Hallucinogen persisting perception disorder (HPPD) is characterised by episodes of altered perception linked to past psychoactive drug use, accompanied by distress and functional impairment. To date, clinical characterisation has been limited in scale. Using TriNetX, a global federated health research network of electronic health records, we conducted a retrospective cohort study comparing clinical associations in individuals with HPPD versus population and psychedelic-using controls. Cumulative incidences of psychiatric and medical disorders were compared. Cox proportional hazards models assessed risk factors for developing HPPD, and odds ratios (ORs) were used to evaluate associated conditions following diagnosis. We identified 25,778 individuals diagnosed with HPPD. Prior to diagnosis, high rates of comorbidities were observed, including depressive episodes (29.2%), anxiety disorders (26.2%), chronic pain (15.9%), headache syndromes (14.7%), post-viral fatigue (12.3%), ADHD (6.6%), and fibromyalgia (6.7%). Anxiety and functional somatic syndromes were significantly more common in the HPPD group than in psychedelic-using controls (p < 0.001). Anxiety (OR 1.5) and post-viral fatigue (OR 1.9) predicted HPPD development in psychedelic users. HPPD diagnosis was associated with increased risk of subsequent functional somatic syndromes (OR 2.0) and psychiatric disorders (OR 1.4) versus psychedelic-using controls. This largest-to-date study of HPPD highlights its psychiatric and somatic complexity, with strong associations with anxiety and functional somatic syndromes. Several methodological limitations are acknowledged. Further research should explore overlapping pathophysiological mechanisms linking HPPD, visual disorders (e.g. visual snow syndrome), anxiety, and functional somatic syndromes.

PurposeFunctional neurological disorder (FND) is a common condition, associated with high disability and healthcare costs, and poor treatment access. This qualitative study aimed to explore participants' experiences of being diagnosed with functional neurological disorder (FND), accessing treatment, and navigating life after diagnosis. Participants were drawn from a randomised feasibility study of eye movement desensitisation and reprocessing therapy for people with FND (MODIFI, Trial Registration: NCT05455450 (www.clinicaltrials.gov)).MethodsReflexive thematic analysis was used to analyse the data from eighteen semi-structured interviews with participants diagnosed with FND.ResultsSix main themes were identified: (1) the process of seeking a diagnosis and initial relief from the physical struggles, (2) receiving a diagnosis of FND, (3) treatment for FND, (4) the burden of FND in day-to-day life, (5) the need to assert agency and return to normal, and (6) hopes for the future.ConclusionThe findings emphasize the need for personalised and compassionate care for individuals suffering from FND, underpinned by increased service provision within the healthcare system.

Background: Functional seizures (FS) and functional motor symptoms (FMS), subtypes of functional neurological disorder, may involve distinct predisposing, precipitating, perpetuating, and triggering (PPPT) factors. This study investigated potential PPPT factors in FS and FMS separately. Methods: Two hundred participants (FS=50, FMS=50, individuals with anxiety and/or depression [CC]=50, healthy controls [HC]=50) completed an in-depth medical history interview and online questionnaires to assess self-reported potential aetiological factors including traumatic/adverse life events, alexithymia, autistic traits, psychological and physical symptoms, illness perceptions, cognitive-behavioural responses, and outcome measures of general functioning, and health-related quality-of-life (HRQoL). Outcomes: Participants with FS more frequently reported traumatic/adverse events and psychopathology (e.g., dissociation, PTSD) as illness causes/precipitating factors, and sensory symptom triggers, relative to FMS and/or CCs. In contrast, participants with FMS endorsed physical illness causes/precipitating factors, and physical activity and emotion-related symptom triggers, more frequently than FS and/or CCs. Physical and dissociative symptoms were elevated, alongside reductions in HRQoL and general functioning, in FS/FMS compared to CCs/HCs. Greater current, threatening illness-related beliefs and cognitions were disclosed in FS/FMS compared to CCs. Negative associations between HRQoL, cognitive-behavioural responses, and traumatic/adverse events were also seen in FS/FMS. Interpretation: Distinct biopsychosocial factors may be involved in the development and maintenance of FS and FMS: traumatic events and psychopathology in FS, and physical illness/injury, physical functioning, and alexithymia in FMS. Unhelpful illness-related beliefs, and impacts on HRQoL and general functioning, are shared between these subtypes. The results of this study provide insight into potential subtype-specific characteristics of FS/FMS, with implications for treatment. Funding: The study is funded by an MRC Career Development Award to SP [MR/V032771/1]. This project also represents independent research part-funded by the NIHR Biomedical Research Centre at South London and Maudsley NHS Foundation Trust and King’s College London.

