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April2014 Vol.51 Issue:      2 Table of Contents
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Cognitive Impairment in Idiopathic Generalized Epilepsies

Mervat Mostafa1, Foraysa Talaat1, Nevin Shalaby1, Neveen El-Fayoumy2, Dalia Labib1

Departments of Neurology1, Clinical Neurophysiology Unit2, Cairo University; Egypt



ABSTRACT

Background: Idiopathic generalized epilepsies (IGEs) are defined by normal imaging as well as normal psychomotor development; yet, cognitive impairments have been described in these syndromes. Objective: To assess the cognitive impairments in IGE patients. Methods: A cross-sectional study conducted on 30 patients with IGEs with ages 16.97±4.47 years and 30 matched healthy volunteers. Patients were subjected to clinical evaluation, electroencephalogram (EEG), neuropsychological battery to assess attention, memory, mental speed, information processing, and visuomotor perception. Results: IGE patients performed significantly poorer than the controls in almost all the tested cognitive domains. Patients with GTCs showed the lowest performance in expressive attention task in comparison to patients with JME and CAE, while JME patients showed the poorest performance in executive functions. Impaired performance in most of tested domains correlated with higher seizure frequency, longer disease duration, and less years of education. Attention was poorer in patients with interictal discharge compared to those with normal interictal EEG. Conclusion: IGE patients may exhibit impaired cognitive function, despite having normal intelligence. The observed cognitive impairments correlated mostly with disease duration, seizure frequency, and educational level. [Egypt J Neurol Psychiat Neurosurg.  2014; 51(2): 215-221]

Key Words: Idiopathic generalized epilepsy, cognitive functions.

 Correspondence to Nevin M Shalaby. Department of Neurology, Cairo University, Egypt. Tel.: +201001493242. Email: nevine.shalaby@kasraliany.edu.eg.





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 combinations. Although patients with IGEs have normal psychomotor development, yet, several studies have pointed to the presence of some form of cognitive impairment in those patients1,2, but their mechanism is unknown. Potential mechanisms, like genetic factors, seizure influence, underlying brain abnormalities, and antiepileptic drug effects, have been implicated 3,4.

In the present work, we tried to assess the cognitive impairments in IGE in a cohort of Egyptian patients.

 

SUBJECTS AND METHODS

 

This was a case control study conducted on 30 patients with IGEs: juvenile myoclonic epilepsy (JME); generalized tonic clonic seizures (GTCs); and childhood absence epilepsy (CAE), each forming 10 patients, diagnosed according to the international classification of epileptic seizures 5 with ages from 11

 

to 25 years (16.97±4.47), they were 23 females (76.67 %) and seven males (23.33 %).  Thirty healthy volunteers age, sex, and educational level matched with patients were also included. All subjects were right handed. The patients were recruited from epilepsy outpatient clinic, Kasr Al-Ainy School of Medicine, Cairo, Egypt, during the period from April 2008 to September 2010.

Inclusion Criteria were age from 10-25 years, normal development prior to seizure onset, normal brain imaging, normal metabolic profile; average IQ (>85%) for patients (using Wechsler intelligence scale for children (WISC) in patients < 16 y, and  Wechsler adult intelligence scale  (WAIS) for patients >16 y). Patients were selected from Arabic speaking schools and with relatively the same socio-economic status.

Exclusion Criteria comprised symptomatic/ syndromic epilepsy, neurological deficits or psychiatric illness, physically handicapped children, drug intake other than AEDs, and illiteracy.

The patients or their guardians signed informed consent, and approval from Cairo University Hospitals Research Ethics Committee was obtained.

Patients were subjected to: 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. Electroencephalogram (EEG) 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 seven patients developed seizures during recording. III. Neuropsychological battery (Arabic version) six was designed by a senior psychologist according to Aldenkamp et al.7 Duration of ≥ 1 week from last seizure was required. The following cognitive domains were assessed: a)   global intellectual functions (both verbal and performance skills); b) specific cognitive functions: such as attention, memory, and other higher order cognitive processes such as mental speed, information processing, and visuomotor perception as follows: Similarity Test and Block Design Test derived from WISC & WAIS to assess selective functions on IQ including the verbal Scale of IQ (VIQ), and Abstraction Abilities, and the performance scale of IQ and the constructional and visuospatial abilities, respectively; The Paced Auditory Serial Addition Test (PASAT); Expressive Attention Task, and Receptive Attention Task (A & B) to assess both sustained and selective attention, in addition to calculation, working memory, and psychomotor speed. Memory was assessed  using Spatial memory test, Incidental (Verbal) Memory Test, and Number Recall to measure visuospatial memory and simultaneous processing; verbal-associate memory; and measure attention, working memory, and sequential processing respectively. Trail Making Test (A & B) and Visual Search Test for Mental Speed and information Processing.

