Transnasal Endoscopic Injection of Botulinum Toxin in Patients with Adductor Spasmodic Dysphonia.

Introduction: Adductor Spasmodic Dysphonia (ADSD) is the most common form of spasmodic dysphonia. It encompasses various symptoms affecting voice and speech. The objective of this study is to report the management of patients with ADSD using the transnasal endoscopic approach for laryngeal Botulinum Toxin (Botox) injection. Materials and Methods: A retrospective chart review of patients with ADSD who underwent transnasal endoscopic laryngeal Botox injection was conducted. Voice outcome measures included the Voice Handicap Index-10 (VHI-10) score and the degree of speech fluency. Results: Eight patients with ADSD who underwent 20 office-based transnasal endoscopic laryngeal Botox injections were included. The most commonly injected sites were the thyroarytenoid muscle (TA) and the false vocal fold in 95% and 55% of the cases, respectively. The mean dose of injected Botox was 2.48 ± 0.55 IU in the TA muscle, and 2.14 ± 0.53 IU in the false vocal fold. The mean amount of Botox injected in the larynx was 7.16 ± 2.42 IU. The mean follow-up period was 17.7 ± 13.3 months. There was marked improvement in speech fluency in 64.7% of the cases and mild improvement in one third of the cases. Marked improvement in speech fluency was recorded in 64.7% of the cases and mild improvement in one third of the cases. The mean VHI-10 score of patients dropped significantly from 22.47±4.08 to 15±4.69 following treatment (p<0.001). Conclusions: The transnasal endoscopic approach is an effective and well-tolerated approach for laryngeal Botox injection in patients with ADSD.

Next move in movement disorders: neuroimaging protocols for hyperkinetic movement disorders.

Introduction: The Next Move in Movement Disorders (NEMO) study is an initiative aimed at advancing our understanding and the classification of hyperkinetic movement disorders, including tremor, myoclonus, dystonia, and myoclonus-dystonia. The study has two main objectives: (a) to develop a computer-aided tool for precise and consistent classification of these movement disorder phenotypes, and (b) to deepen our understanding of brain pathophysiology through advanced neuroimaging techniques. This protocol review details the neuroimaging data acquisition and preprocessing procedures employed by the NEMO team to achieve these goals. Methods and analysis: To meet the study's objectives, NEMO utilizes multiple imaging techniques, including T1-weighted structural MRI, resting-state fMRI, motor task fMRI, and 18F-FDG PET scans. We will outline our efforts over the past 4 years to enhance the quality of our collected data, and address challenges such as head movements during image acquisition, choosing acquisition parameters and constructing data preprocessing pipelines. This study is the first to employ these neuroimaging modalities in a standardized approach contributing to more uniformity in the analyses of future studies comparing these patient groups. The data collected will contribute to the development of a machine learning-based classification tool and improve our understanding of disorder-specific neurobiological factors. Ethics and dissemination: Ethical approval has been obtained from the relevant local ethics committee. The NEMO study is designed to pioneer the application of machine learning of movement disorders. We expect to publish articles in multiple related fields of research and patients will be informed of important results via patient associations and press releases.

Canine paroxysmal dyskinesia-a review.

Paroxysmal dyskinesias (PDs) are a group of involuntary, hyperkinetic movement disorders that recur episodically and may last seconds to hours. An important feature of PD is that there is no loss of consciousness during the episode. Using a clinical classification, three main types of PDs have been distinguished in canine PD: (1) paroxysmal kinesigenic dyskinesia (PKD) that commences after (sudden) movements, (2) paroxysmal non-kinesigenic dyskinesia (PNKD) not associated with exercise and can occur at rest, and (3) paroxysmal exertion-induced dyskinesia (PED) associated with fatigue. Canine PDs are diagnosed based on the clinical presentation, history, and phenomenology. For the latter, a video recording of the paroxysmal event is extremely useful. An etiological classification of canine PDs includes genetic (proven and suspected), reactive (drug-induced, toxic, metabolic, and dietary), structural (neoplasia, inflammatory, and other structural causes), and unknown causes. In this review, an overview of all reported canine PDs is provided with emphasis on phenotype, genotype, and, where possible, pathophysiology and treatment for each reported canine PD.

Hyperkinetic Biliary Dyskinesia: An Underrecognized Problem With Good Surgical Outcomes After Cholecystectomy.

