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April2011 Vol.48 Issue:      2 Table of Contents
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Electrophysiological Changes and Behavior of Children with Acquired Dysphasia

Ann A. Abdel Kader1, Hala R. El-Habashy1, Mohamed N. Sadek2,

Hanaa M. Rashad1, Mye A. Basheer1


Departments of Clinical Neurophysiology Unit1, Psychiatry2, Cairo University; Egypt



Background: Language is a cognitive function of the highest order. Language deficit may be one of the earliest indicators of neurological impairment, often presenting as the first sign of a developmental delay. Epileptiform aphasia refers to a language disorder associated with epileptiform features on EEG. Psychopathology is overrepresented in patients with chronic epilepsy. Objective: To elaborate the presence – or absence- of any impact of electrophysiological changes on behavior of children with acquired dysphasia. Methods: Forty patients with age ranging 3-16 years, with history of acquired language disorder were studied for 1. Sleep and wake EEG, 2. Event Related Potentials (ERPs;P300) 3. Psychometric assessment; Childhood behavior checklist and Vineland Adaptive Behavior Scales. In addition, 20 normal age and sex matched subjects were examined for psychometric assessment and P300. Results: Twenty-six - 65% of- patients had epileptiform discharges and/or epileptic history, with heterogeneous diagnoses. Patients group showed significant sociability affection. Moreover, epileptic patients showed significant behavioral affection. Conclusions: The onset of epilepsy in brain systems involved in social communication and/or recognition of emotions- during the brain developmental period- can initiate speech and language development impairment.  Also, it can occasionally be the cause of -or may aggravate preexisting- behavioral disturbances. [Egypt J Neurol Psychiat Neurosurg.  2011; 48(2): 145-149]


Key Words: Childhood behavior, Checklist, Acquired  childhood dysphasia


Correspondence to Ann A. Abdel Kader, Clinical Neurophysiology Unit, Cairo University, Egypt.

Tel.: +20106063114. Email:



Developmental disorders of speech and language (Dysphasias) occur in 7% of children (in the absence of causal factors such as mental retardation, deafness, neurological deficits or social deprivation1.

It was suggested that Continuous Spike Wave during Sleep (CSWS) and Benign Rolandic Epilepsy (BRE) – both occasionally affect language- are two epileptic syndromes  that lead to psychiatric disorders and lower IQ scores2.

The possible direct role of epilepsy should be evaluated in cognitive and/or behavioral abnormalities, as they can be the presenting, and sometimes the only symptom of an epileptic disorder, or can even be caused by paroxysmal EEG abnormalities without recognized seizures3.

The aim of this work was to elaborate the presence – or absence- of any impact of electrophysiological changes on neurobehavioral performance in children with acquired dysphasia.




This study was designed as an outpatient cross sectional comparative study after approval of the ethical research committee that conforms to the provisions of the world medical association's Declaration of Helsinki. The total sample of the study consisted of 40 subjects who were selected on consecutive referral basis recruited from the University clinics (neurology and psychiatry) in Kasr Al Aini university hospitals and non-governmental rehabilitation centers according to the inclusion criteria in the period from November 2007 and November 2009. All subjects included in this study fulfilled the general inclusion and exclusion criteria: age ranged from 3-16 years, having history of normal developmental milestones, before acquiring language delay or arrest, with (or without) history of epilepsy, were studied. All patients families gave consent to participate in the study after full explanation of procedures was provided. The sample was divided into 2 groups:

a.      Group I: Dysphasic patients with epileptic history or epileptiform EEG; 26 patients.

b.      Group II: Dysphasic patients with neither epileptic history nor epileptiform EEG; 14 patients.  Twenty normal age, sex matched subjects served as a normal control group. The patients were subjected to:

1.      Thorough general and neurological history and examination.

2.      Psychological assessment.

-        Vineland Adaptive Behavior Scales (VABS) 4.

