The Connective IssueThe Fascia Institute & Treatment Center Journal
A weekly report from the line of scrimmage of fascia medicine — where grit, recovery, and getting back in the game meet.
Four patients, four confident answers, and all four were wrong.
This week’s issue has one theme running underneath all of it: the difference between a test result and an explanation. They get confused constantly, and it costs people years.
In football, a “read” is what the quarterback does in the second and a half before the ball leaves his hand. He looks at the defense, decides what it’s doing, and commits. Get the read wrong and it doesn’t matter how good the throw is.
Medicine does the same thing, with the same time pressure and higher stakes. And in musculoskeletal medicine specifically, we have a bad habit: we get a piece of data, we call it the answer, and we commit.
So this week: your lumbar MRI report, and why the degenerative findings on it are almost certainly also on the MRI of the person sitting next to you who feels fine. Then why hypermobility cannot be reduced to a protocol, which is the most common question I get from other clinicians. Then a differential I wish every emergency department knew — the episodes in hypermobile patients that get called seizures or strokes and turn out to be neither. And a case report: facial twitching, a normal brain MRI, and an answer in the trapezius.
A warning about that last one, up front: it’s a single case. I’ll tell you exactly what it can and can’t prove, because a case report that oversells itself is worth less than no case report at all.
Also inside: OxeFit assessments are free for the entire month of September in both cities, and September is now four days away. And the person who makes FIT Therapeutics actually work — Tyler Bazley, who has quietly done nearly every job in the building.
Read the defense before you throw. Let’s kick off.
In This Issue
- Your Back Hurts. Your MRI Isn’t Why. Highlight Reel
- No Two Cases of Hypermobility Are the Same Game Plan
- When It Isn’t a Seizure and It Isn’t a Stroke Special Teams
- Facial Twitching, Normal MRI, and the Trapezius Film Room
- OxeFit Is Free All September Free Kick
- Team Spotlight: Tyler Bazley MVP
- The Ten-Minute Stand Test Two-Minute Drill
Your back hurts. Your MRI probably isn’t why.
Low back pain is the single largest cause of disability on earth. It is also the condition where the gap between what we image and what we explain is widest.
Low back pain is the leading cause of years lived with disability worldwide — ahead of every other condition, accounting for roughly 69 million years lived with disability in 2020 (Global Burden of Disease 2021, Lancet Rheumatology). And one detail from that data undercuts how most people think about it: prevalence doesn’t peak in working-age adults hauling boxes. It peaks at age 85.
So this is not a niche problem, and it is not a young laborer’s problem. It’s nearly everyone’s problem eventually. Which makes it worth being precise about.
The most useful thing I can tell you about your imaging
Someone read your MRI and used words like degenerative disc disease, disc bulge, facet arthropathy. Those words feel like a diagnosis. Here is what happens when you run the same scan on people with no back pain at all.
Systematic Literature Review of Imaging Features of Spinal Degeneration in Asymptomatic Populations
Brinjikji, Luetmer, Comstock, Bresnahan, Chen, Deyo, Halabi, Turner, Avins, James, Wald, Kallmes & Jarvik
American Journal of Neuroradiology · 2015 · 36(4):811–816 · 33 studies, 3,110 people with no symptoms
Every one of those people felt fine. Disc degeneration was present in 37% of asymptomatic twenty-year-olds and 96% of asymptomatic eighty-year-olds. Disc bulges climbed from 30% to 84%. The authors’ own conclusion is the sentence to carry with you: these findings are “likely part of normal aging and unassociated with pain.”
This isn’t new, either. In 1994, researchers scanned 98 people with no back pain and found that only 36% had normal discs at every level (New England Journal of Medicine). Four years before that, a study of 67 people who had never had back pain, sciatica, or claudication found that about a third had a substantial abnormality on MRI (Journal of Bone and Joint Surgery). We have known this for more than thirty years. It has barely changed how reports are written.
