Online ISSN : 1687-8329

    




Quick Search 
 
Author  
Year    
Title  
Vol:  

 
 
April2012 Vol.49 Issue:      2 Table of Contents
Full Text
PDF


Role of Serum S100B Protein in Prediction of Outcome of Malignant Middle Cerebral Artery Infarction: Clinical and Laboratory Study

Wael A. Fadel1, Ashraf A. Abo-El-Safa1, Khalid H. Rashed1,

Gamalat A. El-Saleet2, Morad A. Morad3

Departments of Neuropsychiatry1, Public Health and Community Medicine2,

Clinical Pathology3, Tanta University; Egypt

 



ABSTRACT

Background: Early prediction of outcome in patients with malignant middle cerebral artery infarction may help the proper choice for the therapeutic decision in this stroke subtype. Objective: We attempted to investigate the possible role of serum S100 B protein, beside other clinical and radiological determinants, in prediction of outcome of malignant cerebral infarction. Methods: This study was conducted on 42 stroke patients with clinical and radiological evidence of malignant cerebral infarction (group I), and 20 patients with non malignant cerebral infarction as a morbid control (group II), in addition to 20 individuals as a healthy control (group III). Assessment of the disability was done by modified Rankin Scale, which was performed after one week, then after one month and after three months of admission. Computerized tomography of the brain was done for all patients on admission, and was repeated after one week for group I patients. Serum S100 B protein was measured initially for the three groups and after one week for group I patients. Results: the serum S100B protein value on admission was significantly higher in group I patients when compared to both group II and group III patients. Follow up values were increased but without significant difference from the initial values in group I patients. Moreover, the S100B value was significantly related to the mortality outcome. Conclusion: Serum S100B protein on admission (beside other clinical and radiological predictors) can predict the outcome of malignant middle cerebral artery infarction. [Egypt J Neurol Psychiat Neurosurg.  2012; 49(2): 157-164]

Key words: Malignant infarction, Middle cerebral artery, Serum S100B.

Correspondence to Dr Ashraf A. Aboelsafa, Neuropsychiatry Department, Tanta University; Egypt.

Tel: +20106622792. E-mail: draboelsafa@hotmail.com.





INTRODUCTION

 

Patients having complete middle cerebral artery (MCA), or internal carotid artery occlusion and either occlusion of the anterior cerebral artery or posterior cerebral artery have a higher risk of developing severe midline shift with compression of the basal cisterns and clinical signs of herniation.  This clinical and radiographic condition has been termed the malignant MCA syndrome because many patients will have a mortality rate as high as 80% 1. This clinical syndrome usually initially consists of contralateral hemiparesis, hemianesthesia, conjugate gaze palsy with reduced level of consciousness. In the next three to five days, approximately more than half of these patients deteriorate because of cerebral edema and herniation2,3. Early identification of patients who are likely to develop malignant MCA syndrome is extremely important in determining the amount of hospital  and  social  resources,  immediate intervention,  and in determining prognosis. This may be done by clinical, radiological, or laboratory predictors4. Early clinical predictors of massive brain edema or fatal brain herniation in patients with MCA stroke include drowsiness, asymmetric pupil size, nausea, coma on day of admission, carotid dissection and younger age at onset5. Early radiologic changes can be seen through brain imaging by computed tomography (CT). These include hypodensity of the affected territory, loss of gray/white junction and hyperdense MCA sign less than 6 hours from stroke onset6.

               Moreover, early laboratory predictors are variable; one of them is the astroglial protein S100B, which is released into serum in acute ischemic stroke and most likely reflects astroglial cell death followed by a leakage of this protein through an impaired blood–brain barrier7. It is a member of S100 protein family, which has 21 members discovered to date. These protein members are acid calcium-binding proteins and share substantial amino acid sequence 8.

