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July2005 Vol.42 Issue:      2 Table of Contents
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Relationship between Hyperglycemia on Admission and Severity of Acute First-Ever Anterior Cerebral Circulation Infarction

Bukhary FES1, Soliman WT2, Mohsen AMS3, Al-Sharkawy EA4
Departments of Internal Medicine1, Neurology2, Radiodiagnosis3,Clinical Pathology4, El-Minia University

ABSTRACT

Objective: Ischemic stroke is a leading cause of death and long-term disability; and hyperglycemia is believed to aggravate cerebral ischemia. Aim of the work: To evaluate relationship between admission hyperglycemia and clinical severity; stroke features in brain CT, short-term functional outcome in patients with first-ever acute total anterior cerebral infarction. Subjects and methods: Fifty-five consecutive patients with first -ever acute (< 24 hours) anterior cerebral infarction were included in the study within 72 hours after onset of symptoms. Baseline clinical variables and risk factors were analyzed. National Institute of Health Stroke Scale (NIHSS) was used to asses the clinical severity of neurological deficit on admission and on day 7 after admission. All patients had brain CT without contrast enhancement on day 3 and day 7 after stroke onset. Size of infarction, presence or absence of brain edema, hemorrhagic transformation and degree of X- ray attenuation in centre of infarction were determined. Patients were classified into 2 groups according to their random blood sugar at time of admission; Group I: 17 patients with random blood glucose level<140 mg/dl; and group II: 38 patients with hyperglycemia (level ≥ 140 mg/dl). Both groups were compared in terms of NIHSS score, laboratory data, admission blood pressure, and brain CT findings. The primary outcome was assessed after 30 days of admission by modified Rankin scale (mRsc). Patients with good outcome (grades ≤3; 41 patients) and patients with poor outcome (grades >3 or in-hospital death; 14 patients) were compared as group A and group B respectively. Logistic regression was used to examine the relationship between admission blood glucose level and NIHSS score, CT features and mRsc variables. Results: Group II showed significantly high NIHSS score at 1st day of admission, big infarction size (>6 cm3) at 7th day of admission and high mRSc after one month. Those with past history of diabetes mellitus in group II showed insignificant difference with those non diabetic in the same group. The neurological outcome (mRsc) is strongly influenced by baseline NIHSS score, admission hyperglycemia and higher initial blood pressure. Those with good outcome (group A) were younger and had smaller infarcts volume in brain CT than those with bad outcome (group B). Conclusion: Admission hyperglycemia is an independent determinant of expansion; clinical severity of acute total anterior cerebral infarction and associated with worse functional outcome. NIHSS score in 1st day and infarction size at 7th days of stroke onset had a predominant influence upon in-hospital death and short term outcome. Increased attenuation or hemorrhagic transformation had no predictive value for short term prognosis.

(Egypt J. Neurol. Psychiat. Neurosurg., 2005, 42(2): 453-463).

 




INTRODUCTION

 

In 25% to 40% of patients with ischemic stroke, neurological deficits progress during the initial hours resulting in increased mortality and functional disability.1 Although causes of clinical deterioration have not been identified, many variables were found to be relevant in such deterioration.2 Hyperglycemia in patients with or without history of diabetes is associated with a worse clinical outcome than in patients without hyperglycemia especially in non-lacunar type of stroke.3 It may augment brain injury, predispose to intra-cerebral hemorrhage or both.4 The need for prompt therapeutic decisions emphasizes the importance of early predictors of functional outcome.

The present study is aiming to evaluate the effect of admission hyperglycemia on clinical; radiological severity and short- term outcome of acute first-ever total anterior cerebral circulation infarction patients.

PATIENTS AND METHODS

 

Patients:

Patients were admitted in internal medicine and neurology departments in EL-MINIA University hospital within ≤ 72 hours of start of symptoms. Exclusion criteria were; posterior cerebral circulation infarction (As brain stem is not visualized in CT); non- ischemic stroke(cerebral hemorrhage), old cerebral infarction, delayed hospital admission > 72 hours.

