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Related Experiment Video

Updated: Jun 13, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

Published on: August 21, 2017

Neuromyelitis optica preceded by hyperCKemia episode.

N Suzuki¹, T Takahashi, M Aoki

¹Department of Neurology, Tohoku University School of Medicine, Aoba-ku, Sendai 980-8574, Japan. naoki@em.neurol.med.tohoku.ac.jp

|May 12, 2010

Summary

Elevated creatine kinase (CK) levels, known as hyperCKemia, may precede neuromyelitis optica (NMO) onset in some patients. This transient muscle enzyme elevation warrants further investigation into its role in NMO pathogenesis.

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Last Updated: Jun 13, 2026

Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4

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Published on: August 21, 2017

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients

Dynamic Visual Tests to Identify and Quantify Visual Damage and Repair Following Demyelination in Optic Neuritis Patients

Published on: April 14, 2014

Area of Science:

Neurology
Immunology
Neuroimmunology

Background:

Neuromyelitis optica (NMO) is a central nervous system autoimmune disease.
Anti-aquaporin-4 (AQP4) antibodies are key biomarkers for NMO, targeting astrocytes.
AQP4 is also present in skeletal muscle, but muscle involvement in NMO was previously undescribed.

Observation:

A retrospective analysis of 733 NMO patients with anti-AQP4 antibodies was conducted.
Three female patients presented with significant hyperCKemia and fatigue preceding optic neuritis.
HyperCKemia was transient, resolving without treatment, but recurred in one patient.

Findings:

The study identified a potential association between hyperCKemia and NMO.
Transient elevations in creatine kinase (CK) levels were observed in a subset of NMO patients.
This suggests hyperCKemia may be linked to the underlying pathogenesis of NMO.

Implications:

HyperCKemia might be an unrecognized clinical feature in some NMO cases.
The exact cause of transient hyperCKemia in NMO patients remains unknown.
Further research is needed to determine the frequency and pathogenic role of hyperCKemia in NMO.