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July2011 Vol.48 Issue:      3 (Supp.) Table of Contents
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Long Term EEG Monitoring in Childhood Acquired Dysphasia

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

Amani M. Nawito 1, Mye A. Basheer1


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




Background: Dysphasia is a language disorder with impairment of speech and its comprehension. Acquired childhood aphasia is rare but has important conceptual implications for developmental neuropsychology.  Objective: Studying long term monitoring EEG in patients with acquired dysphasia, with/without history of epilepsy, to know- and calculate the ratios of-  its different EEG pictures, and causes. Methods: Forty patients with age ranging 3-16 years, with history of acquired language disorder were studied for Sleep and wake EEG and Childhood Autistic Rating Scale (CARS). In addition, relevant clinical history of 20 normal age and sex matched subjects were studied. Results: Twenty-six - 65% of- patients had epilepsy by history and/or epileptiform discharges, and had heterogenous diagnoses.  Only 17.5% of patients showed sleep induced potentiation for epileptiform changes. 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. In acquired epileptiform childhood dysphasia there is no specific EEG pattern that can be a clue or applied as a diagnostic criterion for that entity. [Egypt J Neurol Psychiat Neurosurg.  2011; 48(3): 291-294]


Key Words: Landau Kleffner Syndrome, Epileptiform encephalopathies, Pervasive Developmental disorders



Corresponding author: Ann A. Abdel Kader, Clinical Neurophysiology Unit, Faculty of Medicine, Cairo University; Egypt. Tel.: +20106063114. Email:



Aphasia literally means no speech. But the speech impairment in aphasia could range from complete absence of speech to difficulty in naming a few objects. It is caused by brain damage, usually in the left side of the brain which is responsible for language and communication. The word comes from the Greek dys- (impairment) and phasia (speech)1. Developmental disorders of speech and language occur in 7% of children (in the absence of causal factors such as mental retardation, deafness, neurological deficits or social deprivation2.

The differentiation between neurological diseases that can mimic psychiatric disorders, and vice versa, is crucial. Among psychiatric disorders, autism fits this model since it is associated with many organic diseases with different etiologies, including chromosomal disorders, metabolic disorders, congenital infections, neonatal anoxia, prenatal injury and others. Moreover, many children without autism showed severe disturbances of language, cognition, perception deficits associated with other behavioral disorders, which comprise the autistic spectrum disorders. Landau-Kleffner-Syndrome (LKS) of unknown etiology affects previously normal children and

is designed as an epileptic syndrome, characterized by acquired aphasia, EEG abnormalities and epilepsy. In this syndrome, behavioral changes can mimic autistic conditions, especially in patients with autistic regression (AR), since in both there is impairment of language, and behavior3.

The aim of this work was to study long term EEG monitoring in patients with acquired dysphasia, whether giving history of epilepsy or not, to stand on the different EEG pictures related to it, identify their causes and calculate their ratios.




       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. Five patients from the patients of group I showed epileptiform EEG with no epileptic history.

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.            Long term monitoring EEG: awake and sleep.

3.            Childhood Autistic Rating Scale (CARS)4


Statistically, 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.




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

                  There was no significant difference as regarding the maternal age of patients from patients group and control group.

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

2.   Group I versus Group II

The study found significantly decreased mean relative illness duration (P< 0.05), significantly increased Anti-Epileptic-Drugs (AED) intake history (P<0.05), and significantly increased neurological deficits (P<0.05), all in comparison of data from group I to that of group II. As regarding the AED intake history, heterogeneous drug groups were used-at any time of illness- including classic AEDs and new AEDs (e.g Sulthiame).


C)           EEG results

The EEG results in group I were as follows:

§   26 patients had epileptic history and/or epileptiform EEG

§   9 (34.61%) patients having focal epileptiform discharges; 2 patients having right sided discharges; 7 patients having bilateral discharges.

