Familial Congenital Mirror Movements (CMM): Disease Characteristics Research Report

Target disease

• Disease name: Familial Congenital Mirror Movements (CMM)
• Category: Mendelian neurodevelopmental motor disorder

1. Disease information

Overview (current understanding)

Congenital mirror movements (CMM) are involuntary movements of one side of the body that occur simultaneously with intentional movements of the opposite side, classically involving the hands/fingers. The condition is typically apparent in infancy or early childhood and persists lifelong in the congenital/familial form, in contrast to physiologic mirroring in young children which declines with maturation. (meneret2017mutationsinthe pages 1-2, legboUnknownyearmirrormovementsa pages 4-5)

Key identifiers

• OMIM: Congenital mirror movements #157600 (explicitly cited in primary literature) (meneret2017mutationsinthe pages 1-2)
• OMIM: Developmental split-brain syndrome (DSBS) #617542 (related allelic disorder due to biallelic DCC variants, often with corpus callosum agenesis and more severe neurodevelopmental features) (accogli2024arecurrentmcf2 pages 13-16, prato2024paroxysmaldystonicposturing pages 1-2)

Not found in retrieved sources: Orphanet ORPHA code, MONDO ID, MeSH descriptor, and ICD-10/ICD-11 code were not present in the available retrieved texts; therefore they cannot be stated with evidence here. (meneret2017mutationsinthe pages 1-2, accogli2024arecurrentmcf2 pages 13-16)

Synonyms / alternative names

• Congenital mirror movements
• Mirror movement disorder
• Familial mirror movements (These naming variants are used across the clinical and genetics literature discussing “mirror movements disorder” and “congenital mirror movements.”) (meneret2017mutationsinthe pages 1-2, chaudhari2024ahumandcc pages 1-3)

Evidence provenance

Evidence in this report derives from: - Aggregated disease-level resources/reviews (narrative review emphasizing recognition, diagnostics, and management) (legboUnknownyearmirrormovementsaa pages 4-5) - Primary human genetics and mechanistic studies (NTN1, DCC pathway effectors; cohort/family studies) (meneret2017mutationsinthe pages 1-2, schlienger2023geneticsofmirror pages 1-2, chaudhari2024ahumandcc pages 1-3) - Model-organism functional validation studies (mouse, zebrafish, Drosophila) (hu2024ventricularnetrin1deficiency pages 5-6, jain2014mirrormovementlikedefects pages 6-8, chaudhari2024ahumandcc pages 1-3)

2. Etiology

Primary causal factors (genetic)

Familial CMM is genetically heterogeneous but converges strongly on axon guidance and midline-crossing biology involving the netrin-1/DCC pathway, with additional downstream effectors identified recently.

Key genetic causes supported by primary literature in this corpus: - DCC variants are frequently associated with CMM (chaudhari2024ahumandcc pages 1-3, prato2024paroxysmaldystonicposturing pages 1-2) - NTN1 (netrin-1) mutations cause CMM and are associated with abnormal corticospinal tract (CST) anatomy/decussation (meneret2017mutationsinthe pages 1-2) - RAD51 haploinsufficiency causes CMM (referenced in mechanistic genetics context) (accogli2024arecurrentmcf2 pages 13-16)

Recent developments (2023–2024): - ARHGEF7 identified in an autosomal dominant MM pedigree; mechanistic linkage to DCC signaling via a multifunctional ARHGEF7/GIT1 complex (Science Advances, 2023-05; URL in paper metadata) (schlienger2023geneticsofmirror pages 1-2) - A CMM-associated DCC cytoplasmic-tail variant reveals requirement of the WAVE regulatory complex (WRC) via a conserved WIRS motif for netrin-1–DCC axon guidance (Science Signaling, 2024-10; URL in paper metadata) (chaudhari2024ahumandcc pages 1-3) - MCF2 recurrent hemizygous X-linked variant c.31C>T p.(R11W) reported in two unrelated males with CMM/CCA; biochemical evidence shows disrupted MCF2–DCC interaction and decreased GEF activity (preprint, 2024-12; URL in paper metadata) (accogli2024arecurrentmcf2 pages 1-5)

Risk factors

• Genetic: family history consistent with Mendelian inheritance (often autosomal dominant in familial CMM) (legboUnknownyearmirrormovementsac pages 2-4)
• Non-genetic/environmental: No validated environmental risk factors were identified in the retrieved evidence. CMM is typically framed as a neurodevelopmental wiring disorder. (legboUnknownyearmirrormovementsa pages 4-5)

