INTRODUCTION

About 65% of  the epilepsies are idiopathic and  presumed to be genetically determined. In 35% of childhood epilepsy, a neuropathologic lesion has been identified¹. The causes of symptomatic epilepsy are numerous and include all broad groups of abnormality, such as vascular, neoplastic, degenerative, traumatic, post-infective and metabolic causes.²

Although the majority of patients with epilepsy show interictal epileptiform activity at repeated routine electroencephalographic (EEG) recordings, this is not the case in about 15%³. Ictal recordings can sometimes be quite decisive, especially when combined with a simultaneous video recording^4.

The lack of sensitivity for the detection of subtle parenchymal abnormalities renders CT inadequate for evaluating seizure patients. High resolution magnetic resonance imaging (MRI) now allows for diagnosis of previously undetected pathology which is not revealed on computed tomography (CT) scan  or even conventional MRI⁵.

This study has been undertaken to throw light on risks, etiology, different types, different EEG and brain MRI abnormalities among Egyptian children in both urban and rural areas.

SUBJECTS AND METHODS

This study was carried out on 280 epileptic infants and children (142 males and 138 females) attended the Neuropsychiatry Department, Tanta University Hospital over a period of one year. The patients’ age ranged between 4 to 215 months  with a mean of 107.6±60.5 months. 

Patients were categorized as follows:

A)     According to the etiology of epilepsy into two groups (ILAE,1989).

                Group I: Patients with idiopathic epilepsy .

         Group II: Patients with cryptogenic or symptomatic.

B)     According to the age of epilepsy onset based on Robert⁶:

-        Infantile group: Patients who developed epilepsy before the age of one year.

-        Early childhood group : Patients developed epilepsy at age of one year up to twelve years .

-        Late childhood group : Patients developed epilepsy at the age of twelve years and up to eighteen years.

In order to subserve the above categorization each patient was subjected to the following: 

I.       Careful history taking with special emphasis on: (i) perinatal history including prenatal history (premature rupture of membrane “PROM”, drug intake, hemorrhage, infection), natal history (place of labour “hospital or home”, type of labour “normal, instrumented by forceps, ventose or cesarean section”, onset of labour “pre-term, full-term, post-term” and  condition of the baby “injury, asphyxia, weight”). Postnatal history inquiries included: infection, trauma, ischemia or hemorrhage to the baby. (ii) developmental history they were categorized as having a " major disability " when their activities of daily living (such as toileting, dressing or feeding) were impaired to the extent that they could not function independently or appropriately for their age; a "minor disability" implied that the children had signs of motor deficits but were functioning independently. The assessment was independent of cognitive status⁷. (iii) family history  of epilepsy  or other CNS disease. (iv) history of seizure.

II.            Thorough neurological examination.

III.   Electrophysiological studies: Interictal awake or sleep EEG was done for each patient using digital paperless multi-channels EEG equipment (PL-270 WINSOR).   

IV.          Video EEG monitoring.

It was done for selected patients according to the following indications:

1-   Differential diagnosis between epileptics and non epileptic attacks.

2-   Seizure classification

3-   Evaluation  of seizure precipitating factors.

IV.          Neuroimaging (MRI).

The Brain MRI scans were  performed using the General Electric (GE) medical system 1.5 Tesla. MRI of the brain  were obtained for all patients aiming at:⁸

1-   Identification of underlying pathologies, in patients with neurological signs.

2-   Assisting the formulation of syndrome-based on etiological diagnosis.

3-   Getting neuroimaging data in patients with complicated and intractable epilepsies.

VI.          Statistical analysis: The statistical analysis was done through SPSS for Windows, version 7.5.

Table 1. Demographic data of patients in both groups, paternal consanguinity and family history among  patients and perinatal history of the patients.

*=Significant

Table 2. Different seizure types in both groups.

Table 3. Neurological deficits in both groups.

*=Significant

Table 4. Brain MRI abnormality among both groups.

*=Significant

Table 5. EEG pattern in both groups.

*=Significant

Fig (1): Distribution of epilepsies and epileptic syndromes in group I and II.

Table 6. Parental consanguinity, family history, perinatal insults and etiology of epilepsy in the three age groups.

*=Significant

Fig (2): Brain MRI of female child age 12 years presented by severe headache, right side hemiplegia and

recurrent partial seizure with secondary generalization. It shows heterotopia with arachnoid cyst.

