Background: Currently, there is a marked increase of young people with sudden onset of tic‐like behaviors (TLBs) resembling movements and vocalizations presented on social media videos as “Tourette's syndrome.”Objective: To delineate clinical phenomenology of TLBs after social media exposure in comparison with clinical features of Tourette's syndrome.Methods: We compared demographic and clinical variables between 13 patients with TLBs and 13 age‐ and sex‐related patients with Tourette's syndrome.Results: Patients with TLBs had several characteristics allowing to distinguish them from patients with Tourette's syndrome, some of which discriminated perfectly (ie, abrupt symptom onset, lack of spontaneous symptom fluctuations, symptom deterioration in the presence of others) and some nearly perfectly (ie, predominantly complex movements involving trunk/extremities). Also, symptom onset was significantly later.Conclusions: TLBs after social media consumption differ from tics in Tourette's syndrome, strongly suggesting that these phenomena are categorically different conditions. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society

Background: Pathogenic variants in 5 genes (GCH1, TH, PTS, SPR, and QDPR), involved in dopamine/tetrahydrobiopterin biosynthesis or recycling, have been linked to Dopa‐responsive dystonia (DRD). Diagnosis and treatment are often delayed due to high between‐ and within‐group variability.Objectives: Comprehensively analyzed individual genotype, phenotype, treatment response, and biochemistry information.Methods: 734 DRD patients and 151 asymptomatic GCH1 mutation carriers were included using an MDSGene systematic literature review and an automated classification approach to distinguish between different forms of monogenic DRDs.Results: Whereas dystonia, L‐Dopa responsiveness, early age at onset, and diurnal fluctuations were identified as red flags, parkinsonism without dystonia was rarely reported (11%) and combined with dystonia in only 18% of patients. While sex was equally distributed in autosomal recessive DRD, there was female predominance in autosomal dominant DYT/PARK‐GCH1 patients accompanied by a lower median age at onset and more dystonia in females compared to males. Accordingly, the majority of asymptomatic heterozygous GCH1 mutation carriers (>8 years of age) were males. Multiple other subgroup‐specific characteristics were identified, showing high accuracy in the automated classification approach: Seizures and microcephaly were mostly seen in DYT/PARK‐PTS, autonomic symptoms appeared commonly in DYT/PARK‐TH and DYT/PARK‐PTS, and sleep disorders and oculogyric crises in DYT/PARK‐SPR. Biochemically, homovanillic acid and 5‐hydroxyindoleacetic acid in CSF were reduced in most DRDs, but neopterin and biopterin were increased only in DYT/PARK‐PTS and DYT/PARK‐SPR. Hyperphenylalaninemia was seen in DYT/PARK‐PTS, DYT/PARK‐QDPR, and rarely reported in autosomal recessive DYT/PARK‐GCH1.Conclusions: Our indicators will help to specify diagnosis and accelerate start of treatment. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society

The investigation of action control processes is one major field in cognitive neuroscience and several theoretical frameworks have been proposed. One established framework is the “Theory of Event Coding” (TEC). However, only rarely, this framework has been used in the context of response inhibition and how stimulus-response association or binding processes modulate response inhibition performance. Particularly the neural dynamics of stimulus-response representations during inhibitory control are elusive. To address this, we examined n = 40 healthy controls and combined temporal EEG signal decomposition with source localization and temporal generalization multivariate pattern analysis (MVPA). We show that overlaps in features of stimuli used to trigger either response execution or inhibition compromised task performance. According to TEC, this indicates that binding processes in event file representations impact response inhibition through partial repetition costs. In the EEG data, reconfiguration of event files modulated processes in time windows well-known to reflect distinct response inhibition mechanisms. Crucially, event file coding processes were only evident in a specific fraction of neurophysiological activity associated with the inferior parietal cortex (BA40). Within that specific fraction of neurophysiological activity, the decoding of the dynamics of event file representations using temporal generalization MVPA suggested that event file representations are stable across several hundred milliseconds, and that event file coding during inhibitory control is reflected by a sustained activation pattern of neural dynamics. NEW & NOTEWORTHY The “mental representation” of how stimulus input translate into the appropriate response is central for goal-directed behavior. However, little is known about the dynamics of such representations on the neurophysiological level when it comes to the inhibition of motor processes. This dynamic is shown in the current study.

