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July2005 Vol.42 Issue:      2 Table of Contents
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Therapeutic Effect of Repetitive Transcranial Magnetic Stimulation on Motor Function Recovery after Acute Ischemic Stroke

Eman M. Khedr1, Mohamed Abdel Rahman1, Ola A. Shawky1,Nehal Fathy2, Effet Awad3
Departments of Neuropsychiatry1, Physical Medicine2, Physiology3, Assiut University

ABSTRACT

Background and purpose: Repetitive transcranial magnetic stimulation (rTMS) is increasingly used as a therapeutic tool in various neurological and psychiatric disorders1. In the present study we evaluated the effect of rTMS of the primary motor cortex (M1) on motor recovery in 52 consecutive patients with acute ischemic stroke of middle cerebral artery territory as documented by computerized tomography. Methods: Patients were randomly assigned to one of two groups, the groups receiving either real-rTMS (10 trains at 3 Hz, 10 s for each train with an inter-train interval of 60 s and an intensity of 120% of resting motor threshold using a figure-of-eight coil positioned over the M1 of the affected hemisphere) or sham-rTMS for 10 consecutive days. Clinical assessment of motor disability and functional activity using the Scandinavian Stroke Scale (SSS), National Institutes of Health Stroke Scale (NIHSS), and Barthel Index Scale (BI), was done for each patient before rTMS (pre-rTMS), at the end of the last treatment session and 10 days later. Motor evoked potentials (MEP) were recorded from abductor digiti minimi at the time of each motor assessment. Results: There were no significant differences between the two groups of patients in the pre-rTMS assessments. However, a two factor ANOVA on each of the clinical measures revealed a significant “group” X “time” interaction indicating that real and sham rTMS had different effects on SSS, NIHSS, and BI. No subject experienced adverse effects during the study. Conclusion: We conclude that repeated application of rTMS over the primary motor cortex of the affected hemisphere can enhance motor function recovery in patients with acute ischemic stroke.

(Egypt J. Neurol. Psychiat. Neurosurg., 2005, 42(2): 417-428).

 





INTRODUCTION

 

Despite the intense efforts devoted to prevent and abort cerebral ischemia, some individuals will continue to have completed infarctions. Failure of prevention or intervention does not, however, preclude therapeutic approaches to enhance recovery.

Repetitive transcranial magnetic stimulation (rTMS) is a well-established, non-invasive method for cortex stimulation in conscious human subjects2. Depending on the frequency of magnetic stimulation, rTMS of the primary motor cortex has been shown to modulate cortical excitability beyond the time of stimulation3-4. In normal subjects, high-frequency rTMS at frequencies of 5 Hz and higher induces an increase in cortical excitability beyond the time of stimulation5 whereas low-frequency rTMS at 1 Hz gives rise to a lasting decrease in cortical excitability6. The mechanism of the effect is unclear but may be related to phenomena such as long term potentiation and depression observed in animal preparations7. Several recent reports have suggested that this modulation of cortical excitability by rTMS might have a therapeutic potential 6,7,8. Pascual-leone et al.3  and Khedr et al.9 reported a lasting improvement of motor performance after rTMS of primary motor area (M1) in Parkinson's disease (PD), suggesting a possible therapeutic role in this condition.

Several lines of evidence show that the cortex retains its potential for reorganisation after stroke, both on the damaged and on the undamaged hemisphere. For example, Nudo and co-workers10 mapped the motor cortex of squirrel monkeys before and after small ischemic lesions in the hand territory. They showed that the subsequent loss of hand representation around the lesion could be prevented by intensive retraining of hand skills starting 5 days after the injury.  Such an approach might reduce the progressive derangement of tissue around affected areas and the subsequent development of dysfunctional zones that are frequently seen in experiment animals and stroke patients11,12. However, it should be noted that the success of training may depend critically on when training begins. Overuse of the affected limb during the first week after the lesion can increase the volume of lesion (perhaps by glutamatergic excitotoxicity), whereas overuse during the second week does not13. Recently, Brown et al.14 reported a case of right spastic hemiparesis that occurred 19 months ago treated with epidural motor cortex electrical stimulation for three weeks, they found significant improvement in motor scale. Another study, recorded a significant improvement in motor performance of a non human primate model of cortical ischemia, using epidural electrical stimulation of motor cortex with rehabilitative training15.

