There are three main pathophysiological hypotheses for<unk>  that exist. Interhemispheric connections First, some researchers believe that this neurological<unk>  is due to abnormal communication between cerebral hemispheres. They explain the mechanism of the physiological miscommunication with on development. Amongst many neuronal changes in the brain during normal human brain development, researchers claim that the corpus callosum shows a gradual increase number of myelinated axons. This suggests that up until a certain age, the corpus callosum is heavily unmyelinated. This would explain why children during normal development can be seen with CMM<unk>  up to the age of 7 years, likely due to lack of corpus callosum development. The normal disappearance of clinically significant<unk><unk> s after this age is associated with anatomical and functional maturation of interhemispheric connections through the corpus callosum between motor cortices. Researchers hypothesize that this axonal density in the corpus callosum is responsible for the interhemispheric communication that is ultimately responsible for the suppression of<unk><unk> s during voluntary<unk> s in healthy adults. Therefore, disruptions in corpus callosum circuits could lead to CMM. Motor cortex Another pathophysiological explanation that researchers suggest for CMM<unk>  is that there is a miscommunication during motor<unk>  execution. This claim is supported by evidence of structural abnormalities in the primary motor cortex (M1) in CMM patients. These structural abnormalities in the motor cortex might explain why the hands, requiring great motor dexterity and therefore have a large cortical representation, are often the target of and suffer from more severe<unk><unk>  in CMM<unk> . Corticospinal tract A third pathophysiological explanation proposed by researchers has to do with the corticospinal tract (CST). Healthy newborns in fact have ipsilateral CST projections up until the age of around 7. During normal adult development, these axonal projects disappear. This might provide an alternate explanation for the presence of mild<unk><unk> s in normally developing young children that typically disappear before the age of 7. Some researchers propose that DCC mutations cause a reduction in gene expression and less robust midline guidance, which may lead to a partial failure of axonal fiber crossing and encourage development of an abnormal ipsilateral connection. This is confirmed by other researchers who demonstrate that patients with DDC mutants show an increased proportion of ipsilateral axonal projections, and show that even a very small number of aberrant ipsilateral descending axons is sufficient to induce incorrect<unk>  patterns. These findings are corroborated by evidence from mice models, Kanga mice with a deletion of DCC, whose CST has been shown not to be altered, but rather partially rerouted ipsilaterally.
Congenital mirror movement disorder
Athetoid cerebral palsy
Ataxic cerebral palsy
Cerebral achromatopsia
Dorian Gray syndrome
Non-progressive congenital ataxia
Paramyotonia congenita
Acrocallosal syndrome