 

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 of the performance in the cognitive tests in individual patients was defined as a value outside the two SD of the mean of normal controls. A p-value less than 0.05 was considered significant.

 

RESULTS

 

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

EEG Results:

All patients had abnormal EEGs either inter-ictally (23) or ictally (7), in the form of generalized spike-wave or polyspike-wave complexes with a normal background. 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.

 

Psychometric Results:

All IGE patients performed significantly poorer than the controls in global intellectual functions, attention, memory, and mental speed and information processing (Table 2).

Patients with GTC showed the lowest performance in expressive attention task in comparison to patients with JME and CAE. Whereas, CAE showed the best performance in similarities and trail making A tests (Table 3). Table (4) shows the frequency of subjects with abnormal psychometric performance in the whole study group.

Higher seizure frequency correlated with worse performance in block design part of global intellectual function(r=-0.48; P=0.007), attention tests; PASAT (r= -0.53; P=0.002), expressive attention task (r= 0.64; P=0.001); and receptive attention task (r= -0.52; P=0.003);  spatial memory (r= -0.41; P=0.02), and information processing and mental speed: trail making A (r=0.45; P=0.01); Trail making B (r= 0.41; P=0.03), and visual research test (r= 0.52; P=0.003). Whereas, disease duration correlated with worse performance in receptive attention (r= -0.37; P=0.04) and trail making A (r=0.45; P=0.01). A statistically significant negative correlation between the age at seizure onset and visual research test was found, while no statistically significant correlation was observed with other tests (r= -0.42; P=0.02).

A statistically significant correlation between the educational level and the performance in most psychometric tests was found as follows: block design (r=0.542; P=0.002), PASAT (r=0.519; P=0.003), expressive attention task (r=-0.626; P=0.001), receptive attention task (1) (r=0.617; P=0.001), spatial memory (r=0.418; P=0.021), number recall (r=0.501; P=0.005), and trail making B (r=-0.418; P=0.002).

A statistically significant lower performance in expressive attention task in IGE patients with abnormal interictal discharges compared to those with normal interictal EEG (P=0.02).

No significant difference in performance on psychometric tests was found between males and females, or between those on poly or monotherpy (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)

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 (23.3%)

23 (76.6%)

 

2 (20%)

8 (80%)

 

4 (40%)

6 (60%)

 

1 (10%)

9 (90%)

 

6 (20%)

24 (80%)

School years

  12-16 y

  6 y

 

17 (56.7%)

13 (43.3%)

 

8 (80%)

2 (20%)

 

5 (50%)

5 (50%)

 

4 (40 %)

6 (60%)

18 (60%)

12 (40%)

Family history

7 (23.3%)

1(10%)

4 (40%)

2 (20%)

4 (13%)

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

  Monotherapy

  Polytherapy

 

25 (83.3%)

5 (16.7%)

 

8 (80%)

2 (20%)

 

9 (90%)

1 (10%)

 

8 (80%)

2 (20%)

 

-

  VPA

23

7

8

8

-

  CBZ

2

1

1

0

-

  PHT

1

0

1

0

-

  LTG

3

1

0

2

-

  TPM

1

1

0

0

-

AEDs antiepileptic drugs, CBZ carbamazepine, GTCs generalized tonic clonic seizures, LTG lamotrigine, PHT phenytoin, TPM Topiramate. VPA valproic acid

 

Table 2. Comparison between performance of IGE patients and controls in psychometric tests.

