Experimental Model of Brainstem Infarction

Abstract

A new, canine model of brainstem infarction has been developed. The authors describe the production of this model as well as the neurological symptoms, changes invital signs, and extent of infarction observed. Twenty-four mongrel dogs were anesthetized with sodium pentobarbital. After removal of the right zygomatic arch, a small temporal craniectomy was performed. The perforating arteries arising from the bilateral posterior cerebral arteries as far as their junctions with the posterior communicating arteries were occluded by means of a subtemporal approach to the region of the interpeduncular cistern. The animals were divided into three groups. In the acute group (n=6), the brain was perfused with microcarbon or microbarium immediately after occlusion of the perforators. In the chronic group (n=14), the animals were examined daily for neurological alterations and changes in vital signs for 7 to 10 days after the procedure. The remaining 4 animals were controls and underwent a sham procedure. Sagittal and/or serial coronal sections of the fixed brains of all animals were prepared for examination of the extent of defective perfusion or infarction. All of the sham-operated animals survived without any neurological deficit and showed no evidence of pathological lesions. In the acute group, the area not perfused with microcarbon or microbarium was the rostral brainstem, which corresponded to the extent of infarction observed in the chronic animals. Thirteen of the 14 chronic animals survived for more than 1 week, while exhibiting such clinical symptoms as disturbance of consciousness, tetraparesis, oculomotor paralysis, respiratory abnormalities, bradycardia, and arrhythmia. Gross pathological study of the brain sections revealed well defined infarctions, which were consistently located in the posterior thalamus, subthalamus, midbrain, and upper pons in all 14 chronic animals. The lesions were butterflyshaped in the paramedian portion of the thalamus and wedge-shaped at the midbrain and upper pons levels. The clinical features and extent of infarction observed in this model closely resemble those of rostral brainstem infarction in human stroke. Therefore, this model may be useful in the study of the pathophysiology of brainstem ischemia.