Case Report

SYMPTOMATIC EPILEPSY

Arranged by:

Deby Andita
1608438220

Supervisor:

dr. Riki Sukiandra, Sp.S

DEPARTMENT OF NEUROLOGY
MEDICAL FACULTY OF RIAU UNIVERSITY
ARIFIN ACHMAD RIAU PROVINCE GENERAL HOSPITAL
PEKANBARU
2018
 KEMENTERIAN PENDIDIKAN DAN KEBUDAYAAN
FAKULTAS KEDOKTERAN UNIVERSITAS RIAU
SMF/ BAGIAN SARAF
Sekretariat : Gedung Kelas 03, RSUD Arifin Achmad Lantai 04
Jl. Mustika, Telp. 0761-7894000
E-mail : saraffkur@gmail.com
PEKANBARU

I. Patient’s Identity

Name Mr. S
Age 59 years old
Gender Male
Address Jl Tuanku Tambusai – Pekanbaru
Religion Moslem
Marital Status Married
Occupation Entrepreneur
Entry Hospital October, 12th 2018 , 09:00 p.m.
Medical Record 9983XX

II. ANAMNESIS :
Allo anamnesis with his daughter (October, 13th 2018)

Chief Complain
Seizure since 8 hours before admitted to the hospital.

A. Present Illness History

8 hours before admitted to the hospital, the patient’s family complained that the
patient had seizure. The seizure occured 9 times, the duration every seizure under 5
minutes. The seizure occurred 4 times in home, 5 times in Syafira Hospital. Before
seizure, the patient had nausea because of unpleasent smells, did not complain
headache and fever. While seizure occured, the patient felt unconsciousness,
stiffness all over his body, most on left extremities, the eye’s aim to the top, foam
on the mouth (-), bitten tounge (-), The space time between of them were 30
minutes with conscious condition. After the seizure, the patient was conscious. but
1
didn’t recognize his family for few minutes. His left extremities became heavier.
Then patient’s speak became slurred. There is no nausea and vomiting, dyspneu, no
numbness on his both hands and legs. There is no complaints of urination and
defecation. Then the patient reffered immediately to Arifin Achmad General
Hospital

Past Illness History

 February 2018, The patient has complained the parase on left side.
No seizure complaints. The patient was diagnosed with non haemmorrhage
stroke.
 Hypertension (+) 7 months ago
 Seizure on infant/childhood (-)
 Diabetes mellitus (-)
 Trauma history (-)
 Anti epileptic drugs (-)

Socioeconomic History
 The patient working as an entrepreneur
 History of smoking (+) BI: Moderate , consume alcohol (-)

The Family Disease History

 No family history with the same complains.
 A history of hypertension (+Hy)
 A history of stroke (-)
 A history of epilepsy (-)

ANAMNESIS RESUME
Mr. S, 59 years old admitted to the hospital on October, 12th 20178. The
patient’s family has complained that the patient had seizure on his all over body
suddenly 8 hour before admission. The seizure occured 9 times, the durationevery
seizure under 5 minutes and the space time between of them were 30 minutes with
consciousness condition but didn’t recognize his family for few minutes. Before

2
seizure, the patient had nausea because of unpleasent smells While seizure occur,
the patient felt unconsciousness, stiffness all over his body, most on left
extremities, Then patient’s speak became slurred, the eye’s aim to the top. This
is his first seizure complaint. He was diagnosed by stroke on February 2018 with
the same characteristized as recent complaint.

III. Physical Examination (October, 12th 2018)

A. Generalized Condition
Blood Presure : Dextra :180/100 mmHg, sinistra :180/100 mmHg
Heart Rate : Dextra : 90 bpm, sinistra : 90 bpm, regular
Respiratory rate : 22x/minute
Temperature : 36,8°C
Weight : 60 kg
Height : 162 cm
Body Mass Index (BMI) : 22,9 kg/m2 (Normoweight)

B. Neurological status
1) Consciousness : Composmentis, GCS : E4V5M6
2) Noble Function : Normal
3) Meningeal Sign : Nuchal rigidity (-)
Brudzinki I, II, III, IV (-)
4) Cranial Nerves
1. N. I (Olfactorius )
Right Left Interpretation
Sense of Smell Normal Normal Normal

2. N.II (Opticus)
Right Left Interpretation
Visual Acuity >3/60 >3/60
Visual Fields Normal Normal Normal
Colour Recognition No test No Test

