ME/CFS, Long Covid, Fibromyalgia & POTS: Connecting the Dots for Effective Recovery

[@radarashwood5397]

Seriously underrated channel.

[@PsychiatrySimplified]

Appreciate the feedback 🙏🏼

[@daniellelblackwell]

Wow, I wish you were my doctor!! Will definitely consider listening to the full 10 hour lecture to get a deeper understanding. Thankyou for putting this out there 🙏

[@PsychiatrySimplified]

The 10 hour course is for clinicians ; for non clinicians one can view the other videos on this topic that may be used to discuss the condition with one’s doctor potentially? Wish you well.

[@hbly]

Wejow, my man!! You describe exactly what happened to me. Lc-pots keep working drop attacks pem pain fatigue sleep disturbance emotional dysregulation. The way you present it is so much easier to swallow.

[@PsychiatrySimplified]

Glad you found it useful

[@Jules-kp7rw]

Pen and notebook out. I am ready for this comprehensive and complex review of these conditions. I don't expect a miracle pill but I know I will come out with hope, realistic expectations and practical solutions to implement. Thank you sir. My previous research around this topic has been an absolute chaos, the latent brain fog definitely not helping.

[@PsychiatrySimplified]

I hope the video is helpful. Appreciate your interest

[@Dr.M.Shafiq]

Very informative Episode for very little understood disease ME/CFS, Fibro. I an a sufferer, warrior of 50 years for Ds. I m a retired Pathologist, Public Health Consultant from Pakistan. Here few of Medical elite know fibro.and almost no physician, Neurologist, psychiatrist, Physical Therapist Rheumatologist, immunologist know this ds.

[@PsychiatrySimplified]

Its a multisystem condition but in the age of super specialisation; the integration falls behind

[@Jules-kp7rw]

I feel so sad for those suffering from ME. A recent long covid has given me a peak into that experience and it is absolutely disgusting. It's such a profound loss of your abilities and even your identity. It's like losing a limb except nobody understands.

[@Twent25]

I had not heard of cataplexy before. Have been falling for decades but feels like a momentary lack of attention and suddenly there is the ground. Back to rest of your video. Thank you sir.

[@PsychiatrySimplified]

Cataplexy is usually part of narcolepsy but sleep disorders or falls due to POTS or extreme fatigue can occur.

[@Twent25]

​@@PsychiatrySimplified Ok thank you. Good to understand.

[@skeptik-ci5xo]

I have insomnia for over a decade, and nothing I have taken has particularly effective. I'm interested to know which medications might help to counteract amygdala hyperarousal, but don't lower blood pressure. I take Spironolactone, so I can't take another blood pressure med. Thank you as always for providing brilliant content. I wish more physicians would tune in; I think it would significantly improve their practices, leading to better patient outcomes.

[@PsychiatrySimplified]

As I’ve mentioned clonidine or prazosin . Clonidine can be prescribed with spironolactone via dose adjustment. If BP is normal Clonidine does not drop not significantly at low doses. Alternatively Prazosin can be considered as its shorter acting. There are other agents if agitation is present. I’ve done a video on hyperarousal vs agitation. As depending on symptoms the medication choice may differ. Ps not advice

[@skeptik-ci5xo]

@@PsychiatrySimplified Thank you! Just gathering info, no advice taken :)

[@Twent25]

1. Improve sleep/hyperarousal Two pathways guacnifine (sp?) / other pathway meds (Mirtazipine) 2. Improve cognition, pain will now recognize, better express cognition etc issues. Adjunct medicines : dopamine and noradrenagenic potentiators sp?) Duloxetine, (above 90mg for fibromyalgia, need Goldilocks dose for cognition) 3. Emotions (via neurobiology), rooted in limbic system, cumulative molecular load: interception. 50:02 , *Multi modal integrative in patient team approach recomended

[@PsychiatrySimplified]

Good summary . The sleep hyperarousal - there are other medications. Here these are matched to severity. E.g long acting low dose benzodiazepines like clonazepam can be effective. For severe agitation one may need low dose antipsychotic ( at low dose they are anti agitation - not really antipsychotic ) . Mood stabilisers like Lamotrigine can be helpful for mid range and emotional dysregulation, racing thoughts etc . Ps not advice