               The biologic activity of S100B protein has not been completely illuminated, but in general, it has neurotrophic effects in enhancing the survival of neurons, stimulating the outgrowth of neurite, and modulating synaptic function and potassium channels activity. However, upon acute and/or chronic brain injury or under neurodegenerative conditions, excessive production and release of S100B proteins from astrocytes can result in toxic consequences acting like pro-inflammatory cytokine 9. Its high concentrations have a direct neurotoxicity 10-12. It can be measured in arterial and venous blood13.

So, the current study aimed to investigate the role of serum S100B protein (beside other clinical and laboratory factors) in the prediction of outcome in malignant cerebral infarction.

 

SUBJECT AND METHODS

 

               This study was conducted on 42 stroke patients with clinical and radiological evidence of malignant cerebral infarction (Group I), selected from the neurology intensive care unit in Tanta University Hospital from the first of July 2007 till the first of January 2009. The inclusion criteria were: (1) Clinical and CT and/or MRI evidence of acute complete MCA infarction such as hemiplegia with persistent nausea and vomiting, forced head and eye deviation, hyperdense middle cerebral artery sign, attenuation of the lentiform nucleus, hemispheric sulcus effacement, compression of the ipsilateral ventricular system, and/or midline shift; (2) Neurological deterioration compared with the baseline clinical status on admission such as deteriorating consciousness, unequal pupils, conjugate eye deviation, and deteriorating muscle power.

Patients with any previous disabling neurological disease, secondary hemorrhagic infarction, advanced endocrinal, hepatic, or renal diseases, malignancy or autoimmune disorders, and patients with history of drug abuse or alcohol intake were excluded.

Twenty patients with non malignant cerebral infarction were taken as a morbid control (group II), and 20 individuals as a healthy control (group III).

 

All subjects were matched in age and sex, and all patients were subjected to:

1.      Thorough history taking, general medical and neurological examination, with assessment of the degree of disability using the modified Rankin Scale14 which was done initially, then after one, and three months. Glasgow Coma Scale (GCS) was used in initial assessment and in follow-up of the conscious level of the patients.

2.            Early brain CT and/or MRI.

3.      Routine laboratory investigations, including lipid profile, fasting and postprandial blood sugar, erythrocyte sedimentation rate, blood picture, blood urea, serum creatinine, and liver functions.

4.      Investigations to assess the cardiovascular system including electrocardiography, carotid duplex study and echocardiography.

5.      Measurement of serum astroglial S100B protein that was done initially for all groups and after one week for group I survived patients. Blood samples were collected at 7 AM by vein puncture following an overnight fast, centrifuged (4 °C, 5000 rpm, 10 min), to get the serum, then stored at −20 to −70 °C. Serum S100B levels were measured within 1 week by sandwich enzyme-linked immunosorbent assay (ELISA) using a commercially available kit (Adlitteram Diagnostic Laboratories, Inc., San Diego, CA, USA). The antibodies were provided by ADL Inc., and the measurement procedure has been validated in a previous publication15.

 

Statistical Analysis:

The data were collected, and analysed using SPSS software v11.5 (statistical package for social science). Data were expressed as number, percentage and mean ± standard deviation. Qualitative data were assessed using Chi-Square test. P value of <0.05 was considered significant.

 

RESULTS

 

The risk factors and co-morbidity in the studied subjects were presented in table (1). Hypertension was the most prevalent among all groups. Hypertension, atrial fibrillation and valvular lesions were significantly higher in patients of group I compared to the other groups (p=0.005, 0.000 and 0.000 respectively), while diabetes mellitus, ischemic heart disease, smoking and dyslipidemia were non-significantly higher in patients of group II compared with the other groups (p=0.504, 0.526, 0.996, and 0.887 respectively).

