Dynamics of polymorphonuclear leukocyte accumulation in acute cerebral infarction and their correlation with brain tissue damage.
OBJECTIVE
This study was performed to study the dynamics of polymorphonuclear leukocyte (PMNL) accumulation in human cerebral infarction and its association with neurological outcome and brain lesion.


METHODS
A total of 88 patients diagnosed as having hemispheric ischemic stroke were examined. PMNL accumulation was studied using technetium-99m hexamethylpropyleneamine oxime (99mTc HMPAO)-labeled leukocyte brain single-photon emission computed tomography (SPECT). Volume of brain infarction was evaluated by CT scan. The Mathew Scale was used for neurological assessment. Dynamics of PMNL accumulation was studied 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 increased 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 patients were subdivided into three groups: patients with severe PMNL accumulation that dramatically increased within 12 hours after stroke onset and persisted even at 28 to 30 days (group A); those with moderate PMNL accumulation that significantly decreased at 30 days (group B); and those with mild PMNL accumulation that decreased at 6 to 9 days (group C). Baseline neurological deficit and brain tissue damage at admission appear to be at a similar level for all groups of patients. In dynamics, however, in patients with severe PMNL accumulation, neurological outcome was worse and infarction volume larger than in patients with less marked PMNL accumulation.


CONCLUSIONS
The present clinical study confirms that PMNLs intensively accumulate in the regions of cerebral infarction. The present study revealed that this accumulation correlated with the severity of the brain tissue damage and poor neurological outcome.
Akopov
S E
SE
Department of Neurology, Armenian National Institute of Health, Republican Emergency Hospital, Yerevan, Armenia.
Simonian
N A
NA
Grigorian
G S
GS
D000368:Aged; D001921:Brain / Q000000981:diagnostic imaging*; D002544:Cerebral Infarction / Q000000981:diagnostic imaging* / Q000503:physiopathology; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009420:Nervous System / Q000503:physiopathology; D009504:Neutrophils / Q000000981:diagnostic imaging*; D015609:Organotechnetium Compounds; D010091:Oximes; D019690:Technetium Tc 99m Exametazime; D015899:Tomography, Emission-Computed, Single-Photon; D014057:Tomography, X-Ray Computed
D015609:Organotechnetium Compounds; D010091:Oximes; D019690:Technetium Tc 99m Exametazime