FND: Speech & Voice Differential Clinical case Diagnostic Dogma Organic Clues Rule-In Signs Diagnostic Overshadowing Misdiagnosis Clinical Reasoning Diagnostic History

Diagnosed With FND After Her Son’s Suicide. It Was Fatal Frontotemporal Dementia

Author profile image FND Nope Moderator
0 comments

A 47-year-old woman developed progressive neurological symptoms following her son's suicide. Her speech deteriorated, her movements slowed, her coordination worsened, and she eventually became almost completely unable to speak or care for herself. Doctors diagnosed conversion disorder, now commonly called Functional Neurological Disorder (FND). Her son's death became a central part of the explanation for her illness.

She did not have FND. She had a progressive neurodegenerative disease. By the time genetic testing confirmed the underlying condition, she had already been discharged to a dementia care facility, where she died several weeks later. The genetic results arrived after her death.

The case was published in September 2019 in the American Journal of Psychiatry under the title Clinicians and Cognitive Bias: A Case of Frontotemporal Dementia Misdiagnosed as Conversion Disorder. What makes this report particularly revealing is that the treating clinicians themselves examined how their assumptions contributed to the misdiagnosis.


Progressive Neurological Disease, Treated as a Psychiatric Problem

The woman, identified as Ms. A, had experienced approximately two and a half years of worsening symptoms, including depression, anxiety, impaired speech, slowed movement and incoordination. Previous neurological and psychiatric evaluations had been inconclusive. Neuropsychological testing identified abnormalities in memory and speech, but these were interpreted as effort-dependent and attributed to possible conversion disorder. An earlier MRI report had also raised the possibility of cerebral atrophy.

When she was admitted to a psychiatric hospital for further assessment, clinicians considered severe depression with catatonia while retaining the conversion disorder diagnosis. She received benzodiazepines, antidepressants, antipsychotics and electroconvulsive therapy (ECT). None produced meaningful improvement. Meanwhile, neurological investigations identified abnormalities, including increased reflexes, EEG slowing and mildly elevated cerebrospinal fluid protein and neuron-specific enolase. These findings did not immediately establish a specific neurological diagnosis, but neither did they justify continuing to assume that her symptoms were functional.

After two months in hospital, further examination revealed frontal release signs and worsening hyperreflexia. Electromyography identified a chronic, active neurogenic process. A fresh review of her brain scans suggested cortical atrophy inappropriate for her age. Only then did clinicians seriously reconsider the possibility of a neurodegenerative disorder.

Frontotemporal dementia was suspected, and genetic testing was ordered. The results subsequently identified a C9orf72 mutation consistent with familial frontotemporal dementia. Ms. A had died before those results became available.


Her Son's Death Became a Diagnostic Anchor

The authors identified several cognitive biases that had influenced the woman's care. The first was representativeness bias: her symptoms appeared after a devastating personal tragedy, matching the historical stereotype of conversion disorder as a psychological response to trauma. The second was availability bias: her son's suicide was repeatedly emphasised in clinical assessments, while other important details received less attention. The third was anchoring bias: once conversion disorder had been suggested, clinicians continued interpreting subsequent evidence through that diagnosis.

The paper explains that the woman's son's suicide appeared in nearly every evaluation, despite other clinically relevant events receiving less attention. Her depressive symptoms had actually begun years before his death, while her severe speech deterioration occurred approximately a year and a half afterwards. Those distinctions mattered, but the emotionally compelling trauma narrative repeatedly took precedence.

The authors also acknowledged that the association between trauma and conversion disorder was an outdated diagnostic assumption. DSM-5 had already removed the requirement for an associated psychological stressor because it had not been demonstrated to be diagnostically reliable or predictive of outcome.

In other words, the clinicians were influenced by a historical understanding of conversion disorder that the diagnostic criteria themselves had already moved away from. A woman's traumatic experience became a convenient explanation for symptoms that were actually being caused by progressive neurological disease.


The Most Damning Admission: There Was No Positive Evidence

Perhaps the most important admission in the paper is that the clinicians had not established the positive evidence required to diagnose conversion disorder in the first place. The authors explicitly acknowledged that the clinical findings did not demonstrate incompatibility between the patient's symptoms and a recognised neurological or medical condition, as required by DSM-5.

They even identified a specific mistake in their interpretation of her speech. Her speech production was consistently sparse. Had it varied substantially between examinations, that might have provided stronger evidence supporting a functional explanation. But that variability was not documented.

This is not a minor technicality. The diagnosis was retained without the evidence supposedly required to establish it. Meanwhile, abnormal neurological findings, progressive deterioration and failed psychiatric treatments did not prompt sufficiently early reconsideration.

The clinicians identified missed opportunities to obtain complete earlier test reports, reassess abnormal findings and recognise that the patient's progression was inconsistent with the working diagnosis. They acknowledged that the original diagnostic label influenced subsequent assessments even as evidence accumulated against it.

The problem was not simply that frontotemporal dementia can be difficult to diagnose. It can be, particularly in patients with C9orf72 mutations, where psychiatric symptoms may be prominent and early brain imaging can appear relatively normal. The problem was that diagnostic uncertainty was repeatedly handled by retaining a diagnosis that had not been positively demonstrated.


What the Clinicians Admitted

The authors concluded that cognitive bias had contributed to the diagnostic error and argued for greater attention to the evidence required to establish conversion disorder. They also noted that the patient's earlier recognition would not have changed her eventual outcome. That is an important qualification: this report does not establish that the misdiagnosis caused her death or that earlier identification would have saved her life.

But an unchanged ultimate outcome does not make the diagnostic failure acceptable. A woman with a progressive neurological disease spent months receiving psychiatric treatments that did not help her, while her actual illness remained unidentified. Her family was also denied a timely understanding of what was happening to her.

The paper discusses the commonly cited estimate that approximately 4% of conversion disorder diagnoses are subsequently found to be incorrect. Whatever confidence clinicians place in that figure, this case demonstrates something the percentage alone cannot explain: how a diagnosis can become entrenched, how trauma can distort clinical reasoning, and how abnormal findings can fail to dislodge an unsupported assumption.

There is an uncomfortable irony here. Modern FND diagnosis is frequently described as a positive, evidence-based process rather than a diagnosis of exclusion. Yet this woman was diagnosed without the necessary positive evidence, and the label survived repeated assessments, objective abnormalities and worsening disability. The authors' own account shows that knowing the diagnostic criteria and actually applying them are two very different things.

Ms. A's case is not evidence that every FND diagnosis is incorrect. It is evidence of a documented diagnostic failure in which clinicians allowed psychological assumptions and an existing label to interfere with recognition of neurological disease. That failure deserves scrutiny, not excuses.

Her son's suicide was a tragedy. It was not evidence that her neurological symptoms were functional. The clinicians eventually recognised the difference. By then, she was dying.


References