 

Methods:

Full history taking was done including; past history of diabetes mellitus, hypertension, cardiac disease, coronary artery disease and history of transient ischemic attacks (TIA).Neurological deficit severity was evaluated by using the National Institute of Health Stroke Scale (NIHSS) (Severe ≥ 15; mild / moderate  <15).5

Admission blood pressure, random serum blood sugar; routine blood chemistry, basic hematology, and ECG were done to every patient on time of arrival. Non-enhanced brain CT was done at time of admission and on day 3 and day 7 by the radiologist who was blinded of clinical study data. Assessment of infarct volume (in cm3) was done according to the atlas of Gado, Hanaway and Frank.6 Formula 0.5 X a X b X c, where a & b represent the largest perpendicular diameters measured and c the slice thickness; was used. Infarcts were further classified into small and large (≤6 cm3 and > 6 cm3, respectively) in volume.7&8

Focal hypo-density was measured by attenuation coefficient in Hounsfield Units (HU) in the centre of the infarct area and compared to the corresponding zone of the contra-lateral hemisphere.9 Midline shift, hemorrhagic change and mass effect were also assessed.

According to criteria of American Diabetes Association; 10 patients were classified into 2 groups; group I; those having random blood glucose level < 140 mg/dl; and group II; (hyperglycemic); those with glucose level ≥ 140 mg/dl. Both groups were compared as regards clinical and CT signs of severity of cerebral infarction.

 

Outcome:

Modified Rankin scale (mRsc) was applied to each patient one month after infarction onset to evaluate outcome. Patients were classified into six categories:0- no symptoms at all; 1- no significant disability, able to carry the usual activities; 2-slight disability, unable to carry out all previous activities but able to look after his own affairs without assistance, 3- moderate disability, requiring some help but able to walk without assistance, 4- moderate to severe disability, unable to walk without assistance and unable to do his own affairs; 5- severe disability, bedridden, incontinent; 6- in-hospital death.11&5 The studied patients were classified into 2 groups according to mRsc; group A (Score≤3) and group B (Score >3 or in-hospital death). Both groups were compared according to clinical, laboratory data at day of admission and radiological data at 7th day of admission.

 

Statistical studies

Continuous data were expressed as mean ± SD. The X2 test, student t test were used as appropriate. The spearman correlation coefficient was used to analyze the association between NIHSS score and laboratory data and brain CT features. A value of P≤0.05 was established as statistically significant. Neurological worsening and hyperglycemia were assessed by forward stepwise logistic regression analysis.

 

RESULTS

 

Thirty eight out of 55 (69.1%) were found to be hyperglycemic at 1st presentation.  Table (1) showed the demographic and clinical data of the studied groups. The hyperglycemic group (Group I) was significantly older with increase prevalence of diabetes, female gender and showed significant high rate of AF (=0.05), high NIHSS score (=0.0005), serum total cholesterol (=0.01), triglycerides (=0.01) and LDL (=0.05) than group I.  Table (2) showed brain CT findings at 7th day after admission. The hyperglycemic group showed significantly increased infarct size (=0.01) than euglycemic one. Cortical and subcortical sites were the most prevalent sites in hyperglycemic group (=0.02) while capsular site was most prevalent in euglycemic one (=0.007). No significant difference was found between the studied groups as regards mass effect, hemorrhagic transformation or attenuation co-efficient. Table (3) showed patients' characteristics according to mRsc after one month. Fourteen patient out of 55 (25.5%) showed worse outcome (mRsc >3 or in hospital death). Twelve of them (85.7%) had severe NIHSS score. They had significant big infarct size (> 6 cm3) than those with good outcome (mRsc≤3) (=0.005). They were hyperglycemic at admission (=0.002), and showed mixed type of anatomical site of infarction (=0.03). Females had the worse mRsc (p=0.03). Most of those having high mRsc score (Group B) had past history of ischemic heart disease (=0.03) and atrial fibrillation (=0.04) while those with low score (Group A) had past history of TIA (=0.05). Figures from (1) to (6) show different studied cases with different types of infarction with dash arrows to show outlines of the infarction. Among patients of group II the outcome (mRsc) and functional (NIHSS) scores did not differ significantly by having history of diabetes or not (Table 4).


