É uma condição neurológica que afeta os movimentos involuntários. É caracterizada por contrações musculares rápidas, irregulares e que não se repetem. É observada em pessoas com a Doença de Huntington.
Introdução
O que você precisa saber de cara
É uma condição neurológica que afeta os movimentos involuntários. É caracterizada por contrações musculares rápidas, irregulares e que não se repetem. É observada em pessoas com a Doença de Huntington.
Escala de raridade
<1/50kMuito rara
1/20kRara
1/10kPouco freq.
1/5kIncomum
1/2k
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Entender a doença
Do básico ao detalhe, leia no seu ritmo
Preparando trilha educativa...
Sinais e sintomas
O que aparece no corpo e com que frequência cada sintoma acontece
Características mais comuns
Os sintomas variam de pessoa para pessoa. Abaixo estão as 12 características clínicas mais associadas, ordenadas por frequência.
Linha do tempo da pesquisa
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Genética e causas
O que está alterado no DNA e como passa nas famílias
Genes associados
2 genes identificados com associação a esta condição. Padrão de herança: Autosomal dominant.
Catalyzes the formation of the signaling molecule cAMP in response to G-protein signaling (PubMed:15385642, PubMed:24700542, PubMed:26206488). Mediates signaling downstream of ADRB1 (PubMed:24700542). Regulates the increase of free cytosolic Ca(2+) in response to increased blood glucose levels and contributes to the regulation of Ca(2+)-dependent insulin secretion (PubMed:24740569)
Cell membraneCell projection, cilium
Dyskinesia with orofacial involvement, autosomal recessive
An autosomal recessive disorder characterized by abnormal involuntary movements mainly affecting the limbs and causing walking difficulties, oro-facial dyskinesia, and speech delay. Some patients develop neuropsychiatric features. Cardiomyopathy has rarely been described and may be a manifestation of the disorder.
Transcription factor that binds and activates the promoter of thyroid specific genes such as thyroglobulin, thyroperoxidase, and thyrotropin receptor. Crucial in the maintenance of the thyroid differentiation phenotype. May play a role in lung development and surfactant homeostasis. Forms a regulatory loop with GRHL2 that coordinates lung epithelial cell morphogenesis and differentiation. Activates the transcription of GNRHR and plays a role in enhancing the circadian oscillation of its gene exp
Nucleus
Chorea, hereditary benign
A rare autosomal dominant movement disorder, defined by early onset in childhood, a stable or non-progressive course of chorea, and no mental deterioration. Chorea is characterized by involuntary, forcible, rapid, jerky movements that may be subtle or become confluent, markedly altering normal patterns of movement.
Variantes genéticas (ClinVar)
387 variantes patogênicas registradas no ClinVar.
Classificação de variantes (ClinVar)
Distribuição de 56 variantes classificadas pelo ClinVar.
Vias biológicas (Reactome)
18 vias biológicas associadas aos genes desta condição.
Diagnóstico
Os sinais que médicos procuram e os exames que confirmam
Tratamento e manejo
Remédios, cuidados de apoio e o que precisa acompanhar
Onde tratar no SUS
Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)
🇧🇷 Atendimento SUS — Coreia benigna familiar
Selecione um estado ou use sua localização para ver resultados.
Dados de DATASUS/CNES, SBGM, ABNeuro e Ministério da Saúde. Sempre confirme a disponibilidade diretamente com o estabelecimento.
Pesquisa ativa
Ensaios clínicos abertos e novidades científicas recentes
Pesquisa e ensaios clínicos
Nenhum ensaio clínico registrado para esta condição.
Publicações mais relevantes
International Registry of NKX2-1-Related Disorders: Clinical, Genetic, and Imaging Perspectives.
NKX2-1-related disorders result from heterozygous variants in NKX2-1, a gene crucial for brain, lung, and thyroid development. Although movement disorders, hypothyroidism, and neonatal respiratory distress are recognized, the full phenotype and genotype-phenotype relationships remain incompletely defined. To delineate neurological, respiratory, and endocrine features across ages, characterize movement disorder trajectories - particularly chorea - and explore genotype-phenotype associations with clinical relevance. We conducted a multicenter, cross-sectional study recruiting participants through referral clinicians and European networks. Standardized clinical and genetic data were captured in an electronic database and analyzed with descriptive and inferential statistics. Sixty-eight individuals (37 female; median age 16 years, range 2-60 years) were included. Motor delay was the commonest presenting feature (~60%); neonatal respiratory distress syndrome occurred in one-third of cases. The brain-lung-thyroid triad was present in almost half. Chorea affected over 90% and began in early childhood; it was more frequent with single nucleotide variants than with deletions. Deletions are associated with better gross motor function. Frameshift or nonsense variants showed greater respiratory involvement, and variants in the exon-3 homeobox region were associated with age-related reduction of chorea. Neonatal respiratory distress predicted later respiratory symptoms. Greater abnormal involuntary movement severity correlated with poorer manual and gross motor function. Hypotonia and untreated hypothyroidism are associated with more severe chorea. Psychiatric comorbidity occurred in over one-third of cases, mainly attention-deficit/hyperactivity symptoms. This largest cohort to date shows early neurological onset, genotype-specific outcomes, and frequent psychiatric comorbidity in NKX2-1-related disorders, refining clinical expectations and supporting genotype-informed diagnosis, counseling, and management. © 2026 The Author(s). Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
A novel NKX2-1 frameshift variant expanding the genetic landscape of benign hereditary chorea.