-           Child Behavior CheckList (CBCL)5.

3.      Long term monitoring EEG: awake and sleep.

4.      Event Related Potentials (ERPs; P300).


Statistical Methods

All data were expressed as mean and standard deviation. Significance was tested by parametric and non-parametric tests: student's t-test and one way analysis of variance (ANOVA) for ordinal data and Chi square for nominal data. P value less than 0.05 was considered significant, while P value less than 0.001 was considered highly significant. This was in addition to tests for association (correlation studies). Graphic presentation was done using Microsoft office: excel sheets.




A)           Demographic data

Forty patients having acquired dysphasia, 60% were males and 40% were females, with age range 3.6-16 year and mean of 8.5 year. The control group included 20 normal subjects, age and sex matched, with age range 3-15.17 year and mean of 7.94 year. Male/female ratio was 11/15 in group I and 13/1 in group II.

B)           Comparative analysis

1.   Controls  (NCG) versus- all- patients     

The history of the occurrence of the perinatal problems was significantly increased in patients group compared to control group (P <0.05).

P300 amplitude was significantly decreased in patients group compared to control group (P <0.05).

Social quotient and mental age were significantly decreased, while the total CBCL score was significantly increased in the patients group compared to control group.

2.   Group I versus Group II

All performed CBCL scores were significantly increased in patients of group I compared to patients of group II (P <0.005).

N.B.: No other psychometric assessment parameter (in CARS or VABS) show significant change when comparing results from group I and group II patients.

C)           Correlation analysis

         We correlated group I EEG results as regarding the background (wake and sleep), the epileptiform discharges (wake and sleep) and sleep potentiation of the epileptiform discharges, to the results from the psychometric battery. We found that the social quotient value was negatively correlated with the degree of background disorganization in wake and sleep EEG. Organization during wakefulness was judged by visual analysis of posterior rhythm, while during sleep it was judged by the quality of normal sleep changes; Vertex waves, sleep spindles, K-complexes and delta waves, symmetry and synchrony.

D)           The EEG

The EEG results showed 26/40 (65%) patients had epileptiform discharges of variable pictures; during wakefulness and sleep {with only one patient showing epileptiform discharges exclusively during sleep and seven patients with possible Continuous Spike-Wave pattern during Sleep (CSWS)}. Also, 5/40 (12.5%) patients had epileptiform EEG in absence of epileptic history.



Table 1. VABS and CBCL values among patients and Control group.







P value

Social Quotient






≤ 0.05


Mental age






< 0.05


Total CBCL score






< 0.05


CBCL t- externalizing






> 0.05


CBCL t- internalizing






> 0.05


Table 2. Comparison of CBCL values among patients groups.



Group I

Group II

P value

Total score





< 0.001


t- externalizing





< 0.001


t- internalizing





< 0.005







Figure 1. Correlation between social quotient and

EEG wake background disorganization.


Figure 2. Correlation between social quotient and

EEG sleep background disorganization.





The presence of the perinatal problems was the only part of history, in the present work, showing significant increase in patients compared to the controls. Earlier, it was suggested that consistent association of unfavorable events in pregnancy, delivery, and the neonatal phase and the pervasive developmental disorders (PDDs)6. Breech presentation and PDDs were associated in one study, and suggesting a shared etiology rather than causal relationship7. Prenatal stress can cause seizure disorders, cognitive deficits, and abnormalities in immune function, that also have greatly elevated rates in PDDs.8  

In the current work the P300 response amplitude was significantly reduced in the patients group compared to the control group. In autistic patients, studied recently, the absence of response was the most frequently observed alteration followed by the Delayed Latency. These findings suggest that P300 alterations in autistic individuals reflect their cognitive and attention difficulties9. In another earlier study of electrical status epilepticus during sleep (ESES), there is a significant correlation between the length of the ESES period and the extent of residual intellectual deficit at follow-up.10

