#post exertional neuroimmune exhaustion

[chronicallydragons]

Very rude that fun spoons are still spoons

[sapphicautistic]

There's so much to do and so much I WANT to do but i am. sososick

[myalgicencephalomyelitiscfstom]

From "Living in the in between" https://thelowsideblog.com/2022/06/10/living-in-the-in-between/

Author has ME/CFS. He reflects on the strange, liminal world one can feel one is living in when one has a debilitating chronic illness

PEM=Post-Exertional Malaise

PENE=Post-exertional neuroimmune exhaustion

Also: "Life with chronic illness leaves us questioning ultimate reality and whether being stuck in the inbetween, in no man’s land, in purgatory, in limbo, a space between life and death is a place in which we really want to exist"

[longhaulerbear]

The paper presents a systematic review assessing the role of autoimmunity in ME/CFS, specifically focusing on the association of autoantibodies and immune dysregulation with the condition's pathogenesis.

Findings from the review suggest insufficient evidence to classify ME/CFS as an autoimmune disease due to the absence of specific autoreactivity and tissue damage typically seen in autoimmune conditions.

Notable studies within the review explore cytokine signaling, genetic factors, and the prevalence of autoantibodies, with mixed results that highlight the complexity of ME/CFS.

Future research is vital for developing diagnostic and treatment strategies that accurately address the multifactorial nature of ME/CFS, especially as the post-COVID-19 landscape may increase its prevalence.

The evidence as a collective, suggests that immune dysregulation and the presence of AAb in people with ME/CFS may play a role in the contribution to specific symptoms or comorbidities. However, there is a lack of evidence to suggest ME/CFS is an autoimmune condition. It is critical to recognise the broader and more specific limitations of these studies, such as that of small sample sizes and the need for further mechanistic research to establish causal relationships and clinical significance. Notably, the heterogeneity of AAb profiles amongst ME/CFS patients underscores the complexity of this phenomenon and highlights the necessity for personalised approached to diagnosis and treatment.

Whilst there exists evidence suggestive of immune deregulatory phenomena and autoantibodies in ME/CFS patients, these findings cannot deduce ME/CFS to an autoimmune disease. These findings underscore the pressing need for further research to unravel the precise immunological and genetic factors at play in ME/CFS. With direct emphasis on distinguishing autoimmunity from broader immune dysregulation, such targeted efforts will ultimately pave the way for more effective diagnostic and therapeutic strategies in the ongoing quest to understand and manage this enigmatic condition.

[starrynightsdelight]

I do think “post-exertional neuroimmune exhaustion” is a more accurate and intuitive term than post-exertional malaise, but I still can’t commit to it, if only because I don’t think the ICC authors considered what the acronym PENE spells out in one of the most widely spoken languages in the world (Spanish).

[livingdeathdiary]

This is the diary of someone with severe ME. For those unfamiliar ME stands for Myalgic Emcephalomyelitis it is a neuroimmunological disease affecting over 30 million people worldwide. Severe ME refers to patients with ME who are housebound and mostly bedbound. I am completely bedbound and depend on IV fluids.

The defining symptom of ME is PENE or post exertional neuroimmune exhaustion. PENE happens whenever someone with ME "overexerts." The more PENE you experience the worse you get. The last thing I did to trigger PENE was eat some bread with my mum. In other words, if you dare to live, the disease progresses.

To prevent the progression of my disease I spend every day in a dark room resting. I recieve IV fluids through a central line in my chest and take a carefully crafted set of over 20 medications and supplements. I can watch videos, but nothing too exciting. I can talk, but not get emotional. Every action must be accounted for in my balance sheet. Every piece of ATP accounted for.

Then of course the pain. The daily constant migraines. The light, noise, and skin hypersensitivity. The acid burning muscles. The aching joints. The spasms. The stabbing neuropathy. These too take energy to endure. Energy I can't afford.

This is my existance of living death. The girl who once inhabited this body, a girl you will get to know perhaps, is no more. She died a slow painful death. Now I write to you from the living death of severe ME. Not to teach or to shed light or whatever other BS. No. I do my advocacy elsewhere. Simply because even ghosts it seems want to be heard. Because this existance makes you want to shout and curse into the void and you dear reader, if you even exist, you are my void.

