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July2005 Vol.42 Issue:      2 Table of Contents
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Clinical Pattern, MRI and Serum Soluble Intercellular Adhesion Molecule-1 (sICAM-1) in Neuro-Behcet Disease

Adel S. Abdel-Ghaffar1, Dorriya Abdul-Fattah1, Alaa M. Abdel-Ghani1, Mohamad A. Denewar2, Somaya M. Desouky3
Departments of Neurology1, Radiology2, Microbiology & Immunology3, Zagazig Universit

ABSTRACT

Behcet’s disease is a chronic multisystem disease. Neurological manifestations are relatively rare, but they must be investigated due to their grave prognosis. We designed this study to measure serum level of sICAM-1 in patients with neuro-Behcet disease, and investigate the possible relationship between its level, clinical activity of the disease and MRI findings. Twenty-three patients presenting with neuro-Behcet disease participated in this study. They were divided into two groups according to clinical course of the disease: group I, comprised 15 patients with relapse/remission course; group II, comprised 8 patients with progressive course. Serum sICAM-1 level was determined using ELIZA technique at two occasions (before and after treatment) for all patients. The levels were compared with those of 20 control healthy subjects age and sex matched. All patients underwent MRI brain examination for 2 times at corresponding dates for serum analysis of sICAM-1. Similarly, clinical evaluation of patients including the disability status scale was performed at the same occasions. Our patients ages ranged from 25-53 years( mean33.5±10.3) of whom 21 were males(91%) and 2 were females(9%).The mean serum sICAM-1 level was significantly higher in group I and group II patients on admission (375.4±67.4ng/ml and 278.75±41.4ng/ml respectively) than in the control group (205.8±36.6ng/ml). The serum level of sICAM-1 showed significant reduction in group I patients after treatment (remission phase) than before treatment (relapse phase) p<0.001, while in group II patients the reduction in its level did not reach statistical significance p=0.18. MRI brain revealed abnormal findings in all patients, demonstrated as extensive regions with high intensity signals on T2 weighted images. There was closely related association between MRI findings (size and number of lesions), serum levels of sICAM-1and clinical activity of the disease, in which clinically evident remission was associated with reduction in both serum levels and MRI findings. We concluded that both sICAM-1 and MRI study may be useful in assessing disease activity as well as in monitoring response to treatment.

(Egypt J. Neurol. Psychiat. Neurosurg., 2005, 42(2): 279-289).

 




 

INTRODUCTION

 

                Behcet’s disease (BD) is a chronic relapsing multisystem disorder of unknown etiology, affecting the eyes, skin, mucosa, joint, vascular system, gastrointestinal tract and nervous system1.

                The most widely accepted diagnostic criteria are those of the international study group (ISG)2. Although not included in these diagnostic criteria, there are some other features seen in patients with BD; thrombophlebitis, oligo-arthritis, GIT ulcerations and neurological involvement3.

                Neurological involvement is one of the most devasting manifestations of BD(4). The frequency of neurological manifestations- more common in male BD patients is between 5% and 30%5,6,7. Both the central (CNS) and peripheral nervous systems can be involved. CNS manifestations can divided into two main groups: (a) parenchymal involvement (neuroBehcet), which includes brain stem involvement, hemispheric manifestations, spinal cord lesions and meningioencephalitic presentation; (b) non-parenchymal involvement (vascular Behcet) 2ry to major vascular involvement, including dural sinus thrombosis, arterial occlusion, and/ or aneurysms. Peripheral neuropathy and myopathy are relatively rare5.

                The etiopathogenesis of BD remains unknown. When the disease was first reported, viral etiology was suggested, however, there was no evidence of direct infectious cause8,9. Antigenic cross-reactivity seems to be a better explanation, suggesting that BD has an immune nature10. SICAM-1 is a cell surface glycoprotein of endothelial cells that support the adhesion of leukocytes. It is a member of the immunoglobulin supergene family of adhesion molecules and reported to be involved in important steps of human response to infection and injury11.