[@MichaelONeill-s6u]

Very interesting and informative very like Dr Sarno mind body language

[@PsychiatrySimplified]

Glad you found it useful

[@TheStealthPawn]

What about addressing neuropsychiatric complications of long covid? Not necessarily a reaction to the other symptoms, but I mean a direct result of the neuroinflammatory cascade? Some patients they react to it with things like anhedonia and cognitive symptoms like blank mind (loss of inner world, creativity, no inner monologue when one was there) rather than say ME CFS. These symptoms are among the most difficult to treat in psychiatry, especially consummatory anhedonia we don't yet even have any medications that target the endogenous opiod system (besides LDN which is weak). And many times in anhedonia, the reward system can be so blunted that it does not even respond to say alcohol. This kind of neuroinflammatory based anhedonia also is different than vanilla MDD (which may not even have that) and often includes blunted emotions as well to begin with. These patients interestingly respond to benzos/GABAergic agents which is quite peculiar. Ideally a neurosteroid medication like Zuranolone would be there but its not approved outside PPD.

[@PsychiatrySimplified]

They are included in the domains I mentioned. This is why clusters help. When improving cognitive and activity dimensions - we target frontostriatolimbic circuits . Here we have 1. Executive function DLPFC 2. OFC - part of reward network 3. vMPFC - part of fear / anxiety inhibition 2. Ventral striatum - Reward ‘centre’ 3. Dorsal striatum - Goal directed and habit part 4. Amygdala ( limbic ) - arousal , pain, etc So anhedonia can be targeted via these pathways - anticipatory anhedonia , consummatory and motivational. The advantage of what I’ve covered in the video is that we focus on getting the person back to function by looking at broad domains. Cognitive symptoms as part of neuroinflammation have 6-7 different descriptions . You can see my other videos on CFS where I cover the mechanisms.

[@TheStealthPawn]

@ The video did mention the dopaminergic stuff but I am wondering isn’t dopamine more for anticipatory anhedonia and motivation rather than the consummatory “liking” aspect? Stimulants or dopamine agonists can improve the former but don’t necessarily lead to ‘in the moment’ reward. Are there other things that address this? Endogenous opiod system dysfunction seems to be the problem in consummatory anhedonia but besides LDN not much targets this directly yet. Until maybe the Kappa antagonists come out. Currently do the dopaminergic anhedonia medications (MAOIs, stimulants, dopamine agonists) just rely on somehow indirectly balancing this system?

[@AhadKhan-cx6cu]

Dr, for improving cognition, would we need to target both d1 & a2a receptors with different compounds? Are there any drugs that target both?

[@PsychiatrySimplified]

SNRIs, Psychostimulants, Armodafinil / modafinil / NARIs / Bupropion , Vortioxetine would do this . Alpha 2 A selective is Guanfacine. Any agents that significantly increase DA and NA in synaptic clefts would be able to target these receptors. It is best however to consider choice via matching with symptoms ( including their severity)

[@AhadKhan-cx6cu]

@ do you do any consults with other physicians? Even those going through chronic illness?

[@maple7432]

@@PsychiatrySimplified very good answer

[@ethanlubell4774]

Hi Dr can you do a video on the 3-6 month antidepressant chemical rebound phenomenon that occurs for some people that is unrelated to the original condition.

[@PsychiatrySimplified]

kzbin.info/www/bejne/o3Wkp6mZopmbgNksi=2hVbm_cx6FDoU-z8

[@ethanlubell4774]

@@PsychiatrySimplified I already watched that video and dont remember you discussing that at all...

[@prabalpratapsingh3966]

Can plasma glutamate level also help in digging deep ?

