Dystonia Research Articles

Neuropsychological Functioning in Primary Dystonia: Updated and Expanded Multidomain Meta-Analysis.

Primary dystonia is conventionally considered as a motor disorder, though an emerging literature reports associated cognitive dysfunction. Here, we conducted meta-analyses on studies comparing clinical measures of cognition in persons with primary dystonia and healthy controls (HCs). We searched PubMed, Embase, Cochrane Library, Scopus, and PsycINFO (January 2000-October 2020). Analyses were modeled under random effects. We used Hedge's g as a bias-corrected estimate of effect size, where negative values indicate lower performance in dystonia versus controls. Between-study heterogeneity and bias were primarily assessed with Cochran's Q, I2 , and Egger's regression. From 866 initial results, 20 studies met criteria for analysis (dystonia n = 739, controls n = 643; 254 effect sizes extracted). Meta-analysis showed a significant combined effect size of primary dystonia across all studies (g = -0.56, P < 0.001), with low heterogeneity (Q = 25.26, P = 0.15, I2 = 24.78). Within-domain effects of primary dystonia were motor speed = -0.84, nonmotor speed = -0.83, global cognition = -0.65, language = -0.54, executive functioning = -0.53, learning/memory = -0.46, visuospatial/construction = -0.44, and simple/complex attention = -0.37 (P-values <0.01). High heterogeneity was observed in the motor/nonmotor speed and learning/memory domains. There was no evidence of publication bias. Moderator analyses were mostly negative but possibly underpowered. Blepharospasm samples showed worse performance than other focal/cervical dystonias. Those with inherited (ie, genetic) disease etiology demonstrated worse performance than acquired. Dystonia patients consistently demonstrated lower performances on neuropsychological tests versus HCs. Effect sizes were generally moderate in strength, clustering around -0.50 SD units. Within the speed domain, results suggested cognitive slowing beyond effects from motor symptoms. Overall, findings indicate dystonia patients experience multidomain cognitive difficulties, as detected by neuropsychological tests. © 2022 International Parkinson and Movement Disorder Society.

Shedding light on the phenotypic\u2013genotypic correlation of rare treatable and potentially treatable pediatric movement disorders

BackgroundAdvances in genetic science have led to the identification of many rare treatable pediatric movements disorders (MDs). We explored the phenotypic–genotypic spectrum of pediatric patients presenting with MDs. By this, we aimed at raising awareness about such rare disorders, especially in our region. Over the past 3 years, we reviewed the demographic data, clinical profile, molecular genetics and other diagnostic workups of pediatric patients presenting with MDs.ResultsTwelve patients were identified; however, only six patients were genetically confirmed. The phenomenology of MDs ranged from paroxysmal kinesigenic choreoathetosis (1 patient), exercise-induced dyskinesia (2 patients), ataxia (2 patients) and dystonia (2 patients). Whole-exome sequencing in addition to the functional studies for some patients revealed a specific genetic diagnosis being responsible for their MDs. The genetic diagnosis of our patients included infantile convulsions and paroxysmal choreoathetosis syndrome and episodic ataxia due to “pathogenic homozygous mutation of PRRT2 gene,” glucose transporter type 1 deficiency-exercise induced dyskinesia due to “De Novo pathogenic heterozygous missense mutation of exon 4 of SLC2A1 gene,” aromatic L amino acid decarboxylase deficiency due to “pathogenic homozygous mutation of the DDC gene,” myopathy with extrapyramidal signs due to “likely pathogenic homozygous mutations of the MICU1 gene,” mitochondrial trifunctional protein deficiency due to “homozygous variant of uncertain significance (VUS) of HADHB gene” and glutaric aciduria II with serine deficiency due to “homozygous VUS for both ETFDH and PHGDH genes.” After receiving the treatment as per recognized treatment protocols, two patients showed complete resolution of symptoms and the rest showed variable responses.ConclusionIdentifying the genetic etiology of our patients guided us to provide either disease-specific treatment or redirected our management plan. Hence, highlighting the value of molecular genetic analysis to avoid the diagnostic odyssey and identify treatable MDs.

