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July2007 Vol.44 Issue:      2 Table of Contents
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Motor Evoked Potential in Presymptomatic Spondylotic Cervical Cord Compression

Inas Shaheen1, Walid Al Saadany2, Ghada A. Osman3

Departments of Physical Medicine, Rheumatology and Rehabilitation1,

Neurosurgery2, Neurology3, Alexandria University



ABSTRACT

Background: Cervical spondylotic myelopathy (CSM) is the most severe consequence of degenerative disease of cervical spine as it is usually a chronic and progressive disease. Despite advances in diagnosis and surgical treatment, many patients still have severe permanent neurologic deficits caused by this condition. An early measure (s) is highly needed to detect preclinical manifestations of such condition. Aim: is to investigate whether electrophysiological parameters of Motor Evoked potential (MEP) could detect clinically asymptomatic (preclinical) spondylotic cervical cord compression before progression to symptomatic myelopathy and to compare between MEP and Somatosensory Evoked Potential (SEP) in this regard. Subjects: Twenty patients with clinical and radiological (plain X-ray and MRI) features of spondylotic cervical root compression, but without clinical or radiological evidence of cervical myelopathy were included in the study. Fifteen healthy subjects, matching in age and sex were included as a control group. Methods: A modification of the Japanese Orthopedic Association Scale (mJOA) was used to confirm the functional status of the patients. The following procedures were carried out bilaterally for patients and unilaterally for control subjects. Percutaneous transcranial magnetic stimulation (TMS) was carried over the corresponding motor cortices of the upper and lower limbs  to elicit MEP. SEP of both median and posterior tibial nerves was recorded  as well. Results: The mean age of patients was 52.7±6.2 years; the majority of them were males (60%). The mean duration of illness was 3.36±1.5 years. There were 6 patients (30 %) with mJOA score of 17 and 14 patients (70 %) with mJOA score of 18. The mean score of mJOA scale was 17.73±0.45. The mean age of control subjects was 48.8±4.5 years. Both plain X- ray and MRI revealed cervical spondylotic changes from C4 to C7 in the form of intervertebral disc degeneration and osteophytosis of vertebral bodies. Indentations of the dural sac on MRI were observed at C5/6, C6/7 and C4/ 5 intervertebral levels in order of incidence. However, the cord was reportedly normal. Central motor conduction time (CMCT) was prolonged in 6 patients. Three of those patients had bilaterally prolonged CMCT. In the other 3 patients CMCT was unilaterally prolonged. MEP amplitude didn't show significant abnormality among patients. There was no significant difference in patients' SEP latencies or amplitudes when compared to control subjects. Conclusion: MEP provides an objective and quantitative approach to assess the motor functional integrity of the corticospinal pathways. Measurement of CMCT could serve as a detector of subclinical spondylotic cervical cord involvement before progression to symptomatic mylopathy even earlier than SEP can do.

(Egypt J. Neurol. Psychiat. Neurosurg., 2007, 44(2): 713-721)

 




INTRODUCTION

 

Cervical spondylotic myelopathy (CSM) is a condition in which degenerative changes of the cervical vertebral bodies and the intervertebral discs cause disturbances to the spinal cord either by direct mechanical compression or by disturbing the blood supply.1 It is the most severe consequence of degenerative disease of cervical spine as it is usually a chronic and progressive disease.2 Despite advances in diagnosis and surgical treatment, many patients still have severe permanent neurologic deficits caused by that condition.3 An early measure (s) is highly needed to detect preclinical manifestations of such condition.

Involvement of neurologic structures on imaging studies may be asymptomatic, as compression of the spinal cord does not always cause clinical symptoms.4 Multiple dural sac and spinal cord indentations are often observed on magnetic resonance imaging (MRI) in CSM. However, it is rare that all of the indented levels contribute to clinical symptoms. Still the critical degree of spinal cord compression needed to induce pathologic changes is unknown. Moreover it is difficult to infer the degree of dysfunction of the spinal cord from MRI findings alone.5 Signal intensity changes of the spinal cord on MRI in CSM are thought to be indicative of the prognosis. However, the prognostic significance of signal intensity changes remains controversial.6 Some studies have not found a correlation between neurological function and the presence of spinal cord signal change on T2-weighted MRI scans.7,8

Previous studies evaluating neurologic function and predictability of surgical results in CSM patients always depended on the morphologic changes of the cord and spinal structures. Motor Evoked Potential (MEP) is a noninvasive measurement of central motor conduction time (CMCT) that may provide an objective method to evaluate physiologic motor function in CSM patients.9

The aim of this study is to investigate whether electrophysiological parameters of MEP could detect clinically asymptomatic (preclinical) spondylotic cervical cord compression before progression to symptomatic myelopathy and to compare between MEP and Somatosensory Evoked Potential (SEP) in this regard.