[@PsychiatrySimplified]

@@prabalpratapsingh3966 not really as no correlation with symptoms or brain impact. Clinical symptoms / markers as a constellation are often more valuable than biomarkers here once main organic aspects are ruled out

[@prabalpratapsingh3966]

@ Just out of curiosity and to know, if high glutamate indicate excitoxicity / neuro inflammation

[@Sam-n6k1c]

Would guanfacine be dose dependent, I have seen an improvement on 3 but my pots and anxiety is still there just lesser. I am unsure if my pots is hyperadrenergic as all I do is sleep, its not disturbed just not restful

[@PsychiatrySimplified]

It’s difficult to provide individualised advice without knowing the full picture but about 50% of sleep improvement comes from day time improvement of cognition and improving fatigue. A sleep study always helps. Guanfacine does have dose dependent effects. While it can help with sleep , addressing day time fatigue is the other aspect that improves sleep as activity improves. The symptoms during the day provide clues in what may need to be prescribed.

[@AhadKhan-cx6cu]

Hello Dr. Are the medication examples you mentioned temporary to correct problem or permanent for patient?

[@PsychiatrySimplified]

The question is a difficult one to answer because what we mean by temporary and permanent is nuanced. For example is the symptoms are controlled with medication then is that permanent? Or is it conditional on medication being absent. The aim is to help the individual reach a level of recovery. Recovery itself is defined differently by each individual. So its a challenging one to answer as a short yes or no

[@3manifold]

Sir do protracted withdrawal from ssri resolve on its own? I have every symptom low blood pressure, direct cognitive symptom and anhedonia too, like i cant feel music anymore

[@PsychiatrySimplified]

It can yes- but it really depends on the overall constellation of symptoms. Its important to address the picture proactively if it is very distressing and interfering with functioning.

[@AhadKhan-cx6cu]

Hi Dr. I am a clinician, and also a long covid sufferer for 3 years myself. One of the biggest problems I’ve dealt with is sleep problems. Never feeling restored or getting deep sleep which then causes next day fatigue and persistent brain fog/derealization. I dont jolt awake but my brain constantly feels on. No dreams at all. So not classic hyperarousal. Could clonidine still be beneficial for this? Also, at what point would you know when to introduce other drugs after correcting hyperarousal?

[@PsychiatrySimplified]

Yes i mention clonidine/prazosin in the video and the Hyperarousal which is a very common symptom. One is aiming to target the Hyperarousal to reach 50-60% improvement in sleep - cessation of nightmares or vivid dreams ( not everyone has this) , waking up more refreshed. Feeling like sleep is deeper and not superficial ( as dreams may not occur if the person is having significant restless rem sleep). Sunsequent to this one may notice the other symptoms as being more prominent which is when the other targets can be worked on

[@AhadKhan-cx6cu]

@@PsychiatrySimplifiedthank you Dr. Any concern of building tolerance to Clonidine?

[@maple7432]

maybe rule out sleep apnea and uars (which usually causes more microaruasels and the type of sleep fragmantion you are reporting) also look into luteolin.

[@Jules-kp7rw]

Is it possible to have very poor sleep even though you sleep like a hibernating bear ? I also have long covid and sleep extremely well : if I don't put an alarm I can sleep 12 hours in a row without waking up once and still feel absolutely horrible when I wake up. I can really relate to that brain fog / derealization part. A while ago I was doing very intense cognitive work all day and sleeping a lot at night too. In the subway, full of lights and people, I was constantly falling into nothingness, forgetting everything around almost like falling asleep yet it wasn't sleep as I was standing up eyes wide opened. The world around me was fading away... and suddenly coming back, over and over. It felt unreal, similar to how you can feel after not sleeping for 2 nights in a row but without other symptoms of sleep deprivation like extreme emotional dysregulation. If I'm correct, REM sleep if where emotions are processes and deep sleep is more related to mood, memory and cognition. The thing is I wasn't in a bad/depressed mood either like it should have been if it was a lack of deep sleep. Maybe SSRIs (100mg sertraline) prevented that ? I think I had dreams, at least I remembered some but they were very strange and unusual in a way I can't explain as I don't remember them well anymore. Other odd change : I used to wake up at least 1 time to pee during the night. Since covid, it doesn't happen anymore even though my water intake hasn't changed (I drink a lot of water). I just wake up with a painful distended bladder in the morning. I send you my best wishes through my keyboard, this condition is such an invisible curse.