Introduction While surgical indications for symptomatic cholelithiasis and biliary hypokinesia are clear, hyperkinetic biliary dyskinesia (HBD) is an underrecognized condition with poorly defined symptomology and management guidelines. HBD is typically defined as a gallbladder ejection fraction (EF) ≥ 80% on a hepatobiliary iminodiacetic acid (HIDA) scan. We aimed to identify the prevalence and radiographic reporting of HBD, physician referral patterns, and clinical outcomes following cholecystectomy. Methods  A retrospective cohort study of patients with HIDA scans completed over 21 years at our tertiary care hospital was performed. Demographics, symptomatology, referral patterns, and operative data were collected. HBD was defined as HIDA EF ≥80%. Patients with HBD who underwent cholecystectomy were analyzed. ANOVA and chi-square tests were used to compare variables among patients with or without symptom improvement using Statistical Product and Service Solutions (SPSS; IBM SPSS Statistics for Windows, Armonk, NY). Results Of 1,997 patients (73% female, mean age 51.7 years) who had HIDA scans with reported EF, 730 (36.6%) had an EF≥80%. Only 13.7% of HIDA scans with EF≥80% were reported as hyperkinetic, and the rest are "normal". Cholecystectomy was performed in 57 (7.8%) patients with EF≥80%, most being elective (89.5%) and all minimally invasive. Primary care physicians (PCPs) referred most elective cases to surgery (61.4%). The median time from HIDA to cholecystectomy was 146 days. Chronic cholecystitis was common in pathology (82.5%), while 38.6% had cholelithiasis. Overall, 53 patients (93.0%) reported symptom improvement at a median follow-up of 17.0 days. Patients without improvement had a higher prevalence of chronic gastrointestinal conditions (p<0.05), but not significantly more cholelithiasis, cholecystitis, time to surgery, or elective surgery status. Conclusions HBD is common but often underdiagnosed and thus likely underrecognized by treating physicians. Most HBD patients benefit from cholecystectomy, regardless of cholelithiasis. Patients with persistent symptoms after cholecystectomy may have confounding gastrointestinal diagnoses. Increased awareness among radiologists, referring PCPs, gastroenterologists, and surgeons about HBD and postoperative outcomes is needed to ensure that HBD is adequately treated.

Nocturnal paroxysmal dystonia to sleep-related hypermotor epilepsy: A critical review.

Sleep-related paroxysmal motor episodes (SPMEs) have been described by various names, including nocturnal paroxysmal dystonia, nocturnal frontal lobe epilepsy (NFLE), and sleep-related hypermotor epilepsy. The underlying pathophysiology has been debated over the years, with these episodes assumed to be a form of paroxysmal dystonia or parasomnia versus a form of epilepsy. In most studies published on SPMEs and their variants (paroxysmal arousals, nocturnal paroxysmal dystonia, and episodic nocturnal wanderings) in the early 1990s, the authors speculated on the pathophysiology but did not commit to one idea. It was not until the mid-1990s that epilepsy became the leading prospect. We performed a narrative review of the major articles that have described this syndrome in a chronological fashion. We identified three eras, 1972-1993, 1994-1998, and 1999 to the present, each era marked by a landmark study. Our critical review of these early studies shows that the neurophysiological data supporting epilepsy as the sole basis for all SPME cases is very weak. In 1994-1995, a familial pattern of this syndrome was described and the term autosomal dominant NFLE was coined, with the authors claiming that all their patients had a form of frontal lobe epilepsy. With the exception of a few reference cases, the neurophysiological evidence that all patients had frontal lobe epilepsy was very weak. Compared to articles published on surgical series of frontal lobe epilepsy, the percentage of SPME cases with positive interictal/ictal electroencephalograms remained very low, seriously questioning the epileptic basis of the syndrome. Our critical review and analysis of the published literature shows that the evidence presented in favor of SPMEs being a homogenous focal epilepsy syndrome is very weak. Neurologists must recognize that SPMEs could be a form of movement disorder, parasomnia, or epilepsy. We recommend a pragmatic semiology-based classification of these episodes using the four-dimensional classification system.

Symptomatic Treatment of Extrapyramidal Hyperkinetic Movement Disorders.

