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July2007 Vol.44 Issue:      2 Table of Contents
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Progressive Ischemic Cerebrovascular Stroke: Frequency and Predictive Factors

Ahmed Osama, Ahmed Abou Hagar, Raafat Al-Sayed, Mohamed Nigm, Ismail Youssef
Department of Neuropsychiatry, Suez Canal University

ABSTRACT

 

       Objectives: To determine the frequency of progression in patients with ischemic stroke and to identify clinical, laboratory and radiological factors that could lead its to  early prediction. Subjects and Methods: Two hundred patients with ischemic stroke presented within 24 hours from onset of symptoms were included in the study. They were 121 males and 79 females with mean age (60.5±11.2) years. The following predictors were assessed: clinical predictors: age, sex, TIA, cardiac disease, diabetes mellitus, hypertension, cigarette smoking, time to admission, Glasgow coma scale, systolic and diastolic blood pressure and body temperature. Laboratory predictors: random and fasting blood sugar, prothrombin time, partial thromboplastin time, liver enzymes, serum creatinine,  erythrocyte sedimentation rate, serum cholesterol, high and low density lipoprotein, C-reactive protein and serum ferritin. Radiological predictors: early focal hypodensity and initial mass effect in admission CT brain scan and site and size of infarction, mass effect and hemorrhagic infarction in follow up CT scan (7days). Neurological deficits were assessed by Scandinavian Stroke Scale on admission, 24 hours and 7 days after admission to diagnose progressive stroke. Early progressive stroke was considered when progression occurred within 24 hours after admission. Late progressive stroke  was considered when progression occurred between 24 hours and 7 days. Results: The frequency of progressive stroke was 20% (13% early progression and 7% late progression). History of hypertension, high systolic and diastolic blood pressure, low Glasgow coma scale, short time to admission, elevated serum glucose,  cholesterol, C-reactive protein and ferritin, early focal hypodensity in the initial CT and cortico-subcortical and medium size infarction in follow up CT were significantly frequent in patients with progressive stroke. Admission hyperglycemia and high ferritin level were significantly frequent in early progressive stroke patients, while high serum C-reactive protein and cholesterol levels and were significantly frequent in late progressive stroke patients.

(Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 535-544)

 





INTRODUCTION

    

What can be more frustrating for the physicians and for their patients than deterioration during treatment? Expectations are high that patients will get better when they come to the hospital. Unfortunately, progression is common in patients with ischemic stroke despite present treatment.1

Progressive ischemic stroke is a stroke in which the neurological deficit is still increasing in severity or distribution after the patients admittance to observation, i.e. there is worsening of their clinical findings even after medical care.2 Various terms e.g. progressive stroke, stroke-in-evolution, evolving stroke or deteriorating stroke have been proposed for this clinical setting.3

The progression of ischemic stroke can be early (within 24 hours after admission) termed early progressive stroke (EPS) or late (between 24 hours and 7 days) termed late progressive stroke (LPS).4 Progressive stroke severely affects the prognosis of the patients, doubling mortality, discharge rate and length of hospital stay. Furthermore, survivors have more neurological deficits and functional disabilities. Thus, if progression could be prevented or treated the influence on prognosis would be considerable.4

Progressive stroke is poorly understood, it is difficult to be predicted and many factors could play a role in its progression.5 For this purpose, several studies were done to detect its exact incidence with wide variations ranging from 20% to 43%,6-9 and to detect whether cerebral or systemic factors are major determinants of its progression. Some of these factors included: history of diabetes,4,10,11  high body temperature,12 high blood pressure,2,11 low blood pressure,4 high  serum glucose6, C-reactive protein (CRP)13 and plasma ferritin14 and early focal hypodensity with cortical or cortico-subcortical distribution on initial cranial computed tomography (CT).10

To clarify these apparent discrepancies, we decided to determine the frequency of progression in a sample of patients with ischemic stroke and to identify some clinical, laboratory and radiological factors that could predict it earlier.

