epilepsi

Case Report

EPILEPSY IN CHILDHOOD

Presenter : Rizky Indah Soraya

Day/Date :

Supervisor in charge : dr. Hj. Tiangsa Br. Sembiring, M.Ked (Ped), Sp.A (K)

INTRODUCTION

Epilepsy is one of most frequent of all neurologic disorder. Often it is only the

manifestation of a disease state that is otherwise inapparent but persists for lifetime and

requires regular medical care. In many other cases, seizure complete intercurrent medical and

neurologic illnesses or brain injuries.1 As proposed by the International League Against

Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE) in 2005, epilepsy is defined

as a brain disorder characterized by an enduring predisposition to generate epileptic seizures

and by the neurobiologic, cognitive, psychological, and social consequences of this condition. 2, 3

The incidence of epilepsy in children reported from various countries with a wide

variation, about 4-6 per 1000 children, depending on the study design and population age

group. In Indonesia, there are at least 70000-140000 case of epilepsy by increments of 70,000

new cases each year and an estimated 40% -50% occur in children. Most of idiopathic

epilepsy, but often also accompanied by neurological disorders such as mental retardation,

cerebral palsy, and so caused abnormalities in the central nervous system. In addition, also

known as some epilepsy syndromes in children include Ohtahara syndrome, infantile spasms

(West syndrome), Lenox-Gestaut syndrome, benign rolandic epilepsy, and juvenile

myoclonic epilepsy.4

The history can provide important information about the type of seizures. Children who

have a propensity to develop epilepsy may experience the 1st convulsion in association with a

viral illness or a low-grade fever. Seizures that occur during the early morning hours or with

drowsiness, particularly during the initial phase of sleep, are common in childhood epilepsy.5

A prolonged personality change or intellectual deterioration may suggest a degenerative

disease of the CNS, whereas constitutional symptoms, including vomiting and failure to

thrive, might indicate a primary metabolic disorder or a structural lesion. It is essential to

obtain details of prior anticonvulsant medication and the child's response to the regimen and

to determine whether drugs that may potentiate seizures, including chlorpromazine or

methylphenidate, were prescribed. 5

The description of the seizure along with the family history can provide clues to the

presence of possible genetic epileptic syndromes. These include autosomal dominant

nocturnal frontal lobe epilepsy, familial benign neonatal convulsions, familial benign

infantile convulsions, autosomal dominant febrile seizures, partial epilepsy with auditory

symptoms, autosomal dominant frontal lobe progressive epilepsy with mental retardation,

absence epilepsy, and febrile seizures with later partial complex seizures.5

Diagnosis of epilepsy is determined by examination consisting of anamnesis, physical

examination and investigations. The usual investigations consisting of blood tests, urine,

cerebrospinal fluid, electroencephalography and imaging. EEG examination is the best

investigation to establish the diagnosis of epilepsy. The focal abnormalities on EEG showed

the possibility of structural lesions in the brain, while their common abnormality on EEG

showed the possibility of a genetic or metabolic abnormalities.6

The ultimate goal of epilepsy treatment is to free patients from epileptic seizures, without

interfering with the normal function of the CNS so that patients can perform their duties

without interference.7 The type of anti-epileptic drugs is highly dependent on the nature of

epileptic seizures. Most of epilepsy can be treated with phenobarbital, carbamazepine,

primidone, phenytoin, ethosuximide, and valproic acid. 8

Epilepsy prognosis depends on several things, including the type of

epilepsy causes, when treatment is started , and adherence to

medication. In general, the prognosis of epilepsy is quite encouraging. 9

The aim of this paper is to report a case about Epilepsy in a 2 years old girl.

CASE

Name : KA

Age : 2 years 4 months

Sex : Girl

Date of Admission : April, 12nd 2015

Chief Complaint : Seizure

History : Seizures experienced by patient since this day with the frequency 2

times a day. Last seizures experienced one hour before admission to the hospital. Seizures

occur all over the body with duration of 10 minutes and seizures stop with diazepam rectal

administration in the clinic. Patient asleep after had the seizure. Patient experienced the

seizures after preceded by the fever.