A Rare Case of Domperidone-Induced Acute Dystonia in a Young Adult Due to Consumption of Combination Drug (Proton Pump Inhibitors With Domperidone) and Its Possible Pathomechanism

Globally, a substantial number of people are tormented by dystonia. Domperidone, a D-2 receptor antagonist acts outside the blood-brain barrier in the brain stem as well as on the gastrointestinal tract. In India, domperidone is conveniently obtainable over the counter as a combination drug with proton pump inhibitors (PPIs) for dyspepsia and gastro-esophageal reflux disease. We present a rare case of domperidone-induced acute dystonia in a young adult presented within 72 hours after consuming two oral doses of this combination drug (PPIs with domperidone) for dyspepsia. Drug-induced extra pyramidal symptoms (EPS) are often misdiagnosed as some psychiatric condition and undoubtedly its expeditious diagnosis staves off unnecessary investigations and ameliorates prognosis. Our case ignites alertness amongst practitioners in India over the judicious use of PPIs with domperidone as the latter may trigger EPS. Such combination drugs can be prescribed if absolutely mandatory by the treating physician. The possible pathomechanism of this hyperkinetic motor phenomenon, perturbing the equilibrium of the cortical-subcortical circuit and resulting in an overflow of muscular activity, is attempted to be explained here, although the explicit mechanism is still blurry.

Cortical and Subcortical Structural Abnormalities in Patients With Idiopathic Cervical and Generalized Dystonia.

In this study, we sought to investigate structural imaging alterations of patients with idiopathic dystonia at the cortical and subcortical levels. The common and specific changes in two subtypes of dystonia, cervical dystonia (CD) and generalized dystonia (GD), were intended to be explored. Additionally, we sought to identify the morphometric measurements which might be related to patients' clinical characteristics, thus providing more clues of specific brain regions involved in the mechanism of idiopathic dystonia. 3D T1-weighted MRI scans were acquired from 56 patients with idiopathic dystonia and 30 healthy controls (HC). Patients were classified as CD or GD, according to the distinct symptom distributions. Cortical thickness (CT) of 30 CD and 26 GD were estimated and compared to HCs using Computational Anatomy Toolbox (CAT12), while volumes of subcortical structures and their shape alterations (29 CD, 25 GD, and 27 HCs) were analyzed via FSL software. Further, we applied correlation analyses between the above imaging measurements with significant differences and patients' clinical characteristics. The results of comparisons between the two patient groups and HCs were highly consistent, demonstrating increased CT of bilateral postcentral, superiorparietal, superiorfrontal/rostralmiddlefrontal, occipital gyrus, etc., and decreased CT of bilateral cingulate, insula, entorhinal, and fusiform gyrus (PFWE < 0.005 at the cluster level). In CD, trends of negative correlations were found between disease severity and CT alterations mostly located in pre/postcentral, rostralmiddlefrontal, superiorparietal, and supramarginal regions. Besides, volumes of bilateral putamen, caudate, and thalamus were significantly reduced in both patient groups, while pallidum volume reduction was also presented in GD compared to HCs. Caudate volume reduction had a trend of correlation to increasing disease severity in GD. Last, shape analysis directly demonstrated regional surface alterations in bilateral thalamus and caudate, where the atrophy located in the head of caudate had a trend of correlation to earlier ages of onset in GD. Our study demonstrates wide-spread morphometric changes of CT, subcortical volumes, and shapes in idiopathic dystonia. CD and GD presented similar patterns of morphometric abnormalities, indicating shared underlying mechanisms in two different disease forms. Especially, the clinical associations of CT of multiple brain regions with disease severity, and altered volume/shape of caudate with disease severity/age of onset separately in CD and GD might serve as potential biomarkers for further disease exploration.

Optimal deep brain stimulation sites and networks for cervical vs. generalized dystonia

Dystonia is a debilitating disease with few treatment options. One effective option is deep brain stimulation (DBS) to the internal pallidum. While cervical and generalized forms of isolated dystonia have been targeted with a common approach to the posterior third of the nucleus, large-scale investigations regarding optimal stimulation sites and potential network effects have not been carried out. Here, we retrospectively studied clinical results following DBS for cervical and generalized dystonia in a multicenter cohort of 80 patients. We model DBS electrode placement based on pre- and postoperative imaging and introduce an approach to map optimal stimulation sites to anatomical space. Second, we investigate which tracts account for optimal clinical improvements, when modulated. Third, we investigate distributed stimulation effects on a whole-brain functional connectome level. Our results show marked differences of optimal stimulation sites that map to the somatotopic structure of the internal pallidum. While modulation of the striatopallidofugal axis of the basal ganglia accounted for optimal treatment of cervical dystonia, modulation of pallidothalamic bundles did so in generalized dystonia. Finally, we show a common multisynaptic network substrate for both phenotypes in the form of connectivity to the cerebellum and somatomotor cortex. Our results suggest a brief divergence of optimal stimulation networks for cervical vs. generalized dystonia within the pallidothalamic loop that merge again on a thalamo-cortical level and share a common whole-brain network.

