Functional neurological disorder — FND — is the second most common reason for outpatient neurology consultations after headaches. Second most common. So it's not particularly rare. And yet it's one of the most misunderstood diagnoses out there. To be honest with you, a lot of that misunderstanding comes from where the diagnosis came from historically.
So let me break that down.
The Problem With How FND Has Been Understood
Dr. Mark Edwards and Jon Stone did a really good job articulating what FND actually is. What they said was that FND describes motor (so movement) and/or sensory (feeling) symptoms that arise from the voluntary motor or somatosensory nervous system — and they're experienced as involuntary. Let me say that again. The symptoms come from the voluntary motor system or the sensory system, but the patient experiences them as involuntary movements, involuntary sensations.
OK so that's the clinical definition. But here's the part that creates the uphill climb for patients.
FND has been conflated — lumped in — with previous diagnoses like "psychogenic disorders" and "conversion disorders." And what those labels meant historically was malingering. Feigning. Faking symptoms, right? There was actually a study done that showed both neurologists and psychiatrists, when surveyed, considered a proportion of feigning as intertwined with or the same thing as FND.
So you can see, for people that are dealing with functional neurological disorders there's an uphill climb toward a resolution for these — because quite frankly the toolbox is pretty small.
A 17-Year-Old With Fainting and Pseudoseizures
I want to share a case that came through the clinic because I think it makes this real. This was a 17-year-old female with a history of fainting. She'd been subsequently diagnosed with functional neurological disorder. But her fainting wasn't just dropping to the floor — it was associated with a type of pseudoseizure where there was a movement disorder component, a tremor portion. And these episodes were happening several times a day and kept increasing.
They did photic stimulation with an EEG in the hospital — that's where they hook you up and do a flashing light to check for epileptiform activity — and when she went through that, her symptoms actually ramped up. More frequent episodes. More prolonged. More motor involvement.
The types of episodes she was having included mild jerking of her limbs and head. She was having difficulty walking. And here's one that was really important for us: she was drifting to the side as she walked, and she couldn't control it. She felt like her body was just carrying her over.
And when most people look at something like that, it's very easy for their mind to go "oh, that's not real, she's faking it." Right? It's really hard to get a good honest look at a case like this when that's the backdrop.
What We Found When We Actually Looked
Her legs were giving out. Things were worse when standing up. Episodes typically lasted a couple minutes but could go anywhere up to half an hour, an hour. After they were done she'd feel relief. What was interesting was that during these episodes she was non-verbal — couldn't communicate, couldn't move — but she had the perception that she could still hear and be aware of what was going on around her.
Episodes were made worse with too much mental activity or too much physical activity. And then we found something critical in evaluation: simply being upright, being in orthostasis, made things harder for her.
The only thing that helped her feel better was laying down. And while in the hospital, they gave her IV saline and that gave her several hours of relief afterward. That's a clue. That's a really helpful little anecdote for the diagnostic process, right? It didn't last — couple hours, felt really nice — but it tells us something about the pathology.
The orthostatic connection: A physician noticed that her tachycardia and palpitations were mostly happening as a consequence of orthostasis. She could lay down and get relief. She could recover. But when she stood back up — tachycardia, then symptoms would evolve. As long as it didn't progress into the loss of consciousness phase, she could get back down and try to recover. So super helpful.
The Autonomic Findings
We confirmed what the other doctor had already noticed. There was an acceleration of heart rate when she was in an orthostatic position. We saw a baseline level of heart rate activity, baseline blood pressure, and then a drop in blood pressure — not on the scale of orthostatic hypotension, but enough of a dip that she had to have a cardiac response.
Said in easier words: her heart rate wasn't just going rogue on its own. It was compensating for the fact that she wasn't getting adequate blood pressure.
And we were able to measure that with Doppler ultrasound of middle cerebral activity in the brain. We could actually see that she was losing blood flow in her brain. Which makes a lot of sense for the symptoms she was having.
On the tilt table test she developed her symptoms asymmetrically — stereotyped movements in the right leg, posturing overhead to one side, fluttering of her eyes in one direction. These are really helpful in understanding that this isn't like a global hypoxia. We're actually seeing pathway genesis where she's losing blood flow in some specific areas.