Fig. (3): Brain MRI of male child age 13-year old presented with uncontrolled complex partial seizures which started at the age of 6 years. T1  weighted coronal section and T2 weighted image axial section (right mesio-temporal  sclerosis).

DISCUSSION

In this study, the patients’ age ranged between 4 to 215 months  with a mean of 107.6±60.5 months. Of the included group of patients, 142 were males and 138 were females with a male to female ratio of 1.1: 1. Also ,we reported predominance of male in symptomatic and cryptogenic group (59.52%) than in idiopathic group (43.5%) of patients and the difference was significant (Table 1). The predominance of male gender was reported by other studies⁹ among pediatric epileptic patients.   

In the current  study, patients from rural areas were significantly higher in symptomatic group (79.3%) compared to idiopathic group (54.54%) (Table 1). The  predominance of rural areas patients was compatible with that  recorded in other series^7,10. This predominance of patients coming from rural area may refer to the location of our hospital near rural areas. Also,  the ratio of rural to urban population  in Tanta region  is about 1.5:1 and this high ratio of rural population was reflected on the predominance  of rural patient in this study. Also, normal labor by non medical personnel  at home is very common  in rural area in this study (45%) in which the infants suffer from bad perinatal care which is important factor for developing epilepsy especially symptomatic and cryptogenic.

In this study, 21% of the patients had a family history of epilepsy and/or neurological  illness and about 29% had parental consanguinity. Although these parameters were more common in idiopathic group (33% and 29%, respectively) compared to symptomatic group (24% and 10%, respectively) the difference didn’t reach a statistical significance (Table 1). Actually the symptomatic epilepsies are usually acquired disorders where genetic factors play a minor role¹¹. An Egyptian study¹² reported to some extent higher  percentage (40%) of family history of epilepsy among infant and children with idiopathic generalized epilepsies. Also in accordance with data presented in the current study, other studies suggested a strong genetic predisposition for idiopathic epilepsies¹³ and that inheritance is complex than monogenic¹⁴. Parental consanguinity might suggest autosomal recessive disorder¹⁵.

In the current study, home delivery mostly by non-medical personnel together with instrumented and cesarean section “C.S.” delivery were significantly higher among symptomatic epilepsy group patients (Table 1). The latter circumstances contributed to the significantly higher incidence of perinatal insults encountered among the symptomatic epilepsy patients in this study (59.52%) compared to that of the idiopathic group (7.14%) (Table 1). These findings are concordant with that reported by other studies^7,9,16,17 highlighting the fact that perinatal insults contribute markedly in the etiology of symptomatic epilepsy in pediatric age group.   

In this study, generalized seizures were present in 69% of patients while partial seizure in 31% (Table 2). Nearly similar findings were detected by other studies in which generalized seizures were common than partial seizures^7,18. Lower percentage  of generalized seizures, reaching down to 12% and up to 44%, were present in other studies^19-23. This low percentage  of generalized seizures among the previous studies may refer to high percentage  of undetermined seizures in these studies. Also, generalized seizures predominate seizure types among patients of this study explained by high percentage of patients who had mixed generalized seizure types (4.3%) and high percentage of generalized epileptic syndromes ; childhood absence epilepsy (13%) and juvenile absence epilepsy (5.9%). 

In this study, 42% of patients had neurological deficit all of them belong to symptomatic and/or cryptogenic group (Table 3). About 66% of neurological deficit was pyramidal sings either unilateral or bilateral. This was nearly compatible with the result of other series^24,25, who found that 49% of their patients had neurological deficits. Some authors categorized  the epileptic patients as symptomatic cases when epileptic seizure occurred in the presence of neurological abnormalities or a history of brain insult or a disorder associated with an increased risk of epilepsy and which were presumed to be etiologically related to childhood epilepsy²⁴. 

In this study, 41% of patients had abnormal MRI all of them were of symptomatic epilepsy while all of idiopathic and cryptogenic epilepsy had normal MRI (Table 4). This is in agreement with previous studies^24,26, which reported no MRI abnormality in children with EEG confirmed idiopathic epilepsy and only found MRI abnormality in symptomatic epilepsies.