 

Table 1. Univariate analysis of baseline demographic, clinical and laboratory data in the studied groups at 1st day of admission.

 

Variable

Group I

Random blood sugar

< 140 mg/dl

(NO=17)

Group II

Random blood sugar

≥ 140 mg/dl

(NO=38)

P value

Age (Y):                          Range:

                                         Mean± SD

16 - 80

56.9 ± 18.4

24 - 85

64.8 ± 12.9

 

0.05

Gender (M/F)

4 / 13

23 / 15

NS

Past history of diabetes (%):

Duration of diabetes (Y) :Range:

                                         Mean± SD

                                         Oral hypoglycemic drugs:

                                         Insulin therapy:

4 / 17 (23.5%)

1 - 3

2.3 ± 0.03

4 / 17

0

26 / 38 (68.4%)

1 – 10

5.7 ± 1.6

14 / 38

12 / 38 (31.6%)

0.01

 

0.05

NS

 

History of TIA (%):

History of hypertension (%):

History of antiplatelets therapy:

History of anticoagulant therapy:

11/ 17

12/ 17

2/ 17

4/ 17

20 / 38

32 / 38

7/ 38

15 / 38

NS

NS

NS

NS

Smoking:                         Non-smoker

                                          X-smoker

                                          Current smoker

11/ 17

4/ 17

2/ 17

21/ 38

9/ 38

8/ 38

NS

NS

NS

Underlying cardiac disease

Coronary ischemia: (%)

Rheumatic heart disease: (%)

Presence of atrial fibrillation (%)

 

8/ 17

3/ 17

6/ 17 (35.3%)

 

19/ 38

2/ 38

22/ 38 (57.9%)

 

NS

NS

0.05

NIHSS score:                         Range:

                                                Mean ± SD

                                                < 15 (NO)

                                                ≥ 15 (NO)

4 - 16

9.1± 4.4

9/17 (52.9%)

8/17 (47.1%)

3 - 24

13.8 ± 5.9

7 / 38 (10.4%)

31 / 38 (81.6%)

 

 

0.002

0.0005

Systolic Bp:                            Range:

                                                Mean± SD

110 - 200

159.4 ± 21.6

120 - 240

169.5 ± 30.2

 

NS

Diastolic Bp:                           Range:

                                                 Mean ± SD

80 - 140

101.5 ± 12.0

80 - 150

104.7 ± 14.9

 

NS

Serum total cholesterol:         Range:

       ( mg/dl)                             Mean ± SD

178-320

240.00±48.3

230-470.0

320.00±62.9

0.01

Serum triglycerides: (mg\dl)  Range:

                                                  Mean ± SD

75 - 140

113.2 ± 18.6

95 - 585

161.8 ± 32.6

 

0.01

Serum LDL: ( mg/dl)              Range:

                                                  Mean ± SD

80 - 195

145.3 ± 21.3

110 - 480

175.2 ± 1.6

 

0.05

NS=Not significant

Table 2. Brain CT findings in the studied patients groups at 7th day of admission.

 

Variable

Group I

Random blood sugar

< 140 mg/dl (No. = 17)

Group II

Random blood sugar

≥ 140 mg/dl (No. = 38)

P value

Side affected: Right side:

                        Left side:

                        Both sides:

3 / 17

10 / 17

4/ 17

14 / 38

16 / 38

8 / 38

NS

NS

NS

Infarct size(cm3): Range:

                               Mean± SD

                               < 6 cm3 (%)

                               ≥ 6 cm3 (%)

1- 446

48.3 ± 106.4

9 / 17 (52.9%)

8 / 17 (47.1%)

1- 440

77.4 ± 91.5

5 / 38 (13.2%)

33 / 38 (86.8%)

 

< 0.01

< 0.001

< 0.001

Attenuation co-efficient: Range:

                 Mean± SD

8 - 48

20.6 ± 9.7

10 - 52

20.7 ±11.7

 

NS

Hemorrhagic transformation (%)

2 / 17

8 / 38

NS

Site of infarction:* Cortical and subcortical:

        Capsular:

        Mixed:

        Lacunar:

3 / 17 (17.64%)

10 / 17 (58.8%)

12 / 17 (70.6%)

3 / 17

8 / 38 (21.1%)

11 / 38 (28.9%)

17 / 38 (44.74%)

2 / 38

0.02

0.007

0.02

NS

Mass effect in brain CT (%)

6 / 17 (35.3%)

13 / 38  (34.2%)

NS

*More than one finding may be present in the same patient.                   NS = Not significant

 

Table 3. Univariate analysis of patients groups according to mRsc classification after one month of infarct onset.