                MRI is a very sensitive diagnostic method for detecting the CNS lesions of neuro-Behcet disease (NBD)4.

                In this study we measured the serum level of sICAM-1 in patients with NBD in an attempt to find out a possible relation between its level, clinical activity of disease and MRI findings.

 

PATIENTS AND METHODS

 

                We prospectively studied 23 patients with NBD, diagnosed primarily according to the international study group criteria for BD2 (table 1).


 

 

Table 1. International study group for Behat's disease criteria.

 

Recurrent oral ophatae plus two of:

At least three times in a  year

Genital ulcerations:

Active lesion or scar

Skin lesion:

Erythema nodosum, folliculitis, other ulcerations

Eye involvement:

Anterior or posterior uveitis, or retinal vasculitis

Positive pathergy test:

Skin hyper-reactivity to pinprick (Sterile pustule formed 24-48 hours)

 

 


Patients were divided into 2 groups according to the clinical course of the disease:

-       Group I: included 15 patients with relapse/remission course with evolving new neurological symptoms and/or signs of acute or subacute onset, lasting more than 24 hours and occurred at least 2 months after any previous attack.

-       Group II: included 8 patients with progressive course, with slowly evolving and worsening neurological symptoms and signs over months with no preceding attack (1ry progressive) or after at least one previous attack (2ry progressive).

 

Exclusion criteria:

                Patients without any evidence of objective neurological involvement, i.e. those with only headache or vague symptoms such as dizziness, patients who did not show any abnormalities by neurological examination, those with other possible explanation for their symptoms, and those not fulfilling the criteria for BD.

 

All patients were submitted to the following:

-       Careful history taking and full neurological examination, including the mini mental scale for cognitive function assessment, and the disability status scale which is graded from 1-5 according to the physical and mental dependence: 1= self sufficient (not depending on another person or any aid); 2= physically dependent (requiring help for walking or other motor activities); 3= mentally dependent( severe inappropriate behavior or dementia requiring another persons care); 4= both physically and mentally dependent; 5= dead( due to any cause related to BD)5.

-               The following laboratory investigations:

·    Complete blood count, erythrocyte sedimentation rate.

·    Urine analysis.

·    C reactive protein, rheumatoid factor, and antinuclear antibodies.

·    Serum sICAM-1 measurement: using the commercially available enzyme liked immunosorbant assay (ELISA) kit11 (Predica ICAM-1 Genzyme corporation– Cambridge, MAO2139). The test was done according to the manufactures instruction. Blood samples were collected from patients at 2 occasions: immediately after admission (during active or relapse phase) before starting treatment; and after remission or follow up period. Normal value: 140-255 ng/ml.

-       MRI brain was performed to all patients for 2 times using 0.5 T superconductive magnet (signa) GE medical system contour. All patients were examined in supine position using head coil. Sagittal, axial and coronal spin echo-images were obtained using multiple slice thickness varying from 3-7 mm. The sagittal scout T1 was done for localizing subsequent slice. Axial T1-W1 spin-echo pulse sequence was done with TR 1800-2500 msec.and TE 90 msec. Fluid attenuated inversion recovery (FLAIR) pulse sequence was done for all patients with the following parameters: TR 1694, TE 20-30 and T1 500 msec. Intravenous contrast gadolinium – DTPA dimaglumine was injected to all patients with a doze of 0.2 nmol/kg body weight. The method used to measure the total amount of visible MRI abnormality was reported in earlier study(12), in which the size and presence of lesions were recorded in 8 discrete areas of brain parenchyma( internal capsule, basal ganglia, frontal, parietal, temporal and occipital lobes, brain stem and cerebellum) and the periventricular areas. In each area the largest lesion was scored according to the longest diameter using a four point scale (0= 1 mm, 1= 2-5 mm, 2= 6-10 mm, 3> 10 mm). A total lesion score was obtained by adding scores from all the areas. For statistical purpose, lesions of grades 0 and 1 were considered as small sized lesions, lesions of grade 2 considered as medium sized and those of grade 3 large sized lesions.