 

Psychometric test

Patients

Control

P-value

Mean±SD

Mean±SD

Global Intellectual Functions

Block Design

7.16±1.6

9.6±1.4

0.00**

Similarities

8.66±1.7

11±2.2

0.001**

Attention tests

PASAT

18.3±2.9

19.5±1.1

0.05

Expressive Attention Task a

4.9±2.3 €

2.2±1.3

0.001**

Receptive Attention Task (1)

30.6±2.4

31±2.1

0.67

Receptive Attention Task (2) a

4.3±2.6

1.9±0.8

0.001**

Memory tests

Spatial Memory

6.0±2.28

8.2±1.7

0.005**

Incidental Memory

7.5±1.07

8.4±1.1

0.03*

Number Recall

7.5±1.7

9.8±1.7

0.001**

Information processing tests

Trail Making A†

106±34.6†

62±12.6

0.001**

Trail Making B†

202.7±29.4†

114.1±21.2

0.001**

Visual Research†

4.1±1.28†

1.9±0.7

0.001**

aScore is the number of wrong answers, higher scores indicate worse performance

†Scores represent time duration, higher scores indicate worse performance.

PASAT Paced Auditory Serial Addition Test.

*Significant at p<0.05 **Significant at p<0.01

Table 3. Comparison between JME, GTC and CAE regarding psychometric tests.

 

Psychometric test

JME

GTC

CAE

P-value

Mean±SD

Mean±SD

Mean±SD

Global Intellectual functions tests

Block Design

7.1±2.1

6.9±1.5

7.5±1.2

0.728

Similarities

8.1±1.8

8.2±1.3

9.7±1.5

0.04*

Attention tests

PASAT

18.7±2.9

17.1±3.6

19.1±2

0. 297

Expressive Attention Task a

3.8±1.1

6.5±2.7

4.4±1.8

0.017*

Receptive Attention Task (1)

31±2.3

29.8±2.6

31±2.2

0.402

Receptive Attention Task (2) a

5.2±3.3

4.5±2.1

3.4±2

0.312

Memory tests

Spatial Memory

5.8±2.2

5±2.1

7.2±2.1

0.09

Incidental Memory

7.2±1.2

7.3±1

8.1±0.7

0.12

Number Recall

7.9±2.2

6.9±1.7

7.7±1.1

0.426

Information

processing tests

Trail Making A†

127.7±42.8

114.4±16.4

77.7±16.2

0.01**

Trail Making B†

192.3±34.4

216.2±27

199.6±23.5

0.181

Visual Research†

4.6±1. 1

3.3±1.2

4.3±1

0.04*

aScore is the number of wrong answers, higher scores indicate worse performance

†Scores represent time duration, higher scores indicate worse performance.

CAE childhood absence epilepsy, GTCs generalized tonic clonic seizures, JME juvenile myoclonic epilepsy, PASAT Paced Auditory Serial Addition Test.

*Significant at p<0.05 **Significant at p<0.01

 

Table 4. The frequency of subjects with abnormal psychometric performance.

 

Psychometric test

Patients

Control

(n=30)

IGE

(n=30)

JME

(n=10)

GTC

(n=10)

CAE

(n=10)

No (%)

No (%)

No (%)

No (%)

No (%)

Global Intellectual functions tests

Block Design

10 (33.3)

4 (40)

5(50)

1(10)

0(0)

Similarities

2(6.6)

2(20)

0(0)

0(0)

0(0)

Attention tests

PASAT

10(33.3)

3(30)

5(50)

2(20)

0(0)

Expressive Attention Task

15 (50)

3(30)

7(70)

5(50)

1(3.3)

Receptive Attention Task (1)

0 (0)

0(0)

0(0)

0(0)

0(0)

Receptive Attention Task (2)

17 (56.6)

7(70)

6(60)

4(40)

0(0)

Memory tests

Spatial Memory

11(36.6)

4(40)

5(50)

2(20)

0(0)

Incidental Memory

5(16.6)

3(30)

2(20)

0(0)

0(0)

Number Recall

9(30)

3(30)

4(40)

2(20)

0(0)

Information processing tests

Trail Making A

21(70)

10(100)

7(70)

4(40)

0(0)

Trail Making B

27(90)

10(100)

9(90)

8(80)

2(6.6)

Visual Research

20(66.6)

8(80)

8(80)

4(40)

0(0)

CAE childhood absence epilepsy, GTCs generalized tonic clonic seizures, IGE idiopathic generalized epilepsies, JME juvenile myoclonic epilepsy, PASAT Paced Auditory Serial Addition Test.