Protective factors / gene–environment interactions

No protective variants or gene–environment interactions were identified in the retrieved evidence. (legboUnknownyearmirrormovementsa pages 4-5)

3. Phenotypes

Core phenotype

The defining phenotype is involuntary, synchronous “mirrored” activation during voluntary movement, most prominently affecting distal upper limbs (hands/fingers), with variable severity. (prato2024paroxysmaldystonicposturing pages 1-2, legboUnknownyearmirrormovementsaa pages 4-5)

Age of onset, severity, progression

• Onset: infancy/early childhood for congenital/familial cases (legboUnknownyearmirrormovementsa pages 4-5, prato2024paroxysmaldystonicposturing pages 1-2)
• Course: typically lifelong and non-progressive (legboUnknownyearmirrormovementsa pages 4-5)
• Severity: variable within and across families; intrafamilial variability described with DCC variants (prato2024paroxysmaldystonicposturing pages 2-4)

Syndromic/associated findings

• Corpus callosum agenesis/dysgenesis (ACC): may co-occur with mirror movements, especially in DCC-related disease spectra (prato2024paroxysmaldystonicposturing pages 1-2)
• Other syndromic associations are discussed in review-level literature (e.g., Klippel–Feil, Kallmann, Joubert, Moebius) (legboUnknownyearmirrormovementsaa pages 4-5)

Quantitative phenotype statistics from recent/primary sources

• Narrative epidemiology estimates (see Epidemiology) indicate extreme rarity and ascertainment variability. (legboUnknownyearmirrormovementsaa pages 2-4)
• In a 2024 family report that also summarizes prior pediatric cases with DCC variants, among 26 reported children: 25/26 (96%) had mirror movements; 9/26 (35%) had partial/complete ACC; 8/26 (31%) had both mirror movements and ACC. (prato2024paroxysmaldystonicposturing pages 4-6)

Quality-of-life and functional impact

Persistent mirror movements can impair bimanual coordination and fine motor tasks (e.g., writing, manipulating objects) and can carry psychosocial burden (teasing/embarrassment). (legboUnknownyearmirrormovementsaa pages 4-5)

Suggested HPO terms (non-exhaustive; based on phenotypes explicitly described)

• Mirror movements (core concept; HPO term exists but identifier not provided in retrieved sources)
• Abnormality of voluntary movement / involuntary movements
• Abnormality of fine motor coordination
• Agenesis of corpus callosum (ACC) (prato2024paroxysmaldystonicposturing pages 1-2)
• Global developmental delay / developmental delay (prato2024paroxysmaldystonicposturing pages 4-6)
• Hyperreflexia; clonus; hypertonia (prato2024paroxysmaldystonicposturing pages 4-6)
• Dystonia / paroxysmal dystonic posturing (prato2024paroxysmaldystonicposturing pages 4-6)

4. Genetic / molecular information

Table: This table summarizes the main genes implicated in familial congenital mirror movements and the mechanistic evidence linking them to defective axon guidance and corticospinal midline crossing. It highlights inheritance, representative variants, associated phenotypes, and key citations from the provided context.

Key molecular concepts (definitions)

• Axon guidance: developmentally regulated process directing axons to targets; disruption can cause commissural/corticospinal miswiring that manifests as abnormal bilateral motor output. (accogli2024arecurrentmcf2 pages 1-5)
• Netrin-1/DCC signaling: Netrin-1 (ligand) binds DCC (receptor) to attract commissural axons to the midline; defects impair midline crossing and contribute to lateralization failures. (chaudhari2024ahumandcc pages 1-3, hu2024ventricularnetrin1deficiency pages 5-6)
• GEFs and Rho-family GTPases: ARHGEF7 and MCF2 encode GEFs affecting Rac1/Cdc42 activity and cytoskeletal dynamics downstream of DCC signaling. (schlienger2023geneticsofmirror pages 1-2, accogli2024arecurrentmcf2 pages 1-5)

Pathogenic variant types and functional consequences (examples from 2023–2024)

• DCC R1343H: missense in cytoplasmic WIRS motif; disrupts DCC–WRC binding → impaired netrin-1–DCC axon guidance (chaudhari2024ahumandcc pages 1-3)
• MCF2 p.R11W: missense; disrupts DCC interaction and reduces GEF activity (accogli2024arecurrentmcf2 pages 1-5)