Patient had a history of seizures since the age of 5 months with the frequency 5 times daily

with generalized seizure. Seizures occur in the whole body with jerking

movements of the arms and legs repeatedly and accompanied by stiffness

in the whole body. Seizures are not preceded by the fever. Seizures occurred in duration

of 5 minutes.

History of fever was found since one week with a temperature of fluctuation. Fever is not

accompanied by shiver. While in the room, patient is not in the fever state.

History of cough was found since 2 week. No productive.

History of trauma was not found.

History of diarrhea was not found. The frequency of bowel movements in the last 2 days was

as much as 4 times daily with the volume of ¼ cup aqua per times defecating. Consistency of

stool is more watery. Blood was not found in stool.

History of vomiting was found since 2 days ago, especially after the cough. The frequency of

vomiting is 3 times a day with a volume of ½ teaspoon per times vomiting. The vomits

contents of regurgitated food and beverages consumed before.

History of growth: to date patient can only lying to the side.

History of Birth: Second child. Spontaneous birth, not cried immediately as soon as born.

Enough months at birth. Birth weight was 2.4 kg. History of cyanosis was found.

History of previous illness: Epilepsy in neurology unit of Adam Malik’s General Hospital

and regularly controls.

History of previous medication: Valproic acid 2 x 1.6 cc (22 mg / kg / day) and paracetamol

Feeding History

From birth to 5 months : Breast Milk

From 5 months until now (2 years 4 months) : Formula milk + Rice Porridge

History of Growth and Development

Lying to the left/right : 8 months

Crawling : Not yet

Sitting : Not yet

Standing : Not yet

Walking : Not yet

Physical Examination

Generalized status

Body weight: 7,4 kg, Body length: 72 cm, Head circumference: 40 cm, Arm circumference:

14,4 cm

BW/BL : -2 SD < z-score < -1 SD

BW/age : z-score < -3 SD

BL/age : z-score < -3 SD

HC/age : z-score < -2 SD

AC/age : -1 SD < z-score < 0 SD

Presens status

Sensorium : Alert

Blood Pressure: 100/60 mmHg

Heart Rate: 128 x/i

Respiratory Rate: 28 x/i

Body Temperature: 40,1oC.

Anemic (-). Icteric (-). Cyanosis (-). Edema (-). Dyspnea (-).

Localized status

Head : Face : No edema.

Eye : Light reflex (+/+), Isocoric pupil (+), no pale in inferior palpebra

conjunctiva, no icteric sclera and no edema in inferior and superior

palpebra.

Ear / Nose / Mouth : within normal limit.

Neck : No lymph node enlargement.

Chest : Symmetrical fusiformis, no retraction and muscle wasting.

HR: 128 bpm, regular, no murmur.

RR: 28 tpm, reguler, coarse crackles (+/+).

Abdomen : Soepel. Liver and spleen were not palpable. No shifting dullness. Bowel

peristalsis was normal.

Extremities : Pulse was 128 bpm, regular, adequate pressure and volume, warm, CRT <

3”. BP: 100/60 mmHg.

Urogenital : Female. Anus (+).

Neurological Examination

Sensorium : GCS 14 (E4 V4 M6)

Nervus Olfactorius : Normosmia

Nervus Opticus : Light reflexes (+/+), pupils isochoric 3mm

Nervus Oculomotorius, trochlear, abducens: Normal eye movement

Nervus trigeminus : Mastication as well

Nervus Facialis : Symmetrical lip angle

Nervus Auditorius : Normal

Nervus Glossofaringeus, vagus : Uvula in medial

Nervus Accesoriu : Normal

Nervus hipoglossus : Tongue in medial

Motorical Examination : within normal limit

Right/left muscle strength :

Physiological reflexes : Right Left

KPR/APR (+/+) (+/+)

Biceps/Triceps (+/+) (+/+)

Pathological reflexes : Babinsky ( - ) ( - )

55555 55555

55555 55555

Chaddock ( - ) ( - )

Gordon ( - ) ( - )

Oppenheim ( - ) ( - )

Meningeal’s sign : Nuchal rigidity (-), Kernig’s sign (-), Brudzinski I/II (-).

