ArticleJournal of neurology2013
A family with IVIg-responsive Charcot-Marie-Tooth disease.
Article in Journal of neurology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 12 citations in OpenAlex.
- Chronic Inflammatory Demyelinating Polyneuropathy (CIDP): A Comprehensive Review of Types, Pathophysiology, and Treatment Approaches.Brain and behavior · 2026Review
- Tibial to ulnar nerve amplitude ratio as a marker of length-dependent neuropathy.Clinical neurophysiology practice · 2025Article
- Inherited neuropathies: an update.Journal of neurology · 2013Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We report a family of intravenous immunoglobulin (IVIg)-responsive X-linked Charcot-Marie-Tooth disease Type 1 (CMT1X) with a novel gap junction protein 1 mutation. Two of three siblings in the family complained of subacute motor and sensory impairment, and their symptoms improved after the administration of IVIg. Additional IVIg treatment also resulted in similar improvement. The other also showed a mild improvement on IVIg. It has been suggested that an immune-mediated process is involved in the progression of neuropathy in CMT1X. The finding in our report provides evidence of susceptibility to immune-mediated demyelinating neuropathy in some form of CMT1X. Superimposed demyelinating neuropathy as well as a gradual deterioration of neuropathy over decades can be a clinical manifestation of CMT1X.
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Registered trials
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