Diagnostic yield / heterogeneity

Even with known genes, substantial genetic heterogeneity remains; early gene sets explain only a minority of families (reported as ~35% in a primary genetics paper context). (meneret2017mutationsinthe pages 1-2, accogli2024arecurrentmcf2 pages 1-5)

5. Environmental information

No consistent non-genetic environmental contributors were identified in the retrieved evidence; CMM is primarily presented as a genetically driven developmental connectivity disorder. (legboUnknownyearmirrormovementsa pages 4-5)

6. Mechanism / pathophysiology

High-level causal chain (current synthesis)

1. Pathogenic variants in netrin-1/DCC pathway genes (DCC, NTN1) or downstream effectors (ARHGEF7, MCF2) impair attractive signaling and cytoskeletal remodeling required for commissural and corticospinal axons to cross the midline. (chaudhari2024ahumandcc pages 1-3, schlienger2023geneticsofmirror pages 1-2, accogli2024arecurrentmcf2 pages 1-5)
2. This yields abnormal corticospinal tract decussation (pyramidal decussation) and/or ectopic ipsilateral projections and impaired bilateral inhibitory control. (hu2024ventricularnetrin1deficiency pages 5-6, legboUnknownyearmirrormovementsa pages 4-5)
3. The result is bilateral activation of homologous muscles during unilateral voluntary movement, producing mirror movements. (legboUnknownyearmirrormovementsac pages 2-4)

Recent mechanistic advances (2023–2024)

• ARHGEF7/GIT1 effector complex: binds DCC; activates Rac1/Cdc42 and inhibits Arf1; via Arf1 mediates netrin-1–induced increase in cell-surface DCC, connecting receptor signaling to membrane trafficking and actin control. (schlienger2023geneticsofmirror pages 1-2)
• DCC–WAVE regulatory complex linkage: a conserved DCC WIRS motif mediates DCC–WRC interaction; the CMM-associated DCC variant disrupts this, implicating WRC-dependent actin dynamics in netrin-1–DCC guidance. (chaudhari2024ahumandcc pages 1-3)
• MCF2–DCC interaction: MCF2 physically interacts with DCC and influences DCC subcellular localization; R11W disrupts binding and reduces GEF activity, supporting a pathogenic mechanism through weakened DCC signaling. (accogli2024arecurrentmcf2 pages 1-5)

Model-organism evidence and quantitative data

Mouse (Ntn1Gfap conditional knockout; 2024): - CST splits into bundles with a lateral portion failing to decussate and descending ipsilaterally. - Behavioral phenotype includes increased symmetric forelimb movements in an exploratory reaching assay (p < 0.001) and increased homologous LF-RF coupling on gait analysis (p < 0.05). (hu2024ventricularnetrin1deficiency pages 5-6, hu2024ventricularnetrin1deficiency pages 6-7)

Zebrafish dcc mutants (2014): - Mirror-like startle/turning errors arise from a small subset of misprojecting identified reticulospinal neurons; midline-crossing failure produces ipsilateral projections. - Quantitative anatomy/behavior examples: misprojecting axons counted (e.g., 54/138 and 28/66 in two alleles; p = 0.0001 vs wild type); touch-evoked counterbend errors frequent (e.g., 9/12 and 7/7 animals with same-side counterbends). (jain2014mirrormovementlikedefects pages 6-8)

Suggested ontology terms (mechanisms)

• GO Biological Process (examples): axon guidance; commissural neuron axon guidance; actin cytoskeleton organization; regulation of small GTPase mediated signal transduction (schlienger2023geneticsofmirror pages 1-2, chaudhari2024ahumandcc pages 1-3)
• UBERON (examples): corticospinal tract; medulla oblongata; spinal cord; corpus callosum (hu2024ventricularnetrin1deficiency pages 5-6, prato2024paroxysmaldystonicposturing pages 1-2)
• CL (examples): corticospinal neuron; radial glial cell; commissural neuron/commissural interneuron (hu2024ventricularnetrin1deficiency pages 5-6, schlienger2023geneticsofmirror pages 1-2)

7. Anatomical structures affected

Primary structures

• Corticospinal tract (CST) and pyramidal decussation at the ventral medulla (legboUnknownyearmirrormovementsac pages 2-4, hu2024ventricularnetrin1deficiency pages 5-6)

Additional/associated structures

• Corpus callosum (agenesis/dysgenesis in some genetic subtypes, especially DCC-related) (prato2024paroxysmaldystonicposturing pages 1-2, prato2024paroxysmaldystonicposturing pages 4-6)