Laseque sign (-).

Electroencephalography Test Result: July 8th, 2013 in ST. Elisabeth Hospital

- Recording is done in a state of sleep with premedication chloralhydrate syrup. basic

rhythm waves with a frequency of 6-7 cycles per second voltage being mixed with a

frequency of 4-5 cycles per second. Does not seem significant asymmetry. There are

sharp waves and waves of spikes waves in the posterior right temporal and left

frontal. Photic stimulation did not result in any significant change.

- Impression : EEG can be in accordance with the general convulsion disease with

multifocal irritative focus.

Differential Diagnosis:

- Generalized symptomatic epilepsy + Bronchopneumonia + Global Development

Delayed + Cerebral Palsy + Gastroenteritis without Dehydration

- Generalized idiopathic epilepsy + Bronchopneumonia + Global Development Delayed

+ Cerebral Palsy + Gastroenteritis without Dehydration

Working Diagnosis:

- Generalized symptomatic epilepsy + Bronchopneumonia + Global Development

Delayed + Cerebral Palsy + Gastroenteritis without Dehydration

Management:

- O2 ½ L/i nasal canule

- IVFD NaCl 0,9% 10 gtt/i micro

- Injection Paracetamol 100 mg / 8 hour / IV

- Injection Ceftriaxone 400 mg / 12 hour / IV Skin test

- Zinc 1 x 20 mg

- Valproic acid 2 x 1,8 cc (25 mg / kgBW / day)

- Diet : chicken porridge in diluted 740 kcal (100 kcal/ kgBB/ day) with 15 gram protein

Diagnostic Planning:

- Complete Blood Count

- Arterial Blood Gas Analysis

- Serum Electrolytes

- Electroencephalography test

- Thoracic X-ray

- Consul to Neurology division

- Consul to Respirology division

- Consul to Growth and development division

- Consul to Gastroenterohepatology division

April 13rd, 2015

S Fever (-), Seizure (+)

O Sens: GCS 15 (E4 V5 M6), Temp: 37oC. Anemic (-). Icteric (-). Edema (+). Cyanosis (-).

Body weight: 7,4 kg, Body length: 72 cm.

Urine colour : yellowish

Head Light reflex (+)/(+). Conjunctiva palpebra inferior anemic (-). Isochoric

pupil.

Neck Jugular vein pressure R-2 cmH2O. Lymph node enlargement (-).

Thorax Symmetrical fusiformis, no retraction and muscle wasting.



Abdomen Soepel. Liver and spleen were not palpable. No shifting dullness. Bowel


Extremitie

s

Baggy pants (-), thinning of subcutaneous fat (-), muscle hypotrophy (-).

Crazy pavement dermatosis (-). Pulse 140 x/i, regular, adequate p/v,

warm, CRT < 3”. Pitting edema (-) pretibia. BP: 120/70 mmHg.

Genital Female, within normal limit

Laboratory Findings: April, 12nd 2015

Parameters Value Normal Value

Complete Blood Count

Hemoglobin 9,2 gr% 11,3 – 14,1 gr%

Hematocrite 29,2 % 37 – 41%

Erithrocyte 3,4 x 106 /mm3 4,40 – 4,48 x 106 /mm3

Leucocyte 13,8 x 103 /mm3 4,5 – 13,5 /mm3

Trombosit 263.000 /mm3 150000 – 450000 /mm3

MCV 85,90 fl 81 – 95 fl

MCH 27,10 pg 25 – 29 pg

MCHC 31,50 gr% 29 – 31 gr%

RDW 16,70 % 11,6 – 14,8 %

Diftel 0,3 / 0,4 / 72,2 / 19,4 / 7,7

Arterial Blood Gas Analysis

PH 7,436 7,35 – 7,45

pCO2 29,6 mmHg 38 – 42

pO2 188,4 mmHg 85 – 100

Bikarbonat (HCO3) 19,5 mmHg 22 – 26

Total CO2 20,4 mmHg 19 – 25

Base Excess (BE) -3,4 mmHg (-2) – (+2)