In the present study we asked whether rTMS over the damaged hemisphere might also be able to induce beneficial reorganisation of the brain in patients after stroke.

 

MATERIAL AND METHODS

 

Fifty-two right-handed patients (36 males and 16 females) with acute ischemic stroke of middle cerebral artery territory recruited consecutively during the period from January 2002 to March 2003 were included in the study. All patients were admitted at Stroke Unit, Department of Neurology Assiut University Hospital. Each patient fulfilled the inclusion criteria as follows; acute hemiplegia (right or left) with single thromboembolic non haemorrhagic infarction documented by computerized tomography (CT) in the distribution of middle cerebral artery. Exclusion criteria included; brain stem or multiple cerebral lesions, head injury or neurological disease other than stroke, unstable cardiac dysrhythmia, prior administration of major or minor tranquilizer. Patients who were unable to give informed consent because of severe aphasia, ansognosia, or cognitive deficit were not included. All patients provided fully informed consent. The local Ethical Committee had approved the experimental protocol.

Each patient underwent a complete clinical examination and CT of the brain to detect the site of infarction. On the basis of CT findings, a lesion was classified as “cortical” if it involved cortical structures, “subcortical” if it involved corona radiata or internal capsule and “massive” “if it involved both cortical and subcortical structures (complete middle cerebral artery territory infarction)16.

Motor disability and functional ability were assessed using Scandinavian Stroke Scale (SSS)17, National Institutes of Health Stroke Scale (NIHSS)18, and Barthel index scale (BI)19. Resting motor threshold of healthy side  and motor evoked potentials of healthy and hemiplegic sides were recorded from abductor digiti minimi at the 5th-7th day of onset of stroke.

Patients were assigned to one of the two groups (using closed envelopes), real-rTMS linked with rehabilitation (Passive limb movement beginning on the 2nd day, modifying to a more active one as a patients improves at the end of first week) and medical treatment (anticoagulant 'low molecular weight heparin' in the first week and then Asprin and notroopic drugs) and sham-rTMS linked with the same rehabilitation and medical treatment.

Determination of Motor threshold and motor evoked potential:

Patients were seated comfortably in a reclining chair. TMS was delivered through a figure-of-eight coil (9 cm outer diameter of each wing, 1.5 tesla maximum field strength) attached to a Mag-Lite stimulator (Dantec Medical, Skovelunde, Denmark) set to the Keypoint recording equipment (Dantec Medical, Skovelunde, Denmark) with the band-pass ranging from 10 Hz to 1.5 kHz, a sweep time of 500 ms.

Resting motor threshold of the abductor digiti minimi (ADM) of healthy side was determined using pairs of Ag-AgCl surface electrodes taped to the belly and tendon of the muscles. The coil was held tangentially to the skull. The threshold for eliciting an MEP of at least 50 μV in at least five consecutive trails was determined at a provisional point of optimal excitability.  After establishing the threshold intensity, sites adjacent to this point were stimulated in order to exclude the possibility that any more consistent or larger response could be obtained. If any larger responses occurred the threshold was again determined at that point and the procedure was repeated. Ten stimuli were delivered at each site at a frequency of about 0.3 Hz.

We examined whether the focal TMS on the affected hemisphere elicited MEPs in the contralateral paretic ADM in the patients. For this purpose, the stimulus intensity was set at 100% of the output of the stimulator, and MEP s were recorded from the affected ADM while the patients tried to contract the paretic hand. The stimulation site was searched on the scalp around the presumed motor cortex, which was approximately symmetrical to the opposite motor cortex. The hand of the coil was directed posteriorly and 45 away from the parasagittal line to induce maximal MEP responses. This site and direction of the coil are marked by red colour to re-use again for daily rTMS. A ground electrode was placed proximal to the recording sites.

