and take one), and those two can be alternated. Melatonin stops working for me after 1-2 nights, so I don't use it very often.

Some PwMEs also use low dose tricyclic antidespressants as sleep sustainers - things like amitryptiline. Again, they're good in that your don't develop tolerance much. But I don't find them all that effective. Phenergen is better in my experience.

Sometimes I'm so unwell at night, with low grade fevers, aches and pains, that I need something stronger, and then I use zopiclone, which is a prescription-only sleep inducer. I try to use only a fragment (half a pill max), and minimise my use.

PS Many people say good things about Trazadone.

 

[Mij]

I sleep alright sometimes but not as deeply as I used to. When I don't sleep I feel absolutely dreadful. I have been looking at trazadone as a potential sleep aid because it induces stage 3 and 4 sleep, acts as an antidepressant, and calms microglia. But like you were I am a bit hestitant to put another toxin into my body

My overall sleep is ok too but when I can't sleep I love trazodone. I only need 25mg to get deep sleep for 5 1/2 hours. I wake up feeling well rested.

 

[Basilico]

I sleep alright sometimes but not as deeply as I used to. When I don't sleep I feel absolutely dreadful.

@silky , another med to consider for improving the 'deepness' of your sleep is Baclofen. It's not a sleep med, it's an extremely mild non-habit forming muscle relaxer. It actually doesn't work for my muscle spasms at all (the reason I have a rx), but since it's a gaba agonist, it does help me to have very deep sleep, which is what I use it for.

Since it's not a sleeping pill it won't make you fall asleep. It's generally well-tolerated and doesn't have any abuse potential, so doctors are pretty happy to prescribe it. I take 1/2 pill (5mg) when I've been sleeping restlessly, waking up throughout the night, or generally thrashing around, doing weird stuff in my sleep that wakes up my husband and messes up his sleep. Even if you don't have insurance, you can get 30 pills (10mg) for $4 at Target and Walmart with a rx.

I take it when I start having restless sleep and it does a good job. I do sometimes feel a bit groggy in the morning, but I've found that the grogginess wears off pretty quickly (much more quickly than if I'd taken Benadryl) and I can reduce the grogginess by taking it earlier in the evening, rather than right before bed. I never wake up feeling refreshed, but I do feel significantly better if I've taken Baclofen vs. my normal 'light' sleep. Just something to consider.

 

[PhoenixDown]

Some PwMEs also use low dose tricyclic antidespressants as sleep sustainers - things like amitryptiline. Again, they're good in that your don't develop tolerance much.

I developed a strong tolerance to Amitryptiline after only two days.

 

[Woolie]

I developed a strong tolerance to Amitryptiline after only two days.

That's odd. Its supposed to take several weeks to actually start working. As a sleeping med, it doesn't work that great for me.

 

[heapsreal]

@silky , another med to consider for improving the 'deepness' of your sleep is Baclofen. It's not a sleep med, it's an extremely mild non-habit forming muscle relaxer. It actually doesn't work for my muscle spasms at all (the reason I have a rx), but since it's a gaba agonist, it does help me to have very deep sleep, which is what I use it for.

Since it's not a sleeping pill it won't make you fall asleep. It's generally well-tolerated and doesn't have any abuse potential, so doctors are pretty happy to prescribe it. I take 1/2 pill (5mg) when I've been sleeping restlessly, waking up throughout the night, or generally thrashing around, doing weird stuff in my sleep that wakes up my husband and messes up his sleep. Even if you don't have insurance, you can get 30 pills (10mg) for $4 at Target and Walmart with a rx.

I take it when I start having restless sleep and it does a good job. I do sometimes feel a bit groggy in the morning, but I've found that the grogginess wears off pretty quickly (much more quickly than if I'd taken Benadryl) and I can reduce the grogginess by taking it earlier in the evening, rather than right before bed. I never wake up feeling refreshed, but I do feel significantly better if I've taken Baclofen vs. my normal 'light' sleep. Just something to consider.

