NONOCCLUSIVE COMMON CAROTID-ARTERY THROMBOSIS IN THE RAT RESULTS IN REVERSIBLE SENSORIMOTOR AND COGNITIVE-BEHAVIORAL DEFICITS

Background and Purpose Microemboli released during transient ischemic attack, stroke, and cardiac surgery are thought to cause a variety of functional deficits in humans. The purpose of this study was to charac terize the type and extent of neurobehavioral deficits present after p hotochemically induced common carotid artery thrombosis (CCAT), a thro mboembolic model of stroke in the rat that results In shower. Methods Thirty-two male Wistar rats were assigned to four groups 1 (n=8) and 3 (n=8) were long-term (6-week survival) and short-term (2-week surviva l) experimental groups subjected to right CCAT with the use of the pho tochemical technique. Groups 2 (n=8) and 4 (n=8) served as sham-operat ed controls for each experimental group. A battery of behavioral tests was applied daily beginning 24 hours after thrombosis; this consisted of elicited forelimb placing, postural reflex, beam balance, beam wal king, and open Field activity. Cognitive testing with a water maze tas k was performed on post-CCAT days 30 to 33 fur groups 1 and 2 and on p ost-CCAT day 2 for groups 3 and 4. Ten-micrometer coronal brain sectio ns were stained with hematoxylin and eosin, and infarct location and f requency were determined. Results Significant sensorimotor deficits we re observed; which recovered within 2 weeks after CCAT. The data that follow are derived by combining the two experimental groups and compar ing these with the two sham groups. The following tests showed signifi cant effects after CCAT: contralateral elicited forelimb placing, ipsi lateral elicited forelimb placing, beam balance, and beam walking scor e. Cognitive dysfunction was seen acutely (group 3 animals) at 2 days after CCAT; Morris water maze length and latency to target were signif icantly greater in the experimental group. No deficits were seen in po stural reflex, open field activity, or delayed cognitive testing. Hist opathological assessment revealed small infarcts in 11 of 16 thrombose d rats. However, a strong relationship between neurobehavioral deficit s and infarct location was not consistently demonstrated. Conclusions CCAT produces consistent sensorimotor and cognitive behavioral deficit s that recover within 2 weeks of injury. Behavioral outcome was not ne cessarily associated with overt histopathological damage, suggesting t hat reversible injury mechanisms, both vascular and neuronal, may be p artly responsible for the temporary loss of function. These data stren gthen the role of CCAT as a clinically relevant model of thromboemboli c stroke.