Saturasi O2 99,7% 95 – 100

Carbohydrate Metabolism

Blood Glucose ad random 155 mg/Dl < 200

Electrolytes

Sodium (Na) 133 mEq/L 135 – 155

Pottassium (K) 3,6 mEq/L 3,6 – 5,5

Chloride (Cl) 102 mEq/L 96 – 106

Imunoserologi

Procalcitonin 8,72 ng/mL <0,05

Peripheral blood smear: Normochromic normocytic anemia and leukositosis

Faeces: April 12nd, 2015

Macroscopic

Color : yellowish

Consistency : watery

Blood : Negative

Mucous : Negative

Microscopic

Worm’s egg : negative

Amoeba : negative

Eritrocyte : 0-1

Leucocyte : 0-1

A Generalized symptomatic epilepsy + Bronchopneumonia + Global Development Delayed


P Management:

- O2 nasal canule ½ L/i



- Injection Ceftriaxone 400 mg / 12 hour / IV Skin test

- Valproic acid 2 x 1,8 cc (25 mg / kgBB / hari)

- Zinc 1 x 20 mg

- Nebule Ventolin ½ respule + 2,5 cc NaCl 0,9% / 8 jam

- Diet : chicken porridge in diluted 740 kcal (100 kcal/ kgBW/ day) with 15 gram

protein

April 14th, 2015

S Seizure (-), Fever (+), shortness of breath (+)

O Sens: GCS 15 (E4 V5 M6), Temp: 40oC. Anemic (-). Icteric (-). Edema (+). Cyanosis (-).

Body weight: 7,4 kg, Body length: 72 cm.

Urine colour : yelowish to brown


pupil.


Thorax Symmetrical fusiformis, no retraction and muscle wasting.





Extremitie

s

Pulse 165 x/i, regular, adequate p/v, warm, CRT < 3”. BP: 110/70 mmHg.




P Management:


- Injeksi Ceftriaxone 400 mg / 12 hour / IV

- Injeksi Paracetamol 100 mg / 8 hour / IV

- Injeksi Dexamethasone 2 mg/ 8 hour/ IV

- Nebule Flixotide 1 respul / 8 hour

- Valproic Acid 2 x 1,8 cc (25 mg / kgBW / day)

- Chest physiotherapy

- Zinc. 1 x 20 mg

- Diet : chicken porridge 740 kcal with 15 gram protein in diluted 740 cc / day. 123,33

cc / 2 hour ≈ 125 cc / 2 hour.


- Arterial Blood Gas Analysis

- Liver Function Test

- Blood Glucose ad random

- Serum Electrolytes

April 15th, 2015

S Seizure (-), Shortness of breath (+) minimizing, Fever (+)

O Sens: GCS 15 (E4 V5 M6), Temp: 39,0oC. Anemic (-). Icteric (-). Edema (+). Cyanosis

(-).

Body weight: 7,4 kg, Body length: 72 cm. Urine output 2,25 cc/kg/hour

Urine colour : yellowish


pupil.


Thorax Simetris fusiformis. Retraction (-).

HR: 165 bpm, reguler. Murmur (-).

RR: 26 x/i, regular. Coarse crackles (+/+)



Extremitie

s

Baggy pants (-), thinning of subcutaneous fat (-), muscle hypotrophy (-).

Crazy pavement dermatosis (-). Pitting edema (-) pretibia.

Pulse 165 x/i, regular, adequate p/v, warm, CRT < 3”. BP: 120/70 mmHg.