Lateralization

Mirror movements by definition reflect abnormal bilateral activation during unilateral intended movement; mechanisms include abnormal bilateral corticospinal projections and reduced interhemispheric inhibition. (legboUnknownyearmirrormovementsac pages 2-4, legboUnknownyearmirrormovementsa pages 4-5)

8. Temporal development

• Typical onset: congenital/infancy or early childhood (legboUnknownyearmirrormovementsa pages 4-5)
• Course: generally stable/non-progressive, lifelong persistence in congenital forms; physiological mirroring in young children typically resolves with maturation. (legboUnknownyearmirrormovementsa pages 4-5)

9. Inheritance and population

Inheritance

• Familial cases are often described as autosomal dominant in review-level synthesis, consistent with many DCC/ARHGEF7 families. (legboUnknownyearmirrormovementsac pages 2-4, schlienger2023geneticsofmirror pages 1-2)
• X-linked hemizygous inheritance is implicated for the recurrent MCF2 variant reported in males. (accogli2024arecurrentmcf2 pages 1-5)

Epidemiology (statistics)

Reported prevalence estimates vary, likely due to ascertainment and under-recognition: - < 1 per 1,000,000 individuals (review-level estimate) (legboUnknownyearmirrormovementsaa pages 2-4) - Older estimates cited: ~1 in 8,000 men and ~1 in 40,000 women (legboUnknownyearmirrormovementsaa pages 2-4)

Prognosis

Congenital/familial CMM is typically non-progressive and does not shorten life expectancy; many individuals have preserved neurological function and cognition in isolated forms, though syndromic/genetic subtypes may include callosal anomalies and neurodevelopmental issues. (legboUnknownyearmirrormovementsac pages 2-4, prato2024paroxysmaldystonicposturing pages 4-6)

10. Diagnostics

Clinical criteria / recognition

• Identify involuntary mirrored movements during unilateral voluntary actions, especially of hands/fingers; document age of onset and family history; evaluate functional impairment. (legboUnknownyearmirrormovementsa pages 4-5)

Severity scales

• Woods & Teuber classification (used in a 2024 DCC family case report) (prato2024paroxysmaldystonicposturing pages 2-4)
• Cohen Mirror Movement Scale (discussed in review) (legboUnknownyearmirrormovementsa pages 4-5)

Neurophysiology

• TMS/EMG can show bilateral motor-evoked potentials and reduced transcallosal inhibition; review notes symmetric latency of bilateral MEPs as typical. (legboUnknownyearmirrormovementsac pages 2-4, legboUnknownyearmirrormovementsaa pages 4-5)

Imaging

• Brain MRI to detect corpus callosum agenesis/dysgenesis and other malformations in syndromic cases. (prato2024paroxysmaldystonicposturing pages 1-2)
• DTI tractography to assess CST crossing and quantify laterality; one genetics paper describes quantitative tractography and laterality coefficients and extensive sampling (“1 million draws”). (meneret2017mutationsinthe pages 11-12)

Genetic testing approach

• Targeted sequencing/panels including DCC, NTN1, RAD51, and newer genes ARHGEF7 and candidate MCF2; or WES/WGS with segregation analysis in families. (schlienger2023geneticsofmirror pages 1-2, accogli2024arecurrentmcf2 pages 1-5, prato2024paroxysmaldystonicposturing pages 4-6)
• Variant interpretation using ACMG/AMP principles is referenced in clinical genetics reporting. (prato2024paroxysmaldystonicposturing pages 4-6)

Differential diagnosis

• Physiological mirror movements in young children (resolve with maturation) vs congenital persistent CMM. (legboUnknownyearmirrormovementsa pages 4-5)
• Acquired mirror movements in neurological disease (e.g., post-stroke; movement disorders) are discussed as a separate category in review-level synthesis. (legboUnknownyearmirrormovementsa pages 4-5)

11. Outcome / prognosis

• Survival: typically normal life expectancy in isolated familial CMM (legboUnknownyearmirrormovementsac pages 2-4)
• Morbidity: functional impairment in fine bimanual tasks; psychosocial distress possible (legboUnknownyearmirrormovementsaa pages 4-5)
• Complications: primarily functional; syndromic subtypes may have neurodevelopmental impairments (e.g., developmental delay, cognitive impairment in a DCC family with ACC). (prato2024paroxysmaldystonicposturing pages 4-6)

12. Treatment

Current clinical management (real-world implementations)

