Consensus Paper: Latent Autoimmune Cerebellar Ataxia (LACA).

Biomarkers Cerebellar reserve Cerebellum Immune-mediated cerebellar ataxias Latent autoimmune cerebellar ataxia Latent autoimmune diabetes in adults

Journal

Cerebellum (London, England)
ISSN: 1473-4230
Titre abrégé: Cerebellum
Pays: United States
ID NLM: 101089443

Informations de publication

Date de publication:
Apr 2024
Historique:
accepted: 20 03 2023
pubmed: 30 3 2023
medline: 30 3 2023
entrez: 29 3 2023
Statut: ppublish

Résumé

Immune-mediated cerebellar ataxias (IMCAs) have diverse etiologies. Patients with IMCAs develop cerebellar symptoms, characterized mainly by gait ataxia, showing an acute or subacute clinical course. We present a novel concept of latent autoimmune cerebellar ataxia (LACA), analogous to latent autoimmune diabetes in adults (LADA). LADA is a slowly progressive form of autoimmune diabetes where patients are often initially diagnosed with type 2 diabetes. The sole biomarker (serum anti-GAD antibody) is not always present or can fluctuate. However, the disease progresses to pancreatic beta-cell failure and insulin dependency within about 5 years. Due to the unclear autoimmune profile, clinicians often struggle to reach an early diagnosis during the period when insulin production is not severely compromised. LACA is also characterized by a slowly progressive course, lack of obvious autoimmune background, and difficulties in reaching a diagnosis in the absence of clear markers for IMCAs. The authors discuss two aspects of LACA: (1) the not manifestly evident autoimmunity and (2) the prodromal stage of IMCA's characterized by a period of partial neuronal dysfunction where non-specific symptoms may occur. In order to achieve an early intervention and prevent cell death in the cerebellum, identification of the time-window before irreversible neuronal loss is critical. LACA occurs during this time-window when possible preservation of neural plasticity exists. Efforts should be devoted to the early identification of biological, neurophysiological, neuropsychological, morphological (brain morphometry), and multimodal biomarkers allowing early diagnosis and therapeutic intervention and to avoid irreversible neuronal loss.

Identifiants

pubmed: 36991252
doi: 10.1007/s12311-023-01550-4
pii: 10.1007/s12311-023-01550-4
pmc: PMC10060034
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

838-855

Informations de copyright

© 2023. The Author(s).

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Auteurs

Mario Manto (M)

Service de Neurologie, Médiathèque Jean Jacquy, CHU-Charleroi, Charleroi, Belgium.
Service des Neurosciences, University of Mons, Mons, Belgium.

Marios Hadjivassiliou (M)

Academic Department of Neurosciences, Royal Hallamshire Hospital, Sheffield, UK.

José Fidel Baizabal-Carvallo (JF)

Department of Sciences and Engineering, University of Guanajuato, León, Mexico.

Christiane S Hampe (CS)

University of Washington, Seattle, WA, USA.

Jerome Honnorat (J)

French Reference Center on Paraneoplastic Neurological Syndromes, Hospices Civils de Lyon, Hôpital Neurologique, Bron, France.
Institut NeuroMyoGene MELIS INSERM U1314/CNRS UMR 5284, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France.

Bastien Joubert (B)

French Reference Center on Paraneoplastic Neurological Syndromes, Hospices Civils de Lyon, Hôpital Neurologique, Bron, France.
Institut NeuroMyoGene MELIS INSERM U1314/CNRS UMR 5284, Université de Lyon, Université Claude Bernard Lyon 1, Lyon, France.

Hiroshi Mitoma (H)

Department of Medical Education, Tokyo Medical University, Tokyo, Japan. mitoma@tokyo-med.ac.jp.

Sergio Muñiz-Castrillo (S)

Center for Sleep Sciences and Medicine, Stanford University, Palo Alto, CA, USA.

Aasef G Shaikh (AG)

Louis Stokes Cleveland VA Medical Center, University Hospitals Cleveland Medical Center, Cleveland, OH, USA.

Alberto Vogrig (A)

Clinical Neurology, Udine University Hospital, Azienda Sanitaria Universitaria Friuli Centrale (ASU FC), Udine, Italy.
Department of Medicine (DAME), University of Udine, Udine, Italy.

Classifications MeSH