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July2014 Vol.51 Issue:      3 (Supp.) Table of Contents
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Magnetic Resonance Spectroscopy in Idiopathic Generalized Epilepsies

Mervat Mostafa1, Foraysa Talaat1, Ihab Ismail2, Nevin Shalaby1,

Rania Hegazy2, Neveen El-Fayoumy3, Dalia Labib1

Departments of Neurology1, Radiology2, Clinical Neurophysiology Unit3, Cairo University; Egypt



ABSTRACT

Background: The absence of gross structural abnormalities on conventional brain imaging does not preclude the existence of subtle alterations on the neuronal level in case of idiopathic generalized epilepsy (IGE). Objective: To quantify neuronal dysfunction of the thalamus and prefrontal cortex in patients with IGE. Methods: A case control study carried out on 60 subjects; 30 patients with IGE and 30 healthy subjects, age and sex matched. Patients were divided into 3 groups: juvenile myoclonic epilepsy (JME); generalized tonic clonic seizures (GTCs) and childhood absence epilepsy (CAE). Proton magnetic resonance spectroscopy (H1MRS) was done to assess NAA and NAA/Cr in thalamus and prefrontal cortex. Results: A Significant reduction of NAA and NAA/Cr ratio in the thalamus of all IGE patients as well as individual groups compared with controls was found. JME patients had a statistically significant lower mean value of NAA /Cr ratio in prefrontal cortex in comparison to GTCs and CAE. Among all IGE patients and individual groups, a positive correlation was found between NAA& NAA/Cr ratio in the thalamus and prefrontal cortex. Conclusion: The thalamic frontal cortex reduction in NAA supports the notion of abnormal thalamo-cortical circuitry as a substrate of seizure generationin this form of epilepsy. A possible role can be played by the frontal lobe in the pathophysiology of the epileptogenic process in IGEs especially JME. [Egypt J Neurol Psychiat Neurosurg.  2014; 51(3): 265-273]

Key Words: MRS, IGE, Epilepsy.

Correspondence to Nevin Mohieldin Shalaby. Department of Neurology, Cairo University. Tel.: +201001493242          Email: nevinmohy@gmail.com

 






INTRODUCTION

 

Idiopathic generalized epilepsies (IGEs) constitute one third of all epilepsies. IGEs manifest with typical absences, myoclonic jerks, and generalized tonic-clonic seizures, alone or in varying combinations1.

IGE occurs in the absence of any macroscopic brain abnormalities. The absence of gross structural abnormalities on conventional brain imaging does not preclude the existence of subtle alterations on the neuronal level2.

Two strategic brain regions, which are interconnected, are involved in the epileptogenic activity in IGEs; the thalamus and the frontal lobe3. The notion of network connectivity in patients with IGE has been addressed in several studies utilizing functional imaging4,5. A network is a functionally and anatomically connected set of cortical and subcortical brain regions where activity in any one part affects the activity in all others6. The thalamo-

cortical pathway is the most recognized epileptic network. The thalamus is the major source of input to the cortex with multiple reciprocal connections from the cortex back to the thalamus. It has widespread interconnections to the frontal lobe, in addition, its reticular nucleus is formed of GABAergic neurons, with strong inhibitory connections with the relay nuclei, which may serve to regulate cortical excitability and, therefore, seizure threshold7,8.

Nevertheless, the exact origin of the epileptogenic process in IGEs warrants further verification. Assessment of neuronal functions using magnetic resonance spectroscopy (MRS) via quantification of neurometabolites can reveal the possibility of seizures arising from focal brain pathology in what appears otherwise as generalized epilepsy syndromes9,10.

In the present work, we assessed the neurometabolites in the thalamus and the prefrontal cortex in IGE patients to reveal hidden dimensions in the pathophysiologic process in IGE.