[@AhadKhan-cx6cu]

Dr, do you do any email/phone consults with other clinicians?

[@PsychiatrySimplified]

Not unless they are involved in patient care. I do to share knowledge but time restraints often mean I find it challenging to do so. This is the reason why we developed the course so clinicians can learn in a structured manner through case studies. www.academy.psychscene.com/courses/the-neuropsychiatry-of-chronic-fatigue-syndrome-and-long-covid-2/

[@3manifold]

Sir what is the progress of gaze continent music reward therapy?

[@Dr.M.Shafiq]

What does pregablin do in such hyperarousal condition?

[@PsychiatrySimplified]

Pregabalin can also reduce Hyperarousal ( and hence is indicated for anxiety) along with reducing pain. But at higher levels may struggle to do so

[@AhadKhan-cx6cu]

Hi Dr. One of the strangest symptoms I’ve had for 3 years post covid is the ‘dream like state’ or derealization. It happened almost overnight after getting a mild case of cov19. Is this something you’ve seen in practice? Could this be a result of central adrenergic state or overactive amygdala?

[@PsychiatrySimplified]

This is a common description by patients as part of the ‘brain fog’ pn.bmj.com/content/early/2024/09/19/pn-2024-004112.long

[@AhadKhan-cx6cu]

@ so same principles would apply in terms of improving adrenergic state, increasing dopamine in frontal lobe?

[@PsychiatrySimplified]

Yes. One aspect to take into account is trauma exposure at early age or trauma in adulthood as this can be associated with depersonalisation symptoms as part of fear cascade. Treatments are similar but ofcourse trauma informed care is necessary there

[@prabalpratapsingh3966]

Can 24hrs urine catecholamine and their metabolite test can also give a hint of underlying cause ?

[@PsychiatrySimplified]

Not really. To rule out pheochromocytomas perhaps but not necessarily to guide specific treatments.

[@prabalpratapsingh3966]

@@PsychiatrySimplified I meant fractioned catecholamine , which can give noradrenaline levels in periphery , I an just guessing

[@3manifold]

Sir do tardive dystonia got better as your anxiety reduce?

[@PsychiatrySimplified]

Really depends. If mechanism is linked to arousal, then yes. But there may be other associated aspects.

[@3manifold]

@PsychiatrySimplified i think were not on the same page, so dystonia can be from arousal and its not functional dystonia.

[@LittleE28]

can you make a video on the dangers of anti/critical psychiatry

[@PsychiatrySimplified]

I'll add to the list

[@maple7432]

more research about mast cells role in these conditions should be done in my opnion.

[@PsychiatrySimplified]

They are one part of the innate immune system which in initial stages may be a target but as more domains are involved targeting mast cells only is less likely to target all domains as the wider immune dysregulation cascade is set into motion which includes HPA axis dysfunction, brain network involvement etc which is what I've covered.

[@maple7432]

@@PsychiatrySimplified you are definitely right, prof.theoharides research is very interesting tough.

[@Dr.M.Shafiq]

Another troublesome symptom is problem of balance, tinnitis ,internal tremor ,vibration in body , What does Benzo,clonazepam etc do with Dopa and other receptors. and withdrawl of clonazepam ? low grade fever is part of disease or may be wthdrawl of benzo?

[@PsychiatrySimplified]

Part of it is Hyperarousal and with a contribution of ANS dysfunction. Benzodiazepines reduce Hyperarousal ( indirectly reducing dopamine, noradrenergic, glutamatergic potentiation ) ; so withdrawal can lead to agitation.

[@Jules-kp7rw]

Why do you mention benzos ? I already answered you under your other comment. I happen to have a very peculiar reaction to benzos. They turn me from an introverted socially anxious person who doesn't have much to say to the most extroverted talkative guy. It's quite incredible. When I got covid, I was coincidentally very high on benzos as I had found a full bottle of bromazepam, a long acting benzo, and completely megadosed on it because I'm an addicted idiot. I took 180mg in the span of 2 days which is about 5 times the maximum recommended posology. I wonder if it could have lead to my current long covid.

