Evidence map›Paper›PMID 20443018›Full record

ArticleJournal of neurology2010

Clinical progression in Charcot-Marie-Tooth disease type 1A duplication: clinico-electrophysiological and MRI longitudinal study of a family.

José Berciano, Elena Gallardo, Antonio García, César Ramón, Jon Infante, Onofre Combarros

Abstract read
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Article in Journal of neurology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.6field-weighted citation impact, top 39% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

6 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Review
  3. Biomarkers predict outcome in Charcot-Marie-Tooth disease 1A.Journal of neurology, neurosurgery, and psychiatry · 2017
    Article
  4. Observational
  5. Article
  6. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 1 country.

José BercianoService of Neurology, University Hospital Marqués de Valdecilla (IFIMAV), University of Cantabria and Centro de Investigación Biomédica en Red de Enfermedades Neurodegenerativas, 39008, Santander, Spain. jaberciano@humv.es
Elena Gallardo
Antonio García
César Ramón
Jon Infante
Onofre Combarros
Universidad de Cantabria · ESFundación Marques de Valdecilla · ESMarqués de Valdecilla University Hospital · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-term follow-up studies in Charcot-Marie-Tooth disease type 1 duplication (CMT1A) are scanty. Here we describe a longitudinal study in a CMT1A pedigree. Our CMT1A pedigree comprised 11 examined patients, ages between 13 and 83 (median, 36) years, serially evaluated for up to 26 years. In all 11 patients we carried out electrophysiological evaluation, and in three of them magnetic resonance imaging (MRI) of lower-limb musculature. The 54-year-old proband patient, yearly examined as of age 28, developed at age 48 gradual and progressive distal lower-leg weakness ascending to thigh musculature. His serial electrophysiological studies showed diffuse slowing of motor conduction velocity, absence or severe attenuation of distal compound muscle action potentials, and spontaneous muscle activity in the tibialis anterior and rectus femoris. Two MRI studies of lower limbs, at ages 51 and 54, showed extensive fatty atrophy of lower-leg musculature, and progressive and distally accentuated fatty atrophy of anterior and posterior femoral muscles. An outstanding finding in the first MRI was the presence of marked edema of anterior femoral musculature, which to a great degree was replaced by fatty atrophy in the second study. Muscle edema was also noted in lower-leg and posterior femoral musculature. There was minimal fatty atrophy of the gluteus maximus, the remaining pelvic muscles being preserved. The other ten patients showed mild or moderate phenotype, which remained quiescent over the period of observation. Electrophysiological studies disclosed diffuse and uniform slowing of nerve conduction velocities; in no case was spontaneous muscle activity recorded. MRI showed the CMT1A characteristic pattern of distally accentuated fatty atrophy involving foot and lower-leg musculature with preservation of thigh musculature. We conclude that a small proportion of patients with CMT1A develop a late progression of disease manifested with accentuated distal leg weakness ascending to involve thigh musculature, and that long-term follow-up is essential for its detection.

Indexed as

Charcot-Marie-Tooth DiseaseElectrophysiologyFamily HealthMagnetic Resonance ImagingAdultChromosome AberrationsChromosomes, Human, Pair 17Disease ProgressionFemaleHumansLongitudinal StudiesMaleMiddle AgedMyelin ProteinsProteinsCDRT1 protein, humanMyelin ProteinsPMP22 protein, humanProteins

Identifiers

PMID20443018
OpenAlexW2038896613

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.