 

SUBJECTS AND METHODS

 

Two hundred patients with ischemic stroke presented within 24 hours from onset of symptoms and admitted to the Neuropsychiatry department of Suez Canal University Hospital were included in the study. They were 121 (60.5%) males and 79 (39.5%) females with mean age (60.54±11.25) years. Patients with coma, previous stroke, cerebral hemorrhage and previous disability precluding assessment of changes in neurological deficits (e.g. old polio) were excluded.  

Neurological deficits were assessed by the Scandinavian Stroke Scale (SSS)15 on admission,  24 hours and 7 days after admission. Progressive stroke was diagnosed when  repeated evaluation of the patient by Scandinavian Stroke Scale (SSS) revealed dropping of speech score 3 points or more or dropping of arm, hand or leg scores 2 points or more.4 Early progressive stroke (EPS) was considered when progression occurred within 24 hours after admission. Late progressive stroke (LPS) was considered when progression occurred between 24 hours and 7 days. Patients who died within the first 24 hours were classified in the EPS group.    

 

The following predictors were assessed for all the patients:

1-      Clinical predictors: age, sex, history of transient ischemic attack (TIA), diabetes mellitus, hypertension and cardiac disease, time to admission (from onset of symptoms to initiation of treatment), Glasgow coma scale, systolic (SBP) and diastolic blood pressure (DBP) on admission and body temperature.

2-      Laboratory predictors: random and fasting blood sugar, prothrombin time, partial thromboblastin time, aspartate amino-transferase, alanin amino-transferase, serum creatinine, erythrocyte sedimentation rate, serum cholesterol, high and low density lipoprotein, C-reactive protein and serum ferritin.

3-      Radiological predictors: early focal hypodensity and initial mass effect in brain CT brain scan done on admission and site and size of  infarction, mass effect, and hemorrhagic infarction in follow up CT scan done on the 7th days.

 

The site of infarction was classified as follows:16

(1)     Subcortical: Involvement of deep branch of middle cerebral artery (MCA) or internal border zone areas.

(2)     Cortical: Involvement of the territory of superficial branch of MCA.

(3)     Corticosubcortical: With concomitant involvement of deep and superficial branches of  MCA.

(4)     Other territories: Involvement of other supratentorial non-MCA areas.

 

The size of infarction was quantified as follows:17

(1)     Small: <1/2 of a lobe or consistently normal CT scans.

(2)     Medium: 1/2 of a lobe to 1 lobe.

(3)     Large: >one lobe.

The mass effect was  quantified as follows:17

(1)     Slight: Sulcal effacement or compression of ventricles without dislocation.

(2)     Moderate: Between slight and severe.

(3)     Severe: Partial or total ventricular shift across the midline.

 

During hospitalization, patients received the medical conservative treatment that is required for the treatment of the concomitant disease. Anti-hypertensive drugs for hypertension, short acting insulin for diabetes mellitus. Intravenous or subcutaneous heparin has been given for neurological worsening in patients with supposed thrombus propagation or with cardioembolism. Oral aspirin (150 mg) has been given systematically to all patients.

Data entry and verification was done by using the SPSS software version 6.1. Students t-test was used as a significance test to compare the means of the various continuous variables. The Chi-squared test and fisher exact test were used to find out the significant difference between qualitative data. P value was set at <0.05 for significant results and <0.01 for highly significant results.

 

RESULTS

 

The frequency of progressive stroke is 20% (13% early and 7% late) (Table 1). Sex and age distribution shows no statistical significant difference between progressive and non-progressive patients or between EPS and LPS patients (Table 2).

Past history of hypertension, short time to admission, low GCS and high systolic and diastolic blood pressure at admission are significantly high (P<0.01) and more frequent in progressive than in non-progressive patients. Short time to admission and high systolic and diastolic blood pressure are significantly more frequent in EPS than in LPS patients (P<0.05) (Tables 3 and 4).