Now the honest other half
I’m not going to tell you imaging is useless, because that’s the opposite error and it’s also wrong. The same research group ran the reverse comparison — people with back pain against people without — and some findings really do track with pain. In adults aged 50 and under, disc extrusion was roughly four times more common in people with back pain, Modic type 1 changes about four times, disc protrusion about two and a half times, disc degeneration about two and a quarter times.
Note what’s on that list and what isn’t. Extrusion matters. A bulge — the single most common word on the reports I read — did reach statistical significance, but with a confidence interval so wide that the true size of the effect is barely pinned down at all. And the study only covered people 50 and under; nobody should stretch it past that.
So the accurate statement isn’t “MRIs are meaningless.” It’s this: a lumbar MRI is very good at finding things and quite poor at telling you which of those things is generating your pain. Which is exactly why getting one early doesn’t help you. Six randomized trials covering 1,804 patients compared immediate imaging against usual care for back pain, and found no benefit in pain or function, short-term or at a year (Lancet, 2009). In one of those trials, the group that got rapid MRI had more lumbar operations — 10 versus 4 — a difference that didn’t reach statistical significance, but points in a direction worth noticing.
What the surgical trials actually say
“Non-surgical” is in the title of the article this piece comes from, so let me be careful and fair here, because surgery is sometimes exactly right and I refer patients for it.
For sciatica from a disc herniation: surgery is faster, not better
283 patients with severe sciatica were randomized to early surgery or prolonged conservative care (New England Journal of Medicine, 2007). Median time to recovery was 4.0 weeks with surgery versus 12.1 weeks without — a real, meaningful difference if you’re the one in pain. But at one year, the probability of perceived recovery was 95% in both groups, and the difference in disability across the whole year wasn’t statistically significant. Surgery bought time. It didn’t buy a better destination.
The big American discectomy trial can’t answer the question
The SPORT trial randomized 501 patients — and then half the surgical group and 30% of the non-surgical group crossed over within three months. The authors say so themselves, plainly: because so many patients crossed in both directions, “conclusions about the superiority or equivalence of the treatments are not warranted.” Anyone quoting SPORT as proof either way hasn’t read the discussion.
For back pain from degeneration, fusion is a different story
The UK’s Spine Stabilisation Trial (349 patients, BMJ 2005) found fusion beat rehabilitation by 4.1 disability points — described by its own authors as “marginal and only just” at the threshold of clinical meaning, against a roughly 11% surgical complication rate. Two Norwegian trials found no advantage over cognitive treatment plus exercise. A 2018 review in the Internal Medicine Journal concluded there are “no high-quality systematic reviews” and that the evidence “does not support a benefit from spine fusion compared to non-operative alternatives for back pain associated with degeneration.” The UK’s national guideline is blunter: do not offer spinal fusion for low back pain except as part of a randomized trial.
And more fusion is not better fusion
A 2016 New England Journal of Medicine trial of 247 patients found that adding fusion to decompression did not improve outcomes at two or five years — while more than doubling blood loss and adding roughly an hour to the operation. Meanwhile, Medicare data showed complex fusion rates rising fifteen-fold in six years, with life-threatening complications climbing from 2.3% to 5.6% and average charges from about $24,000 to about $81,000.
None of that means don’t have surgery. It means the burden of proof has been quietly reversed in most people’s minds. Surgery is presented as the definitive option and conservative care as the thing you try while you wait. For disc-related sciatica, the trials say conservative care gets most patients to the same place more slowly. For back pain attributed to degeneration, they say fusion has not earned its reputation.
What guidelines actually recommend first
The American College of Physicians reviewed this in 2017 and put non-drug treatment first for acute and subacute low back pain — superficial heat, massage, acupuncture, or spinal manipulation — with medication as the fallback rather than the opening move. For chronic low back pain, the first-line list is exercise, multidisciplinary rehabilitation, acupuncture, and mindfulness-based stress reduction, followed by a longer list of lower-certainty options including yoga, tai chi, motor control exercise, cognitive behavioral therapy, and spinal manipulation.
