(Jeff Wood’s remarkable recovery following spinal surgery to correct craniocervical instability (CCI) and tethered cord shocked the ME/CFS community. It’s safe to say that almost no one saw that coming.  In this piece Jeff – the former ME/CFS patient who started all this off – proposes that the pain, fatigue, etc. in ME/CFS could potentially all be explained mechanically.)

I invite you to engage with me in a thought experiment.

connective tissue

Connective tissue is pervasive throughout the body. Could problems with it be causing ME/CFS?

One of the central puzzles of myalgic encephalomyelitis is that multiple triggering events can lead to ME — viral infections, Fluroquinolone antibiotics, impact trauma, surgery, pregnancy, overtraining, m­­old exposure, and others — yet the symptoms of ME are consistent.

I have a proposal that might possibly explain this: Perhaps all these triggers lead to a failure of the body’s connective tissue, and perhaps some people’s connective tissues are more vulnerable to failure in response to these triggers.

We often associate connective tissue with ligaments and tendons, but it’s more pervasive than that. The three membranes that envelop the brain and spinal cord, for instance, are composed of connective tissues. The blood vessels, too, are composed of connective tissue.

In turn, every symptom of ME could be accounted for as a chronic, ongoing brain and spinal cord injury that occurs as a result of connective tissue failure. Exertion would result in physical trauma to those neural tissues.

A Hypothesis to Explain ME

I am proposing that ME, as defined by any current or historical criteria, is a chronic, ongoing traumatic brain injury and spinal cord injury – that often results from connective tissue damage.

More specifically:

  • There is chronic, ongoing mechanical distortion of neural tissue that is further distorted by movement.
    • The area impacted by the distortion can be the brainstem (including the cranial nerves), the spinal cord, or, perhaps likely, both.
  • There is chronic, ongoing disturbance of blood flow and cerebral spinal fluid flow (these two concepts are together described as “craniospinal hydrodynamics”).

Let me acknowledge explicitly: I don’t have proof at this point that this hypothesis is true. My purpose here is to suggest reasons that this hypothesis might be true, and that we should follow up on the idea with research to confirm or disprove it.

Also, please understand I’m not suggesting that neurosurgery is the only solution for mechanical conditions. While a number of people with ME have corrected their underlying mechanical conditions with neurosurgery, there is an expanding universe of creative ideas for addressing mechanical conditions without neurosurgery.

Part of what I hope will come from exploring a mechanical paradigm of the disease is the development of methods less invasive, and less expensive, than neurosurgery.

Ongoing Traumatic Brain Injury: The Potential Role of Faulty Connective Tissue

Brain injury

Could every movement be producing a micro-traumatic brain or spinal injury? (Image by kalhh from Pixabay)

A traumatic brain injury (TBI) is traditionally thought of as a onetime occurrence: say, someone falls down, hits their head, and suffers a concussion. A spinal cord injury, too, is usually thought of as a onetime event.

I’m proposing, though, for someone with ME, these injuries aren’t “one and done” events. They are ongoing events, perpetuated by small daily micro-TBIs and spinal cord injuries that occur when we physically move.

My hypothesis is these micro-TBIs result from a failure of our connective tissue to hold our body in place. In turn, every time someone with ME engages in exertion, their neural tissue is essentially getting battered and “beaten up” and their blood and cerebral spinal fluid are being disturbed. Every time we move, we give ourselves a micro-TBI and spinal cord injury.

If that’s true, then post exertional malaise (PEM) could be considered a consequence of mechanical trauma. PEM would be the unavoidable consequence of experiencing a brain or spinal cord injury.

In the past few years, multiple people, including myself, have recovered from ME by treating craniocervical instability (CCI), and this condition illustrates one way that micro-TBIs could perpetuate one’s illness. In the case of CCI, the ligaments and joints of our skull and upper cervical vertebrae are no longer holding our skull and upper neck in place. These damaged ligaments allow excess motion at the junction of the head and neck, and this motion can mechanically beat up the brainstem, deforming it. This could explain the 1995 finding of brainstem hypoperfusion, or a lack of blood flow to the brainstem, in ME patients. (See: Brainstem perfusion is impaired in chronic fatigue syndrome).

Instability of the skull and upper neck could also explain how in people with more severe ME, even such minor exertion as talking softly while lying in bed or chewing a soft meal can exacerbate symptoms.