Prepulse inhibition reflects subcortical sensory integration, where a low-intensity peripheral stimulus (prepulse) reduces the amplitude of a reflex response to a subsequent high-intensity stimulus. As a measure of pre-attentive sensory gating, prepulse inhibition has been found to be altered in small cohorts of patients with functional disorders, including functional motor disorder and fibromyalgia, suggesting a shared deficit in sensory information processing. However, prior studies have not demonstrated consistent associations between prepulse inhibition abnormalities and clinical measures. We hypothesized that widespread pain and somatic symptoms in somatic symptom disorders may result from a general deficit in the interpretation of bodily signals, potentially linked to abnormalities in sensory filtering as measured by prepulse inhibition. In this study, we examined 140 participants across four age- and sex-matched groups: 35 patients clinically categorized with functional motor disorder without fibromyalgia, 35 with both functional motor disorder and fibromyalgia, 35 with fibromyalgia only, and 35 healthy controls. A weak electrical stimulus to the index finger served as the prepulse, delivered 100 ms before supraorbital nerve stimulation to elicit the R2 component of the blink reflex. Prepulse inhibition was calculated as the percent reduction in R2 amplitude. Across all groups, lower prepulse was significantly associated with higher scores on the Fibromyalgia Severity Scale, consisting of Widespread Pain Index and Symptom Severity Scale. In patients with functional motor disorder, no association was found between prepulse inhibition size and objectively rated motor symptom severity. These findings suggest that impaired early sensory processing at subcortical level is related to “fibromyalgianess” in people with functional motor disorder and fibromyalgia. Abnormal prepulse inhibition may serve as an objective transdiagnostic marker of fibromyalgia symptomatology or fibromyalgianess, including widespread pain and other non-motor symptoms in functional disorders, highlighting a potential role of sensory gating deficits in the pathophysiology of fibromyalgia-spectrum manifestations.

This cohort study compared the prevalence of neurological comorbidities among people with functional neurological disorder versus those with epilepsy and multiple sclerosis.