Random blood sugar, fasting blood sugar and serum cholesterol are significantly (P<0.05) higher in progressive than in non-progressive patients. C-reactive protein and serum ferritine are significantly higher (P<0.01) in progressive than in non-progressive patients. Random and fasting blood sugar and Serum ferritine are significantly higher in early progressive than in late progressive patients (P<0.05). While, serum cholesterol and C-reactive protein are significantly higher in late progressive than in early progressive patients (P<0.05) (Table 5).

Early focal hypodensity in initial CT scan and cortico-subcotical and medium size infarctions are significantly more frequent in progressive than in non-progressive patients (P<0.05). While small size infarction is significantly predominating in non-progressive patients (P<0.05) (Tables 6 and 7).


 

Table 1. Frequency of progressive ischemic stroke (early and late).

 

 

N=200

(%)

Progressive

Early Progressive     

Late  Progressive        

40

26

14

(20%)

(13%)

(7%)

Non-Progressive

160

(80%)

                  

Table 2. Sex and age distribution in non-progressive and progressive patients.

 

 

Sex

Age

Male N(%)

Female N(%)

Mean + SD(Years)

Non- Progressive (n=160)

100 (62.5%)

60 (37.5%)

60.75+10.86

Progressive (n=40)

Early Progressive (n=26)

Late  Progressive (n=14)

21 (52.5%)

13 (50%)

8 (57.1%)

19 (47.5%)

13 (50%)

6 (42.9%)

60.32+11.65

60.29+13.65

60.35+10.7

Table 3. Frequency of risk factors in non progressive and progressive patients.

 

 

Non- Progressive n=160

Progressive

n=40

EPS

n=26

LPS

n=14

TIA

32 (20%)

9 (22.5%)

6 (23.1%)

3 (21.4%)

Diabetes Mellitus      

58 (36.3%)

13 (32.5%)

11(42.3%)

2 (14.3%)

Hypertension

34 (21.3%)

29 (72.5%) *

19 (73%)

10 (71.4%)

Smoking

86 (53.7%)

18 (45%)

10 (38.5%)

8 (57.1%)

Cardiac disorders     

38 (23.7%)

5 (12.5%)

3 (11.5%)

2 (14.3%)

Atrial fibrilation       

24 (15%)

4 (10%)

4(15.4%)

0 ( 0 %)

(EPS): Early progressive stroke, (LPS): Late progressive stroke.

X2 test, (*) P< 0.01 compared to non-progressive group.

 

Table 4. Clinical parameters (Mean±SD) of non-progressive and progressive patients.

 

 

Non- Progressive

Progressive

EPS

LPS

Time to admission  (hours)

23.3±8.1

18.7±6.3*

17.3±5.4a

19.4±6.6

Glasgow Coma Scale         

14.3±0.7

13.9±0.7*

13.7±0.7

13.9±0.7

Systolic Blood Pressure

154.8±22.5

168.9±15.1*

174.5±14.8a

164.1±15.3

Diastolic Blood Pressure

91.7±10.5

100.8±11.1*

105.5±11a

97.2±12.1

Temperature

37.4±0.22

37.4±0.2

37.5±0.2

37.4±0.2

(EPS): Early progressive stroke, (LPS): Late progressive stroke

Unpaired t test, (*) P<0.01  compared to non-progressive group. (a) P<0.05  compared to late progressive group.

 

Table 5. Biochemical parameters (Mean±SD) of non-progressive and progressive patients.

 

 

