ABSTRACT: BACKGROUND: The widespread use of tissue plasminogen activator (tPA), the only FDA-approved acute stroke treatment, remains limited by its narrow therapeutic time window and related risks of brain hemorrhage. Normobaric oxygen therapy (NBO) may be a useful physiological strategy that slows down the process of cerebral infarction, thus potentially allowing for delayed or more effective thrombolysis. In this study we investigated the effects of NBO started simultaneously with intravenous tPA, in spontaneously hypertensive rats subjected to embolic middle cerebral artery (MCA) stroke. After homologous clot injection, animals were randomized into different treatment groups: saline injected at 1 hour; tPA at 1 hour; saline at 1 hour plus NBO; tPA at 1 hour plus NBO. NBO was maintained for 3 hours. Infarct volume, brain swelling and hemorrhagic transformation were quantified at 24 hours. Outcome assessments were blinded to therapy. RESULTS: Upon clot injection, cerebral perfusion in the MCA territory dropped below 20% of pre-ischemic baselines. Both tPA-treated groups showed effective thrombolysis (perfusion restored to nearly 100%) and smaller infarct volumes (379+/-57 mm3 saline controls; 309+/-58 mm3 NBO; 201+/-78 mm3 tPA; 138+/-30 mm3 tPA plus NBO), showing that tPA-induced reperfusion salvages ischemic tissue and that NBO does not significantly alter this neuroprotective effect. NBO had no significant effect on hemorrhagic conversion, brain swelling, or mortality. CONCLUSION: NBO can be safely co-administered with tPA. The efficacy of tPA thrombolysis is not affected and there is no induction of brain hemorrhage or edema. These experimental results require clinical confirmation.

BACKGROUND AND PURPOSE: Early neurological deterioration (END) is a relatively common unfavorable course after anterior circulation ischemic stroke that can lead to worse clinical outcome. None of the END predictors identified so far is sufficiently reliable to be used in clinical practice and the mechanisms underlying END are not fully understood. We review the evidence from the literature for a role of hemodynamic and perfusion abnormalities, more specifically infarction of the oligemia, in END. Summary of Review-After an overview of the neuroimaging, including perfusion imaging, predictors of END, we review the putative mechanisms of END with a special focus on hemodynamic factors. The evidence relating perfusion abnormalities to END is addressed and potential hemodynamic mechanisms are suggested. CONCLUSIONS: Hemodynamic factors and perfusion abnormalities are likely to play a critical role in END. Infarction of the oligemic tissue surrounding the penumbra could be the putative culprit leading to END as a result of perfusion, but also physiological and biochemical abnormalities. Further studies addressing the role of the oligemia in END and developing measures to protect its progression to infarction are now needed.

Early blood-brain barrier (BBB) disruption resulting from excessive neurovascular proteolysis by matrix metalloproteinases (MMPs) is closely associated with hemorrhagic transformation events in ischemic stroke. We have shown that normobaric hyperoxia (NBO) treatment reduces MMP-9 increase in the ischemic brain. The aim of this study was to determine whether NBO could attenuate MMP-9-mediated early BBB disruption following ischemic stroke. Rats were exposed to NBO (95% O(2)) or normoxia (30% O(2)) during 90-min middle cerebral artery occlusion, followed by 3-hour reperfusion. NBO-treated rats showed a significant reduction in Evan's blue extravasation in the ischemic hemisphere compared with normoxic rats. Topographically, Evan's blue leakage was mainly seen in the subcortical regions including the striatum, which was accompanied by increased gelatinolytic activity and reduced immunostaining for tight-junction protein, occludin. Increased gelatinolytic activities and occludin protein loss were also observed in isolated ischemic microvessels. Gel gelatin zymography identified that MMP-9 was the main enzymatic source in the cerebral microvessels. Incubation of brain slices or isolated microvessels with purified MMP-9 revealed specific degradation of occludin. Inhibition of MMP-9 by NBO or MMP-inhibitor, BB1101, significantly reduced occludin protein loss in ischemic microvessels. These results suggest that NBO attenuates early BBB disruption, and inhibition of MMP-9-mediated occludin degradation is an important mechanism for this protection.