[idlespright]

ME/CFS Awareness

Myalgic Encephalomyelitis, that’s what the abbreviation M.E. stands for, has many other names. One is CFS (chronic fatigue syndrome), another SEID (systemic exertion intollerance disorder). Since the late 1960s it’s classified by the WHO as a neurological disorder.

Main symptom, and what distinguishes ME from many other debilitating illnesses, is post exertional neuroimmune exhaustion (PENE, also called PEM). That means: worsening of symptoms of ME after doing even small tasks, like, brushing your teeth, taking the dog for a walk or sitting up. This worsening of symptoms is delayed, that is, it sets in later than the actual task. Sometimes a few hours later, sometimes days. And stays from days to weeks and even months.

Most patients have flu like symptoms all the time, with sore throat, backache, stomach cramps, muscle weakness, brain fog and feeling feverish.

For many, this means they are unable to read, listen to music, watch videos, etc. Imagine having the flu so bad, that you can’t even watch cartoons. That’s M.E.

The illness is characterized by better and worse days. Some people can’t get out of bed and have to lay in darkness in absolute noise isolation on their bad days. Sometimes those periods last years. If they neverthess attempt to get up they get what’s called a flare up. Their immune system acts up resulting in severe muscle pain, lymph node pain and migraine like headaches. And more.

It is important to note, that while there is up to now no single cause identified (the most promising research points in the direction of a partly inherited autoimmune dysfunction that is activated by going through common infectious deseases like Eppstein Barr), no serious, up to date study points to it being a psychological issue or treatable via psychotherapy/psychiatry. To distinguish between ME and depression is easy, ME patients do not lose incentive. They want to get up and work - and do so! To the point, that most crash regularly. “Crash” describing what leads to the above mentioned flare up, doing too much so their symptoms worsen again.

Many doctors don’t know about this illness. And some who have heard of it believe, that it is a mental health issue. Their believe is often based on the infamous PACE study of some UK psychiatrists that was discovered to be a huge fraud years ago. As with the idea of autism being connected to vaccines (also based on fraudulent research), it’s hard to get rid of those rumours once they are started.

But it means, that ME patients are still treated with behaviour therapy and activation therapy. Resulting in renewed flare ups and some times long term worsening of their symptoms. While talking to a therapist can, in some cases, help to cope with this disabling illness, it can’t cure it. And going out to weekly appointments can be too much for many patients, making their illness actually worse than better. When those patients stop seeing their therapist because it didn’t help or made their symptoms worse, the medical system is used to treat these dropouts as success of their method (as in ”Didn’t need to come to therapy any more. Was cured.”). Others get their disability benefits revoked because they refuse to do “therapy” that further damages their body. They then have to go on living with this condition, in isolation and pain, without any financial support. Treating this illness as a mental health issue and refusing to treat the physical symptoms (sleep disturbance, POTS, inflammation) with accurate medication is one reason the suicide rate in ME patients is about 21%

Another 21% die of heart failure. All ME patients have a greatly reduced life expectancy and greatly increased risk to die from cancer. The life expectancy of ME patients with cancer is 20 years less than that of “healthy” cancer patients.

Through this Covid pandemic people realized what it means having to stay inside when you want to go out. Abled people know now why it isn’t always fun to stay in bed when you want to go to the gym instead. Or meet with friends. ME/CFS patients have to live like this for years. Some all their life.

There is currently no causal treatment (although clinical trials with immune modulators and hemodialysis are ongoing, e.g. at Charite, Berlin) because funding for ME research is notoriously low. But we need more knowledge. We need to convince young scientists, that this is a rewarding field of study. ME is not a rare illness. More wide spread than breast cancer in women (data from Germany estimates for ME 300.000 cases). Finding a cure could be worth millions for big pharma. But there is so much to do to get there. And many prejudices to correct.

Spread the word! End this scandal!