Non- Progressive

Progressive

EPS

LPS

RBS

188.1±27.3      

208.9±22.3*      

218±24.9a        

197.1±19.6

FBS

167.2±23.1          

188.8±18.9*         

196.6±16.2a        

183.7±20.9

PT

13.4±1.1             

13.7±1.1              

13.9±1.1             

13.6±1.2

PTT

29.6±2.2             

29.4±2.5             

30.29±3.8        

 28.9±1.5

AST

26.8±12.5           

27.5±8.3                  

28±9.4            

27.4±7.7

ALT

26.2±15.4           

28.1±10.8           

28.36±9.96       

27.85±10.73          

Serum Cholesterol

184.2±25.2            

209±24.1*          

201.9±26.2       

220.2±22b

HDL

44.4±13.9            

44.8±12.1           

44.29±13.4         

45.2±11.5

LDL

124.2±39.9        

129.3±46               

132.6±42.1      

127.5±48.7

Serum Creatinine

1.1±0.4              

1.2±0.5               

1.19±0.43        

1.16±0.56

ESR-1

24.5±10.8           

27.7±12.7           

30.36±14.8     

26.35±11.5

ESR-2

52.9±13.2          

58.4±18.8             

60.8±21.5       

56.2±17.6

CRP

3.4±1.4              

8.9±1.8**                      

8.1±1.5       

10.49±1.7b

Serum Ferritine

152.9±38.7         

190.6±33.8**         

203.7±37.9a   

168.8±28.2

(EPS): Early progressive stroke, (LPS): Late progressive stroke, (RBS) Random blood sugar,  (FBS) Fasting blood sugar,  (PT) Prothrombin time,  (PTT) Partial thromboblastin time,  (AST) Aspartate aminotransferase, (ALT)  Alanin aminotransferase,  (HDL) High density lipoproteins,  (LDL) Low density lipoprotein, (ESR) Erythrocyte sedimentation rate,  (CRP) C-reactive protein.

Unpaired t-test, (*) P< 0.05 compared to non-progressive group (**) P< 0.01 compared to non-progressive group, (a) P< 0.05  compared to late progressive group. (b) P< 0.05  compared to early progressive group

Table 6. Computed Tomography at hospital admission in non-progressive and progressive patients.

 

 

Non- Progressive

n=160

Progressive

n=40

EPS

n=26

LPS

n=14

Early focal hypo-density    

26 (16.3%)           

14 (35%)*       

9 (34.6%)       

5 (35.7%)

Initial mass effect         

10 (6.3%)             

7 (17.5%)        

5 (19.2%)       

2 (14.3%)

(EPS): Early progressive stroke, (LPS): Late progressive stroke

X2 test (*) P< 0.05 compared to non-progressive group.

 

Table 7. Follow up Computed Tomography (after 1 week) in progressive and non-progressive patients.

 

 

Non- Progressive

n=160

Progressive

n=40

EPS

n=26

LPS

n=14

Site of infarction

        

 

 

 

Subcortical

Cortical

Cortico-subcortical

Non MCA

50 (31.3%)

54 (33.8%)               

12 (7.5%)             

10 (6.3%)               

15  (37.5%)

8 (20%)        

11 (27.5%)*      

4 (10%)         

11 (42.3%)

5 (19.3%)             

6  (23%)         

2 (7.7%)             

4 (28.6%)

3 (21.4%)

5 (35.7%)

2 (14.3%)

Size of infarction

 

 

 

 

Small

Medium

Large

86(68.3%)

36 (28.6%)

4 (3.1%)

18 (47.4%)*

19 (50%)*

1 (2.6%)

13 (54.2%)

10 (41.7%)

1 (4.1%)

5 (35.7%)

9 (64.3%)

0 (0 %)

Mass effect

 

 

 

 

Slight

Moderate

Severe

94 (74.7%)

28 (22.2%)

4 (3.1%)

26 (68.4%)

11 (29%)

1  (2.6%)

18 (75%)

5 (20.9%)

1 (4.1%)

8 (57.1%)

6 (42.9%)

0 (0%)

Hemorrhagic Infarction

6 (4.8%)             

5  (13.1%)          

3 (12.5%)

2 (14.2%)

(EPS): Early progressive stroke, (LPS): Late progressive stroke, MCA= middle cerebral artery.

X2 test, (*)P< 0.05 compared to non-progressive group.

 

 


DISCUSSION

 

In the present study, the frequency of progressive stroke is 20% (13% early progression and 7% late progression). Similar results were reported by Mohr et al.18 (20%) and Audebert et al.8 (24%). Other studies reported higher frequencies up to 43%.7,9,19-21 Low frequency in our study can be explained by late admission of some patients after onset of symptoms thus they were mistakenly classified into non-progressive group and the evaluation could not confirm progression in the early stages after onset. This explanation can be supported by the finding that mean time to admission is significantly lower in progressive than in non-progressive patients. Price22 supported this finding as he assumed that the earlier we see patients with stroke after onset, the higher the rate of progression.