CCI is not the only way that mechanical problems of the craniocervical junction can cause ME symptoms. Distortions in blood or cerebrospinal fluid (CSF) through this area due to Chiari malformation, CCI, or other problems can also occur. Some problems involving craniospinal hydrodynamics include:

  • Too much blood backing up in the brain due to lack of outflow.
  • Too much cerebral spinal fluid, resulting in increased intracranial pressure.
  • Cerebral spinal fluid leaking from a hole in the dura (connective tissue membrane), resulting in intracranial hypotension.

These are all mechanical problems — and this is just a partial listing. There are additional mechanical problems that can affect other parts of the nervous system, too.

Connective Tissue Problems With No Known Connective Tissue Disorder

Mechanical problems of this kind are better understood in Ehlers Danlos Syndrome (EDS) – a connective tissue disorder. Dr. Ron Davis has estimated 50% of people with ME meet the hypermobile hEDS criteria. However, many people who have developed ME – including myself – do not.

A surprise that’s emerged in the last few years is that some of us with ME, who don’t meet the criteria for hEDS or for any other known connective tissue disorder, nonetheless have faulty connective tissues. I believe that the criteria used to diagnose known connective tissue disorders may not capture all of us.

Until my own case, it was broadly believed that the only way anyone could develop CCI was from impact trauma (like a car accident), rheumatoid arthritis, Downs Syndrome, or through having a known connective tissue disorder. Since my case, though, we’ve seen multiple ME patients, both with and without known connective tissue disorders, recover from ME when their mechanical problems were addressed.

Many Mechanical Conditions

Spinal stenosis - Rowe

Spinal stenosis in a person with ME/CFS who recovered following surgery.

I use the term “mechanical” because it captures the nature of an ongoing, chronic traumatic brain and spinal cord injury, exacerbated by movement. While there’s been a recent focus on CCI, multiple structural neurological conditions can exist in our population, and each of these is caused by problems with the connective tissue. In addition to CCI, here are some of the mechanical problems we’ve been seeing in ME patients: Tethered cord syndrome, Chiari malformation, cervical stenosis, venous stenosis, median arcuate ligament syndrome (MALS), and Eagles syndrome.

These mechanical conditions can lead to:

  • Chronic distortion of neural tissue in the brain, brainstem, cranial nerves, spinal cord, etc.
    • Compression, stretching, and other mechanical forces can cause problems.
  • Not enough blood getting to the brain in the proper way (cerebral hypoperfusion).
  • Too much blood backing up in the brain.
  • A nuanced, fluctuating combination of the above.
  • An overall dysregulation of blood flow and cerebral spinal fluid, along with mechanical neural tension deranging the nervous system.
    • In turn, this can activate, strain, and derange the mechanisms the body mounts to compensate, e.g., attempting to achieve functional homeostasis.

Dr. Peter Rowe believes connective tissue/nerve elongation problems are causing symptoms of pain, fatigue, brain-fog, light-headedness, nausea, sweating and flushing, headache, etc. in young people with ME/CFS when they move. Additionally, Dr. Rowe has published a case series of women who recovered from severe ME after treating cervical stenosis.

In 2020, Swedish researcher Bjorn Bragee found that 80% of ME patients had craniocervical obstructions, 83% had signs of intracranial hypertension, and 50% had hypermobility. These are all mechanical conditions, and they are all associated with connective tissue problems.

The good news is that these mechanical problems are identifiable, measurable, and treatable. Over just the last year, mechanical problems have been found to be causing, or contributing to, ME symptoms in hundreds of people. The number continues to grow as more people with ME pursue evaluation. But at this point, only a small percentage of us have been evaluated.

But, What About the ME Outbreaks?

Some mechanical problems can result in disturbed blood or spinal fluid flow.

Many ME patients — including those with a confirmed mechanical basis to their ME — have had viral onsets. At first, it might seem like viruses are unrelated to connective tissue damage. But in fact, we know that the immune molecules released to defend ourselves against viruses also damage collagen, a key ingredient in connective tissue. Whether an infection is tick born, viral, bacterial, doesn’t seem to matter. Any of those infections could initiate a breakdown of collagen.

It is not hard to imagine that the outbreaks throughout documented ME history could have a connective tissue component because of, rather than despite, the infectious component.