Edit:

Sources for this article include:

pubmed - Beyond ME/CFS: Redefining an illness

CDC on ME/CFS

NIH working group on ME/CFS

Euromene - European research network for ME

Bayrischer Rundfunk (German) on a possible blood test for ME/CFS from Stanford University

Deutsche Gesellschaft für ME/CFS (German)

fatigatio (German) Bundesverband Chronisches Erschöpfungssyndrom

[compare-wp10]

Into the looking glass: Post-viral syndrome post COVID-19

See on Scoop.it - COMPARE RISK COMMUNICATION

Letter to the Editor We are writing to highlight the potential for a post-viral syndrome to manifest following COVID-19 infection as previously reported following Severe Acute Respiratory Syndrome (SARS) infection, also a coronavirus [1]. After the acute SARS episode some patients, many of whom were healthcare workers went on to develop a Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) – like illness which nearly 20 months on prevented them returning to work [2]. We propose that once an acute COVID-19 infection has been overcome, a subgroup of remitted patients are likely to experience long-term adverse effects resembling CFS/ME symptomatology such as persistent fatigue, diffuse myalgia, depressive symptoms, and non-restorative sleep. Post-mortem SARS research indicated the virus had crossed the blood brain barrier into the hypothalamus via the olfactory pathway [2]. The pathway of the virus seemed to follow that previously suggested in CFS/ME patients, involving disturbance of lymphatic drainage from the microglia in the brain [3].One of the main pathways of the lymphatic drainage of the brain is via the perivascular spaces along the olfactory nerves through the cribriform plate into the nasal mucosa [4]. If the pathogenesis of coronavirus affects a similar pathway, it could explain the anosmia observed in a proportion of COVID-19 patients. This disturbance leads to a build-up of pro-inflammatory agents, especially post-infectious cytokines such as interferon gamma, and interleukin 7 [5], which have been hypothesized to affect the neurological control of the ‘Glymphatic System’ as observed in CFS/ME [3]. The build up of cytokines in the Central Nervous System (CNS) may lead to post viral symptoms due to pro-inflammatory cytokines passing through the blood brain barrier in circumventricular organs such as the hypothalamus, leading to autonomic dysfunction manifesting acutely as a high fever and in the longer term to dysregulation of the sleep/wake cycle, cognitive dysfunction and profound unremitting anergia, all characteristic of CFS/ME. As happened after the SARS outbreak, a proportion of COVID-19 affected patients may go on to develop a severe post viral syndrome we term ‘Post COVID-19 Syndrome’ – a long term state of chronic fatigue characterised by post-exertional neuroimmune exhaustion [6]. Clinically, one of the authors (RP) has already seen a patient with possible post COVID-19 syndrome. A 42 year old male, married with 5 children who was fit and healthy with no prior existing symptoms with the exception of mild anxiety 10 years previously and a month of fatigue following a viral infection 4 years previously. He contracted the virus, showing symptoms from 3 to 15th April 2020, during which time he was virtually bed bound for about 2 weeks. At the end of April, he contacted the osteopathic clinic and scored 164/324 regarding the severity of symptoms on the validated rating scale Profile of Fatigue Related States (PFRS) [7]. The PFRS consists of 54 symptoms each with a score of 0–6 where 0 = no symptom, 3 = moderate and 6 = extreme. Twenty four of his symptoms initially scored high i.e. 4, 5 and 6 on the scale. He was seen in clinic on 5th May, complaining of severe physical fatigue, insomnia, difficulty reading with brain fog, general myalgia, dry skin and increased anxiety. On physical examination he had a restricted and inflamed mid-thoracic spine, engorged varicose lymphatics in the chest with severe tenderness in the left breast lateral and superior to the left nipple. Marked tenderness was also felt in the coeliac plexus. These signs have utility in aiding the diagnosis of CFS/ME [3]. Manual treatment was provided to aid central lymphatic drainage, improve mechanics and reduce the inflammation of the spine and reduce the allostatic load by improving the sympathetic tone. Three treatments were completed, once a week and the patient followed a self-massage routine to aid lymph drainage along with gentle exercises to improve thoracic spinal mobility. By the third treatment (27th May) his symptom severity had reduced significantly with a follow-up PFRS score of 75/324 with all but five of the very severe symptoms relating to physical and mental fatigue reducing from 4, 5 or 6 to only mild / moderate complaints i.e. 1–3 on the severity scale. He remains in active follow-up. It may be that early intervention and supportive treatments at the end of the acute phase of COVID-19 can help overcome acute phase symptoms and prevent them in becoming longer-term consequences. Without this, in a contracted future economy (at least in the short to intermediate term), managing these likely Post COVID-19 syndrome cases, in addition to existing CFS/ME cases will place additional burden on our already hard pressed healthcare system. In the light of this and similar cases and in the context of the available evidence for SARS, we suggest that priority should be given to examine the prevalence of fatigue related symptoms following COVID-19 infection and to explore pragmatic relatively low cost techniques to treat post-viral fatigue, to alleviate symptoms and improve the quality of life for those affected by the longer term sequelae of COVID-19. Let’s start the preparations now for what may come in due course.