 

 

 

SUBJECTS AND METHODS

 

This was a case control study conducted on 60 right handed Egyptian subjects, including 30 patients with idiopathic generalized epilepsy (IGE), diagnosed on clinical and EEG basis according to the international classification of epileptic seizures1,with age ranging from 11 to 25 years with a mean of  16.97±4.47 years, they were  23 females (76.67%) and 7 males (23.33%). They were divided into three groups; group 1: juvenile myoclonic epilepsy (JME); group 2: patients with generalized tonic clonic seizures (GTCs); and group 3: childhood absence epilepsy (CAE), each including 10 patients, in addition to 30 healthy volunteers age, sex, and educational level matched with patients. The patients were recruited from epilepsy outpatient clinic, Kasr Al-Aini School of Medicine during the period from April 2008 to September 2010.

Informed written consent was taken from patients or their guardians, and approval from Cairo University Hospitals Research Ethics Committee was obtained.

Inclusion criteria were age from 10-25 years, normal development prior to seizure onset, normal MRI of the brain, normal metabolic profile.

Exclusion criteria comprised symptomatic/ syndromic epilepsy, neurological deficits or psychiatric illness, physically handicapped children, drug intake other than anti epileptic drugs (AEDs).

 

Participants were subjected to the following: I. Clinical evaluation: History was based on interview with patients and an eyewitness. Seizure frequency was considered that of GTCs as myoclonic jerks and absence attacks could not be quantified. None reported history of status. II. Conventional electroencephalogram (EEG): Inter-ictal assessment was carried out at the clinical neurophysiology unit in Kasr Al-Aini hospital, using Nihon Kohden 14-channels EEG machine. EEG electrodes were placed according to the international 10-20 system using a cap, referential and bi-polar montages were used. EEGs were carried out under standard conditions. Hyperventilation and intermittent photic stimulation were used as provocative tests. When interictal EEG was normal, it was repeated after sleep deprivation, where 7 patients had their EEGs performed during the ictus. III. Magnetic Resonance Imaging and Magnetic resonance spectroscopy Imaging as follows:

 

1.      Conventional MRI: Non-enhanced MRI of the brain was performed for all subjects in the MRI unit of radiodiagnosis department in Kasr Al-Aini Hospital using a1.5 Tesla whole-body system (ACS-NT 15 model; Philips Medical Systems, Best, Netherlands). Protocol: Axial and Coronal (T1, T2, FLAIR-weighted images), and sagittal (T1, T2 weighted images).

2.      MR spectroscopy (MRS): The proton MR spectroscopy (1H-MRS) was performed with a single voxel technique using a1.5 Tesla whole-body system  in the interictal period (>24 h since last seizure) to all patients and control subjects. 

 

Preparation:

Axial, Coronal and sagittal T2-weighted images were used to place the volume of interest (VOI) in 3 planes with an average volume of 8 ml (20 × 20 × 20 mm). The VOI were placed over the right thalamus and prefrontal cortex. The thalamus VOI covered all thalamic nuclei. The prefrontal VOI was placed anterior to the corpus callosum by using the plane of anterior and posterior cerebral commissure as the caudal border, and including the craniolateral portion of the frontal lobe. The caudomesial portion of the frontal lobe was avoided to reduce distortions of the spectra due to susceptibility artifacts in the vicinity of bone and air.

 

Imaging:

MRI spectroscopy (PRESS) pulse sequence was used with the following parameters: repetition time (TR) = 2000 msec, 2048 data points, measurement of 128. Before recording the spectrum, the homogeneity of the magnetic field over the VOIs was optimized (shimming) automatically, water suppression was achieved using chemical shift selective (CHESS) radiofrequency pulses before PRESS excitation.

A short echo time (31 ms) and long echo time (272 ms) were used to study peak of N-acetyl aspartate (NAA) and NAA/Cr ratio as shown in Figure (1). Peak areas of metabolites were quantified and then the position (the place as parts per million (ppm) and amplitude (as maximum intensity) of the metabolites were held. All acquisition and analyses were performed by a single operator with an average total scan time for the whole study of about 50 minutes. A neuroradiologist interpreted the MRI and MRS.