Oxygen is frequently administered to patients with suspected stroke. However, the role of oxygen therapy in ischemic stroke remains controversial in light of the failure of three clinical trials of hyperbaric oxygen therapy to show efficacy, and the fear of exacerbating oxygen free radical injury. The previous trials had several shortcomings, perhaps because they were designed on basis of anecdotal case reports and little preclinical data. Most animal studies concerning oxygen therapy in stroke have been conducted over the last 6 years. Emerging data suggests that hyperbaric and even normobaric oxygen therapy can be effective if used appropriately, and raises the tantalizing possibility that hyperoxia can be used to extend the narrow therapeutic time window for stroke thrombolysis. This article reviews the history, rationale, mechanisms of action and adverse effects of hyperoxia, the key results of previous hyperoxia studies, and the potential role of oxygen therapy in contemporary stroke treatment.

Preventing death and limiting handicap from ischaemic stroke are major goals that can be achieved only if the pathophysiology of infarct expansion is properly understood. Primate studies showed that following occlusion of the middle cerebral artery (MCA)--the most frequent and prototypical stroke, local tissue fate depends on the severity of hypoperfusion and duration of occlusion, with a fraction of the MCA territory being initially in a 'penumbral' state. Physiological quantitative PET imaging has translated this knowledge in man and revealed the presence of considerable pathophysiological heterogeneity from patient to patient, largely unpredictable from elapsed time since onset or clinical deficit. While these observations underpinned key trials of thrombolysis, they also indicate that only patients who are likely to benefit should be exposed to its risks. Accordingly, imaging-based diagnosis is rapidly becoming an essential component of stroke assessment, replacing the clock by individually customized management. Diffusion- and perfusion-weighted MR (DWI-PWI) and CT-based perfusion imaging are increasingly being used to implement this, and are undergoing formal validation against PET. Beyond thrombolysis per se, knowledge of the individual pathophysiology also guides management of variables like blood pressure, blood glucose and oxygen saturation, which can otherwise precipitate the penumbra into the core, and the oligaemic tissue into the penumbra. We propose that future therapeutic trials use physiological imaging to select the patient category that best matches the drug's presumed mode of action, rather than lumping together patients with entirely different pathophysiological patterns in so-called 'large trials', which have all failed so far.British Journal of Pharmacology advance online publication, 26 November 2007; doi:10.1038/sj.bjp.0707530.

Normobaric hyperoxia is under investigation as a treatment for acute ischaemic stroke. In experimental models, normobaric hyperoxia reduces cerebral ischaemic injury and improves functional outcome. The mechanisms of neuroprotection are still debated because,(i) inhalation of 100% O(2) does not significantly increase total blood O(2) content;(ii) it is not known whether normobaric hyperoxia increases O(2) delivery to the severely ischaemic cortex because of its short diffusion distance; and (iii) hyperoxia may reduce collateral cerebral blood flow (CBF) to ischaemic penumbra because it can cause vasoconstriction. We addressed these issues using real-time two-dimensional multispectral reflectance imaging and laser speckle flowmetry to simultaneously and non-invasively determine the impact of normobaric hyperoxia on CBF and oxygenation in ischaemic cortex. Ischaemia was induced by distal middle cerebral artery occlusion (dMCAO) in normoxic (30% inhaled O(2), arterial pO(2) 134 +/- 9 mmHg), or hyperoxic mice (100% inhaled O(2) starting 15 min after dMCAO, arterial pO(2) 312 +/- 10 mmHg). Post-ischaemic normobaric hyperoxia caused an immediate and progressive increase in oxyhaemoglobin (oxyHb) concentration, nearly doubling it in ischaemic core within 60 min. In addition, hyperoxia improved CBF so that the area of cortex with </=20% residual CBF was decreased by 45% 60 min after dMCAO. Furthermore, hyperoxia reduced the frequency of peri-infarct depolarizations (PIDs) by more than 60%, and diminished their deleterious effects on CBF and metabolic load. Consistent with these findings, infarct size was reduced by 45% in the hyperoxia group 2 days after 75 min transient dMCAO. Our data show that normobaric hyperoxia increases tissue O(2) delivery, and that novel mechanisms such as CBF augmentation, and suppression of PIDs may afford neuroprotection during hyperoxia.