 

Variable

Group A

mRsc 0- 3 (No. = 41)

Group B

mRsc > 3 or death (No. = 14)

P value

Age (Y): Range:

              Mean± SD

24-80

62.4±14.8

16-85

62.4±16.6

 

NS

Gender (M/F)

24/17

3/11

0.03

Past history of hypertension (%):

Past history of ischemic heart disease (%):

Past history of atrial fibrillation (%):

Past history of diabetes (%):

Past history of TIA (%):

History of anti-platelets therapy (%):

History of anticoagulants treatment (%):

33/ 41

16/ 41(39%)

17/ 41(41.5%)

21/ 41 (51.2%)

26/ 41(63.4%)

6/ 41

13/ 41

11/14

11/14 (78.6%)

11/14 (78.6%)

6/14 (42.9%)

5/14 (35.7%)

3/14

6/14

NS

0.03

0.04

NS

0.05

NS

NS

Smoking (%):                    Non-smoker:

                                            X-smoker:

                                            Current smoker:

21/41

11/41

9/41 (22%)

1/14

2/14

11/14 (78.6%)

NS

NS

0.08

NIHSS score at admission:        Range:

Mean± SD

<10

≥10

3-12

10.6± 4.9

14/ 41(34.1%)

27/ 41(65.9%)

11-24

17.3±5.6

2/14 (14.3%)

12/14 (85.7%)

 

0.001

0.003

0.000

Blood sugar at admission:         Range:

                                                     Mean± SD

                                                     < 140 mg\dl (%)

                                                     ≥ 140 mg\dl (%)

69-187

110.8±19.6

15 \ 41 (36.6%)

26 \ 41(63.4 %)

140 - 564

238.3± 106.9

2 \ 14 (14.3 %)

12 \ 14 (85.7%)

 

0.002

0.01

0.01

Infarct size at 7th day of  admission (cm3):  Range:

                                                                        Mean± SD

1-205

33.8±43.4

26 - 446

161.6±139.5

 

0.005

Attenuation co-efficient  at 7th day of admission: Range:

                                                                          Mean± SD

8-52

19.3±12.3

12-29

24.8± 4.3

 

NS

Hemorrhagic transformation (%):

7 / 41(17.1%)

3 / 14 (21.4%)

NS

Side of infarction:              Right:

                                             Left:

                                             Both sides:

12 / 41

19 / 41

9 / 41

5 /14

7/14

1/14

NS

NS

NS

Mass effect (%):

12 / 41(29.3%)

7/14 (50%)

0.05

Site of infarction:*  Cortical and subcortical:

                                             Capsular:

                                             Mixed:

                                             Lacunar:

11/ 41

18/ 41(43.9%)

29/ 41(70.7%)

3/ 41

5 /14

10 / 14 (71.43%)

12 / 14 (85.7%)

0 /14

NS

0.04

0.03

NS

*More than one finding may be present in the same patient.                   NS=Not significant

 

 

                     

Fig. (1) (A & B): Patient with subacute ischemic hemorrhagic infarction at right anterior parietal

region (high parietal) involving centrum semiovale (*NIHSS= 19 & **RBS= 348 mg/dl).

 

Fig. (2): Patient with lacunar infarct in anterior part of right corona radiate (*NIHSS=12 & **RBS=129 mg/dl).

Fig. (3): Patient with non-hemorrhagic infarction in anterior part of left internal capsule and anterior parietal region with no mass effect (*NIHSS= 18 & **RBS=278 mg/dl).

 

 

 

 

 

Fig. (4) (A & B): Hemorrhagic infarction in right frontoparietal region with mass effect.

(C): Extension to high parietal region (*NIHSS=22 & **RBS=469 mg/dl).