 

PATIENTS AND METHODS

 

Twenty patients with clinical and radiological (plain X-ray and MRI) features of spondylotic cervical root compression10,11, but without clinical or radiological evidence of cervical myelopathy were selected from those attending the outpatient clinic of Physical Medicine, Rheumatology and Rehabilitation, Neurosurgery and Neurology Departments, Faculty of Medicine, University of Alexandria. Radiologic features of spondylotic cervical radiculopathy were obtained by MRI that also revealed absence of either T1 or T2 weighted images cervical cord compression but just dural indentations.7,12

A modification of the Japanese Orthopedic Association Scale (mJOA) for functional assessment of cervical spondylotic myelopathy was used to confirm patients' functional status.13 The scale assess motor dysfunction of the upper extremities (0-5 scores) and lower extremities (0-7 scores), as well as sensory dysfunction of the upper extremities (0-3 scores), in addition to sphincter dysfunction (0-3 scores). The maximum score is 18 which denotes absence of any motor, sensory or sphincter dysfunction.  

Patients were excluded if they had other central or peripheral neurological conditions or subjected to previous cervical spine surgery and/or trauma. Those having any contraindication for transcranial magnetic stimulation (TMS) were also excluded.14

Fifteen healthy subjects, matching in age and sex were included as a control group. They were included on the basis of absence of clinical or radiological manifestations of spondylotic cervical radiculopathy or myelopathy.

 

The following procedures were carried out bilaterally for each patient and unilaterally for control subjects:

1-      Percutaneous TMS over the corresponding motor cortices of the upper and lower limbs to elicit MEP in order to evaluate the neurofunctional integrity of the central motor pathway.15 Stimulation was performed by a single pulse stimulator, Magstim 200 (Magstim company, Whitland, Wales, UK), equipped with a high power 90 mm circular coil, capable of generating 2 tesla maximum field intensity. Testing protocol was carried out according to the International Federation of Clinical Neurophysiology criteria for magnetic stimulation of the brain.16

Muscle responses (MEP) were recorded on a Nihon Kohden (Neuropack 2) electrophysiological apparatus, with 7 mm surface disc electrodes. The active electrode was placed over the belly of the abductor pollicis brevis (APB) and abductor hallucis (AH) muscles (belly-tendon montage). Filter was set to 3 Hz- 3 KHz. Gain was set at 0.5-2 mV/division, according to the amplitude of the response. Time base was set at 5 -10 ms/ division for upper and lower limbs respectively.16

Compound muscle action potential (CMAP) and F-wave were recorded from APB and AH muscles with unchanged recording electrodes position following supramaximal electrical stimulation of median and posterior tibial nerves at the wrist and ankle respectively.17,18 Peripheral conduction time, which included synaptic delay in spinal motor neurons, was measured as follow (latency of CMAPs + latency of F-wave + 1)/2 (ms). The central motor conduction time was measured by subtracting the peripheral conduction time from the shortest onset latency of the MEP.19 The cut off value for CMCT was calculated as the mean CMCT + 2SD of the healthy control group.

The peak to peak maximal amplitude of MEPs was determined and expressed as a ratio of the peak to peak amplitude of CMAP as follow (MEP maximal amplitude / CMAP maximal amplitude).16 The cut off value for MEP amplitude was calculated as the mean amplitude ratio - 2SD of the healthy control group.