 

Follow up:

                All patients were followed up for a period ranging from 6-33 months, i.e. after clinical remission regarding group I patients, and 9 months after receiving treatment regarding group II patients. After the follow up period all patients were submitted to:

-               Clinical evaluation including the mini mental state and the disability state scale.

-               Serum sICAM-1 measurement.

-               MRI brain.

                All patients received high dose corticosteroids immediately after extraction of the fist blood sample, MRI performance and clinical evaluation and then received maintenance dose.

                Finally, data were collected and data base processing was done using statistical package of social sciences and statistical analysis was performed by paired sample t test, unpaired t test, and Mc'Nemar chi-square (P<0.05) was considered significant.

 

RESULTS

 

                Twenty three patients with NBD participated in this study, of whom 21(91%) were males and 2 (9%) were females. Their mean age at the first evaluation was (33.5±10.3) ranging from 25-53 years. Mean age at onset of BD was 25.8±7.8 years and mean age at onset of neurological manifestations was 31.5±8.9 years with no significant difference between both groups of patients regarding age at onset of neurological manifestations .In 14 patients (61%) the neurological presentation was after the onset of other systemic symptoms of BD; in 5 patients (22%) the neurological onset was concomitant with the onset of BD; 4 patients (17%) had their neurological presentation as the first manifestation of BD, the other features appeared later.

                The mean duration of the disease was 4.6 years (ranging from 8 months to 11 years). Four patients (17%) had their disease for less than 12 months, 5 (22%) for between 12 and 24 months, 8 (35%) > 2 to5 years, and 6 (26%) for more than 5 years. The mean duration for first neurological presentation was 3.25 years. All patients were followed up for a mean period of 20.7 months (range from 6-33 months).

                The pattern of the first neurological presentation (table 2), included 3 well defined clinical forms: brain stem syndrome, cerebral stroke like and diffuse features. The characteristic features of these forms were as follows:

-       Brain stem syndrome (14 patients): characterized by sudden or acute onset , taking days to reach the peak deficit. The findings were commonly bilateral combination of cranial nerves (other than optic), cerebellar, or pyramidal signs. However, only 8 patients of these had isolated brain stem involvement. The remaining 6 patients had additional cognitive and psychiatric impairment (brain stem plus).

-       Cerebral-stroke like i.e. hemispheric involvement (6 patients): acute onset of unilateral neurological findings highly suggestive of stroke, with features suggesting cerebral involvement as seizures, which occurred in 2 patients.

-       Diffuse form (3 patients): pseudobulbar signs including emotional lability, spastic dysarthria, swallowing difficulty, exaggerated jaw jerk. In these cases other features of CNS involvement were reported including pyramidal signs, sphincteric disturbances and cerebellar signs.

               

Slowly evolving signs and symptoms were evident in 3 patients (namely those with the  primary progressive course).

                As regards the clinical signs and symptoms (table 3), the most common findings were; pyramidal signs, which were bilateral in 74% of cases. Eleven patients (48%) had various cranial nerves involvement including different types of ophthalmoplegias other than internuclear ophthalmoplegia, facial nerve affection either unilateral or bilateral, trigeminal nerve, bulbar signs, either isolated or in combinations. Cognitive impairment evolving over few weeks or months were present in 3 patients (13%) affecting predominantly memory and attention span, and one patient showed disinhibited behavior as noticed by his family.