Non-invasive brain stimulation techniques including repetitive transcranial magnetic stimulation (rTMS), continuous theta-burst stimulation (cTBS), paired associative stimulation (PAS), and transcranial direct current stimulation (tDCS) have been applied over the cerebellum to induce plasticity and gain insights into the interaction of the cerebellum with neo-cortical structures including the motor cortex. We compared the effects of 1 Hz rTMS, cTBS, PAS and tDCS given over the cerebellum on motor cortical excitability and interactions between the cerebellum and dorsal premotor cortex / primary motor cortex in two within subject designs in healthy controls. In experiment 1, rTMS, cTBS, PAS, and tDCS were applied over the cerebellum in 20 healthy subjects. In experiment 2, rTMS and PAS were compared to sham conditions in another group of 20 healthy subjects. In experiment 1, PAS reduced cortical excitability determined by motor evoked potentials (MEP) amplitudes, whereas rTMS increased motor thresholds and facilitated dorsal premotor-motor and cerebellum-motor cortex interactions. TDCS and cTBS had no significant effects. In experiment 2, MEP amplitudes increased after rTMS and motor thresholds following PAS. Analysis of all participants who received rTMS and PAS showed that MEP amplitudes were reduced after PAS and increased following rTMS. rTMS also caused facilitation of dorsal premotor-motor cortex and cerebellum-motor cortex interactions. In summary, cerebellar 1 Hz rTMS and PAS can effectively induce plasticity in cerebello-(premotor)-motor pathways provided larger samples are studied.

Background: Functional movement disorders (FMD) are associated with considerable morbidity and impairment of quality of life. Specialized treatment is scarce and data on efficacy of different therapies are limited.Objective: To evaluate a multi‐modal inpatient treatment program for patients with FMD.Methods: Thirty‐one patients with FMD were analyzed before (t1) and after multi‐modal inpatient treatment (t2) by a blinded video rating using the Psychogenic Movement Disorder Rating Scale (PMDRS), the simplified Functional Movement Disorder Rating Scale (S‐FMDRS), and the Clinical Global Impression Scale of Severity (CGI‐S), as well as patients' self‐rating. In 23 out of 31 patients a 5 months follow‐up investigation was performed (t3). Wilcoxon signed‐rank test and Friedman test were used for rating scale and self‐rating comparisons over time. Spearman correlation was used for correlation of symptom improvement and clinical characteristics.Results: Video rating revealed significant reduction of scores after therapy (median PMDRS t1 = 24, t2 = 8, P = 0.0006; S‐FMDRS t1 = 11, t2 = 4, P = 0.008; CGI‐S t1 = 4, t2 = 3, P = 0.000136) with sustained score decrease in follow‐up evaluations (PMDRS t1 = 31, t2 = 8, t3 = 7, P = 0.000032; S‐FMDRS t1 = 12, t2 = 4, t3 = 3, P = 0.000888; CGI‐S t1 = 4, t2 = 3, t3 = 3, P = 0.000032). Patients reported a stable reduction of symptoms in the self‐rating (CGI‐S t1 = 5, t2 = 4, t3 = 4, P = 0.016). Age correlated with treatment response with older patients showing better improvement, but disease duration did not correlate with outcome. Patients who suffered from physical trauma, sexual or physical abuse had smaller score reductions.Conclusion: Blinded video and self‐rating assessment showed significant score reduction in patients with FMD after an individualized interdisciplinary inpatient intervention.

Transcranial current stimulation (tCS) techniques have been shown to induce cortical plasticity. As an important relay in the motor system, the cerebellum is an interesting target for plasticity induction using tCS, aiming to modulate its excitability and connectivity. However, until now it remains unclear, which is the most effective tCS method for inducing plasticity in the cerebellum. Thus, in this study, the effects of anodal transcranial direct current stimulation (tDCS), 50 Hz transcranial alternating current stimulation (50 Hz tACS), and high frequency transcranial random noise stimulation (tRNS) were compared with sham stimulation in 20 healthy subjects in a within-subject design. tCS was applied targeting the cerebellar lobe VIIIA using neuronavigation. We measured corticospinal excitability, short-interval intracortical inhibition (SICI), short-latency afferent inhibition (SAI), and cerebellar brain inhibition (CBI) and performed a sensor-based movement analysis at baseline and three times after the intervention (post1 = 15 min; post2 = 55 min; post3 = 95 min). Corticospinal excitability increased following cerebellar tACS and tRNS compared to sham stimulation. This effect was most pronounced directly after stimulation but lasted for at least 55 min after tACS. Cortico-cortical and cerebello-cortical conditioning protocols, as well as sensor-based movement analyses, did not change. Our findings suggest that cerebellar 50 Hz tACS is the most effective protocol to change corticospinal excitability.