2-      Mixed nerve SEPs of the median and posterior tibial nerves were recorded to evaluate the neurofunctional integrity of the central sensory pathway.20 Scalp- scalp montage (10-20 system)21 was used for recording of SEPs; where C3'- Fz and C4'- Fz were the recording montage for right and left upper limbs respectively. Cz - Fpz was the recording montage for lower limbs. Median nerve was electrically stimulated at wrist; posterior tibial nerve was stimulated at ankle.22 Testing protocol was carried out according to the Evoked potentials Committee of the American Association of Electromyography and Electrodiagnosis.23 Parameters of SEP included latency (N 20 & P37 for upper & lower limbs respectively) and peak to peak amplitude. The cut off value for SEP latency was calculated as the mean latency + 2SD, while that for SEP amplitude was calculated as the mean amplitude - 2SD of the healthy control group.

All patients and control group were informed about the nature of the study and written acceptance consent was signed by each subject.

 

Statistical Methods:

All statistical procedures were performed using SPSSTM version 11.0. Descriptive statistics were used to present the sample characteristics. Case - control comparisons were done using Student's t-test. P values ≤ 0.05 were considered statistically significant.

 

RESULTS

 

The mean age of patients was 52.7±6.2 years; the majority of them were males (60 %). The mean duration of illness was 3.36±0.5 years. There were 6 patients (30 %) with mJOA score of 17 and 14 patients (70 %) with mJOA score of 18. The mean score of mJOA scale was 17.73±0.45.

The mean age of control subjects was 48.8± 4.5 years; the majority of them were males (60%). No statistically significant difference was found between patients and control subjects as regards age and sex (p>0.05).

The most frequent presenting symptom was upper extremity sensory complaints (100 %) (8 patients (40%) had bilateral brachialgia and 12 patients (60 %) had unilateral brachialgia). The majority of patients with unilateral brachialgia had right side affection (8 patients), while the left side was involved in 4 patients. Neck pain was present in 11 patients (55%).

Objective sensory deficits were present in the form of hypoesthesia in 6 patients (3 patients had hypoesthesia at C6,7 distribution, 2 patients at C5,6 distribution and one patient at C7 distribution). Hyperesthesia was found in 2 patients (one patient at C6 and the other one at C7 distribution). No objective motor weakness was encountered.

Deep tendon reflexes were damped in 5 patients. Right biceps reflex was damped in two patients and it was bilaterally damped in one patient. Left triceps reflex was damped in 2 patients.

Neither sphincter nor lower limb dysfunction was encountered among all patients.

Both plain X- ray and MRI revealed cervical spondylotic changes from C4 to C7 in the form of intervertebral disc degeneration and osteophytosis of vertebral bodies in all patients.

Indentations of the dural sac on MRI were observed at C5/6, C6/7 and C4/ 5 intervertebral levels, in order of incidence. However, the cord was reportedly normal. The C4-5 intervertebral level was involved in 3 patients, who were 60 year old and older.

Table (1) demonstrates normal MEP and SEP parameters in control subjects and their cut off values.

CMCT1: CMCT calculated after median nerve stimulation. Amp1: amplitude ratio of MEP after median nerve stimulation. CMCT2: CMCT calculated after posterior tibial nerve stimulation. Amp2: amplitude ratio of MEP after posterior tibial nerve stimulation.

Lat1: SEP latency recorded by median nerve stimulation. Ampl1: amplitude of SEP recorded by median nerve stimulation. Lat2: SEP latency recorded by posterior tibial nerve stimulation. Ampl2: amplitude of SEP recorded by posterior tibial nerve stimulation.

The calculated CMCT after stimulation of both median and posterior tibial nerves was abnormally prolonged in 6 patients. Three of those 6 patients had bilaterally prolonged CMCT, they were the same elderly patients with C4-5 involvement. In the other 3 patients CMCT was unilaterally prolonged (2 patients had right side prolonged CMCT and 1 patient had left side prolongation). On the other hand, MEP amplitude and SEP parameters were within the normal limits in those patients. Table 2 presents the MEP and SEP parameters of those 6 patients.

CMCT1: CMCT calculated after median nerve stimulation. Amp1: amplitude ratio of MEP after median nerve stimulation. CMCT2: CMCT calculated after posterior tibial nerve stimulation. Amp2: amplitude ratio of MEP after posterior tibial nerve stimulation.

Lat1: SEP latency recorded by median nerve stimulation. Ampl1: amplitude of SEP recorded by median nerve stimulation. Lat2: SEP latency recorded by posterior tibial nerve stimulation. Ampl2: amplitude of SEP recorded by posterior tibial nerve stimulation.

