Progression in lacunar stroke is related to elevated acute phase parameters.
OBJECTIVE
Despite the small size of lacunar infarcts, progression of neurological deficits is a common problem in this stroke subtype. This investigation studied the frequency and the course of neurological deterioration as well as predictors and possible underlying pathomechanisms of early progression in lacunar stroke.


METHODS
Fourty-six consecutive patients with acute lacunar stroke were prospectively evaluated by daily clinical neurological examination including the National Institutes of Health Stroke Scale (NIHSS) and follow-up using the Barthel Index after 3 months. Progressive neurological deficit was defined as worsening by > or =1 point in the NIHSS for motor function. Progressive and stable patients were compared regarding clinical profile, inflammatory parameters (leukocytes, body temperature, C-reactive protein), coagulation parameters (fibrinogen, D-dimer, vWF, PTT), and glutamate plasma concentration, as well as blood glucose and blood pressure.


RESULTS
Eleven patients (23.9%) showed progression of stroke symptoms, 9 of these within the first 24 h after admission. The score on the NIHSS on admission was similar in patients with progressive stroke and stable patients, but significantly higher in the progressive stroke group on days 2 (p = 0.01), 3 (p = 0.001) and at discharge (p = 0.003). Deterioration was significantly associated with a higher leukocyte count (p = 0.012), higher body temperature (p = 0.031) and a higher fibrinogen concentration (p = 0.046) on admission. Barthel Index at discharge (p = 0.001) and after 90 days (p < 0.001) was significantly worse in the progressive stroke group.


CONCLUSIONS
Progression in lacunar stroke usually occurs within 24 h and may be related to an acute-phase response. The long-term prognosis of progressive stroke patients is persistently worse compared with patients with nonprogressive stroke.
Audebert
Heinrich J
HJ
Städtisches Krankenhaus München-Harlaching, München, Deutschland. neuro.audebert@khmh.de
Pellkofer
Tina S
TS
Wimmer
Martin L
ML
Haberl
Roman L
RL
D000368:Aged; D001831:Body Temperature / Q000502:physiology; D020520:Brain Infarction / Q000175:diagnosis* / Q000209:etiology; D016022:Case-Control Studies; D018450:Disease Progression; D005260:Female; D005340:Fibrinogen / Q000378:metabolism; D005500:Follow-Up Studies; D006801:Humans; D007249:Inflammation / Q000150:complications / Q000503:physiopathology; D007962:Leukocytes / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009043:Motor Activity / Q000502:physiology; D009460:Neurologic Examination; D018377:Neurotransmitter Agents / Q000097:blood; D011379:Prognosis; D011446:Prospective Studies; D012307:Risk Factors; D012720:Severity of Illness Index; D020521:Stroke / Q000175:diagnosis* / Q000503:physiopathology; D013997:Time Factors
D018377:Neurotransmitter Agents; D005340:Fibrinogen