Similar experience to you with baclofen, doesnt put me to sleep but it improves sleep quality.

Its suppose to work on gaba B receptors and traditional benzos used for sleep work on gaba A receptors. I think the different gaba receptor it works on his why theres no withdrawal issues and other issues seen with normal sleep meds.

A supplement called phenibut also works on gaba B receptors. In some countries its classed as a drug and others its a supplement. It does seem to work differently than baclofen. Phenibut i needed larger doses than normal to have any effect and for me there was some delayed actions where it seemed to kick in after 8hrs and be very sleepy all day. It was ok for sleep but too long acting for me. Many others find it works well and havent heard of anyone else having this delayed type reaction although some get a hangover effect.

 

[Basilico]

Phenibut i needed larger doses than normal to have any effect and for me there was some delayed actions where it seemed to kick in after 8hrs and be very sleepy all day. It was ok for sleep but too long acting for me. Many others find it works well and havent heard of anyone else having this delayed type reaction although some get a hangover effect.

I had a similar reaction to Phenibut! I tried it years ago, and there was such a delayed reaction, I was having to take it in the early afternoon for it to start working by nighttime.

 

[PhoenixDown]

That's odd. Its supposed to take several weeks to actually start working.

I've never taken an antidepressant that hasn't affected me the same day I started it. I've never believed all that it takes weeks to start working bullshit. There's a real danger of letting a coincidence fool you in to thinking the antidepressant had an affect.

 

[silky]

Point 1: People mistakenly telling you ME is largely a benign recoverable condition.

The rousing discussion you speak of is false science, because the people you are talking with cannot give you any data on PWME having a largely benign condition, because it is exceptionally rare PWME are autopsied. In the people who do die young, inflammation is found in the brain (see UK cases) and in the heart (see case of Casey Fero). This is probably 8 people. We need 8,000 people who's brains or bodies are analyzed.

So you have to be mindful that these minor changes people tell you about are people concluding on medical syndromes without data. That facts we do know is: CFS is not ME but a syndrome of unexplained chronic tiredness according to CDC.(CFS doesn't even require chronic pain) - pain is always present in an encephalomyeltiis, both in the muscles and brain, CFS doesn't require the hallmarks of ME either: Dysautonomia, Post Exertional Relapse, Orthostatic Intolerance. One exception to the rule is British CFS/ME (NHS criteria) does require PEM, but PEM is not relapse, it's feeling worse after doing something. Neurotics feeling worse after doing something, as do people with other mental health conditions based on activity phobias. So PEM is not reflective of probably or likely having an 'ME'. Having difficulty standing up is. Yet this isn't a requirement of British CFS/ME or American CFS either.

But the real elephant in the room, is ME has no test and has become CFS due to politics.
ME used to be tied to PVFS (Post Viral Fatigue Syndrome). CFS does not require any association to a virus whatsoever, and neither does British CFS/ME used by the NHS. So the waters are muddied, ruined actually, in terms of research.

You have to look at this logically and without bias which the other thread is full of because 'CFS' patients are feeding you the information. They are biased, as they aren't bedridden with ME and also they aren't deceased.

*A CFS or ME/CFS or CFS/ME patient is not a confirmed ME patient, no one is.

*Patients in neuroimaging studies are NOT severely affected. Severely affected are too sick to be under a brain scanner. In medicine, you always study the most severely affected to find out what a disease and you certainly do not exlude patients with any sign of disease and call these people ME. - Which is what ME/CFS does and what CFS/ME does.This is because....

*At time of diagnosis No one with ME/CFS or CFS/ME is a allowed to have anything wrong with them. Patients with ME have masses of things wrong them, all of which can be diagnosed in a doctors office.

*These people are excluded from research. Ergo, no large study size, quality ME research has ever taken place, because the patients then breach the criteria of CFS.