Altered Structural Brain Network Topology in Patients With Primary Craniocervical Dystonia.

PurposeRegional cortical thickness or volume analyses based upon structural MRI scans have been employed to study the pathophysiology of primary craniocervical dystonia (CCD). In the present study, brain connectivity network analyses based upon morphological distribution similarities among different brain areas were used to study the network disruption in individuals affected by CCD.MethodsThe T1 MRI scans were completed for 37 patients with CCD and 30 healthy controls, with individual brain structural networks being constructed based upon gray matter (GM) similarities in 90 regions within the brain. Area under the curve (AUC) values for each network parameter were determined, and the GRETNA program was used to conduct a graph theory-based measurement of nodal and global network properties. These properties were then compared between healthy controls and those with CCD. In addition, relationships between nodal properties and the severity of clinical dystonia were assessed through Spearman's correlation analyses.ResultsRelative to individuals in the control group, patients with CCD exhibited decreased local nodal properties in the right globus pallidus, right middle frontal gyrus, and right superior temporal pole. The degree of centrality as well as the node efficiency of the right globus pallidus were found to be significantly correlated with ocular dystonic symptom. The node efficiency of right middle frontal gyrus was significantly related to the total motor severity. No nodal properties were significantly correlated with oral dystonic motor scores. Among CCD patients, the right hemisphere exhibited more widespread decreases in connectivity associated with the motor related brain areas, associative cortex, and limbic system, particularly in the middle frontal gyrus, globus pallidus, and cingulate gyrus.ConclusionsThe assessment of morphological correlations between different areas in the brain may represent a sensitive approach for detecting alterations in brain structures and to understand the mechanistic basis for CCD at the network level. Based on the nodal properties identified in this study, the right middle frontal gyrus and globus pallidus were the most severely affected in patients with CCD. The widespread alterations in morphological connectivity, such as the cortico-cortical and cortico-subcortical networks, further support the network mechanism as a basis for CCD.

EP257: A homozygous nonsense variant in DNAJC30 causes Leigh-like phenotypes

A single exon protein coding gene, DNAJC30, encodes a chaperone protein which enriches in neurons, involves in ATP biosynthesis, and is a regulator of mitochondrial respiration. Here, we report a 12-year-old boy of Guatemalan ancestry who had acute dystonia onset at age 10. Brain MRI showed bilateral basal ganglion and thalamic hyperintensities. He developed bilateral optic atrophy and rapidly progressive vision loss. He also was diagnosed with autism spectrum disorder. Whole exome sequencing analysis of his peripheral blood sample revealed a homozygous nonsense variant, c.24G>A (p.W8X), in the DNAJC30 gene.

Organic Acidemias.

Organic Acidemias.

Functional writer's cramp as psychogenic focal dystonia

We present a description of a functional writer's cramp case. The disease manifested as pain and tension in the right hand when writing; thus, we suspected kinesigenic dystonia in the form of writer's cramp. However, the motor pattern and the presence of additional manifestations made it possible to assume the neurotic nature of hyperkinesis. A psychiatrist diagnosed a combined conversion motor and undifferentiated somatoform disorder as a part of personality dynamics of the dramatic cluster at the involutionary age. Treatment included cognitive-behavioral therapy and periciazine administration with a positive effect. We discuss the aspects of hyperkinesis and mental status, which help differentiate the kinesigenic form of dystonia (writer's cramp) and functional movement disorder.

The Parasomnias and Sleep Related Movement Disorders—A Look Back at Six Decades of Scientific Studies

The objective of this article is to provide a comprehensive personal survey of all the major parasomnias with coverage of their clinical presentation, investigation, physiopathogenesis and treatment. These include the four major members of the slow-wave sleep arousal parasomnias which are enuresis nocturna (bedwetting), somnambulism (sleepwalking), sleep terrors (pavor nocturnus in children, incubus attacks in adults) and confusional arousals (sleep drunkenness). Other parasomnias covered are sleep-related aggression, hypnagogic and hypnopompic terrifying hallucinations, REM sleep terrifying dreams, nocturnal anxiety attacks, sleep paralysis, sleep talking (somniloquy), sexsomnia, REM sleep behavior disorder (RBD), nocturnal paroxysmal dystonia, sleep starts (hypnic jerks), jactatio capitis nocturna (head and total body rocking), periodic limb movement disorder (PLMs), hypnagogic foot tremor, restless leg syndrome (Ekbom syndrome), exploding head syndrome, excessive fragmentary myoclonus, nocturnal cramps, and sleep-related epileptic seizures. There is interest in the possibility of relationships between sleep/wake states and creativity.