Background and Objectives Functional neurological disorder (FND) is one of the most common causes of neurological symptoms and disability, but much remains unknown about its pathophysiology. In both clinical conversations and research publications, clinicians and researchers imply a variety of models for onset of the condition with respect to both the process culminating in its onset, and the distribution of susceptibility to the condition across the population. Here we used population-level data as evidence to arbitrate between these generative models of the condition. Methods We identified six hazard distributions corresponding to different pathophysiological processes, and four distributions of population susceptibility, as the assumptions underlying the range of plausible generative models resulting in the observed distribution of age of onset of FND. We combined these model families into 24 parametric proportional hazards models, and fitted each to the observed distribution of reported age at onset in two large FND datasets, one for functional movement disorders (FMD) and one for functional seizures (FS). Out-of-sample predictive accuracy for these models was compared using Bayesian model comparison. Results Strong trends were seen across model families with different distributions of population susceptibility to FND. For both datasets, the best-fitting model family overall was the mixture-cure family, which represents susceptibility as binary, with a susceptible and an unsusceptible proportion of the population. For the FMD dataset, some models in the log-normal frailty family had comparable fits to the mixture-cure models, and for the FS dataset, a number of the gamma frailty family had comparable fits. The variance parameters for each of these frailty distributions were so large as to imply binary risk, approximating mixture-cure models. Models with exponential hazard distributions--which correspond to a generative process where a single trigger in a susceptible person brings about the condition--were universally poor fits for the observed data. Other hazard distributions were insufficiently distinguished by their out-of-sample predictive accuracy to make further inference as to the underlying process resulting in onset of FND in susceptible individuals. Interpretation Our results suggest that susceptibility to FND is approximately binary, with the susceptible proportion of the population extremely likely to develop FND in their lifetime. The results also argue strongly against a generative model where a single trigger is sufficient to cause the onset of FND in a susceptible person. ### Competing Interest Statement M.J.E. does medical expert reporting in personal injury and clinical negligence cases. M.J.E. has shares in Brain & Mind, which provides neuropsychiatric and neurological rehabilitation in the independent medical sector. M.J.E. has received financial support for lectures from the International Parkinson's and Movement Disorders Society and the FND Society (FNDS). M.J.E. receives royalties from Oxford University Press for his book The Oxford Specialist Handbook of Parkinson's Disease and Other Movement Disorder. M.J.E has received honoraria for medical advice to Teva Pharmaceuticals and educational events. M.J.E. receives grant funding from the National Institute for Health and Care Research (NIHR). M.J.E. is an associate editor of the European Journal of Neurology. M.J.E is a board member of the FNDS. M.J.E. is on the medical advisory boards of the charities FND Hope UK and the British Association of Performing Arts Medicine. ### Funding Statement This work was supported by the Canadian Institute for Advanced Research (CIFAR). JBM was supported by a National Health and Medical Research Council (Australia) Investigator Grant (2010141). ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: This work was exempted from ethical review by the University of Queensland's Human Research Ethics Committee (ref: 2026/HE010662). I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes The study used publicly available datasets. Analysis code is available through the Open Science Framework at https://doi.org/10.17605/OSF.IO/E4TDM.

Functional neurological disorder (FND) is one of the most common, but least researched, conditions in neurology. It can cause a broad range of sensory, motor, and constitutional symptoms, with the underlying mechanism of symptom-generation proposed to be an abnormality of perceptual inference. Debate exists as to whether the clinical entity referred to as FND is truly a single disorder or is in fact multiple entities which have been erroneously amalgamated into the same condition. We sought to provide empirical evidence on this question by treating it as a problem of model comparison. We formulated statistical models equivalent to: (1) FND being a single entity with variation in phenotype, represented by latent trait models, and (2) FND being multiple discrete entities, represented by latent class models. We fitted these models to data on the symptoms experienced by 697 people with FND from the FND Research Connect database (www.fnd-research.org) and used Bayesian model comparison to compare their likelihoods. All but one of the latent trait models, representing FND as a single entity with heterogeneous phenotype, fit the data better than all the latent class models. Furthermore, secondary analysis of the latent class models showed results compatible with the models discretising continuous variation rather than capturing true discrete categories. Our results are most compatible with the hypothesis that the symptom structure of FND is the result of a single pathophysiological process, either as a single entity, or a common pathway preceded by multiple causative processes where the common pathway is solely responsible for the phenotype.

BACKGROUND:Functional neurological disorder (FND) is a disabling condition often presenting with motor impairments, including gait disturbance and postural instability. Data on the prevalence and predictors of falls in people with FND are limited. This study aimed to investigate the prevalence of self-reported falls among individuals with motor FND and identify factors associated with falling. METHODS:Adults with motor FND were recruited from a tertiary neurology centre in London, UK, December 2021 to August 2024. Participants reported falls within the previous 6 months and completed assessments of sensory impairment, mobility, pain, fatigue, depression and anxiety. Group differences between recurrent fallers (≥ 2 falls) and those with one or no falls were examined, and logistic regression analyses identified predictors of recurrent falls. RESULTS:One hundred participants (81% female, mean age 43.7 ± 14.2 years) were included. Falls were reported by 62%, and 56% reported recurrent falls. Among fallers, 64% reported injuries including bruising (39%), laceration (8%) and fracture (6%). Recurrent fallers had poorer plantar sensation and vibration detection, as well as worse scores for anxiety, depression, pain and functional mobility. A multivariable regression model indicated that absent plantar sensation (OR = 5.30, 95% CI [1.37, 20.44], p = 0.015), greater pain severity (OR = 1.25, 95% CI [1.05, 1.48], p = 0.011) and greater anxiety (OR = 1.09, 95% CI [1.004, 1.18], p = 0.040) were associated with increased odds of recurrent falls. CONCLUSION:Falls are common among individuals with motor FND. Absent plantar sensation, pain and anxiety were independently associated with recurrent falls, supporting a multidimensional approach to falls assessment and rehabilitation.

