Clinical Neurophysiology最新文献

Objective: Mirror movements are involuntary, task-coupled contractions in contralateral homologous muscles during unilateral movement. While often described as a developmental remnant or rare clinical sign, mirror movements offer insight into the physiological mechanisms that underlie motor lateralization and interhemispheric balance. This review aimed to synthesize the available neurophysiological evidence-primarily from transcranial magnetic stimulation (TMS)-and propose a structured, mechanism-based framework for interpreting mirror movements across neurological conditions.

Methods: A structured narrative review was conducted of studies published between 1966 and November 2025 using TMS in individuals with congenital, developmental, or acquired mirror movements. Studies using neuroimaging or peripheral electrophysiology were included selectively to support anatomical or functional interpretation of TMS findings. Data were organized into three mechanistic layers based on prevailing neurophysiological signatures rather than etiology alone.

Results: Three non-mutually exclusive mechanisms were identified: (I) persistent fast-conducting ipsilateral corticospinal projections, primarily in congenital mirror movement syndromes and early brain injury; (II) deficient transcallosal inhibition, observed in conditions affecting interhemispheric balance such as amyotrophic lateral sclerosis, multiple sclerosis, Parkinson's disease, and callosal agenesis; and (III) bilateral overactivation of premotor and supplementary motor areas, especially under conditions of impaired motor program selection or increased task demands.

Conclusions: Mirror movements can be interpreted within a tri-layer model reflecting distinct disruptions in corticospinal connectivity, interhemispheric inhibition, and supraspinal motor control.

Significance: This framework provides an integrative model for interpreting neurophysiological findings in mirror movements, offering insight into hierarchical motor control without implying specific diagnostic or therapeutic applications.

Objectives: Corticospinal excitability of the motor cortex (M1) hand representation is predicted by phase and power of the sensorimotor mu-rhythm in EEG-TMS studies. Here we address for the first time corticospinal excitability prediction of the M1 leg representation.

Methods: In 16 healthy subjects, 1,000 trials of single-pulse navigated focal TMS to the hot spot of the tibialis anterior muscle were obtained during motor evoked potential (MEP) and EEG recording, using Hjorth montages centered over sensorimotor cortex, ipsilateral to the hemisphere that was targeted by TMS.

Results: Power in the high gamma frequency bands correlated directly, and power in the beta band inversely with MEP amplitude. The phase of the mu-rhythm had no effect but a significant interaction between mu-power and mu-phase was observed: with high mu-power, largest MEPs occurred during the early peak, while with low mu-power largest MEPs were observed during the late peak.

Conclusions: Findings demonstrate that an interaction of mu-power and -phase, and power in other frequency bands of the EEG signal from the sensorimotor cortex prior to the TMS pulse predict corticospinal excitability of the M1 leg representation.

Significance: Findings may inform brain-state dependent stimulation of M1 leg representation for treatment of gait or balance disorders.

Introduction: Chronic pain is a major public health issue due to limited treatment efficacy. Within the IMI-PainCare project, we aimed to identify spinal biomarkers reflecting nociceptive processing and responsive to analgesics. Standardization and pharmacological validation are key for advancing analgesic development and improving care.

Methods: In a multi-center, randomized, double-blind, placebo-controlled crossover trial in healthy subjects, we assessed single doses of tapentadol (primary endpoint), lacosamide, and pregabalin (secondary endpoints) on two spinal biomarkers: RIII flexion reflex area and N13 somatosensory evoked potentials (N13-SEP), after hyperalgesia induction via high-frequency stimulation (HFS). Exploratory analyses included RIII reflex threshold and pain ratings.

Results: Twenty-four participants were enrolled. Tapentadol and pregabalin reduced the RIII flexion reflex area on the HFS sensitized side, 60 min after drug, compared to placebo, but the predetermined level of significance (p = 0.025) was not reached. No drug affected N13-SEP amplitude. All drugs significantly increased RIII threshold vs. placebo. Tapentadol and pregabalin also reduced RIII pain ratings.

Conclusions: Although primary and secondary endpoints were not met, tapentadol and pregabalin reduced the RIII flexion reflex area with medium, non-significant effect sizes. Exploratory analysis showed all drugs significantly increased the RIII threshold in HFS-induced hyperalgesic condition. N13-SEP amplitudes remained unchanged, questioning its reliability as a spinal biomarker.

Significance: Our findings support the RIII threshold as an objective spinal biomarker to assess antihyperalgesic drug effect. This study informs future choices of biomarkers, optimal timing, and analysis strategies in analgesic research.

Introduction: Transcranial magnetic stimulation (TMS) of the primary motor area induces a brief suppression of voluntary muscle activity in electromyography (EMG), known as the ipsilateral silent period (iSP). The iSP reflects transcallosal inhibitory interaction between motor cortices. However, protocols vary, and systematic studies on how stimulation intensity influences the iSP are lacking.

Methods: In 100 healthy young adults, we applied line based neuronavigated single-pulse TMS to both primary motor hand areas at 90-230% of resting motor threshold (RMT). iSPs were recorded at each intensity, and summary statistics were calculated for common parameters. A multilevel mixed-effects model identified variables contributing to differences in outcomes.

Results: We obtained 197 complete datasets (2116 iSPs). iSP duration and depth increased non-linearly with intensity, while onset remained unchanged. Consistently detectable iSPs (>80% occurrence) were observed at 120% RMT. Variability increased at higher intensities, interacting with pre-stimulation EMG.

Conclusion: iSP parameters show a non-linear relationship with intensity, except for onset, with greater variability at higher levels. To minimize variability, we recommend 120-140% RMT.

Significance: This first systematic evaluation of stimulation intensity on iSPs in the largest cohort to date provides recommendations for future TMS studies.