Long-term effects of pallidal deep brain stimulation in tardive dystonia: a follow-up of 5–14 years

IntroductionPallidal DBS is an established treatment for severe isolated dystonia. However, its use in disabling and treatment-refractory tardive syndromes (TS) including tardive dyskinesia and tardive dystonia (TD) is less well investigated and long-term data remain sparse. This observational study evaluates long-term effects of deep brain stimulation (DBS) of the globus pallidus internus (GPi) in patients with medically refractory TS.MethodsWe retrospectively analyzed a cohort of seven TD patients with bilateral GPi-DBS. Involuntary movements, dystonia and disability were rated at long-term follow-up (LT-FU) after a mean of 122 ± 33.2 SD months (range 63–171 months) and compared to baseline (BL), short-term (ST-FU; mean 6 ± 2.0 SD months) and 4-year follow-up (4y-FU; mean 45 ± 12.3 SD months) using the Abnormal Involuntary Movement Scale (AIMS) and the Burke–Fahn–Marsden Dystonia Rating Scale (BFMDRS), respectively. Quality of life and mood were evaluated using the SF36 and Beck Depression Index (BDI) questionnaires, respectively.ResultsAt LT-FU patients had improved by 73% ± 14.2 SD in involuntary movements and 90% ± 1.0 SD in dystonia. Mood had improved significantly whereas quality of life remained unchanged compared to baseline. No serious long-lasting stimulation-related adverse events (AEs) were observed. Three patients of this cohort presented without active stimulation and ongoing symptom relief at long-term follow-up after 3–10 years of continuous DBS.ConclusionPallidal DBS is a safe and effective long-term TD treatment. Even more interesting, three of our patients could stop stimulation after several years of DBS without serious relapse. Larger studies need to explore the phenomenon of ongoing symptom relief after DBS cessation.

Pearls & Oy-sters: Grisel Syndrome Presenting as Pseudodystonia: A Twist in the Neck.

Pseudodystonia is a term that describes abnormal postures, repetitive movements, or both, where clinical analysis, imaging, laboratory, or electrophysiologic investigations indicate that these movements are not consistent with dystonia. Grisel syndrome (GS), characterized by rotatory subluxation of the atlantoaxial joint (AAJ) due to nontraumatic causes, is a cause of pseudodystonia. GS is seen in children less than 12 years of age and should be suspected in patients with acute onset of painful torticollis. We report 2 girls, aged 9 and 6 years, who developed painful torticollis following upper respiratory tract infection. They were thought to have cervical dystonia and referred to a movement disorder specialist for botulinum neurotoxin therapy (BoNT). MRI of the cervical spine showed type I and type II rotary AAJ subluxation, respectively, which confirmed the diagnosis of GS. Short tau inversion recovery hyperintensity was noted suggesting AAJ edema without any bone erosion or cord compression. Abruptness of onset, presence of severe pain, resistance to passive neck movements, fixed postures present equally in rest and action, absence of sensory trick, and persistence in sleep favor pseudodystonia. Both subjects improved with conservative treatment, which included temporary immobilization of the cervical spine and anti-inflammatory drugs. Early identification and treatment is imperative to avoid neurologic complications, like high cervical compressive myelopathy, which can lead to quadriplegia and respiratory distress. Prominent sternocleidomastoid contraction ipsilateral to the rotated chin helps to clinically identify GS.

Clinical spectrum and management of dystonia in patients with Japanese encephalitis: A systematic review.