 

 

 

 

Figure 1. MRS brain axial and coronal images (MRS at TE 31, 272 on Rt thalamus (A, B)

and on the prefrontal cortex (C, D).

 

 


Statistical Methods

Numerical data were expressed as mean and standard deviation (SD), median, minimum and maximum. Qualitative data were expressed as frequency and percentage. For quantitative data, comparison between two groups was done using independent t-test. Comparisons between more than two groups were done using ANOVA test. Correlation between variables was tested using Pearson’s correlation coefficient (r) test. Abnormality in the regional concentration of a given metabolite in individual patients was defined as a value outside the 2 SD of the mean of normal controls. A p-value less than 0.05 was considered significant.

 

RESULTS

 

Demographic data of the study subjects and patients clinical Characteristics are illustrated in Table (1).

 

EEG Results:

All patients had abnormal EEGs either inter- ictally (23 patients) or ictally (7 patients), in the form of generalized spike-wave or polyspike-wave complexes.  The frequency of generalized discharges in JME was 4-6 cycles/sec; in GTC patients was 3-4 cycles/sec; and in CAE patients was 2.5-4 cycles/sec.

 

MRS Results:

MRS neurometabolites in IGE patients & controls:

IGE patients had generally had lower mean values of NAA and NAA/Cr ratio than controls in prefrontal area and in thalamus, which were statistically significant (P<0.05) at certain ETs, and tended to be statistically significant (P-0.05) at other ETs (Table 2).

 

MRS Findings in Individual Patients Groups Vs Controls:

In JME, all prefrontal and thalamic NAA and NAA/Cr were lower than controls (Table 3).

In GTCS, all thalamic parameters were lower while none of the prefrontal was significantly lower than controls (Table 4).

In CAE, thalamic NAA at ET 272 & 31, and prefrontal NAA/Cr were lower than controls (P=0.01; 0.02; 0.01 respectively).

 

Frequency of subjects with abnormal values of neurometabolites within the study groups:

Abnormality of the MRS metabolites in individual patients was defined as a value outside the 2 SD of the mean of normal controls. Percentage of subjects with abnormal values of neurometabolites is shown in Table (5).

 

Comparison between JME, GTC and CAE regarding MRS metabolites:

A statistically significant difference was found between the three groups in NAA/Cr ratio at TE (272) in prefrontal area (0.04), where the lowest mean value was found in JME group (1.8±0.79), whereas the value was equal in both GTCs and CAE (1.97±0.28).

 

Correlations within the Epileptic Network in All Patients:

At ET 272 the NAA in the prefrontal cortex correlated positively with that in the thalamus (r=0.37, P=0.04). Also, at ET 31 the  NAA in the prefrontal cortex correlated positively with NAA and NAA/Cr in the thalamus (r=0.42, P=0.01; r=0.50, P=0.005). In contrast, no correlation was observed in controls between thalamus and prefrontal cortex neurometabolites.

 

Correlations within the Epileptic Network in Individual Patients Groups:

JME: A positive correlation was found between prefrontal NAA/CR at ET 31 and the thalamic NAA (r=0.69, P=0.025).

GTCs: At ET 272, the prefrontal NAA/Cr correlated positively with thalamic NAA/Cr (r=0.64, P=0.04), and the prefrontal NAA correlated positively with thalamic NAA at ET 31 (r=0.85, P=0.002).

CAE: At ET 272, the prefrontal NAA and NAA/Cr correlated positively with the thalamic NAA (r=0.72, P=0.02; r= 0.63,P=0.049).

 

Relation of MRS Findings and Clinical Data:

There was no statistically significant correlation between the age at seizure onset or disease duration and the MRS metabolites mean values (P>0.05). However, a statistically significant negative correlation existed only between NAA/Cr ratio at TE (31) in prefrontal area (r=-0.433; P=0.01) and thalamus and the frequency of seizure (r=-0.511; P=0.004).

 

MRS and Gender:

A statistically significant lower mean value of NAA/Cr ratio in males in comparison to females in thalamus at TE (272) (P=0.01), otherwise, no statistically significant difference was found between both genders.