There is no disease-modifying therapy established in the retrieved evidence; management is supportive and function-oriented: - Rehabilitation / occupational therapy / physical therapy to improve function and compensate for bimanual limitations (legboUnknownyearmirrormovementsa pages 4-5, legboUnknownyearmirrormovementsa pages 5-6) - Patient education and psychosocial support (legboUnknownyearmirrormovementsa pages 4-5) - Surgical approaches (e.g., corpus callosotomy) have been largely abandoned historically. (legboUnknownyearmirrormovementsa pages 4-5)

MAXO term suggestions (examples)

• Occupational therapy; Physical therapy; Rehabilitation therapy
• Genetic counseling; Cascade genetic testing
• Magnetic resonance imaging; Diffusion tensor imaging
• Transcranial magnetic stimulation; Electromyography (Intervention names are supported as management/diagnostic categories in the review/case literature.) (legboUnknownyearmirrormovementsa pages 4-5, legboUnknownyearmirrormovementsac pages 2-4)

13. Prevention

No primary prevention is established; prevention centers on genetic risk management: - Genetic counseling for affected families and at-risk relatives - Cascade testing once a familial pathogenic variant is identified (legboUnknownyearmirrormovementsa pages 4-5, prato2024paroxysmaldystonicposturing pages 4-6)

14. Other species / natural disease

No naturally occurring non-human disease epidemiology was identified in the retrieved evidence. Mechanistic conservation is supported by vertebrate models (mouse, zebrafish) showing analogous midline-crossing defects producing mirror/symmetric motor output. (hu2024ventricularnetrin1deficiency pages 5-6, jain2014mirrormovementlikedefects pages 6-8)

15. Model organisms

Zebrafish

Zebrafish dcc mutants show mirror movement–like startle/turning phenotypes due to ipsilateral misprojection of specific descending hindbrain neurons; quantitative axon misprojection rates and behavioral misdirection were reported, and targeted ablation rescues directional control. (jain2014mirrormovementlikedefects pages 6-8, jain2014mirrormovementlikedefects pages 8-8)

Mouse

Conditional deletion of ventricular-zone netrin-1 (Ntn1Gfap CKO) causes defective pyramidal decussation and increased symmetric forelimb movements with preserved general locomotion, consistent with a selective lateralization defect. (hu2024ventricularnetrin1deficiency pages 5-6)

Drosophila

A conserved mechanism for attractive midline signaling is supported by the requirement of the Drosophila DCC ortholog (Fra) WIRS motif for in vivo midline attraction, paralleling the 2024 DCC–WRC findings. (chaudhari2024ahumandcc pages 1-3)

Key recent sources prioritized (2023–2024)

• Schlienger et al., Science Advances, 2023-05. “Genetics of mirror movements identifies a multifunctional complex required for Netrin-1 guidance and lateralization of motor control.” https://doi.org/10.1126/sciadv.add5501 (schlienger2023geneticsofmirror pages 1-2)
• Prato et al., Journal of Clinical Medicine, 2024-02. “Paroxysmal dystonic posturing… with DCC mutation, callosal agenesis and mirror movements.” https://doi.org/10.3390/jcm13041109 (prato2024paroxysmaldystonicposturing pages 1-2, prato2024paroxysmaldystonicposturing pages 4-6)
• Hu et al., Cell Death & Disease, 2024-05. “Ventricular Netrin-1 deficiency leads to defective pyramidal decussation and mirror movement in mice.” https://doi.org/10.1038/s41419-024-06719-1 (hu2024ventricularnetrin1deficiency pages 5-6)
• Chaudhari et al., Science Signaling, 2024-10. “A human DCC variant… reveals that the WAVE regulatory complex mediates axon guidance by netrin-1–DCC.” https://doi.org/10.1126/scisignal.adk2345 (chaudhari2024ahumandcc pages 1-3)
• Accogli et al., preprint, 2024-12. “A recurrent MCF2 variant… disrupts DCC binding…” https://doi.org/10.21203/rs.3.rs-5227743/v1 (accogli2024arecurrentmcf2 pages 1-5)

Evidence-supported figure note

Cropped figure panels from Hu et al. (2024) directly visualize CST decussation failure and quantify increased symmetric movements/homologous limb coupling in the Ntn1 conditional knockout model, supporting the mechanistic link between midline crossing defects and mirror-like motor output. (hu2024ventricularnetrin1deficiency media 43ad5fdf, hu2024ventricularnetrin1deficiency media 169a53b2)

Limitations of this report

• Orphanet, MONDO, MeSH, and ICD codes were not present in the retrieved texts, so they cannot be cited here.
• Some mechanistic and genetic claims (e.g., RAD51 primary data) are referenced but not fully extracted from their original primary papers within the current retrieved evidence set.
• Quantitative epidemiology is limited to narrative estimates; robust population-based incidence/prevalence data for genetically confirmed familial CMM remains sparse in the retrieved corpus.