Extrapyramidal hyperkinetic movement disorders comprise a broad range of phenotypic phenomena, including chorea, dystonia, and tics. Treatment is generally challenging and individualized, given the overlapping phenomenology, limited evidence regarding efficacy, and concerns regarding the tolerability and safety of most treatments. Over the past decade, the treatment has become even more intricate due to advancements in the field of deep brain stimulation as well as optimized dopamine- depleting agents. Here, we review the current evidence for treatment modalities of extrapyramidal hyperkinetic movement disorders and provide a comprehensive and practical overview to aid the choice of therapy. Mechanism of action and practical intricacies of each treatment modality are discussed, focusing on dosing and adverse effect management. Finally, future therapeutic developments are also discussed.

Exploring the Genetic Landscape of Chorea in Infancy and Early Childhood: Implications for Diagnosis and Treatment.

Chorea is a hyperkinetic movement disorder frequently observed in the pediatric population, and, due to advancements in genetic techniques, an increasing number of genes have been associated with this disorder. In genetic conditions, chorea may be the primary feature of the disorder, or be part of a more complex phenotype characterized by epileptic encephalopathy or a multisystemic syndrome. Moreover, it can appear as a persistent disorder (chronic chorea) or have an episodic course (paroxysmal chorea). Managing chorea in childhood presents challenges due to its varied clinical presentation, often involving a spectrum of hyperkinetic movement disorders alongside neuropsychiatric and multisystemic manifestations. Furthermore, during infancy and early childhood, transient motor phenomena resembling chorea occurring due to the rapid nervous system development during this period can complicate the diagnosis. This review aims to provide an overview of the main genetic causes of pediatric chorea that may manifest during infancy and early childhood, focusing on peculiarities that can aid in differential diagnosis among different phenotypes and discussing possible treatment options.

Hyperkinetic Movement Disorder Caused by the Recurrent c.892C>T NACC1 Variant.

BACKGROUND: Genetic syndromes of hyperkinetic movement disorders associated with epileptic encephalopathy and intellectual disability are becoming increasingly recognized. Recently, a de novo heterozygous NACC1 (nucleus accumbens-associated 1) missense variant was described in a patient cohort including one patient with a combined mitochondrial oxidative phosphorylation (OXPHOS) deficiency. OBJECTIVES: The objective is to characterize the movement disorder in affected patients with the recurrent c.892C>T NACC1 variant and study the NACC1 protein and mitochondrial function at the cellular level. METHODS: The movement disorder was analyzed on four patients with the NACC1 c.892C>T (p.Arg298Trp) variant. Studies on NACC1 protein and mitochondrial function were performed on patient-derived fibroblasts. RESULTS: All patients had a generalized hyperkinetic movement disorder with chorea and dystonia, which occurred cyclically and during sleep. Complex I was found altered, whereas the other OXPHOS enzymes and the mitochondria network seemed intact in one patient. CONCLUSIONS: The movement disorder is a prominent feature of NACC1-related disease.

Case Report: Chorea as a Rare Manifestation of Secondary Adrenal Insufficiency.

The word "chorea" comes from the Latin word "choreus," which means dancing movement. Chorea is defined as a hyperkinetic movement disorder characterized by uncontrolled, unintended, jerky, brief, irregular, random movements involving the limbs or facial muscles. Here, we discuss the case of a 48-year-old male with hypothyroidism for two years, which is well-controlled with medication. He presented with behavioral disturbances for the past seven months and choreiform movements affecting all four limbs, his tongue, and his face for the past six months. Investigations revealed hyponatremia and low serum osmolality. An MRI of the brain showed the empty sella sign. Further investigations revealed low levels of adrenocorticotropic hormone (ACTH), prolactin, and testosterone. Considering the diagnosis of chorea with euvolemic hyponatremia due to secondary adrenal insufficiency, the patient was started on tetrabenazine, trihexyphenidyl, oral hydrocortisone, and gradual correction of sodium level. The patient's condition improved during the hospital stay, and he continues to do well in routine follow-ups.

Botulinum neurotoxin as early treatment in acute-onset lesional hemiballism.

