Mirror Movements in Acquired Neurological Disorders: A Mini-Review

Mirror movements (MMs) are specifically defined as involuntary movements occurring on one side of homologous muscles when performing unilateral movements with the contralateral limb. MMs have been considered a kind of soft neurological signs, and the persistence or reappearance of MMs in adults is usually pathologic. In addition to some congenital syndrome, MMs have been also described in age-related neurological diseases including pyramidal system diseases (e.g., stroke, amyotrophic lateral sclerosis) and extrapyramidal disorders (e.g., Parkinson's disease, essential tremor). With the advances in instrumentation and detection means, subtle or subclinical MMs have been deeply studied. Furthermore, the underlying mechanism is also being further elucidated. In this mini-review, we firstly discuss the MM examination means, and then review the literature regarding MMs in individuals with acquired neurological disorders, in order to further understand the pathogenesis of MMs.

Congenital Mirror Movements Associated With Brain Malformations

Background: Congenital mirror movements are involuntary movements of a side of the body imitating intentional movements on the opposite side, appearing in early childhood and persisting beyond 7 years of age. Congenital mirror movements are usually idiopathic but have been reported in association with various brain malformations. Methods: We describe clinical, genetic, and radiologic features in 9 individuals from 5 families manifesting congenital mirror movements. Results: The brain malformations associated with congenital mirror movements were: dysplastic corpus callosum in father and daughter with a heterozygous p.Met1* mutation in DCC; hypoplastic corpus callosum, dysgyria, and malformed vermis in a mother and son with a heterozygous p.Thr312Met mutation in TUBB3; dysplastic corpus callosum, dysgyria, abnormal vermis, and asymmetric ventricles in a father and 2 daughters with a heterozygous p.Arg121Trp mutation in TUBB; hypoplastic corpus callosum, dysgyria, malformed basal ganglia and abnormal vermis in a patient with a heterozygous p.Glu155Asp mutation in TUBA1A; hydrocephalus, hypoplastic corpus callosum, polymicrogyria, and cerebellar cysts in a patient with a homozygous p.Pro312Leu mutation in POMGNT1. Conclusion: DCC, TUBB3, TUBB, TUBA1A, POMGNT1 cause abnormal axonal guidance via different mechanisms and result in congenital mirror movements associated with brain malformations.