There was a statistically significant difference in the calculated CMCT after stimulation of both median and posterior tibial nerves of patients as compared to control subjects (p = 0.021 & 0.035 respectively) while, the amplitude of MEP didn't show statistically significant difference between patients and control subjects (Table 3).

CMCT1: CMCT calculated after median nerve stimulation. Amp1: amplitude ratio of MEP after median nerve stimulation. CMCT2: CMCT calculated after posterior tibial nerve stimulation. Amp2: amplitude ratio of MEP after posterior tibial nerve stimulation.

There was no significant difference in the median or posterior tibial SEP latency and amplitude among patients and control subjects (Table 4).

Lat1: SEP latency recorded by median nerve stimulation. Ampl1: amplitude of SEP recorded by median nerve stimulation. Lat2: SEP latency recorded by posterior tibial nerve stimulation. Ampl2: amplitude of SEP recorded by posterior tibial nerve stimulation.

Table 1: Motor Evoked Potential(MEP) and Somatosensory Evoked Potential(SEP) parameters in control subjects.

 

Parameters

Controls

N=15

Cut off value

Mean ± SD

+2SD

-2 SD

CMCT1(ms)

3.64 ± 0.69

5.02

 

Amp1

0.48 ± 0.09

 

0.30

CMCT2(ms)

11.20 ± 0.77

12.74

 

Amp2

0.12 ± 0.03

 

0.06

Lat1(ms)

20.19 ± 0.89

21.97

 

Ampl1(µV)

5.72 ± 0.32

 

5.08

Lat2(ms)

41.20± 1.91

45.02

 

Ampl2(µV)

7.14± 1.11

 

4.92

 


Table 2: Motor Evoked Potential and Somatosensory Evoked Potential parameters of 6 patients with abnormally prolonged central motor conduction time(CMCT).

 

Patient

Side

CMCT1

(ms)

Amp1

CMCT2

(ms)

Amp2

Lat 1

(ms)

Ampl1

(µV)

Lat 2

(ms)

Ampl2

(µV)

1

Rt

8.20

0.31

18.5

0.10

19.9

6.00

38.0

7.00

Lt

8.65

0.34

18.0

0.20

18.8

6.20

39.0

6.05

2

Rt

10.4

0.61

17.0

0.08

19.8

5.90

42.2

8.30

Lt

11.7

0.50

17.3

0.08

20.0

5.10

43.0

8.75

3

Rt

12.6

0.32

18.9

0.10

20.1

5.80

40.0

7.30

Lt

11.8

0.30

18.3

0.20

20.2

5.80

40.5

7.20

4

Rt

7.85

0.70

16.4

0.08

21.2

7.50

39.0

6.00

Lt

4.30

0.60

10.9

0.10

20.1

6.30

39.4

7.60

5

Rt

7.60

0.80

15.6

0.07

21.0

6.10

42.5

5.50

Lt

4.20

0.71

12.2

0.08

18.9

5.70

41.5

5.80

6

Rt

4.80

0.42

10.0

0.05

19.8

5.90

40.9

6.83

Lt

9.70

0.40

14.9

0.09

20.8

5.60

42.0

8.00

 

Table 3: Central motor conduction time (CMCT) and Motor Evoked Potential(MEP) amplitude in patients and control subjects.

 

Variables

Patients

N=40

Controls

N=15

t

P

Mean

Std. Deviation

Mean

Std. Deviation

CMCT1(ms)

5.56

3.06

3.64

0.69

2.393*

0.021

Amp1

0.46

0.14

0.48

0.09

0.365

0.717

CMCT2(ms)

12.93

3.00

11.20

0.77

2.178*

0.035

Amp2

0.11

0.07

0.12

0.03

0.431

0.668

P: significant if ≤ 0.05.

Table 4. Somatosensory Evoked Potential(SEP) latency and amplitude in patients and control subjects.

 

Variables

Patients

N=40

Controls

N=15

t

P

Mean

Std. Deviation

Mean

Std. Deviation

Lat1(ms)

20.14

0.84

20.19

0.89

0.183

0. 855

Ampl1(µV)

5.78

0.45

5.72

0.32

0.479

0. 635

Lat2(ms)

40.98

1.78

41.20

1.91

0.381

0. 705

Ampl2(µV)

7.11

1.07

7.14

1.11

0.112

0. 911

P: significant if ≤ 0.05.