BackgroundJapanese encephalitis (JE) is a potentially fatal viral infection with a wide range of manifestations and can also present with a variety of movement disorders (MD) including dystonia. Dystonic features in JE are uncommon. Here, we have tried to summarize the clinical features and management of dystonia among JE patients with a comprehensive literature search.MethodsVarious databases, including PubMed, Embase, and Google Scholar, were searched against the predefined criteria using suitable keywords combination and boolean operations. Relevant information from observational and case studies was extracted according to the author, dystonic features, radiological changes in the brain scans, treatment options, and outcome wherever provided.ResultWe identified 19 studies with a total of 1547 JE patients, the diagnosis of which was confirmed by IgM detection in serum and/or cerebrospinal fluid in the majority of the patients (88.62%). 234 (15.13%) of JE patients had dystonia with several types of focal dystonia being present in 131 (55.98%) either alone or in combination. Neuroimaging showed predominant involvement of thalami, basal ganglia, and brainstem. Oral medications including anticholinergics, GABA agonists, and benzodiazepines followed by botulinum toxin were the most common treatment modalities.ConclusionDystonia can be a disabling consequence of JE, and various available medical therapies can significantly improve the quality of life. Owing to insufficient studies on the assessment of dystonia associated with JE, longitudinal studies with a larger number of patients are warranted to further clarify the clinical course, treatment, and outcome of dystonia.

DYT6 mutated THAP1 is a cell type dependent regulator of the SP1 family

DYT6 dystonia is caused by mutations in the transcription factor THAP1. THAP1 knock-out or knock-in mouse models revealed complex gene expression changes, which are potentially responsible for the pathogenesis of DYT6 dystonia. However, how THAP1 mutations lead to these gene expression alterations and whether the gene expression changes are also reflected in the brain of THAP1 patients are still unclear. In this study we used epigenetic and transcriptomic approaches combined with multiple model systems [THAP1 patients' frontal cortex, THAP1 patients' induced pluripotent stem cell (iPSC)-derived midbrain dopaminergic neurons, THAP1 heterozygous knock-out rat model, and THAP1 heterozygous knock-out SH-SY5Y cell lines] to uncover a novel function of THAP1 and the potential pathogenesis of DYT6 dystonia. We observed that THAP1 targeted only a minority of differentially expressed genes caused by its mutation. THAP1 mutations lead to dysregulation of genes mainly through regulation of SP1 family members, SP1 and SP4, in a cell type dependent manner. Comparing global differentially expressed genes detected in THAP1 patients' iPSC-derived midbrain dopaminergic neurons and THAP1 heterozygous knock-out rat striatum, we observed many common dysregulated genes and 61 of them were involved in dystonic syndrome-related pathways, like synaptic transmission, nervous system development, and locomotor behaviour. Further behavioural and electrophysiological studies confirmed the involvement of these pathways in THAP1 knock-out rats. Taken together, our study characterized the function of THAP1 and contributes to the understanding of the pathogenesis of primary dystonia in humans and rats. As SP1 family members were dysregulated in some neurodegenerative diseases, our data may link THAP1 dystonia to multiple neurological diseases and may thus provide common treatment targets.

The effect of antipsychotic-induced extrapyramidal disorders on patient’s compliance with schizophrenia (a clinical case)

Extrapyramidal disorders are common adverse events in antipsychotic therapy. However, their diagnosis is difficult due to broad differential diagnosis, and often their specific clinical variant is not recognized, and timely intervention is not performed, which leads to severe patient suffering. This affects the quality of life of patients with schizophrenia and leads to their refusal to receive therapy, which aggravates the course of the disease. The article presents a clinical case of a 33-year-old patient at a psychiatric hospital with schizophrenia combined with such rare severe extrapyramidal disorders as antipsychotic-induced tardive dyskinesia and tardive dystonia.The diagnosis was carried out in accordance with the criteria of the International Classification of Diseases, Tenth Revision (ICD-10). The intensity of clinical manifestations was assessed using the Positive and Negative Syndrome Scale (PANSS), the Abnormal Involuntary Movement Scale (AIMS), and the Barnes Akathisia Rating Scale (BARS). Compliance was assessed using the Method for Measuring Medication Adherence in Psychiatry. Detailed differential diagnosis of tardive dyskinesia and tardive dystonia with akathisia and Huntington’s disease was presented. Substantiated treatment strategy and positive clinical dynamics with increased compliance were described.