References

1. (meneret2017mutationsinthe pages 1-2): Aurélie Méneret, Elizabeth A. Franz, Oriane Trouillard, Thomas C. Oliver, Yvrick Zagar, Stephen P. Robertson, Quentin Welniarz, R.J. MacKinlay Gardner, Cécile Gallea, Myriam Srour, Christel Depienne, Christine L. Jasoni, Caroline Dubacq, Florence Riant, Jean-Charles Lamy, Marie-Pierre Morel, Raphael Guérois, Jessica Andreani, Coralie Fouquet, Mohamed Doulazmi, Marie Vidailhet, Guy A. Rouleau, Alexis Brice, Alain Chédotal, Isabelle Dusart, Emmanuel Roze, and David Markie. Mutations in the netrin-1 gene cause congenital mirror movements. Journal of Clinical Investigation, 127:3923–3936, Sep 2017. URL: https://doi.org/10.1172/jci95442, doi:10.1172/jci95442. This article has 79 citations and is from a highest quality peer-reviewed journal.

2. (legboUnknownyearmirrormovementsa pages 4-5): J Legbo. Mirror movements: a narrative review of an under-recognized pediatric disorder in sub-saharan africa. Unknown journal, Unknown year.

3. (accogli2024arecurrentmcf2 pages 13-16): Andrea Accogli, Victoria Veas Roy, Patricia Yam, Nassima Addour-Boudrahem, Jean-Francois Michaud, Sabrina Schlienger, Judith St-Onge, Oriane Trouillard, Caroline Dubacq, Emmanuel Roze, Catherine Fallet-Bianco, Joke Verheij, Mirthe Schoots, Evan McNabb, Veronique Fortier, Alex Wong, Jesse Klostranec, Dorothy Barthelemy, Frederic Charron, and Myriam Sr. A recurrent mcf2 variant which disrupts dcc binding leads to congenital mirror movements and corpus callosum agenesis. Dec 2024. URL: https://doi.org/10.21203/rs.3.rs-5227743/v1, doi:10.21203/rs.3.rs-5227743/v1.

4. (prato2024paroxysmaldystonicposturing pages 1-2): Adriana Prato, Lara Cirnigliaro, Federica Maugeri, Antonina Luca, Loretta Giuliano, Giuseppina Vitiello, Edoardo Errichiello, Enza Maria Valente, Ennio Del Giudice, Giovanni Mostile, Renata Rizzo, and Rita Barone. Paroxysmal dystonic posturing mimicking nocturnal leg cramps as a presenting sign in an infant with dcc mutation, callosal agenesis and mirror movements. Journal of Clinical Medicine, 13:1109, Feb 2024. URL: https://doi.org/10.3390/jcm13041109, doi:10.3390/jcm13041109. This article has 2 citations.

5. (chaudhari2024ahumandcc pages 1-3): Karina Chaudhari, Kaiyue Zhang, Patricia T. Yam, Yixin Zang, Daniel A. Kramer, Sarah Gagnon, Sabrina Schlienger, Sara Calabretta, Jean-Francois Michaud, Meagan Collins, Junmei Wang, Myriam Srour, Baoyu Chen, Frédéric Charron, and Greg J. Bashaw. A human dcc variant causing mirror movement disorder reveals that the wave regulatory complex mediates axon guidance by netrin-1–dcc. Science Signaling, Oct 2024. URL: https://doi.org/10.1126/scisignal.adk2345, doi:10.1126/scisignal.adk2345. This article has 4 citations and is from a domain leading peer-reviewed journal.

6. (legboUnknownyearmirrormovementsaa pages 4-5): J Legbo. Mirror movements: a narrative review of an under-recognized pediatric disorder in sub-saharan africa. Unknown journal, Unknown year.

7. (schlienger2023geneticsofmirror pages 1-2): Sabrina Schlienger, Patricia T. Yam, Nursen Balekoglu, Hugo Ducuing, Jean-Francois Michaud, Shirin Makihara, Daniel K. Kramer, Baoyu Chen, Alfonso Fasano, Alfredo Berardelli, Fadi F. Hamdan, Guy A. Rouleau, Myriam Srour, and Frederic Charron. Genetics of mirror movements identifies a multifunctional complex required for netrin-1 guidance and lateralization of motor control. Science Advances, May 2023. URL: https://doi.org/10.1126/sciadv.add5501, doi:10.1126/sciadv.add5501. This article has 21 citations and is from a highest quality peer-reviewed journal.