                When comparing serum sICAM-1 levels between both groups of our patients and control group (table 4), we found that the mean levels were significantly higher in group I patients during the active phase (relapse) and group II patients before starting treatment on one hand than in the control group on the other hand. However, when we compared the change in serum sICAM-1 levels on admission and after follow up period in each group of patients (table 5), we found significant reduction in serum levels among group I patients in the remission or inactive phase than in the relapse or active phase. Group II patients did not show significant reduction in sICAM-1 levels after the follow up period than before treatment. There was a positive relation between the clinical course of the disease and the sICAM-1 levels in which the reduction in serum levels was accompanied by marked improvement of the neurological deficit (according to the disability status scale) in group I patients with complete remission in most patients after receiving treatment, except for 4 patients who experienced subsequent relapse later on due to discontinuation of corticosteroid therapy. On the other hand, no significant clinical improvement was detected in group II patients, moreover, three patients had subsequently undergone progressive deterioration leading to severe disability.

                MRI brain was done for all patients on admission (first time) and after the follow up period for a second time. Abnormal findings were detected in all patients; these findings are summarized in table (6). The most common lesion type was located in the basal ganglion region or in the brain stem extending to the diencephalic structures. The next most common lesion type was small scattered lesions in the basal ganglia, brain stem, hemispheric white matter lesions either periventricular or apart from the ventricles. As regards number of lesions in each group of patients, there was significant reduction in total lesion number in group I patients in the second MRI examination (after remission) than that performed on admission, while no marked reduction was noticed in group II patients. When we compared lesions size in each group of patients before and after the follow up, we found significant reduction in lesions size in group I patients in the second MRI, no lesions had enlarged, small new lesions were found in 5 patients and were asymptomatic clinically, new medium or large sized lesions were detected in 3 patients who had stopped treatment and had neurological relapse.


 

Table 2. Pattern of first neurological presentation in all patients.

 

Pattern

No. of patients (%)

Brain stem syndrome

14 (60.9%)

             - Isolated brain stem

8 (57.1%)

             - Brain stem plus

6 (42.9%)

Cerebral stroke like

6 (26.1%)

Diffuse

3 (13.0%)

Total

23 (100%)

 

 

Table 3. Cumulative frequency of neurological signs and symptoms in all patients.

 

Clinical features

No. of patients (%)

Pyramidal signs:

 

             - Bilateral

17 (73.9%)

             - Hemiparesis

6 (26.1%)

Cranial nerves

11 (47.8%)

Sphincter/impotance

6 (26.1%)

Cerebellar

6 (26.1%)

Pseudobulbar

3 (13.0%)

Sensory symptoms

4 (17.4%)

Psychiatric

3 (13.0%)

Cognitive

3 (13.0%)

Seizures

2 (8.7%)

 

 

Table 4. Mean serum sICAM-1 levels in both groups of patients on admission and in control group.

 

Groups

sICAM-1 mean±SD (Range)

t

P

Group I

375.4±67.4 (270-480)

8.57

<0.001

Group II

278.75±41.4 (210-335)

4.88

<0.001

Control

205.8±36.6 (140-254)

 

 

Table 5. Mean serum sICAM-1 levels in both groups of patients on admission (before-treatment) and after follow-up (after treatment).

 

sICAM-1

Groups

On admission

mean±SD (Range)

After follow-up

mean±SD (range)

Paired t

P

Group I

375.4±67.4 (270-480)

296.3±57.1 (215-380)

10.1

<0.001

Group II

278.4±41.4 (210-335)

268.5±41.1 (200-330)

1.3

0.10

 

Table 6. MRI findings on admission and after follow-up in both groups of patients.

 

Groups

 

MRI findings

Group I

Group II

On admission

After follow

P

On admission

After follow

P

No

%

No

%

No

%

No

%

Size of lesions

 

 

 

 

 

 

 

 

 

 

   - Small

25

34

39

66

<0.001

26

39.4

30

50

>0.05

   - Medium

32

43

13

22

<0.001

24

36.4

21

35

>0.05

   - Large

17

23

7

17

<0.001

16

24.2

9

15

>0.05

No. and site:

 

 

 

 

 

 

 

 

 

 

   - Brain stem

24

32

20

34

>0.05

30

46

31

52

>0.05

   - Basal ganglia

22

30

17

29

>0.05

18

27

13

22

>0.05

   - Cerebellum

19

26

18

31

>0.05

18

27

16

26

>0.05

   - Cortical and subcortical

5

7

2

3

>0.05

 

 

 

 

 

   - Periventricular

4

5

2

3

>0.05

 

 

 

 

 

Total

74

100

59

100

<0.05

66

100

60

100

>0.05

 

 

Fig. (1): T2WI of the brain of NBD showing multiple small periventricular hyperintense lesions.

