Misdiagnosis of functional neurological symptom disorders in paediatrics: Narrative review and relevant case report

Abstract

Functional neurological symptom disorders (FNSD) pose a common challenge in clinical practice, particularly in pediatric cases where the clinical phenotypes can be intricate and easily confused with structural disturbances. The frequent coexistence of FNSDs with other medical disorders often results in misdiagnosis. In this review, we highlight the distinctions between FNSD and various psychiatric and neurological conditions. Contrary to the misconception that FNSD is a diagnosis of exclusion, we underscore its nature as a diagnosis of inclusion, contingent upon recognizing specific clinical features. However, our focus is on a critical learning point illustrated by the case of a 14-year-old male initially diagnosed with FNSD, but subsequently found to have a rare primary monogenic movement disorder (paroxysmal kinesigenic dyskinesia, PKD). The crucial takeaway from this case is the importance of avoiding an FNSD diagnosis based solely on psychiatric comorbidity and suppressible symptoms. Instead, clinicians should diligently assess for specific features indicative of FNSD, which were absent in this case. This emphasizes the importance of making a diagnosis of inclusion. Extended follow-up and clinical-oriented genetic testing might help identify comorbidities, prevent misdiagnosis, and guide interventions in complex cases, which cannot be simply classified as “functional” solely because other conditions can be excluded.

Plain language summary

Understanding and Avoiding Mistakes in Diagnosing Children with Functional Neurological Symptom Disorders: A Review and Case Report: This article discusses Functional Neurological Symptom Disorders (FNSDs), focusing on misdiagnosis, differential diagnosis, and other diagnostic challenges, particularly in pediatric cases. FNSDs involve motor or sensory symptoms that are inconsistent over time and unexplained by neurological disease, often associated with psychosocial factors. The article highlights the complexity of distinguishing FNSDs from other neurological and psychiatric conditions, emphasizing the importance of careful evaluation. The authors review various conditions that can mimic FNSDs, such as epileptic seizures, syncope, and different motor disorders. They emphasize the need to consider psychiatric conditions in the differential diagnosis, including factitious disorders, and malingering. The article presents a case study of a 14-year-old with involuntary movements, initially diagnosed as having a Functional Movement Disorder. After careful evaluation, the patient was diagnosed with a genetic dystonia (PRRT2 mutation). The case shows the importance of not rely solely on psychological problems, bizarre presentations or suppressible symptoms when diagnosing FNSDs.

Keywords

Functional neurological symptom disorder conversion disorder paediatric movement disorder proline-rich transmembrane protein 2 paediatric dystonia

Introduction

Functional Neurological Symptom Disorders (FNSDs), as defined in DSM-5 TR (and previously known as conversion disorder) (American Psychiatric Association, 2022), encompass variable and common conditions including Functional Seizures (FS), also known as psychogenic non-epileptic seizures, and Functional Motor Disorders (FMDs), but also chronic dizziness and cognitive dysfunction (Hallett et al., 2022). FNSDs are commonly associated in clinical practice with psychosocial and psychiatric comorbidities, disability, and relevant health costs. (Kozlowska et al., 2007) Despite involving all ages, a high prevalence of FNSD has been reported in young females (Yong et al., 2023).

Functional Neurological Symptom Disorders (FNSDs) mainly refer to incongruent and time-inconsistent motor or sensory symptoms, that are unexplained by neurological disease and caused by altered brain networking, rather than structural abnormalities. However, the pathophysiological processes are still largely unknown (Hallett et al., 2022).

Functional dystonia was the first FNSD described with specific diagnostic criteria (Fahn & Williams, 1988), later adapted by other authors for other FNSDs as well (Ganos et al., 2014; Gupta & Lang, 2009; LaFrance et al., 2013). However, neurological signs and symptoms in children are often complex, thereby challenging classical diagnostic criteria for FNSDs. In this regard, a recent systematic review found significant variability and low reproducibility of diagnostic criteria for paediatric FMDs (Kirkwood & Mark, 2022).

