Background and Purpose: 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 ≧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.

Lodder J, Gorsselink EL: Progressive stroke caused by CT-verified small deep infarcts; relation with the size of the infarct and clinical outcome. Acta Neurol Scand 1985;71:328–330.
Nakamura K, Saku Y, Ibayashi S, Fujishima M: Progressive motor deficits in lacunar infarction. Neurology 1999;52:29–33.
Fisher CM: Lacunar strokes and infarcts: A review. Neurology 1982;32:871–876.
Asplund K: Any progress on progressing stroke? Cerebrovasc Dis 1992;2:317–319.
Dávalos A, Castillo J: Potential mechanisms of worsening. Cerebrovasc Dis 1997;7(suppl 5):19–24.
Gautier JC: Stroke-in-progression. Stroke 1985;16:729–733.
Yamamoto H, Bogousslavsky J, van Melle G: Different predictors of neurological worsening in different causes of stroke. Arch Neurol 1998;55:481–486.
Toni D, Fiorelli M, Gentile M, Bastianello S, Sacchetti ML, Argentino C, Pozzilli C, Fieschi C: Progressing neurological deficit secondary to acute ischemic stroke. Arch Neurol 1995;52:670–675.
Gan R, Sacco RL, Kargman DE, Roberts JK, Boden-Albala B, Gu Q: Testing the validity of the lacunar hypothesis: The Northern Manhattan Stroke Study experience. Neurology 1997;48:1204–1211.
Castillo J, Dávalos A, Noya M: Progression of ischaemic stroke and excitotoxic amino acids. Lancet 1997;349:79–83.
Akopov SE, Simonian NA, Grigorian GS: Dynamics of polymorphonuclear leukocyte accumulation in acute cerebral infarction and their correlation with brain tissue damage. Stroke 1996;27:1739–1743.
Vila N, Castillo J, Dávalos A, Chamorro A: Proinflammatory cytokines and early neurological worsening in ischemic stroke. Stroke 2000;31:2325–2329.
Dávalos A, Castillo J, Pumar JM, Noya M: Body temperature and fibrinogen are related to early neurological deterioration in acute ischemic stroke. Cerebrovasc Dis 1997;7:64–69.
Castillo J, Dávalos A, Noya M: Aggravation of acute ischemic stroke by hyperthermia is related to an excitotoxic mechanism. Cerebrovasc Dis 1999;9:22–27.
Reith J, Jørgensen HS, Pedersen PM, Nakayama H, Raaschou HO, Jeppesen LL, Olsen TS: Body temperature in acute stroke: Relation to stroke severity, infarct size, mortality, and outcome. Lancet 1996;347:422–425.
Audebert HJ, Rott MM, Haberl RL: Post-stroke inflammation depends on stroke volume (abstract). Stroke 2002;1:413.
Audebert HJ, Rott MM, Haberl RL: Successful thrombolysis leads to a significant reduction of post-stroke inflammation (abstract). Stroke 2003;1:311–312.
Boysen G, Christensen H: Stroke severity determines body temperature in acute stroke. Stroke 2001;32:413–417.
Qizilbash N, Duffy S, Prentice CRM, Boothby M, Warlow C: Von Willebrand factor and risk of ischemic stroke. Neurology 1997;49:1552–1556.
Giroud M, Dutrillaux F, Lemesle M, Volot F, Lorenzini JL, Becker F, Dumas R: Coagulation abnormalities in lacunar and cortical ischemic stroke are quite different. Neurol Res 1998;20:15–18.
Uchiyama S, Yamazaki M, Hara Y, Iwata M: Alterations of platelet, coagulation, and fibrinolysis markers in patients with acute ischemic stroke. Semin Thromb Hemost 1997;23:535–541.
Steinke W, Ley SC: Lacunar stroke is the major cause of progressive motor deficits. Stroke 2002;33:1510–1516.
Fisher M, Minematsu K: Lacunar stroke: Diagnosis, evaluation, and management. Heart Dis Stroke 1992;1:353–356.
Mahoney FI, Barthel DW: Functional evaluation: The Barthel index. Md Med J 1965;14:61–65.
Britton M, Rödén A: Progression of stroke after arrival at hospital. Stroke 1985;16:629–632.
Rödén-Jüllig A: Progressing stroke: Epidemiology. Cerebrovasc Dis 1997;7(suppl 5):2–5.
Dávalos A, Cendra E, Teruel J, Martinez M, Genís D: Deteriorating ischemic stroke: Risk factors and prognosis. Neurology 1990;40:1865–1869.
Toni D: Predictors of stroke deterioration. Cerebrovasc Dis 1997;7(suppl 5):10–13.
Fisher M, Garcia JH: Evolving stroke and the ischemic penumbra. Neurology 1996;47:884–888.
Ginsberg MD, Belayev L, Zhao W: Recruitment of the ischemic penumbra into the necrotic core. Cerebrovasc Dis 1997;7(suppl 5):14–18.
Castellanos M, Castillo J, Garcia MM, Leira R, Serena J, Chamorro A, Dávalos A: Inflammation-mediated damage in progressing lacunar infarctions: A potential therapeutic target. Stroke 2002;33:982–987.
Grotta J, Ostrow P, Fraifeld E, Hartman D, Gary H: Fibrinogen, blood viscosity, and cerebral ischemia. Stroke 1985;16:192–198.
Castillo J, Dávalos A, Naveiro J, Noya M: Neuroexcitatory amino acids and their relation to infarct size and neurological deficit in ischemic stroke. Stroke 1996;27:1060–1065.
Serena J, Leira R, Castillo J, Pumar JM, Castellanos M, Dávalos A: Neurological deterioration in acute lacunar infarctions. The role of excitatory and inhibitory neurotransmitters. Stroke 2001;32:1154–1161.
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