               The clinical signs in patients of group I and II on admission were described in table (2), after one month in table (3) and after three months in table (4). GCS less than 10 (or less than 7 aphasic) was significantly higher in group I compared to group II on admission only (p<0.001). Modified Rankin Scale more than 3 was significantly higher in group I compared to group II on admission (p<0.001) and after one month of follow up (p=0.006), but did not show any significant difference between the two groups on further follow up after three months (p=0.179). Also, conjugate head and eye deviation was significantly higher in group I compared to group II on admission (p<0.001) and after one month of follow up (p=0.010) as well, but did not show any significant difference between the two groups on further follow up after three months (p=0.144).

               Neuroimaging findings on admission, done within 24 hours from onset, were seen in table (5). Tempro-parietal infarction was the most seen site found in patients of group I (38.09%) and II (85%).

               The follow up CT scan after one week was done for survivors of group I (n=12), revealed that brain edema was stationary in 9 (75%) patients, and increased in 3 (25%) patients. Brain shift was stationary in two cases (16.66%) and appear recently in one case (8.33%). Hemorrhagic transformation occurred only in one case (8.33%).

               The serum S100B value on admission was significantly higher in patients of group I compared to group II and group III (p<0.001). Moreover, there was significant difference between group I and both groups II and III (p= 0.015 and p=<0.001 respectively), while there was no significant difference between group II and group III (p=0.501), as shown in table (6). The S100B values were increased after one week than on admission but without significant difference (p=0.061), as shown in table (7).

               The relation between risk factors and mortality was seen in tables (8) and (9). The mean of GCS scores was significantly higher in survivors than deaths (p= 0.014). On the other hand, the mean S100B values was significantly higher in deaths than survivors (p=0.002), as seen in table (8). Midline shift in initial CT scan was absent totally in the survivors with a highly significant difference between deaths and survivors (p=0.003). Other risk factors failed to show any significant difference between survivors and deaths.


 

Table 1. Risk factors and co-morbidity among the studied groups.

 

Risk factors and

co-morbidity

Group I

(n=42)

Group II

(n=20)

Group III

(n=20)

Chi-square

N

%

N

%

N

%

X2

p-value

Hypertension

27

64.29

11

55.00

4

20.00

10.786

0.005*

Atrial fibrillation

20

47.62

2

10.00

1

5.00

16.464

0.000*

Valvular lesion

10

23.81

1

5.00

0

0.00

29.525

0.000*

Transient ischemic attacks

8

19.05

2

10.00

0

0.00

3.965

0.138

Diabetes mellitus

7

16.67

6

30.00

3

15.00

1.371

0.504

Ischemic heart disease

6

14.29

3

15.00

1

5.00

1.285

0.526

Smoking

6

14.29

4

20.00

3

15.00

0.008

0.996

Dyslipidemia

5

11.90

3

15.00

2

10.00

0.240

0.887

* Significant at p<0.01.

 

Table 2. Clinical signs on admission among the patients of group I and II.

 

Clinical signs on admission

Group I

(n=42)

Group II

(n=20)

Chi-square

N

%

N

%

X2

p-value

GCS less than 10 (or less than 7 aphasic)

37

88.10

0

0.00

40.11

<0.001*

Modified Rankin Scale more than 3

42

100.00

11

55.00

16.981

<0.001*

Conjugate head and eye deviation

27

64.29

3

15.00

17.633

<0.001*

Pupillary changes

6

14.29

0

0.00

1.740

0.187

Lateralization

Right

22

52.83

9

45.00

4.645

0. 310

Left

20

47.62

11

55.00

* Significant at p<0.01.

 

Table 3. Clinical signs after one month in survivors of group I and II patients.

 

Clinical signs after one month

Group I

(n=9)

Group II

(n=19)

Chi-square

N

%

N

%

X2

p-value

GCS less than 10 (or less than 7 aphasic)

1

11.11

0

0.00

0.152

0.697

Modified Rankin Scale more than 3

9

100.00

7

36.84

7.536

0.006**

Conjugate head and eye deviation

4

44.44

0

0.00

6.557

0.01*

Pupillary changes

0

0.00

0

0.00

2.893

0.089

Lateralization

Right

4

44.44

9

47.37

0.068

0.794

Left

5

55.56

10

52.63

* Significant at p<0.05 ** Significant at p<0.01.