3. N.III (Oculomotorius)
Right Left Interpretation
Ptosis - - Normal
3
 Pupil isokor isokor
Shape Round Round
Side Φ2mm Φ2mm
Pupillary reaction to light
direct + +
Indirect + +

4. N. IV (Trokhlearis)
Right Left Interpretation
Extraocular movement Normal Normal Normal

5. N. V (Trigeminus)
Right Left Interpretation
Motoric Normal Normal
Sensory Normal Normal Normal
Corneal reflex + +

6. N. VI (Abduscens)
Right Left Interpretation
Extraocular
Normal Normal
movement
(-) (-) Normal
Strabismus
(-) (-)
Deviation

7. N. VII (Facialis)
Right Left Interpretation
Tic (-) (-)
Motoric
1. Frowning Normal Normal
2. Raised eye brow Normal Normal
3. Close eyes Normal Normal
4. Corners of the Extracted (-)
Parese central type
mouth
5. Nasolabial fold Deeper (-) of left N.VII

Sense of Taste Normal Normal

Chvostek Sign
(-) (-)

4
 8. N. VIII (Akustikus)
Right Left Interpretation
Hearing sense Normal Normal Normal

9. N. IX (Glossofaringeus)
Right Left Interpretation
Arcus farings Normal Normal
Flavour sense Normal Normal Normal
Gag Reflex Normal Normal

10.N. X (Vagus)
Right Left Interpretation
Arcus farings Normal Normal
Normal
Dysfonia - -

11.N. XI (Assesorius)
Right Left Interpretation
Motoric Normal Norma;
Non Interpretabe
Trophy Eutrophy Eutrophy

12.N. XII (Hipoglossus)

Right Left Interpretation
Motoric Normal Deviation
Trophy Eutrophy Eutrophy Parese N.XII Sinistra
Tremor - -
Disartria - -

5) MOTORIC
Right Left Interpretation
Upper Extremity
Strength
5 2
Distal
5 2
Medial
5 2 Hemiparese
Proximal
Normal Normal sinistra
Tone
Eutrophy Eutrophy
Trophy
(-) (-)
Involuntary movements
(-) (-)
Clonus
Lower Extremity
Strength 5 2
Distal 5 2

5
 Medial 5 2
Proximal Normal Normal
Tone Eutrophy Eutrophy
Trophy (-) (-)
Involuntary movements (-) (-)
Clonus
Body
Trophy Eutrophy Eutrophy
Involuntary movements (-) (-)
Normal
Abdominal Reflex (+) (+)
Cremaster Reflex (+) (+)

6) SENSORY
Right Left Interpretation
Touch Normal Normal
Normal,
Pain Normal Normal
except the
Temperature No test No test
temperature
Proprioceptive
and vibration
 Position Normal Normal
test was
 Two point Normal Normal
difficult to
discrimination
assess
 Stereognosis Normal Normal
 Graphestesia Normal Normal
 Vibration No test No test

7) REFLEX
Right Left Interpretation
Physiologic
Biseps + + Physiologic reflex
Triseps + + (+)
Patella + +
Achilles + +
Pathologic
Babinsky (-) (-)
Chaddock (-) (-) Pathological Reflex
HoffmanTromer (-) (-) (-)
Openheim (-) (-)
Schaefer (-) (-)
Primitive Reflex
Palmomental (-) (-) Primitive Reflex (-)
Snout (-) (-)

6
8) COORDINATION
Right Left Interpretation
Point to point movement (+) NT
Walk heel to toe (+) NT Non Interpretable
Gait NT NT
Tandem NT NT
Romberg NT NT

9) AUTONOM
Urinate : Urine catheterized (+)
Defecate : Normal
Erection : Normal

10) OTHERS EXAMINATION

a. Laseque : Not Limited >700
b. Kernig : Not Limited >1350
c. Patrick : -/-
d. Kontrapatrick : -/-
e. Valsava test :--
C. GAJAH MADA STROKE ALGORITHM

GAJAH MADA STROKE ALGORYTHM (ASGM)

Loss of conciousness (-) Headache (-) Babinski reflex (-)

Non hemorrhage stroke

D. SIRIRAJ SCORE
Siriraj Stroke Score
Consciousness (C) : Composmentis (0)
Vomitting (V) : No (0)
Headache within 2 hours (H) : No (0)
Diastolic blood pressure (DBP) : 100 mmHg (100)
Atheroma (A) : Hypertension(1)
SSS = 2,5 C + 2 V + 2 H + 0,1 DBP - 3 A - 12
7
 = 2,5 (0) + 2 (0) + 2 (0) + 0,1 (100) - 3 (1) - 12
= - 5 (non hemorrhage stroke)