The item with the most solid evidence on that entire list is supervised active rehabilitation. It is also the least marketable thing in medicine, which is roughly why you’ve heard less about it than about everything else.
Where fascia comes in — and where it doesn’t yet
This is my field, so I’m going to hold it to a stricter standard than I’d hold anyone else’s.
What is well established: the thoracolumbar fascia — the broad sheet across your low back — is densely innervated, and the nerve endings that signal pain are concentrated in its outer layers. That work was quantified in animal tissue with a preliminary human examination alongside it (Neuroscience, 2011). More directly: when researchers injected irritant saline into twelve healthy volunteers’ muscle, fascia, and the tissue just under the skin, the fascia injections hurt longer, radiated further, and were described as burning and stinging more than the muscle injections (Pain, 2014). Fascia is not inert packing material. It generates pain.
What is suggestive: people with chronic low back pain appear to have less fascial glide. In a study of 121 people, ultrasound measured shear strain during passive trunk flexion at 56.4% in the back pain group versus 70.2% in those without — roughly a fifth less movement between layers. A companion study of 107 people found the fascia about 25% thicker and more echogenic in back pain patients, though that finding correlated strongly with body mass index, which complicates it. The authors themselves decline to say which came first — abnormal movement patterns or the tissue changes.
What is not settled: whether hands-on fascial treatment reliably reduces back pain. Two meta-analyses published in the same year reached opposite conclusions. One pooled eight trials of 375 patients and found a small benefit for pain. The other found no significant effect on pain intensity at all — and, tellingly, found that adding myofascial release on top of spinal manipulation added nothing measurable. That is the honest state of the evidence, and I’d rather you hear it from me.
So what do we actually do differently
Two things, and neither is a machine.
First, we examine before we image, and we image dynamically. Diagnostic ultrasound lets us watch tissue move while you move it, which is where gliding problems reveal themselves and where a static MRI is structurally unable to help. Its limits are real and worth stating: ultrasound cannot see the spinal canal, the disc itself, bone, or marrow. It is not a replacement for MRI. It answers a different question.
Second, we do not tell you your problem is whatever we happen to own. Several of the treatments we offer — shockwave, PEMF, TECAR, hydrodissection, prolotherapy, PRP — do not appear in the ACP or UK guidelines for low back pain at all. That absence is a fact you should know before you consent to any of them. We use some of them, selectively, on the basis of anatomy and clinical judgment rather than on the basis of trial evidence that does not yet exist for this indication. Anyone telling you these are “proven” or “evidence-based” for back pain is telling you something that isn’t true.
That’s a strange thing for a clinic to put in a newsletter. I’d rather you decide with the real numbers.
Educational information only, not medical advice, and not a recommendation for or against any procedure. Back pain with fever, unexplained weight loss, a history of cancer, progressive weakness, numbness in the saddle area, or loss of bowel or bladder control needs urgent in-person evaluation — not a newsletter. Prolotherapy, PRP, and hydrodissection are not FDA-approved for these indications and are generally not covered by insurance.
No two cases of hypermobility are the same.
The question I get most often from other clinicians is what our hypermobility protocol is. The honest answer is that we don’t have one, and that the wish for one is the problem.
A protocol is a good thing. It reduces variation, it prevents forgetting, and it works beautifully when you have a reasonably uniform population and a reasonably predictable disease. Hypermobility is neither.
Look at what the surveys find. In one large global survey of people meeting hypermobile Ehlers-Danlos criteria, the average patient carried around two dozen comorbid conditions. In a registry study of 505 people with clinically confirmed hEDS, the average was more than ten separate co-diagnoses per person, with anxiety in 75%, depression 68%, migraine 67%, POTS 61%, and irritable bowel syndrome 57%.
Now imagine writing one protocol for that. Two patients both labeled “hypermobile” can share almost nothing clinically: one has debilitating gut dysmotility and stable joints, the other dislocates a shoulder reaching for a seatbelt and has a perfectly ordinary GI tract. Averaging them produces a plan that fits neither.
