**5. Conclusions**

The aetiology of CP is attributed to the interaction of multiple risk factors which through complex causal pathways within a limited duration disrupt brain development or augment the risk of damage to the motor system in the foetal/infant brain. It has remained a challenge to identify with certainty the timing of these non-progressive disturbances. Nevertheless, the increasing role of genetic susceptibility in CP causation is evolving.

A link between neuropathology and the clinical-neurological features of CP (neuromuscular deficits, accompanying impairments, severity/functional level, clinical types) exists. However, limitations currently remain in devising a comprehensive neuropathologic classification of CP due to inconsistent structure-function correlations and difficulties in estimating timing of insults. Overall, a gap currently exists in our understanding of the aetiology and pathogenesis of CP despite the pivotal roles of advanced neuroimaging and evolving genomics.
