Raras
Buscar doenças, sintomas, genes...
Displasia cortical focal
ORPHA:65683CID-10 · Q04.8CID-11 · LA05.51DOENÇA RARA

A Displasia Cortical Focal Isolada é uma rara malformação cerebral, de origem genética e não associada a outras síndromes. Ela surge de um problema no movimento e organização das células nervosas (neurônios) durante o desenvolvimento do cérebro. Caracteriza-se por malformações de tamanhos variados e localizadas em pontos específicos da camada mais externa do cérebro (o córtex cerebral). Essa condição se manifesta com epilepsia de difícil controle com medicamentos (que geralmente leva a deficiência intelectual) e problemas de comportamento. A ressonância magnética do cérebro geralmente mostra alterações, como: sinais anormais em certas áreas de matéria branca e/ou cinzenta, a fronteira entre essas duas substâncias borrada, diminuição de volume em pontos específicos, espessamento do córtex, um padrão incomum das dobras cerebrais (giros) e alterações no hipocampo. Além disso, a análise do tecido cerebral (biópsia) pode apresentar diferentes padrões.

Mantido por Agente Raras·Colaborar como especialista →

Introdução

O que você precisa saber de cara

📋

A Displasia Cortical Focal Isolada é uma rara malformação cerebral, de origem genética e não associada a outras síndromes. Ela surge de um problema no movimento e organização das células nervosas (neurônios) durante o desenvolvimento do cérebro. Caracteriza-se por malformações de tamanhos variados e localizadas em pontos específicos da camada mais externa do cérebro (o córtex cerebral). Essa condição se manifesta com epilepsia de difícil controle com medicamentos (que geralmente leva a deficiência intelectual) e problemas de comportamento. A ressonância magnética do cérebro geralmente mostra alterações, como: sinais anormais em certas áreas de matéria branca e/ou cinzenta, a fronteira entre essas duas substâncias borrada, diminuição de volume em pontos específicos, espessamento do córtex, um padrão incomum das dobras cerebrais (giros) e alterações no hipocampo. Além disso, a análise do tecido cerebral (biópsia) pode apresentar diferentes padrões.

Publicações científicas
7 artigos
Último publicado: 2018 Jan

Escala de raridade

CLASSIFICAÇÃO ORPHANET · BRASIL 2024
Unknown
Ultra-rara
<1/50k
Muito rara
1/20k
Rara
1/10k
Pouco freq.
1/5k
Incomum
1/2k
Prevalência
0.0
Worldwide
Início
All ages
🏥
SUS: Cobertura mínimaScore: 15%
CID-10: Q04.8
🇧🇷Dados SUS / DATASUS
PROCEDIMENTOS SIGTAP (5)
0202010503
Cariótipo — bandas G, Q ou Rgenetic_test
0202010600
Pesquisa de microdeleções/microduplicações por FISHlab_test
0202010694
Sequenciamento completo do exoma (WES)rehabilitation
0202010260
Dosagem de alfa-fetoproteína
0301070040
Atendimento em reabilitação — doenças raras
Você se identifica com essa condição?
O Raras está aqui pra te apoiar — com ou sem diagnóstico

Encontrou um erro ou informação desatualizada? Sugira uma correção →

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

Partes do corpo afetadas

🧠
Neurológico
18 sintomas
🦴
Ossos e articulações
2 sintomas

+ 7 sintomas em outras categorias

Características mais comuns

90%prev.
Convulsão
Muito frequente (99-80%)
90%prev.
Morfologia neuronal anormal
Muito frequente (99-80%)
90%prev.
Anormalidade do sistema nervoso
Muito frequente (99-80%)
90%prev.
Anormalidade em imagem cerebral
Muito frequente (99-80%)
90%prev.
Deterioração psicomotora
Muito frequente (99-80%)
55%prev.
Giração cortical anormal
Frequente (79-30%)
27sintomas
Muito frequente (5)
Frequente (10)
Ocasional (6)
Sem dados (6)

Os sintomas variam de pessoa para pessoa. Abaixo estão as 27 características clínicas mais associadas, ordenadas por frequência.