 

 


DISCUSSION

 

Cervical spondylotic myelopathy (CSM) is a condition; where the vascular and neural structures are compressed by bony spurring and soft tissue hypertrophy as well as intervertebral disc; which causes ischemic damage to the spinal cord. The diagnosis is often missed since the initial symptoms are subtle and the condition usually presents with associated conditions such as nerve root involvement.24 Combined CSM (Lateral & Medial) which includes both nerve root and asymmetric long tract damage, is by far the most common type of CSM. Clinically, patients with combined CSM may present with what appears to be simple cervical nerve root involvement.25

Early diagnosis of CSM is important since failure to recognize and properly treat the disorder can result in permanent cord damage with irreversible related neurologic deficits. Previous studies evaluating neurologic function and predictability of surgical results in cervical spondylotic myelopathy patients always depended on the morphologic changes of the cord and spinal structures.13 Motor Evoked Potential study and noninvasive measurement of CMCT provide an objective method to evaluate physiologic motor function in CSM patients.9

In this study, eight patients had objective sensory deficits, no motor or sphincter disturbance was encountered. The functional status of patients was not affected by their cervical pathology. The mean score of mJOA scale came out high due to the good functional status of all patients under the study.

T1 and T2-weighted MRI did not show any cervical cord compression or vascular insult in all patients under this study, but just dural indentations at C5/6, C6/7 and C4/5 intervertebral levels. However, six patients showed variable degrees of CMCT abnormalities. The recent study of Fernandez et al.26 and the earlier study of Yone et al.27 have reported that the presence or absence of a high intensity area on T2-weighted images did not correlate with the severity of myelopathy or with surgical results in CSM patients.

Patient- control comparison revealed a significant difference regarding CMCT after stimulation of both median and posterior tibial nerves, while SEP did not show this difference. This could be due to the fact that, the pathologic course of cervical spondylotic myelopathy is characterized by early involvement of the corticospinal tracts and later destruction of anterior horn cells, demyelination of lateral and dorsal tracts.28-30 As ischemic damage in CSM is often greatest in the anterolateral white and the central gray matter of the cord, the pyramidal tracts are often the first to be involved, and often most severely, next the spinothalamic tracts and later possibly the posterior columns.28 Patients under this study may also show SEP changes if their disease course progress worse. Follow up of those patients for at least one year is recommended to detect any subsequent clinical or electrophysiological changes.

In the present study, MEP showed abnormalities in CMCT but not in amplitude. CMCT represents conductivity in corticospinal tracts, while MEP amplitude measures excitability of cortical motor neurons.14  Previous studies have shown that demyelination was distributed in the lateral white matter of CSM patients, with the existence of thin myelinated fibers. This indicates that focal demyelinating and remyelinating processes occur in CSM.12,31 It appears that these two processes are responsible for CMCT prolongation.

In the current study, 3 patients had C4-5 intervertebral level involvement; they were 60 year old and older. Previous studies have found that the upper disc levels of C3-4 and C4-5 have a tendency to be involved in the elderly patients, with higher incidence of spinal cords compression as compared with the younger patients.32 In elderly patients the lower cervical segments show less mobility than the upper cervical segments reflecting the degree of bony degeneration. By contrast, an excessive compensatory movement imposed on the C3-4 and the C4-5 segments that would cause instability, leading to spinal cord compromise.33 Those patients also showed bilaterally prolonged CMCT which could be explained by the high vulnerability of the upper cervical cord levels to vascular ischemia. Ischemic compression of the anterior spinal artery, that supplies 60% - 70% of the cord, mainly the pyramidal, spinothalamic tracts and the anterior horns, is the primary cause of the myelopathy in elderly patients.4 

Patients with subclinical CSM who had abnormally prolonged CMCT have to be followed up for at least one year to record their neurological and functional status and properly managed.  

 

Conclusion:

MEP provides an objective and quantitative approach to assess the motor functional integrity of the corticospinal pathways. Measurement of CMCT could serve as a detector of subclinical spondylotic cervical cord involvement before progression to symptomatic myelopathy even earlier than SEP can do.