 

MRS and Anti epileptic drugs (AEDs):

A statistically significant lower mean value of NAA in IGE patients receiving polytherapy in comparison to those on monotherapy in thalamus at TE (272) (P=0.006), otherwise, no statistically significant difference was found between both groups.

 

MRS and Interictal EEG:

No statistically significant difference in NAA or NAA/Cr in patients with normal interictal EEG recording and those with abnormal interictal recording (P>0.05).


 

 

Table 1. Demographic Data of Subjects and Patients’ Clinical Characteristics.

 

 

All IGE

(30)

JME

(10)

GTC

(10)

CAE

(10)

Controls

(30)

Age (y)

(Mean±SD)

11-25

(16.97±4.5)

16-25

(19.5±3)

11-23

(18.4±3.3)

11-20

(13±4.1)

14-23

(19±2.9)

Sex

      M/F  

 

7/23

 

2/8

 

4/6

 

1/9

 

6/24

Age of onset   (y)

(Mean±SD)

6-22

(12.3±4.2)

11-18

(15±2.6)

6-22

(13.5±5.5)

7-10

(8.4±1.9)

-

Disease duration (y)

(Median)

0.25-15

(5)

0.25-10

(4.5)

0.25-15

(7)

0.25-10

(4)

-

 

Associated GTCs

20 (66.6%)

8 (80%)

10 (100%)

2 (20%)

-

Seizure frequency (GTCs)/mo (Median)

0-4

(2)

1-2

(1)

0-4

(2)

0-1

(0)

-

AEDs

    Montherapy

    Polytherapy

 

25 (83.3%)

5 (16.7%)

 

8 (80%)

2 (20%)

 

9 (90%)

1 (10%)

 

8 (80%)

2 (20%)

-

 

Table 2. Comparing MRS results of all IGE patients and control subjects.

 

ROI location

IGE Patients

Mean±SD

Control

Mean±SD

P-value

Prefrontal(272)NAA

0.57±0.3

0.63±0.37

0.05

Prefrontal(272)NAA/Cr

1.97±0.28

2.48±0.51

0.003**

Prefrontal(31)NAA

1.1±0.48

1.53±0.35

0.03*

Prefrontal(31)NAA/Cr

1.51±0.39

1.63±0.43

0.05

Thalamus(272)NAA

0.33±0.23

0.45±0.35

0.05

Thalamus(272)NAA/Cr

2.61±1.01

3.0±1.3

0.01**

Thalamus(31)NAA

0.49±0.3

0.64±0.42

0.05

Thalamus(31)NAA/Cr

1.51±0.37

1.83±0.43

0.03*

* Statistically significant at P<0.05 ** Statistically significant at P<0.01

 

Table 3. Comparison between MRS results of JME group and control subjects.

 

ROI

JME

Mean±SD

Control

Mean±SD

P-value

Prefrontal(272)NAA

0.53±0.21

0.63±0.37

0.01**

Prefrontal(272)NAA/Cr

1.8±0.79

2.48±0.51

0.05*

Prefrontal(31)NAA

1.02±0.44

1.53±0.35

0.01**

Prefrontal(31)NAA/Cr

1.4±0.45

1.63±0.43

0.02*

Thalamus(272)NAA

0.34±0.09

0.45±0.35

0.03*

Thalamus(272)NAA/Cr

2.9±0.83

3.0±1.3

0.00**

Thalamus(31)NAA

0.63±0.19

0.64±0.42

0.02*

Thalamus(31)NAA/Cr

1.52±0.49

1.83±0.43

0.04*






* Statistically significant at P<0.05 ** Statistically significant at P<0.01

 

Table 4. Comparison between MRS results of GTC group and control subjects.