Repetitive transcranial magnetic stimulation:

TMS was performed with a commercially available 90 mm figure-of-eight coil connected to Mag-Lite stimulator. Real-rTMS was applied for 10 trains, each one for 10 sec with 60 sec intervals. The rate of stimulation was set at 3 Hz at 120% of the resting motor threshold using a figure of-eight-coil positioned over the primary hand area of the affected hemisphere with the same orientation which previously determined. In patients who had no MEPs response we, positioned the coil at a approximately hand area of the opposite motor cortex.  Sham-rTMS was applied using the same parameters but with the coil elevated and angled away from the head to reproduce the subjective sensation of rTMS but to avoid induction of current in the brain 20 . These sequences were applied for 10 consecutive days. During rTMS, all patients wore earplugs in order to protect the ears from the acoustic artefact associated with the discharge of the stimulation coil. The patients didn't know whether they are receiving real or sham-rTMS.

Patients were followed-up after 10th session, and another 10 days after the last session of rTMS, using motor disability and functional activity scales besides measuring MEPs in the hemiplegic side. Evaluation of these measures was performed blindly by the neurologist without knowing the type of rTMS.

 

Data analysis

Before starting rTMS, after the 10th rTMS session, and 10 days after the last session, disability was assessed using the three scales. At the baseline assessment (i.e. before 3 Hz rTMS), the mean values of different disability scales (SSS, NIHSS, and BI) between both groups were compared using Student's-test for independent samples. Mean + SD were used to represent data. Differences between subgroups were assessed using Chi-square test. 

The level of significance was set at P < 0.05. ANOVA for repeated measurements analysis for variance was used for statistical analysis. Conditional on a significant ANOVA, a post-hoc t-test for paired sample was performed. Two factor ANOVA with the stimulation condition as the main factor was used to compare the differential effect of the rTMS conditions (real-rTMS vs. sham-rTMS) on changes of disability (i.e. changes in SSS, NIHSS, and BI).

 

RESULTS

 

The study included 24 patients presented with right-sided and 28 with left-sided hemiplegia. They were distributed into two groups, matched for age, age of onset, sex, side of hemiplegia, and site of infarction. The mean (SD) age of patients under real was 53.5 (9.5) and 52.2 (8.4) years for sham group. The mean (SD) age of onset at time of first assessment was 7.12 (1.4) for patients under real and 7.3 (1.5) days under sham stimulation. The mean (SD) amplitude of MEPs was 0.35 (0.4), 0.72 (1.6), and 0.96(1.4) mV for the 1st, 2nd, and 3rd assessments of patients under real and 0.45 (0.43), 0.85 (1.1), and 0.92 (1.2) mV for patients under sham stimulations with no significant changes on follow up between them, despite the presence of more improvement of amplitude in real group (Fig. 1). There are significant correlations between different scales in the 1sr, 2nd, and 3rd assessment (P < 0.0001 for all of them). Fifteen patients had cortical infarction, 26 patients had subcortical infarction and 11 had both cortical and subcortical infarction (middle cerebral artery occlusion). Twenty-three of all patients didn’t' have MEPs at 1st assessment (6 had cortical infarction, 6 had subcortical infarction and all patients with cortical and subcortical infarction). Details of individual data of both groups illustrated in Table (1) and (2). 

The mean (SD) SSS, NIHSS and BI at baseline measurement showed no significant differences between the patients under real and sham groups (P = 0.15, 0.36 and 0.338, respectively). On follow up ANOVA for repeated measurements for each group separately, revealed a significant time effect for the SSS, NIHSS, and BI during the course of the study in both groups. However, a two factor ANOVA on each of the clinical measures revealed a significant “group” X “time” interaction indicating that real and sham rTMS had different effects on SSS, NIHSS, and BI (F=14.5, DF =1.3; P<0.0001, for SSS, F= 16.8, DF =1.4; P<0.0001 for NIHSS, and  F= 26.0, DF =1.5; P<0.0001, for BI). It demonstrated that there was a differential effect of the rTMS condition on the three scales, revealing greater improvement in all scales after real-rTMS as compared with the sham-rTMS as shown in figures 2,3,4. Post hoc testing showed that real-rTMS led to a greater improvement in all scales than sham-rTMS. However, 11 patients who had an occlusion of main stem of middle cerebral artery (6 of them received true rTMS, and the other 5 patients received sham rTMS) showed no significant improvement in both groups. None of them had a MEP response of ADM at initial assessment. The mean (+ SD) SSS, NIHSS, and BI of those patients at initial assessment were 24.6+4.7, 14.9+1.1, and 21.8+4.0 respectively.