Laboratory Findings: April, 14th 2015

Parameters Value Normal Value

Blood Gas Analysis

pH 7,428 7,35 – 7,45

pCO2 31,9 mmHg 38 – 42

pO2 145,4 mmHg 85 – 100

Bikarbonat (HCO3) 20,6 mmHg 22 – 26

Total CO2 21,6 mmHg 19 – 25

Kelebihan Basa (BE) -3,3 mmHg (-2) – (+2)

Saturasi O2 99,3 % 95 – 100

Liver

Total Billirubin 0,26 mg/dL <1

Direct Billirubin 0,03 mg/dL 0 – 0,2

Alkaline phospatase (ALP) 103 U/L < 281

AST/SGOT 27 U/L < 32

ALT/SGPT 15 U/L < 31

Albumin 2,8 g/dL 3,8 – 5,4

Carbohydrate Metabolism

Blood Glucose ad random 98,20 mg/dL < 200

Electrolytes

Natrium (Na) 131 mEq/L 135 – 155

Kalium (K) 3,6 mEq/L 3,6 – 5,5

Chloride (Cl) 100 mEq/L 96 – 106



P Management:


- Injection Ceftriaxone 400 mg / 12 hour / IV


- Injection Dexamethasone 2 mg/ 8 hour/ IV

- Nebule Flexotide 1 respul / 8 hour + ventoline 1 respule / 8 hour

- Valproic acid 2 x 1,8 cc (25 mg / kgBW / day)

- Zinc. 1 x 20 mg

- Diet : chicken porridge 740 kcal with 15 gram protein in diluted 740 cc / day. 123,33

cc / 6 hour ≈ 125 cc / 6 hour.


- Hyponatremia correction

Natrium need = (135 – 131) x 7,4 x 0,6 = 17,76 mEq

Natrium maintanance need = 2 – 4 mEq/kgBB = 14,8 – 29,6 mEq

Total Natrium needs = 32,56 – 47,36 mEq ≈ 45 mEq

Natrium correction with 0,9% NaCl IVFD 12 cc/hour in 24 hour

Start at 16.00 (15-4-2015) until 16.00 (16-4-15)

- Hypoalbuminemia correction = (3 – 2,8) x 7,4 x 0,8 = 1,184 gr

Albumin 20% = (1,184/20) x 100 cc = 5,92 cc ≈ 6 cc

Albumin 25% = (1,184/25) x 100 cc = 4,726 cc ≈ 5 cc

Discussion

Epilepsy is defined as a condition characterised by recurrent epileptic seizures. An

epileptic seizure is a clinical manifestation presumed to result from an abnormal and

excessive discharge of a set of neurones in the brain. (10) Symptomatic generalized epilepsy

is caused by widespread brain damage. Injury during birth is the most common cause of

symptomatic generalized epilepsy. In addition seizures, these patient often have other

neurological problems, such as mental retardation or cerebral palsy. These epilepsies include

different subtypes and the most commonly known type is the Lennox-Gastaut syndrome:

multiple types of seizures are common in these patient and can be difficult to control. 11

Overall, seizures are a paroxysm of high-frequency or synchronous low frequency

high-voltage electrical discharge that cause a sudden alteration in the CNS. Three conditions

are involved: (1) population of pathologically excitable neurons, (2) an increase in excitatory

glutaminergic activity, and (3) reduction of inhibitory GABAergic projections. In SGE, an

underlying structural or metabolic derangement also present. EEG findings reflect age-related

changes as the brain matures. 12

Assessing the frequency of symptomatic generalized epilepsy (SGE) is difficult

because the definition varies and can be more or less inclusive. It refer to age at onset. In

adulthood, most patient with SGE have a less well-defined syndrome that still has the

characteristics of SGE and is closest to a Lennox-Gastaut syndrome (intractable multiple

seizures types, mental retardation, and cerebral palsy). In infancy, SGE progress to a west

syndrome. In childhood, SGE will proggess to be an epilepsy with myoclonic atonic seizures,

epilepsy with myoclonic absence, and Lennox-Gastaut syndrome. In adolescence-adults, it

will progresses into progressive myoclonic epilepsies. 12

The child 's age and developmental factors affect whether there will be epileptic or not.

In this case, the age of patient’s first seizure are at the age of 5 months and

patient does not have a history of preterm birth. This is consistent with

the theory that suggests that epilepsy is seizures less frequently found in

premature babies because their nervous system has not developed but more common in

infants age. Epileptic seizure is relatively rare in the first months of age, and more often

between the ages of 4 months to 4 years. 13

Epileptic seizures are categorised as either focal or generalised epileptic seizures and

epileptic syndromes. Focal epileptic seizures arise in specific loci in one part of the cerebral

cortex that carry with them identifiable clinical features either subjective or observed.