 

ROI

GTC

Mean±SD

Controls

Mean±SD

P-value

Prefrontal(272)NAA

0.59±0.12

0.63±0.37

0.76

Prefrontal(272)NAA/Cr

1.97±0.28

2.48±0.51

0.43

Prefrontal(31)NAA

0.95±0.5

1.53±0.35

0.05*

Prefrontal(31)NAA/Cr

1.54±0.5

1.63±0.43

0.65

Thalamus(272)NAA

0.26±0.12

0.45±0.35

0.02*

Thalamus(272)NAA/Cr

2.04±1.0

3.0±1.3

0.04*

Thalamus(31)NAA

0.34±0.17

0.64±0.42

0.002**

Thalamus(31)NAA/Cr

1.42±0.41

1.83±0.43

0.04*






* Statistically significant at P<0.05 ** Statistically significant at P<0.01

 

 

Table 5. Frequency of subjects with abnormal lower MRS metabolites using a 2 SD cutoff from the mean of normal controls.

 

ROI

Patients

 

Control

(n=30)

IGE

(n=30)

JME

(n=10)

GTC

(n=10)

CAE

(n=10)

No (%)

No (%)

No (%)

No (%)

No (%)

Prefrontal(272)NAA

6 (20)

3(30)

2(20)

1(10)

0(0)

Prefrontal(272)NAA/Cr

3(10)

2(20)

1(10)

0(0)

0(0)

Prefrontal(31)NAA

6(20)

4(40)

1(10)

1(10)

0(0)

Prefrontal(31)NAA/Cr

2(6.6)

1(10)

0(0)

1(10)

0(0)

Thalamus(272)NAA

3(10)

0(0)

2(20)

1(10)

0(0)

Thalamus(272)NAA/Cr

4(16.6)

1(10)

3(30)

0(0)

0(0)

Thalamus(31)NAA

4(16.6)

0(0)

4(40)

0(0)

0(0)

Thalamus(31)NAA/Cr

2(6.6)

1(10)

1(10)

0(0)

0(0)

 

 


DISCUSSION

 

Over the last decade 1H-MRS has contributed toward understanding the changes in brain metabolism associated with IGE. Nevertheless, there is relative inhomogeneity in studied IGE groups, and thus the results have been highly variable.

In the present study, we measured NAA, NAA/Cr ratio, using single voxel proton MRS technique, in the right thalamus and the prefrontal cortex. The choice of those two locations was based on an analogous study, in IGE patients, which did not report any abnormalities of NAA/Cr in the insular cortex, posterior temporal lobe white matter, splenium of the corpus callosum, cerebellum, or occipital cortex compared to healthy controls10. Fojtikova et al. showed a symmetrical distribution of NAA/Cr ratio in both thalami11.However, another study concluded that the visual-spatial function was more affected with relative sparing of language in epileptic patients indicating more involvement of right hemisphere12; thus, we selected the right thalamus, rather than the left in this study.

NAA is found exclusively in neurons and neuronal processes, whereas Cr is relatively homogeneously distributed throughout the brain and can be affected by confounding factors, such as neuronal shrinkage or increase/decrease in water content13, 14.  Thus, the choice of quantification of NAA besides NAA/Cr ratio providesa more reliable data.

Our spectroscopic analysis revealed a significant reduction of mean NAA and NAA/Cr ratio in the right thalamus of IGE patients compared with controls, with low thalamic NAA and NAA/Cr ratio in 16.6% of patients, which agrees with other studies13,15,16 which implies neuronal metabolic dysfunction and/or neuronal loss.

On comparing individual groups of patients, we found a significant reduction of thalamic NAA and NAA/Cr ratio compared with controls. Ten percent of JME patients, 40% of GTC and 10% of CAE had abnormally low thalamic NAA and NAA/Cr ratio, with no significant inter group difference in the mean thalamic NAA or NAA/Cr ratio. Some studies reported that single voxel MRS showed abnormally low NAA/Cr levels in JME patients16,17. In addition, progressive thalamic atrophy was reported by others18,19. A significant thalamic reduction of NAA was also observed in pure primarily GTC epilepsy15, and in patients with typical absence11.The MRS findings, in this study, confirm theories stating that the thalamus plays an important role in the pathogenesis of generalized epilepsies20.