8. (hu2024ventricularnetrin1deficiency pages 5-6): Ling Hu, Xi-Yue Liu, Li Zhao, Zhi-Bin Hu, Ze-Xuan Li, Wei-Tang Liu, Ning-Ning Song, Yun-Qing Hu, Luo-Peng Jiang, Lei Zhang, Yun-Chao Tao, Qiong Zhang, Jia-Yin Chen, Bing Lang, Yu-Bing Wang, Lei Yue, and Yu-Qiang Ding. Ventricular netrin-1 deficiency leads to defective pyramidal decussation and mirror movement in mice. Cell Death & Disease, May 2024. URL: https://doi.org/10.1038/s41419-024-06719-1, doi:10.1038/s41419-024-06719-1. This article has 5 citations and is from a peer-reviewed journal.

9. (jain2014mirrormovementlikedefects pages 6-8): Roshan A. Jain, Hannah Bell, Amy Lim, Chi-Bin Chien, and Michael Granato. Mirror movement-like defects in startle behavior of zebrafish dcc mutants are caused by aberrant midline guidance of identified descending hindbrain neurons. The Journal of Neuroscience, 34:2898-2909, Feb 2014. URL: https://doi.org/10.1523/jneurosci.2420-13.2014, doi:10.1523/jneurosci.2420-13.2014. This article has 32 citations.

10. (accogli2024arecurrentmcf2 pages 1-5): Andrea Accogli, Victoria Veas Roy, Patricia Yam, Nassima Addour-Boudrahem, Jean-Francois Michaud, Sabrina Schlienger, Judith St-Onge, Oriane Trouillard, Caroline Dubacq, Emmanuel Roze, Catherine Fallet-Bianco, Joke Verheij, Mirthe Schoots, Evan McNabb, Veronique Fortier, Alex Wong, Jesse Klostranec, Dorothy Barthelemy, Frederic Charron, and Myriam Sr. A recurrent mcf2 variant which disrupts dcc binding leads to congenital mirror movements and corpus callosum agenesis. Dec 2024. URL: https://doi.org/10.21203/rs.3.rs-5227743/v1, doi:10.21203/rs.3.rs-5227743/v1.

11. (legboUnknownyearmirrormovementsac pages 2-4): J Legbo. Mirror movements: a narrative review of an under-recognized pediatric disorder in sub-saharan africa. Unknown journal, Unknown year.

12. (prato2024paroxysmaldystonicposturing pages 2-4): Adriana Prato, Lara Cirnigliaro, Federica Maugeri, Antonina Luca, Loretta Giuliano, Giuseppina Vitiello, Edoardo Errichiello, Enza Maria Valente, Ennio Del Giudice, Giovanni Mostile, Renata Rizzo, and Rita Barone. Paroxysmal dystonic posturing mimicking nocturnal leg cramps as a presenting sign in an infant with dcc mutation, callosal agenesis and mirror movements. Journal of Clinical Medicine, 13:1109, Feb 2024. URL: https://doi.org/10.3390/jcm13041109, doi:10.3390/jcm13041109. This article has 2 citations.

13. (legboUnknownyearmirrormovementsaa pages 2-4): J Legbo. Mirror movements: a narrative review of an under-recognized pediatric disorder in sub-saharan africa. Unknown journal, Unknown year.

14. (prato2024paroxysmaldystonicposturing pages 4-6): Adriana Prato, Lara Cirnigliaro, Federica Maugeri, Antonina Luca, Loretta Giuliano, Giuseppina Vitiello, Edoardo Errichiello, Enza Maria Valente, Ennio Del Giudice, Giovanni Mostile, Renata Rizzo, and Rita Barone. Paroxysmal dystonic posturing mimicking nocturnal leg cramps as a presenting sign in an infant with dcc mutation, callosal agenesis and mirror movements. Journal of Clinical Medicine, 13:1109, Feb 2024. URL: https://doi.org/10.3390/jcm13041109, doi:10.3390/jcm13041109. This article has 2 citations.

