Literature DB >> 26799151

Cortical hyperexcitability in patients with C9ORF72 mutations: Relationship to phenotype.

Olivia Schanz1, Devin Bageac1, Laura Braun1, Bryan J Traynor2, Tanya J Lehky3, Mary Kay Floeter1.   

Abstract

INTRODUCTION: Patients with mutations in C9orf72 can have amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), or ALS-FTD. The goals were to establish whether cortical hyperexcitability occurs in C9orf72 patients with different clinical presentations.
METHODS: Cortical thresholds and silent periods were measured in thenar muscles in 19 participants with C9orf72 expansions and 21 healthy controls using transcranial magnetic stimulation (TMS). El Escorial and Rascovsky criteria were used to diagnose ALS and FTD. Fourteen participants with C9orf72 expansions were re-tested 6 months later. Correlations with finger-tapping speed, timed peg test, the ALS functional rating scale, and Dementia Rating Scale were examined.
RESULTS: Most participants with C9orf72 expansions had normal or low cortical thresholds. Among them, ALS patients had the lowest thresholds and significantly shorter silent periods. Thresholds correlated with timed peg-test scores. TMS did not correlate with the Dementia Rating Scale.
CONCLUSIONS: TMS measures of cortical excitability may serve as noninvasive biomarkers of ALS disease activity. Muscle Nerve, 2016 Muscle Nerve 54: 264-269, 2016.
© 2016 Wiley Periodicals, Inc.

Entities:  

Keywords:  ALS; C9orf72; amyotrophic lateral sclerosis; cortical hyperexcitability; cortical silent period; frontotemporal dementia; transcranial magnetic stimulation

Mesh:

Substances:

Year:  2016        PMID: 26799151      PMCID: PMC4940214          DOI: 10.1002/mus.25047

Source DB:  PubMed          Journal:  Muscle Nerve        ISSN: 0148-639X            Impact factor:   3.217


  45 in total

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Authors:  A Eisen
Journal:  Semin Neurol       Date:  2001-06       Impact factor: 3.420

2.  Corticomotor threshold is reduced in early sporadic amyotrophic lateral sclerosis.

Authors:  K R Mills; K A Nithi
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3.  The corticomotor threshold is not dependent on disease duration in amyotrophic lateral sclerosis (ALS).

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4.  Impaired motor cortex inhibition in patients with amyotrophic lateral sclerosis. Evidence from paired transcranial magnetic stimulation.

Authors:  U Ziemann; M Winter; C D Reimers; K Reimers; F Tergau; W Paulus
Journal:  Neurology       Date:  1997-11       Impact factor: 9.910

5.  Double cortical stimulation in amyotrophic lateral sclerosis.

Authors:  T Yokota; A Yoshino; A Inaba; Y Saito
Journal:  J Neurol Neurosurg Psychiatry       Date:  1996-12       Impact factor: 10.154

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7.  Covariation of corticospinal efficiency and silent period in motoneuron diseases.

Authors:  S Attarian; J Pouget; A Schmied
Journal:  Muscle Nerve       Date:  2006-08       Impact factor: 3.217

8.  Changes in motor cortex inhibition over time in patients with amyotrophic lateral sclerosis.

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Journal:  J Neurol       Date:  2002-12       Impact factor: 4.849

9.  Intrinsic membrane hyperexcitability of amyotrophic lateral sclerosis patient-derived motor neurons.

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10.  Characterization of frontotemporal dementia and/or amyotrophic lateral sclerosis associated with the GGGGCC repeat expansion in C9ORF72.

Authors:  Bradley F Boeve; Kevin B Boylan; Neill R Graff-Radford; Mariely DeJesus-Hernandez; David S Knopman; Otto Pedraza; Prashanthi Vemuri; David Jones; Val Lowe; Melissa E Murray; Dennis W Dickson; Keith A Josephs; Beth K Rush; Mary M Machulda; Julie A Fields; Tanis J Ferman; Matthew Baker; Nicola J Rutherford; Jennifer Adamson; Zbigniew K Wszolek; Anahita Adeli; Rodolfo Savica; Brendon Boot; Karen M Kuntz; Ralitza Gavrilova; Andrew Reeves; Jennifer Whitwell; Kejal Kantarci; Clifford R Jack; Joseph E Parisi; John A Lucas; Ronald C Petersen; Rosa Rademakers
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1.  The C9ORF72 Gene, Implicated in Amyotrophic Lateral Sclerosis and Frontotemporal Dementia, Encodes a Protein That Functions in Control of Endothelin and Glutamate Signaling.

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Review 4.  Considerations for Amyotrophic Lateral Sclerosis (ALS) Clinical Trial Design.

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5.  C9orf72 Dipeptide Repeats Cause Selective Neurodegeneration and Cell-Autonomous Excitotoxicity in Drosophila Glutamatergic Neurons.

Authors:  Wangchao Xu; Jin Xu
Journal:  J Neurosci       Date:  2018-07-23       Impact factor: 6.167

Review 6.  Synaptic dysfunction and altered excitability in C9ORF72 ALS/FTD.

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Journal:  Brain Res       Date:  2018-02-14       Impact factor: 3.252

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8.  Effects of mexiletine on hyperexcitability in sporadic amyotrophic lateral sclerosis: Preliminary findings from a small phase II randomized controlled trial.

Authors:  Michael D Weiss; Eric A Macklin; Courtney E McIlduff; Steve Vucic; Brian J Wainger; Matthew C Kiernan; Stephen A Goutman; Namita A Goyal; Seward B Rutkove; Shafeeq S Ladha; I-Hweii Amy Chen; Matthew B Harms; Thomas H Brannagan; David Lacomis; Sasha Zivkovic; Maxwell Ma; Leo H Wang; Zachary Simmons; Michael H Rivner; Jeremy M Shefner; Merit E Cudkowicz; Nazem Atassi
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Review 9.  Insights into C9ORF72-Related ALS/FTD from Drosophila and iPSC Models.

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10.  Cell-type specific differences in promoter activity of the ALS-linked C9orf72 mouse ortholog.

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