The specific molecular mechanism that underpins this<unk><unk>  is not well known. However, most researchers suggest that it follows an autosomal dominant genetic inheritance pattern in which mutations in certain genes give rise to structural abnormalities in nervous system networks responsible for voluntary skeletal muscle<unk> , which, in turn, result in the functional<unk>  abnormalities seen in patients. Despite being autosomal dominant, it is important to note that the disease has variable expressivity. That is, patients who have inherited a mutated dominant allele, along with their genetically affected parent, can be symptomatic or asymptomatic for CMM<unk> . The genes that currently have evidence to be associated with CMM<unk>  include DCC (deleted in colorectal carcinoma), DNAL4 (dynein axonemal light chain 4), and RAD51 (recombination protein A). DCC encodes a receptor for NTN1 (netrin-1), a protein thought to be responsible for axon guidance and neuronal cell migration during development. A mutation of this gene (including nonsense, splice site mutation, insertions, frameshift) has been identified as a possible cause for CMM<unk> . Experiments in mice also support the claim that CMM<unk>  is associated with genetic mutations in DCC. Kanga mice, lacking the P3 intracellular domain of the DCC receptor, show a hopping gait, moving their hind legs in a strictly paired fashion, as do kangaroos. DNAL4 encodes a component of dynein motor complex in commissural neurons of the corpus callosum. In contrast to DCC, DNAL4 is thought to have a recessive inheritance pattern for the CMM<unk> . In CMM<unk>  patients, researchers found splice site mutations on DNAL4, which caused skipping of exon 3, and thereby omission of 28 amino acids from DNAL4 protein. This mutant DNAL4 protein, in turn, could lead to faulty cross-hemisphere wiring, resulting in CMM. RAD51 maintains genome integrity by repairing DNA double-strand breaks through homologous recombination. RAD51 heterozygous mutations, specifically premature termination codons, have been found in many CMM<unk>  patients through genome-wide linkage analysis and exome sequencing. In a mouse model, researchers also found RAD51 products in corticospinal tract axons at the pyramidal decussation. They therefore suggest that RAD51 might be a gene that, when haploinsufficient, causes CMM<unk>  in humans. Despite identification of three prospective genes, no genotype–phenotype correlations have yet been found. That is, the severity of clinical signs and symptoms does not correlate with the type of genetic variant. Mutations in the above genes account for a total of about 35 percent of cases. Mutations in other genes that have not been identified likely account for the other cases of this<unk> .
Congenital mirror movement disorder
Athetoid cerebral palsy
Ataxic cerebral palsy
Cerebral achromatopsia
Dorian Gray syndrome
Non-progressive congenital ataxia
Paramyotonia congenita
Acrocallosal syndrome