PURPOSE OF REVIEW: Hyperoxic inspired gas is essential for patients with hypoxic respiratory failure; it is also suspected, however, as a contributor to the pathogenesis of acute lung injury. Several recent studies in humans, animals, and cell culture have identified mechanisms by which hyperoxia may exert deleterious effects on critically ill patients. This review identifies relevant new findings regarding hyperoxic lung injury in the context of providing guidance for future clinical studies. RECENT FINDINGS: Recent studies have clarified the roles of both receptor-mediated and mitochondrial cell death pathways in experimental hyperoxic lung injury. Studies in animals demonstrate that hyperoxia interacts with mechanical stretch to augment ventilator-induced lung injury. Finally, studies in humans implicate hyperoxia in impairment of host defense responses to infections. SUMMARY: Although hyperoxia has not been conclusively identified as a clinically important cause of lung injury in humans, animal data strongly implicate it. Reports of interaction effects between hyperoxia and both mechanical ventilation and host defense suggest that clinical studies of hyperoxia must take these variables into account. Accumulating data about how hyperoxia initiates cell death provide guidance for development of both biomarkers to identify hyperoxia-induced injury and pharmacological interventions to limit hyperoxia's adverse effects.

BACKGROUND: Standard 12-lead electrocardiography is a routine and mandatory cardiovascular examination in the evaluation of stroke patients. This study investigates the relationship of electrocardiography findings and first-ever ischemic stroke. METHODS: This hospital-based case-control study consisted of 238 consecutively hospitalized cases of first-ever ischemic stroke and 238 healthy age- and sex-matched control subjects. Multivariate logistic regression analyses were performed to evaluate the risk factors and electrocardiography findings. RESULTS: Atrial fibrillation [odds ratio (OR)= 6.8, 95% confidence interval (CI)=1.90-24.45], myocardial ischemic change (OR = 5.0, 95% CI = 2.22-11.06), left ventricular hypertrophy (OR = 3.9, 95% CI = 2.02-7.39) and sinus bradycardia (OR = 0.37, 95% CI = 0.18-0.79) were significantly related with first-ever ischemic stroke. CONCLUSIONS: Electrocardiography findings of atrial fibrillation, myocardial ischemic change and left ventricular hypertrophy as risk factors for ischemic stroke were similar to those from other studies. Additional studies are needed to assess the role of sinus bradycardia for ischemic stroke, which was less common in patients with stroke than in controls.

BACKGROUND: Teaching inexperienced nurses to assess neurologic function of acute ischemic stroke patients poses challenges to educators in Taiwan. OBJECTIVES: The purpose of this study was to examine the effectiveness of two programs that teach nurses the use of the Chinese version of the National Institute of Health Stroke Scale (C-NIHSS), and to evaluate the level of learner satisfaction with these teaching programs. DESIGN: An experimental research design with two groups, one pre-test and two post-tests was utilized. SETTING: Six neurology and neurosurgery wards at two hospitals in southern Taiwan. PARTICIPANTS: Participating nurses were stratified based on their clinical level of experience and prior training on the National Institute of Health Stroke Scale (NIHSS). They were randomly assigned to either the experimental C-NIHSS interactive computer assisted instruction (ICAI) group (n=44) or the Instructor-led videotape learning program (IVLP) group (n=40) to learn the C-NIHSS. METHODS: The measurement tools included the score verification unit (SVU)(score range from 0 to 45, content validity index, CVI=0.96, percentage agreement=84%) and the learner satisfaction scale (CVI=0.92, Cronbach's alpha=0.97). RESULTS: Both groups' scores on the assessment of correctness significantly increased (F=35.50, p=0.00) after intervention. However, there was an insignificant difference between the changes in the two groups (F=0.02, p=0.89). After using one-way ANCOVA analysis, and adjusting for the length of experience in neurological nursing, the results showed that in the second post-test, the ICAI group's score was significantly higher than that of the IVLP group (F=4.81, p=0.03). There was a positive correlation between assessment correctness on the second post-test and length of experience in neurological nursing (r=0.35, p<0.05). It was concluded that nurses with less experience in neurological nursing, who receive ICAI will perform a better assessment of stroke patients than those who received IVLP. CONCLUSION: The C-NIHSS ICAI teaching program contributed to better assessment correctness after adjusting for the length of experience in neurological nursing, and to some extent increased satisfaction for the participating nurses. Therefore it is worth promoting the use of ICAI for in-service education of nurses, especially for nurses with less experience in neurological nursing, in order to enhance long-term effects of learning.