Benign hereditary chorea (BHC) is a rare childhood-onset hyperkinetic disorder caused by pathogenic variants in NKX2-1. It typically follows a stationary or only mildly progressive course and may be associated with thyroid and respiratory involvement, constituting the "brain-lung-thyroid" syndrome. We report the case of a girl carrying a novel heterozygous NKX2-1 frameshift variant. Clinical assessment included longitudinal neurological examinations, neuroimaging, laboratory testing, cardiological evaluation, and genetic analysis. A 6-year-old girl, first evaluated at age 3 for delayed psychomotor milestones, showed choreiform movements with motor impersistence, milkmaid's grip, and imbalance, sparing the forehead. Brain MRI was normal. Thyroid dysfunction was documented since foster care, while no respiratory involvement was reported. Genetic testing in August 2024 identified a novel heterozygous NKX2-1 frameshift variant (c.246_250del p.Met83AlafsTer354), classified as likely pathogenic. At last follow-up, movements persisted but remained non-progressive. This case expands the mutational spectrum of NKX2-1-related disorders. The stationary course of chorea, together with thyroid involvement and absence of pulmonary disease, aligns with previous literature. Recognition of novel NKX2-1 variants is essential to improve genotype-phenotype correlations, avoid misdiagnosis with progressive pediatric choreic or ataxic syndromes, and provide accurate prognostic counselling, as most affected individuals achieve a favorable long-term functional outcome.
Update on Genetic Chorea.
Hereditary choreas are a clinically and genetically heterogeneous group of monogenic disorders in which chorea constitutes the core or an early-dominant feature. These conditions result from various genetic mutations affecting the structures and pathways involved in movement control, primarily the caudate and putamen, ultimately impairing the basal ganglia circuits involved in the regulation of movement, cognition, and behavior. This review focuses on the main forms of hereditary choreas, including Huntington's disease, neuroacanthocytosis syndromes, Huntington's disease phenocopies, benign hereditary chorea, and other less common genetic disorders presenting with chorea. We discuss the clinical, genetic, and pathophysiological features of each condition, alongside key aspects of phenomenology, examination, and complementary tests-including laboratory findings-to guide phenotype-driven genetic testing. We detail the characteristic features of key disorders while also highlighting less common but emerging conditions. This review aims to assist neurologists in recognizing and diagnosing hereditary choreas efficiently, including guidance on the selection of appropriate genetic tests, thereby reducing diagnostic delays, informing accurate counseling, and facilitating access to disease-specific interventions and clinical trials.
Respiratory and other organ manifestations in NKX2-1-related disorders: a systematic review.
NKX2-1-related disorders (NKX2-1-RD) encompass a spectrum of conditions arising from pathogenic deletions or variants in the NKX2-1 gene, crucial for thyroid, lung, and brain development. Respiratory manifestations in NKX2-1-RD range from neonatal respiratory distress to severe lung diseases, constituting a leading cause of mortality. This study will review and synthesize NKX2-1-RD respiratory phenotypes, genetic alterations, and long-term trajectories. We conducted a systematic review using PRISMA and PICO question formats. From January 2002 to July 2023, major biomedical databases and rare disease resources were searched. Genetically confirmed NKX2-1-RD patients with respiratory symptoms were eligible for this study. Out of 4,569 studies, 38 met inclusion criteria, predominantly case reports and series. The study included 148 patients, revealing diverse respiratory phenotypes and treatments. Respiratory manifestations emerged at various ages, with neonatal respiratory distress, asthma, interstitial lung disease, and lung cancer observed. Nonsense mutations in NKX2-1 were linked to lung cancer. Treatment varied, including oxygen supplementation, ventilation, antibiotics, and lung transplantation. Long-term follow-up disclosed heterogeneous respiratory outcomes, with some patients asymptomatic while others faced chronic insufficiency or recurrent infections. The overall survival of informed cases was about 60%. This study highlights the complex respiratory manifestations of NKX2-1-RD and their impact on patient outcomes. The findings support standardized respiratory follow-up protocols and provide clinical management insights despite study quality and sample size limitations. We discuss the challenges of treating diverse respiratory conditions in this rare clinical entity and lay the groundwork for future research.