In this study, EEG showed that 80% of all patients had abnormal EEG pattern (Table 5). This result is in accordance with a previous study⁷, which reported abnormal EEG in 83% of patients. On comparison between symptomatic and idiopathic groups we found that ,abnormal EEG was more common among symptomatic epilepsy groups (88%) compared to idiopathic epilepsy group (73.5%).

In this study , 20% of all the patients could be diagnosed as specific epileptic syndromes. These data are  concordant with another study²⁷, who could diagnose 20.9% of patients as specific epileptic syndromes. On the other hand, other study²⁸, reported much higher percentage (52%) because they did not exclude provoked seizures from their work. In this study (Fig. 1), 31% of all the patients had localized related epilepsies and epileptic syndromes ;16% were idiopathic and 15.3% were symptomatic or cryptogenic epilepsies and epileptic syndromes. Generalized related epilepsy and epileptic syndromes were present in 68% of patients; 39% were idiopathic and 29% were symptomatic or cryptogenic generalized related epilepsies and epileptic syndromes and finally, 1% had syndromes undetermined whether focal or generalized.

After  patients had been categorized  according  to their age of epilepsy onset  , it was apparent that 3.92% of patients developed epilepsy before the age of one year, 77.14% between the age of 1 to 12 years and 18.2% developed  it between 12 -18 years (Table 6). This is in agreement with other series^10,25, which reported highest incidence of epilepsies in the early childhood period. Such finding might be attributed to the high percentage of patients in this group exposed  to different perinatal insults.     

In this study, Most of patients belong to infantile age group (73%) or early childhood group (68%) were from rural area while 49% of patients in late childhood group were from rural area (Table 6). This finding is in accordance with other study⁷, which found 70% of patients at infantile age group and 61% of early childhood group were from rural area. This high percentage of patients from rural area in both groups reflect the major role of home delivery under supervision of non medical personnel, which is common in rural area, for developing symptomatic epilepsy as a result of poor perinatal care. 

In the current study, parental consanguinity was more prevalent (39.62%) among late childhood group and also family history of epilepsy (32.07%) compared to both infantile and early childhood groups (Table 6). These results agree with a previous study²⁹, who found parental consanguinity in 36% of patients who developed epilepsy at late childhood period. This can explain the high percentage of idiopathic epilepsies among the late childhood grouping where  genetic factor plays an important role. Consequently, paying more attention and awareness of young individuals about the increased risk of epilepsy after familial marriage, as well as pre-marital counseling for couples who have a family history of epilepsy are necessarily as an effective protective program.

About 91% of infant and 29% of early childhood age group had history  of perinatal troubles (Table 6) and this agree with previous series^7,30 which reported that perinatal insults among  patients who developed epilepsy at infant (<1 year) and from (1-12 years) were 80% and 35% respectively. This indicate the importance of perinatal  insults  in developing symptomatic epilepsy at these age groups. This was evident  in this study where symptomatic epilepsy was prominent among infantile age group (72.81%) and early childhood group (41.22%) compared to late childhood group (35.8%).

REFERENCES

1.      Painter MI and Bregman I (2004): Central nervous system disease. In: Nilson (ed.) Essential of Pediatrics (4^th ed). Philadelphia, New York; pp. 718-723.

2.      Wright NB (2001): Imaging in epilepsy: A pediatric perspectives. BJM; (74) 575-589.

3.      John R. (1998): Normal Rhythm. In :John R (ed). EEG in clinical practice 2^nd ed. Butter worth-Heinemann, USA,PP 55-98.

4.      Oguni H, Hayoshi K, Awaya Y et al., (2001): Severe myoclonic epilepsy in infants. A review based on Tokoya women’s Medical University series of 84 cases. Brain Dev; 23 (7) : 736-48

5.      Weishmann UC (2003): Clinical application of neuroimaging in epilepsy. Neurology, Neurosurgery and Psych.; 74: 466-470.

6.      Robert Needlman (2003): Growth and Development: Overview and assessment of variability. In: Richard E (ed) Nelson textbook of Pediatrics (17^th edition), Saunders Company; pp. 23-66.

7.      Selina H, Nalia Z, Mahmoda H, Anisa F and Louis G (2003): Profile of childhood epilepsy in Bangladesh. Developmental Medicine and Child Neurology; 45(7): 477-482.

8.      Johs Duncan(1997):Imaging and epilepsy. Brain, 120: 339-59.

9.      Hauser WA, Annergers JP, and Kurland LT.(1993): Incidence of epilepsy and unprovoked seizures in Rochester, Minnesot (a 1935-1984). Epilepsia ; 34 (3) : 453-463.