Furthermore, it has also been outlined that some patients with presumed functional symptoms revealed unexpected non-functional diagnoses during follow-up (Stone et al., 2009). These conditions are often rare and genetically based disorders, usually detected by the increasing use of genetic testing tools.

Finally, as frequently occurs for FS and epileptic manifestation, functional and neurological motor symptoms may coexist in some patients, making the differential diagnosis even more challenging for clinicians (Hallett et al., 2022; Kurtis & Pareés, 2021).

Here we present a brief review of available literature regarding misdiagnosis, differential diagnosis, and other diagnostic issues involving FNSDs, particularly in paediatric age. We then propose a relevant case of a young patient with a rare monogenic neurological disorder, previously supposed as FMD and mistreated over 10 years, highlighting the importance of careful evaluation and prolonged follow-up.

Functional neurological symptom disorder mimics

Functional Neurological Symptom Disorders (FNSDs) are a complex and multifaceted group of conditions that have been the subject of extensive scientific interest in recent years.

While some might assume that FNSDs are frequently misdiagnosed due to the absence of specific instrumental or laboratory findings, this is not necessarily the case. Some authors (Stone et al., 2009) conducted a prospective cohort study involving 1444 patients referred from primary care to neurology clinics. They found that only 0.4% of these patients had an unexpected structural non-functional diagnosis that could explain their initial symptoms at follow-up. Similarly, other authors (Walzl et al., 2019) observed that a comparable percentage of patients initially diagnosed with a structural neurological disease were later identified as having a functional diagnosis that better explained their symptoms. As shown by a previous systematic review and metanalysis (Stone et al., 2005), the relatively low rate of misdiagnosis of functional symptoms since 1970s (similar to other neurological or psychiatric conditions) could be due to improved diagnostic accuracy or better study methods.

However, van der Salm et al. (van der Salm et al., 2013) highlighted that even experienced movement disorder specialists sometimes disagree on the clinical diagnosis of FS. Furthermore, there are documented instances of misdiagnosis related to FNSD (van der Feltz-Cornelis et al., 2020) that suggest the hypothesis that the actual number of diagnostic errors might be underestimated.

In particular, misdiagnosis of FNSD has become a growing concern within emergency rooms, inpatient or outpatient units, and other clinical contexts (Yong et al., 2023). Despite the recent attention to FNSD and the development of clear diagnostic criteria, there is still a significant challenge in diagnosing these disorders due to their resemblance to other medical conditions. This risk of misdiagnosis is particularly concerning in paediatric populations. Therefore, it is important to approach these cases with caution and to consider the possibility of either missing an FNSD diagnosis or misdiagnosing another neurologic disorder as FNSD.

There are specific conditions that are more at risk of being misdiagnosed. These include disorders that have no specific signs and those whose specific clinical signs are difficult to obtain. For example, in some cases, specific tools or skills may be required, including genetic analysis or neuroimaging techniques. Furthermore, there may be conditions where the signs are ambiguous or unknown to the clinician, therefore differentiating functional presentations from traditional neurological diseases necessitates a diagnostician’s ability to identify the subtle distinctions between them.

FNSD and psychiatric differential diagnoses

When considering the differential diagnosis of FNSD is crucial to take into account not only other neurological disorders but also other psychiatric or behavioral conditions.

With regard to the latter, the most important distinction to make is between functional disorder, factitious disorder, and simulation or malingering. The distinction between the three conditions is significant as it may determine further workup and treatment (Bass & Halligan, 2016). In this context, another condition, not explored in detail here, is Factitious Disorder Imposed on Another (FDIA), where, for instance, a caregiver actively produces factitious symptoms in a child. However, in FDIA, the diagnosis is potentially assigned to the caregiver rather than the minor, and the diagnostic-therapeutic path differs significantly from the other conditions we are about to discuss (Walters et al., 2019).