Neuroleptic-induced tardive dystonia in young patients suffering from psychosis

Tardive dystonia is one of the extrapyramidal syndromes that start after long-term use of dopamine receptor antagonists. Tardive dystonia is underdiagnosed and often misdiagnosed; some of the treatment possibilities are hardly known among psychiatrists and are notorious for being resistant to treatment. Here, we present a set of two cases who had come with neuroleptic-induced tardive dystonia, initially given oral tetrabenazine and injectable botulinum toxin, but they did not respond. They got better after treatment with the combination of oral baclofen and electroconvulsive therapy (ECT). ECT is thought to prevent the super sensitization of postsynaptic dopamine receptors that contribute to the development of tardive states. Baclofen is a presynaptic gamma-aminobutyric acid receptor agonist primarily used to treat spasticity. Both may have acted synergistically to treat the dystonia. Tardive dystonia needs to be ruled out in patients with a history of long-term antipsychotic medication use. Consultant liaison with psychiatrists will be of paramount importance in the timely management of these cases. The combination of ECT and baclofen may be an effective choice for patients of schizophrenia with tardive dystonia developed in the course of neuroleptic treatment. However, further controlled studies are needed to develop and refine the guidelines for managing it.

Lithium-associated movement disorder: A literature review.

In 1949, Cade described “sedative effects” after injecting guinea pigs intraperitoneally with lithium (LTM) carbonate. Based on his experiments, he began treating psychiatric patients with LTM. This literature review aims to evaluate the clinical epidemiological profile, pathological mechanisms, and management of LTM-associated movement disorder (MD). Relevant reports in six databases (Excerpta Medica, Google Scholar, Latin American and Caribbean Health Sciences Literature, Medline, Scientific Electronic Library Online, and ScienceDirect) were identified and assessed by two reviewers without language restriction from 1949 to 2021. A total of 250 reports containing 1100 individuals who developed MD associated with LTM were identified. The MDs encountered 148 parkinsonism (PKN), 114 dyskinesia (DKN), 97 myoclonus, 22 dystonia (DTN), 20 Creutzfeldt–Jakob-like syndrome, 11 akathisia, 10 restless legs syndrome (RLS) symptoms, 6 tics, 5 cerebellar syndromes, and 3 stuttering. In the subgroup of cases not clearly defined, there were 320 individuals with extrapyramidal symptoms, 135 with DTN, 37 with DKN, 24 with PKN, and 7 with RLS. Other 141 individuals were only described as presenting an abnormal involuntary movement without further explanation. The mean age was 53.06 years (standard deviation [SD]: 15.64) and the predominant sex was female, i.e., 56.20% (154/274). The mean LTM dose was 963.03 mg/day (SD: 392.03). The mean serum LTM level was 1.53 mEq/L (SD: 1.08). The median onset time was 3 months (1 day to 40 years). The mean recovery time was 0.94 months (SD: 0.87). 45.94% had a full recovery. LTM-induced MD was extensively reported in the literature. Only general terms were used in the majority of the reports. LTM polytherapy probably affected the identification of the MD cause.

Chapter 14 - Neuroplasticity in dystonia: Motor symptoms and beyond

This chapter first focuses on the role of altered neuroplasticity mechanisms and their regulation in the genesis of motor symptoms in the various forms of dystonia. In particular, a review of the available literature about focal dystonia suggests that use-dependent plasticity may become detrimental and produce dystonia when practice and repetition are excessive and predisposing conditions are present. Interestingly, recent evidence also shows that functional or psychogenic dystonia, despite the normal plasticity in the sensorimotor system, is characterized by plasticity-related dysfunction within limbic regions. Finally, this chapter reviews the non-motor symptoms that often accompany the motor features of dystonia, including depression and anxiety as well as obsessive-compulsive disorders, pain, and cognitive dysfunctions. Based on the current understanding of these symptoms, we discuss the evidence of their possible relationship to maladaptive plasticity in non-motor basal ganglia circuits involved in their genesis.

Tardive dyskinesia and dystonia – Clinical case review and grand rounds

Tardive dyskinesia and dystonia – Clinical case review and grand rounds

Treatment of tardive dystonia due to risperidone use with single-dose botulinum toxin

Late-onset dystonia occurs after long-term antipsychotic treatment or after discontinuation of treatment. Being young, male gender, mental retardation, and mood disorder are risk factors. By considering the dystonic complaints and psychotic symptoms of the patient who had a diagnosis of schizoaffective disorder and had risperidone 8 mg/day tablet use for 3 months, it was planned to continue treatment with clozapine. When the dystonic complaints did not improve, botulinum toxin was applied and recovery was achieved. In most cases, botulinum toxin can provide a dramatic improvement in the treatment of tardive dystonia, which is very difficult to treat and causes significant loss of functionality and poor quality of life. For this reason, botulinum toxin application should come to mind in the treatment of tardive dystonia.