Raras
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Coreia benigna familiar
ORPHA:1429CID-10 · G25.5CID-11 · 8A01.0DOENÇA RARA

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.

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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.

Publicações científicas
121 artigos
Último publicado: 2026 Apr

Escala de raridade

CLASSIFICAÇÃO ORPHANET · BRASIL 2024
<1 / 1 000 000
Ultra-rara
<1/50k
Muito rara
1/20k
Rara
1/10k
Pouco freq.
1/5k
Incomum
1/2k
Prevalência
0.02
Worldwide
Início
Childhood
+ infancy
🏥
SUS: Cobertura mínimaScore: 15%
CID-10: G25.5
🇧🇷Dados SUS / DATASUS
PROCEDIMENTOS SIGTAP (2)
0202010694
Sequenciamento completo do exoma (WES)genetic_test
0301070040
Atendimento em reabilitação — doenças rarasrehabilitation
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Entender a doença

Do básico ao detalhe, leia no seu ritmo

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Sinais e sintomas

O que aparece no corpo e com que frequência cada sintoma acontece

Características mais comuns

90%prev.
Anormalidade do movimento
Muito frequente (99-80%)
90%prev.
Distúrbio da marcha
Muito frequente (99-80%)
Coreia
Demência
Atraso motor
Quedas frequentes
12sintomas
Muito frequente (2)
Sem dados (10)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 12 características clínicas mais associadas, ordenadas por frequência.

Anormalidade do movimentoAbnormality of movement
Muito frequente (99-80%)90%
Distúrbio da marchaGait disturbance
Muito frequente (99-80%)90%
CoreiaChorea
DemênciaDementia
Atraso motorMotor delay

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa1desde 2026
Total histórico121PubMed
Últimos 10 anos41publicações
Pico20167 papers
Linha do tempo
2026Hoje · 2026📈 2016Ano de pico
Publicações por ano (últimos 10 anos)

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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.

ADCY5Adenylate cyclase type 5Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

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)

LOCALIZAÇÃO

Cell membraneCell projection, cilium

VIAS BIOLÓGICAS (10)
ADORA2B mediated anti-inflammatory cytokines productionG alpha (i) signalling eventsG alpha (z) signalling eventsG alpha (s) signalling eventsGPER1 signaling
MECANISMO DE DOENÇA

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.

OUTRAS DOENÇAS (4)
dyskinesia with orofacial involvement, autosomal dominantdyskinesia with orofacial involvement, autosomal recessiveneurodevelopmental disorder with hyperkinetic movements and dyskinesiachoreatic disease
HGNC:236UniProt:O95622
NKX2-1Homeobox protein Nkx-2.1Disease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

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

LOCALIZAÇÃO

Nucleus

VIAS BIOLÓGICAS (2)
Regulation of gene expression in endocrine-committed (NEUROG3+) progenitor cellsRegulation of gene expression in beta cells
MECANISMO DE DOENÇA

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.

EXPRESSÃO TECIDUAL(Tecido-específico)
Tireoide
352.6 TPM
Pulmão
89.7 TPM
Hipotálamo
5.6 TPM
Brain Caudate basal ganglia
3.5 TPM
Brain Nucleus accumbens basal ganglia
3.3 TPM
OUTRAS DOENÇAS (6)
brain-lung-thyroid syndromehereditary progressive chorea without dementiaathyreosisdifferentiated thyroid carcinoma
HGNC:11825UniProt:P43699

Variantes genéticas (ClinVar)

387 variantes patogênicas registradas no ClinVar.

🧬 NKX2-1: NM_001079668.3(NKX2-1):c.292T>C (p.Tyr98His) ()
🧬 NKX2-1: NM_001079668.3(NKX2-1):c.428G>A (p.Trp143Ter) ()
🧬 NKX2-1: NM_001079668.3(NKX2-1):c.611A>G (p.Tyr204Cys) ()
🧬 NKX2-1: NM_001079668.3(NKX2-1):c.671T>C (p.Leu224Pro) ()
🧬 NKX2-1: NM_001079668.3(NKX2-1):c.470G>C (p.Arg157Pro) ()
Ver todas no ClinVar

Classificação de variantes (ClinVar)

Distribuição de 56 variantes classificadas pelo ClinVar.