Functional disorder implies the sunintentional production of neurological symptoms (American Psychiatric Association, 2022). In contrast, factitious disorder and malingering represent the voluntary production of symptoms with internal (emotional) or external (e.g. pecuniary) incentives, respectively (Bass & Halligan, 2016; Galli et al., 2018). Assessing these possibilities can assist in avoiding a misdiagnosis as well as mismanagement. To investigate the possibility of factitious disorder or malingering, it could be useful, for instance, to include psychological evaluation and testing for secondary gain (Kemp et al., 2008; van Impelen et al., 2017). Table 1 summarises the main differences between these three conditions.

Table 1.

Differential Diagnosis Between Functional Neurological Symptom Disorder, Factitious Disorder, and Malingering.

	Symptom production	Motivation	Gain	Agrees to diagnostic/therapeutic procedures	Diagnosis (DSM-5-TR)
Medically unexplained neurological symptoms	Unconscious	Unconscious	None	Yes	Functional neurological symptom disorder
	Intentional	Unconscious	Internal/Primary (e.g. psychological goal)	Yes	Factitious disorder imposed on self
	Intentional	Intentional	External/Secondary (e.g. monetary)	No	Malingering

Despite the clear theoretical distinction between these conditions, it should be noted that differentiating among them in children and adolescents can be difficult (Kozlowska, 2014). This is particularly true from a semeiological standpoint, where functional and simulated movement disorders can be impossible to differentiate, even if several functional magnetic resonance imaging (fMRI) studies have shown differences in regions of activation (Hassa et al., 2016; Perez et al., 2021). Additionally, an accurate psychosocial history must be taken when evaluating these conditions, as both functional and factitious disorders often have experienced traumatic adverse events in childhood (Hausteiner-Wiehle & Hungerer, 2020; Peebles et al., 2005; Steffen-Klatt et al., 2019).

Moreover, as it has been pointed out (Kozlowska, 2014), distinguishing between volitional and non-volitional processes is already a challenge in adults, let alone in children and adolescents. The adaptive use of dissimulation and deception can develop very early before explicit cognitive processes arise, which makes differential diagnosis even more complex. These difficulties probably contribute to relatively low rates of factitious disorders in neurology settings (Kanaan, 2022; Kanaan & Wessely, 2010). For this reason, it is essential to involve different specialists in the assessment of children and adolescents with neurological symptoms, given that the interaction between biological, psychological, and social factors should always be considered (Hallett et al., 2022; Onofrj et al., 2023).

Differential diagnoses of Functional Seizures

In the realm of FS, a broad spectrum of conditions emerges as potential differential diagnoses. Beyond epileptic seizures, clinicians must be vigilant to other paroxysmal non-epileptic events. These encompass a range of conditions such as syncope, sleep disorders, movement disorders, ischemic attacks, migraines, transient global amnesia, and other psychogenic episodes like panic attacks, as well as metabolic disorders, which include hypo/hyperglycemia and electrolyte disturbances (Malmgren et al., 2012; Volbers et al., 2022). The diagnostic landscape becomes even more intricate in infancy and early childhood. Here, one must also consider physiological startle responses, benign neonatal sleep myoclonus, shuddering or shivering attacks, Sandifer syndrome, dystonic spasms seen in spastic or dyskinetic cerebral palsy, opsoclonus-myoclonus, paroxysmal extreme pain syndrome, and maladaptive daydreaming (Malmgren et al., 2012). The cornerstone of accurate diagnosis lies in meticulous history-taking and keen observation of clinical characteristics. These usually suffice to delineate most of these conditions. For a more structured comparison, Table 2 elucidates the primary clinical data instrumental in differentiating FS, epileptic seizures, and syncope (Ali et al., 2011; Leibetseder et al., 2020; Malmgren et al., 2012; Volbers et al., 2022).

Table 2.

Main diagnostic characteristics used to differentiate functional seizures (FS) from two other common paroxysmal events (Epileptic seizures and syncope).