15. (jain2014mirrormovementlikedefects pages 1-2): Roshan A. Jain, Hannah Bell, Amy Lim, Chi-Bin Chien, and Michael Granato. Mirror movement-like defects in startle behavior of zebrafish dcc mutants are caused by aberrant midline guidance of identified descending hindbrain neurons. The Journal of Neuroscience, 34:2898-2909, Feb 2014. URL: https://doi.org/10.1523/jneurosci.2420-13.2014, doi:10.1523/jneurosci.2420-13.2014. This article has 32 citations.

16. (jain2014mirrormovementlikedefects pages 8-8): Roshan A. Jain, Hannah Bell, Amy Lim, Chi-Bin Chien, and Michael Granato. Mirror movement-like defects in startle behavior of zebrafish dcc mutants are caused by aberrant midline guidance of identified descending hindbrain neurons. The Journal of Neuroscience, 34:2898-2909, Feb 2014. URL: https://doi.org/10.1523/jneurosci.2420-13.2014, doi:10.1523/jneurosci.2420-13.2014. This article has 32 citations.

17. (hu2024ventricularnetrin1deficiency pages 6-7): Ling Hu, Xi-Yue Liu, Li Zhao, Zhi-Bin Hu, Ze-Xuan Li, Wei-Tang Liu, Ning-Ning Song, Yun-Qing Hu, Luo-Peng Jiang, Lei Zhang, Yun-Chao Tao, Qiong Zhang, Jia-Yin Chen, Bing Lang, Yu-Bing Wang, Lei Yue, and Yu-Qiang Ding. Ventricular netrin-1 deficiency leads to defective pyramidal decussation and mirror movement in mice. Cell Death & Disease, May 2024. URL: https://doi.org/10.1038/s41419-024-06719-1, doi:10.1038/s41419-024-06719-1. This article has 5 citations and is from a peer-reviewed journal.

18. (meneret2017mutationsinthe pages 11-12): Aurélie Méneret, Elizabeth A. Franz, Oriane Trouillard, Thomas C. Oliver, Yvrick Zagar, Stephen P. Robertson, Quentin Welniarz, R.J. MacKinlay Gardner, Cécile Gallea, Myriam Srour, Christel Depienne, Christine L. Jasoni, Caroline Dubacq, Florence Riant, Jean-Charles Lamy, Marie-Pierre Morel, Raphael Guérois, Jessica Andreani, Coralie Fouquet, Mohamed Doulazmi, Marie Vidailhet, Guy A. Rouleau, Alexis Brice, Alain Chédotal, Isabelle Dusart, Emmanuel Roze, and David Markie. Mutations in the netrin-1 gene cause congenital mirror movements. Journal of Clinical Investigation, 127:3923–3936, Sep 2017. URL: https://doi.org/10.1172/jci95442, doi:10.1172/jci95442. This article has 79 citations and is from a highest quality peer-reviewed journal.

19. (legboUnknownyearmirrormovementsa pages 5-6): J Legbo. Mirror movements: a narrative review of an under-recognized pediatric disorder in sub-saharan africa. Unknown journal, Unknown year.

20. (hu2024ventricularnetrin1deficiency media 43ad5fdf): Ling Hu, Xi-Yue Liu, Li Zhao, Zhi-Bin Hu, Ze-Xuan Li, Wei-Tang Liu, Ning-Ning Song, Yun-Qing Hu, Luo-Peng Jiang, Lei Zhang, Yun-Chao Tao, Qiong Zhang, Jia-Yin Chen, Bing Lang, Yu-Bing Wang, Lei Yue, and Yu-Qiang Ding. Ventricular netrin-1 deficiency leads to defective pyramidal decussation and mirror movement in mice. Cell Death & Disease, May 2024. URL: https://doi.org/10.1038/s41419-024-06719-1, doi:10.1038/s41419-024-06719-1. This article has 5 citations and is from a peer-reviewed journal.

21. (hu2024ventricularnetrin1deficiency media 169a53b2): Ling Hu, Xi-Yue Liu, Li Zhao, Zhi-Bin Hu, Ze-Xuan Li, Wei-Tang Liu, Ning-Ning Song, Yun-Qing Hu, Luo-Peng Jiang, Lei Zhang, Yun-Chao Tao, Qiong Zhang, Jia-Yin Chen, Bing Lang, Yu-Bing Wang, Lei Yue, and Yu-Qiang Ding. Ventricular netrin-1 deficiency leads to defective pyramidal decussation and mirror movement in mice. Cell Death & Disease, May 2024. URL: https://doi.org/10.1038/s41419-024-06719-1, doi:10.1038/s41419-024-06719-1. This article has 5 citations and is from a peer-reviewed journal.

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