[@daniellelblackwell]

Have any of your patients benefited from a ketogenic diet as part of the physical strategies to improve this condition? Or theoretically do you think it could be a useful tool? I appreciate your time and thoughts 🙏

[@PsychiatrySimplified]

There is evidence for it . However at the severe end of the spectrum there are 1. Challenges implementing the diet 2. Risks with diet itself . I’ve covered ketogenic diet in more detail here psychscenehub.com/psychinsights/brain-insulin-resistance-2/

[@allTheRobs]

Interesting stuff. Appreciate the biological take. The assertion that inappropriate amygdala response is the basis of PEM/PESE is just wrong though, in my body anyway. I can be calm/clear of mind and still exacerbate POTS to the point of PEM/PESE. I can also happily and calmly use my brain to the point of getting a concussion by doing 15-20mins of a technical task, even fun stuff. Music and interesting visuals can trigger nausea. If this is excitotoxicity, I'd like to deactivate my microglia please! 😅

[@PsychiatrySimplified]

Amygdala response is not always overt. In the video I cover interception and allostatic load which the amygdala mediates. The behavioural response can be very ‘core’ -I talk about it in the form of a thermostat. Fatigue / PEM has multifactorial aetiology but the behavioural response embedded over time in ‘chronic’ conditions can be shaped by interoception.

[@allTheRobs]

@@PsychiatrySimplified put it this way: I know how I experience fear, and I'm still capable of feeling afraid in a way that is subjectivity identical to before I fell ill. Telling me the amygdala response/setpoint is not always overt renders your model unfalsifiable from my perspective (as the ill person) and disenfranchises me as a reliable narrator for the state of my body and mind--this puts a tremendous amount of responsibility on the clinician as the sole arbiter of truth about not only pathophysiology, but essentially any sensation or experience. I don't believe this can be justified. The burden of proof ought to be very high to make this kind of claim. No doubt that psychological state affects interoception, and vice versa, and this may be a factor exacerbating underlying pathology in some people some of the time, but it IS NOT the "basis" of PEM/PESE/PENE--this claim is basically unfounded, no? Also, PEM et al. and fatigue are not the same. There's a semantic barrier between patients and doctors because the doctors almost always have no analogous experience (but don't know this).

[@seanm.collins9888]

​@@PsychiatrySimplifiedAre you a grifter and a scammer?

[@PsychiatrySimplified]

@ this isn’t about true or false and it’s difficult to explain it on a message like this. The original point was about PEM and amygdala activation. My reading of your post was related to amygdala ‘ feeling calm ‘ therefore unlikely to be related to PEM or fatigue. Fatigue , PEM or any other phenomenon for that matter that has a behavioural component, has multiple factors playing a part. For example in fever - the amygdala is activated - I can be fatigued and feel exhausted but slowed down. No hyperarousal being present. We are not looking at single aetiology to explain a behavioural component - that is what I explain in the later half of the video . The correlation is misleading. It’s about examining the patterns of behaviours in context of allostatic load. These behaviours that are consolidated are underpinned by safety behaviours. I’m not trying to negate or disprove someone’s experience - if the behaviour persists , we have to consider a multi factorial understanding esp one that takes into account interoception , emotions etc.

[@allTheRobs]

@@PsychiatrySimplified PEM is no more behavioural than limping with a broken ankle is. I'm not saying there isn't a behavioural component to limping, and accept that limping can occur after a break has healed for neuro-driven protective reasons, but want to stress the important fact that limping is not the "basis" of a broken ankle. In people with POTS/ME the ankle hasn't healed; the pathology is untreated, and the "limping" is entirely warranted due to the physical damage incurred by exertion/stress/allostatic load. It is about true and false, because you're proposing a hypothesis for a disease pathology, and made a claim about PEM. HPA dysregulation is only a hypothesis, and not the only one. There are a lot of processes in the loop for any person at any time, whether healthy or disabled by illness. My point is that locating the nexus of the problem in POTS/ME/Fibro in the amygdala is like identifying limping as the cause of a broken ankle.