As regard to outcome there were a significantly higher percentage of independent (good to excellent outcome) patients who had BI < 75 21   in patients under real r TMS compared with those under sham rTMS. Also, in SSS there was a significant higher percentage of mild disability (50 – 58) in patients under real rTMS22 compared with the other group (Table 3).

Concerning MEPs of abductor digiti minimi, the following were observed: in group of patients under real rTMS; 12 patients had no MEP responses and 14 patients had responses (either normal or delayed responses) at initial assessment. While in the 2nd and 3rd assessment, there was nearly significant increased number of patients with responses. No such changes were observed in the other group. No subject experienced adverse effects during study (Table 4).

 

 

 

Table 1: Individual data of stroke patients under real rTMS:

No Side of  hemi plegia  Age Sex Time of treat ment (day) MEP amp1 (mV) MEP amp2 (mV) MEP amp3 (mV) SS S1 SS S2 SS S3 NIH SS1 NIH SS2 NIH SS3 BI1 BI2 BI3 Site of infa rction
1 RT 58 M 8 1.60 7.30 6.40 34 49 49 11 5 2 25 55 65 C
2 RT 40 F 8 .70 .80 1.00 28 50 56 11 4 1 25 60 80 SC
3 LT 35 F 9 NR NR .10 26 39 42 12 7 6 25 50 60 C
4 RT 35 M 7 NR .10 .10 25 36 41 15 9 7 20 45 60 SC
5 RT 65 F 7 NR .10 .10 26 36 40 15 9 8 20 45 55 M
6 LT 49 M 7 NR .10 .10 36 47 53 12 4 2 40 60 90 C
7 LT 60 M 6 .10 .40 1.30 37 50 53 12 3 2 40 80 90 SC
8 RT 55 M 7 .10 .10 .30 20 50 53 15 3 2 40 80 90 C
9 LT 60 M 6 NR NR 1.90 20 38 52 14 5 3 20 55 70 C
10 LT 48 M 7 NR .10 .20 28 41 48 14 5 5 25 60 60 SC
11 LT 36 F 6 .50 .60 2.10 26 43 55 14 7 2 20 40 65 SC
12 RT 45 F 7 NR NR NR 20 26 26 14 14 14 15 25 25 M
13 RT 50 M 5 .10 .30 .30 40 53 57 8 1 .00 40 90 100 SC
14 LT 55 M 6 .30 .10 .20 33 54 57 9 1 .00 50 80 100 C
15 LF 60 M 7 NR NR .10 33 44 49 9 7 5 30 45 70 SC
16 RT 55 M 10 NR NR NR 20 32 42 14 10 8 20 25 45 M
17 LT 60 M 9 NR NR NR 28 26 30 13 13 12 20 25 28 M
18 LT 60 F 7 .10 1.10 2.50 28 44 55 13 6 3 20 55 75 SC
19 RT 65 M 6 NR NR NR 14 26 40 14 14 9 20 25 40 M
20 LT 50 M 7 .20 .30 .40 29 46 51 11 6 3 25 60 70 SC
21 RT 45 M 10 NR NR NR 29 35 43 11 8 7 25 45 50 M
22 LF 55 F 7 .10 .20 .50 30 44 49 13 9 6 20 40 55 C
23 LF 25 M 5 .10 .30 1.20 25 47 57 12 6 .00 30 60 100 SC
24 LF 60 M 6 .30 .40 .40 45 52 52 6 2 2 60 70 90 C
25 RT 62 M 6 .30 .30 .40 28 50 52 13 3 2 25 65 80 SC
26 RT 65 M 9 .40 .40 .50 26 36 40 14 11 6 20 35 65 SC

 

 

 

 

 

SSS1, SSS2 and SSS3: 1st, 2nd and 3rd assessment, NIHSS1; NIHSS2 and NIHSS3; 1st, 2nd and 3rd assessment, BI1, BI2 and BI3; 

1st, 2nd and 3rd assessment, NR; no response, LT; left hemiplegia, RT; right hemiplegia,C; cortical infarction, SC; subcortical infarction ,

M; massive infarction cortical + subcortical infarction

Table 2. Individual data of stroke patients under sham rTMS.