*Patients are diagnosed with a feeble requirement of 'Chronic Fatigue'. CF is not a disease, and thus your would expect the minor changes your sources have tried to influence you with. Yet your sources on the other thread are failing to adhere to even basic scientific principles.


Point 2: ME more curable than other 'conditions'?

Currently the official diagnosis in use for CFS, CFS/ME, ME/CFS, doesn't require a single abnormal test finding, which means misdiagnosis and guess work is normal for the physicians seeing their patients with 'ME', and thus we have no idea who has ME and who is cured because we never know if they had it or not!

So, unfortunately, if we are to remove our own biases, then no one has ever been cured of ME as to confirm ME outright you'd have to be dead and have an autopsy and brain/spinal tissue would need to be studied under a microscope and so forth, same with Alzheimers and vCJD.

But...as technology, specifically imaging technology advances and at the same time, scientists can determine what would cause this form of an encephalomyeltis found on scans (e.g. a specific pathogen agreed upon by multiple groups of researchers is known to damage neuron type X), then the damage ME causes should be able to be confirmed in patients who are alive.

These patients can then be given treatments and we can see over decades who is cured, (if at all) and compare these statistical rates in order to be able to honestly answer your question.

Then and only then can we see who is 'cured' who 'recovers' in the same way we can say with confidence who has Parkinson's and who is cured and recovered from PD.

Ergo no one has ever been cured of ME, as first you have to be able to accurately diagnose it, and observe an encephalomyelitis state.

@Research 1st said this in the other thread is it true?

 

[Woolie]

I've never taken an antidepressant that hasn't affected me the same day I started it. I've never believed all that it takes weeks to start working bullshit. There's a real danger of letting a coincidence fool you in to thinking the antidepressant had an affect.

My apologies, @PhoenixDown - we should never buy the "party line" on what the meds are and aren't supposed to do. My experience is also that they don't work very well as sleep aids (which is all I've ever used them for). Some OTC meds are much better.

 

[silky]

Got another for you my friend @Woolie

This is from the prestigious 2011 Canadian Consesus Criteria. What do you think?

If I had to guess it's more disparate non-replicated studies as you said earlier, but... why would they include them in a definition of ME that everyone swears by?

Neurological impairments

Some viruses and bacteria can infect immune and neural cells and cause chronic inflammation. Structural and functional pathological abnormalities [3] within the brain and spinal cord suggest dysregulation of the CNS control system and communication network [62], which play crucial roles in cognitive impairment and neurological symptoms [20]. Neuroinflammation of the dorsal root ganglia, gatekeepers of peripheral sensory information travelling to the brain, has been observed in spinal autopsies (Chaudhuri A. Royal Society of Medicine Meeting 2009). Identified cerebrospinal fluid proteomes distinguish patients from healthy controls and post-treatment Lyme disease [63]. Neuroimaging studies report irreversible punctuate lesions [64], an approximate 10% reduction in grey matter volume [65, 66], hypoperfusion [50, 67–71] and brain stem hypometabolism [1]. Elevated levels of lateral ventricular lactate are consistent with decreased cortical blood flow, mitochondrial dysfunction and oxidative stress [72]. Research suggests that dysregulation of the CNS and autonomic nervous system alters the processing of pain and sensory input [29, 47, 73, 74]. Patients’ perception that simple mental tasks require substantial effort is supported by brain scan studies that indicate greater source activity and more regions of the brain are utilized when processing auditory and spatial cognitive information [75–77]. Poor attentional capacity and working memory are prominent disabling symptoms [20, 75, 78].

 

[Woolie]

Some of these studies I can't comment on because I don't have the skills. I can only comment on the neuroimaging and neuropsyc ones.

Neuroimaging studies report irreversible punctuate lesions [64], an approximate 10% reduction in grey matter volume [65, 66], hypoperfusion [50, 67–71] and brain stem hypometabolism [1].