ConvulsãoSeizure
Muito frequente (99-80%)90%
Morfologia neuronal anormalAbnormal neuron morphology
Muito frequente (99-80%)90%
Anormalidade do sistema nervosoAbnormality of the nervous system
Muito frequente (99-80%)90%
Anormalidade em imagem cerebralBrain imaging abnormality
Muito frequente (99-80%)90%
Deterioração psicomotoraPsychomotor deterioration
Muito frequente (99-80%)90%

Linha do tempo da pesquisa

Publicações por ano — veja quando o interesse científico cresceu
Anos de pesquisa8desde 2018
Total histórico7PubMed
Últimos 10 anos4publicações
Pico20182 papers
Linha do tempo
20202018Hoje · 2026🧪 2009Primeiro ensaio clínico
Publicações por ano (últimos 10 anos)

Encontrou um erro ou informação desatualizada? Sugira uma correção →

Genética e causas

O que está alterado no DNA e como passa nas famílias

Genes associados

4 genes identificados com associação a esta condição.

MTORSerine/threonine-protein kinase mTORDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Serine/threonine protein kinase which is a central regulator of cellular metabolism, growth and survival in response to hormones, growth factors, nutrients, energy and stress signals (PubMed:12087098, PubMed:12150925, PubMed:12150926, PubMed:12231510, PubMed:12718876, PubMed:14651849, PubMed:15268862, PubMed:15467718, PubMed:15545625, PubMed:15718470, PubMed:18497260, PubMed:18762023, PubMed:18925875, PubMed:20516213, PubMed:20537536, PubMed:21659604, PubMed:23429703, PubMed:23429704, PubMed:257

LOCALIZAÇÃO

Lysosome membraneEndoplasmic reticulum membraneGolgi apparatus membraneCell membraneMitochondrion outer membraneCytoplasmNucleusNucleus, PML bodyMicrosome membraneCytoplasmic vesicle, phagosome

VIAS BIOLÓGICAS (10)
MacroautophagyEnergy dependent regulation of mTOR by LKB1-AMPKmTORC1-mediated signallingRegulation of PTEN gene transcriptionMTOR signalling
MECANISMO DE DOENÇA

Smith-Kingsmore syndrome

An autosomal dominant syndrome characterized by intellectual disability, macrocephaly, seizures, umbilical hernia, and facial dysmorphic features.

EXPRESSÃO TECIDUAL(Ubíquo)
Testículo
35.5 TPM
Cerebelo
27.1 TPM
Cérebro - Hemisfério cerebelar
26.0 TPM
Útero
20.1 TPM
Nervo tibial
19.8 TPM
OUTRAS DOENÇAS (7)
isolated focal cortical dysplasia type IImacrocephaly-intellectual disability-neurodevelopmental disorder-small thorax syndromeobsolete cerebral malformationovergrowth syndrome and/or cerebral malformations due to abnormalities in MTOR pathway genes
HGNC:3942UniProt:P42345
TSC1HamartinDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Non-catalytic component of the TSC-TBC complex, a multiprotein complex that acts as a negative regulator of the canonical mTORC1 complex, an evolutionarily conserved central nutrient sensor that stimulates anabolic reactions and macromolecule biosynthesis to promote cellular biomass generation and growth (PubMed:12172553, PubMed:12271141, PubMed:12906785, PubMed:15340059, PubMed:24529379, PubMed:28215400). The TSC-TBC complex acts as a GTPase-activating protein (GAP) for the small GTPase RHEB, a

LOCALIZAÇÃO

Lysosome membraneCytoplasm, cytosol

VIAS BIOLÓGICAS (5)
MacroautophagyEnergy dependent regulation of mTOR by LKB1-AMPKTP53 Regulates Metabolic GenesInhibition of TSC complex formation by PKBTBC/RABGAPs
MECANISMO DE DOENÇA

Tuberous sclerosis 1

An autosomal dominant multi-system disorder that affects especially the brain, kidneys, heart, and skin. It is characterized by hamartomas (benign overgrowths predominantly of a cell or tissue type that occurs normally in the organ) and hamartias (developmental abnormalities of tissue combination). Clinical manifestations include epilepsy, learning difficulties, behavioral problems, and skin lesions. Seizures can be intractable and premature death can occur from a variety of disease-associated causes.