No Side of hemi plegia Age Sex Time of trea tment (day) MEP amp1 (mV) MEP amp2 (mV) MEP amp3 (mV) SS S1 SS S2 SS S3 NIH SS1 NIH SS2 NIH SS3 BI1 BI2 BI3 Site of infar ction
1 LT 59 F 9 NR NR NR 26 26 31 14 14 13 20 20 25 M
2 RT 45 F 7 NR NR NR 22 30 36 15 12 10 25 25 28 SC
3 LT 67 M 6 NR NR NR 40 44 46 10 9 8 50 52 55 C
4 LT 60 F 7 NR NR NR 28 28 30 14 14 11 20 25 30 SC
5 LT 69 M 9 .70 .60 .70 54 54 56 2 2 1 80 80 90 C
6 RT 55 M 7 .10 .20 .30 30 48 54 12 6 2 30 55 80 C
7 RT 46 M 5 1.00 1.50 1.50 30 40 45 12 10 7 30 45 65 SC
8 LT 35 F 8 .20 .30 .50 26 40 51 15 10 4 28 50 60 SC
9 LT 45 F 7 .10 .10 .10 41 42 42 10 10 10 45 50 50 SC
10 RT 56 M 9 NR NR .10 24 36 40 15 11 10 25 40 42 M
11 RT 55 F 9 NR NR NR 28 30 30 14 12 11 20 25 28 M
12 RT 54 M 7 NR NR NR 28 30 40 1 12 9 28 32 45 C
13 LT 52 M 5 .20 .20 .20 28 32 34 13 11 10 30 32 30 SC
14 LT 50 M 6 .10 .20 .20 24 30 32 13 10 10 28 30 30 SC
15 RT 65 M 7 1.20 4.10 4.20 38 40 45 10 9 8 38 42 42 SC
16 RT 60 M 8 1.20 3.00 4.20 38 44 45 11 9 8 35 40 42 C
17 LT 46 M 7 .20 .30 .20 30 40 50 12 10 5 30 45 70 C
18 LT 55 M 7 .20 .20 .20 30 40 47 12 10 8 30 45 55 C
19 RT 50 M 10 NR NR NR 28 32 42 14 11 9 25 35 50 M
20 RT 55 M 8 NR NR NR 33 42 46 11 9 6 35 50 60 SC
21 LT 55 M 5 .10 .10 .20 28 30 35 15 12 11 30 35 40 M
22 RT 46 M 10 1.00 1.50 1.50 30 40 45 11 9 6 30 45 65 SC
23 LT 45 F 5 .20 .30 .50 26 40 45 15 9 7 25 50 60 SC
24 RT 47 M 8 1.00 1.50 1.50 30 40 45 12 9 8 32 45 55 SC
25 LT 35 F 7 .20 .30 .50 26 40 51 15 9 6 25 50 60 SC
26 LT 49 F 6 .10 .10 .10 41 42 42 8 7 7 55 60 60 SC

SSS1, SSS2 and SSS3: 1st, 2nd and 3rd assessment, NIHSS1; NIHSS2 and NIHSS3; 1st, 2nd and 3rd assessment, BI1, BI2 and BI3;  1st, 2nd and 3rd assessment, NR;

no response,  LT; left hemiplegia, RT; right hemiplegia,C; cortical infarction, SC; subcortical infarction , M; massive infarction cortical + subcortical infarction

   

Table 3. Comparison between the outcomes of patients under real- and sham-rTMS according to Barthel Index Scale and Scandinavian Stroke Scale.

 

Scales

 

Real-rTMS

N = 26

Sham-rTMS N = 26

Chi-square

P value

Barthel Index

 

      Good – excellent outcome   > 75

9 (34.6 %)

2 (7.7%)

0.0175

       Moderate – severe disability   < 75

17 (65.4 %)

24 (92.3 %)

Scandinavian Stroke Scale

 

      Mild disability <  50

13 (50 %)

5 (19.2 %)

0.019

       Severe disability > 50

13 (50 %)

21 (80.8 %)

 

 

Table4: Sequence of motor evoked potential responses among patients under real- and sham-rTMS.