§   5 (19.23%) patients having generalized discharges; 2 patients having awake secondary generalized (secondary bilateral synchrony of) discharges.

§   2 (7.7%) brother patients having multifocal epileptiform discharges.

§   7 (26.92%) patients showing potentiation of the focal discharges and/or generalizations during sleep.

§   5 (19.23%) patients having nonspecific focal or diffuse slowing.

§    1 (3.8%) patient having epileptiform discharges exclusively during sleep.

N.B.: The EEG results of the five patients with epileptiform EEG in absence of epileptic history were as follows:

§   1 (3.8%) patient showing a picture suggestive of absence epilepsy

§   1(3.8%) patient showing a generalized epileptogenic dysfunction.

§   1 (3.8%) patient showing a right centro-temporal epileptogenic dysfunction.

§   1 (3.8%) patient showing right postero-temporal epileptogenic dysfunction

§   1 (3.8%) patient showing bilateral temporal epileptogenic dysfunction with secondary generalization.




In this study, there was increased male ratio in group II (non epileptic, dysphasic patients); mainly composed of patients having Autism Spectrum disorders (ASDs), compared to group I (epileptic dysphasic patients). Predominance in males is noticed in ASDs) (all except Rett syndrome)5.

The current study reported no significant difference between maternal age; of patients vs. control group subjects, or patients from different groups. The association between parity and autism is complicated by the difficulty in separating parity effects from the possible effects of maternal age6.

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. Prenatal stress can cause seizure disorders, cognitive deficits, and abnormalities in immune function7.

       The mean relative duration of the illness (acquired language impairment) was significantly increased among patients in group II compared to patients from group I. We are hypothesizing that epileptic patients are diagnosed and treated earlier in their life than autistic patients. This is possibly due to the more noticeable symptomatology of epilepsy, especially when having motoric semiology, compared to less noticeable signs of autism spectrum disorders.

One of the patients of this study- from group I- was diagnosed formerly as benign focal epilepsy of childhood, experienced dramatic language impairment following the administration of sulthiame. Antiepileptic drugs can sometimes worsen epileptic seizures. As an example, lamotrigine (LTG) was associated with seizure worsening in a female child with benign partial epilepsy that evoluted towards a Landau-Kleffner-like syndrome8.

Neurological deficits were significantly increased among patients of group I compared to group II. In autism, there is no agreement on the anatomical extent, timing, and consistency of the biological abnormalities across subjects, although magnetic resonance imaging studies have highlighted structural pathologies9.

Recently, Landau-Kleffner was seen as the rare and severe end of a spectrum of cognitive-behavioral symptoms that can be seen in idiopathic focal epilepsies of childhood, the benign end being the more frequent typical rolandic epilepsy. The severity and type of deterioration correlate with the site and spread of the epileptic spikes recorded on the EEG within the perisylvian region10. 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 epilepsy11.

In a recent study- on epileptic Autistic Spectrum Disorders (ASD) patients- the EEG results were variable. Of the patients, 23.3% showed a slow background rhythm for age, 9.9% showed asymmetry, 10% showed slow and disorganized background rhythm, 50% showed focal spikes or sharps, 6.6% showed generalized sharp and wave discharges, and 20% exhibited continuous sharp and slow waves during slow sleep (CSWS)12. In the present study, the EEG results of group II patients varied too. At the mildest form it was focal epileptiform discharges; right sided or bilateral, mainly at the temporal region. Generalized epileptiform discharges, slowing; focal or diffuse were also concluded. Even multifocal epileptiform discharges and potentiation of epileptiform discharges during sleep were found in a considerable percentage of the patients. Although seen in only one patient, epileptiform discharges occurring exclusively during sleep were also found. Hence, in acquired epileptiform childhood dysphasia there is no specific EEG pattern that can be a clue or applied as a diagnostic criterion for that entity.