The mean time to admission is significantly lower in EPS than in LPS patients. This finding supports the evidence that both EPS and LPS has different mechanisms. Asplund3 assumed that the cause of EPS is due to propagation of the thrombus in the perforating arteries in the lack of collaterals and impairment in autoregulation leading to cerebral ischemia that initiates cascade of chemical reactions and development of brain edema leading to progression. While, LPS is attributed to cerebral edema and inflammatory process that may occur late in stroke. Experimental studies23,24 proved that neuronal death after transient ischemia may be caused by 2 different mechanisms, firstly necrosis within the ischemic core and secondly apoptosis at the borders of infarct volume. The latter process can develop in delayed fashion i.e. between 3 days and 2 weeks which may add another explanation for the mechanism of LPS.    

In agreement with all previous studies there is no significant gender difference between all groups. There is also no significant age difference between them. This finding comes in accordance with Yamamoto et al.19. In contrast, Toni et al.6 and Davalos et al.10 found that progressive stroke and specially EPS patients were significantly older. In these studies, the mean age is collectively higher (68 years) than of our study (60 years). As elderly patient tend to come in more sever state on admission (coma) so they were excluded from our study. Older age can predispose to progression by the co-morbid association of age with other risk factors specially atherosclerosis and by increased excitotoxicity of excitatory amino acids  and glutamate which is higher in elderly.25 Davalos and Castillo26 found that glutamate level increases after ischemic stroke and this increase dropped to normal values in less than 6 hours in non-progressive patients, while it persists for at least 24 hours in EPS patients. This maintained excitotoxicity leads to the progression of ischemic process in the penumbra over a period of several hours, adding another mechanism which can explain the cause of EPS.          

Past history of hypertension is significantly frequent in progressive than in non-progressive patients. This finding is matched with Yamamoto et al.19. The prevalence of other risk factors such as TIA, smoking and cardiac disorders is not significantly differ between progressive and non-progressive patients or between EPS and LPS.  This finding matched with Toni et al.6 and Wolfgang and Stephan27.

GCS is significantly reduced in progressive than in non-progressive patients. This comes in accordance with Wolfgang and Stephan27. Reduced level of consciousness at admission in patients with progressive stroke may be due to large infarction volume, this assumption is matched with our finding that medium size infarction are more frequent in progressive patients compared to small size infarction which are more frequent in non-progressive patients.

Systolic and diastolic blood pressure on admission are significantly higher in progressive and early progressive than in non-progressive patients. This can be attributed to impairment of autoregulation as cerebral perfusion often varies with the systemic blood pressure.11 This finding matched with Davalos et al.2 and Barber et al.11. In contrast, Jorgensen et al.4, suggested that the higher the blood pressure, the lower was the risk of progression. While, Nakamura et al.28 reported that, neither systolic or diastolic blood pressure at entry nor changes in blood pressure within the first 24 hours were associated with progression.

Body temperature in this study shows no significant difference between progressive and non-progressive patients. This come in keeping with Davalos et al.12, and in contrast to Audebert et al.8, who found that progressive stroke were associated with higher body temperature on admission.

Frequency of atrial fibrillation and other cardiac disorders shows no significant difference between progressive and non-progressive patients. Wolfgang and Stephan27 found more occurrence of AF in non-progressive stroke. Yamamoto et al.19, reported that patients with cardio embolic infarcts had a stabilized course of stroke more than other patients denoting that emboli can not be included in the mechanism of progressive stroke. While, Itoh et al.29, found that progressive stroke was seen frequently in patients with AF. They explained this finding by the chronically reduced cerebral blood flow in patients with AF compared patients with sinus rhythm.