Consciousness may or may not be retained or there may be partial loss of awareness.

Generalised epileptic seizures involve large areas of brain from the outset, usually both

hemispheres, and are associated with early impairment of consciousness. There range from

absence characterised only by impairment consciousness, to generalised tonic-clonic seizures

in which widespread convulsive activity takes place. Myoclonic, tonic and clonic seizures are

all types of generalised seizures.

Another classification is epileptic syndromes which have been defined by the

commision in Classification and Terminology of the International League against Epilepsy

(ILAE) as a complex of sign and symptoms that defined a unique epilepsy condition. 10

Symptomatic generalized epilepsy (SGE) encompases a group of challenging epilepsy

syndromes. As a group, SGE has 3 main features: (1) multiple seizure types, especially

generalized tonic and atonic seizures; (2) brain dysfunction other than the seizures, in the

intellectual domain (mental retardation or developmental delay) and in the motor domain

(cerebral palsy); and (3) EEG evidence of diffuse brain abnormality. Examples of epilepsy

syndromes that are include in the category of SGE are early myoclonic encephalopathy, early

infantine epileptic encephalopathy with suppression bursts or Ohtahara syndrome, west

syndrome, epilepsy with myoclonic atonic seizures, epilepsy with myoclonic absence,

lennox-gastaut syndrome, and progressive myoclonic epilepsies. 12

Seizure types that exist in these patients is generalized tonic-clonic seizures because

seizures occured in the whole body with jerking movements of the arms and legs repeatedly

and accompanied by stiffness in the whole body. The types of seizures seen in SGE are in the

following: (1) Myoclonic presents with brief muscle jerks, single or in clusters, affecting any

group of muscles, usually in trunks and limbs; (2) Clonic presents with repetitive and

rhytrmic jerking of limbs, neck, or face; (3) Tonic presents with symmetric or asymmetric

stiffening or posturing; (4) Atonic presents with abrupt loss of muscle tone, usually truncal

and resulting in a head drop or a fall; (5) Generalized tonic-clonic seizures; (6) Atypical

absence is similar to abscence seizure but longer and with less clear onset; 12 Absence is

described as episodes of abrupt psychomotor arrest lasting 5-15 second in younger children,

but can be longer in the older child and can be associated with retropulsion of the head,

upward deviation of eyes and eyelid, or perioral myoclonia. 14

The history is the most important diagnostic tool and should include birth, mother’s

pregnancy, and developmental history, CNS infection, head trauma, family history of

seizures, and seizure description by witness. 12 In this case, patient history at birth were not

immediately cry as soon as born and cyanosis showed signs of neonatal asphyxia. Asphyxia

can cause lesions in the hippocampus and the lesions can become the epileptogenic focus.

Asphyxia will cause hypoxic ischemic encephalopathy resulting neuropathological

abnormalities. Neurological disorders can be caused by non-progressive neurological

disorders such as seizures, mental retardation, psychomotor developmental disorders and

motoric disorder. Hypoxia and ischemia will causing elevation of intracellular Na fluid

resulting in brain edema which can cause brain damage. Areas that are sensitive to hypoxia

are the cores in the brainstem, thalamus, and inferior colliculi, while against ischemia is

'watershead area' is the area of the brain hemispheres that gets the least vascularization.

Hypoxia, as previously described, may cause damage or increasing factor inhibition and

excitation functions of the neurons so easily arise epilepsy when there is adequate

stimulation. Babies born with low birth weight will soon be able to experience hypoxia

ischemia, and or intraventricular hemorrhage, with clinical manifestations such as seizures

and can progress to epilepsy later in life. 15

Staring or blank spells, particularly in children with learning difficulties, often cause

diagnostic difficulty. Factors more likely to be indicative of non-epileptic staring include:

staring interrupted by voice or touch, staring associated with rocking and initially noticed by

a professional carer rather than the family. While factors more likely to be an indicative of

epileptic staring include: short, frequency (daily) events, interruption of play and speech,

automatisms, and association with up-gaze and/or urinary incontinance. 10

Investigations were carried out to confirm the diagnosis of epilepsy include

electroecephalography (EEG) and brain imaging. An EEG contributes to identification of

features of a focal or of a generalised epilepsy, syndromes diagnosis, choice of further

investigation, making therapeutic management of epilepsy and making prognosis of epilepsy. 10

