Abstract
Interventions to treat cerebral palsy should be initiated as soon as possible in order to restore the nervous system to the correct developmental trajectory. One drawback to this approach is that interventions have to undergo exceptionally rigorous assessment for both safety and efficacy prior to use in infants. Part of this process should involve research using animals but how good are our animal models? Part of the problem is that cerebral palsy is an umbrella term that covers a number of conditions. There are also many causal pathways to cerebral palsy, such as periventricular white matter injury in premature babies, perinatal infarcts of the middle cerebral artery, or generalized anoxia at the time of birth, indeed multiple causes, including intra-uterine infection or a genetic predisposition to infarction, may need to interact to produce a clinically significant injury. In this review, we consider which animal models best reproduce certain aspects of the condition, and the extent to which the multifactorial nature of cerebral palsy has been modeled. The degree to which the corticospinal system of various animal models human corticospinal system function and development is also explored. Where attempts have already been made to test early intervention in animal models, the outcomes are evaluated in light of the suitability of the model.
Highlights
It is widely accepted that research with animal models is crucial to developing and testing new therapies
MODELS OF PERIVENTRICULAR WHITE MATTER INJURY Based on the various risk factors discussed in Section “Cerebral Palsy in Humans,” various animal models have been developed in different species but mostly rodents, including models of hypoperfusion and models using infectious agents, bacterial products, or excitotoxic insults
When considering the outcome of testing experimental therapies for cerebral palsy in animal models it is important to ask a number of questions
Summary
It is widely accepted that research with animal models is crucial to developing and testing new therapies. It is important not to fall into the traps identified in pre-clinical adult stroke research, which may explain the massive failure rate in clinical trials of novel neuroprotective agents identified in animal experiments [1]. These include omission of fundamental aspects of experimental design such as blinding, randomization, exclusion reporting, and sample size, and “cherry picking” the data to publish to maximize impact [2]. We ask what exactly are we trying to model? How similar are our animal models to the human condition? What have our animal models told us so far, and what outcomes should we be measuring in order to gage the likely success of our proposed therapies?
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