In the present study, the patients' social quotient, mental ages were significantly lower in comparison to the normal control subjects. While the t-total score in the CBCL, was significantly higher in the patients compared to the normal control subjects. Expectedly, the measures of social cognition differentiate the performance of individuals with autism and controls11. In epileptic patients, countless factors can affect neuropsychological performance: age at onset of seizures, duration of the disorder, type, frequency, seriousness and the total number of seizures, damage to the subjacent brain structure and etiology, location of the electroencephalographic focus, and duration of treatment.12      

The CBCL t-total, t-externalizing, t-internalizing scores were significantly higher among group I patients, compared to group II. In continuous spike-wave pattern during sleep (CSWS) sustained epileptic activity is related to cognitive and behavioral decline. Treatment extends beyond the control of the seizures to amelioration of the continuous epileptiform discharge to improve neuropsychological outcome.13

It was also an interesting finding; the presence of a negative correlation between the EEG disorganization and the social quotient. The relation between EEG and sociability was studied differently in and earlier pilot study showing a greater relative right resting frontal EEG activity (a trait marker of stress) in shy schizophrenic patients.14

Except for some cases, No direct relation could have been confirmed between epilepsy and language disorders15. The occurrence of sleep EEG abnormalities in some children with specific language impairment, the various forms of language dysfunction patterns seen in children with benign childhood epilepsy with centrotemporal spikes, and finally the acquired aphasia in LKS indicate a large spectrum of interactions between language and epilepsy.16

For children with acquired dysphasia it is advised to integrate the efforts of parents, physicians (pediatricians, neurologists, and psychiatrists), psychologists, educators, speech and language pathologists, social workers, audiologists, even an obstetrician at the beginning of the subject's life to achieve an optimum outcome.


[Disclosure: Authors report no conflict of interest]




1.      Watkins KE, Dronkers NF, Vargha-Khadem F. Behavioural analysis of an inherited speech and language disorder: comparison with acquired aphasia. Brain. 2002; 125(3): 452-64.

2.      Taner Y, Erdoğan-Bakar E, Turanlı G, Topçu M. Psychiatric evaluation of children with CSWS (continuous spikes and waves during slow sleep) and BRE (benign childhood epilepsy with centrotemporal spikes/Rolandic epilepsy) compared to children with absence epilepsy and healthy controls. Turk J Pediatr. 2007; 49: 397-403.

3.      Deonna T, Roulet E. Autistic spectrum disorder: evaluating a possible contributing or causal role of epilepsy. Epilepsia. 2006; 47(2):79-82.

4.      Roszkowski, MJ. Concurrent Validity of the Adaptive Behavior Scale as Assessed by the Vineland Social Maturity Scale. Am J Mental Def. 1980; 85 (1): 86-9.

5.      Achenbach TM. Manual for Child Behavior Checklist/ 4-18 and 1991 Profile. Burlington, VT: University of Vermont, Dept. of Psychiatry; 1991.

6.      Meador KJ, Baker GA, Browning N, Clayton-Smith J, Combs-Cantrell DT, Cohen M, et al. Cognitive Function at 3 Years of Age after Fetal Exposure to Antiepileptic Drugs. N Engl J Med. 2009; 16; 360(16): 1597–605.

7.      Bilder D, Pinborough-Zimmerman J, Miller J, McMahon W. Prenatal, perinatal, and neonatal factors associated with autism spectrum disorders. Pediatrics. 2009; 123(5):1293-300.

8.      Kinney DK, Munir KM, Crowley DJ, Miller AM. Prenatal stress and risk for autism. Neurosci Biobehav Rev. 2008; 32(8):1519-32.

9.      Magliaro FC, Scheuer CI, Assumpção Júnior FB, Matas CG. Study of auditory evoked potentials in autism. Pro Fono. 2010; 22(1):31-6.

