Morvan syndrome

disease
On this page

Also known as limbic encephalitis-neuromyotonia-hyperhidrosis-polyneuropathy syndromeMorvan's fibrillary chorea

Summary

Morvan syndrome (MONDO:0008718) is a disease. A subtype of muscular channelopathy — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

At a glance

  • Prevalence: <1 / 1 000 000 (Worldwide) [Orphanet-validated]
  • Phenotypes (HPO): 1

Clinical features

Epidemiology

Prevalence records

2 prevalence record(s), Orphanet:

TypeClassValueGeographyValidation
Cases/families60WorldwideValidated
Point prevalence<1 / 1 000 000WorldwideValidated

Signs & symptoms

Clinical features (HPO)

1 HPO clinical features (Orphanet curated; top 1 by frequency):

HPO IDTermFrequency
HP:5000005Anti-CASPR2Frequent (30-79%)

Identifiers

Disease identifiers

FieldValue
Canonical nameMorvan syndrome
Mondo IDMONDO:0008718
EFOEFO:1001897
Orphanet83467
SNOMED CT763803004
UMLSC3854373
MedGen1632829
GARD0009766
Is cancer (heuristic)no

Also known as: limbic encephalitis-neuromyotonia-hyperhidrosis-polyneuropathy syndrome · Morvan’s fibrillary chorea

Disease family

This is a subtype of muscular channelopathy. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: disease › human disease › disease by body system or component › nervous system disorderneuromuscular diseasemuscular channelopathyMorvan syndrome

Related subtypes (11): Andersen-Tawil syndrome, Thomsen and Becker disease, malignant hyperthermia of anesthesia, Isaac syndrome, RYR1-related myopathy, CNGB3-related retinopathy, SCN4A-related channelopathy, neurological muscular channelopathy due to a genetic sodium channel defect, neurological muscular channelopathy due to a genetic chloride channel defect, neurological muscular channelopathy due to a genetic calcium channel defect, neurological muscular channelopathy due to a genetic potassium channel defect

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.

No linked Atlas pages yet — the cross-entity mesh grows as the corpus expands.