 

  

Fig. (2): T1WI brain of NBD after IV contrast showing few occipital subcortical enhanced lesions.

 

 

 

 

Fig. (3): FLAIR of brain of NBD showed multiple brain stem and temporal lobe.

 

 

 

Fig. (4)

 

 

 

Fig. (5)

 

Figs. (4 and 5): FLAIR of brain showing two cases of NBD with multiple periventricular

and subcortical hyperintense lesions.


DISCUSSION

 

                The parenchymal CNS pattern is the most common form of presentation of BD with neurological manifestation7,13,14, while non-parenchymal form was reported in less than 20% of patients3.

                Our study included 23 patients with NBD (parenchymal form). The clinical pattern of presentation included 3 well defined clinical forms, namely; brain stem syndrome, cerebral stroke like and diffuse features. The incidence of brain stem involvement was high (60.9%), either isolated or combined with other features. This is in agreement with earlier studies5,15 who stated that NBD is commonly a motor-mental disorder with a predilection for the brain stem region. BD patients who complained of headache with no other neurological signs and symptoms were excluded from our study to avoid confusion and overestimation of neurological presentation of the disease, as these were mainly patients with primary headache syndromes (migraine and tension type headache). These types of headache are known to be prevalent in BD, but it is generally believed that they are not related to a direct involvement of the nervous system by this disorder5,6,16.

                Signs of motor dysfunction as manifested by the pyramidal signs and symptoms, were the most common cumulative neurological findings during the course of the illness (73.9%) - in agreement with previous reports5,6,7 - as these are the main disabling features of the parenchymal CNS presentation. Cranial nerves involvement including the optic nerve, cerebellar signs were next in frequency after the pyramidal findings, while sensory deficit was not common (17.4%). Interestingly, non of our patients had extrapyramidal features- despite the common involvement of the basal ganglia on MRI - a finding that was supported by previous study7, whereas hemichorea, hemiballismus and hemidystonia were encountered in 6% of cases in a previous report5. The neurological relapses in the course of the disease (group I) commonly took the same pattern as the presentation, but less commonly different patterns had occurred. The same finding was reported by others4,13,15. Assessing the cognitive and neuropsychological status of our patients revealed memory impairment, attention span deficit, disinhibited behavior  and psychotic features in the same order regarding frequency of presentation. The neuropsychological status deteriorated insidiously during the follow up period especially in group II patients, a finding that is supported by a previous author17, who postulated that the late stages of the disease seem to be reflected on MRI as an enlargement of the third ventricle and atrophy of the upper brain stem, which could be compatible with memory loss.

                Serum sICAM-1 levels were higher in patients than in controls. The difference was more marked between group I patients during the relapse and control subjects. Moreover, serum levels were significantly higher in the same group of patients during the relapse phase than those in remission. We found positive relation between clinical course of the disease and serum sICAM-1 levels, in which marked improvement of the clinical status was associated with significant reduction in serum levels. This is in agreement with earlier reports18,19,20 who added that, the elevated levels of sICAM-1 may be due to endothelial cell activation and/or damage, or may be the result of inflammation. As regards patients with the progressive course(group II), there was no noticeable reduction in sICAM-1 levels before and after the follow up period and was associated with lack of clinical improvement or even progressive increase in the disability state.