I suspect that some people already have vulnerable connective tissue prior to an infection. They would be more prone to connective tissue breakdown from an infection, or the infection might be the straw that broke the camel’s (connective tissue laden) back.

But viruses aren’t the only thing that lead to connective tissue damage, and that could explain how the experience of patients with viral ME onsets can be similar to those without them.

Traumatic Brain Injury: Physical and Cognitive Fatigue

A considerable body of scientific literature connects TBIs to fatigue. This literature generally discusses the TBI as a “one and done” event, resulting in a temporary aftermath of physical fatigue. But what might happen if we were experiencing a perpetual series of TBIs, made worse every time we move or exert ourselves?

What might living with ongoing micro-TBIs feel like?

It might leave us in an ongoing state of fatigue, lasting years, reliably worsened by exertion.

We can also see, in the published literature, that brain injuries result not only in physical fatigue. They can also result in cognitive fatigue. Many of us experience PEM following cognitive work. The overlap between TBI and ME symptoms is striking.

Through a Mechanical Lens: Graded Exercise Therapy (GET) and Pacing

Jeff proposes that mechanical problems could explain why graded exercise approaches fail.

Consider: Why might graded exercise therapy (GET) be harmful for many people with ME? The mechanical paradigm offers an explanation. By forcing someone with ME to move their body and exert themselves, GET could perpetuate connective tissue injury and ongoing micro-TBIs and spinal cord strain, as well as further derange cerebral spinal fluid and blood flow. This could, in turn, worsen the baseline condition of people with ME.

Also consider: Why might pacing, or intentionally limiting physical exertion, help protect people with ME from getting worse? The lack of exertion would prevent a person with ME from giving themselves micro-TBIs, spinal cord strain, and deranged cerebral spinal fluid and blood flow. Through limiting these mechanical harms, pacing would then reduce the severity of symptoms, or even maintain or increase a person’s baseline functioning.

Neuroinflammation, Immune Dysfunction, and Mast Cells

Within the ME community, among scientists and patients alike, there is an understanding that people with ME can exhibit the following: neuroinflammation, immune dysfunction, and mast cell activation.

Interestingly, traumatic brain injuries of any kind lead to neuroinflammation, immune dysfunction, and mast cell activation. Some consistencies between ME and traumatic brain injury can be seen in the article, “Mast Cell Activation, Neuroinflammation, and Tight Junction Protein Derangement in Acute Traumatic Brain Injury”:

TBI activates glial cells and immune and inflammatory cells, including mast cells in the brain associated with neuroinflammatory responses. This can, in turn, cause secondary brain damage.

TBI can cause mast cell activation, neuroinflammation, and a derangement of the tight junction proteins, and this is associated with increased [blood-brain barrier] BBB permeability.

Deeper Questions: Connective Tissue

Solutions other than neurosurgery currently exist. For example, regenerative medicine treatments can sometimes strengthen the connective tissue.

This brings us to some deeper questions: If ME can result from connective tissue failure, then what exactly is causing our connective tissues to fail? To fail badly enough that we develop ME?

What are the necessary elements to brew this terrible storm? What combination of genetics, epigenetics, environment, and specific events? How do these interact?

How do we arrest this process? How do we reverse it? How do we prevent it?

And by exactly what mechanism(s)?

I think the answers to these questions could be central to reversing, and even preventing, ME. As we live through the discovery process of finding these answers, we will learn so much more.

And how many surprising, related mysteries could we unlock along the way?


Jeff Wood

After uncovering the mechanical problems behind his severe ME/CFS, Jeff Wood completely recovered.

Jeff Wood is the creator of MechanicalBasis.org. In early 2017, after extensive research, Jeff figured out the cause of his own ME and has remained in remission since his craniocervical instability (CCI )and tethered cord surgeries. His experience has lead to a re-evaluation of both what constitutes ME/CFS and how CCI occurs as well. 

Jeff developed the Mechanical Paradigm in 2018 which proposes a connection exists between ME and mechanical neurological conditions – specifically those associated with connective tissue disorders.

He has been calling for more research into these connections.

Check out blogs and other resources including Jeff’s startling story in Health Rising’s Fibromyalgia and ME/CFS Spinal Resource Center

Fibromyalgia and ME/CFS Spinal Resource Center


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