When FND Overshadowed an Axonal Neuropathy: A Case of AMSAN

A 2026 case report describes a 22-year-old woman admitted to inpatient rehabilitation with Functional Neurological Disorder (FND) as her primary diagnosis. Her neurological disability was severe, but during rehabilitation the pattern of her symptoms and her failure to improve increasingly challenged that explanation. Further neurological investigation eventually identified extensive motor and sensory axonal damage consistent with Acute Motor and Sensory Axonal Neuropathy (AMSAN), an axonal variant within the Guillain-Barré spectrum.

The authors ultimately retained FND alongside AMSAN, but they also explicitly describe what happened as diagnostic overshadowing. Their concern was that the existing FND diagnosis and psychiatric comorbidity influenced how the patient's neurological symptoms were interpreted, delaying recognition of an underlying neurological disease.

FND was already the primary diagnosis

By the time the patient reached inpatient rehabilitation, FND was not merely one possibility on a differential diagnosis. It was her primary diagnosis. Rehabilitation therefore began within an established functional framework, even though the patient had profound neurological disability requiring inpatient care.

This is important because diagnoses do more than name symptoms. They influence what clinicians expect to see next, which findings are considered significant and when further investigation appears necessary. Once neurological disability has been classified as functional, new symptoms can potentially be interpreted as further manifestations of the existing diagnosis rather than evidence that the diagnosis itself needs reconsideration.

The pattern increasingly pointed elsewhere

During rehabilitation, the patient's clinical course became increasingly difficult to reconcile with the existing explanation. She made little functional progress, while her weakness and sensory disturbance showed a largely bilateral and symmetrical pattern. The symptoms followed an ascending distribution and affected the lower extremities more severely than the upper extremities.

These were not isolated abnormalities appearing after an otherwise successful rehabilitation course. They formed an increasingly coherent neurological pattern. The combination of ascending weakness, sensory disturbance and poor progress prompted clinicians to reconsider whether an underlying peripheral neurological disorder had been missed.

The EMG changes the case

Electromyography and nerve conduction studies provided the critical objective evidence. Testing demonstrated extensive axonal damage involving both motor and sensory nerves. The findings were considered consistent with Acute Motor and Sensory Axonal Neuropathy.

At this point, the diagnostic landscape had materially changed. The patient no longer simply had unexplained neurological symptoms occurring in the context of an FND diagnosis. There was physiological evidence of widespread peripheral nerve injury capable of explaining major components of her neurological disability.

She was urgently transferred back to acute hospital care for further neurological investigation. CT imaging of the head, MRI of the brain and cervical spine, lumbar puncture and paraneoplastic investigations did not identify another explanation, while the electrodiagnostic findings supported presumed AMSAN.

Treatment changes the trajectory

The patient was treated with intravenous immunoglobulin (IVIG), a disease-directed treatment used in Guillain-Barré spectrum neuropathies. The authors report improvement in proximal upper-extremity strength and increased participation in rehabilitation following treatment.

The change in her rehabilitation trajectory is particularly notable. Before AMSAN was recognised, she had made minimal functional gains and discharge to a subacute rehabilitation facility was being considered. After recognition and treatment of the neuropathy, her recovery progressed sufficiently for her to be discharged home approximately three weeks later, although she continued to require assistance and equipment.

The sequence is difficult to ignore: an FND diagnosis was already established, rehabilitation produced little improvement, the neurological pattern prompted reassessment, electrophysiology demonstrated extensive motor and sensory axonal damage, AMSAN was treated with IVIG, and the patient's rehabilitation course subsequently improved.

The authors call it diagnostic overshadowing

The significance of this case does not depend on imposing a critical interpretation on an otherwise routine diagnostic revision. Diagnostic overshadowing is the authors' own description of what occurred. They specifically discuss the risk that neurological disease may be missed when symptoms are interpreted through an existing FND diagnosis and psychiatric history.

That is important because it demonstrates how an established diagnosis can alter the evidential threshold applied to later findings. Symptoms that might otherwise trigger investigation can appear less surprising once a patient has already been classified as having a functional neurological disorder.

The danger is not merely that a rare disease might occasionally be missed. The deeper problem is diagnostic direction. Once FND becomes the organising explanation, clinicians need to remain willing to recognise when the accumulating evidence points somewhere else.

What remains functional?

The authors did not discard FND after diagnosing AMSAN. They concluded that the patient had both conditions. That conclusion creates another question that deserves the same evidential scrutiny as the AMSAN diagnosis: which findings independently established the remaining functional component?

AMSAN was supported by a neurological pattern and objective electrophysiological abnormalities. The attribution of any remaining symptoms to FND therefore needs its own evidential basis. The discovery of AMSAN does not automatically answer that question, but neither does the statement that the disorders coexist.

This distinction becomes particularly important after a diagnosis has already contributed to diagnostic overshadowing. If the original framework delayed recognition of neurological disease, retaining part of that framework should involve explicit reassessment of the evidence that originally supported it.

FND as a diagnosis of inclusion

Modern descriptions of FND frequently emphasise that it should be diagnosed positively rather than simply because neurological investigations are unrevealing. This case demonstrates why that distinction matters in practice. Before the peripheral neuropathy was identified, FND provided an explanation for severe neurological disability. After electrodiagnostic testing, a substantial part of that disability had an objective neurological correlate.

The relevant question is therefore not simply whether FND and AMSAN are theoretically capable of occurring together. It is whether the evidence in this particular patient demonstrated both conditions independently. If AMSAN was established through its characteristic clinical pattern and electrophysiology, the remaining FND attribution should likewise be traceable to evidence that positively supports it.

Why this case matters

This case provides an unusually direct example of diagnostic closure being recognised from within the clinical literature itself. A young woman entered rehabilitation with FND as her primary diagnosis while an axonal peripheral neuropathy remained unidentified. Her failure to progress and increasingly coherent neurological pattern eventually prompted further investigation, and EMG/NCS demonstrated extensive motor and sensory axonal damage consistent with AMSAN.

The diagnosis mattered because it changed management. The patient received IVIG and subsequently progressed sufficiently to return home rather than proceeding to the subacute rehabilitation placement being considered before the neuropathy was recognised.

Perhaps the most important part of the case is very simple. The evidence stopped fitting the existing explanation, and somebody eventually looked again. The authors themselves describe what preceded that reassessment as diagnostic overshadowing.

That leaves two separate questions on the table: why was AMSAN initially obscured by the FND framework, and after AMSAN was demonstrated, what positive evidence independently justified retaining FND? Both are questions about evidence, and neither is answered merely by saying that the two diagnoses can coexist.

Source

Diagnostic Overshadowing in Functional Neurological Disorder Leading to a Diagnosis of Acute Motor and Sensory Axonal Neuropathy: A Case Report, Roldan A, Shulman J, Singh R, Dayon E, Abdou A, Hartnett J, Trovato EL. Journal of Clinical Medicine. 2026;15(9):3501.