Neural Noise

TMS and concomitant medications: drug interactions and clinical management

2 min read

  • A report of three cases in Clinical Neurophysiology addresses whether lamotrigine should be discontinued before TMS treatment.1
  • TMS is a form of non-invasive neuromodulation; drug interactions with anticonvulsants such as lamotrigine are relevant for clinical and BCI/neurotech practice.1 1

Gardner updates

  • Whether lamotrigine should be discontinued before TMS was addressed in a report of three cases (Clinical Neurophysiology, April 2026). 1

  • A case report in Clinical Neurophysiology (April 2026) addresses whether lamotrigine should be discontinued before TMS treatment, reporting three cases. 1

Weekly enrichment (2026-07-20)

  • The source is a case report titled “Should lamotrigine be discontinued before TMS treatment: A report of three cases” in Clinical Neurophysiology (2026); it is indexed on PubMed as a Letter with no abstract available, so specific per-case numeric outcomes are not reported in accessible metadata.23
  • Lamotrigine is an antiepileptic drug that acts primarily by blocking voltage-dependent sodium channels, stabilizing neuronal membranes and reducing release of excitatory neurotransmitters such as glutamate.45
  • In TMS studies this mechanism appears as a dose-dependent increase in the resting motor threshold (RMT), a standard marker of reduced motor-cortical excitability.4
  • A randomized, placebo-controlled crossover study in 16 male volunteers (single 325 mg dose or graded cumulative dosing) found lamotrigine serum levels and RMT both rose dose-dependently with a significant linear correlation (P < 0.0001), though with high inter-individual variability.4
  • In six patients with complex partial seizures, loading doses of lamotrigine monotherapy titrated from 25 mg/day toward 200 mg/day significantly raised motor threshold from about 2 weeks, while MEP amplitude and the cortical silent period were unchanged.6
  • Sodium-channel-blocking antiepileptics (carbamazepine, lacosamide, lamotrigine, phenytoin) all increase RMT relative to drug-naïve patients, and the effect is reversible upon medication withdrawal.5
  • Because a higher motor threshold raises the stimulator output needed to reach threshold, lamotrigine can shift TMS motor-threshold-based dosing; TMS is generally well tolerated with very low seizure risk, and NIH consensus safe-stimulation parameters govern repetitive TMS.7
  • Clinical/BCI implication: the case report weighs whether to hold lamotrigine before TMS, while the wider TMS pharmacology literature indicates its excitability effect is dose-dependent and reversible—relevant both for motor-threshold calibration and for interpreting TMS-derived excitability biomarkers used in neuromodulation and BCI protocols.25

Footnotes

  1. https://www.sciencedirect.com/science/article/pii/S138824572600204X?dgcid=rss_sd_all ↩ ↩2 ↩3 ↩4 ↩5

  2. https://doi.org/10.1016/j.clinph.2026.2111705 ↩ ↩2

  3. https://pubmed.ncbi.nlm.nih.gov/41719897/ ↩

  4. https://www.sciencedirect.com/science/article/abs/pii/S0920121103001505 ↩ ↩2 ↩3

  5. https://www.frontiersin.org/journals/integrative-neuroscience/articles/10.3389/fnint.2019.00057/full ↩ ↩2 ↩3

  6. https://doi.org/10.1111/j.1528-1157.1999.tb00711.x ↩

  7. https://pmc.ncbi.nlm.nih.gov/articles/PMC321221/ ↩

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