Evidence map›Paper›PMID 17395141›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2007

Autoimmune and paraneoplastic channelopathies.

Steven Vernino

Open access · bronzeAbstract readReview
PubMed Publisher
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
3.8field-weighted citation impact, top 7% 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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 50 citations in OpenAlex.

  1. Guideline
  2. Guideline
  3. Autoimmune autonomic ganglionopathy associated with monoclonal gammopathy of undetermined significance: a case report.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2019
    Article
  4. Review
  5. Article
  6. Review
  7. Ion channelopathies of the immune system.Current opinion in immunology · 2018
    Review
  8. Review
  9. Article
  10. Review
  11. Article
  12. Toxic role of K+ channel oxidation in mammalian brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    Article
  13. Article
  14. Review
  15. Challenges in the design and conduct of therapeutic trials in channel disorders.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2007
    Review
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

1 author at 1 institution in 1 country.

Steven VerninoDepartment of Neurology, University of Texas Southwestern Medical Center, Dallas, Texas 75390-9036, USA. steven.vernino@utsouthwestern.edu
Southwestern Medical Center · US

Funding

Experimental Dysautonomia: Pathogenesis and TreatmentR01NS048077 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI VERNINO, STEVEN A · 2004 to 2006
$630k
SCALA TYMPANI ELECTRODE ARRAYSN01NS032353 · NINDS · UNIVERSITY OF CALIFORNIA SAN FRANCISCO · PI MERZENICH, MICHAEL M · 1985 to 1987
–
NINDS NIH HHS P50NS32353NINDS NIH HHS R01NS48077
6 · The paper itself

Abstract

Thirty years ago, antibodies against the muscle acetylcholine receptor (AChR) were recognized as the cause of myasthenia gravis. Since then, there has been great interest in identifying other neurological disorders associated with autoantibodies. Several other antibody-mediated neuromuscular disorders have been identified, each associated with an antibody against a ligand- or voltage-gated ion channel. The Lambert-Eaton syndrome is caused by antibodies against voltage-gated calcium channels and often occurs in patients with small cell lung cancer. Acquired neuromyotonia is caused by voltage-gated potassium channel antibodies, and autoimmune autonomic ganglionopathy is caused by antibodies against the neuronal AChR in autonomic ganglia. There is good evidence that antibodies in these disorders cause changes in synaptic function or neuronal excitability by directly inhibiting ion channel function. More recently, studies have identified ion channel antibodies in patients with certain CNS disorders, such as steroid-responsive encephalitis and paraneoplastic cerebellar ataxia. It remains unclear if antibodies can gain access to the CNS and directly cause ion channel dysfunction. Treatment of autoimmune channelopathies includes drugs that help restore normal neuronal function and treatments to remove pathogenic antibodies (plasma exchange) or modulate the immune response (steroids or immunosuppressants). These disabling neurological disorders may be dramatically responsive to immunomodulatory therapy. Future studies will likely lead to identification of other ion channel antibodies and other autoimmune channelopathies.

Indexed as

AntibodiesAutoimmune DiseasesCalcium ChannelsChannelopathiesHumansMuscle, SkeletalParaneoplastic PolyneuropathyPotassium Channels, Voltage-GatedReceptors, NicotinicAntibodiesCalcium ChannelsPotassium Channels, Voltage-GatedReceptors, Nicotinic

Identifiers

PMID17395141
OpenAlexW2159521444

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.