E. MMSE

5
4

2
2
2
1

2
1

24

11). EXAMINATION RESUME (October, 12th 2018)

Generalized Condition
Consciousness : Composmentis GCS E4M6V5
Blood Presure : 180/100 mmHg
Heart Rate : 90 bpm regullar
Respiratory rate : 22 x/s ,
Temperature : 36,8°C
Weight : 60 kg
Height : 162 cm
Body Mass Index (BMI) :22,9 (Normoweight)
Noble Function : No cognitive impairment
Meningeal Sign : (-)
Cranial Nerve : Parese central type N.VII sinistra, Parese N.XII sinistra
8
Motoric : Hemiparese sinistra
Sensory : Normal
Coordination : Non - interpretable
Autonom : Urine catheterized (+)
Reflex : Physiology (+), Pathology (-)
Gajah Mada Stroke Algorithm : Non haemorrhage stroke
Siriraj score : Non haemorrhage stroke

C. WORKING DIAGNOSE
CLINICAL DIAGNOSE : Symptomatic Epilepsy
TOPICAL DIAGNOSE : Intracranial (Carotid system)
ETIOLOGICAL DIAGNOSE : Post Non Haemmorrhage Stroke
DIFFERENTIAL DIAGNOSE : Idiopathic Epilepsy
SECONDARY DIAGNOSE : Hypertension grade II

D. SUGGESTION EXAMINATION
 Blood routine
 Blood Glucose Profile
 Electrolyte
 Chest X-Ray
 Head CT-Scan
 Electroencephalogram (EEG)

E. MANAGEMENT
1) Bed rest
2) Airway Management
3) Nasal Canule O2 2-4 l/minute
4) Pharmacology
 IVFD RL 16 dpm
 Injection Phenytoin 3 x100 mg Normal Saline 20 ml iv
 Injection Diazepam 10 mg prn iv
 Injection Citicolin 2 x 500mg iv
 Injection Ranitidin 2 x 30 mg iv
 Amlodipin 1 x 10 mg po
 Aspilet 2 x 80 mg po

9
LABORATORIUM FINDING :
1. Blood routine (October, 12th 2018)
Hb : 8,2 g/dL
Leucosyte : 12.200/mm3
Trombocyte : 158.000/uL
Hematocryte : 23.8%
Interpretation : Anemia ec Low intake

2. Blood Glucose Profile Chemistry (October, 12th 2018)

- Glucose : 107 mg/dl

Interpretation : in normal limit

3. Electrolyte (October, 12th 2018)
- Na : 138 mmol/L
- K : 4.00 mmol/L
- Cl : 103 mmol/L
 Interpretation : in normal limit

4. Chest Xray (October, 12th 2018)

Interpretation :

Cardiomegaly

10
 5. Head CT Scan (October, 12th 2018)

Interpretation :
Old infarct on right frontaparietal lobes, atrophy cerebri

FINAL DIAGNOSE :
SYMPTOMATIC EPILEPSY EC NON HAEMMORRHAGE STROKE +
HYPERTENSION GRADE II + ANEMIA EC LOW INTAKE

FOLLOW UP
October 13th 2018
S : Seizure (-) fever (-) left extremities felt heavy, speech difficult
O : GCS E4M6V5
Blood Pressure :170/100 mmHg
Heart Rate : 92 bpm
Respiratory Rate : 22 tpm
Temperature : 36,5°C

11
 Cognitive Function : Normal
Neck Stiffness : Negative
Cranial Nerves : Parese central type of N VII sinistra
Motoric : Hemiparese sinistra
Motoric strength :
5 2
5 2
Sensory : Normal
Coordination : Normal
Autonomy : Urine catheterized (+), concentrated yellow urine
Reflex : Normal

A : Symptomatic Epilepsy ec Non Haemmorrhagee Stroke

Hypertension gr II
P :
 Continue therapy
 Observe seizure
 Suggested to do physiotheraphy
 Suggested to consul nutrisionist