BACKGROUND: Hemiballism (HB) and hemichorea (HC) are the most frequent secondary movement disorders, usually caused by cerebrovascular diseases. In only a minority of cases, these involuntary movements are not self-limited, and they may severely compromise patients' quality of life, so that symptomatic treatments are required. Typical and atypical neuroleptics as well as tetrabenazine are considered therapies of choice. However, anecdotal reports of antiseizures medications and botulinum neurotoxin injection effectiveness have been described. METHODS: We described a case of severely disabling acute-onset lesional HB/HC, where high dosage of first- and second-line therapies was contraindicated due to patient's comorbidities. RESULTS: After botulin neurotoxin (BoNT) injections in his left upper limb muscles (biceps brachii, triceps brachii, teres major, and deltoid), the patient experienced gradual reduction of hyperkinetic movements. The gradual discontinuation of topiramate (TPM) did not worsen the clinical picture. DISCUSSION: The reduction of hyperkinetic movements led to rhabdomyolysis resolution as well as cutaneous injuries healing with renal function improvement, so that the patient was able to be eligible for rehabilitation, which was prevented by HB/HC itself. The clinical improvement was consistent with BoNT pharmacokinetic. The administration of BoNT early after the onset of lesional HB/HC remarkably modified the clinical management and drove toward comorbidities resolution and rehabilitation. CONCLUSION: The present case highlights the effectiveness of unconventional therapeutic options in disabling acute onset lesional HB/HC when first-line therapies are contraindicated. Particularly, this report may encourage BoNT application in the early stage of movement disorder emergencies.

Flapping Tremor: Unraveling Asterixis-A Narrative Review.

Asterixis is a subtype of negative myoclonus characterized by brief, arrhythmic lapses of sustained posture due to involuntary pauses in muscle contraction. We performed a narrative review to characterize further asterixis regarding nomenclature, historical aspects, etiology, pathophysiology, classification, diagnosis, and treatment. Asterixis has been classically used as a synonym for negative myoclonus across the literature and in previous articles. However, it is important to distinguish asterixis from other subtypes of negative myoclonus, for example, epileptic negative myoclonus, because management could change. Asterixis is not specific to any pathophysiological process, but it is more commonly reported in hepatic encephalopathy, renal and respiratory failure, cerebrovascular diseases, as well as associated with drugs that could potentially lead to hyperammonemia, such as valproic acid, carbamazepine, and phenytoin. Asterixis is usually asymptomatic and not spontaneously reported by patients. This highlights the importance of actively searching for this sign in the physical exam of encephalopathic patients because it could indicate an underlying toxic or metabolic cause. Asterixis is usually reversible upon treatment of the underlying cause.

DHDDS-related disease; biallelic missense novel variant causing major severity with an early-onset epilepsy and hyperkinetic movement disorder.

BACKGROUND: Dehydrodolichyl diphosphate synthase complex is encoded by DHDDS. De novo mutations in this gene are associated with epilepsy, movement disorders, intellectual and motor disabilities. The clinical picture is commonly identified in children and shows variations in terms of age of onset, severity, seizure types, and types of dyskinesia. CASE: we present a case with a infantile- onset epilepsy and severe global developmental delay, caused by a novel, de novo homozygous variant (c.425C > T, p.Thr142Met) in DHDDS. Clinical improvement was achieved with valproate and tetrabenazine treatments in the 2-year-old male patient with drug-resistant epilepsy, hyperkinetic movement disorder and myoclonus. CONCLUSION: Despite being rare, DHDDS-related diseases should be considered in patients with movement disorders, seizures and global developmental delay in infancy in differential diagnosis of patients resembling neuronal ceroid lipofuscinosis or progressive myoclonic epilepsies.

Analysis of characteristics of movement disorders in patients with anti-N-methyl-D-aspartate receptor encephalitis.