42
14
Patogênica (75.0%)
VUS (25.0%)
VARIANTES MAIS SIGNIFICATIVAS
NKX2-1: NM_001079668.3(NKX2-1):c.671T>C (p.Leu224Pro) [Likely pathogenic]
NKX2-1: NM_001079668.3(NKX2-1):c.182del (p.Gly61fs) [Likely pathogenic]
NKX2-1: NM_001079668.3(NKX2-1):c.521del (p.Gly174fs) [Pathogenic]
NKX2-1: NM_001079668.3(NKX2-1):c.572G>T (p.Arg191Leu) [Pathogenic/Likely pathogenic]
NKX2-1: NM_001079668.3(NKX2-1):c.43_64dup (p.Pro22fs) [Pathogenic]

Diagnóstico

Os sinais que médicos procuram e os exames que confirmam

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Tratamento e manejo

Remédios, cuidados de apoio e o que precisa acompanhar

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Onde tratar no SUS

Hospitais de referência no Brasil e o protocolo oficial do SUS (PCDT)

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Ensaios clínicos abertos e novidades científicas recentes

Pesquisa e ensaios clínicos

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Publicações mais relevantes

📖Melhor nível de evidência: Revisão
Timeline de publicações
42 papers (10 anos)
#1

International Registry of NKX2-1-Related Disorders: Clinical, Genetic, and Imaging Perspectives.

Movement disorders : official journal of the Movement Disorder Society2026 Jan 19

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.

#2

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 Neurophysiology2025 Dec 22

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.

#3

Update on Genetic Chorea.

European journal of neurology2025 Oct

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.

#4

Respiratory and other organ manifestations in NKX2-1-related disorders: a systematic review.

Frontiers in medicine2025

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.

#5

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.

Neurosurgical review2024 Nov 28

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

Ver todas no PubMed

📚 EuropePMC70 artigos no totalmostrando 39

2026

International Registry of NKX2-1-Related Disorders: Clinical, Genetic, and Imaging Perspectives.

Movement disorders : official journal of the Movement Disorder Society
2025

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

Update on Genetic Chorea.

European journal of neurology
2025

Respiratory and other organ manifestations in NKX2-1-related disorders: a systematic review.

Frontiers in medicine
2024

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.

Neurosurgical review
2024

Differential diagnosis of Huntington's disease- neurological aspects of NKX2-1-related disorders.

Journal of neural transmission (Vienna, Austria : 1996)
2024

A Case of Chorea with Slow Saccades Caused by NKX2-1 Mutation.

Movement disorders clinical practice
2024

The First Indian Patient With Benign Hereditary Chorea due to a De Novo Mutation in the NKX2-1 Gene.

Journal of movement disorders
2023

A Teenager with Benign Hereditary Chorea and Selective Tooth Agenesis Type 3.

Movement disorders clinical practice
2023

Genetic screening for Huntington disease phenocopies in Sweden: A tertiary center case series focused on short tandem repeat (STR) disorders.

Journal of the neurological sciences
2023

Thyroid Disorders and Movement Disorders-A Systematic Review.

Movement disorders clinical practice
2023

Benign Hereditary Chorea as a Manifestation of HPCA Mutation.

Movement disorders clinical practice
2022

Persisting embryonal infundibular recess in a case of TITF-1 gene mutation.

Neuroradiology
2022

Altered pituitary morphology as a sign of benign hereditary chorea caused by TITF1/NKX2.1 mutations.

Neurogenetics
2022

Growth 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 &amp; metabolism : JPEM
2021

Homozygous 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 Neurophysiology
2021

Deletion of conserved non-coding sequences downstream from NKX2-1: A novel disease-causing mechanism for benign hereditary chorea.

Molecular genetics &amp; genomic medicine
2020

Combined mutations of NKX2-1 and surfactant protein C genes for refractory low oxyhemoglobin saturation and interstitial pneumonia: A case report.