The definition itself moves
Here’s the part that should give anyone pause. Depending on which study you read, “hypermobile” means a Beighton score of 4 or more, or 5 or more, or a five-question self-report survey, or the full 2017 diagnostic checklist. These are not the same population.
The consequence is visible in the literature. A recent systematic review pooling more than 8,000 EDS patients and nearly 13,000 POTS patients found that the reported rate of POTS among EDS patients ranged from 17.5% to 92.7% across studies. That is not biological variation. That is mostly definitional drift — different studies counting different people and using the same word.
What replaces a protocol
Not improvisation. A protocol answers what do we do. What these patients need answered first is what is actually going on with you — and that requires an ordered way of looking, not an ordered way of treating.
- Which joints are actually unstable, and in which direction — not a global score. A Beighton number is a screening tool. It tells you almost nothing about which structure is failing under load.
- Whether the autonomic system is involved — and if so, how much of the fatigue, brain fog, and exercise intolerance belongs to that rather than to the joints. See the next section; this is frequently the biggest single contributor and the most frequently missed.
- What the connective tissue looks like under ultrasound — imaged while it moves, since laxity is a behavior rather than an appearance.
- Whether a genetic evaluation would change management — which is the only good reason to order one. Some hypermobility syndromes carry vascular or cardiac risk that changes what we do and how urgently. Most do not. Finding out which you have is worth the visit.
- What the metabolic picture is — because tissue that cannot heal often has a reason, and it is frequently a correctable one.
- What the patient has already been told — which sounds soft and is not. Most of these patients arrive after years of being disbelieved, and that history shapes what they will report to you and what they will leave out.
Then, and only then, the treatment plan — which will be different for the person with a lax shoulder and the person with orthostatic collapse and the person with both. Same diagnosis on the chart. Different problem in the room.
Comorbidity figures above come from patient registries and specialty-clinic surveys, which recruit people who are already symptomatic and already seeking answers. Real-world community rates are almost certainly lower. Genetic testing is appropriate in selected cases, not as a routine screen.
When it isn’t a seizure, and it isn’t a stroke.
Four very different things can look nearly identical from the foot of the bed. Telling them apart is most of the job — and in hypermobile patients, it goes wrong often.
A patient goes down. There’s jerking. Someone calls it a seizure, and from that moment forward the chart says seizure, and everything that follows — the EEG, the medication, the driving restriction, the years — follows from that word.
Sometimes it’s right. Often enough that it should worry all of us, it isn’t.
Start with the most misread sign in medicine
In 1994, researchers deliberately induced fainting in healthy volunteers and filmed it. Of 42 complete faints, 38 — ninety percent — involved myoclonic jerking. These were healthy people with no neurological disease whatsoever. The unconsciousness lasted an average of about twelve seconds.
Jerking during a faint isn’t a warning sign. It’s the norm.
What distinguishes it is the character and the count. A 2018 study in Neurology compared 65 tilt-induced faints against 50 convulsive seizures on video with simultaneous EEG. The faints produced a median of 2 jerks, essentially never more than about ten, brief and disorganized, with loss of muscle tone. The seizures produced a median of 48, rhythmic and sustained. Those distributions barely overlap.
That last number deserves its own paragraph. In a 2000 study in the Journal of the American College of Cardiology, 74 patients who already carried a diagnosis of epilepsy were put on a tilt table with simultaneous heart and brain monitoring. An alternative diagnosis was found in 31 of them — 41.9%. The most common alternative was ordinary vasovagal syncope. Nineteen patients had profound drops in blood pressure or heart rate on tilt. Some had been taking anticonvulsants for years.
Where hypermobility enters
Two separate connections, and they should not be blurred together.
The orthostatic one. POTS and hypermobility travel together. In one tilt-table study of 35 adults with hypermobile Ehlers-Danlos, 49% met POTS criteria; in a study looking the other direction, 31% of 91 POTS patients met the clinical criteria for hEDS. Depending on how it’s measured and who’s counted, roughly a third to two-thirds of hypermobile patients have POTS, and roughly a third of POTS patients are hypermobile. Anyone quoting you a single precise percentage is quoting one study out of dozens.