Table 4. Clinical signs after three month in survivors of group I and II.

 

Clinical signs after three months

Group I

(n=8)

Group II

(n=19)

Chi-square

N

%

N

%

X2

p-value

GCS less than 10 (or less than 7 aphasic)

1

12.50

0

0.00

0.207

0.649

Modified Rankin Scale more than 3

5

62.50

5

26.32

1.800

0.179

Conjugate head and eye deviation

2

25.00

0

0.00

2.132

0.144

Pupillary changes

0

0.00

0

0.00

3.704

0.054

Lateralization

Right

3

37.50

9

47.37

0.002

0.962

Left

5

62.50

10

52.63

 

Table 5. Neuroimaging on admission among patients of group I and II.

 

Group II (n=20)

Group I (n=42)

Neuroimaging on admission

 

 

%

No

%

No

 

85.0%

17

38.09%

16

Temproparietal

Site of infarction

 

15.0%

3

35.71%

15

Frontotemproparietal

 

0%

0

26.19%

11

Hemispheric

 

0%

0

100%

42

Associated brain edema

 

0%

0

100%

42

Compression on ipsilateral ventricle

 

0%

0

52.38%

22

Midline shift











 

Table 6. S100B serum level on admission in patients of the studied groups.

 

Groups

S100B in ug/L

ANOVA

Range

Mean ± SD

f

p-value

Group I (n=42)

0.67 - 1.74

1.184 ± 0.364

9.997

<0.001**

Group II (n=20)

0.02 - 2.86

0.704 ± 0.684

Group III (n=20)

0.02 - 0.77

0.428 ± 0.229

Tukey's test

Group I & Group II

Group I & Group III

Group II & Group III

0.015*

<0.001**

0.501








* Significant at p<0.05 ** Significant at p<0.01

Table 7. Comparison of S100B mean levels in patients of group I on admission (n=42) and after one week (n=12).

 

Timing

S100B in ug/L

Paired t-test

Range

Mean ± SD

t

p-value

On admission

0.67 - 1.74

1.184 ± 0.364

-2.082

0.061

After one week

0.78 - 1.82

1.238 ± 0.338

 

Table 8. Relation between risk factors (numerical data) and mortality in group I patients (n=42).

 

Risk factor

Deaths (n=34)

Survivors (n=8)

t-test

Mean ± SD

Mean ± SD

t

p-value

Age

63.174 ± 10.439

65.500 ± 7.407

-0.579

0.567

GCS

8.657 ± 1.070

9.925 ± 1.923

2.558

0.014*

S100B

1.928 ± 0.843

0.889 ± 0.141

3.432

0.002*

* Significant at p<0.05 ** Significant at p<0.01

Table 9. Relation between risk factors (non-numerical data) and mortality in group I patients (n=42).

 

Risk factor

Mortality

Chi-square

Deaths (n=34)

Survivors (n=8)

X2

p-value

Sex

Male

21 (80.77%)

5 (19.23%)

0.134

0.714

Female

13 (81.25%)

3 (18.75%)

Hypertension

11.11 (24.00%)

3 (3.00%)

88.89

0.714

Diabetes mellitus

18.18 (9.00%)

2 (2.00%)

81.82

0.718

Atrial fibrillation

10.00 (18.00%)

2 (2.00%)

90.00

0.303

Valve lesion

12.50 (7.00%)

1 (1.00%)

87.50

0.657

Midline shift in initial CT

0.00 (22.00%)

0 (0.00%)

100.00

0.003*

The side of  hemiplagia

Right

19 (86.36%)

3 (13.64%)

0.039

0.842

Left

15 (75.00%)

5 (25.00%)

* Significant at p<0.01

 


DISCUSSION

              

The main aim of this study was to study some predictors of malignant cerebral infarction, and to study their role in early diagnosis and outcome of this important type of stroke. The rationale for this effort was to provide clinicians caring for acute stroke patients with early prognostic factors that may influence their treatment decisions.               