Medicine
2020

Benign hereditary chorea: From benign to serious.

Revue neurologique
2019

PNKP deficiency mimicking a benign hereditary chorea: The misleading presentation of a neurodegenerative disorder.

Parkinsonism &amp; related disorders
2018

Methylphenidate Can Improve Chorea in NKX2.1 and ADCY5 Mutation-positive Patients-A Report of Two Children.

Movement disorders clinical practice
2019

A Not So Benign Family Pedigree With Hereditary Chorea: A Broader Phenotypic Expression or Additional Picture?

Child neurology open
2019

Is Benign Hereditary Chorea Really Benign? Brain-Lung-Thyroid Syndrome Caused by NKX2-1 Mutations.

Movement disorders clinical practice
2019

Restless Legs Syndrome in NKX2-1-related chorea: An expansion of the disease spectrum.

Brain &amp; development
2018

NKX2-1 New Mutation Associated With Myoclonus, Dystonia, and Pituitary Involvement.

Frontiers in genetics
2018

Benign hereditary chorea and deletions outside NKX2-1: What's the role of MBIP?

European journal of medical genetics
2018

l-Thyroxine-responsive drop attacks in childhood benign hereditary chorea: A case report.

Brain &amp; development
2016

A Video Report of Brain-Lung-Thyroid Syndrome in a Japanese Female With a Novel Frameshift Mutation of the NKX2-1 Gene.

Child neurology open
2017

A further case of brain-lung-thyroid syndrome with deletion proximal to NKX2-1.

European journal of medical genetics
2016

Benign hereditary chorea related to NKX2-1 with ataxia and dystonia.

Neurology. Genetics
2016

Phenotypic insights into ADCY5-associated disease.

Movement disorders : official journal of the Movement Disorder Society
2016

ADCY5 mutations are another cause of benign hereditary chorea.

Neurology
2015

ADCY5 Mutations and Benign Hereditary Chorea.

Pediatric neurology briefs
2016

Benign hereditary chorea, not only chorea: a family case presentation.

Cerebellum &amp; ataxias
2016

Huntington's Disease, Huntington's Disease Look-Alikes‎, and Benign Hereditary Chorea: What's New?

Movement disorders clinical practice
2016

Functional characterization of two novel mutations in TTF-1/NKX2.1 homeodomain in patients with benign hereditary chorea.

Journal of the neurological sciences
2015

ADCY5 identified as a novel cause of benign hereditary chorea.

Movement disorders : official journal of the Movement Disorder Society
2015

Benign Hereditary Chorea: An Update.

Tremor and other hyperkinetic movements (New York, N.Y.)
2015

Isolated and combined dystonia syndromes - an update on new genes and their phenotypes.

European journal of neurology
Ver todos os 70 no EuropePMC

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Doenças relacionadas

Doenças com sintomas parecidos — ajudam quem ainda está buscando diagnóstico

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.

  1. 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
  2. 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
  3. Update on Genetic Chorea.
    European journal of neurology· 2025· PMID 41104576mais citado
  4. Respiratory and other organ manifestations in NKX2-1-related disorders: a systematic review.
    Frontiers in medicine· 2025· PMID 40395234mais citado
  5. 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.
    Neurosurgical review· 2024· PMID 39604647mais citado

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:1429(Orphanet)
  2. MONDO:0001595(MONDO)
  3. GARD:15152(GARD (NIH))
  4. Variantes catalogadas(ClinVar)
  5. Busca completa no PubMed(PubMed)
  6. Artigo Wikipedia(Wikipedia)
  7. 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

Coreia benigna familiar
Compêndio · Raras BR

Coreia benigna familiar

ORPHA:1429 · MONDO:0001595
Prevalência
<1 / 1 000 000
Herança
Autosomal dominant
CID-10
G25.5 · Outras formas de coréia
CID-11
Início
Childhood, Infancy
Prevalência
0.02 (Worldwide)
MedGen
UMLS
C0008489
EuropePMC
Wikidata
Wikipedia
Papers 10a
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