Why it matters here: a patient with orthostatic intolerance faints more, faints upright, faints in heat and after standing in line — and faints with jerking, ninety percent of the time. That is a pattern that looks like epilepsy to anyone who wasn’t watching closely.
The functional one. Functional seizures — also called dissociative or non-epileptic seizures — also cluster with hypermobility. In a 2022 study in Epilepsy & Behavior, 57% of 42 patients with functional seizures met criteria for joint hypermobility, against 21% of 34 matched controls. Note the careful wording: they met criteria for joint hypermobility on examination. Nobody diagnosed them with hEDS.
Functional seizures are real, and they are not voluntary
This needs saying plainly, because the way this diagnosis gets delivered causes enormous damage. A functional seizure is not faking. It is not attention-seeking. It is an involuntary event produced by a genuine disruption in how the brain processes and predicts signals from the body, and imaging studies find measurable differences in patients who have them. The evidence that patients aren’t feigning is partly behavioral: people with functional neurological disorders relentlessly pursue investigation and treatment, which is the opposite of what feigning looks like. In one registry of people with hEDS, a functional neurological disorder diagnosis was rejected by 95% of those who received it — the highest rejection rate of any diagnosis they had been given. A label that gets refused by 95% of recipients is being delivered badly, and that is a separate question from whether it is accurate.
The four things that look alike
| Epileptic seizure | Convulsive faint | Functional seizure | Stroke-like spell | |
|---|---|---|---|---|
| Position at onset | Any — including lying down or asleep | Almost always upright; often heat, dehydration, standing still, pain, a blood draw | Any; often situational | Any |
| Warning | Aura, or none at all | Distinct fade: lightheaded, greying vision, sound going distant, sweating, nausea | Variable; may build over minutes | Symptoms march over minutes — visual, then sensory, then speech |
| Time unconscious | Roughly one to three minutes | About twelve seconds | Often much longer | Usually awake throughout |
| Jerking | Rhythmic, sustained, slowing — median 48 jerks | Brief, disorganized, with loss of tone — median 2 jerks | Often asynchronous; side-to-side head movement; stopping and restarting | Absent |
| Recovery | Confused for minutes; headache, soreness, sleepiness | Reorients within seconds once flat; drained for hours | Variable; may recall the event; may not be confused | Clears over minutes to hours, often with headache |
| Better lying flat? | No | Yes — the defining feature | Not characteristically | No |
Two features get over-read constantly and belong in every version of this conversation. Incontinence does not distinguish these — it happens in epileptic, syncopal, and functional events alike, and it is routinely treated as proof of epilepsy. And jerking, as above, is the most over-read sign of all. The feature that genuinely earns its reputation is a bite to the side of the tongue, which is uncommon but, when present, points strongly toward an epileptic seizure.
The cheapest useful test in this entire differential
A ten-minute stand. Heart rate and blood pressure lying down, then again on standing at one, three, five, and ten minutes. The 2015 expert consensus criteria for POTS are a heart rate rise of at least 30 beats per minute within ten minutes of standing (at least 40 for ages 12 to 19), with orthostatic symptoms and without a drop in blood pressure that would define orthostatic hypotension instead.
It requires a blood pressure cuff and a clock. It is frequently just not done. There’s a version of it you can do at home in this week’s Two-Minute Drill.
Four things I am not saying
- I am not saying hypermobility causes seizures. These are associations found largely in specialty referral clinics and patient registries — populations enriched for exactly these overlaps. The mechanism people propose involves interoception, the brain’s reading of its own internal state, which we covered back in Vol. X. It is a plausible hypothesis and it is not a demonstrated causal chain.
- I am not saying hypermobile people don’t get epilepsy. They do, at whatever the background rate is. There is also a genuine but rare structural link between certain connective tissue disorders and epilepsy, involving a specific gene and a specific brain malformation — and it is a distinct condition, not hEDS. If your events are epileptic, they need epilepsy treatment.