EXPRESSÃO TECIDUAL(Ubíquo)
Cerebelo
59.5 TPM
Cérebro - Hemisfério cerebelar
57.4 TPM
Nervo tibial
37.5 TPM
Ovário
36.5 TPM
Tireoide
35.7 TPM
OUTRAS DOENÇAS (7)
tuberous sclerosis 1isolated focal cortical dysplasia type IIlymphangioleiomyomatosistuberous sclerosis
HGNC:12362UniProt:Q92574
TSC2TuberinDisease-causing germline mutation(s) inAltamente restrito
FUNÇÃO

Catalytic component of the TSC-TBC complex, a multiprotein complex that acts as a negative regulator of the canonical mTORC1 complex, an evolutionarily conserved central nutrient sensor that stimulates anabolic reactions and macromolecule biosynthesis to promote cellular biomass generation and growth (PubMed:12172553, PubMed:12271141, PubMed:12842888, PubMed:12906785, PubMed:15340059, PubMed:22819219, PubMed:24529379, PubMed:28215400, PubMed:33436626, PubMed:35772404). Within the TSC-TBC complex

LOCALIZAÇÃO

Lysosome membraneCytoplasm, cytosol

VIAS BIOLÓGICAS (6)
Energy dependent regulation of mTOR by LKB1-AMPKTP53 Regulates Metabolic GenesInhibition of TSC complex formation by PKBTBC/RABGAPsAKT phosphorylates targets in the cytosol
MECANISMO DE DOENÇA

Tuberous sclerosis 2

An autosomal dominant multi-system disorder that affects especially the brain, kidneys, heart, and skin. It is characterized by hamartomas (benign overgrowths predominantly of a cell or tissue type that occurs normally in the organ) and hamartias (developmental abnormalities of tissue combination). Clinical manifestations include epilepsy, learning difficulties, behavioral problems, and skin lesions. Seizures can be intractable and premature death can occur from a variety of disease-associated causes.

EXPRESSÃO TECIDUAL(Ubíquo)
Cerebelo
133.2 TPM
Cérebro - Hemisfério cerebelar
103.9 TPM
Pituitária
94.3 TPM
Tireoide
88.0 TPM
Testículo
86.3 TPM
OUTRAS DOENÇAS (9)
lymphangioleiomyomatosistuberous sclerosis 2isolated focal cortical dysplasia type IItuberous sclerosis
HGNC:12363UniProt:P49815
SLC35A2UDP-galactose translocatorCandidate gene tested inAltamente restrito
FUNÇÃO

Transports uridine diphosphate galactose (UDP-galactose) from the cytosol into the Golgi apparatus, functioning as an antiporter that exchanges UDP-galactose for UMP (PubMed:12682060, PubMed:9010752). It is also able to exchange UDP-galactose for AMP and CMP, and to transport UDP-N-acetylgalactosamine (UDP-GalNAc) and other nucleotide sugars (PubMed:11784306, PubMed:12682060). As a provider of UDP-galactose to galactosyltransferases present in the Golgi apparatus, it is necessary for globotriaos

LOCALIZAÇÃO

Endoplasmic reticulum membraneGolgi apparatus membrane

VIAS BIOLÓGICAS (1)
Transport of nucleotide sugars
MECANISMO DE DOENÇA

Congenital disorder of glycosylation 2M

An X-linked dominant, severe neurologic disorder characterized by developmental delay, hypotonia, ocular anomalies, and brain malformations. Othere more variable clinical features included seizures, hypsarrhythmia, poor feeding, microcephaly, recurrent infections, dysmorphic features, shortened limbs, and coagulation defects. Congenital disorders of glycosylation are caused by a defect in glycoprotein biosynthesis and characterized by under-glycosylated serum glycoproteins and a wide variety of clinical features. The broad spectrum of features reflects the critical role of N-glycoproteins during embryonic development, differentiation, and maintenance of cell functions.

