DYNAMICS OF POLYMORPHONUCLEAR LEUKOCYTE ACCUMULATION IN ACUTE CEREBRAL INFARCTION AND THEIR CORRELATION WITH BRAIN-TISSUE DAMAGE

Background and Purpose This study was performed to study the dynamics of polymorphonuclear leukocyte (PMNL) accumulation in human cerebral i nfarction and its association with neurological outcome and brain lesi on. Methods A total of 88 patients diagnosed as having hemispheric isc hemic stroke were examined. PMNL accumulation was studied using techne tium-99m hexamethylpropyleneamine oxime ((TC)-T-99m HMPAO)-labeled leu kocyte brain single-photon emission computed tomography (SPECT). Volum e of brain infarction was evaluated by CT scan. The Mathew Scale was u sed for neurological assessment. Dynamics of PMNL accumulation was stu died at 3 to 6, 6 to 12, and 12 to 24 hours and 6 to 9, 28 to 30, and 90 days after stroke onset. In parallel, at admission, at 6 to 9 days, and at 28 to 30 days neurological outcome and infarction volume were evaluated. Results Generally, PMNL accumulation progressively increase d during 6 to 24 hours after stroke, remained at a high level up to 6 to 9 days and then declined. With the use of cluster analysis, all pat ients were subdivided into three groups: patients with severe PMNL acc umulation that dramatically increased within 12 hours after stroke ons et and persisted even at 28 to 30 days (group A); those with moderate PMNL accumulation that significantly decreased at 30 days (group B); a nd those with mild PMNL accumulation that decreased at 6 to 9 days (gr oup C). Baseline neurological deficit and brain tissue damage at admis sion appear to be at a similar level for all groups of patients. In dy namics, however, in patients with severe PMNL accumulation, neurologic al outcome was worse and infarction volume larger than in patients wit h less marked PMNL accumulation. Conclusions The present clinical stud y confirms that PMNLs intensively accumulate in the regions of cerebra l infarction. The present study revealed that this accumulation correl ated with the severity of the brain tissue damage and poor neurologica l outcome.