Thread by @jenbrea

So excited to watch this interview between @polybioRF s @microbeminded2 and @MS_SouthNassau’s @RuhoyMD that I’m going to live tweet it. Dr. Ruhoy is a neurologist with a Ph.D in environmental medicine who works with #longCOVID #mecfs #EDS patients.

Ruhoy describes her long-standing interest in integrative medicine, natural approaches, and environmental medicine. She’s even a certified medical acupuncturist! She now helps lead a neurosurgery practice. 😍😍😍

Ruhoy: “I was an environmentalist from when I was very young and I believe that the world around us plays a role in our health. Even before I was a doctor, I would always try to find ways of living a healthier life. I saw no reason why I couldn’t combine it.”

“We’re not an individual organ. I know even as a neurologist, we’re not just our brains and our cords. We are an integrated organism, so our care should be integrated as well.” @RuhoyMD

On structural issues: “I got into it because I was getting a lot of referrals for complex, neurological presentations that didn’t localize all that well. Neurologists…we like to localize things. If there is this symptom, where does it localize to?”

“It didn’t really localize. It didn’t make sense. It didn’t really fit into a nice little box.” @RuhoyMD #mespine #EDS

“And I started to notice that a lot of these patients were very flexible. This was several years ago. I do autonomic testing in my clinic. They would often meet the criteria for POTS and often have other types of autonomic dysfunction”

“I started looking at the correlation and lead me down the path of hypermobile type EDS (#hEDS). In residency training, you learn about #vEDS because of the risk of aneurysm, but in neurology, you don’t really learn a whole lot about hypermobility.”

“What I found was that the vast majority of these patients—not all of them—were hypermobile. (Which is sort of an interesting question on its own—what is going on with [those patients who aren’t hypermobile]? 😍)”

“So I started to learn more about EDS, and more about its manifestations, and more about how connective tissue holds things together. And then when you think about where connective tissue lies, not only is it holding our joints together…”

[Connective tissue] is holding our organs to our skeleton, the meninges are connective tissue, the vasculature holds connective tissue. So I started to see where the neurological systems can play a role in a connective tissue disorder…

And then I came across Dr. Bolognese one day, and I became very, very interested in how the change in alignment and the structural issues with laxity of the ligaments, hence, the difficulty of the ability to hold its alignment well, can result in neurological manifestations.

We’re writing a lot of papers about how and why it actually DOES ”localize” in the end. At the beginning it was like, ‘this doesn’t localize, this doesn’t make any sense’ but now it actually does localize the more you understand about connective tissue.

Amy: “When you say localize, do you mean the craniocervical junction? I guess what people are hearing more about these days is craniocervical instability.”

The C0-C1 joint and C1-C2 holds very important anatomy. It actually holds the bottom part of our brainstem. The medulla oblongata sits there. And within that space is vascular use: arteries that feed the brain, veins that drain the brain…

It holds CSF (cerebrospinal fluid) compartments…So it has important anatomy to our nervous system.

On the craniocervical junction: ”When a joint is unstable—and that joint is so critical, it’s actually held together by almost 20 different ligaments—and you are born with ligamentous laxity, right there you are at risk.“

“I don’t think it’s necessarily pathologic to be born hypermobile, but I think that predisposition is that 1st hit. And then there’s something that becomes that 2nd hit, whether it’s infection or exposure to an environmental contaminant, or even physical trauma.” #MEspine #hEDS

“A lot of these patients will report changes in symptoms in certain positions: flexion/extension, turning right and turning left. So in certain positions, that anatomy is compressed. It’s really that simple. There’s mechanical compression.”

“That is why craniocervical instability can play a role in a lot of the manifestations #EDS and #MECFS patients present with.”

Discussing provocative testing and traction trials: “We try to see if we create space in this joint to see is there a change in symptoms? Is there an improvement in symptoms.” #MEspine

.@microbeminded2 talking about how she and @MBVanElzakker had believed for a long time that the brainstem and vagus nerve played a major role in #MECFS. Learning about CCI was an “aha” moment for them.