Background Functional neurological disorder (FND) is a common neurological condition characterised by symptoms which vary characteristically with attention. In the sensory realm, these symptoms frequently take the form of 'phantom' perception in the absence of sensation. While the condition is generally regarded not to cause auditory symptoms, tinnitus is a phantom perception which varies with symptom-focused attention, and is suggested to have similar underlying mechanisms to those proposed for FND. Based on this, we hypothesized that tinnitus might reflect the same underlying process as FND, and that it would therefore be more common in people with FND (pwFND). Methods Using an international database, we compared the proportions of pwFND who reported tinnitus with a control group. To ensure that observed differences were not attributable to agreement bias in symptom reporting, we also conducted an experiment where pwFND and controls were asked to report which symptoms they had experienced in the past month, 14 of which were symptoms of FND, and 7 of which were unrelated. Results Rates of tinnitus were significantly higher in the FND group (54% HDI 50 - 57%, n=732) than the control group (17% HDI 8.5 - 25%, n=59). In the symptom reporting experiment, pwFND (n=38) reported more FND-related symptoms than controls (n=38), but there was no between-group difference in reporting of non-FND related symptoms. Discussion Based on the markedly higher prevalence of tinnitus in pwFND than controls, and the substantial overlap in mechanisms and phenomenology, we believe tinnitus should be considered a possible symptom of FND, where both conditions reflect a failure of symptom resolution after incitement by a peripheral stimulus. ### Competing Interest Statement D.D.G.P is the unpaid project lead at FND Research Connect. M.J.E. does medical expert reporting in personal injury and clinical negligence cases. M.J.E. has shares in Brain & Mind, which provides neuropsychiatric and neurological rehabilitation in the independent medical sector. M.J.E. has received financial support for lectures from the International Parkinson's and Movement Disorders Society and the FND Society (FNDS). M.J.E. receives royalties from Oxford University Press for his book The Oxford Specialist Handbook of Parkinson's Disease and Other Movement Disorder. M.J.E has received honoraria for medical advice to Teva Pharmaceuticals and educational events. M.J.E. receives grant funding from the National Institute for Health and Care Research (NIHR). M.J.E. is an associate editor of the European Journal of Neurology. M.J.E is a board member of the FNDS. M.J.E. is on the medical advisory boards of the charities FND Hope UK and the British Association of Performing Arts Medicine. ### Funding Statement This work was supported by the Canadian Institute for Advanced Research (CIFAR). JBM was supported by a National Health and Medical Research Council (Australia) Investigator Grant (2010141). ### Author Declarations I confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained. Yes The details of the IRB/oversight body that provided approval or exemption for the research described are given below: The Human Research Ethics Committee of the University of Queensland Health gave ethical approval for this work with reference 2024/HE000730. I confirm that all necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived, and that any patient/participant/sample identifiers included were not known to anyone (e.g., hospital staff, patients or participants themselves) outside the research group so cannot be used to identify individuals. Yes I understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance). Yes I have followed all appropriate research reporting guidelines, such as any relevant EQUATOR Network research reporting checklist(s) and other pertinent material, if applicable. Yes Anonymised data and analysis scripts are available online through the Open Science Framework at https://doi.org/10.17605/OSF.IO/9CXJT