                In our study MRI brain showed positive findings in all cases, in which the plaques were recognized as hyperintense parenchymal lesions on T2 weighted images and bright focal lesions on FLAIR sequence. In acute lesions edema and enhancement were present in the majority of cases. The most prevalent lesions were located in the brain stem and basal ganglia, with the periventricular distribution being uncommon (5%). This is in agreement with other studies6,7 who reported that the most common lesions were located in the brain stem, basal ganglia and internal capsule, next to these are scattered lesion in the hemispheric white matter either periventricular or away from the ventricles. Where as in other papers no periventricular lesions – which are characteristic to multiple sclerosis- were observed in their series7,15.

                Evaluation of treatment choices is beyond the scope of this paper, however after high doze corticosteroid treatment, patients within group I showed marked clinical improvement, MRI lesions gradually reduced in size and were no longer enhanced. These findings suggest that abnormal MRI features in NBD are potentially reversible and that radiographic improvement parallels clinical improvement. This is in consistency with others21,22 who reported that at least partial disappearance of abnormal MRI findings takes place after resolution of clinical attack. On the other hand, in group II patients no such improvement could be detected in both clinical manifestations and MRI study after the follow up period. These findings suggest that NBD should comprise two distinct immuno-pathogenetic stages, that is a relatively steroid- responsive stage with relapsing/ remitting clinical course and a late steroid- non responsive stage with a chronic progressive course.

                We conclude that serum sICAM-1 seems to be related to disease activity in NBD, and that both brain MRI and sICAM-1 may be useful in monitoring the clinical status of patients and therapeutic response for this disease. 

 

REFERENCES

 

1.      Yazici h, Yurdacul S, and Hamury V (1999). Behcet’s syndrome. Rheumatol; 11:53-57.

2.      International study group for Behcet’s disease (1990). Criteria for diagnosis of Behcet’s disease. [review]. Lancet; 335:1087-1080.

3.      Hamuryudan V, Mat C, Saip S, Ozyazgan Y, and Siva Y (1998). Thalidomide in the treatment of the mucocutaneous lesions of Behcet’s syndrome. Ann Intern Med; 128: 443-450.

4.      Serdaroglu P (1998). Behcet’s disease and nervous system. J Neurology, April; 245(4): 197-205.

5.      Akman-Demir G, Serdaroglu P, Tasci B, and the neuro-Behcet study group (1999). Clinical patterns of neurological involvement in Behcet’s disease: evaluation of 200 patients. Brain; 122; 2171-2181.

6.      Kidd D, Steuer A, Denmam AM, and Rudge P (1999). Neurological complications in Behcet’s syndrome. Brain; 122: 2183-2194.

7.      Al-Araji A, Sharquie K, and Al-Rawi Z (2003). Prevalence and patterns of neurological involvement in Behcet’s disease: a prospective study from Iraq. J Neurol Neurosurg Psychiatry ; 74: 608-613.

8.      Eglin RP, Lehner T, Subak-Sharpe JH (1982). Detection of RNA complementary to herpes simplex virus in mononuclear cells from patients with Behcet’s syndrome and recurrent oral ulcers. Lancet; 2: 1356-1361.

9.      Behcet’s disease research committee of Japan (1989). Skin hypersensitivity to streotococcal antigens and the induction of systemic symptoms by the antigens in Behcet’s disease- a multicenter study. J Rheumatol; 16: 506-511.

10.    Saruhan- Direskeneli, Akman-Demir G, Tascib, Sedaroglu P, Eraksoy M (1996). Local synthesis of oligoclonal IgG is infrequent in Behcet’s disease . Rev Rheumatol; 63 Suppl: 552.

11.    Bevillacque MP (1993). Intracellular adhesion molecule-1; Eliza for quantitation of ICAM-1. Ann Rev Immunol; 11: 767.

12.    Ormerod IEC, Miller DH, Mc Donald WZ (1987). The role of MR imaging in the assessment of multiple sclerosis and isolated neurological lesions: a quantitative study. Brain; 110: 1597-1616.

13.    Serdaroglu P, Yazici H, Ozdemir C (1989). Neurological involvement in Behcet syndrome: a prospective study. Arch Neurol; 46: 265-269.