10.    Ayse AD, Serdargale A, Tezcan S and Terihd K (2004): Prevalence of epilepsy in Turkish children between age of O and 18 years . J. Child Neurol ;19 : 271-279.

11.    Scheffer LE and Berkovic SF (2000):Rational diagnosis of genetic epilepsies. In:Schmidt D and Schachter S.C. (eds), epilepsy problem solving in clinical practice. Martin Dunitz It., Chap. 9 PP. 111-135.

12.    Shoib T.M (1995): Does the interictal EEG Have a role in the diagnosis of epilepsy :M.sc thesis, Ain Shams University Egypt.

13.    Szptowski P (2000): The genetics of human epilepsies. Ann Acod Med Singapore; 29(3): 284-284.

14.    Berkovic SF (2000): Familial epilepsies quality of life issues in genetic research. Neurology; 55 (5): 53-58.

15.    Delgado Escueta AV ,Derratosa J Mand Median MT (1996): Myoclonic seizures and progressive myoclonic epilepsy  syndromes. In Wyllie E. (ed.) the treatment of epilepsy principles and practice, 2^nd ed., Williams & Wilins, 32: 467-483.

16.    Sander V, Taevilk T and Kassik AE (1997): Epidemiology of childhood Epilepsy in Estonia does it differ from data from developed Europe. Epilepsia; 38(3): 256 .

17.    Khamitous GR Yuldashev VL and Magzhanov RU (1997): The epidemiology of epilepsy in children in the republic of Bashkortostan. Epilepsia; 38 : 257.

18.    Ojuawoh. Joiner KT (1997): Childhood Epilepsy in African, Nigeria, East Afr. Med. J; 74:72-5.

19.    El-Khayate H, El-Hodhod MA and Adel Aziz H (1994): Prevalence and epidemiology of epilepsy among Egyptian infant and children .Scl. Med. J. Cai Synd ; 6(2): 93-101.

20.    Berg AT, Shinnar S, Levy SR and Testa FM (1999): Newly diagnosed epilepsy in children : presentation at diagnosis. Epilepsia ; 40 : 445-452.

21.    Zarrelli MM, Beghi Eand Rocca WA.(1999): Incidence of Epileptic syndromes in Rochester, Minnesota 1980-1484. Epilepsia ;40:1708-1714.

22.    Shinnar S, O’Dell C and Berg AT (1999) : Distraction of epilepsy syndromes in a cohort of children prospectively monitored from the time of the first unprovoked seizure . Epilepsia; 40: 445-452.

23.    Freitag CM, May TW , Pfulfflin M, Konig S and David F (2004): Incidence of epilepsies  and epileptic syndromes in children and adolescence population based study in Germany. Epilepsia; 42(8): 979-985.

24.    Berg AT, Shinnar S, Levy SR and Testa FM (1999): Newly diagnosed epilepsy in children : presentation at diagnosis. Epilepsia; 40: 445-452.

25.    Amal Bassil,Tarek Omar,Adel Zaki,Motaz Abdel-Fatah et al.,(2002):Pattern of diagnostic and therapeutic care of childhood epilepsy in Alexandria ,Egypt. International Journal for Quality in Health Care ;14(4):277-284

26.    King MA, MR and Graeme GD.(1998): Epileptology of the first seizure presentation : a clinical electroencephalographic and magnetic resonance study of 300 consecutive cases. Lancet; 352: 1007-1011.

27.    Jallon M (2005): Epilepsy and epileptic disorders, an epidemiological markers: Contribution of descriptive epidemiology. Epileptic disorder ;14 (1): 1-13.

28.    Loiseau P and Loiseau J(2002):Newly diagnosed epileptic seizures: presentation and diagnosis in Carole study. Epilepsia; 42: 464-475.

29.    Asadi AA and Hojabri K(2005):Risk factors for childhood epilepsy: a case control study. Epilepsy Behav; 6(2): 203-6

30.    Panayiotopoulos CP (2005): Clinical Aspects of the diagnosis of epileptic seizures and epileptic syndromes. In Panayiotopolos (ed.) .The epilepsies (1^st ed.). NBN international Ltd., Estover Road,  Ply mouth, UK, pp. 1-23.