Background Functional seizures (FS) and functional motor symptoms (FMS), subtypes of functional neurological disorder, may involve shared and distinct predisposing, precipitating, perpetuating and triggering (PPPT) factors. This study investigated potential self-reported PPPT factors in FS and FMS separately. Methods 200 participants (FS=50, FMS=50, individuals with anxiety and/or depression (clinical controls [CC]=50, healthy controls [HC]=50) completed an in-depth medical history interview and online questionnaires to assess potential aetiological factors including traumatic/adverse life events, alexithymia, autistic traits, psychological and physical symptoms, illness perceptions, cognitive-behavioural responses and outcome measures of general functioning and health-related quality of life (HRQoL). Results Participants with FS more frequently reported traumatic/adverse events and psychopathology (eg, dissociation, posttraumatic stress disorder) as possible illness causes/precipitating factors and sensory symptom triggers, relative to FMS and/or CCs. In contrast, participants with FMS endorsed physical illness causes/precipitating factors and physical activity and emotion-related symptom triggers more frequently than FS and/or CCs. Physical and dissociative symptoms were elevated, alongside reductions in HRQoL and general functioning in FS/FMS compared with CCs/HCs. Greater current, threatening illness-related beliefs/cognitions were disclosed in FS/FMS compared with CCs. Negative associations between HRQoL, cognitive-behavioural responses and traumatic/adverse events were also seen in FS/FMS. Conclusions Traumatic events and psychopathology may be more prominently involved in the development/maintenance of FS and physical illness/injury, physical functioning and alexithymia may be more central to FMS. Unhelpful illness-related beliefs and impacts on HRQoL and general functioning are shared between these subtypes. The results of this study provide insight into potential unique and overlapping characteristics of FS/FMS, with implications for treatment.

OBJECTIVES:Functional neurological symptoms that do not meet clinical definitions of functional neurological disorder (FND) are common in clinical practice. Understanding the distinction between these "benign" functional symptoms and FND is crucial in defining FND as an entity for study and a clinical syndrome. We aimed to measure the frequency of functional symptoms in people who do not have FND. METHODS:A survey was administered to 95 clinicians who attended an international conference on FND. Participants were asked to report the occurrence and characteristics of experiences with features of functional sensory or motor symptoms, or dissociation, which they had experienced at any time. RESULTS:Of the 95 people who responded to the survey, 57.4% reported having experienced any functional symptoms, and 47.9% reported having experienced functional motor or sensory symptoms. The symptoms reported were generally short-lived and caused only mild distress and disruption. Most respondents who reported having experienced a functional symptom reported having had multiple events through their lives. CONCLUSIONS:The results suggest that the lifetime occurrence of functional neurological symptoms is at least an order of magnitude higher than FND. The high prevalence of functional symptoms in people who have never had FND challenges the assumption that the occurrence of functional neurological symptoms is synonymous with FND. We propose that FND is better conceived of as a failure of the mechanisms by which functional neurological symptoms resolve, rather than the occurrence of functional symptoms per se. This reconceptualization implies new research directions for the underlying etiology of FND.

Previous research has indicated possible implications for altered interoceptive processing in functional neurological disorder. This study investigated dimensions of interoception in functional seizures (FS, n=50) and functional motor symptoms (FMS, n=50) relative to healthy (HC, n=50) and clinical controls with anxiety disorders/depression (CC, n=50), before and after a physiological autonomic arousal induction (isometric hand-grip). Measures of cardiac interoceptive accuracy and insight (heartbeat tracking task [HTT] with confidence ratings) and in-the-moment ratings of functional neurological symptoms (FNS) were completed pre/post-arousal induction. Baseline interoceptive sensibility (Multidimensional Assessment of Interoceptive Awareness-2) was altered in FS/FMS relative to HC/CC (ps<.004, η2>.07) across ‘Not-Distracting,’ ‘Not-Worrying,’ ‘Attention-Regulation,’ ‘Self- Regulation,’ and ‘Trusting’ subscales. There were no baseline group differences in interoceptive accuracy, confidence, or insight (ps>.13, η2<.05) and no change in FNS (FS/FMS), interoceptive accuracy, or confidence (all groups) post-arousal induction. This study replicates reports of altered interoceptive sensibility alongside intact interoceptive accuracy in FND.