When a first seizure has been diagnosed as epileptic, an EEG may be considered for the

purposes of assesing recurrence risk, making a syndromic diagnosis, and identifying

precipitating factors. It should not be used to guide a decision on whether or not to commence

antiepileptic drug medication. 10

But in other cases, age specific patterns may be misinterpreted as epileptiform

discharges. Around 40% of children with seizures will have a normal record on a first

standard EEG recording. Otherwise, the EEG shows paroxysmal activity or background

changes up to 32% of normal children that could be misinterpretated as abnormal.

Epileptiform abnormalities are seen up to 5% of normal children which are higher in rates

than children with epilepsy. So an EEG should only be requested after carefull clinical

evaluation by someone with expertise in childhood epilepsy. 10

Magneting resonance imaging (MRI) scanning is superior to computed tomography

(CT) scanning in elective imaging to identify abnormalities underlying epilepsy and avoids

radiation. Most children with epilepsy should have an elective MRI brain scan. But children

with idiopathic (primary) generalised epilepsies and benign childhood epilepsy with

centrotemporal spikes do not need brain imaging. 10

Other investigations (eg. Cytogenetic, molecular genetic and metabolic) may be

indicated to identify specific aetologies of symptomatic epilepsies and for children with

moderate or severe learning difficulties or cognitive regression. 10 The most common side

effects of valproic acid is severe hepatic toxicity, weight gain, and osteopenia so do liver

function tests while the patient control is recommended. 16

Bronchopneumonia in a patient's diagnosis is made by history, physical examination,

and investigations. From history taking, productive cough, shortness of breath and high fever

were found. In the physical examination, there are symptoms of respiratory distress such as

tachypnea and retraction subkostal, and the coarse crackles in both lung fields. On chest X-

ray examination found the bronchopneumonia appearance that is characterized by diffuse

opacification evenly on both lungs resembling the ground-glass appearancs of respiratory

distress syndrome, patchy infiltrates, accompanied by an increase of peribronchial air-

bronchograms appearance. 17, 18

Cerebral palsy diagnosis in this patients is generally made based on the clinical

pictures. It begins with history of gross motor developmental delay in the first year of life,

abnormal muscle tone, definite hand preference before age 1 year, asymmetrical crawling or

failure to crawl, growth disturbance, increased reflexes, and underdevelopment or absence of

postural or protective reflexes.19 Gross motor milestones of concern with cerebral palsy

include head control at age 2 months, rolling at age 4 months, sitting at age 6 months, and

walking at age 1 year. Infants with cerebral palsy may have significantly delayed gross motor

milestones or show an early hand preference when younger than 1.5 years, suggesting the

relative weakness of one side (eg, reaching unilaterally).19, 20 The patient can only lying to the

right and left since the age of 8 months. Speech and language were under development. Until

the age of 2 years old, patients could only say a word like " ma " and " gak ". In addition to

those mentioned above, The patient’s overall gait pattern should be observed, and each joint

in the lower and upper extremity should be assessed for signs of cerebral palsy, including: (1)

Hip presents with excessive flexion, adduction, and femoral anteversion make up the

predominant motor pattern; scissoring of the legs is common in spastic cerebral palsy; (2)

Knee presents with flexion and extension with valgus or varus stress occur. (3) Foot present

with equinus, or toe walking, and varus or valgus of the hindfoot which is common in

cerebral palsy. Presentation of the hip was found in this patient. 19

Short stature in patients is determined by nutritional status examination showed that the

height is under percentile 3 or below -2 standard deviation. 21 Global Development delay is

the delay in development on two or more aspects where these aspects consists of gross motor,

fine motor, speech or social. Speech delay often encountered in patients with cerebral palsy.