[chronicallydragons]

Me, a chronically ill girlie who just spent the whole weekend traveling and talking to people and moving around and being upright: why do I feel sick today??

[chronicallydragons]

migraine cravings be like "I know we're super nauseous right now. I know it's 10pm. But if we don't go make some French Toast immediately, we're going to die"

[chronicallydragons]

I learned that post exertional malasie/post exertional neuroimmune exhaustion from ME/CFS can cause or worsen dyslexia and WOOOO BOY does that explain a LOT

[chronicallydragons]

Idk if you can answer this question, but I need some answer on this bc a lot of ppl say no but others say yes

BUT

Does exercise help with POT's??

I'm definitely not a doctor, so this isn't medical advice, and I strongly encourage finding a knowledgeable doctor and even a knowledgeable PT about this, but I understand that's really hard to do, so I'll try my best to answer! It's also probably a really unsatisfying answer because it just depends. It'll depend on the individual and other comorbidities you have going on! In theory it's supposed to help, but only if you do it right and take it slow enough--if our ANS isn't going to constrict our blood vessels for us, then having the thigh and core strength to squeeze blood back into our brains manually is good enough! And exercising will help make that easier! There are lots of great resources on how to slowly scale from recumbent exercises to eventually being able to exercise upright and what muscles to specifically target to help--I remember the dysautonomia international website has a CHOP protocol template that a lot of people swear by!

However, if you experience a worsening of symptoms within a few days of exercising, you may be experiencing Post Exertional Malaise/Post Exertional Neuroimmune Exhaustion (PEM and PENE respectively--it's the same thing, some people just prefer different terms) which may suggest ME/CFS as a comorbidity. ME/CFS is super commonly connected with POTS/other types of dysautonomia causing orthostatic intolerance, so if you have POTS, it's important to try to rule out ME/CFS because graded exercise programs like you might find with POTS exercise therapies can really cause a lot of genuine physical harm if you have ME/CFS as well. If you do have ME/CFS, it's extra important to have a care team that knows ME/CFS so you can figure out how to pace yourself correctly depending on your severity so you don't make yourself worse. But if you're not getting significantly worse after a recumbent exercise (some soreness and maybe increased tachycardia is to be expected for a day or two, but if you feel like you've been hit by a truck and thinking is exhausting, that's a sign it could be PEM/PENE), it may be worth trying it out and seeing if it helps you! (I'm currently in a PEM crash, so can't track down references right now, but if you need anything else, let me know, and I'll get to it when I can!)

[sapphicautistic]

I'm in pretty bad post exertion neuroimmune exhaustion (PENE/PEM, it's an M.E. symptom) so my throat hurts sooo bad, I overdid it cleaning and stuff before the surgery and then surgery was even more strain on the system 😅 I'm actually surprised the pain from the surgery is this easy to manage so far, I feel like a lot of what I'm feeling is just M.E. stuff

[longhaulerbear]

While the pathogenesis of ME/CFS and post-COVID-19 syndrome remain poorly understood, it seems that the underlying pathology involves the CNS; the autonomic nervous system; and a persistent, dysregulated immune and metabolic response to the infectious agents [10]. Previous studies have shown a high propensity of patients with ME/CFS to be misdiagnosed with a psychiatric condition.

We hypothesized that ME/CFS and post-COVID syndrome are not primary mental health conditions but share some clinical features and common pathophysiological mechanisms related to autonomic dysfunction and microcirculation disorder.

We assessed microcirculation by amplitude–frequency wavelet analysis of blood flow oscillations with laser Doppler flowmetry (LDF) [24]. Because of the proven parallelism between microcirculatory changes in the skin and inner organs, we investigated forearm blood flow in the participants with «LASMA MC-1» peripheral blood and lymph flow laser diagnostic complex.

…the belonging of four symptoms to the domain of “sleep disturbance” and one symptom to the domain of “pain syndromes” confirms the validity of the treatment approach to ME/CFS, described in the recent guidelines from the European Network on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (EUROMENE). According to this approach, to reduce the severity of fatigue, patients are provided first of all with symptomatic help to normalize sleep and combat pain.

