New animal model to mimic spastic cerebral palsy: the brain-damaged pig preparation.

Objective.  Classically, a decerebrated animal by mesencephalic lesioning is considered the paradigm for experimental study of spasticity that accompanies cerebral palsy, but, the model does not actually correspond with anatomical and pathologic realities. Therefore, a new and novel animal model is needed. Our objective was to create a more adapted animal model to be used in neuromodulation and functional electrical stimulation research. Materials and Methods.  Our new model in pigs closely simulates cortical and subcortical lesions produced by perinatal anoxic brain damage, which is present in spastic cerebral palsy and other spastic conditions. Our surgical lesions were produced by means of resecting the rolandic and perirolandic areas (cortical lesion) and aspiration and coagulation of white matter and deep gray nuclei. This model results in anatomic and pathologic configurations that are similar to human spastic cerebral palsy. We physiologically tested our model both in the pre- and postoperative situations. After experimental stimulation in nonoperated animals to establish mean latencies for preoperative bilateral cervical motor-evoked potentials and to confirm the absence of abnormally propagated electromyographic activity, another group of animals were retested using the same experimental variables before and after creation of the surgical lesioning in cortical and subcortical pyramidal areas. Results.  Normal latencies and no propagated electromyographic responses were found in sham animals. There were significant differences found in both latencies for motor-evoked potentials and electromyographic propagated responses when compared to pre- and postoperative values, which signaled abnormal physiology. Conclusions.  This animal model presents anatomic similarities to lesions currently present in cerebral palsy and related diseases. The model also shows electrophysiologic differences that signal chronic brain damage. Therefore, this method is useful in research when spastic syndromes produced by upper motor lesions need to be modeled.