               Hypertension, atrial fibrillation and valvular heart lesions are the main risk factors for large artery strokes including malignant cerebral infarction, while diabetes mellitus, smoking, transient ischemic attacks and dyslipidemia may be present in any stroke subtype16,17. This is going with findings of the current study. Hypertension may predispose to large artery strokes through potentiating atherosclerosis of the aorta and large cerebral arteries, causing arteriosclerosis and promoting the occurrence of other heart diseases16,17.

               High systolic blood pressure and elevated blood sugar concentration were independently related to deterioration in the first 48 hours after malignant middle cerebral infarction,18 however in our patients there was no significant difference in the prevalence of DM between malignant and non malignant groups, as seen also in another study (19).  This may be explained by that in our study other risk factors than DM like smoking, age and dyslipidemia were included.

               In the present study, clinical assessment of stroke severity of our patients on admission and during follow up was done depending upon Glasgow Coma Scale (GCS), modified Rankin Scale of disability (mRS), presence of conjugate head and eye deviation, and pupillary changes. We considered the findings of severe stroke in the present study to be GCS less than 10 or less than 7 if aphasic, mRS scores more than 3, presence of conjugate head and eye deviation, and pupillary changes.

               In the current study findings of severe stroke  were  significantly present in group I patients on admission  and in the survived patients of group I during the  initial  follow up after two days and after one week (both GCS  and  mRS were significant), also during the follow up after one month  (only mRS was significant). While in the follow up after three months there was no significant difference regarding the stroke severity between the survived patients of group I and group II.

               These findings indicated that the stroke severity in group I patients reached the peak in the first week. Follow up of these severe cases showed that all cases with pupillary changes died by the first month and this, in our opinion, may indicate that cases presented initially with signs of transtentorial herniation were the most severe form and all were died.

               Also we found the mortality in group I patients jumped by the end of the first week to 71.43 %, the value which were not highly far from the three months mortality of 80.95 %. This can be explained by the fatal brain edema reached the peak in the first week. In the current study the relation between the above mentioned findings of stroke severity and mortality were of non significant value except for low GCS which was found to be of significant value.

               Similar to our results but with little differences, Scott et al20 found that neither the level of consciousness nor the stroke severity on presentation was associated with neurological death, and they referred this lack of association to the limited statistical power to their study. However, others21,22 found that the National Institute of Health Stroke Scale (NIHSS) score at admission, and within 48 hours of stroke onset, was strongly associated with the outcome.

               Radiographic factors appear to play a major role in determining the patients at risk for subsequent fatal ischemic brain swelling. Non contrast CT scans are readily available in emergency departments and are prerequisite for treatment of acute stroke patients. The sensitivity and prognostic value of early CT in MCA occlusion have been extensively investigated. There is controversy in the literature regarding the importance of signs for cerebral ischemia. Von Kummer et al.6 and Tomsick et al.23 did not demonstrate a good correlation between hyperdense MCA sign and poor outcome and said that this sign may lack specificity given the location, surrounding bone artifacts, and frequent calcification of the artery in this location.

               In the current study, associated brain edema and midline shift in the initial CT scans showed a highly significant relation to the mortality and poor outcome after malignant cerebral infarction. This is also ongoing with previous studies24,25 that refer the neurological deterioration to massive brain edema more than the infarct size. However, Krieger et al26 found that the early CT hypodensity findings were not significantly associated with herniation, but when combined as a more than 50% hypodensity, this was shown to be a strong predictor.