In the present study, there was a significant negative correlation between the thalamic NAA/Cr ratio and the seizure frequency in the whole patients group, but no such correlation was found with the age at seizure onset nor with the duration of epilepsy. On the other side, in individual groups a significant negative correlation existed between the thalamic NAA/Cr ratio at TE (31) and the frequency of seizure and disease duration in GTC patients. Bernasconi et al.13 found a negative correlation between thalamic NAA/Cr and the duration of epilepsy in IGE patients.

On assessment of prefrontal cortex neurometabolites, there was a significant reduction of NAA and NAA/Cr in patients compared with controls. Moreover, 20% of IGE patients had abnormally low prefrontal NAA and NAA/Cr ratio. This goes in accordance with Simister et al.21, who reported that IGE patients had bilateral frontal lobe metabolite changes in the form of reduction in NAA, which may indicate reduced overall neuronal numbers or neuronal dysfunction. Some studies22,23 supported this observation when they found that IGE patients were exhibiting elevated frontal lobe fraction of CSF and reduced fraction of gray matter.

On analyzing findings in individual groups, we found a significant reduction of prefrontal cortex NAA and NAA/Cr ratio among JME, GTC and CAE patients compared with controls. This agrees with other studies which found reduction of absolute NAA values in the frontal lobes of patients with JME 15, 24.Also, Lin et al.16, found that more than 20% of patients with JME had abnormal NAA/Cr levels ratio in bilateral medial prefrontal cortices. Moreover, Tae et al.25 reported reduction in the cortical thicknesses of frontal in patients with JME.

Our results showed that the JME patients showed a significantly lower mean value of prefrontal NAA/Cr ratio compared with the other two groups. This agrees with Savic et al.15 who found that patients with JME had reduced frontal lobe NAA in relation to GTC patients.

A significant negative correlation was noticed between prefrontal cortex NAA/Cr ratio and the seizure frequency in patients with IGE, but such correlation was not observed neither with age at seizure onset nor with duration of epilepsy. On the other hand, Simister et al.21 reported that seizure frequency, age of onset, and epilepsy duration did not affect the metabolite changes of the prefrontal cortex in IGE patients.

Considering JME group individually, patients showed lower prefrontal NAA/Cr ratio with increasing seizure frequency. This agrees with Lin et al16. Conversely, Bernasconi et al.13 observed the lack of difference of NAA/Cr between JME patients with adequate seizure control and those with persistent seizures.

Strikingly, a significant positive correlation existed between the duration of epilepsy and the prefrontal NAA/Cr in CAE patients, which may suggest the lack of a significant impact of prolonged seizure activity on the prefrontal cortex in the absence of GTCs. To our knowledge according to available literature, no studies addressed the prefrontal metabolites in CAE except in the context of IGE and not individually.  

In the current study, the presence of a positive correlation between NAA and NAA/Cr in the thalamus and the NAA in the prefrontal cortex in patients was observed, meanwhile such correlation was absent in controls, which indicates structural and functional alterations in the thalamo-cortical pathway in patients with generalized epilepsy. However, this finding does not point clearly whether these changes are the result of spread of seizure activity to the frontal cortex or that they do play a role in the generation of seizure activity itself. The presence of neurometabolic alterations in regions other than the thalamus, in our case; the prefrontal cortex, would imply the existence of multiple epileptic foci in IGE. This can be particularly true for JME, and to a lesser extent for GTC, as the lowest mean of prefrontal NAA/Cr ratio relative to control as well as to GTC and CAE was present in the JME, with 40% of patients having absolutely abnormal low levels.  Lin et al.16 reported that the identification of a specific network of neurochemical dysfunction in patients with JME with diverse involvement of particular structures within the thalamocortical circuitry, suggests that cortical hyperexcitability is not necessarily diffuse, but it may indicate that JME is a multifocal rather than a truly generalized syndrome, supporting the knowledge that the focal/generalized distinction of epileptogenesis should be reconsidered. The lack of difference of NAA/Cr between JME patients with adequate seizure control and those with persistent seizures, as reported by Bernasconi et al.13, supports the idea that neuronal dysfunction in JME could be related primarily to the underlying epileptogenic process rather than to the effect of the seizures themselves or to interictal activity. On the other hand, the positive correlation between neurometobolites in prefrontal cortex and disease duration in patients with CAE makes a role played by the prefrontal lobe in generation of absence seizure activity unlikely.