 

 


DISCUSSION

 

This study has shown that patients with IGE can show subtle cognitive impairments including attention deficit type, memory deficit type, and speed factor type, which goes with the postulation by Aldenkamp et al.7.

Results of our study showed that although patients with IGE may demonstrate normal IQ ranges and average scholastic achievements, yet, they differ significantly from controls in several cognitive domains.

The patients' performance in global intellectual functions, attention, memory, and mental speed and information processing was variable; some showed marked impairment and others less marked affection, with highest frequency of impairment recorded in mental speed and information processing.  These types of impairment were also observed by others8-10.

Generally, patients performed significantly poorer than controls in global intellectual function tests. This agrees with Jeong et al.11. On the contrary, Kim et al.12 found the IQ scores did not differ between the JME patients and controls.

Up to 56% of IGE patients performed worse than controls in attention tests where the difference reached statistical significance in nonverbal attention tests. These observations are consistent with previous reports in which similar tests were administered and IGE patients performed poorer in both non-verbal and verbal attention tests2,8. GTC had the poorest performance in non-verbal attention  relative to JME and CAE, while JME patients showed the poorest performance in Trail-Making A test, which assesses attention, visuomotor abilities, and mental flexibility. This was consistent with Kim et al.12 who reported attention deficits in JME patients. On the other hand, Henkin et al.8 reported that no difference in performance in attention tests in IGE with only typical absence and those with GTC only. The underlying neurological mechanism for an attention deficit in epileptic patients is thought to originate from thalamic or other subcortical levels. This might be derived from the fact that the cortex is believed to be the main generator of the three per second spike and wave discharges, with a special role attributed to thalamo-cortical oscillating circuits13. Some evidence exists that interictal epileptiform activity impairs sustained attention when it occurs in the right hemisphere. Some evidence also exists that ongoing epileptiform discharges during sleep may impair attention14.

More than one third of patients had abnormal lower performance in immediate memory tests. Patients with IGE performed significantly poorer in verbal (auditory) and nonverbal (visual) immediate memory. This was consistent with what was reported by Schouten et al. 15. Patients’ groups did not differ in their performance in relation to each other. In agreement with our findings, Sonmez et al.16 and Pascalicchio et al.17 found a statistically significant difference between JME patients and controls in verbal and visual memory. Henkin et al.12, found a significantly poorer verbal memory in patients with CAE than controls. On the other hand, no significant difference among controls and IGE groups regarding nonverbal memory. The hypothesis most frequently used to explain memory deficits in patients with epilepsy is that memory problems are more marked in focal compared to generalized epilepsies, particularly short-term memory. The impairment is related to the laterality with a verbal learning deficit in the dominant lobe and a figural learning deficit in the nondominant lobe. Impairment is more pronounced in dominant mesio-temporal lobe (MTL) epilepsy; however, memory deficits are also described in extra-temporal epilepsy. Attention and language problems may be, at least in part, responsible for the memory deficits18.

The most severely affected cognitive domain, in IGE patients in our study, was mental speed and information processing, where up to 90% of patients had marked impairment. This goes with previous reports indicating that executive function is a vulnerable domain of cognition among pediatric epilepsy patients regardless of epilepsy syndrome19, 20.

Interestingly, in this work patients with JME showed the poorest performance in trail making A and visual research tests, examining executive functions, relative to GTC and CAE groups. Recent evidence is built up to point to a focal prefrontal dysfunction in JME patients on the basis of frontal lobe neurometabolite changes (which will be handled in details in the part concerning MRS later on). (Pre) frontal lobe dysfunction is responsible for disturbances in executive functions by direct dysfunction (epilepsy focus) or indirect due to the seizure spread and secondary abnormal circuitry. Frontal lobes seem to be the preferred target of ictal and interictal spreading of focal epilepsy as well as idiopathic generalized epilepsies18,21.