- I am not saying hypermobility causes strokes. Meaningful arterial risk lives in vascular EDS, a different and rarer diagnosis. In one review of 258 patients referred to a hypermobility clinic, spontaneous coronary or cervical artery dissection occurred in 5 of 258 — 1.9%. Small, real, not zero.
- And I am not saying treating POTS will stop functional seizures. I looked for that evidence specifically and it does not exist. What does exist: a randomized trial of 223 patients found that simple physical counterpressure maneuvers cut vasovagal syncope recurrence from 50.9% to 31.6%. And for functional seizures, the largest randomized trial to date found that CBT did not significantly reduce monthly seizure frequency at a year, though it improved several other outcomes that patients care about. If the mechanism is orthostatic, treat the orthostatic problem. If it’s functional, that’s a different road, and honesty about how hard that road is serves people better than optimism.
There’s an opposite error worth naming too, and it’s the one I worry about in my own patients. Once POTS or hEDS is written on a chart, every new symptom risks being filed under it. A genuinely new focal deficit in a hypermobile patient is not automatically dysautonomia. Given that dissection figure, that assumption can be expensive.
This is educational information, not a diagnostic tool, and the table above is a teaching aid rather than a checklist to apply to yourself or anyone else. Loss of consciousness, convulsive events, and new neurological symptoms require in-person evaluation. Sudden weakness on one side, facial droop, or trouble speaking is a medical emergency — call 911.
Facial twitching, a normal MRI, and an answer in the trapezius.
One patient. A clean brain scan. A finding nobody had looked for. And a set of limits I want to state before the story, not after it.
Let me put the caveat first, because it belongs first. This is a single case. A case report can show that something happened. It cannot show that it happens generally, that it will happen for you, or that what we did is what caused it. And there is a specific confounder here that I want on the table: benign muscle twitching is extremely common — fasciculations occur in something like 70% of healthy people — and it usually resolves on its own. A patient whose twitching stopped after treatment cannot be cleanly distinguished from a patient whose twitching stopped on schedule.
With that said, this case is worth publishing, because the reasoning it illustrates generalizes even where the outcome doesn’t.
What a normal brain MRI does and doesn’t settle
Facial twitching gets imaged, appropriately, because the differential includes things you must not miss. A normal scan meaningfully lowers the probability of a tumor, a demyelinating lesion, or a gross vascular anomaly. That is real reassurance and it matters.
What it does not do is identify a cause. It doesn’t even exclude the most common structural explanation. In hemifacial spasm, the classic mechanism is a blood vessel contacting the facial nerve — and that same contact is present in roughly 37% to 53% of people with no symptoms at all. A finding that common in healthy people cannot carry a diagnosis. Meanwhile, a routine brain MRI — often not the thin-slice posterior-fossa protocol required to see the relevant anatomy — misses a meaningful minority of true compressions.
So a normal MRI converts the question from where is the lesion to what else could be driving this. In this patient, nobody had asked the second question.
The mechanism that makes the neck a reasonable place to look
Here is the part that’s solid, and it isn’t a fascia argument — it’s brainstem neuroanatomy.
The nerves carrying sensation from your face and the nerves carrying sensation from your upper neck do not stay separate. The trigeminal sensory nucleus is continuous with the dorsal horn of the top three cervical segments, forming one uninterrupted column called the trigeminocervical complex. Facial and upper-cervical inputs converge onto the same second-order neurons there. This has been mapped directly in animal recordings: stimulating the greater occipital nerve at the back of the head increases the responsiveness of neurons receiving input from the covering of the brain, and the effect runs both directions.
That explains face and head pain from a neck source. The step that makes this case plausible is a human study that went further.
Functional connectivity between trigeminal and occipital nerves revealed by occipital nerve blockade and nociceptive blink reflexes
Busch, Jakob, Juergens, Schulte-Mattler, Kaube & May
Cephalalgia · 2006 · 26(1):50–55 · 15 healthy subjects
Fifteen healthy volunteers had one greater occipital nerve blocked with local anesthetic. The researchers then measured the blink reflex — a circuit that comes in on the trigeminal nerve and goes out on the facial nerve to the muscle around the eye. On the injected side, the reflex response shrank and slowed. On the other side, nothing changed. Sensory and pain thresholds were unaffected.