What the Eye Movements Told Us
We looked at her oculography — her eye movement testing — and this is where it gets really interesting. We had her do vertical saccades, which are eye movements jumping to targets up and down, randomly spaced throughout the vertical plane. What you'd want to see is crisp, sharp movements. What we saw was slow, delayed movements. And at one point her eyes did this little swirl.
That little swirl is really helpful. It tells us about the integration happening between areas in the cerebellum, the brainstem, and the frontal lobe — the pathway that helps your eyes move in that plane. So her eyes were slow going down, slow going up. They should snap. Snap, snap. Instead we see that swirl, and then her eyes drift with her head movement. She develops a right head turn and her eyes drift over to the left side.
These little subtle indicators tell us these pathways in the brain are not working optimally. And this test was done seated — so she's in a degree of orthostasis, not purely laying down.
We also tested pursuit movements — smooth tracking instead of jumps. Pursuits come from a different mechanism, generated largely based on information your visual system takes in through the parietal eye fields rather than the frontal eye fields. When you compare how those two different pathways perform, you start to understand what's going on. Her eyes were jumpy and they were jumpy side to side — which, if you're following a target going straight up and down, there's no reason for your eyes to move side to side and do those swirls.
We also found with the Maddox Rod test that her eyes were skewed — at 20 feet away they didn't aim at the same spot. They aimed at slightly different places. This tells us about how her brain is directing the whole symphony of eye movement coordination, posture coordination, and delivering blood to her brain.
How We Treated It (With a Caveat)
Before I get into the treatment, I want to be really clear: this is what we did in this case. It's not an invitation to try this on everybody you see or to try it on yourself. It's an invitation to understand how I thought about a case. Don't run and do this at home.
So what we noticed was the point in her orthostasis where things start to fail. We started at the very baseline — laying flat, zero degrees — and worked on subtle head movements, side to side, opposite of the plane where she had the hyperkinetic movement. Just simple gaze fixation with her head turning only about three degrees in either direction.
And I did it passively. That's the key. If I turn her head slightly and control the rotation of her spine with my hands while she looks at a target, she is not generating the movement. She's getting feedback about the movement from her body. Remember from the definition — there's a mismatch between what's experienced as voluntary versus the outputs from the motor system or the inputs from the sensory system. So we are commandeering the sensory system. We're taking it over.
And when we did that, she was able to generate smoother movements. We could then bring her up incrementally — watching for the stereotyped movements in her legs, watching for acuity in her eyes, making sure she didn't fall into a convergent spasm.
We did that slowly over the course of days. She could sit up and move and walk without drifting to the side. Longer time periods between episodes. She was able to tolerate movement with her eyes and a moving environment better and better and better, sequentially.
The objective evidence: When we repeated the vertical pursuit test a couple days in, you could compare the eye movements directly. Still not perfectly smooth yet — but the horizontal deviations were gone. No more swirling. Even though it wasn't a perfect home run, the objective signs were starting to transfer into her experience of her subjective reality. Which is awesome.
Getting to Upright, Getting to Life
We continued until we got her to an upright position and she was able to actively turn her own head. Then we transitioned to exercises in our whole body rotation device — a chair with goggles on, fixated on a target, rotating back and forth. It's a little harder than me doing it passively, but it's still her body getting a stimulus. That stimulus allowed her to attenuate — to calm down — the hyperkinetic myoclonus she was experiencing.
We did this over the course of a couple weeks and then transferred it to tools she could use at home. So that she could get out of the wheelchair. Be able to go to school. Sit through class with all of the movement and sensory information. Walk to class without getting triggered. And then ultimately pursue higher education and the extracurricular activities she was involved in.
Why This Matters: The Blood Flow Connection
Here are the key points. We could find the levels of orthostasis where her symptoms were brought out by positioning — where her brain doesn't understand how to get blood into the head. That further exacerbates the firing rates she experiences with the syndrome. She has these symptoms, but the pathway responsible for them — when you take blood away from it, it's going to do worse.
So by allowing blood flow to exist in that pathway and then slowly exercising that pathway, she was able to get some purchase. She was able to get some momentum in being able to rehabilitate that and take part in the process and solve it herself. Which is pretty beautiful.
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