POTS Found After FND: Comorbidity, or a Common Phenotype?
FND Nope
Moderator
A 2026 case report in the American Journal of Case Reports describes an 18-year-old woman diagnosed with Functional Neurological Disorder (FND) whose persistent orthostatic symptoms were eventually investigated with formal autonomic testing. The result was not ambiguous. Her heart rate rose from 95 beats per minute while supine to 144 within ten minutes of a 70-degree head-up tilt, without the blood pressure fall required for orthostatic hypotension. Her typical symptoms were reproduced during testing. She was diagnosed with Postural Orthostatic Tachycardia Syndrome (POTS), and subsequent evaluation also produced diagnoses of hypermobile Ehlers-Danlos syndrome and chronic migraine.
The authors present this as a case of coexisting FND and POTS. That is certainly one interpretation. It is not, however, something this single case actually proves.
The patient had originally been diagnosed with FND because her motor symptoms were variable and examinations showed findings regarded as positive functional signs. In the later assessment described in the paper, she had fluctuating give-way weakness, inconsistent effort, preservation of automatic movement during distraction, and a gait that varied across tasks and improved with distraction. Under the current diagnostic framework, those findings support FND.
But alongside those signs was another remarkably consistent pattern. Her episodes were triggered by fatigue and prolonged standing. She experienced lightheadedness. Her dizziness and leg weakness worsened with standing and heat. Symptoms improved when she lay down. She had chronic fatigue, brain fog and exercise intolerance. These symptoms had been present for years.
And they had not been properly explained.
“These symptoms had largely been attributed to anxiety, deconditioning, or her functional neurologic diagnosis.”
That sentence is probably the most important one in the report. The patient did not suddenly develop POTS after her FND diagnosis. The orthostatic symptoms were already there. They were interpreted through the diagnoses she already carried. Earlier bedside orthostatic measurements had not met the criteria for POTS, but the authors note that the duration of upright posture during that assessment was limited. Formal autonomic testing was only performed later.
When it was finally done, an objective physiological abnormality appeared. Her heart rate increased by 49 beats per minute during tilt, her characteristic symptoms were reproduced, and the authors concluded that the findings were consistent with POTS.
The unanswered question
The authors therefore frame the case as diagnostic overshadowing caused by comorbidity: the FND diagnosis was correct, POTS was also present, and clinicians mistakenly attributed symptoms of the second disorder to the first. That is possible. But there is another possibility that the case report does not test.
What if variability, distractibility, give-way weakness and inconsistent gait are not sufficiently specific to establish an independent second disorder in someone already suffering from a physiological condition capable of producing weakness, fatigue, exercise intolerance, presyncope, cognitive impairment and major changes in function?
Finding a sign that medicine currently classifies as a “positive functional sign” establishes that the sign was present. It does not by itself establish why that sign occurred. Even reviews of positive FND signs acknowledge that no individual sign is pathognomonic and that findings such as give-way weakness and gait inconsistency can occur in other circumstances, including pain and musculoskeletal disorders.
This matters because the two interpretations are fundamentally different:
Comorbidity model:
POTS + positive functional signs = POTS and a separate FND.
Common phenotype hypothesis:
POTS or associated disease + positive functional signs = a neurological phenotype that overlaps with the phenotype currently classified as FND.
This case cannot tell us which model is correct. To answer that question, researchers would need to take people with objectively established POTS who had not already been selected for FND, systematically examine them for distractibility, variability, give-way weakness, gait inconsistency and other positive FND signs, and compare the results with appropriate neurological and healthy control groups. If these signs are genuinely rare in POTS, the comorbid-FND interpretation becomes considerably stronger. If they are common, calling every occurrence “comorbid FND” becomes circular.
There is already reason not to simply assume that FND is a common POTS comorbidity. A 2024 paper by Blitshteyn and colleagues, written by clinicians with expertise in autonomic disorders, noted that three POTS datasets containing a combined 5,214 patients did not identify FND as a common comorbidity. The authors were careful about what could be concluded from this: those studies were not specifically designed to measure FND prevalence in POTS, so the actual prevalence remains unknown. They explicitly called for studies comparing FND prevalence in POTS with appropriately matched controls.
That missing denominator is important. Without it, finding an FND sign in a patient with POTS and declaring the result “comorbidity” risks assuming the very thing that needs to be demonstrated.
What happened after POTS was recognised?
The patient's subsequent course makes the question even harder to ignore. Treatment included POTS-specific measures such as fluid and sodium optimisation, compression, graded recumbent exercise progressing towards upright activity, and low-dose propranolol. Physical therapy was also reintroduced and she continued receiving care through an FND clinic, so this was not a controlled experiment and the improvement cannot honestly be attributed to POTS treatment alone.
Nevertheless, the change was substantial. The patient initially required a wheelchair because of lower-extremity weakness and orthostatic symptoms. During follow-up, orthostatic tolerance improved, presyncopal and paroxysmal symptoms became less frequent and less severe, and she became capable of prolonged independent standing. Approximately six months after the POTS diagnosis and introduction of propranolol, her COMPASS-31 autonomic symptom score had fallen from 63.4 to 30 and she no longer required a wheelchair.