TMS can be considered as an effective, rapid, inexpensive and non-invasive technique for screening patients for cervical cord abnormalities before MRI studies in the clinical setting.

The findings in this study have relevant implications in the pathophysiology, management, and health costs of cervical spondylotic myelopathy.

 

REEFRENCES

 

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8.      Morio Y, Yamamoto K, Kuranobu K, et al. Does increased signal intensity of the spinal cord on MR images due to cervical myelopathy predict prognosis?. Arch Orthop Trauma Surg 1994; 5:254-9.

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الملخـص العربى

 

 الجهد الحركى المستحث فى ما قبل ظهور أعراض انضغاط الحبل الشوكى العنقى الروماتيزمى العظمى المفصلى

 

الخلفية :

انضغاط الحبل الشوكى العنقى الروماتيزمى العظمى المفصلى يعد من اكثر تبعيات انحلال الفقرات العنقية خطورة, حيث أنه يعد مرضا مزمنا ومتزايدا. وعلى الرغم من التقدم فى أساليب التشخيص والعلاج إلا أن كثيرا من المرضى يعنون من عجز عصبى نتيجة هذا المرض. لذلك وجبت الحاجة الى وسيلة للكشف عن أعراض ذلك المرض قبل حدوثها, حيث أن الرنين المغناطيسى وحده لا يستطيع تحيد درجة تأثر الحبل الشوكى بمثل هذا المرض من الناحية الوظيفية.

هدف البحث :

معرفة اذا كان الجهد الحركى المستحث قادرا على كشف انضغاط الحبل الشوكى العنقى الروماتيزمى العظمى المفصلى قبل ظهور أعراضه وكذلك المقارنة بينه وبين الجهد الحسى المستحث فى هذا الغرض.

أشخاص البحث :

عشرون مريضا يعانون من ضغط بجذور الأعصاب العنقية نتيجة الروماتيزمى العظمى المفصلى بدون اعراض سريرية إو إشعاعية لانضغاط الحبل الشوكى العنقى. بالإضافة الى 15 شخصا يضاهونهم فى السن و الجنس كمجموعة ضابطة.

طرق البحث :

تم قياس الحالة الوظيفية للمرضى باستخدام المعيار المحور للجمعية اليابانية للعظام. كما أجرى تنبيه مغناطيسى للقشرة المخية للمرضى للطرفين العلويين والسفليين لاستثارة جهد حركى لتقييم سلامة الوظيفة العصبية للمسار الحركى المركزى. كذلك تم قياس الجهد الحسى المستحث لعصبى الوسطى والعصب الساقى الخلفى لتقييم سلامة الوظيفة العصبية للمسار الحسى المركزى. كما أجريت تلك الاختبارات للمجموعة الضابطة.

النتائج :

كان متوسط عمر المرضى 52,7 ± 6,2 سنة و كان معظمهم من الرجال (58%). لم يظهر أى أختلاف ذو دلالة احصائية بين المرضى والمجموعة الضابطة من حيث السن والجنس. التقييم الوظيفى للمرضى كان جيدا كما أظهره المعيار المحور للجمعية اليابانية للعظام. أظهرت الوسائل الاشعاعية وجود تأثر روماتيزمى عظمى مفصلى عنقى فى الفقرات الرابعة وحتى السابعة لدى جميع المرضى. كما أظهر الرنين المغناطيسى وجود ضغط على اغشية  الحبل الشوكي (الام الجافية) عند مستويات الفقرات العنقية الخامسة والسادسة, السادسة والسابعة وكذلك الرابعة والخامسة. بينما لم يظهر أى ضغط على الحبل الشوكى. زاد وقت التوصيل الحركى المركزى فى 6 مرضى بينما لم يقل مقدار الجهد الحركى المركزى بين المرضى. كذلك لم يختلف مقدار أو زمن الجهد الحركى المستحث فى المرضى عند مقارنتهم بالمجموعة الضابطة.

الخلاصة :

ان الجهد الحركى المستحث يعد من الوسائل التقييمية الكمية لوظيفة المسار الحركى المركزى حيث أنه يستطيع الكشف عن أعراض انضغاط الحبل الشوكى العنقى الروماتيزمى العظمى المفصلى قبل حدوثها حتى قبل أن يستطيع الجهد الحسى المستحث ذلك.



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