GDD diagnosis in a patient is determined by the status of its growth and development in

which the patient can only speak one or two words at age 2 years. at the age of 2 years the

patient should be able to speak more than one hundred words or 2-3 sentences. in addition,

gross motor development such as walking and climbing did not exist in the patient. 20

Diagnosis of gastroenteritis without dehydration in this patient is determined based on

history, physical examination, and investigations. The frequency of bowel movements in the

last 2 days was as much as four times per day. Consistency of stool is more watery. a history

of vomiting in patients also present. The degree of dehydration is determined based on the

criteria. Criteria without dehydration showed fluid loss is less than 5 percent of body weight.

Degrees without dehydration characterized by the discovery of the main signs and additional

signs, general condition is good, sunken eyes were not found, the oral mucosa does not dry,

skin turgor was good, normal bowel peristaltic, and extremities was warm. 22

The choice of treatment for the various pediatric epilepsies depend on the type of

seizure or epilepsy syndrome. For symptomatic generalized seizures among children,

valproate has been the treatment of choice (first-line monotherapy). For children of any age,

it is recommended that therapy should begin with at least two and possibly three trials of

monotherapy, before trying at least two or possibly three combination of 2 antiepileptic

drugs. If combination therapy with 2 agents is ineffective, then a combination of 3

antiepileptic drugs is recommended. Other drugs which can be used are lamotigrine,

levetiracetam, and topiramate. However, valproate stands out as a broad-spectrum

antiepiletic-drug. Also, it is the treatment of choice as preventive therapy for febrile seizures

and childhood epilepsy with centro-temporal spikes. 23, 24

Valproic acid may increase levels of the inhibitory neurotransmitter gamma-

aminobutyric acid (GABA) in brain; may enhance or mimic action of GABA at postsynptic

receptor sites; and may also inhibit sodium and calcium channels. As adjunctive therapy,

valproic acid may be added to the patient’s regimen at 10-15 mg/kgBW/day and may increase

by 5-10 mg/kgBW/week to achieve optimal clinical response. Ordinarily, optimal clinical

response is achieved at daily doses of less than 60 mg/kgBW/day.12 In this case, the patient

had a history of using valproic acid as much as 22 mg/kgBW/day in divided doses. In terms

of the number of doses consumed, the patient is no longer in a period of initial drug therapy.

At the treatment of seizures when admitted to the hospital, valproic acid dose is increased as

much as 3 mg/kgBW/day to 25 mg/kgBW/ day in divided doses. On the fifth day of

hospitalization, valproic acid dose was increased to 30 mg/kgBW/day in divided doses. This

is in line with the theory that if a seizure occurs again, the drug dose may be increased

gradually up to a maximum dose of 60 mg/kgBW/day.

In addition to medicines, other treatments may be added to help reduced the frequency

and severity of epileptic seizures including ketogenic diet, vagus nerve stimulation, brain

surgery, anterior-temporal lobectomy, hemispherectomy, and corpus callosotomy. Surgery

for epilepsy may involve removing an area of abnormal tissue in the brain (such as a tumor or

scar tissue) or the specific area of brain tissue where seizures begin. Hemispherectomy is a

commonly used surgical technique in children with severe epilepsy. In this procedure, the

damaged side of the brain is removed. Corpus collostomy, another common surgery,

disconnect the two sides (hemispheres) of the brain to prevent generalized seizures in

children. Surgery does not help with partial seizures. 11

At 50-70% of epileptic attacks can be prevented with medications,

while about 50 % at a time will be able to stop taking medication. Primary

epileptic seizures, both generalized seizures and attacks flax or absence

has the best prognosis. Instead epileptic attack first began at the age of 3

years old or accompanied by neurological disorders or mental retardation

have a relatively bad prognosis. 9

Result

It has been reported, an toddler girl with the main complain of seizure and was diagnosed

with generalized symptomatic epilepsy. The diagnose was established based on history

taking, clinical manifestation, laboratory finding, and electroencephalography. The patient

got antiepileptic drug and still need to be followed up.

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