…the belonging of four symptoms to the domains associated with disorders of the nervous system (autonomic, sensory, and motor functions) confirms the classification of ME/CFS in ICD-10, where it belongs to the chapter G—“Diseases of the nervous system”.

Our data, therefore, not only agree with the concept of ME/CFS as a disease with neuroimmune pathogenesis but also allow us to make assumptions about approaches to diagnosis and treatment of this disease, as well as the most effective organization the patient care in ME/CFS, which optimally should be provided by neurologists.

In the past, ME/CFS has often been misdiagnosed as a psychiatric disorder of the affective spectrum, leading to mismanagement and deterioration of the patient’s health [31]. Today, it is believed that anxiety and depressive symptoms, which are common in ME/CFS [32,33], should not always be considered as a sign of an alternative diagnosis.

it should be remembered that recent research data on this topic suggests that depression and anxiety in ME/CFS are associated with the neuroinflammation process, pain syndromes, psychological distress due to the inability to return to work, and reduced physical functioning, social isolation, as well as insufficient knowledge of medical specialists about the disease. Consequently, they are deontologically vulnerable and have skeptical attitudes toward the patient’s problems.

POTS itself often develops following infectious diseases and, at least in some cases, may be associated with the production of autoantibodies against adrenergic and cholinergic receptors.

…in ME/CFS that developed after COVID-19, there is a more pronounced increase in heart rate starting from the 6th minute of the test compared to the control group. This allowed us to assume that POTS is one of the key characteristics of ME/CFS of post-COVID genesis. It is important to note that in 4/13 people who met POTS criteria in our study, the required increase in heart rate was achieved only at the 8–10th minute of the active orthostatic test. This confirms the practice of carrying out the test in its complete (within 10 min) and not abridged (5 min) version.

The rhythmic characteristics of oscillatory processes in the microcirculation system are useful for the diagnosis of many diseases related to the changes in the microcirculation [36]. The LDF method allows a non-invasive assessment of human blood microcirculation system disturbances. In this work, LDF was applied to assess the dynamic characteristics of microcirculation in ME/CFS, including post-COVID genesis (in the latter subgroup—it was done for the first time, to the best of our knowledge). A change in the microcirculation index (increase or decrease) characterizes, respectively, an increase or decrease in perfusion. Its increase can be associated with a lower tonus of the arterioles, which leads to an arterial hyperemia, or with the congestion of blood in the venules and venous hyperemia. Regarding the regulation of microcirculation, there are “active” and “passive” mechanisms. The “passive” mechanisms include external factors that act outside the microcirculatory bed: a pulse wave and the suction action of the “respiratory pump” from the veins. “Active” factors directly affect the vessels of the microvasculature by periodically changing the resistance of blood vessels to blood flow through vasomotions and creating transverse fluctuations in blood flow. These active factors are sympathetic nerve fibers, smooth muscle cells of the vascular wall, and endothelium-derived regulatory molecules. When carrying out spectral analysis, the active factors correspond to low-frequency oscillations [37]. There are several forms of microcirculation disorders: arterial hyperemia, venous hyperemia, combined hyperemia, ischemia, and stasis [38]. The changes identified in this study in ME/CFS, including ME/CFS of post-COVID-19 nature, correspond to the hyperemic form of microcirculation disorders, which is characterized by increased blood flow into the microcirculatory bed. It is distinguished by a significant increase in the number of functioning capillaries, an increase in tortuosity, vasodilation, and an increase in the permeability of the vascular wall. This form of microcirculation disorder is usually observed in acute inflammatory response or other conditions of decreased systemic vasoconstriction.

Bond et al. showed that chronic oxidative stress could contribute significantly to the development of ME/CFS symptoms due to the development of endothelial dysfunction [39]. The relationship between chronic inflammatory processes and increased arterial stiffness is well-known [40]. An increase in vascular resistance in cohort 1 compared to cohort 2 may reflect the contribution of the chronic inflammatory process of a long course to microcirculation disorders and suggests the existence of long-term consequences of ME/CFS, in particular, an increased risk of cardiovascular diseases.

Changes in microcirculation in ME/CFS (including ME/CFS of the post-COVID-19 nature) identified with the LDF method correspond to the hyperemic form of microcirculation disorders which is generally observed in acute inflammatory response or in case of the systemic vasoconstriction failure. It seems that increased vascular resistance may occur later in the disease course due to the chronic inflammatory process.