TY - JOUR
T1 - Neurophysiology in the mirror
T2 - A tri-layer model of mirror movements informed by TMS evidence
AU - Sebastianelli, Luca
AU - Versace, Viviana
AU - Ferrazzoli, Davide
AU - Ortelli, Paola
AU - Trinka, Eugen
AU - Sellner, Johann
AU - Nardone, Raffaele
N1 - Trinka: Nardone: Department of Neurology, Neurocritical Care, and Neurorehabilitation, Center for Cognitive Neuroscience, Member of European Reference Network EpiCARE, Christian Doppler University Hospital, Paracelsus Medical University, Salzburg, Austria
Trinka: Neuroscience Institute, Center for Cognitive Neuroscience, Christian Doppler University Hospital, Paracelsus Medical University, Salzburg, Austria Karl Landsteiner Institute for Clinical Neuroscience, Salzburg, Austria; Sellner: externe Aff.;
Lehr-KH Hospital of Merano (SABES-ASDAA), Merano-Meran, Italy und Hospital of Vipiteno (SABES-ASDAA), Vipiteno-Sterzing, Italy
PY - 2026/4
Y1 - 2026/4
N2 - 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.
AB - 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.
KW - Interhemispheric inhibition
KW - Ipsilateral corticospinal tract
KW - Mirror movements
KW - Motor control
KW - Motor overflow
KW - Movement disorders
KW - Neuroplasticity
KW - Pathophysiology
KW - Supplementary motor area
KW - Transcranial Magnetic Stimulation
UR - https://www.webofscience.com/api/gateway?GWVersion=2&SrcApp=pmu_pure&SrcAuth=WosAPI&KeyUT=WOS:001686733400001&DestLinkType=FullRecord&DestApp=WOS_CPL
U2 - 10.1016/j.clinph.2026.2111692
DO - 10.1016/j.clinph.2026.2111692
M3 - Original Article
C2 - 41653702
SN - 1388-2457
VL - 184
JO - CLINICAL NEUROPHYSIOLOGY
JF - CLINICAL NEUROPHYSIOLOGY
M1 - 2111692
ER -