Neural Noise

Sensory and motor cortical hyperexcitability in ALS (TMS)

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  • Sensory and motor cortical hyperexcitability can be assessed with TMS in amyotrophic lateral sclerosis (ALS).1
  • A prospective pilot study examined whether sensory and motor cortical hyperexcitability are related in ALS.1 1

Weekly enrichment (2026-07-20)

  • The study is a prospective pilot examining whether sensory and motor cortical hyperexcitability are related in ALS; it enrolled 26 ALS patients and 18 healthy controls (Clinical Neurophysiology / PMID 41520601).2
  • Motor cortex excitability was quantified by transcranial magnetic stimulation (TMS) as a motor evoked potential (MEP) suppression ratio, while somatosensory cortex excitability was assessed with upper-limb somatosensory evoked potentials (SEPs) using conventional and paired-pulse techniques.2
  • ALS patients showed a significantly reduced MEP suppression ratio (p < 0.001) that discriminated patients from controls with 100% accuracy in this sample.2
  • The SEP suppression ratio was also significantly lower in ALS (p < 0.001), with diagnostic sensitivity 76.3%, specificity 91.7% and overall accuracy 84%.2
  • In the subgroup with “giant” SEPs, MEP and SEP suppression ratios were strongly inversely correlated (r = −0.70, p < 0.001), suggesting an interconnected, possibly compensatory sensorimotor cortical interplay rather than fully independent mechanisms.2
  • The authors conclude that MEP and SEP suppression ratios are robust biomarkers of cortical dysfunction in ALS and reveal subgroup-specific heterogeneity of cortical involvement.2
  • Context: a meta-analysis of ~2,500 participants (1,530 ALS patients, 1,102 controls) across 25 threshold-tracking TMS studies found reduced short-interval intracortical inhibition (SICI, ISI 1–7 ms) to be the single most sensitive TMS marker of ALS cortical hyperexcitability (standardized mean difference −0.994).3
  • Context: prospective cohort work (345 ALS patients, 99 mimics) shows cortical hyperexcitability is present across all disease stages and intensifies with longer disease duration via cortical disinhibition and increased corticomotoneuronal excitability, supporting TMS metrics as diagnostic and prognostic BCI-adjacent biomarkers.4

Footnotes

  1. https://www.sciencedirect.com/science/article/pii/S1388245725013379?dgcid=rss_sd_all ↩ ↩2 ↩3

  2. https://pubmed.ncbi.nlm.nih.gov/41520601/ ↩ ↩2 ↩3 ↩4 ↩5 ↩6

  3. https://pmc.ncbi.nlm.nih.gov/articles/PMC11235657/ ↩

  4. https://doi.org/10.1002/acn3.51039 ↩

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