Regarding gender differences, we found a statistically significant lower mean thalamic NAA/Cr ratio in males compared with females in the whole patients´ group. On the other hand, Komoroski et al.26reported no significant differences in any region for any metabolite ratio between males and females; however, the female to male ratio in our study is about 3:1 which may not serve for a fair comparison in this respect.

A statistically significant lower mean thalamic NAA in patients receiving polytherapy in comparison to those receiving monotherapy was found. On the contrary, many authorities15-17,24 did not detect such difference. Again, the small number of patients on polytherapy (5/30) relative to those on monotherapy can offer a possible explanation for such discrepancy.

The presence of abnormal interictal discharges did not have an impact on mean NAA or NAA//Cr ratio when compared with normal interictal EEG, in agreement with Bernasconi et al.13, we found no statistically significant difference in between patients with and those without interictal EEG activity.

 

Conclusion

H1-MRS has the ability to demonstrate subtle neurochemical changes in subjects with IGE at the time conventional MRI results are negative. IGE was associated with thalamic/frontal cortex reduction in NAA implying reduced overall neuronal numbers or neuronal dysfunction supporting the notion of abnormal thalamo-cortical circuitry as a substrate of seizure generation in this form of epilepsy. A possible role can be played by the frontal lobe in the pathophysiology of the epileptogenic process in IGEs especially JME.

 

[Disclosure: Authors report no conflict of interest]

 

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الملخص العربى

 

الرنين الطيفي فى مرضى النوبات الصرعية الكلية المجهولة السبب

 

خلفية البحث: فى مرضى الصرع الكلى المجهول السبب لا تظهر تغيرات مرئية فى المخ ولكن هذا لا ينفى وجود تغيرات وظيفية. هدف البحث: دراسة نسبة المواد التى تعكس وظيفية المهاد والقشرة المخية الأمام أمامية فى مرضى النوبات الصرعية الكلية المجهولة السبب. طريقة البحث: اشتمل البحث على 30 مريضا بالصرع العام مابين صرع الرجفة الفتياني والصرع ذي التشنجات الارتجافية الكاملة وصرع الغيبة الصبياني، حيث حوت كل مجموعة 10 أفراد تراوحت أعمارهم مابين 11-25 سنة. شملت المجموعة 7 ذكور و23 انثى. تمت مقارنة المرضى مع مجموعة من الأفراد الأصحاء المطابقين لهم فى السن والنوع ومستوى التعليم كمجموعة ضابطة. تم عمل تقييم إكلينيكي ورسم مخ كهربائي للمرضى كما خضع جميع المشاركين لفحص المخ بواسطة الرنين المغناطيسي والرنين المغناطيسي الطيفي لقياس نسبة الان ايه ان ونسبة الايه ان ايه على الكرياتين فى القشرة المخية الأمام أمامية والمهاد. نتائج البحث: وجد انخفاض ذو دلالة فى نسبة الان ايه ان ونسبة الايه ان ايه على الكرياتين فى المهاد فى كل المرضى وأيضا المجموعات منفصلة بالمقارنة بالمجموعة الضابطة. كما اظهر المرضى ذوي صرع الرجفة الفتياني انخفاضا ملحوظا فى نسبة الايه ان ايه على الكرياتين فى القشر المخية الأمام أمامية مقارنة بمجموعتي المرضى ذوي التشنجات الارتجافية الكاملة وصرع الغيبة الصبياني. وجدت علاقة طردية مباشرة بين نسب الايه ان ايه ونسبة الايه ان ايه على الكرياتين فى كل من القشرة المخية الأمام أمامية والمهاد.



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