   Although past history of diabetes mellitus is not significantly related to progressive stroke, admission blood glucose level is highly significantly higher in progressive patients especially EPS. This finding comes in accordance with Kagansky et al.30, who found that admission hyperglycemia in patients with or without diabetes was more commonly associated with progression than in patients without hyperglycemia. Hyperglycemia exaggerates the following damaging processes which in turn can lead to progression of stroke: intracellular acidosis, accumulation of extracellular glutamate, brain edema formation, blood-brain barrier disruption, and tendency for hemorrhagic transformation.30 Bomont and Mackenzie31, in their animal model of cerebral infarction found increase in the size of infarction in rats with hyperglycemia and diabetes when compared to the size of infarction in normoglycemic rats. Their use of N-methyl-D-aspartate (NMDA) antagonists reduced the size of infarction in these groups, indicating that NMDA excitotoxicity may play a role in hyperglycemia induced damage in cerebral ischemia.

Serum cholesterol level on admission is significantly higher in progressive patients, especially LPS. Advanced atherosclerosis which causes loss of local autoregulation of cerebral blood vessels and loss of collateral blood supply to the ischemic area may be the explanation for this finding. On the other hand, Nakamura et al.28, found no role of hypercholesterolemia in progressive stroke.

C-reactive protein is significantly higher in progressive patients especially LPS. These findings may give a clue that EPS and LPS have different mechanisms and the inflammatory process that take place late in the stroke reflected by high C-reactive protein may be the mechanism of LPS. Petito33 supported this hypothesis when he mentioned that during the first week of stroke, there is a transient inflammatory reaction, especially around blood vessels and in the meninges, due to release of arachidonic acid and other fatty acids. Wolfgang and Stephan27 found similar results. While, DiNapoli et al.34 found that increase in C-reactive protein was associated with stroke occurrence but not with stroke progression.

Serum ferritin level is significantly higher in progressive patients especially EPS. Davalos et al.14, suggested that increase of plasma ferritin within the first 24 hours of the onset of symptoms will increase the risk of progressive stroke, independent of other predictors. Possible mechanism is that high ferritin levels have an indirect relation with some of the multiple molecular and cellular mechanisms that may lead to the expansion of tissue necrosis.35 Increased body iron stores, and consequently increased brain iron content, might enhance brain damage because of the formation of free radicals, excitatory amino acid release and apoptosis. Ferrous iron released from intracellular stores such as ferritin during ischemia, catalyzes the generation of radical hydroxyl, which has been suggested as a possible mediator of the tissue injury in ischemia/reperfusion.36 Free radicals can attack proteins, deoxynucleic acids, and lipid membranes, disrupting cellular functions and integrity thus disrupting the blood brain barrier and promoting brain edema.37 On the other hand, Armengou et al.38, suggested that high plasma ferritin concentration on admission were associated with larger infarct volume but not with progression.

This study, like most of the previous studies,10,27,28 there is no significant  statistical difference detected between progressive and non-progressive patients in relation to prothrombin time, partial thromboblastin time, aspartate amino-transferase, alanin aminotransferase, high and low density lipoproteins, serum creatinin, and erythrocyte sedimentation rate.

Results of admission CT scan proved that presence of an early focal hypodensity is significantly more frequent in progressive patients, regardless of the type of progression (EPS or LPS). An early focal hypodensity is thought to be a sign of intracellular edema which in turn is thought to be an important suggested mechanism of progression. This finding is matched with findings of previous studies.5,10,39

Results of follow up CT scan proved that lesions in the anterior circulation are  more frequent in patients with progressive stroke than lesions in the posterior circulation. This comes in agreement with Jorgensen et al.4 and Toni et al.5. In contrast, Yamamoto et al.19 reported that posterior circulation infarction were more frequent in progressive stroke. While, Davalos et al.2 found no difference in lesion topography between patients with and without progression. Low frequency of posterior circulation infarction in our study whether in progressive and non-progressive stroke could be explained by: most of posterior circulation infarction patients were presented in more severe  form (coma) that were excluded from  the study from the start.

