Chronic cough without clear cardiopulmonary pathology poses diagnostic and therapeutic challenges in children and adolescents. While psychosocial factors play a crucial role in its pathogenesis, historical labels such as "habit cough" or "psychogenic cough" have often been vague and stigmatizing. Despite contemporary consensus guidelines advocating for the term "somatic cough syndrome," unified diagnostic criteria and standardized care pathways remain lacking. A rapid review approach was employed to search the PubMed database for empirical studies published between 2021 and May 2026 on chronic cough related to psychological factors, using terms including "psychogenic cough," "somatic cough," "habit cough," "somatic cough syndrome," and "tic cough." After screening 2134 records, 20 articles were included. The literature showed substantial heterogeneity in chronic cough presentations and provided complementary evidence regarding psychological morbidity, cough-related sensations and triggers, tic-like features, and behavioral treatment response. Most studies involved adults, and direct pediatric evidence was limited. Integrating these findings with established cough guidelines and relevant literature on tic, somatic symptom, and obsessive-compulsive disorders, we propose an evidence-informed tripartite framework comprising three candidate phenotypes: tic cough, psychogenic (somatic) cough, and compulsive cough. The framework emphasizes distinct sensory, affective, and cognitive-behavioral drivers and their implications for multidisciplinary management. Grounded in the clinical realities of pediatric general hospitals, this review provides a practical framework for non-mental health specialists, such as pulmonologists, to facilitate the early identification of psycho-behavioral drivers in functional cough. We call for a clinical paradigm shift from a passive "diagnosis of exclusion" to active "phenotypic identification," thereby promoting truly integrated, multidisciplinary management. What is Known: • Chronic cough without clear cardiopulmonary pathology may be associated with psychosocial factors. • Terms such as habit cough, psychogenic cough, somatic cough syndrome, and tic cough are inconsistently applied. What is New: • We propose a pediatric tripartite framework: tic, psychogenic (somatic), and compulsive cough. • This framework links distinct psycho-behavioral drivers to targeted multidisciplinary management.

Tourette syndrome is characterized by the presence of motor and phonic tics. Individuals with Tourette syndrome can have a spectrum of related behaviours including attention deficit hyperactivity features, obsessions, compulsions, impulsions and complex tics. The pathophysiology of Tourette syndrome is thought to reflect genetic influences on the development and function of cortical-striatal-thalamic-cortical and broader cortical-subcortical circuitry implicated in motor and inhibitory control and interoceptive processing, which may contribute to the characteristic 'urge-tic-relief' cycles. Shared genetic risks resulting in pleiotropy and overlapping neurocircuitry could explain some of the psychiatric comorbidities of Tourette syndrome. Management typically includes education, psychosocial support and behavioural therapy alongside pharmacotherapy for those with more severe tics or those unresponsive to behavioural therapy. Deep brain stimulation is used in severe, incapacitating and treatment-refractory cases persisting into adult life. Approaches aimed at improving quality of life and management of psychiatric comorbidities are also critically important. Future research should include considering refining the diagnostic criteria and delineating functional tic disorders, as well as the tic-related obsessive-compulsive behaviours, as this may have implications for treatment, understanding the underlying neurobiology, and the development of personalized interventions focusing on core tic-related features, psychiatric comorbidities and improving quality of life.

In 1961, Jean-Noël Seignot (1925-2022) published a clinical observation in the Annales Médico-Psychologiques of a patient with a severe form of Gilles de la Tourette syndrome. He included the results of his clinical test with R.1625, a new compound then in an experimental phase, developed by Janssen Laboratories in Belgium-that is, haloperidol. Seignot's article is constantly cited in the bibliographies on the treatment of this syndrome. Here, I present the first-ever complete translation of Seignot's publication, followed by his biography, based on family archives kindly made available to me. This account is accompanied by a brief history of the discovery of haloperidol. Seignot saw that Gilles de la Tourette syndrome was not just a disease but "a whole mode of being." His foresight in the care and treatment of his seriously ill patient deserves a commemorative biography.

Tourette syndrome (TS) is a neurodevelopmental disorder characterized by motor and vocal tics that are modulated by internal physiological state and interoceptive state, including premonitory urges and associated changes in short-timescale parasympathetic variability. Since tic expression is thought to be linked to fluctuations in autonomic state, understanding how brain networks integrate physiological signals may provide insight into the neural mechanisms contributing to tic generation and suppression. In recent years, there has been increasing interest in understanding interactions between the brain and autonomic physiology, given their shared central role in shaping cognition, emotion, and behavior. Methodological advances have enabled the study of brain-heart coupling, yet much of this work has focused on static or region-based approaches, limiting insight into how autonomic fluctuations are integrated within dynamic, large-scale brain networks. Here, we examined time-resolved brain-heart interactions using densely sampled resting-state fMRI data and concurrent pulse oximetry in two sibling pairs (n = 4) discordant for Tourette syndrome (TS). Using two targeted network analyses organized around interoceptive/urge awareness and inhibitory control/action regulation processes, we quantified coupling between pulse-derived RMSSD and between-network functional connectivity using sliding-window analyses and Bayesian linear mixed-effects models. We observed marked individual variability in functional network organization and autonomic measures. The most consistent observation was a pattern of opposing coupling directions between individuals with and without TS: those with TS showed positive associations between pulse-derived RMSSD with connectivity between internal-state and attentional networks, as well as among action-related systems, while unaffected siblings showed positive associations along broader integrative pathways linking internal-state and action-control networks. These preliminary findings generate hypotheses regarding individualized patterns of brain-heart coupling in TS and illustrate the potential value of integrating individualized network mapping with time-resolved physiological measures in clinical populations.