               Many markers of ischemic brain damage have been investigated in cerebrospinal fluid and serum after acute ischemic stroke both experimentally and in patients. These include lactate and various brain specific proteins like S100B protein. The current study revealed that the mean value of serum S100B protein on admission was significantly higher in patients with malignant cerebral infarction compared with both non-malignant infarction and healthy controls.  This might be referred to the initial metabolic responses in the infarcted tissue. Follow up values, after one week, were increased but without significant difference if compared with the initial values. This increase could be explained by completion of the pathophysiological cascade and glial reaction to cerebral ischemia. Also in our study the relation of S100B value to the mortality showed significant results.

               Similar results were reached by Foerch et al.7, who also reported that the serum marker S100B can predict a malignant course of infarction in proximal MCA occlusion with sensitivity of 0.94 and specificity of 0.83 in the first 24 hours. However, other authors27-29 reported that the rise in serum S100B protein was significant within two days of onset when it reached its maximum level, and was significantly correlated with the neurological state of the patients as assessed by NIHSS, and with the functional status of the patient on discharge and after two months assessed by the mRS29, while no significant difference could be detected in its level between malignant and non malignant infarction at the time of admission.

               In conclusion, the current study identified some predictors that may be helpful in predicting which patients with large hemispheric ischemic strokes are at highest risk for death due to progressive fatal brain edema. In patients with malignant cerebral infarction, hypertension, atrial fibrillation, valvular lesions and transient ischemic attacks are the most prevalent risk factors and co-morbidity. Additionally, the presence of deep coma on admission (GCS less than 10 or less than 7 if aphasic), the presence of midline shift on initial CT scans and elevated serum level of S100B protein on admission are the most important and significant predictors of poor outcome in such patients.

 

[Disclosure: Authors report no conflict of interest]

 

REFERENCES

 

1.      Hacke W, Schwab S, Horn M. Malignant cerebral artery territory infarction: clinical course and prognostic signs. Arch Neurol. 1996; 53:309–15.

2.      Adams HP Jr, Adams RJ, Brott T, del Zoppo GJ, Furlan A, Goldstein LB, et al. Guidelines for the early management of patients with ischemic stroke: a scientific statement from the Stroke Council of the American Stroke Association. Stroke. 2003; 34:1056–83.

3.      Qureshi SE, Suarze JI, Abutaher MY. Timing of neurologic deterioration in massive middle cerebral artery infarction: A multicentre review. Critical Care medicine. 2003; 31:272-7.

4.      Heinsius T, Bogous SJ, Vanmelle G. Large infarcts in the middle cerebral artery territory: Etiology and outcome pattern. Neurology. 1998; 50:341-50.

5.      Ropper A, Shafran B. Brain edema after stroke: clinical syndrome and intracranial pressure. Arch Neurol. 1994; 41:26–9.

6.      von Kummer R, Meyding-Lamadé U, Forsting M, Rosin L, Rieke K, Hacke W, et al. Sensitivity and prognostic value of early CT in occlusion of the middle cerebral artery trunk. AJNR. 1999; 15: 9–15.

7.      Foerch C, Otto B, Singer OC, Neumann-Haefelin T, Yan B et al. Serum S100B predicts a malignant course of infarction in patients with acute middle cerebral artery occlusion. Stroke. 2004; 35:2160-73.

8.      Lima JE, Walz R, Tort A, Souza D, Portela L, Bianchin MM, et al. Serum and cerebrospinal fluid S100B concentrations in patients with neurological disorders. Braz J Med Biol Res. 2006; 39(1):129-35.

9.      Bánfalvi T, Gergye M, Beczássy E, Gilde K, Ottó S. Role of S100B protein in neoplasms and other diseases. Magy Onkol. 2004; 48(1): 71-4.

10.    Rothermundt M, Peters M, Prehn JH, Arolt V. S100B in brain damage and neurodegeneration. Microscopy Res Technique. 2003; 60 (6):614-632.

11.    Michetti F, Gazzolo D. S100B protein in biological fluids: a tool for perinatal medicine. Clin Chem. 2002; 48 (12): 2097-104.