Observation		Epileptic Seizure	FS	Syncope
Environmental features at the onset
Stressful events		Usually no	Frequently yes (e.g. medical practice, emotional aspects)	Frequently yes (e.g. blood sampling) or non-stressful circumstances (e.g. urination, postural changes)
Photosensibility		Yes	No (but possible suggestibility)	No
Sleep/Awake cycle		Sometimes also only during sleep	Rarely during sleep^a	Not during sleep
Ovarian cycle		Worsens	Worsens	Worsens
Pre-ictal features
Onset		Sudden or gradual	Sudden or gradual (if gradual often lasts a few minutes)	Gradual (pre-symptomatic symptoms), duration of a few minutes
Perceptual alterations		Possible and difficult to explain	Possible and very detailed	Rare
Prodromal symptoms		Possible focal motor or non-motor onset (aura), typically <30	Dysautonomic symptoms (tachycardia, dry mouth, tremor, sweaty hands) associated with poor awareness of anxiety	Heat, sweating, blurred vision, distant, muffled or distorted sounds
Ictal features
Motor activity		Typical ictal pattern (tonic, clonic, T-C)	Commonly fluctuating motor activity, sometimes with sudden breaks but stable frequency; Typical waxing-waning movements	Common myoclonic jerks (short duration, rapid recovery), after loss of postural tone
Asynchronous movements of upper/lower limbs		Not typical	Common	Possible (multifocal myoclonus)
Voluntary movements		Very rare	Occasional	Rare
Pelvic thrusts		Rare	Occasional	Absent
Arc de cercle		Very rare	Occasional	Occasional (“decerebrate posture")
Lateral movements (?)		Possible	Frequent (especially marked right-left head movements)	Rare
Falling from sitting position		Common	Rare	Common
Ictal hyperventilation		Exceptional	Frequent	Absent
Vocalizations		“Epileptic scream”; possible but rare crying, laughter (dacristic, gelastic seizures)	Crying, screaming	Typically absent
Skin		Common cyanosis	No cyanosis, despite the prolonged duration	Pallor, hyperhidrosis
Closed eyes		Rare	Very frequent	Rare
Resistance to eye-opening		Very rare	Common	Very rare
Photomotor pupillary reflex		Often abolished	Very commonly preserved (beware of sympathetic hyperactivation mydriasis)	Commonly preserved
Ictal reactivity		Rarely preserved	Occasionally partially preserved (typical guarding response to corneal contact)	Rarely preserved
Overall duration >2 min.		Uncommon	Common (duration up to hours)	Very uncommon (only if the pz remains in orthostatism)
Post-ictal features
General post-ictal symptoms		Drowsiness, asthenia, disorientation, anterograde amnesia, focal paresis (Todd’s P.) lasting minutes	Absent or less marked (confusion or drowsiness), emotional outbursts (crying/laughter)	Possible confusion <1 minute, recurrence of loss of consciousness if rapid recovery of standing position
Tongue bites		Frequent (lateral)	Occasional (tip)	Rare (tip)
Other objective lesions		Frequent (also major injuries)	Rare (mild as bruises, grazes)	Rare if vasovagal
Post-ictal respiratory pattern	Stertorous breath	Possible (generalized crisis)	No	No
Post-ictal respiratory pattern	Rapid and shallow breathing	No	Possible (about 1 min)	No
Sphincter release		Common	Rare but possible (refractory or chronic FS)	Possible
Cough and rhinorrhoea		Possible (temporal crisis)	No	No
Patient’s description of the event
Description of subjective symptoms		Voluntary and accurate description of details	Avoid description of symptoms, report few details, describe the environment	Accurate description of presyncopal symptoms
Attempts to stop the seizure		Voluntarily reported (if recognisable)	Not mentioned	Voluntarily
Use of metaphors		Metaphors in which the attack is agent/force or event/situation	Metaphors of space/place; catastrophization of the episode	—
Description of the loss of consciousness		Often exact and precise description	Limited description	Often exact and precise description

^aPossible “pseudo pre-critical sleep”: at behavioral level it seems a normal sleep (immobile body, closed eyes), while the EEG shows signs of wakefulness (alpha rhythm and rapid eye movement). 56% sensitivity and 100% specificity for FS.