Read that again, because it’s the whole basis of looking at the neck in a facial movement problem: changing input from the back of the neck measurably changed the excitability of a facial motor reflex in living humans.
One correction I want to make in print
There is a version of this story that gets told wrong, and I’d rather correct it than let it circulate. The nerve to the trapezius — the spinal accessory nerve — is purely motor. It supplies the trapezius and the sternocleidomastoid and nothing else. It carries no sensory fibers and it innervates no facial muscle. Irritating it cannot produce facial twitching.
The plausible route is not that nerve. It’s the sensory roots of the upper cervical spine feeding into the trigeminocervical complex. If anyone explains a case like this to you by way of the accessory nerve, they’ve got the anatomy backwards.
What the trapezius region does supply is the setting. The greater occipital nerve passes through the semispinalis capitis in about 90% of people and through the trapezius in about 45% — so muscle and fascia there are genuinely positioned to affect a nerve. And in a study of 25 patients with chronic trapezius myofascial pain, nerve conduction was measurably delayed on the symptomatic side, with 7 of 25 showing delayed latency. Tissue in that region can compromise nerves. That is established.
Why the exam missed it, and why that’s normal
My favorite study on this point is thirty years old. A hundred whiplash patients were investigated with controlled diagnostic blocks; 27% turned out to have headache arising from a single small cervical nerve. The authors’ conclusion was that there were no distinguishing features on history or examination that identified them beforehand.
A common, treatable, cervical source of head symptoms — invisible to history and physical exam. That is not a criticism of anyone’s clinical skill. It’s an argument for a different kind of looking.
Where I have to stop
Now the gap in the story, stated plainly, because papering over it would make everything above less credible.
Referred pain from the neck to the face is well established. Referred movement is not. There is no demonstrated pathway by which a neck muscle generates involuntary contraction in a facial muscle. The Busch study shows the neck can modulate the gain of a facial reflex — not that it can generate spontaneous twitching from nothing. And I found no published case of trapezius or cervical fascial treatment resolving facial twitching. Not a series, not a trial. The nearest thing in the literature is a single case of ear twitching after a whiplash injury that improved with manual therapy and exercise.
I should also note that the trigger-point framework often used to explain cases like this rests on shakier ground than its confidence suggests: when researchers pooled studies of examiners trying to agree on where trigger points are, agreement was moderate at best, and the specific features clinicians rely on most were the least reliable of all.
So what is this case actually good for? It is a documented instance of a patient with a normal brain MRI, a symptom nobody could explain, a cervical finding nobody had looked for, and improvement after that finding was addressed. That is worth writing down. It is worth other clinicians knowing to look. It is not worth a protocol, a claim, or a promise, and you should be skeptical of anyone who converts it into one.
Published with the patient’s permission. A single case report cannot establish that a treatment works, and this one does not. Individual results vary. New or changing facial movements, facial weakness, facial numbness, hearing change, or twitching that spreads or involves both sides warrant neurological evaluation — do not substitute this article for one.
Last call before the free month starts.
This is the final issue before September. For the whole month, OxeFit assessments cost nothing — New Orleans and Beverly Hills both.
The cover story argued that the problem with back pain care is measuring the wrong thing and then committing to it. This is the cheap version of measuring the right thing.
Most people have no objective idea how their body is performing. You know whether something hurts. You don’t know whether your left side is quietly doing sixty percent of the work, whether your force production has dropped since last year, or where you’re compensating in a way you can’t feel.
OxeFit gives you that in numbers — how you produce and absorb force, strength, balance, symmetry between sides, movement quality — and turns it into a baseline you can act on and re-check later.
- Anyone with a back that’s been bothering them — a starting point that isn’t a disc bulge you share with most people your age.