OBJECTIVE: To evaluate the adequacy of management of modifiable risk factors (MRF) in a group of ischemic stroke outpatients and the value of pharmacist intervention in a randomized controlled study in a tertiary referral hospital. METHODS: 160 ischemic stroke outpatients from the same catchment area and with the same financial arrangements for healthcare, went through a 6-month equal allocation stratified randomized study. Routine practice was not altered except for a monthly 1-hour pharmacist-intervention education programme. We evaluated the differences in blood pressure (BP), blood glucose and lipid profiles before and after study. The proportion of patients with adequate management of MRF was studied. RESULTS: There were no differences in the demographic characteristics, MRF and medications prescribed throughout the study. Before the study, the proportions of adequate control of BP in the control and intervention groups were 43% vs. 40%(P = 0.64), lipid 27% vs. 13%(P = 0.09) and glucose 36% vs. 21%(P = 0.15). At the end of the study, the corresponding proportions were for BP 43% vs. 83%(P = 0.00), lipid 27% vs. 40%(P = 0.16) and glucose 46% vs. 35%(P = 0.40). CONCLUSION: Pharmacist intervention was associated with improved BP control but not with the other MRF. Earlier initiation and longer duration of intervention may improve the outcome further, and whether targeting of high-risk subjects may be particularly rewarding is worthy of investigation.

OBJECTIVES: In-hospital initiation and maintaining of lipid-lowering therapy (LLT) after discharge is recommended for dyslipidemic stroke patients. However, little is known about actual adherence to treatment in Taiwan. This study aims to describe the current practice of lipid testing and LLT and to identify predictors for patient to receive LLT. METHODS: Between February 2001 and December 2002, a total of 1105 consecutive ischemic stroke patients were prospectively registered. Dyslipidemic ischemic stroke patients were recruited and followed over a 6 months period. RESULTS: In-hospital lipid testing was performed in 91% of all patients and LLT was initiated in 74%(350/476) of dyslipidemic patients. During the 6 months follow-up period, lipid testing was performed in 77%(266/345) and LLT was maintained in 45%(154/345) of patients. However, the target LDL cholesterol level (<100mg/dL) was achieved in only 30%(78/255) of patients. Older patients had a lower chance to receive LLT. CONCLUSIONS: The in-hospital initiation of LLT and lipid testing was considered adequate as compared to other studies. However, after discharge from the hospital, many patients, especially older patients remained untreated. Efforts to close treatment gaps in lipid management require sustained quality improvement efforts. More awareness in this area is needed.

A 26-year-old young man, had Graves' disease in hyperthyroid state, presented with frequent episodic transient left hemiparesis and mild slurred speech lasting for few minutes to 2 hours for one month. Infarction at posterior limb of right internal capsule was found on brain MRI. Angiography revealed multiple intracranial arteries stenoses around the circle of Willis. After treatment with propylthiouracil and aspirin, his thyroid function returned to normal and the patient remained free from stroke.

BACKGROUND: The clinical course of patients with acute ischemic stroke tends to be unstable. Understanding the factors contributing to the progression of stroke is important for the appropriate management of patients. This study investigated the factors related to 3-month mortality at admission in patients with first-ever acute ischemic stroke. METHODS: Patients with first-ever acute ischemic stroke consecutively admitted to a medical center in Taiwan within 48 hours after stroke onset were prospectively followed-up for 3 months. All deaths during this 3-month post-stroke period were analyzed. We evaluated only those characteristics that could be assessed at admission. Multivariate logistic regression analysis was used to identify the main predictors of 3-month stroke-related mortality. RESULTS: In the 360 enrolled patients, the inhospital mortality rate was 7.8%(28 deaths), and the 3-month mortality rate was 9.7%(35 deaths). Twenty-seven deaths (77%) were stroke-related. Risk factors for mortality at 3 months included sex (odds ratio [OR], 3.18; 95% confidence interval [CI], 1.08-9.41; p=0.036), National Institutes of Health Stroke Scale (NIHSS) at admission (per unit increase: OR, 1.17; 95% CI, 1.12-1.22; p<0.001), history of cardiac disease (OR, 2.73; 95% CI, 1.04-7.16; p=0.042), and posterior circulation stroke (OR, 5.25; 95% CI, 1.92-14.36; p=0.001). CONCLUSION: This study of hospital-based data on patients with first-ever acute ischemic stroke in Taiwan found that initial NIHSS, posterior circulation stroke and history of cardiac disease were risk factors for 3-month mortality.

