The Embodiment Crisis: FNDs in Parkinson’s

Functional Neurological Disorders (FNDs) frequently co-occur with Parkinson’s disease, yet they remain systemically misdiagnosed and severely misunderstood in clinical settings. The failure of the medical establishment to adequately address FNDs is not merely a gap in clinical knowledge; it is a structural flaw in how modern medicine conceptualizes human disease.

Linked below is a talk from three years ago that I recently returned to—a presentation by Peter Gilli on the organic roots of functional disorders—in it he brilliantly pinpoints this failure directly. He argues that the rigid distinction between “functional” and “organic” conditions does not clarify the clinical picture, but rather renders functional disorders unintelligible to physicians. When a patient with Parkinson’s presents with functional symptoms, the current medical paradigm short-circuits.

To understand why FND is so frequently misdiagnosed, we have to look at the strongest defense of the current medical framework. The biomedical model is historically optimized for identifying structural pathology. It operates on the premise of identifying a mechanical failure and applying a targeted intervention—a “lever” that reliably modulates the disease state, such as dopamine replacement in Parkinson’s.

The model struggles with FND because there is no single, identifiable neuroanatomical lesion or reliable pharmacological lever. Furthermore, differentiating functional symptoms from the natural, variable progression of Parkinson’s disease is objectively difficult. Clinicians are rightly cautious; misattributing genuine neurodegenerative disease progression to a functional overlay could result in withholding necessary adjustments in dopaminergic therapy, directly harming the patient.

However, this structural optimization comes at a cost. When medicine relies exclusively on localized lesions to validate a symptom’s existence, conditions that lack them are relegated to the realm of “stress” or delusion. The baggage of Jean-Martin Charcot’s search for dynamic lesions and Sigmund Freud’s theories of repressed trauma still fracture neurology and psychiatry today, as Gilli notes. The result is a system that dismisses millions of patients, creating what Gilli rightly terms a human rights crisis of neglect and abuse.

As detailed in the presentation, FND is not a diagnosis of exclusion. It is a neuropsychiatric disorder of embodiment that accepts “tributaries” from multiple sources, including physical injury, trauma, and crucially, the underlying neurological dynamics of other conditions like Parkinson’s. Parkinson’s profoundly disrupts the brain’s sensory-motor networks. It is a logical downstream consequence that a nervous system already under the stress of neurodegeneration would become vulnerable to software-level functional network failures.

This functional overlay is not simply a psychological reaction to the ‘stress’ of neurodegeneration; it is a direct consequence of the circuitry involved. The basal ganglia—the primary region degraded by dopamine loss in Parkinson’s—does not merely execute movement; it is a critical filter for the brain’s predictive processing and sensory gating. When this physical ‘hardware’ degrades, it feeds noisy, unreliable sensory-motor data to the rest of the nervous system. To compensate for this corrupted input, the brain’s higher-order ‘software’ overcorrects. It generates rigid, maladaptive predictions about movement and sensation, essentially locking the system into abnormal motor patterns or perceived paralysis. FND in Parkinson’s occurs because the brain’s predictive software is forced to operate on a degraded data stream.

The core issue requires a reevaluation of life and illness. Later in the lecture, Gilli proposes a process-oriented view: if life is a collection of self-regulating processes like allostasis (maintaining stability through change) and autopoiesis (self-organization), then illness is simply a harmful alteration to these processes at any level of scale.

This perspective dismantles the functional/organic binary entirely. All illnesses are organic; the question is not whether they are organic, but how. FND is a disruption in the processes of embodiment—the mechanisms that allow a human being to process sensation, exert voluntary control, and feel a sense of affinity with their own living body. In Parkinson’s, the body already feels alienated, resistant, and unpredictable. An FND overlay is a severe compounding of this loss of embodiment. It represents a breakdown in the brain’s predictive systems as it attempts to manage a body that no longer responds to its commands.

To properly diagnose and treat FNDs in Parkinson’s, the medical field must discard its reliance on strict structural pathology as the sole arbiter of legitimacy. By adopting the embodiment framework Gilli advocates for throughout his presentation, clinicians can finally bridge the gap between objective disease states and the subjective human experience of illness.

The Clinical Reality: Identifying FND in Parkinson’s

For those with Parkinson’s disease, here are four concrete examples of FND manifestations that warrant a discussion with your doctor. Before detailing these, a crucial clinical caveat from Peter Gilli must be noted: while these presentations are highly characteristic of FND and look mechanically different from neurodegeneration, a physician must still assess the total picture. Symptoms like “give-way” weakness can occasionally be caused by unrelated issues, such as joint pain making it difficult to maintain force. Accurate differential diagnosis is essential because many of these functional overlays are treatable with the correct therapy.

1. The Entrainable (or Distractible) Tremor A classic Parkinson’s resting tremor has a steady, rhythmic beat (4-6 Hz) that temporarily suppresses intentional movement. A functional tremor might look identical at first glance but is subject to “entrainment” or distraction. If a physician asks the patient to tap out a complex, changing rhythm with their “good” hand, a functional tremor in the affected limb will do one of three things: it will completely stop, it will automatically sync its frequency to match the tapping hand, or the patient will be entirely unable to perform the tapping task. A true PD resting tremor, however, will maintain its own independent beat regardless of what the rest of the body is doing.

2. The “Dragging Leg” and Astasia-Abasia Parkinson’s typically causes a slow, shuffling walk with shortened steps, stiffness, and occasional “freezing” episodes driven by a lack of dopaminergic signaling. In contrast, functional gait issues present mechanically incongruent patterns. One common presentation is a monoplegic “dragging leg,” where the patient pulls the limb behind them flat on the floor like a dead weight. Another is astasia-abasia: a wildly erratic, lurching, “acrobatic” walk where the patient expends massive amounts of energy catching themselves at the very last second, yet rarely actually falls.

3. Fixed Functional Dystonia Parkinson’s can cause painful muscle cramping or twisting (dystonia), such as early morning toe-curling, but these mobile cramps typically fluctuate and correlate directly with the timing of levodopa medication cycles. A functional dystonia, however, is a sudden, rigid, and fixed posture—frequently a severely clenched fist or a continuously inverted ankle. It does not fluctuate or respond to Parkinson’s drugs. It locks in place for days or months, representing a software glitch in the brain’s predictive processing of motor control rather than a lack of dopamine.

4. “Give-Way” Weakness and Hoover’s Sign While Parkinson’s causes severe slowness and rigidity, making movement difficult to initiate, the raw power of the muscle itself usually remains intact when tested directly. A patient with an FND overlay, however, might present with profound weakness or apparent paralysis in a limb. Clinical testing often reveals “give-way” weakness: the muscle initially provides normal resistance before suddenly and completely collapsing. This is definitively diagnosed via Hoover’s sign: if the patient is asked to extend their “paralyzed” leg, they cannot. But when the physician asks them to forcefully flex their “good” hip against resistance, the “paralyzed” leg automatically and involuntarily extends with normal force. The hardware (motor pathways) is completely intact; the brain’s software (the ability to voluntarily access them) is what is disrupted.

The persistent division between “organic” disease and “functional” overlay is a relic of an obsolete biomedical model that actively fails patients navigating the complexities of Parkinson’s disease. By recognizing FNDs not as structural anomalies, but as predictive software failures triggered by the hardware degradation of neurodegeneration, clinicians can bridge the gap between theory and practice. Embracing this embodiment framework is not merely an academic exercise; it is a clinical necessity to ensure patients receive accurate diagnoses and targeted therapies rather than dismissal.

for more on FNDs Peter Gilli’s blog fndportal.org is an exceptional resource.