12.    Persson L, Hårdemark HG, Gustafsson J, Rundström G, Mendel-Hartvig I, Esscher T, et al. S-100 protein and neuron-specific enolase in cerebrospinal fluid and serum: markers of cell damage in human central nervous system. Stroke 1997; 18: 911-8.

13.    Van Eldik IJ, Wainwright MS. The Janus face of glial derived S100B: beneficial and deterimental functions in the brain. Restor Neurol Neurosci. 2003; 21 (34): 97-108.

14.    Frankel MR, Morgenstern LB, Kwiatkowski T, Lu M, Tilley BC, Broderick JP, et al. Predicting prognosis after stroke. A placebo group analysis from the National Institute of Neurological Disorders and Stroke rt-PA Stroke Trial. Neurology. 2000; 55: 952–9.

15.    Leite MC, Galland F, Brolese G, Guerra MC, Bortolotto JW, Freitas R, et al. A simple, sensitive and widely applicable ELISA for S100B: Methodological features of the measurement of this glial protein. J Neurosci Methods. 2008;169:93–9

16.    Thomas H, Bogousslavskyy JG. Large infarction in the middle cerebral artery: etiology and outcome patterns. Neurology. 1998; 50:341-50.

17.    Lawes CMM, Bennett DA, Feigin VL, Rodgers A. Blood pressure and stroke: an overview of published reviews. Stroke. 2004; 35:776–85.

18.    Toni D, Fiorelli M, Bastianello S, Falcou A, Sette G, Ceschin V, et al. Acute ischemic stroke improving during the first 48 hours of onset: predictability, outcome and possible mechanisms; comparison with early deteriorating stroke. Stroke. 1997; 28:10-14.

19.    Serena J, Blanco M, Castellanos M, Silva Y, Vivancos J, Moro MA et al. The prediction of malignant cerebral infarction by molecular brain barrier disruption markers. Stroke. 2005; 36: 1921-6.

20.    Kasner SE, Demchuk AM, Berrouschot J, Schmutzhard E, Harms L, Verro P, et al Predictors of fatal brain edema in massive hemispheric ischemic stroke, Stroke. 2001; 32: 2117.

21.    Kwan J, Hand P. Early neurological deterioration in acute ischemic stroke clinical characteristics and impact on outcome. QJM. 2006; 99(9): 625-33.

22.    Tesing MC, Chang KC. Stroke severity and early recovery after first ever ischemic stroke: results of hospital based study in Taiwan. Health Policy. 2006; 79 (1): 73-80.

23.    Tomsick TA, Brott TG, Chambers AA, Fox AJ, Gaskill MF, Lukin RR, et al. Hyperdense middle cerebral artery sign on CT: efficacy in detecting middle cerebral artery thrombosis. AJNR. 1999; 11: 473-7.

24.    Oppenheim C, Samson Y, Manaï R, Lalam T, Vandamme X, Crozier S, et al. Prediction of Malignant middle cerebral infarction by diffusion weighted imaging. Stroke. 2005; 31(9): 2175-81.

25.    Pullicino PM Alexandrov AV, Shelton JA. Mass effect and death after acute stroke. Neurology. 1997; 49: 1090-5.

26.    Krieger DW, Demchuk AM, Kasner SE, Jauss M, Hantson L. Early clinical and radiological predictors of fatal brain swelling in ischemic stroke. Stroke. 1999; 30: 287–92.

27.    Foerch C, Singer OC, Neumann-Haefelin T, du Mesnil de Rochemont R, Steinmetz H, Sitzer M. Evaluation of serum S100B as a surrogate marker for long term outcome and infarct volume in acute middle cerebral artery infarction. Arch Neurol. 2007; 62 (7): 1130-40.

28.    Dohmen C, Sakowitz OW, Fabricius M, Bosche B, Reithmeier T, Ernestus RI, et al. Spreading depolarizations occur in human ischemic stroke with high incidence. Ann Neurol. 2008; 63: 720-8.