EXPRESSÃO TECIDUAL(Ubíquo)
Fibroblastos
22.3 TPM
Pituitária
20.4 TPM
Esôfago - Mucosa
16.9 TPM
Pulmão
16.7 TPM
Glândula salivar
16.6 TPM
OUTRAS DOENÇAS (2)
SLC35A2-congenital disorder of glycosylationisolated focal cortical dysplasia type Ia
HGNC:11022UniProt:P78381

Variantes genéticas (ClinVar)

4,204 variantes patogênicas registradas no ClinVar.

🧬 SLC35A2: NM_005660.3(SLC35A2):c.1151C>T (p.Pro384Leu) ()
🧬 SLC35A2: NM_005660.3(SLC35A2):c.100C>A (p.Arg34Ser) ()
🧬 SLC35A2: NC_000023.11:g.48902933C>T ()
🧬 SLC35A2: NM_005660.3(SLC35A2):c.761A>G (p.Glu254Gly) ()
🧬 SLC35A2: NM_005660.3(SLC35A2):c.424C>T (p.Gln142Ter) ()
Ver todas no ClinVar

Classificação de variantes (ClinVar)

Distribuição de 1,406 variantes classificadas pelo ClinVar.

914
492
Patogênica (65.0%)
VUS (35.0%)
VARIANTES MAIS SIGNIFICATIVAS
TSC1: NM_000368.5(TSC1):c.631G>T (p.Glu211Ter) [Pathogenic]
TSC2: NM_000548.5(TSC2):c.4618_4619del (p.Tyr1540fs) [Pathogenic]
TSC2: NM_000548.5(TSC2):c.1445_1448del (p.Glu482fs) [Likely pathogenic]
TSC2: NC_000016.9:g.(?_2131598)_(2138613_?)del [Pathogenic]
MIR1225: NC_000016.9:g.(?_2120457)_(2185690_?)del [Pathogenic]

Diagnóstico

Os sinais que médicos procuram e os exames que confirmam

Carregando...

Tratamento e manejo

Remédios, cuidados de apoio e o que precisa acompanhar

Pipeline de tratamentos
Pipeline regulatório — de medicamentos já aprovados a drogas em pesquisa exploratória.
·Pré-clínico1
Medicamentos catalogadosEnsaios clínicos· 0 medicamentos · 1 ensaio
Carregando informações de tratamento...

Onde tratar no SUS

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

🇧🇷 Atendimento SUS — Displasia cortical focal

🗺️

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

🟢 Recrutando agora

1 pesquisa recrutando participantes. Converse com seu médico sobre a possibilidade de participar.

Outros ensaios clínicos

🧪 Está conduzindo uma pesquisa?
Divulgue para pacientes e familiares que acompanham esta doença.
Divulgar pesquisa →

Publicações mais relevantes

Timeline de publicações
4 papers (10 anos)
#1

Childhood-Onset Epileptic Encephalopathy Associated With Isolated Focal Cortical Dysplasia and a Novel TSC1 Germline Mutation.

Clinical EEG and neuroscience2018 May

Tuberous sclerosis complex (TSC) is an autosomal-dominant inheritable neurocutaneous disease due to mutations within the TSC1 and TSC2 genes. Many patients present with West syndrome, a severe epilepsy syndrome characterized by the triad of infantile spasms, an interictal electroencephalogram (EEG) pattern termed hypsarrhythmia (continuous slow activity with an amplitude higher than 300 µV and multiregional spikes/polyspikes/sharp waves) and developmental regression. In this study, we report on a previously healthy patient with positive family history of epilepsy with new-onset epileptic encephalopathy at the age of 9 years. Clinical signs alone were not sufficient to establish the diagnosis of TSC but epilepsy panel screening revealed a novel frameshift mutation (c.90delA; p.Glu31Argfs*12) within the TSC1 gene. Segregation gene analysis detected the same mutation in the mother. Cranial magnetic resonance imaging (MRI) studies from the index patient and his mother revealed a similar pattern of isolated subcortical white matter lesions resembling most likely focal cortical dysplasia (FCD) type IIb. In summary, in these 2 related patients, a novel TSC1 frameshift mutation was associated with an isolated FCD type IIb in the absence of further CNS abnormalities usually encountered in patients with TSC, fostering our understanding of the broad mutation spectra in the TSC1 gene and the close relationship between cortical tubers and FCD type IIb.