14.    Al- Fahad S, Al-Ragi A (1999). Neuro-Behcet’s disease in Iraq: a study of 40 patients. J Neurol Sci; 170: 105-111.

15.    Coban O, Bahar S, Akman-Demir G, Serdaroglu P, Baykan-Kurt B (1999). Masked assessment of MRI findings: is it possible to differentiate NBD from other central nervous system diseases?. Neuroradiology; 41: 255-260.

16.    Siva A, Kantarci OH, Scip S (2001). Behcet’s disease: diagnostic and prognostic aspects of neurological involvement. J Neurol; 248: 95-103.

17.    Oktem- Tanor O, Baykan- Kurt B, Gurvit IH, Akman- Demir G, Serdaroglu P (1999). Neuro-psychological follow up of 12 patients with neuro-Behcet disease. J Neurol. Feb; 246(2): 133-119.

18.    Aydintug AO, Tokgoz G, Ozoran K, Duzgun N, Gurler A, Tutkak H (1995). Elevated levels of soluble intercellular adhesion molecule-1 correlate with disease activity in Behcet’s disease. Rheumatol Int; 15(2): 75-78.

19.    Verity DH, Wallace GR, Seed PT, Kanawati CA, Ayesh I, Holland- Gladwish J, Stanford MR (1998). Soluble adhesion molecules in Behcet’s disease. Occul Immunol Inflamm. June; 6 (2): 81-92.

20.    Saglam K, Yilmaz MI, Saglam A, Ulgey M, Bulucu F, Baykal Y (2002). Levels of circulating intercellular adhesion molecule-1 in patients with Behcet’s disease. Rheumatol Int. Jan; 21(4): 146-148.

21.    Lee SH, Yoon PH, Park Sg (2001). MRI findings in neuro- Behcet’s disease. Clin Radiol; 56: 485-494.

22.    Kocer N, Islak C, Siva A, Saip S, Akman C, Rantarci O, Hamuryudan V (1999). CNS involvement in neuro-Behcet syndrome: an MRI study. Am J NR; 20: 1015-1024.


 

 

الملخص العربي

 

الشكل الإكلينيكي والرنين المغناطيسي والجزىء الإلتصاقي الخلوي الذائب-1

للظواهر العصبية في مرضي بهجت

 

          اشتملت هذه الدراسة على ثلاثة وعشرين مريضا يعانون من مرض بهجت مصحوبا بالأعراض العصبية وتم تقسيمهم إلى مجموعتين على أساس تطور المرض. المجموعة الأولي: تضم خمسة عشر مريضا وكان تطور المرض بهم ما بين زيادة وكمون. أما المجموعة الثانية: تضم ثمانية مرضي وكان تطور المرض بهم في زيادة مستمرة. بالإضافة إلى المجموعة الثالثة الضابطة.

          وتم إجراء الفحص الإكلينيكي والفحص بالرنين المغناطيسي للمخ وقياس مستوي الجزئ الالتصاقي الخلوي الذائب-1 في مصل المرضي مرتين علي مدار تطور المرض بالإضافة إلى الفحوصات العادية لهذا المرض.

          ولقد أظهرت الدراسة ارتفاع ذو دلالة إحصائية في مستوي الجزئ الإلتصاقي الخلوي الذائب-1  في مصل كل المرضي بالمقارنة بالمجموعة الضابطة وقد أرتبط ذلك المستوي بشدة المرض.

          وقد أظهرت الدراسة أيضاً الدور المهم للرنين المغناطيسي في تحديد ومتابعة التغيرات الباثولوجية لإصابات المخ المؤدية إلى التطور الإكلينيكي لهذا المرض.

          وبذلك يتضح أنه هناك علاقة متوازية بين التغيرات الموجودة بالرنين المغناطيسي للمخ ومستوي الجزئ الإلتصاقي الخلولي الذائب-1 وتطور الأعراض العصبية في مرضي بهجت.



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