[1] Unlike spastic or ataxic cerebral palsies, ADCP is characterized by both hypertonia and hypotonia, due to the affected individual's inability to control muscle tone.

[2] Clinical diagnosis of ADCP typically occurs within 18 months of birth and is primarily based upon motor function and neuroimaging techniques.

[2] Classification based on motor characteristics classifies CP as occurring from damage to either the corticospinal pathway or extrapyramidal regions.

[1] Involuntary movements often increase during periods of emotional stress or excitement and disappear when the patient is sleeping or distracted.

[1] Patients experience difficulty in maintaining posture and balance when sitting, standing, and walking due to these involuntary movements and fluctuations in muscle tone.

[6] CP in general is a non-progressive, neurological condition that results from brain injury and malformation occurring before cerebral development is complete.

[1] Bilirubin encephalopathy leading to cerebral palsy has been greatly reduced by effective monitoring and treatment for hyperbilirubinemia in preterm infants.

[1][2] ADCP is typically characterized by an individual's inability to control their muscle tone, which is readily assessed via these classification systems.

[4] MRI also has the ability to detect brain malformation, periventricular leukomalacia (PVL), and areas affected by hypoxia-ischemia, all of which may play a role in the development of ADCP.

[2] The MRI detection rate for ADCP is approximately 54.5%, however this statistic varies depending on the patient's age and the cause of the disease and has been reported to be significantly higher.

[10] Treatment of muscle tone issues via deep brain stimulation typically targets the global pallidus and has shown to significantly improve symptoms associated with ADCP.

[10] DBS of the globus pallidus interna improves dystonia in people with dyskinetic CP in 40% of cases, perhaps due to variation in basal ganglia injuries.