Differential diagnoses of functional motor disorders

While there is extensive literature discussing FNSD with seizure presentations and their mimics, there is a relative paucity of literature on mimics of FNSD with motor presentations or FMD.

Reports of misdiagnosis of FMD as other disorders include multiple sclerosis (Walzl et al., 2022), stroke (Gibson & Whiteley, 2013; Jones et al., 2020; Popkirov et al., 2020; Sequeira et al., 2018), myelopathy (Ginsberg, 2017; Teasell & Shapiro, 2002), myasthenia gravis (Harrison et al., 2023), serotonin syndrome (Nisbet & Penfil, 2008), autoimmune encephalitis (Flanagan et al., 2023; Wilkinson-Smith et al., 2020), sarcoma-induced osteomalacia, cerebellar medulloblastoma, Huntington’s chorea, dystonia (Teasell & Shapiro, 2002), astasia-abasia (Stanković et al., 2015), paresis/paralysis (Gelauff et al., 2019).

On the other hand, reports of misdiagnosis of other neurological disorders as FMD include the following: prionic disorders (Gómez-Mayordomo et al., 2023; Jiang et al., 2019), dystonia (Erro et al., 2014; Yilmaz et al., 2011), Kleine-Levin syndrome (Masi et al., 2000), acute disseminated encephalomyelitis (Abay et al., 2005), paresis/paralysis (Fishbain & Goldberg, 1991), Guillain-Barrè syndrome (Edelsohn, 1982; Wherry et al., 1991), progressive supranuclear palsy (van Meerkerk-Aanen et al., 2017), spinal cord arteriovenous malformation (Spratt & Thomas, 2008).

Furthermore, with specific regard to neurodevelopmental age, there has been recent interest in functional stereotypies and tic-like disorders (Forsyth, 2021; Martino et al., 2023; Pringsheim et al., 2023).

This brief synopsis underscores the importance of thorough differential diagnosis and the potential pitfalls in diagnosing FMD.

Moreover, the most recent systematic review on criteria for diagnosing FMDs (Kirkwood & Mark, 2022) has highlighted that such criteria must refrain from employing subjective and unscientific language, such as “bizarre” and “unusual”, and avoid labeling symptoms as being incongruent with other neurological conditions. On the contrary, FMDs should be diagnosed through the detection of specific clinical positive signs.

With the aim to assist physicians with this complex task, Aybek and coll. (Aybek & Perez, 2022) systematically reviewed 37 bedside clinical tests or test groups for FMD, specifically functional weakness and functional movement disorder, that underwent some form of formal validation. The findings revealed that while the specificities of validated signs were impressively high, spanning 64% to 100%, their sensitivities were more variable, oscillating between 9% and 100%. The inter-rater reliability of these signs was generally found to be good to excellent. However, an overreliance on a singular sign can inadvertently lead to false positives. For instance, in a cohort of 190 patients diagnosed with a neurological disorder, 37 (20%) exhibited at least one positive functional neurological sign (Aboud et al., 2019). For a structured overview, Table 3 delineates the primary clinical signs instrumental in diagnosing FMD.

Table 3.

Some relevant bedside clinical signs to diagnose functional movement disorders (FMDs) adapted from Aybek and Perez (2022). Specificity, sensibility, and specific reference for each sign are reported as well.