PURPOSE: Emergency medical services (EMS) play an important role in acute stroke therapy. The goal of this study was to investigate the roles and determinants of EMS in stroke in Southern Taiwan, Kaohsiung. METHODS: We enrolled stroke patients who arrived at emergent department (ED) of the study hospital within 48 hours after the onset of symptoms. Patients were categorized into arriving by EMS or not EMS. Potential determinants of EMS use for stroke were examined by multivariable analyses and the role of EMS in stroke was discussed. RESULTS: Among 197 stroke patients enrolled, only 44 (22%) patients arrived by EMS at ED. Multivariable logistic regression analysis revealed that the determinants of EMS use were stroke severity measured by NIHSS and non-family member who decided to seek help. Using EMS or not was not associated with the earlier presentation after stroke within 2 hours after attack. CONCLUSION: EMS use was far from sufficient. The transportation time was not the major component of prehospital delay. Both EMS and other vehicles provided prompt delivery. The public should rush to ED either by EMS or other transportation modes when stroke occurred unless use of EMS is proved to provide better outcome in stroke patient in the future study.

A transition of T to C at nucleotide position 16189 in mitochondrial DNA (mtDNA) has attracted biomedical researchers for its probable correlation with the development of diabetes mellitus in adult life. In diabetes, persistent hyperglycemia may cause high production of free radicals. Reactive oxygen species are thought to play a role in a variety of physiologic and pathophysiologic processes in which increased oxidative stress may play an important role in disease mechanisms. The aim of the present study was to clarify the degree of oxidative damage and plasma antioxidant status in diabetic patients and to see the potential influence of the 16189 variant of mtDNA on the oxidative status in these patients. An indicative parameter of lipid peroxidation, malondialdehyde (MDA), and total free thiols were measured from plasma samples of 165 type 2 diabetic patients with or without this variant and 168 normal subjects. Here we report an increase in the plasma levels of MDA and total thiols in type 2 diabetic patients compared with control subjects. The levels of plasma thiols in diabetic patients with the 16189 variant of mtDNA were not different from those in controls. These results suggest an increase in the oxidative damage and a compensatory higher antioxidative status in patients with type 2 diabetes. Harboring the 16189 mtDNA variant may impair the ability of a cell to respond properly to oxidative stress and oxidative damage.

BACKGROUND: Numerous population-based epidemiological studies have shown the prevalence and strength of vascular risk factors for stroke but little is known about risk factors of stroke in Taiwan. The aim of this study was to identify vascular risk factors in a group of first-ever ischemic stroke patients in Taiwan. METHODS: The study consisted of 228 consecutively hospitalized cases of first-ever ischemic stroke and 228 healthy age- and sex-matched control subjects. Conditional logistic regression analyses were performed to evaluate the risk factors. RESULTS: Significant risk factors included hypertension (odds ratio [OR] 2.7, 95% confidence interval [CI]= 1.53-4.80), atrial fibrillation (OR 14.8, 95% CI = 2.32-94.73), ischemic heart disease (OR 4.4, 95% CI = 1.48-13.38), cigarette smoking (OR 2.3, 95% CI = 1.10-4.96), left ventricular hypertrophy (OR 2.7, 95% CI = 1.18-6.16), and other abnormal electrocardiographic findings (OR 2.1, 95% CI = 1.11-3.80). CONCLUSIONS: Several vascular risk factors of first-ever ischemic stroke were identified. A population-based study involving more vascular risk factors is needed for generalization.

PURPOSE: Ethnic differences in the distribution of atherosclerosis in the brain-supplying vessels are well described. However, only scarce data exist on the prevalence of extracranial carotid artery stenosis in Taiwanese patients who have had a single ischemic stroke. METHODS: Color-coded duplex sonography was used to evaluate the carotid arteries in a hospital-based study on 276 consecutive first-time Taiwanese stroke patients. Significant atherosclerotic lesions of the internal carotid arteries (ICA) were defined as a stenosis of more than 50% or an occlusion. RESULTS: The prevalence of significant carotid lesions was 6%(35/552) in the entire cohort and 8%(17/224) in patients with hemispheric strokes. Among patients with large-artery atheroscleroses, according to criteria of the Trial of Org 10172 in Acute Stroke Treatment, only 27% had significant extracranial ICA disease whereas 69% had intracranial vessel stenoses. Older patients tended to have more severe ICA lesions, while other risk factors were not correlated with carotid stenosis. CONCLUSION: The prevalence of more than 50% ICA stenosis was low in Taiwanese patients with first hemispheric ischemic strokes, indicating that it is not a major cause of ischemic stroke in this population.