 

 

 

 

 

 

Fig. (5) (A & B): Patient with ischemic non-hemorrhagic infarction in anterior part of right internal capsule. (C & D): Multiple lacunar infarcts in right corona radiate &right centrum semiovale. Another small one is seen at left high parietal region (*NIHSS=19 & **RBS=458 mg/dl). 

 

 

 

 Fig. (6) (A, B & C): Non-hemorrhagic big sized infarction in right temporo-parietal region in the territory of right middle cerebral artery with mass effect (*NIHSS=24 & **RBS= 362 mg/dl).

*NIHSS = National Institute of Health Stroke Scale

**RBS= Random Blood Sugar at 1st presentation

 

 

Table 4. Study of the hyperglycemic group according to past history of diabetes.

 

Variables

Group II-a

(12\38)

Group II-b

(26\38)

P

NIHSS

Mean± SD

 

14.2 ± 6.6

 

13.5± 5.4

 

NS

MRsc

Mean± SD

 

3.3±2.2

 

2.7± 1.9

 

NS

IIa=No past history of diabetes

IIb=past history of diabetes


DISCUSSION

 

The severity of the clinical deficits in cerebral infarction was considered the major determinant of short-term functional outcome.5,12,13,14 Ages < 70 years, low NIHSS score ≤15, were considered independent predictors of good prognosis.15Low consciousness level on admission was found to reflect severe brain damage and predispose to the functional dependence of the survivors.16

In the present study 39 out of 55 patients (70.9%) were found to have NIHSS score ≥ 15 and 31 0f them (56.4%) were hyperglycemic at first presentation. This result agreed with previous works who found more than one third of patients (42.5%) admitted with acute stroke was hyperglycemic at presentation.17,18

In recent study; diabetes was present in 21% of cases of stroke.19 They found that stroke in diabetes had a specific clinical pattern and a poor prognosis in terms of motor function, which emphasize the need for early diagnosis and treatment. Hyperglycemia at admission was found to be significant predictor of functional outcome in acute cerebral infarction.14 It is associated with enhanced neuronal cell death and increased serum neuron specific enolase concentration.20 It leads to enhanced accumulation of extracellular concentration of excitatory aminoacids (glutamate) and such increase may correlate with histopathological outcome.21 It increases intracellular acidosis, brain edema formation, blood-brain barrier disruption, and tendency for hemorrhagic transformation.3 Insulin resistance and associated hyper-insulinemia have been observed in athero-embolic cerebral infarction suggesting endothelial dysfunction.22

In the present study; most of hyperglycemic group showed moderate to severe mRsc score (31.6% & 23.7% respectively, p<0.05). Els et al.23, study suggested that hyperglycemia in patients with a focal middle cerebral artery (MCA) ischemia can cause a worse clinical outcome despite re-canalization.

Admission hyperglycemia inversely correlated with NIHSS score in re-perfused cases as it counterbalances early restoration of blood flow.18 Hyperglycemia during acute cerebral infarction is detrimental only with reperfusion. This association appears to be linear in the glucose ranges tested (normal to high).23 In addition, there is an association between admission hyperglycemia and hemorrhagic conversion of an acute cerebral infarct when thrombolytics are used.24

In the present study; female patients showed significant worse outcome than male patients (p<0.03) (Table 3). Such result was documented before as female gender being significant predictor of handicap status.25

In the present study, the hyperglycemic group showed significant increased ages, high rate of atrial fibrillation (p<0.05) than euglycemic group (Table 1).

Old age, atrial fibrillation and level of consciousness are the major contributing factors for early and one year mortality.14,18,26,27 Other less common variables affecting outcome were leukocytic count, coronary artery disease and heart failure.14

In the study of deJong et al.28, they stated that diabetes, age, stroke subtype and initial clinical severity were independent predictors of 30- days case fatality. High urate level had greater effect on cerebral strokes in presence of diabetes.29

In the present study history of TIA was significant predictor of good outcome (p<0.05). Meanwhile; others stated that repeated TIA reflects the presence of active, unstable atherosclerotic plaque.14