Bilateral deep brain stimulation (DBS) of globus pallidus internus (GPi) for the treatment of benign hereditary chorea and other childhood onset choreas: a single-center experience.
Chorea is a clinical sign characterized by involuntary, rapid, unpredictable, and irregular muscle movements that can affect various parts of the body. It can be seen in various medical conditions, both neurological and systemic, of genetic and acquired etiology. Deep brain stimulation (DBS) of the globus pallidus internus (GPi) has been used to treat various types of chorea. The aim of this study was to evaluate the efficacy of GPi DBS for chorea in pediatric patients. The authors undertook a single-center retrospective study of all pediatric patients who underwent DBS in the period from July 2017 to April 2024 to identify those presenting with chorea. Three patients with chorea underwent bilateral posteroventral GPi DBS without surgical complications. The mean age at operation was 14.2 years (range: 1.5 years), and the mean follow-up was 49 months (range: 15 months). Two of the 3 patients experienced a positive effect on chorea with an improvement in functional status. In one patient, the pre- and postop Gross Motor Function Classification System (GMFCS) score was 4, while his Burke-Fahn-Marsden Dystonia Scale (BFMDS) score improved from 102/20 pre- to 53.5/20 postop. In the other patient the GMFCS score improved from 4 preop to 3 postop. His preop BFMDS score was not available, postop it was 83/120. In the patient who did not experience a positive effect on chorea the pre- and postop GMFCS score was 4, her BFMDS score was 84.5/120 pre- and 100/120 postop. Bilateral GPi DBS can be safely administered to pediatric patients with choreiform movement disorders, and it could be an effective treatment option for managing chorea in certain patients.
Publicações recentes
International Registry of NKX2-1-Related Disorders: Clinical, Genetic, and Imaging Perspectives.
A novel NKX2-1 frameshift variant expanding the genetic landscape of benign hereditary chorea.
📖 RevisãoUpdate on Genetic Chorea.
Respiratory and other organ manifestations in NKX2-1-related disorders: a systematic review.
Bilateral deep brain stimulation (DBS) of globus pallidus internus (GPi) for the treatment of benign hereditary chorea and other childhood onset choreas: a single-center experience.
🥈 Observacional📚 EuropePMC70 artigos no totalmostrando 39
International Registry of NKX2-1-Related Disorders: Clinical, Genetic, and Imaging Perspectives.
Movement disorders : official journal of the Movement Disorder SocietyA novel NKX2-1 frameshift variant expanding the genetic landscape of benign hereditary chorea.
Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical NeurophysiologyUpdate on Genetic Chorea.
European journal of neurologyRespiratory and other organ manifestations in NKX2-1-related disorders: a systematic review.
Frontiers in medicineBilateral deep brain stimulation (DBS) of globus pallidus internus (GPi) for the treatment of benign hereditary chorea and other childhood onset choreas: a single-center experience.
Neurosurgical reviewDifferential diagnosis of Huntington's disease- neurological aspects of NKX2-1-related disorders.
Journal of neural transmission (Vienna, Austria : 1996)A Case of Chorea with Slow Saccades Caused by NKX2-1 Mutation.
Movement disorders clinical practiceThe First Indian Patient With Benign Hereditary Chorea due to a De Novo Mutation in the NKX2-1 Gene.
Journal of movement disordersA Teenager with Benign Hereditary Chorea and Selective Tooth Agenesis Type 3.
Movement disorders clinical practiceGenetic screening for Huntington disease phenocopies in Sweden: A tertiary center case series focused on short tandem repeat (STR) disorders.
Journal of the neurological sciencesThyroid Disorders and Movement Disorders-A Systematic Review.
Movement disorders clinical practiceBenign Hereditary Chorea as a Manifestation of HPCA Mutation.
Movement disorders clinical practicePersisting embryonal infundibular recess in a case of TITF-1 gene mutation.
NeuroradiologyAltered pituitary morphology as a sign of benign hereditary chorea caused by TITF1/NKX2.1 mutations.
NeurogeneticsGrowth hormone deficiency in a child with benign hereditary chorea caused by a de novo mutation of the TITF1/NKX2-1 gene.