The first reference is to a review written in 1998. It describes some early studies (before the advent of modern neuroimaging) that used clinical methods to count white matter lesions. Two out of three studies found more such lesions in CFS patients than in controls (ppl in both groups had lesions, but in some studies, there were more CFS patients with lesions than controls). These studies looked at white matter, not grey matter.

The second set of references is to studies reporting grey matter volume loss, not white matter. These are the two studies we have already talked about (de Lange and Okada).

I think the last two sets of references - to hypoperfusion studies - are in better agreement and are likely to be saying something real about reduced blood flow in some brain areas in CFS. But for the reasons I mentioned earlier, you should not assume these functional brain differences implicate the brain as the source of the disease. They are more likely to be documenting the effects of a disease process that involves some other system.

Patients’ perception that simple mental tasks require substantial effort is supported by brain scan studies that indicate greater source activity and more regions of the brain are utilized when processing auditory and spatial cognitive information [75–77]. Poor attentional capacity and working memory are prominent disabling symptoms [20, 75, 78].

I think this bit is reliable, as a number of studies have reproduced these findings.

Research suggests that dysregulation of the CNS and autonomic nervous system alters the processing of pain and sensory input [29, 47, 73, 74].

I am not a fan of this bit, as I don't consider that a causal relationship has been properly established in these studies between CNS/ANS dysfunction and pain processing.

My conclusion from the parts of the research in this review that I'm qualified to comment on is that brain function is affected by CFS. The specific cognitive profile associated with CFS has been repeatedly and reliably documented, and the studies showing blood flow changes are also probably onto something. The blood flow findings provide a complete and highly plausible explanation for the cognitive impairments.

But the brain is unlikely to play a causal role in the disease.

 

[silky]

great analysis! thanks @Woolie

 

[halcyon]

@Research 1st said this in the other thread is it true?

The problem is that you rapidly devolve into the no true Scotsman fallacy when talking about this. There is a point to this argument though. Several studies have shown that, at least in the UK and Australia, there is a very high misdiagnosis rate of CFS. Conceivably these are some of the people that go on to "recover from CFS". This of course tell us nothing about ME.

It's difficult to make blanket statements about who has been included in what research. You really have to analyze each study on its own and see what criteria they used and exactly how they used it. For the most part though I agree that there has been no large scale study on well defined classic ME patients. And I also agree that you cannot at this time prove that anybody has recovered from ME because you can't prove that they had ME in the first place.

 

[silky]

The problem is that you rapidly devolve into the no true Scotsman fallacy when talking about this.

this gave a good laugh, yes I agree

And I also agree that you cannot at this time prove that anybody has recovered from ME because you can't prove that they had ME in the first place.

Ah but my dear halcyon, what then of the great Dr Hyde who says that some true ME patients with enterovirus in the stomach and hypoporfusion to the brainstem do recover?

 

[Sidereal]

The definition of encephalitis has in recent years been expanded to include various autoantibody-mediated diseases of the CNS where there is no inflammation (as classically understood in the sense of tissue damage and elevated CRP, sed rate etc.) and few or no objective neurological signs. The symptoms appear to be mediated by direct action of antibodies on various receptors or ion channels and are not caused by inflammation. Symptoms in many cases don't look very neurological and seem entirely "psychiatric" in nature. The best studied of these clinical entities is the anti-NMDA receptor encephalitis but there are many other lesser known ones. So yes, someone trained 30 years ago will tell you that encephalitis can only mean massive irreversible brain damage (and ME/CFS is definitely NOT that) but in the last 10 years or so there has been huge progress made in academic psychiatry. Of course, it usually takes decades for things to trickle down to the average doctor.

 

[halcyon]

Ah but my dear halcyon, what then of the great Dr Hyde who says that some true ME patients with enterovirus in the stomach and hypoporfusion to the brainstem do recover?

Still doesn't prove that enterovirus + hypoperfusion = ME, but I think it's a great start. Drawing a line in the sand and picking a subgroup based on biomarkers is the way forward in my opinion.