Objective: Movement disorders (MDs) are common in anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis but are poorly studied. This study aimed to investigate the clinical characteristics of MDs and the clinical differences between patients with and without MDs in anti-NMDAR encephalitis. Methods: A retrospective study was conducted on patients with anti-NMDAR encephalitis who were first diagnosed and treated in the First People's Hospital of Yunnan Province from January 2017 to September 2022. According to the presence or absence of MDs, all patients were divided into two groups, and the clinical manifestations, auxiliary examinations, and prognosis of the two groups were compared. Patients in the MDs group were further subgrouped by different ages (<12 years, 12-17 years, and ≥ 18 years) and genders, and the prevalence of each MD was compared in different age and gender groups. Results: (1) In our study there were 64 patients, of whom 76.6% (49/64) presented with MDs; the median age of onset in patients with MDs was 21 (15,35) years and 65.3% (32/49) were female. The three most common MDs were orofacial dyskinesia (OFLD) (67.3%), dystonia (55.1%), and stereotypies (34.7%). Patients <12 years were more likely to experience chorea than patients in other age groups (p = 0.003). (2) Compared with the non-MDs group, patients in the MDs group showed higher rates of prodromal manifestations, autonomic dysfunction, consciousness disorders, as well as pulmonary infection and gastrointestinal dysfunction (all p < 0.05). Peripheral blood neutrophil to lymphocyte ratio (NLR) (p = 0.014), the proportion of cerebrospinal fluid (CSF) NMDAR antibody titers ≥1:32 (p = 0.047), ICU admission rate (p = 0.04), length of stay (p = 0.007), maximum mRS score in the course of disease (p = 0.001) and mRS score at discharge (p = 0.006) in the MDs group were significantly higher than the non-MDs group. Conclusion: MDs associated with anti-NMDAR encephalitis were predominantly hyperkinetic. Chorea occurred more commonly in patients aged <12 years. Patients with MDs were prone to autonomic dysfunction, consciousness disorders, pulmonary infection, and gastrointestinal dysfunction; they had more intense inflammation, more severe disease, and a poorer short-term prognosis.

Genetic testing for non-parkinsonian movement disorders: Navigating the diagnostic maze.

Genetic testing has become a valuable diagnostic tool for movement disorders due to substantial advancements in understanding their genetic basis. However, the heterogeneity of movement disorders poses a significant challenge, with many genes implicated in different subtypes. This paper aims to provide a neurologist's perspective on approaching patients with hereditary hyperkinetic disorders with a focus on select forms of dystonia, paroxysmal dyskinesia, chorea, and ataxia. Age at onset, initial symptoms, and their severity, as well as the presence of any concurrent neurological and non-neurological features, contribute to the individual clinical profiles of hereditary non-parkinsonian movement disorders, aiding in the selection of appropriate genetic testing strategies. There are also more specific diagnostic clues that may facilitate the decision-making process and may be highly specific for certain conditions, such as diurnal fluctuations and l-dopa response in dopa-responsive dystonia, and triggering factors, duration and frequency of attacks in paroxysmal dyskinesia. While the genetic and mutational spectrum across non-parkinsonian movement disorders is broad, certain groups of diseases tend to be associated with specific types of pathogenic variants, such as repeat expansions in many of the ataxias. Some of these pathogenic variants cannot be detected by standard methods, such as panel or exome sequencing, but require the investigation of intronic regions for repeat expansions, such as Friedreich's or FGF14-linked ataxia. With our advancing knowledge of the genetic underpinnings of movement disorders, the incorporation of precise and personalized diagnostic strategies can enhance patient care, prognosis, and the application and development of targeted therapeutic interventions.

Prevalence and prognosis of hyperdynamic left ventricular systolic function in septic patients: a systematic review and meta-analysis.

PURPOSE: The prevalence of hyperdynamic left ventricular (LV) systolic function in septic patients and its impact on mortality remain controversial. In this systematic review and meta-analysis, we investigated the prevalence and association of hyperdynamic LV systolic function with mortality in patients with sepsis. METHODS: We searched MEDLINE, Cochrane Central Register of Controlled Trials, and Embase. Primary outcomes were the prevalence of hyperdynamic LV systolic function in adult septic patients and the associated short-term mortality as compared to normal LV systolic function. Hyperdynamic LV systolic function was defined using LV ejection fraction (LVEF) of 70% as cutoff. Secondary outcomes were heart rate, LV end-diastolic diameter (LVEDD), and E/e' ratio. RESULTS: Four studies were included, and the pooled prevalence of hyperdynamic LV systolic function was 18.2% ([95% confidence interval (CI) 12.5, 25.8]; I2 = 7.0%, P < 0.0001). Hyperdynamic LV systolic function was associated with higher mortality: odds ratio of 2.37 [95%CI 1.47, 3.80]; I2 = 79%, P < 0.01. No difference was found in E/e' (P = 0.43) between normal and hyperdynamic LV systolic function, while higher values of heart rate (mean difference: 6.14 beats/min [95%CI 3.59, 8.69]; I2 = 51%, P < 0.0001) and LVEDD (mean difference: - 0.21 cm [95%CI - 0.33, - 0.09]; I2 = 73%, P < 0.001) were detected in patients with hyperdynamic LV systolic function. CONCLUSION: The prevalence of hyperdynamic LV systolic function is not negligible in septic patients. Such a finding is associated with significantly higher short-term mortality as compared to normal LV systolic function.