Journal of pediatric endocrinology & metabolism : JPEMHomozygous ADCY5 mutation causes early-onset movement disorder with severe intellectual disability.
Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical NeurophysiologyDeletion of conserved non-coding sequences downstream from NKX2-1: A novel disease-causing mechanism for benign hereditary chorea.
Molecular genetics & genomic medicineCombined mutations of NKX2-1 and surfactant protein C genes for refractory low oxyhemoglobin saturation and interstitial pneumonia: A case report.
MedicineBenign hereditary chorea: From benign to serious.
Revue neurologiquePNKP deficiency mimicking a benign hereditary chorea: The misleading presentation of a neurodegenerative disorder.
Parkinsonism & related disordersMethylphenidate Can Improve Chorea in NKX2.1 and ADCY5 Mutation-positive Patients-A Report of Two Children.
Movement disorders clinical practiceA Not So Benign Family Pedigree With Hereditary Chorea: A Broader Phenotypic Expression or Additional Picture?
Child neurology openIs Benign Hereditary Chorea Really Benign? Brain-Lung-Thyroid Syndrome Caused by NKX2-1 Mutations.
Movement disorders clinical practiceRestless Legs Syndrome in NKX2-1-related chorea: An expansion of the disease spectrum.
Brain & developmentNKX2-1 New Mutation Associated With Myoclonus, Dystonia, and Pituitary Involvement.
Frontiers in geneticsBenign hereditary chorea and deletions outside NKX2-1: What's the role of MBIP?
European journal of medical geneticsl-Thyroxine-responsive drop attacks in childhood benign hereditary chorea: A case report.
Brain & developmentA Video Report of Brain-Lung-Thyroid Syndrome in a Japanese Female With a Novel Frameshift Mutation of the NKX2-1 Gene.
Child neurology openA further case of brain-lung-thyroid syndrome with deletion proximal to NKX2-1.
European journal of medical geneticsBenign hereditary chorea related to NKX2-1 with ataxia and dystonia.
Neurology. GeneticsPhenotypic insights into ADCY5-associated disease.
Movement disorders : official journal of the Movement Disorder SocietyADCY5 mutations are another cause of benign hereditary chorea.
NeurologyADCY5 Mutations and Benign Hereditary Chorea.
Pediatric neurology briefsBenign hereditary chorea, not only chorea: a family case presentation.
Cerebellum & ataxiasHuntington's Disease, Huntington's Disease Look-Alikes, and Benign Hereditary Chorea: What's New?
Movement disorders clinical practiceFunctional characterization of two novel mutations in TTF-1/NKX2.1 homeodomain in patients with benign hereditary chorea.
Journal of the neurological sciencesADCY5 identified as a novel cause of benign hereditary chorea.
Movement disorders : official journal of the Movement Disorder SocietyBenign Hereditary Chorea: An Update.
Tremor and other hyperkinetic movements (New York, N.Y.)Isolated and combined dystonia syndromes - an update on new genes and their phenotypes.
European journal of neurologyAssociações
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Referências e fontes
Bases de dados externas citadas neste artigo
Publicações científicas
Artigos indexados no PubMed ligados a esta doença no grafo RarasNet — título, periódico e PMID direto da fonte, sem intermediação de IA.
- International Registry of NKX2-1-Related Disorders: Clinical, Genetic, and Imaging Perspectives.Movement disorders : official journal of the Movement Disorder Society· 2026· PMID 41552915mais citado
- A novel NKX2-1 frameshift variant expanding the genetic landscape of benign hereditary chorea.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology· 2025· PMID 41423511mais citado
- Update on Genetic Chorea.
- Respiratory and other organ manifestations in NKX2-1-related disorders: a systematic review.
- Bilateral deep brain stimulation (DBS) of globus pallidus internus (GPi) for the treatment of benign hereditary chorea and other childhood onset choreas: a single-center experience.
Bases de dados e fontes oficiais
Identificadores e referências canônicas usadas para montar este verbete.
- ORPHA:1429(Orphanet)
- MONDO:0001595(MONDO)
- GARD:15152(GARD (NIH))
- Variantes catalogadas(ClinVar)
- Busca completa no PubMed(PubMed)
- Artigo Wikipedia(Wikipedia)
- Q1076421(Wikidata)
Dados compilados pelo RarasNet a partir de fontes abertas (Orphanet, OMIM, MONDO, PubMed/EuropePMC, ClinicalTrials.gov, DATASUS, PCDT/MS). Este conteúdo é informativo e não substitui avaliação médica.
Conteúdo mantido por Agente Raras · Médicos e pesquisadores podem colaborar