BACKGROUND:Cervical dystonia (CD) has a varied motor presentation, combining abnormal postures with complex involuntary head movements. Classification of these motor patterns remains imprecise, relying on descriptive terminology without robust definitions. OBJECTIVES:To provide a kinematically-grounded description of the motor phenomenology of CD. METHODS:Sixty-two patients with CD and 32 age-matched controls were recorded wearing inertial sensors. Voluntary movement was assessed during a head-turning task, including velocity, range of motion, smoothness, and trajectory. Kinematic metrics were extracted from samples of involuntary movements and cluster analysis was applied to identify different patterns. These were then compared with clinical appraisal of movement phenotype. Exploratory factor analysis was conducted to investigate the relationship between motor characteristics. RESULTS:Voluntary deficits included impaired velocity, range, smoothness, and symmetry, with no evidence of sequence effect. Three distinct clusters of involuntary head movement were identified: low-frequency oscillations with a sawtooth waveform consisting of alternating fast and slow phases (Cluster 1); erratic mid-frequency movements with constant changes in speed, waveform profile, and axis (Cluster 2); and high-frequency sinusoidal movements (Cluster 3). Cluster 2 was specifically associated with a 'jerky' clinical phenotype, while Cluster 3 was associated with a 'tremulous' phenotype. Factor analysis identified distinct latent components driving variation in voluntary deficits and involuntary movement. CONCLUSIONS:CD is characterized by a heterogeneous combination of oscillatory movements and impairments in voluntary head control. Kinematic analysis has the potential to refine disease classification and support the development of objective instrumental outcome measures for clinical assessment and research. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.

Many chronic neurological, psychiatric and interface disorders can be understood as conditions where maladaptive homeostatic set points become entrenched, driving pathological states that resist spontaneous resolution. This paper proposes a novel conceptual framework, the therapeutic reset, which unifies diverse interventions that transiently disrupt pathological equilibria, thereby leveraging the intrinsic plasticity of biological systems to facilitate recalibration toward healthier set points. Drawing insights from active inference, dynamical systems theory and nested somatic collective intelligences, we illustrate how treatments such as electroconvulsive therapy, psychedelics, inflammatory perturbations and anaesthetic interventions create brief periods of heightened plasticity. We argue that the reset itself and plasticity more generally do not necessarily incline in the direction of better health and that therapeutic efficacy may depend especially on the quality of contextual elements including preparation, support and post-intervention scaffolding that guides the system towards an adaptive equilibrium. Future research should prioritise mechanistic studies to identify biomarkers of plasticity and delineate intervention-responsive signalling pathways, alongside clinical studies refining precise dosage and anatomical targeting, and identifying therapeutically salient parameters of the scaffolding around high-plasticity states. By strategically harnessing systems’ inherent capacity for correction, this framework offers transformative potential for treating otherwise intractable disorders through proactive, precision-based recalibration of maladaptive homeostatic networks.

BACKGROUND:Cognitive symptoms are common in functional neurological disorder (FND), yet evidence of impaired neurocognitive test performance is variable. We aimed to assess self-reported cognitive symptoms, neurocognitive test performance, and metacognitive confidence in patients with functional seizures (FS) and functional motor symptoms (FMS). METHODS:Participants with FS (n = 50) and FMS (n = 50) were compared to age- and gender-matched healthy controls (HC, n = 50), and clinical controls with depression and/or anxiety disorders (CC, n = 50). The Cambridge Neuropsychological Test Automated Battery was used to examine response speed, working memory, executive functions, and social-emotional processing, with subjective confidence rated for each test. Intellectual functioning, performance validity, and self-reported cognitive symptoms were also assessed. RESULTS:The FND groups reported elevated cognitive symptoms compared to HC and CC (p-values<0.001). Impaired performance was demonstrated in both FND groups on tests of sustained attention (p-values = 0.03- < 0.001) and set-shifting (p-values = 0.01-0.001). Performance validity was comparable between groups (p = 0.64). The FND groups reported reduced post-diction confidence for sustained attention (p < 0.001). Executive performance deficits correlated with reduced test-specific confidence in FS/FMS (p-values = 0.02- < 0.001). In FMS, post-diction confidence for sustained attention performance correlated negatively with cognitive symptoms (p = 0.002). Cognitive symptoms were associated with psychological/physical symptom load, quality-of-life, and/or general functioning in FND and CC groups (p-values = 0.04- < 0.001). CONCLUSIONS:Patients with FS and FMS displayed localized deficits on tests of executive functioning, with reduced domain-specific metacognitive confidence, alongside significant cognitive symptoms. These neurocognitive features were associated with poorer clinical status, warranting interventions targeting cognitive control and/or cognitive symptoms in everyday life.

