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

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.

to

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 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 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 Maliks 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 :

5555555555
5555555555

Physiological reflexes :

Pathological reflexes :

Right

Left

KPR/APR

(+/+)

(+/+)

Biceps/Triceps

(+/+)

(+/+)

Babinsky

(-)

(-)

Meningeals sign

Chaddock

(-)

(-)

Gordon

(-)

(-)

Oppenheim

(-)

(-)

Nuchal rigidity (-), Kernigs 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 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

Neck
Thorax

pupil.
Jugular vein pressure R-2 cmH2O. Lymph node enlargement (-).
Symmetrical fusiformis, no retraction and muscle wasting.
HR: 138 bpm, regular, no murmur.

Abdomen

RR: 40 tpm, reguler, coarse crackles (+/+).

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

Extremitie

peristalsis was normal.

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

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

Genital

warm, CRT < 3. Pitting edema (-) pretibia. BP: 120/70 mmHg.
Female, within normal limit

Laboratory Findings: April, 12nd 2015

Parameters
Complete Blood Count
Hemoglobin
Hematocrite
Erithrocyte
Leucocyte
Trombosit
MCV
MCH
MCHC
RDW
Diftel
Arterial Blood Gas Analysis
PH
pCO2
pO2
Bikarbonat (HCO3)
Total CO2
Base Excess (BE)
Saturasi O2
Carbohydrate Metabolism
Blood Glucose ad random
Electrolytes

Value

Normal Value

9,2 gr%
29,2 %
3,4 x 106 /mm3
13,8 x 103 /mm3
263.000 /mm3
85,90 fl
27,10 pg
31,50 gr%
16,70 %

11,3 14,1 gr%

37 41%
4,40 4,48 x 106 /mm3
4,5 13,5 /mm3
150000 450000 /mm3
81 95 fl
25 29 pg
29 31 gr%
11,6 14,8 %

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

7,436
29,6 mmHg
188,4 mmHg
19,5 mmHg
20,4 mmHg
-3,4 mmHg
99,7%

7,35 7,45
38 42
85 100
22 26
19 25
(-2) (+2)
95 100

155 mg/Dl

< 200

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
Worms egg : negative
Amoeba

: negative

Eritrocyte

: 0-1

Leucocyte : 0-1
A Generalized symptomatic epilepsy + Bronchopneumonia + Global Development Delayed
+ Cerebral Palsy + Gastroenteritis without Dehydration
P

Management:
-

O2 nasal canule L/i

IVFD NaCl 0,9% 10 gtt/i micro
Injection Paracetamol 100 mg / 8 hour / IV
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 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
Head

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

Neck
Thorax

pupil.
Jugular vein pressure R-2 cmH2O. Lymph node enlargement (-).
Symmetrical fusiformis, no retraction and muscle wasting.

HR: 165 bpm, regular, no murmur.

Abdomen

RR: 26 tpm, reguler, coarse crackles (+/+).

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

Extremitie

peristalsis was normal.

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

s
Genital
Female, within normal limit
A Generalized symptomatic epilepsy + Bronchopneumonia + Global Development Delayed
P

+ Cerebral Palsy + Gastroenteritis without Dehydration

Management:
-

IVFD NaCl 0,9% 10 gtt/i micro

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.

Diagnostic Planning:
-

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
Head

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

Neck
Thorax

pupil.
Jugular vein pressure R-2 cmH2O. Lymph node enlargement (-).
Simetris fusiformis. Retraction (-).
HR: 165 bpm, reguler. Murmur (-).

Abdomen

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

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

Extremitie

peristalsis was normal.

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.
Genital
Female, within normal limit
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
A Generalized symptomatic epilepsy + Bronchopneumonia + Global Development Delayed
P

+ Cerebral Palsy + Gastroenteritis without Dehydration

Management:
-

IVFD NaCl 0,9% 10 gtt/i micro

Injection Ceftriaxone 400 mg / 12 hour / IV
Injection Paracetamol 100 mg / 8 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.

Diagnostic Planning:
-

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 patients 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, mothers
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 Xray 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 airbronchograms 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 patients 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 gammaaminobutyric 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 patients 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.

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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