Psychoeducation for adult ADHD: a scoping review about characteristics, patient involvement, and content.

BACKGROUND: Psychosocial interventions such as psychoeducation are increasingly being used to treat adult ADHD, both as an alternative and as a supplement to pharmacotherapy. A thorough overview of the literature on psychoeducation for adult ADHD is lacking. The objectives of this scoping review were therefore to identify the characteristics of psychoeducation interventions designed for adults with ADHD, examine how the patient experience or perspective is considered during the intervention's development and implementation, determine the typical themes covered, and explore how 'psychoeducation' is defined in these interventions. METHODS: A comprehensive search was performed to identify records in MEDLINE, Embase, PsycINFO, Web of Science, Cochrane CENTRAL, AMED, and ClinicalTrials.gov. Two or more reviewers were included in every step of the screening process and the final selection of included studies. The Preferred Reporting Items for Systematic reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) checklist (Supplementary Material 1) was used to report the results, and the framework developed by Arksey and O'Malley was used as a guide throughout the scoping process. RESULTS: A total of 2121 records were identified through the literature search. After screening and full-text analysis, ten studies were included for final analysis. Most studies were conducted in Europe and followed a group format. Seven main themes were identified: Information about the diagnosis, treatment options, somatic health and ADHD, the insider perspective, ADHD and social life, coping and psychological skills, and ADHD and work. There was significant overlap in themes covered, but coverage of each theme varied. Themes deemed important by newer research, such as sexuality and gender-specific issues, were missing. Only one intervention involved patients in its development and implementation, and two interventions involved family members. There was variation in how psychoeducation was defined in the included studies, and the implications of this are discussed. CONCLUSION: The literature on psychoeducation for adult ADHD is not ready for any systematic effect estimation. Before such estimations are conducted, a shared understanding and definition of psychoeducation are needed. The involvement of end users in the development and delivery of interventions may aid reach this goal but results from this review indicate that such practices are rare.

Challenges in Interpreting Norwegian Child and Adolescent Mental Health Records.

The Electronic Health Record system BUPdata served Norwegian Child and Adolescent Mental Health Services (CAMHS) for over 35 years and is still an important source of information for understanding clinical practice. Secondary usage of clinical data enables learning and service quality improvement. We present some insights from explorative data analysis for interpreting the records of patients referred for hyperkinetic disorders. The major challenges were data preparation, pre-analysis, imputation, and validation. We summarize the main characteristics, spot anomalies, and detect errors. The results include observations about the patient referral diversity based on 12 different variables. We modeled the activities in an individual episode of care, described our clinical observations among data, and discussed the challenges of data analysis.

Co-morbid tics and stereotypies: a systematic literature review.

BACKGROUND: Tics and stereotypies are childhood-onset repetitive behaviours that can pose significant diagnostic challenges in clinical practice. Both tics and stereotypies are characterised by a complex co-morbidity profile, however little is known about the co-occurrence of these hyperkinetic disorders in the same patient population. OBJECTIVE: This review aimed to assess the relationship between tics and stereotypies when these conditions present in co-morbidity. METHODS: We conducted a systematic literature review of original studies on co-morbid tics and stereotypies, according to the standards outlined in the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. RESULTS: Our literature search identified six studies of suitable sample size (n ≥ 40) presenting data on the association between tics and stereotypies in otherwise typically developing patients. A considerable proportion (23%) of patients diagnosed with stereotypic movement disorder present with co-morbid tics (range 18-43%). Likewise, the prevalence of primary stereotypies is increased in patients with tic disorders such as Tourette syndrome (8%, range 6-12%). DISCUSSION: Tics and stereotypies can often develop in co-morbidity. The association of tics and stereotypies in the same patient has practical implications, in consideration of the different treatment approaches. Future research should focus on the assessment and management of both conditions, particularly in special populations (e.g. patients with pervasive developmental disorders).