The authors appropriately state that this is a temporal association rather than proof of causation because POTS treatment, physical therapy and FND-directed treatment occurred during the same period. But the opposite conclusion is equally unavailable: the case cannot tell us how much of the disability previously regarded as functional was actually independent of the untreated autonomic disorder.
That distinction becomes particularly important when considering the patient's leg symptoms. During tilt testing she developed heaviness of the head and legs, followed by generalized heaviness, pallor and slowed speech. Returning her to the supine position improved the symptoms. Earlier in her history, prolonged standing and heat had also worsened her leg weakness. Those observations do not prove that POTS caused every motor symptom, but they make it difficult to cleanly divide the presentation into “functional weakness over here” and “POTS over there.”
The real danger is stopping at FND
Whatever interpretation is ultimately correct, the case demonstrates a much less theoretical problem. Once FND was in the patient's record, physiological symptoms were attributed to it, along with anxiety and deconditioning. The authors themselves call this diagnostic overshadowing and conclude that an FND diagnosis should not prevent investigation for objectively measurable disease.
This is exactly where the distinction between comorbidity and common phenotype becomes clinically important. If positive functional signs are treated as highly specific evidence of an independent FND, clinicians can reassure themselves that they have already explained weakness, gait disturbance or attacks. Subsequent symptoms can then be divided into either more FND or, if sufficiently obvious objective evidence eventually appears, a new “comorbidity.” The original attribution is rarely forced back onto the table.
There is already literature demonstrating how messy that boundary can become. A systematic review of FND and multiple sclerosis found substantial clinical overlap, documented misdiagnosis in both directions and described comorbidity as poorly studied. The problem is therefore not unique to POTS. Neurological diseases can produce fluctuating, multifocal and otherwise confusing presentations, while the FND framework relies heavily on clinical signs intended to identify inconsistency with recognised disease.
The common phenotype hypothesis asks a straightforward question that the comorbidity framework can too easily bypass: what if some of those signs are not evidence of another disease at all?
This case does not answer that question. It does, however, demonstrate why answering it matters. A young woman had years of orthostatic symptoms, weakness and attacks. She acquired an FND diagnosis. Symptoms compatible with autonomic disease were subsequently attributed to FND, anxiety and deconditioning. Formal testing eventually demonstrated POTS. Treatment was broadened and her disability substantially improved.
Calling that simply “FND with comorbid POTS” may be correct. But it is a conclusion, not the experiment.
Before medicine can confidently distinguish comorbidity from common phenotype, it needs to establish how often these supposedly positive functional signs occur across objectively diagnosed neurological and autonomic diseases. Until then, finding the sign and applying another diagnosis does not settle the question.
References
Das S, Yerraballa SRN, Shekhawat P. Coexisting Postural Orthostatic Tachycardia Syndrome on Autonomic Reflex Testing in Functional Neurologic Disorder. American Journal of Case Reports. 2026;27:e953323. Full text.
Blitshteyn S, Treisman GJ, Ruhoy IS, et al. Postural orthostatic tachycardia syndrome and other common autonomic disorders are not functional neurologic disorders. Frontiers in Neurology. 2024;15:1490744. Full text.
Walzl D, Solomon AJ, Stone J. Functional neurological disorder and multiple sclerosis: a systematic review of misdiagnosis and clinical overlap. Journal of Neurology. 2022;269:654–663. Full text.
Positive Clinical Signs in Functional Neurological Disorders: A Narrative Review and Development of a Clinical Decision Tool. Brain Sciences. 2025;15(9):997. Full text.
:::writing I deliberately kept the strongest claim at **“the case cannot distinguish comorbidity from common phenotype”**, rather than claiming POTS caused the functional signs. That makes the criticism much harder to dismiss: the objective POTS is demonstrated; the independence of the supposed FND is the inference being challenged.
On October 5, neurologist Michael Stingl questioned why the gait disorder in this case report was attributed to FND rather than POTS. It was a straightforward question about diagnostic attribution, particularly relevant given the patient's documented orthostatic symptoms and subsequent improvement.
Physiotherapist Zachary Grin responded:
He then accused clinicians of attributing symptoms to POTS without evidence or biological plausibility, before questioning whether Stingl ever diagnoses FND, considers it in his differential, or even knows how to diagnose it.
And there it is. A neurologist asks how the authors established which condition explains the patient's gait disturbance, and the response shifts to whether that neurologist understands FND. Yet the case itself documents leg heaviness during tilt testing, worsening weakness with prolonged standing, and improvement when supine. None of this proves POTS caused the entire gait disorder, but it certainly makes the attribution worth examining.
More importantly, identifying positive functional signs does not automatically establish that they represent a separate disorder independent of the patient's objectively demonstrated autonomic dysfunction. That is precisely the unresolved question discussed throughout this article. Grin's response assumes the distinction has already been established rather than explaining how it was established in this patient.
Questioning the attribution is not denying FND. It is asking for evidence. If the response to that question is to challenge the clinician's competence instead of addressing the uncertainty, perhaps the problem is not the question.