Positive sign	Specificity/Sensibility %	Reference
General signs
Distractibility	100/58	(Baizabal-Carvallo & Jankovic, 2017)
Variability	100/84	(Baizabal-Carvallo & Jankovic, 2017)
Convergence spasms	87/15	(Fekete et al., 2012)
Disproportionate effort to the task	95/55	(Daum et al., 2015)
Gait disorders
Falls toward support	93/19	(Daum et al., 2015)
Excessive slowness	94/32	(Daum et al., 2015)
Non-economic posture	100/21	(Daum et al., 2015)
Sudden knee buckling	95/21	(Daum et al., 2015)
Monoplegic leg dragging	100/9	(Daum et al., 2015; Stone et al., 2010)
Lack of balance
Functional Romberg^a	100/39	(Daum et al., 2015)
Limb weakness
Hoover sign^b	99.5/61	(Daum et al., 2015; McWhirter et al., 2011; Sonoo, 2004; Stone et al., 2010; Tinazzi et al., 2008)
Abductor sign^c	100/100	(Sonoo, 2004)
Abductor finger sign^c	100/100	(Tinazzi et al., 2008)
Tremor
Distractibility	92/94	(van der Stouwe et al., 2016)
Increase amplitude with weight	92/22	(van der Stouwe et al., 2016)
Entrainment^d	91/91	(van der Stouwe et al., 2016)
Combination of at least 2/3 of the above features	93/100	(van der Stouwe et al., 2016)

^aLarge disbalance displayed during Romberg task, without falling; usually improved by distraction.

^bFor unilateral leg weakness. Ask to flex the healthy leg against resistance and observe/feel the strength of hip extension of the controlateral weak leg. Cmpare with voluntary hip extension of the weak leg: if involuntary strength is higher than voluntary strength, the sign is positive.

^cAsk to abduct both legs/fifht hand finger against resistance: observe/feel if involuntary abduction of the weak leg/hand occurs (functional) or not (structural or non-functional).

^dTapping motion with one hand induces change in tremor frequency on the other upper limb (usually synchronous to the tapping frequency).

FNSD comorbidities

Building on the diagnostic complexities of FNSDs, it is crucial to consider that the DSM-5-TR’s Criterion C, which states that “the symptom or deficit is not better explained by another medical or mental (health) disorder”, should not be misconstrued. It does not imply that a patient cannot simultaneously have FNSD and other coexisting neurological or psychiatric conditions. Understanding FNSD comorbidities is vital for a comprehensive differential diagnosis.

For instance, recently, a group of authors (Carle-Toulemonde et al., 2023) provided a narrative review that highlighted several comorbidities associated with FNSD, including fatigue, cognitive symptoms, and psychiatric disorders (ranging from 40% to 100% of FNSD patients, with anxiety disorders being the most common). The presence of non-functional disorders, including neurological conditions like epilepsy in patients with FS (20%) and FMD in Parkinson’s disease (7%), was also noteworthy. Furthermore, somatic symptom disorders and hypermobile Ehlers-Danlos Syndrome were also frequently linked to FNSD, with a prevalence of about 50% each.

Case report

We report the case of a 14-year-old male born to healthy non-consanguineous parents. Their family history was unremarkable. Delivery and neonatal period were uneventful. Motor milestones were on time, while a mild language delay was reported. The first involuntary movements arose at the age of 5 years, diagnosed as stereotyped movements, mainly involving the right lower limb (LL) but also the right upper limb (UL). At the age of 8, he underwent his first hospitalization due to further involuntary movements, clinically characterized by progressive involvement of LLs and trunk with an axial twisting, till opisthotonus, sometimes associated with fallings, without loss of consciousness. These episodes were usually triggered by excitement, anxiety, or stress, typically lasting less than 1 minute and occurring 3-4 times a day. The boy reported that each episode was preceded by a physical sensation and urge, suppressible only for a little time. Physical and neurological examinations revealed only mild motor coordination difficulties.

A normal neurocognitive profile was found, while at the psychopathological evaluation, a social anxiety disorder was revealed. Laboratory tests and electroencephalograms were unremarkable.

At the age of 10 years, he was diagnosed with FMD, because of the bizarre clinical presentation, characterized by involuntary movements, partly suppressible, linked with emotional triggers, and for the related psychopathological features. Thus, cognitive behavioral therapy was suggested and administered for over 3 years.