OBJECTIVE: Free radicals are important in causing neural cell injury during cerebral infarction. Although there was a randomized, placebo-controlled, double-blind study at multiple centers in Japan showing the efficacy of the free radical scavenger, edaravone, in acute cerebral infarction, to date the clinical studies are few. This study investigated the effect of edaravone on the outcome of patients with acute lacunar infarction. METHODS: We retrospectively evaluated 124 consecutive patients with first-ever acute lacunar infarctions who were admitted to our hospital within 24 hours after the onset between January 2004 and June 2007. Of these, 59 patients received both edaravone and conventional therapy (edaravone group), and the other 65 underwent conventional therapy only (non-edaravone group). There was no significant difference in patients' baseline characteristics in the two groups. The clinical outcome was assessed by the National Institutes of Health Stroke Scale (NIHSS). RESULTS: The reduction of NIHSS scale during hospitalization (1.5+/-1.0 vs. 1.0+/-1.1; p = 0.007), especially that of the motor palsy scale (1.0+/-1.0 vs. 0.5+/-1.0; p = 0.006) was significantly larger, and the percentage of patients with a favorable outcome (NIHSS at discharge < or =1)(91.5% vs. 78.5%; p = 0.044) was significantly better in the edaravone group. CONCLUSION: Edaravone improves the outcomes of patients with acute lacunar infarction, especially motor palsy, without regard to the conventional therapy performed concomitantly.

The space-occupying so-called "malignant" middle cerebral artery infarction is-besides acute basilar artery occlusion-the most devastating form of ischemic stroke. Until recently, there was no proven treatment. In 2007, results from randomized controlled trials provided evidence for the benefit of early hemicraniectomy with respect to mortality after 3 months. This review focuses on current treatment options for malignant ischemic brain infarction, especially hemicraniectomy. Moreover, major unsolved problems and open questions regarding the disease are discussed, and perspective is given on future clinical studies.

Presence of central nervous system by extrapulmonary tuberculosis is an infrequent disease specially among non HIV infected patients, and it is associated with poor prognosis and high mortality rates. We report a case with a middle cerebral artery ischemic strocke as a first symptom of miliar tuberculosis.

OBJECTIVES: Cerebral microbleeds (MBs) are known to be indicative of bleeding-prone microangiopathy and may predict incident intracerebral hemorrhage. However, there is controversy concerning the causal relationship between the presence of MBs and hemorrhagic transformation (HTf) after ischemic stroke. METHODS: Of the 1,034 patients with acute ischemic stroke who were consecutively admitted to our hospital, 377 patients with stroke due to large artery atherothrombosis or cardioembolism were selected for participation in this study. We examined the MBs using T2*-weighted gradient-echo MRI performed within 24 hours after admission, and the incidence of HTf was assessed using follow-up brain MRI during the hospitalization period. RESULT: Of the 377 patients with stroke, 234 were male (62.1%) and the mean age was 66.2+/-11.7 years. MBs were initially found in 109 patients (28.9%), and newly incident HTf was noted during the hospitalization period in 74 patients (19.6%). The presence of MBs was not increased in the patients with HTf (24.3% vs. 30.0% in the patients without HTf: p=0.331). In addition, the number of MBs was not higher in the patients with HTf (0.7+/-1.5 vs. 1.8+/-8.1: p=0.234). This lack of significance between MBs and HTf persisted after stratification by stroke mechanism. CONCLUSIONS: This study suggests that underlying MBs do not predict incident HTf after acute ischemic stroke. The clinical significance of MBs should be differentially evaluated according to the type of disease (intracerebral hemorrhage vs. HTf).

A study was conducted for 121 patients (55 female, 66 male; age 68.7 +/- 10.4 years) with first-ever ischemic stroke to investigate the frequency and risk factors of early neurological deterioration (ND). The initial evaluation was carried out within 24 hours of stroke onset. National Institutes of Health Stroke Scale score and Barthel index were used to evaluate patients for a period of 2 months. Thirty-eight patients (31.4%) showed early ND and 83 patients (68.6%) were stable or improved. Among the 38 patients with ND, 25 (65.8%) patients occurred within 48 hours after initial evaluation. In most patients, ND began on the first day and ceased on the third day after stroke onset. Neurological function started to improve after ND reaching the nadir. The mortality rate was 13.2%(5/38) for patients with ND and 1.2%(1/83) for patients without deterioration. At the end of the study, the functional ability and motility of patients were lower in the progressive group than in the non-progressive/stable group. Results of this study seem to indicate that an elevated C-reactive protein level and total anterior circulation infarction are risk factors for ND. The results also suggest that more aggressive and early treatments are needed for stroke patients to prevent disease progression.