#2

Surgical outcome and predictive factors of epilepsy surgery in pediatric isolated focal cortical dysplasia.

Epilepsy research2018 Jan

Focal cortical dysplasia (FCD) is a common cause of medically intractable epilepsy in children. Epilepsy surgery has been a valuable treatment option to achieve seizure freedom in these intractable epilepsy patients. We aimed to present long-term surgical outcome, in relation to pathological severity, and to assess predictive factors of epilepsy surgery in pediatric isolated FCD. We retrospectively analyzed the data of 58 children and adolescents, with FCD International League Against Epilepsy (ILAE) task force classification types I and II, who underwent resective epilepsy surgery and were followed for at least 2 years after surgery. The mean age at epilepsy onset was 4.3 years (0-14.2 years), and mean age at epilepsy surgery was 9.4 years (0.4-17.5 years). The mean duration of postoperative follow-up was 5.1±2.6 years (2-12.4 years). Of 58 patients, 62% of patients achieved Engel class I at 2 years postoperatively, 58% at 5 years postoperatively, and 53% at the last follow up. Forty eight percent of our cohort successfully discontinued antiepileptic medication. Of 30 patients with seizure recurrence, 83% of seizures recurred within 2 years after surgery. We observed that FCD type IIb was significantly associated with a better surgical outcome. At fifth postoperative year, 88% of FCD IIb patients were seizure free compared with 21% of type I and 57% of type IIa patients (P=0.043). By multivariate analysis, lesion on MRI (P=0.02) and complete resection (P<0.01) were the most important predictive factors for a seizure-free outcome. Epilepsy surgery is highly effective; more than half of medically intractable epilepsy patients achieved seizure freedom after surgery. In addition, we found significant difference in surgical outcomes according to the ILAE task force classification. Lesion on MRI and complete resection were the most important predictive factors for favorable seizure outcome in isolated FCD patients.

#3

Outcome of surgery for temporal lobe epilepsy in adults - A cohort study.

International journal of surgery (London, England)2016 Dec

The aim of the current study was to evaluate the factors associated with post-operative outcome in patients with temporal lobe epilepsy (TLE) undergoing Surgery. We analyzed data of 288 consecutive patients operated for drug-resistant TLE. All the patients had at least one year post surgery follow-up. Logistic regression model was used to evaluate the predictive value of different factors for outcome. The mean age at onset of epilepsy of the study population was 15.51 ± 9.79 years; whereas the mean age at surgery was 32.16 ± 9.45 years, with 125 (43.4%) women. The age at surgery was significantly lower in the patients with favourable outcome (30.26 ± 9.05 vs. 34.06 ± 9.85 years; p = 0.007). The mean duration of epilepsy with age of onset below 12 years was higher than the rest (19.84 ± 7.30 vs. 13.00 ± 8.45 years; p < 0.001). The histopathology showed hippocampal sclerosis in 203 (70.4%) of the patients; isolated focal cortical dysplasia was associated with unfavourable outcome (9.3% vs.2.6%; p = 0.036). The duration of follow up ranged from 1 to 10.3 years. Three patients died late in the follow up. At the last follow 73% were seizure free and Engel's favourable outcome was noted in 82%. Duration of epilepsy greater than ten years (β = 6.997; 95%CI; 2.254-21.715; p = 0.01), younger age of onset of epilepsy (β = 1.07; 95%CI; 1.014-1.132; p = 0.015) and acute post operative seizures (APOS) (β = 4.761; 95%CI; 1.946-11.649; p = 0.001) were the predictors of unfavourable outcome. Following surgery for TLE, 73% were seizure free and Engel's favourable outcome was noted in 82%. The predictors of unfavourable outcome were younger age of onset, pronged duration and of epilepsy and APOS.

#4

Cytochrome c oxidase deficit is associated with the seizure onset zone in young patients with focal cortical dysplasia Type II.