29.    Abdel-Azeim H, Soliman V, Kamel A, Abdel-Aziz S, and EL-Taqrhony S. Early predictors of malignant course of middle cerebral artery infarction: clinical, laboratory and radiological study. Egypt J Neurol Psychiat Neurosurg. 2007; 44(2): 437-47.


 

 


الملخص العربى

 

دور البروتين "اس 100 ب" فى توقع مآل الاحتشاء الخبيث للشريان الأوسط المخى:

دراسة سريرية ومختبرية

 

يطلق مصطلح الاحتشاء المخى الخبيث على الاحتشاء المخى الكامل الناتج عن انسداد الشريان الأوسط المخى أو جلطة بنهاية الشريان السباتى الداخلي، وتصل نسبة الوفاة فيه إلى حوالى 80 %، ويصاحب هذا المرض بزيادة في ضغط المخ الناتجة عن الارتشاح التسممى في خلايا المخ وهو السبب المؤدى إلى الوفاة في مثل هذه الحالات. تهدف هذه الدراسة إلى دراسة بروتين "اس 100 ب" كأحد دلائل الأحتشاء المخى الخبيث و دوره  مع بعض الدلالات السريرية والتصويرية فى التشخيص المبكر والتنبؤ بمآل هذا المرض الهام. وتم تقسيم هؤلاء المرضى إلى ثلاثة مجموعات جميعهم متكافئون فى السن والجنس: (أ) المجموعة الأولى وتشمل 42 مريضا بالأحتشاء المخى الخبيث. (ب) المجموعة الثانية وتشمل 20 من مرضى الأحتشاء الجزئي البسيط. (ج) المجموعة الثالثة وهى المجموعة الضابطة وتشمل 20 من الأصحاء. وقد خضع المرضى إلى الفحص السريرى الشامل وتقييم حالة الإعاقة بإتباع تقييم رانكن المعدل ، كما خضعوا الى تصوير المخ بالأشعة المقطعية أوالرنين المغناطيسي فى بداية الحالة وبعد أسبوع بالنسبة لمرضى المجموعة الأولى. كما خضعوا أيضا الى تقييم نسبة البروتين "اس 100 ب"  فى الدم  وذلك فى بداية البحث وبعد أسبوع بالنسبة لمرضى المجموعة الأولى أيضا. وقد أظهرت نتائج هذه الدراسة: وجود العديد من عوامل الخطورة المؤدية إلى هذا النوع من الجلطات منها ما هو ذو دلاله إحصائية بين المجموعتين الأولى والثانية مثل ارتفاع ضغط الدم  وأمراض صمامات القلب وعدم انتظام ضربات القلب ومنها ما هو ليس ذو دلاله إحصائية بين المجموعتين الأولى والثانية مثل مرض السكري واضطراب دهون الدم والاحتشاءت المخية اللحظية. كما وجد أن درجة الوعي أثناء دخول المستشفى تتناسب إحصائيا مع نسب الوفيات في هذا النوع من الجلطات وأن أعلى نسب الوفيات قد حدثت بنهاية الأسبوع الأول و بدراسة نتائج تصوير المخ وجد أن وجود ارتشاح شديد يؤدي الى انحراف بخط توسيط المخ لمرضى المجموعة الأولى يرتبط ارتباطا ذا دلالة إحصائية مع حدوث الوفيات، كما أظهرت الدراسة وجود ارتباط ذى دلالة إحصائية بين البروتين "اس 100 ب" وبين حدوث هذا النوع من الجلطات الخبيثة و نسب الوفيات بها. و توصى هذه الدراسة بتطبيق العمل بدلالات حدوث الجلطة الخبيثة على المرضى المشتبه اصابتهم بهذا المرض وذلك بهدف التشخيص المبكر والتدخل العلاجى السريع لهذا المرض الخطير.



2008 � Copyright The Egyptian Journal of Neurology,
Psychiatry and Neurosurgery. All rights reserved.

Powered By DOT IT