 

MEP responses

Real-rTMS

Normal or delayed  response

Real-rTMS

Absence response

Sham-rTMS

Normal or delayed response

Sham-rTMS

Absence

response

Upper limbs

1st assessment

 

14 (53.8 %)

 

12 (46.2 %)

 

17 ( 65.4  %)

 

9 ( 34.6  %)

2nd assessment

18 (69.2 %)

8 (30.8 %)

17 (65.4   %)

9 (34.6 %)

3rd assessment

21 (80.8 %)

5 (19.2 %)

18 (69.2 %)

8 (30.8 %)

Chi-square

P value

P = 0.059

P = 0.94

 

 

Fig. (1): MEPs recording, at 1st , 2nd and 3rd assessment from male patient with right sided hemiparses under real rTMS, upper trace illustrated small MEP (0.1 mV, peak-to- peak) with long latency (28 ms), the middle trace (0.3 mV, and 24 ms) and third trace (0.3mV and 23.5 ms) appeared larger than upper one.

 

 

 

 

Fig. (2): The mean value of SSS in the 1st, 2nd and 3rd assessments of patients under real rTMS and patients under sham stimulation. It illustrated a significant time effect in the first group compared to second group despite the equality at first assessment.

 

 

 

Fig. (3): The mean value of NIHSS in the 1st, 2nd and 3rd assessments of patients under real rTMS and patients under sham stimulation. It illustrated a significant time effect in the first group compared to second group despite the equality at first assessment.

 

 

 

Fig. (4): The mean value of BI in the 1st, 2nd and 3rd assessments of patients under real rTMS and patients under sham stimulation. It illustrated a significant time effect in the first group compared to second group despite the equality at first assessment.

 

 


DISCUSSION

 

In recent years, increasing interest in the areas of neuroplasticity and neurorehabilitation has been prompted by several important discoveries. Functional recovery frequently occurs following injuries to the nervous system such stroke but the extent of recovery is highly variable. While some patients with initial hemiparesis may eventually achieve full recovery, others have little or no improvement and remain severely disabled. It is thought that the extent of brain reorganization after the injury is an important factor that influences recovery23. The aim of the present study was to examine whether repeated sessions of rTMS to the affected hemisphere of stroke patients could speed up the process of recovery.

rTMS has been used by several groups to produce changes in the excitability of the motor cortex. In these experiments, high frequency stimulation has tended to have an excitatory effect whereas low frequency rTMS suppresses excitability. Cortical excitability can be easily addressed by paired pulse,25'26 and due to technical limitations we were not able to do this in the present study.

Although the effects of rTMS  in healthy subjects have usually been small and short lasting, there is some evidence that more powerful changes may be seen in a compromised nervous system. For example, temporary ischemic nerve deafferentation of the forearm and hand is an established experimental model of cortical plasticity in humans27,28. Ziemann et al.28, found  that very low frequency (0.1 Hz) rTMS, that had no effect on  intact subjects, was applied during ischemia, enhanced the magnitude of the changes induced by temporary ischemic nerve deafferentation alone.

To our knowledge there have been no previous studies to evaluate the effect of  rTMS to enhance motor recovery in acute ischemic stroke. The nearest parallels are two very brief reports of the effects of high frequency epidural stimulation of motor cortex in a single human stroke patient and in an animal model of acute stroke. In the latter, Plautz et al.15 combined 50 Hz epidural stimulation of motor cortex at subthreshold intensities with rehabilitative training to enhance behavioral and cortical plasticity in non human primate model of cortical ischemia. Their results suggest that the addition of cortical stimulation increased the speed of recovery from the cortical damage. Brown et al.14 published a case report of a 65-year-old patient who had a subcortical infarction and right spastic hemiparesis that occurred 19 months before implantation with an epidural motor cortex stimulator. As in the monkey experiment, low intensity stimulation at 50 Hz during rehabilitative training improved the patient’s motor performance despite it having been apparently stable in over the previous months.

Safety concerns prevented us from using such high frequency stimulation with rTMS, and we opted to test the effectiveness of 3 Hz rTMS on motor function recovery in acute ischemic stroke. The results show that there was a beneficial effect of rTMS on motor function recovery in the real versus sham group. This is supported by the following data: firstly, there was greater improvement in all scores of motor disability and functional activity recorded in patients under real-rTMS compared with patients under sham-rTMS despite the equality at the baseline assessment.  Interestingly, patients who had occlusion of main stem of middle cerebral artery (11 patients with cortical and subcortical infarctions) and SSS < 28 showed no significant improvement in both groups. This may indicate that the benefit of rTMS is limited to patients with smaller infarctions. Secondly, a significantly higher percent of good to excellent outcome was recorded in patients under real-rTMS compared with the other group. Thirdly, MEP responses improved more in patients under real-rTMS than the other group.  