Metabolic brain disease2015 Oct

It has been postulated that mitochondrial dysfunction may be an important factor in epileptogenesis of intractable epilepsy. The current study tests the hypothesis that mitochondrial Complex IV (CIV) or cytochrome c oxidase dysfunction is associated with the seizure onset zone (SOZ) in patients with focal cortical dysplasia (FCD). Subjects were selected based on: age <19y; epilepsy surgery between May, 2010 and October, 2011; pathological diagnosis of isolated focal cortical dysplasia Type I (FCDI) or Type II (FCDII); and sufficient residual cortical tissue to conduct analysis of electron transport chain complex (ETC) activity in SOZ and adjacent cortical regions. In this retrospective study, patients were identified who had sufficient unfixed, frozen brain tissue for biochemical analysis in tissue homogenates. Specimens were subtyped using ILAE classification for FCD, and excluded if diagnosed with FCD Type III or dual pathology. Analysis of ETC activity in resected tissues was conducted independently and without knowledge of the identity, diagnosis, or clinical status of individual subjects. Seventeen patients met the inclusion criteria, including 6 FCDI and 11 FCDII. Comparison of adjacent cortical resections showed decreased CIV activity in the SOZ of the FCDII group (P = 0.003), but no significant CIV difference in adjacent tissues of the FCDI group. Because of the importance of CIV as the terminal and rate-limiting complex in the mitochondrial electron transport chain, these authors conclude that 1) a deficit of CIV is associated with the SOZ of patients with FCDII; 2) CIV deficiency may contribute to the spectrum of FCD neuropathology; and 3) further investigation of CIV in FCD may lead to the discovery of new targets for neuroprotective therapies for patients with intractable epilepsy.

Publicações recentes

Ver todas no PubMed

Associações

Organizações que acompanham esta doença — pra ter apoio e orientação

Ainda não temos associações cadastradas para Displasia cortical focal.

É de uma associação que acompanha esta doença? Fale com a gente →

Comunidades

Grupos ativos de quem convive com esta doença aqui no Raras

Ainda não existe comunidade no Raras para Displasia cortical focal

Pacientes, familiares e cuidadores se organizam em comunidades pra compartilhar experiências, fazer perguntas e se apoiar. Você pode ser o primeiro.

Tire suas dúvidas

Perguntas, dicas e experiências compartilhadas aqui na página

Participe da discussão

Faça login para postar dúvidas, compartilhar experiências e interagir com especialistas.

Fazer login

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. Childhood-Onset Epileptic Encephalopathy Associated With Isolated Focal Cortical Dysplasia and a Novel TSC1 Germline Mutation.
    Clinical EEG and neuroscience· 2018· PMID 28762286mais citado
  2. Surgical outcome and predictive factors of epilepsy surgery in pediatric isolated focal cortical dysplasia.
    Epilepsy research· 2018· PMID 29197666mais citado
  3. Outcome of surgery for temporal lobe epilepsy in adults - A cohort study.
    International journal of surgery (London, England)· 2016· PMID 25979111mais citado
  4. Cytochrome c oxidase deficit is associated with the seizure onset zone in young patients with focal cortical dysplasia Type II.
    Metabolic brain disease· 2015· PMID 25957585mais citado
  5. Cerebral glucose hypometabolism is associated with mitochondrial dysfunction in patients with intractable epilepsy and cortical dysplasia.
    Epilepsia· 2014· PMID 25053176recente

Bases de dados e fontes oficiais

Identificadores e referências canônicas usadas para montar este verbete.

  1. ORPHA:65683(Orphanet)
  2. MONDO:0019009(MONDO)
  3. GARD:16671(GARD (NIH))
  4. Variantes catalogadas(ClinVar)
  5. Busca completa no PubMed(PubMed)
  6. Q1316942(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

Displasia cortical focal
Compêndio · Raras BR

Displasia cortical focal

ORPHA:65683 · MONDO:0019009
Prevalência
Unknown
CID-10
Q04.8 · Outras malformações congênitas especificadas do encéfalo
CID-11
Início
All ages
Prevalência
0.0 (Worldwide)
MedGen
UMLS
C1846385
EuropePMC
Wikidata
Papers 10a
DiscussaoAtiva

Nenhuma novidade ainda. O agente esta monitorando.

0membros
0novidades