The quest for patterns in dyskinetic cerebral palsy

In most individuals with cerebral palsy (CP), spasticity is the dominant neurological finding. Consequently, followup programmes and interventions are mostly designed for people with spastic CP. However, there are those who do not fit the template. Dyskinetic CP is less researched and the particular consequences and needs of individuals with dyskinetic CP are less known. Assessment tools have been scarce. Monbaliu et al. have made a commendable effort to highlight the functional profiles of individuals with dyskinetic CP in a more detailed way, using the Dyskinesia Impairment Scale (DIS), together with well-known classifications of motor function and communication. The DIS may be helpful in discriminating the different features of dyskinetic CP in a structured way, increasing our knowledge, which in turn may have implications for future research and hopefully resulting in more appropriate interventions for people with dyskinetic CP. However, the nature of the movement pattern needs to be linked to the consequences for function, activities, and participation. The majority of individuals with dyskinetic CP have dystonia which involves getting into involuntary postures that are probably painful at times, thus impeding activities and reducing quality of life. Communication, both with speech and augmentative and alternative communication, is often hampered by the involuntary movements and dystonia. The neck, mouth, and eye regions are particularly important, as Monbaliu et al. point out. However, any emotion, positive or negative, and the importance of prerequisites such as an adequate sitting position, may affect the whole body in an individual with dyskinetic CP. Consequently, the ability to communicate will be affected by many variables. Thus, essentially all body regions assessed by the DIS are important! Future studies may also shed more light on the underlying lesions. Previous studies have shown that the basal ganglia and thalamus lesions are often accompanied by cortical and subcortical lesions in more severe cases of dyskinetic CP. Surprisingly, in the study by Monbaliu et al. the white matter lesions are more frequent. A common and structured classification of neuroimaging findings, as the one used in this study, is needed to evaluate such differences further. The ‘pure’ basal ganglia/thalamus lesions, associated with choreoathetosis in this study, seem to correspond well with the ‘mild’ form of basal ganglia/ thalamus lesions described in the reference and training manual of the Surveillance of Cerebral Palsy in Europe. Given the large age range of the participants (5–22 years), differences in the causes of the lesions may be expected. As perinatal care develops, preventive strategies against immunization and interventions for hyperbilirubinemia and perinatal asphyxia are changing part of the causal panorama behind dyskinetic CP. The natural course of dyskinetic CP is not the focus of this particular study. We receive no information about previous signs of dystonia or choreoathetosis in the participants. However, from a clinical point of view, this subject is highly interesting. Does the clinical picture change from more to less hyperkinetic? When and where do typical contractures appear? Which interventions are effective for this particular group (and its subgroups) and which interventions should be avoided? We know that survival is decreased in the group with dyskinetic CP. Does this mainly concern those with dystonia, which Monbaliu et al. have shown to be the more disabling form of dyskinetic CP? Many questions remain, but structured studies such as the one by Monbaliu et al. are needed to map out the partly unknown territory of dyskinetic CP.