CT scan was believed to have limited value for early prognostic purposes.30 It is well accepted that infarct size as detected by non- enhanced CT is a strong predictor of clinical outcome.12,31 Persistent hyperglycemia on serial glucose monitoring is an independent determinant of infarct expansion and is associated with worse functional outcome.32

Despite lacunar stroke had the lowest mortality; it cannot be regarded as a mild stroke type as >25% of such patients had died after 2 years.28

In the present study, the infarction volume in 7th day of admission increased significantly in hyperglycemic patients compared to normoglycemic group (p<0.01) and in those with worse clinical outcome despite medical re-canalization (p<0.007). Those with bad outcome showed significant mass effect than those with less mRsc (p<0.05) (Tables 2 and 3).

This result agreed with that of Engelter et al.31, who found that infarct volume ranged from 0.2 to 187 cm3 and correlated significantly with neurological deficit severity and outcome.

Dora et al.33, results have shown that hyperglycemia in the early subacute period after cerebral infarction is associated with more pronounced cerebral edema and has an adverse effect on short term prognosis. This may be explained by an accentuated lactate accumulation and PH decrease by elevated energy levels which cannot be compensated by restoration of blood flow alone.23,32

Haemorrhagic transformation affects treatment and prognosis in patients with acute cerebral infarction.34

In the present study; both groups (I & II) showed insignificant difference as regards hemorrhagic transformation, hypo-attenuation co-efficient on CT findings with no effect on outcome (Tables 2 and 3).

This result disagreed with that of Çelik et al.34, who concluded that there were independent relationships between mean blood glucose level on admission, mRsc, presence of diabetes mellitus, and MCA stem infarction and development of haemorrhagic transformation in patients with MCA territorial infarction.

DeReuck et al.9, found that patients in groups mRsc 0-1 had less X-ray attenuation on day 3, but no significant difference was found between the other 3 groups; despite being significantly correlated with severity of disability on day 10.

X-ray hypo-attenuation on CT is indicative of extended volumes of critically hypo-perfused cortical tissue35 and reflects the severity of ischemic damage.9 It also reflects the cytotoxic edema secondary to failure of ion pumps in response to inadequate supply of adenosine triphosphate.36 An increase in tissue water content by 1% results in a 2.5 HU decrease in parenchymal attenuation that corresponds to 3%-5% decrease in X –ray attenuation.37

Increase of X-ray attenuation on day 10 is known as the fogging effect and appears to be a favorable prognostic factor. Fogging is due to macrophage invasion and proliferation of capillaries within the infarct area and/or partial restoration of some viable tissue.9

Patients with hypoattenuation area ≥ one third of MCA territory should not prone to thrombolytic therapy.36  Patients with NIHSS score ≥ 20 with left or ≥ 15 with right cerebral infarction and > 50% MCA territory hypodensity are at high risk of fatal brain edema.38

Among the patients with hyperglycemia at admission (group I), the outcome and functional score did not differ significantly by past history of diabetes or not (Table 3).

 

Conclusion

Random blood  sugar level at time of acute cerebral infarction provides clinician with a low-cost test at a time when brain CT usually underestimate the real extent of brain infarction to early predict the severity of neurological deficits and short term outcome. Further studies are needed to show whether admission hyperglycemia has a role in pathophysiology of acute cerebral infarction and whether aggressive treatment of hyperglycemia would influence outcome. NIHSS score measurement is also beneficial but needs well training.

 

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الملخص العربى

 

العلاقة بين ارتفاع مستوى سكر الدم وقت دخول المستشفي

وشدة احتشاء الدورة الدموية المخية الأمامية الحاد الذى يحدث لأول مرة

 

تعتبر الصدمات المخية سببا رئيسيا للوفاة أو الاعاقة طويلة المدي- ويعتقد أن ارتفاع سكر الدم العشوائي وقت بداية الاصابة يتسبب في ازدياد سوء حالة  الأحتشاء المخي والناتج الوظيفي.

ولقد استهدفت الدراسة بحث العلاقة بين ارتفاع مستوي سكر الدم لحظة دخول المستشفي وسوء الحالة السريرية وتغيرات الأشعة المقطعية علي المخ والناتج الوظيفي قصير المدي – في مرضي الأحتشاء الحاد في الدورة الدموية المخية  الأمامية والذى يحدث لأول مرة.