“You could get to a set of symptoms in which the brainstem, which has really important nuclei that control autonomic function can result in these sets of symptoms that we are seeing in patients with an #MECFS diagnosis.” jenbrea.medium.com/pathology-part…

Ruhoy: “There are also nuclei that have a direct relationship to the hypothalamus, so there is a neuroendocrine abnormality that we often see. In addition, when there is a connective tissue problem, you often find cranial settling, or low lying cerebellar tonsils…”

“…or an outright Chiari. So the posterior fossa, which is the back of the brainstem…now there is further reason for compression. It just becomes crowded and tight. And if you add an unstable joint on top of it…then you can have lots of different types of symptoms.”

Proal: CSF has to flow between the brainstem and the [cerebellar tonsils] and it’s this tiny, little, space. And you can see how a tiny [compression] could cause [huge problems]

Ruhoy: It could be completely gone. With the right level of compression, that space no longer exists

Amy: “[It’s like] nature created a liability in that area. You look at that and go, “A little bit of a problem could cause a dramatic amount of symptoms, and we see that in #MECFS patients with that diagnosis.”

On diagnosis, @RuhoyMD describes three components:
[1] imaging
[2] a clinical history (“I don’t treat MRIs, I treat the patient.”)
[3] a response to traction

Not every neurosurgeon requires the traction trial. “We do because it’s another parameter to support the diagnosis because the fusion is not to be taken lightly. This is a significant surgical intervention. If we are going to recommend fusion, we want to be sure of the diagnosis”

On alternatives to surgery, @RuhoyMD discusses the role of inflammation in making ligaments in people born with EDS even more “loosey-goosey.” “We try other means of reducing inflammation, of [addressing] anything that is causing further inflammatory assault on the ligaments.”

“A lot of the inflammation comes from mast cell degranulation. We work as a team to help patients reduce inflammation.“ (Team includes Dr. Maitland, an immunologist and #MCAS expert who works with
@RuhoyMD and Dr. Bolognese). Also discusses autoimmunity, infection, exposure.

“There is a high incidence of patients who have symptomatic flares from things like mold exposure or patients with a history of Lyme, bartonella, and babesiosis. We try to identify if any of these things exist and we try to treat to see how much symptomatic relief they can get.”

“I don’t think we ever really cure the symptoms of #CCI and/or #MECFS but we can definitely improve upon them, where patients feel like, OK, this is as good as I have felt in a really long time, and I’m not thrilled with surgery just yet, so I am going to hold off for now.”

Also discusses (different groups) working on injection therapies (platelet-rich plasma therapy, stem cells). Has had a lot of patients travel to centers that do these injections. Has had some good feedback. (My note: I think results are mixed but some have great outcomes.)

“The jury is still out on whether it obviates the need for surgery forevermore, it is still too soon [to know] but patients are reporting some benefits.” Is hopeful for more nonsurgical treatment options.

On research: “The holy grail is really to understand enough that we can be preemptive in this so patients don’t develop full-blown CCI and need surgical intervention. Better to treat them earlier on. The holy grail question would be, “How do we treat their connective tissue?”

.@microbeminded2 on the infection angle: “Most pathogens actually degrade connective tissue as part of their lifecycle.” @RuhoyMD “It’s how they make entry, right?” #longCOVID #mecfs

.@RuhoyMD “Mast cells are a primary source of a protease that is known to break down certain collagen types (i.e., MMP-9)...”

“…and when we start to have any kind of degradation of tissue in our bodies, cellular debris floating around, it becomes a trigger for autoimmunity (and #MCAS). It is a vicious cycle.”

At 26 minutes, @RuhoyMD talks about developing a brain tumor after she had already become a neurologist. She spent a year knowing something was wrong but because her neuro exam was normal, she was told she was just working too hard, that she was just “stressed out.”