The cortico-subcortical involvement of MCA is significantly more frequent in progressive patients. This finding comes in accordance with Toni et al.6. They stated that early focal hypodensity and cortico-subcortical distribution considered an independent predictor of progressive stroke. While Jorgensen et al.4 and Itoh et al.29 found that cortical involvement was more frequent in progressive patients.

The medium size infarction is significantly frequent in progressive patients. This comes in accordance with Davalos et al.2 and Yamamoto et al.19. Nakamura et al.28, suggested that, the size of the infarction, but not the site, is responsible for progression. The occluded portion of the artery may be one of the factors that regulate the duration of progression. That is, occlusion at the proximal portion of a perforating artery produces a large ischemic area which requires much time to complete an infarction, which recognized clinically as progression.

Hemorrhagic transformation of the infarct did not appear to have any role in the early or late progression in our patients. This finding come in accordance with Bazzao et al.40 and Toni et al.5. On the other hand, Jorgensen et al.4, suggested that hemorrhagic transformation is a possible cause of both EPS and LPS. 

In conclusion, although progressive stroke is a multi-factorial event that is difficult to  predict , it can be partially predictable based on some clinical, laboratory and imaging data. Progressive stroke can be predicted early on admission in patients with: past history of hypertension, high systolic and diastolic blood pressure on admission, low Glasgow coma scale, short time to admission,  elevated blood glucose, cholesterol, C-reactive protein and serum ferritin and with early focal hypodensity in the initial CT scan. Admission hyperglycemia and high ferritin level are strong predictors of EPS, while, high serum C-reactive protein and cholesterol levels are strong predictors for LPS.

 

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الملخـص العربـى

 

تم إجراء هذا البحث بهدف معرفة معدل انتشار السكتة الدماغية الإنسدادية المتطورة في مرضى السكتة الدماغية ولمعرفة بعض العوامل الإكلينيكية والمعملية في محاولة للتنبؤ المبكر بها.

وقد تم إجراء الدراسة على 200 مريضا وتم تقييم المرضى باستخدام المقياس الإسكندنافيِ للسكتة الدماغية وذلك لتشخيص السكتة المتطورة وذلك عند حدوث نقص في درجة المقياس خلال 24 ساعة من دخول المستشفى (السكتة الدماغية الانسدادية المتطورة المبكرة) أو نقص في درجة المقياس بعد 24 ساعة من الدخول وخلال أسبوع (السكتة الدماغية الانسدادية المتطورة المتأخرة).

وتم دراسة العوامل الإكلينيكية والمعملية الأشعة المقطعية على المخ عند الدخول وبعد أسبوع من الدخول المختلفة لاستخدامها كمنبئات للسكتة الدماغية الإنسدادية المتطورة:

وقد أثبتت الدراسة أن معدل حدوث السكتة الدماغية الانسدادية المتطورة  يبلغ 20٪ ( 13٪ مبكرة و7٪ متأخرة).

كما أثبتت أن المنبئات المبكرة للسكتة المتطورة هي: تاريخ سابق لارتفاع ضغط الدمِ، ارتفاع ضغط الدم عند الدخول، انخفاض درجة الوعي، انخفاض متوسط وقت الدخولِ، ارتفاع نسبة الجلوكوز العشوائي بالدمِ، ارتفاع مُستَوَى الكُولِسترولِ، ارتفاع مستوى بروتين سي التفاعلي بالدم, ارتفاع مُستَوَى الفيرِّيتين بالدم, وجود الآثار المبكرة لحدوث السكتة  الدماغية الناتجة عند عمل أشعة مقطعية وقت الدخولِ، حجم جلطة المخ متوسطة وامتداد الجلطة من القشرة المخية إلى ما تحت القشرة المخية.  

لم تجد الدراسة اختلاف  في العوامل الأخرى مثل الانسداد العابر للدورة الدموية المخية، التدخين، مرض السكر، أمراض القلب, درجةِ الحرارة، زَمَنُ البروثرومبين والبروثرومبين الجزئي، وظائف الكبد، مستوى الكرياتينينِ بالدم، سرعة الترسيب بين المريضِ بالسكتة المتطورة وغيرِ المتطورة.



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