10.    García-Peñas JJ. Neurocognitive dysfunction in electrical status epilepticus during slow-wave sleep syndrome: Can the natural course of the syndrome be modified with early pharmacological treatment? Rev Neurol. 2010; 50 (3):S37-47.

11.    Losh M, Adolphs R, Poe MD, Couture S, Penn D, Baranek GT, et al. Neuropsychological profile of autism and the broad autism phenotype. Arch Gen Psychiatry. 2009; 66(5):518-26.

12.    de Oliveira EP, Neri ML, de Medeiros LL, Guimarães CA, Guerreiro MM. School performance and praxis assessment in children with Rolandic Epilepsy. Pro Fono. 2010; 22(3):209-14.

13.    Magliaro FC, Scheuer CI, Assumpção Júnior FB, Matas CG. Study of auditory evoked potentials in autism. Pro Fono. 2010; 22(1):31-6.

14.    Jetha MK, Schmidt LA, Goldberg JO. Resting frontal EEG asymmetry and shyness and sociability in schizophrenia: a pilot study of community-based outpatients. Int J Neurosci. 2009; 119(6):847-56.

15.    Campos-Castelló J. Epilepsies and language disorders. Rev Neurol. 2000; 30 Suppl 1:S89-94.

16.    Billard C, Fluss J, Pinton F. Specific language impairment versus Landau-Kleffner syndrome. Epilepsia. 2009; 50 Suppl. 7: 21-4.



الملخص العربى


التغيرات الكهروفسيولوجية وسلوك الأطفال مرضى إضطراب التحدث المكتسب


اللغة من أعلى القدرات المعرفية مقاما, وقد يكون أول علامات الخلل العصبي و تأخر النمو هو تأثر اللغة, هذا ومن أنواع اضطرابات التحدث ما هو مصاحب لتغيرات صرعية برسم المخ, وحيث أن الاعتلال النفسي متواجد و بقوة في أعراض الصرع المزمن, لذا فقد هدف هذا البحث إلى إيضاح وجود تأثير للتغيرات الكهروفسيولوجية على سلوك الأطفال مرضى إضطراب التحدث المكتسب من عدمه.

تم البحث بدراسة أربعين مريضا, ذكورا وإناثا, تتراوح أعمارهم من 3 إلى 16 سنة, يعانون من إضطراب مكتسب في التحدث, وتم عمل رسم مخ طويل المدى أثناء النوم وأثناء الاستيقاظ, هذا وقد تم عمل تقييمات نفسية للمرضى متضمنة تقييم عمرهم العقلي, قياس معامل ذكائهم الاجتماعي وملئ قائمة لوصف سلوك الأطفال والمراهقين, هذا بالإضافة لإجراء الجهود المثارة السمعية المتأخرة. وتم مقارنة نتائج هؤلاء المرضى ( تقييم العمر العقلي, قياس معامل  الذكاء الاجتماعي, ملئ قائمة لوصف سلوك الأطفال والمراهقين والجهود المثارة السمعية) بنتائج 20 شخص طبيعي من ذات الفئة العمرية وبذات نسبة النوع.

تم أيضا تقسيم المرضى إلى مجموعتين بناءا علي وجود تاريخ مرضي لنوبات صرعية أو وجود تغيرات كهربائية في رسم المخ (المجموعة الأولى) أو عدم وجود أي منهما (المجموعة الثانية), مما بين وجود صور عدة لتغيرات رسم المخ في المجموعة الأولى. هذا وقد وجد تأثر اجتماعي ملحوظ في مجموعة المرضي وتأثر سلوكي ملحوظ في المجموعة الثانية.

وقد تم استنتاج أن بدء الصرع في أنظمة المخ المعنية بالتواصل الاجتماعي والمعرفة والعواطف أثناء فترة التطور العقلي قد يؤثر علي التطور الطبيعي للتحدث واللغة, وعادة ما يحدث أو يزيد من الإضطرابات السلوكية.

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