Our results denoted that the duration of epilepsy and the frequency of epileptic seizures had a bad impact on cognitive functions of the epileptic patients, while age of onset was only negatively correlated with visual research test for information processing and mental speed.  In agreement with our results, Kim et al.12 reported that lower IQ scores were observed in JME patients with a younger age at onset, more frequent seizures, and longer duration of seizures. In addition, Calpan et al.1 found that worse performance in IQ test in CAE patients with longer duration of illness and uncontrolled seizures. Pavone et al.22 and Sonmez et al.16 found that younger age at seizure onset had negative effects on attention. In addition, Kim et al.12 added that longer duration of disease had harmful effects on attention. In the current study, it is worth noticing that seizure frequency in JME and CAE patients could not be estimated accurately as the occurrence of attacks of myoclonus and absence was usually overlooked by parents who were only concerned with reporting GTCs. Several studies confirmed the parallelism between cognitive impairment and the frequency of epileptic seizures23-25. This parallelism can be explained by the potential brain damage and ischemic cellular changes caused by frequent seizures resulting in cognitive impairment25, 26.

 

In our patients, a significant correlation between the educational level and the performance in most psychometric tests was observed, which goes in accordance with what was previously documented by other studies which reported that individuals with less educational attainment (low cerebral reserve) exhibit poor cognitive function in association with chronicity of epilepsy24,27,28. It is not known whether brain structure or education plays the major role. If continuous education or mental exercise induces neurogenesis in the aged, then it is a possible mechanism in epilepsy. Education may make brains smart and make “good” brains even smarter.

In the current study, it was observed that the presence of interictal epileptiform activities was associated with poorer performance in attention while other domains were not influenced by presence or absence of interictal epileptic discharges. Also, Henkin et al.8 noted that although half of their epilepsy group remained seizure free, yet, their cognitive function were still impaired, and they attributed this to the possibility that some of them might have suffered from interictal epileptic activity. Aldenkamp and Arends29 mentioned that the effect of epileptiform EEG discharges on cognitive function is mild and limited to transient mechanistic cognitive processes like alertness.

Our results showed no significant difference between IGE patients receiving monotherapy and those receiving polytherapy as regards their psychometric performance. This finding was debated by Aldenkamp et al.30 and Mula and Trimble31 who reported that patients with multiple drug therapy (polytherapy) have more cognitive impairment than those with one drug. However, a possible explanation for this discrepancy is that the number of patients on polytherapy, in our study, was small (5/30) relative to those on monotherapy. In the current study, about 93% of our patients were on valproate, hence we are not in place to compare its impact on cognition versus other AEDs. 

 

Conclusion

IGE patients may exhibit impaired cognitive function, despite having normal intelligence. The observed cognitive impairments correlated mostly with disease duration, seizure frequency, and educational level.

 

[Disclosure: Authors report no conflict of interest]

 

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الملخص العربى

 

القصور المعرفي فى مرضى النوبات الصرعية العامة الغير مسببة

 

هدف البحث: تقييم القدرات المعرفية فى مرضى النوبات الصرعية العامة الغير مسببة.

طريقة البحث: اشتمل البحث على 30 مريضا بالصرع العام مابين صرع الرجفة الفتيانية والصرع ذي التشنجات الارتجافية الكاملة وصرع الغيبة الصبيانية، حيث حوت كل مجموعة 10 أفراد تراوحت اعمارهم 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 لبطارية من الاختبارات النفسية لتقييم الوظائف المعرفية بصورة عامة ووظائف الذاكرة (اللفظية والبصرية) والانتباه وسرعة البديهة ومعالجة المعلومات. النتائج: قل اداء المرضى بشكل ملحوظ عن المجموعة الضابطة فى الوظائف المعرفية العامة. مرضى الصرع ذي التشنجات الارتجافية الكاملة قل أداؤهم فى بعض اختبارات الاتنباه عن المجمعتين الاخرين من المرضى. فى حين كان اداء المرضى ذوي الرجفة الفتيانية الأقل فى معالجة المعلومات وسرعة الاداء. سوء الأداء فى الاختبارات المعرفية اتصل بشكل واضح بارتفاع معدل حدوث النوبات ومدة المرض وانخفاض مستوى التعليم. المرضى الذين كانوا يعانون من نشاط كهربائي فى المخ بين النوبات كان اداؤهم المعرفي أقل من هؤلاء الذين لم يعانوا من مثل هذا النشاط.  لم يوجد فارق بين النوعين او الذين يتناولون أكثر من عقار مقارنة بالعقار الواحد.



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