The underlying mechanism of the beneficial effect of 3 Hz rTMS remains to be established. The enhanced  motor recovery may be attributed to a lasting increase in cortical excitability, and the enhancement of the  regional blood flow around ischemic area (rCBF). Pascual-Leone et al.20 and Paus et al.29  studies, which noted a significant positive correlation between rCBF (as measured by single photon emission  tomography (SPECT) and positron emission tomography) and the number of TMS pulse trains at the stimulation site. Since the improvement occurred rapidly, it probably resulted from enhancing the strengthening of specific connections between neurons, rather than from sprouting of new connections.

These connections could be mediated by different mechanisms: increase in the excitatory neurotransmitter released at the synapse, increase the local density of postsynaptic receptors, changes in membrane conductance properties that could enhance the effect of weak or distant inputs. It could be increase in  axonal collateral of horizontal pathways. The improvement may contributed partially to the effect of  rTMS on mood, as many studies5,30,31 reported that rTMS treatments to the left dorsolateral prefrontal cortex  had antidepressant effect, and because it is known that less-depressed stroke patients comply  better and react better to rehabilitation. 

Unfortunately we did not assess depression in this study. rTMS may potentiat all these possibilities . In conclusion rTMS may be able to change brain circuity as well as strengthen connections that enhance  motor function recovery. Further studies are recommended on a large number of selected stroke patients with EEG monitor and assessment of cortical excitability and depression beside long term follow up.

 

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الملخص العربى

 

التأثير العلاجى للتنبيه المغناطيسى المتكرر عبر الجمجمة على عودة الوظيفة الحركية

بعد السكتة الدماغية الحادة الناتجة من السدة الوعائية

 

يستخدم التنبيه المغناطيسى المتكرر عبر الجمجمة كطريقة للعلاج لمختلف الأمراض العصبية والنفسية. فى هذه الدراسة تم تقييم تأثير التنبيه المغناطيسى المتكرر عبر الجمجمة لمركز الحركة الأولى فى القشرة المخية على عودة الحركة فى إثنين وخمسين مريضاً بالسكتة الدماغية الحادة نتيجة للسدة الوعائية للشريان المخى الأوسط كما ثبت بالأشعة المقطعية. وقد قسم المرضى عشوائياً إلى مجموعتين، أحد المجمعتين طبق عليها استخدام التنبيه المغناطيسى الحقيقى المتكرر عبر الجمجمة لتنبيه مركز الحركة الأولى فى القشرة المخية لفص الخ المصاب باستخدام ملف على شكل فراشة (عشرة تنبيهات متتابعة، الفرق بين كل منها ستون ثانية وكل تنبيه مدتة عشر ثوانى بتردد 3 هرتز وقوة 120% من مستوى السكون الحركى) أما المجموعة الثانية فقط طبق عليها التنبيه المغناطيسى غير الحقيقى المتكرر عبر الجمجمة. وفى كلتا المجموعتين أستخدم التنبيه لمدة عشر أيام متتابعة. وقد تم تقييم العجز الحركى والنشاط الوظيفى لكل مريض قبل وبعد نهاية جلسات التنبيه باستخدام مقياس اسكاندنيفيا للسكتة الدماغية ومقياس السكتة الدماغية لمعهد الصحة القومى ومقياس بارثل. وسجل الجهد المستشار الحركى للعضلة المبعدة لخنصر اليد فى كل مرة تم فيها التقييم الحركى. وقد أوضحت نتائج هذه الدراسة أنه لا توجد فروق بين المجموعتين فى بداية الدراسة قبل استخدام التبيه بينما وجدت فروق ذات دلالة إحصائية بين المجموعة التى طبق عليها التنبيه المغناطيسى الحقيقى وتلك التى طبق عليها التنبيه غير الحقيقى. ونستنتج من هذه الدراسة أن استخدام التنبيه المغناطيسى المتكرر عبر الجمجمة لمركز الحركة الأولى فى القشرة المخية لفص المخ المصاب يحفز عودة الوظيفة الحركية لمرضى السكتة الدماغية الحادة الناتجة من السدة الوعائية.



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