وتمت الدراسة علي خمس وخمسين من المرضي المصابين باحتشاء حاد ( أقل من 24 ساعة) في الدورة الدموية الأمامية المخية في خلال 72 ساعة الأولي من بداية الأعراض0 وتم فحصهم سريريا ثم تحديد نوع الآصابة ومكانها في المخ - ثم تم تقييم شدة الحالة السريرية باستعمال مقياس الجمعية القومية لصحة الصدمات(NIHSS) لتحديد مدي اصابة الجهاز العصبي في اليوم السابع من الدخول.

وتم عمل أشعة مقطعية علي المخ بدون صبغة لجميع المرضي في اليوم الثالث واليوم السابع من بداية الصدمة المخية ومن خلالها تم قياس حجم الاحتشاء ورصد وجود الأوديما المخية أو وجود أية تغيرات نزفية وتم ايضا قياس درجة وهن الأشعة في منتصف الآحتشاء.

وتم تقسيم مجموعة المرضي الي مجموعتين حسب مستوى سكر الدم العشوائي وقت دخول المستشفي – المجموعة الأولي (1) وتكون من 17 مريضا (سكر الدم العشوائي أقل من 140 مج%) والمجموعة الثانية (2)  وتتكون من 38 مريضا (سكر الدم العشوائي 140 مج % فأكثر).

تمت مقارنة المجموعتين من حيث مقياس (NIHSS) والنتائج المعملية وضغط الدم الشرياني وقت دخول المستشفي وتغيرات الأشعة المقطعية0 ثم تمت متابعة الحالات لمدة شهر من تاريخ الدخول لتحديد الناتج الوظيفي باستخدام مقياس رانكين المعدل0 ثم تم تقسيم المرضي مرة أخري بناء علي نتائج مقياس رانكن الي مجموعتين: المجموعة (أ) وهم 41 مريضا أصحاب الناتج الأقل (3 فأقل) والمجموعة (ب) وهم 14 مريضا أصحاب الناتج الأعلي (أكثر من3 أو الوفاة داخل المستشفي) وتمت المقارنة بين المجموعتين مرة اخري لبحث العلاقة بين نتائج مقياس رانكن مع مستوي سكر الدم عند دخول المستشفي ومقياس(NIHSS)  وتغيرات الأشعة المقطعية.

وقد أظهرت النتائج أن الناتج الوظيفي حسب مقياس رانكن يتأثر احصائيا بمقياس (NIHSS ) الأولي وبمستوي سكر الدم العشوائي عند دخول المستشفي وضغط الدم المرتفع وحجم الاحتشاء في الأشعة المقطعية في اليوم الثالث من بداية الاصابة0 وأظهرت النتائج أيضا أن المجموعة (أ) كانوا أقل عمرا ومصابين باحتشاءات ذات احجام صغيرة عن المجموعة (ب) وأن المرضي الحاصلين علي (NIHSS)  15 درجة فأكثر كانوا مصابين باحتشاء المخ الأيسر وأوديما المخ0 ولوحظ أن التاريخ المرضي لمرض البوال السكري في المرضي من مجموعة (2) ليس له تأثير إحصائى علي شدة الإصابة أو الناتج الوظيفي.

 وقد خلصت الدراسة في أن قياس مستوي السكر العشوائي في الدم لمرضي الأحتشاء المخي الحاد للدورة الدموية المخية الأمامية عند دخولهم المستشفي يعتبر دلالة مستقلة تؤشر الي مدي سوء الحالة الإكلينيكية والمستقبل الوظيفي للاصابة وأن استخدام مقياس (NIHSS)   يقل في الأهمية عن مقياس السكر العشوائي لأنه يحتاج الي تدريب وخبرة اكلينيكية- ويعتبر حجم الأحتشاء في الأشعة المقطعية ايضا مؤشرا علي مدي شدة الإصابة الا أنه صعب القياس قبل 72 ساعة من بدء الاصابة0 أما عن وهن الأشعة في منتصف الأحتشاء أو التحول النزفي فلم يكن لهم دلالة إحصائية مؤشرة.



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