For children with acquired dysphasia, a mandatory Long-term EEG monitoring (wake and sleep EEG) is recommended for an optimum diagnosis.


[Disclosure: Authors report no conflict of interest]




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3.      Ribeiro KM, Assumpção FB Jr., Valente KD. Landau-Kleffner and autistic regression: the importance of differential diagnosis. Arq Neuropsiquiatr. 2002; 60(3-B):835-9.

4.      Schopler E, Reichler RJ, DeVellis RF, Daly K. Toward objective classification of childhood autism: Childhood Autism Rating Scale (CARS). J Autism Dev Disord. 1980; 10 (1): 91–103.

5.      Chiu S, Hagerman RJ. Pervasive Developmental Disorder [Internet]. New York: WebMD LLC, Medscape LLC. [Cited 2010 October 29]. Available from:

6.      Juul-Dam N, Townsend J, Courchesne E. Prenatal, Perinatal, and Neonatal Factors in Autism, Pervasive Developmental Disorder-Not Otherwise Specified, and the General Population. Pediatrics. 2001; 107(4): e63.

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

8.      Battaglia D, Iuvone L, Stefanini M, Acquafondata C, Lettori D, Chiricozzi F, et al. Reversible aphasic disorder induced by lamotrigine in atypical benign childhood epilepsy. Epilep Dis. 2001; 3(4):217-22.

9.      Brun CC, Nicolson R, Leporé N, Chou YY, Vidal CN, DeVito TJ, et al. Mapping brain abnormalities in boys with autism. Hum Brain Mapp. 2009; 30(12): 3887-900.

10.    Deonna T,  Roulet-Perez E. Early-onset acquired epileptic aphasia (Landau-Kleffner syndrome, LKS) and regressive autistic disorders with epileptic EEG abnormalities: the continuing debate. Brain Dev. 2010; 32(9):746-52.

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

12.    Lee H, Kang HC, Kim SW, Kim YK, Chung HJ. Characteristics of late-onset epilepsy and EEG findings in children with autism spectrum disorders. Korean J Pediatr. 2011; 54(1): 22–8.




الملخص العربي


رسم المخ طويل المدى فى مرض اضطراب التحدث المكتسب في الطفولة


اضطراب التحدث المكتسب في فترة الطفولة هو مرض قليل الحدوث, وعلى الرغم من ذلك فهو ذو تأثير فائق على التطور العصبي والنفسي لذا فقد هدف هذا البحث إلى دراسة رسم المخ طويل المدى لمرضى اضطراب التحدث المكتسب ,مع وجود نوبات صرعية في التاريخ المرضي أو لا, وذلك لمعرفة أسباب المرض, ومعرفة نسبة حدوث هذه الأسباب, بالإضافة إلى معرفة التغيرات المحتملة في رسم المخ طويل المدى.

تم البحث بدراسة أربعين مريضا, ذكورا وإناثا, تتراوح أعمارهم من 3 إلى 16 سنة, يعانون من اضطراب مكتسب في التحدث, وتم عمل رسم مخ طويل المدى أثناء النوم وأثناء الاستيقاظ, هذا و قد تم ملئ استمارة تقييم مقياس التوحد في الطفولة, هذا بالإضافة لإجراء الجهود المثارة السمعية المتأخرة. و تم مقارنة التاريخ المرضي لهؤلاء بتاريخ 20 شخص طبيعي من ذات الفئة العمرية و بذات 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, وأسباب متعددة للمرض ووجد لدى سبعة مرضي تزايد ملحوظ في التغيرات الكهربائية في رسم المخ أثناء فترة النوم مقارنة برسم المخ أثناء فترة الاستيقاظ, في حين انتمت غالبية المرضى من المجموعة الثانية إلى الطيف التوحدي.

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 و أنه لا توجد تغيرات محددة في رسم المخ قابلة للتطبيق كمعيار تشخيصي لمرض اضطراب التحدث المكتسب في الطفولة.


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