BACKGROUND:Functional neurological disorder (FND) is a common neurological presentation and can be associated with high disability, high healthcare costs and difficulty accessing treatment. Effective treatments are still being established. A feasibility study evaluating eye movement desensitisation and reprocessing (EMDR) therapy as a treatment for FND (MODIFI) demonstrated positive outcomes. The experiences of EMDR for people with FND have not been previously reported. AIMS:We aimed to explore the experiences of participants who had completed EMDR therapy in the MODIFI trial. METHOD:Participants who completed EMDR therapy in MODIFI were invited to take part in semi-structured interviews on completion of the trial. Eleven participants consented to take part and were interviewed. Interviews were analysed with reflexive thematic analysis. RESULTS:Analysis was organised into four main domains: (a) expectations before the trial; (b) preparedness for EMDR; (c) mysterious but unique journey and (d) it was hard, but worth it - 'a rewarding challenge'. Within these domains, we identified ten themes. CONCLUSIONS:Participants reported limited understanding of why or how EMDR might be helpful, but were still motivated to take part. Participants expressed that they had felt anxious about focusing on memories of past experiences. However, they described feeling safe and in control in the therapy, despite it being difficult at times. Overall, participants reported positive effects, and that perceived costs were worthwhile. These results add further support that a full-scale trial evaluating FND-focused EMDR is justified.

BACKGROUND:Childhood trauma is common in functional motor disorder (FMD), but it is unclear whether specific trauma dimensions are differentially linked to symptom burden, and whether depression, anxiety, or multimorbidity can mediate these associations. METHODS:We conducted a cross-sectional case-control study including 322 patients with clinically definite FMD and 215 neurologically healthy controls, balanced with respect to age and sex. Six outcomes - motor symptom severity, cognitive complaints, depression, anxiety, fatigue, and pain - were jointly modeled using Bayesian multivariate regression with Childhood Trauma Questionnaire subscales as predictors. Bayesian structural equation modeling tested mediation by depression, anxiety, and multimorbidity. RESULTS:In FMD, emotional abuse was the most consistent trauma correlate, associated with higher depression (β = 0.37, 95% CrI 0.22-0.51), anxiety (β = 0.32, 95% CrI 0.16-0.47), cognitive complaints (β = 0.27, 95% CrI 0.11-0.42), fatigue (β = 0.17, 95% CrI 0.03-0.32), and motor symptom severity (β = 0.15, 95% CrI 0.04-0.25). Mediation analyses indicated that affective symptoms fully accounted for trauma-symptom associations (indirect effect β = 0.42, 95% CrI 0.27-0.56). Multimorbidity was associated with more severe affective symptoms (β = 0.24, 95% CrI 0.12-0.37) and FMD symptoms (β = 0.24, 95% CrI 0.07-0.42) but did not mediate trauma-symptom relationships. CONCLUSIONS:Emotional abuse is a key developmental risk factor for FMD, with its effects on symptom severity mediated by depression and anxiety. Multimorbidity increases symptom burden but is not a primary pathway linking trauma to FMD. Findings support routine trauma and affective symptom screening in FMD and targeted psychotherapeutic interventions.

Schizophrenia is a common and often disabling neuropsychiatric condition. Whilst sensorimotor abnormalities such as dyskinesia, parkinsonism and motor incoordination are prevalent in schizophrenia, they are often attributed to medication side effects or classified as neurological soft signs or catatonic phenomena. Here, we outline the prevalence, characteristics and challenges in accurate phenotyping of sensorimotor disturbances in schizophrenia, including amongst medication-naïve individuals, demonstrating that sensorimotor dysfunction may be an integral manifestation of the disease process. We then review how current understanding regarding the pathogenesis of schizophrenia supports this possibility and consider how better characterization of sensorimotor dysfunction may improve management and the development of novel treatments for schizophrenia, playing particular attention to the role of instrumental sensorimotor assessment.