- Hypermobility and connective-tissue patients — a stability and control baseline that’s notoriously hard to capture any other way, and one of the measurements the section above is built on.
- Anyone coming back from injury — objective proof of where recovery actually stands, not just how it feels.
- Anyone over 40 — the earliest strength and balance changes are the ones worth catching.
September starts Tuesday and a free month tends to fill. Pick your city and get on the calendar — first come, first served.
September 1–30, 2026 · by appointment and subject to availability. An assessment is not a diagnosis and does not predict injury.
Beverly Hills
The Fascia Institute LA
Same assessment, same offer, on the West Coast.
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Tyler Bazley · Practice Operations Manager, FIT Therapeutics
Every clinic has one person who knows where everything is and how everything works. Ours has been here more than four years and has done nearly every job in the building.
Most of what patients notice about a clinic has nothing to do with medicine. The room is clean or it isn’t. The thing your clinician reaches for is stocked or it isn’t. Someone knew you were coming, or someone didn’t. Those are the details that decide whether you feel cared for, and they are almost never the doctor’s doing.
At FIT Therapeutics they’re Tyler’s.
Tyler is our Practice Operations Manager, and his job description is short and enormous: every patient who walks in is treated like a VIP. The space is clean. It’s stocked. The experience holds to FIT standards on a Tuesday afternoon in the middle of a hard week, not just when someone’s watching. Standards are easy to write down and brutally hard to maintain, and maintaining them is the entire job.
Why he can do the job
Tyler has been with us more than four years and has worked most of the jobs at FIT along the way. That’s the part I’d point to. You cannot run an operation you’ve only ever seen from above — you need to have stood in each position and felt where it breaks. He understands the system because he has been most of the system. Which is why he’s the person everyone goes to, for everything, and why the answer is usually already handled by the time it reaches me.
I’ve called him our go-to guy for years, and I want to be more specific than that, because “go-to guy” undersells it. Tyler is one of the most reliable employees I have ever had. Not the most reliable this year — ever. In a field with the turnover ours has, that is not a small sentence and I don’t hand it out.
If you’ve been to FIT and the visit simply worked, you’ve already met his work. Say hello to him next time.
The ten-minute stand test.
The single most informative thing you can measure at home about orthostatic intolerance. It needs a blood pressure cuff, a clock, and someone in the room with you.
Read this part first. If you have fainted before, do not do this alone — have someone with you, and do it where you can sit or lie down immediately. If you feel lightheaded, hot, nauseated, or your vision starts to grey out, stop and lie down. The point is to gather information, not to push through to a faint. And if you have a heart condition or you’re unsure whether this is safe for you, ask your physician before trying it.
The protocol. Lie flat and quiet for five minutes. Take your heart rate and blood pressure. Then stand up, stay still, and take both again at one, three, five, and ten minutes. Write all five sets down. That’s the whole thing.
What it’s looking for. The expert consensus criteria for POTS involve a sustained heart rate rise of at least 30 beats per minute within ten minutes of standing — at least 40 for ages 12 to 19 — along with orthostatic symptoms, and without the blood pressure drop that would indicate orthostatic hypotension instead. The reason the ten-minute mark matters is that plenty of people look fine at one minute and don’t at eight.
What to do with it. Bring the numbers to your appointment. A written page of five paired readings is far more useful than “I get dizzy when I stand up,” and it’s the kind of data that gets a conversation moving after years of it not moving.
What it is not. Not a diagnosis, and not a substitute for a proper evaluation. A single abnormal reading proves nothing — heart rate on standing varies with heat, illness, hydration, sleep, caffeine, and where you are in your cycle. A normal result doesn’t rule anything out either. It’s one input.
Not medical advice. This is an educational description of a clinical test, not an instruction to self-diagnose or self-treat. Do not start, stop, or change any treatment based on the result. Anyone under 18 should do this only with a parent present and discuss it with their pediatrician.
Missed last week? Catch up on Vol. XII — what the evidence really shows about creatine and fascia hydration, the whole diagnostic playbook, and a high hamstring injury resolved in two visits.