SLC6A1-related neurodevelopmental disorder (SLC6A1-NDD) is emerging as a leading genetic cause of epilepsy, autism spectrum disorder (ASD), and NDD caused by monoallelic loss of function variants in SLC6A1 (solute carrier family 6 member 1) which encodes a gamma-aminobutyric acid (GABA) transporter (GAT1). Descriptions of SLC6A1-NDD have centered around epilepsy, but caregivers report other features that drive key aspects of the disease burden. This retrospective chart review and prospective natural history study (NHS) aims to highlight the nonseizure clinical features of SLC6A1-NDD.

Individuals with chronic tic disorder (CTD) frequently report sensory over-responsivity, defined as heightened awareness of and/or behavioral reactivity to stimuli that are non-aversive to most neurotypical individuals. Within CTD populations, sensory over-responsivity is associated with severity of tics and co-occurring psychiatric symptoms. Despite its prevalence and association with core facets of the phenotype, the neurobiological basis of sensory over-responsivity in CTD remains unclear. Sensory gating, the physiological process of filtering out repetitive stimuli in early perceptual stages to facilitate attention to more salient stimuli, is one potential mechanism underpinning sensory over-responsivity in CTD. The current study sought to quantify somatosensory gating of pneumatic stimuli in adults with CTD using dense-array EEG and to determine the relationship between somatosensory gating and self-reported tactile responsivity. Neurotypical adults (n = 34) and adults with CTD (n = 28) completed a self-report and rater-administered neuropsychiatric evaluation, followed by an event-related potential somatosensory gating paradigm. Contrary to our hypotheses, somatosensory gating, as quantified by gating differences and regression analysis marginal effects, did not differ between groups for P50, N140, or P300 components, and gating indices were not associated with tactile responsivity. However, relative to neurotypical adults, adults with CTD had significantly smaller P50 amplitudes following S1, the first of the paired pneumatic stimuli. Moreover, adults with CTD with smaller S1 P50 amplitudes reported greater tactile responsivity. No other component amplitudes differed between groups. Findings suggest that adults with CTD have altered pre-conscious processing of non-noxious tactile stimuli and that this is linked with tactile over-responsivity.

Background/Objectives: Behavioral disturbances are common in Gilles de la Tourette syndrome (GTS) and can include risky impulsive behaviors (RIBs), but RIB classification remains unclear. This study aims to define the epidemiology of RIB in GTS and to assess its relationship with tic severity and the prevalence of comorbid psychiatric disorders. Methods: The study was structured as a cross-sectional registration study, with each patient enrolled into the database during a single clinical visit. The study included 365 participants with GTS (272 males, 74.5%), of whom 278 (76.2%) were children and adolescents. The mean age at evaluation was 14.4 ± 9.8 years (range 4-64). Clinical data on RIB were obtained during routine outpatient visits using semi-structured questionnaires developed by the authors. Results: RIB was reported in 64 (17.6%) patients with GTS, a group composed of 19 (29.7%) adults and 45 (70.3%) minors. RIB commenced at a mean age of 8.1 ± 5.4 years (range 2-30). The mean age at onset of RIB was 2.6 ± 4.9 years after the onset of tics. Of the patients with RIB, 84.4% had at least one comorbid psychiatric disorder, whereas 15.6% of RIB patients had no psychiatric comorbidity. Multivariable logistic regression showed significant associations between RIB and YGTSS (p = 0.02, OR = 1.02), ADHD (p < 0.01, OR = 2.91), and ODD (p = 0.01, OR = 3.02). Conclusions: RIB may occur early in the course of GTS, typically beginning during childhood, and was identified in 17.6% of patients. Its occurrence was associated with the presence of comorbid psychiatric disorders, particularly ADHD and ODD. Greater tic severity was also statistically associated with RIB, although the effect was small and of limited clinical significance.

Tourette syndrome is characterized by involuntary motor and vocal tics, which are challenging to monitor objectively. This study evaluated convolutional neural networks (CNNs) and Transformer models on EMG and video data ('Rest', 'Tic', and 'Voluntary Movement') for detection and prediction. We hypothesized that EMG windows <5s would better capture tics and improve detection and prediction accuracy. 685 EMG recordings (n=16 participants) were each segmented into 1-, 5-, and 10-second windows. Each model was trained on clinical EMG and validated on held-out data, using corresponding expert-annotated video labels as ground truth. We evaluated model performance using the area under the receiver operating characteristic curve (AUROC) with 95% confidence. Detection performance exceeded prediction across models. The temporal CNN achieved the highest detection performance (mean AUROC 0.66±0.05), with optimal results in 5s windows (AUROC up to 0.82 for tic detection). In contrast, tic prediction performance was lower (best 1s-AUROC 0.66 (0.65-0.68)). Contrary to our hypothesis, longer temporal windows (≥5s) improved tic detection, suggesting that tic-related EMG patterns benefit from extended temporal context, whereas prediction relied on short-term, 1-second signal dynamics. These findings help define a benchmark and suggest that future progress will depend on multimodal integration, patient-specific adjustments, and advanced temporal modeling.

Functional Neurological Disorders, or FND, have become accepted in the vernacular of medicine. Although in the past, they were considered less valid than other conditions, now they are present among the differential diagnoses of most illnesses in neurology and psychiatry. Diagnostic approaches have markedly changed as phenotypic profiles become more consistent. Treatment strategies include pharmacologic and non-pharmacologic techniques and have a burgeoning presence in medical literature. Above all, conceptualization of FND has advanced to a sophisticated perspective that incorporates neural circuitry and roles of default mode systems as well as salience networks in the brain. The progress made has been groundbreaking and represents a blossoming field, which will require that clinicians update their acumen accordingly.