At the age of 13, he was admitted to our Paediatric Movement Disorders (MD) Unit, because of the recurrence of twisting-like movements, which also involved progressively the ULs. The frequency was 3-4 times per week, mainly during school activities. The patient also described recurrent headaches and increasing social and school anxiety with panic attacks due to his motor disorder, and a consequent significant daily life impairment. Furthermore, the constant oversight of caregivers also caused a severe limitation in his personal autonomy.

According to the anamnesis and the clinical evaluation he presented a characteristic involvement of the right part of the body, with a following caudo-rostral progression. Moreover, during the paroxysmal episodes, the motor manifestations were not stoppable or modulated by distractible maneuvers; in subsequent evaluations, no signs of inconsistency were found.

Prolonged clinical observation and home video analysis also revealed that episodes of involuntary movement attacks were triggered by sudden voluntary movements.

In the suspect of paroxysmal kinesigenic dyskinesia, a Next Generation Sequencing (NGS) panel for genetic MDs was carried out, revealing a de novo heterozygous pathogenic variant in the PRRT2 gene (c.649delC; p.Arg217fs*12), compatible with the diagnosis of genetic dystonia type 10 (DYT-10).

Mutation of the proline-rich transmembrane protein 2 (PRRT2) gene has been widely studied as a causative gene of paroxysmal kinesigenic dyskinesia and clinical data showed an effective response to very low doses of carbamazepine (Ebrahimi-Fakhari et al., 1993; Méneret et al., 2012).

Consequently, carbamazepine was titrated up to 100 mg/day, with a dramatic improvement of the symptomatology, presenting after the first week of pharmacological treatment a complete remission of symptoms. He still reports the sporadic presence of premonitory urges without consequent motor manifestations.

Discussion

The presented case highlights the challenging differential diagnosis between structural and functional motor disorders, often due to atypical presentations and overlapping features occurring in paediatric neurology, as discussed above. Non-specific and complex clinical pictures at onset may result in misdiagnosis and subsequent errors up to adulthood (Ganos et al., 2014). In our patient, red flags for non-functional MD, such as the early onset of motor symptoms and their stereotyped phenomenology, emerged after repeated evaluations, leading to a revision of the diagnosis. As it is known, clinical onset of FMD is commonly reported in early adolescence, but rarely in childhood. Furthermore, the motor symptoms are mainly inconsistent over time, presenting high clinical variability with respect to motor patterns and triggers, differently from our case. The duration of the episodes was also evaluated, revealing that all attacks typically lasted less than 1 minute in our patient. FMDs, on the contrary, usually show higher variability in the duration of episodes in the same patient (e.g. between seconds and hours/days) (Gupta & Lang, 2009; Yong et al., 2023).

Moreover, the abnormal movements of the boy did not really change nor were suppressed during complex tasks and, although they tended to generalize, they did not vary much over time, consistently with non-functional MDs (Table 4).

Table 4.

Differential Diagnosis Between Non-functional Movement Disorders (MD) and Functional Movement Disorders (FMD).

Supportive signs of non-functional MD	Diagnostic criteria of FMD
Early-age onset	Onset after puberty
No variability in duration and/or distribution	Variability in duration and/or distribution
No entrainment or full suppressibility	Entrainment or full suppressibility
No distractibility	Distractibility
	Inconsistency and incongruence over time

Confounding features in this case were represented instead by psychopathological issues that led clinicians to consider FNSD. Anxious disorder and significant impairment of the quality of life and daily autonomy probably arose as secondary symptoms, due to the chronic disease experience and to the concern associated with the involuntary manifestations. Considering a broader lens, it is essential to acknowledge the potential impact of psychopathological factors and consider a more multidisciplinary approach in the differential diagnosis, particularly when confounding features such as anxious disorder or overprotective parents significantly impact the patient’s quality of life.