Her brain tumor undiagnosed, she was told to leave her neurological fellowship “because clearly me, as a woman, couldn’t handle the stress…”😳

“I was told that I knew too much. ”Clearly, you’re letting your mind get away from you…’”

“And no one would order an MRI.”

Turns out…

“I had a 7 cm meningioma. There was a lot of swelling. The left side of my brain was on the right. So, I know what it is like to not be believed.”

“So when patients tell me about a symptom they are experiencing…I knew my body better, they know their body better…I believe them until I have reason not to, which I very rarely do.” @RuhoyMD

What about somatoform disorders? Talks about FND and knows a lot of people given this diagnosis (or conversion disorder) and says while there are a lot of people studying it and there is some research, “I know know that they did not have that.”

“I think there is a blurry line here now and I’m not yet ready to say that FND doesn’t exist at all but I do know for a fact that many patients are given that diagnosis but they do not have that.” @RuhoyMD

Re: learning about FND as a student: “Are we giving that diagnosis because we just don’t know enough? Maybe we have to do some more research. Maybe the research just hasn’t caught up. Maybe we don’t know the answers but it doesn’t mean [a distinct pathology] doesn’t exist.”

Amy asks about Bragee & Bertilson study, which found signs of intracranial hypertension on MRI in 83% of #MECFS patients. Ruhoy talks about how the patients she sees often don’t have certain classic signs of IH (e.g., papilledema) @ 32 min frontiersin.org/articles/10.33…

YES YES YES!! @RuhoyMD Talks about patients who on LP have LOW pressure in the spinal canal and but evidence of HIGH pressure in the brain.

Our fluid flow IN COMPARTMENTS. This is often forgotten in diagnosis.

At 35:30 the convo shifts to tethered cord syndrome @RuhoyMD talks about how inflammation can also cause the filum (terminal end of spinal cord composed of connective tissue) to tether to the canal wall.

.@RuhoyMD Talks about how fusion surgery can worsen tethered cord, but how tethered cord release can also worsen craniocervical instability. (This is why patients with both pathologies often need both surgeries.) #MEspine

Hmm..I’m not sure about the body “feeling more” of one issue after the first surgery @microbeminded2. I think it’s more that your posture fundamentally changes after one issue, exacerbating the other problem.

In believe that in a lot of cases:

1) Fusion lengthens the canal, increasing tension on the tethered cord

2) Tethered cord release increases mobility in the spine (in often deconditioned patients), making instability in upper levels worse

.@RuhoyMD “We’re in this for the long haul. This is not about who has #CCI, let’s surgically correct them. This is about #EDS and what happens to the body when you have EDS, and when you are exposed to things that are inflammatory to your body, and what we can do about it.”

.@RuhoyMD “And also just to understand, again, why does CCI develop? What is that about, really? We have theories as to why, but I want to prove it, that’s what we’re setting out to do, along with @polybioRF’s help.”

.@microbeminded2 describes their collaboration to take CCI surgical samples (e.g., ligament tissue) and small fibre (nerve) punches to do sophisticated analyses like whole-genome sequencing and microbe discovery, to develop a full genetic, immune, and infectious profile.

.@RuhoyMD & team are also using transcranial Doppler to measure cerebral blood flow velocity in their patients. Very eager to see if they are able to partially replicate and expand upon this work: sciencedirect.com/science/articl… #MECFS #longCOVID #NEISvoid

Oh wow. She’s saying they have also found #vasculitis of the small vessels (presumably this is in non-#longCOVID patients). This would not surprise me but I am curious to hear more! @RuhoyMD cc: @ahandvanish

Thank you so much for this great interview @RuhoyMD @microbeminded2! Can’t wait from more interviews from @polybioRF (you can check out their YouTube channel here: youtube.com/channel/UC0OFV…)