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.

Lateral cord stimulation decreases spastic electromyographic spreading: responses in a brain-damaged pig preparation.

Objective. The aim of our work was to investigate whether lateral stimulation of the spinal cord, lateral cord stimulation (LCS), results in inhibition of the spastic phenomena of upper motor lesions in an animal model. Methods. This study was conducted using an animal model consisting of surgically brain damaged pigs subjected to unilateral cortical and subcortical brain lesions. A double laminectomy at cervical (C3-C4) and lumbar (L3-L6) was performed, and spastic thresholds of abnormal electromyographic responses, disseminated to adjacent segments, facilitated by spinal liberation, and produced by extradural electrical stimulation of the fourth lumbar root, were measured before and after cervical stimulation of the LCS. The variable studied was the minimal amount of current of LCS necessary to abolish electromyographic responses in the L7 myotome, away from the stimulated L4 nerve root. Results. Experiments in 12 animals showed a significant increase of threshold after LCS, with a marked posteffect, signaling a less abnormal threshold. Conclusions. This experiment demonstrated that LCS produces threshold increases to abolish abnormally propagated electromyographic evoked responses induced by the electrical stimulation of the fourth lumbar root in pigs with experimental cortical and subcortical brain lesions.

Neuropatías periféricas en las paraproteinemias / Peripheral neuropathies in paraproteinemias

Las paraproteinemias presentan en el curso de su evolución una manifestación neurológica no demasiado frecuente: las neuropatías periféricas. A pesar de que éstas tienen una incidencia menor que la compresión medular y los síndromes radiculares, pueden ser la manifestación, aun subclínica de una paraproteinemia. La patogenia de estas entidades ha sido motivo de largas discusiones, considerándolas algunos autores como alteraciones debidas a los efectos remotos de una neoplasia, y por otros por la producción de sustancias por parte del tumor. Se describe el cuadro clínico de un grupo de pacientes portadores de una paraproteinemia asociada a una neumopatía periférica, analizándose su fisiopatogenía y cuadro electrofisiológico

Neuropatías periféricas en las paraproteinemias / Peripheral neuropathies in paraproteinemias

Las paraproteinemias presentan en el curso de su evolución una manifestación neurológica no demasiado frecuente: las neuropatías periféricas. A pesar de que éstas tienen una incidencia menor que la compresión medular y los síndromes radiculares, pueden ser la manifestación, aun subclínica de una paraproteinemia. La patogenia de estas entidades ha sido motivo de largas discusiones, considerándolas algunos autores como alteraciones debidas a los efectos remotos de una neoplasia, y por otros por la producción de sustancias por parte del tumor. Se describe el cuadro clínico de un grupo de pacientes portadores de una paraproteinemia asociada a una neumopatía periférica, analizándose su fisiopatogenía y cuadro electrofisiológico (AU)