In literature, PRRT2 mutations are largely reported as a major cause of paroxysmal kinesigenic dyskinesia (Ebrahimi-Fakhari et al., 1993; Méneret et al., 2012; Ohira et al., 2023), and the genetic confirmation is fundamental because of the possibility of available treatment with a positive outcome. Moreover, paroxysmal kinesigenic dyskinesias (PKD) have frequently been noted as prone to misdiagnosis, particularly given their occasional association with anxious-depressive symptoms (Junewtar et al., 2014; Pan et al., 2018; Cao et al., 2021). Therefore, despite being rare conditions, genetic MDs should be carefully considered as a differential diagnosis of FMDs, especially when clinical and anamnestic data are limited and inconclusive.

Notably, the same genetic condition has been very recently reported in the literature in comorbidity to FNSD (Ohira et al., 2023). The authors described a case of a young woman with paroxysmal kinesigenic dyskinesia genetically determined with functional weakness that significantly worsened the whole clinical presentation. In our paediatric case, on the contrary, FNSD should be more accurately considered as a misdiagnosis, given that his symptoms were better explained by the PRRT2 mutation and highly responsive to a specific treatment. In conclusion, our presented case underscores the intricate challenges in distinguishing between functional and non-functional motor disorders in paediatric neurology, emphasizing the need for a meticulous diagnostic approach. It is imperative to recognize that FNSD is a diagnosis of inclusion based on typical clinical features, cautioning against its sole reliance on unusual, unexplained, or psychologically triggered symptoms.

Therefore, we suggest that child psychiatrists, paediatric neurologists and other clinicians should consider careful evaluation of typical features and possibly prolonged follow-up, combined with clinical-oriented genetic testing, in children presenting with apparent FNSDs, to avoid misdiagnosis and to promote accurate treatment strategies. This approach may help to achieve a correct diagnosis and the development of tailored treatment for young patients.

Footnotes

Author contributions

Research project: Conception (VB, DE), Organization and Execution (VB, KB, DE, MN, VZ). Manuscript Preparation: Writing of the first draft (KB, DE, MN), Review and Critique (VB, SG). All authors have read and agreed to the published version of the manuscript.

Declaration of conflicting interests

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Funding

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Institutional review board statement

All procedures performed in this study were in accordance with the ethical standards of the institutional and national research committee and with the 1964 Helsinki Declaration and its later amendments. We confirm that we have read the Journal’s position on issues involved in ethical publication and affirm that this work is consistent with those guidelines.

Informed consent

Informed consent was obtained from all subjects involved in the study and their parents when required.

ORCID iD

Dario Esposito

Author biographies

Valentina Baglioni (MD PhD) is a paediatric neurologist, working in the Unit of Child Neurology and Psychiatry of the Department of Human Neuroscience –Sapienza University of Rome. Her fields of research and clinical work are on behavioural neurology and neuropsychiatry, with special focus on the behavioural aspects of movement disorders and epilepsy.

Dario Esposito (MD) is a child and adolescent neuropsychiatrist, interested in functional somatic medicine and its relationship with psychiatric and neurodevelopmental conditions.

Katerina Bernardi is an MD in training to become a child and adolescent neuropsychiatrist, with a particular focus on paediatric neurology.

Maria Novelli is a child neuropsychiatrist and PhD student in clinical experimental neuroscience and psychiatry at Sapienza university of Rome.

Valerio Zaccaria is a child neuropsychiatrist and PhD student in clinical experimental neuroscience and psychiatry at Sapienza university of Rome.

Serena Galosi (MD PhD) is a paediatric neurologist, working in the Unit of Child Neurology and Psychiatry of the Department of Human Neuroscience –Sapienza University of Rome. Her fields of research and clinical work are on paediatric movement disorders, neurometabolic disorders and genetic movement conditions.

Francesco Pisani (MD PhD) is professor of Child Neurology and Psychiatry, in the Department of Human Neuroscience –Sapienza University of Rome.

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