October 14th 2018

S : Seizure (-) fever (-) left extremities felt easier
O : GCS E4M6V5
Blood Pressure :170/100 mmHg
Heart Rate : 92 bpm
Respiratory Rate : 22 tpm
Temperature : 36,5°C
Cognitive Function : Normal
Neck Stiffness : Negative
Cranial Nerves : Parese central type of N VII sinistra
Motoric : Hemiparese sinistra
Motoric strength :
5 3
5 3

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 Sensory : Normal
Coordination : Normal
Autonomy : Urine catheterized (+), concentrated yellow urine
Reflex : Normal

A : Symptomatic Epilepsy ec Non Haemmorrhagee Stroke

Hypertension gr II
P :
 IV plug
 Continue therapy
 Observe seizure

October 15th 2018

S : Seizure (-) fever (-) left extremities felt easier
O : GCS E4M6V5
Blood Pressure :160/100 mmHg
Heart Rate : 90 bpm
Respiratory Rate : 22 tpm
Temperature : 36,5°C
Cognitive Function : Normal
Neck Stiffness : Negative
Cranial Nerves : Parese central type of N VII sinistra
Motoric : Hemiparese sinistra
Motoric strength :
5 4
5 4
Sensory : Normal
Coordination : Normal
Autonomy : Normal
Reflex : Normal

A : Post Stroke Epilesy

Hypertension
P :

13
  Bed rest
 Injection Phenytoin 3 x100 mg Normal Saline 20 ml iv
 Injection Citicolin 2 x 500mg iv
 Injection Ranitidin 2 x 30 mg iv
 Amlodipin 1 x 10 mg po
 Aspilet 2 x 80 mg po

 Observe seizure
 Patient discharge

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 DISCUSSION

Epilepsy
1. Definition
Epilepsy is a chronic brain disorder characterized by repetitive unprovoked
seizures more than two times in more than 24 hours in less than 6 months, which
result from paroxysmal uncontrolled discharges of neurons within the central
nervous system (grey matter disease).1 Symptomatic epilepsy defined as an epilepsy
of an acquired or genetic cause, associated with gross anatomic or pathologic
abnormalities, and/or clinical features, indicative of underlying disease or
condition. 


2. Epidemiology
Epilepsy occurs in men and women at all ages, but is most frequently
diagnosed in early childhood (70% are below the age of twenty years) and old age.
Anyone can potentially develop seizures.
Studies indicate that the annual incidence of epilepsy ranges between 50 per
100,000 populations in developed countries to 82 per 100,000 populations in
resource poor countries. This regional disparity in the incidence of epilepsy is
attributed to the higher prevalence of risk factors or conditions which can lead to
permanent brain damage.2
Frontal lobe epilepsies may start at any age and both sexes are equally affected.
They are probably rare, accounting for about 1–2% of all epilepsies, though they
are second in prevalence, after temporal lobe epilepsies, in neurosurgical series. In
a prospective community-based study. the prevalence of frontal seizures (22.5%)
among focal epilepsies was comparable to that of temporal lobe (27%) and central
sensorimotor (32.5%) localisation. Seizure onset from the frontotemporal (5.6%),
parietal (6.3%) or posterior cortex (6.3%) was less common.3

3. Etiology
 Idiopathic : there are no structural lesions in the brain or neurological
deficits. The cause is unknown, thought to have a genetic predisposition.

15
 Cryptogenic : Sympomatic, but the cause is unknown, including here the
western syndrome, lennox-gastaut syndrome, and myoclonic epilepsy. The
clinical presentation corresponds to diffuse encephalopathy.
 Symptomatic : caused by abnormalities or lesions of the central nervous
system such as head trauma, nervous system infection (CNS), congenital
abnormalities, splitting lesions, cerebral circulatory disturbances, toxic
(alcohol, drug), metabolic, or neurodegenerative disorders. In resource-poor
countries, parasitic infestations such as malaria, neurocysticercosis and
paragonimiasis are important risk factors. Most epilepsies starting in adult
life are symptomatic and investigations to detect any underlying aetiology
are mandatory.5 Thromboembolic events and cerebral haemorrhage are
important causes of symptomatic epilepsy starting in later life, where they
are responsible for up to 50% cases. It is estimated that approximately 15%
of people with strokes will eventually develop epileptic seizures. Vascular
malfor- mations and cerebral aneurysms may also cause sympto- matic
epilepsy, whether or not haemorrhage has occurred.

16
4. Classification
 Focal seizure
These originate in neural networks limited to one hemisphere that may be
discrete or more diffuse and not necessarily confined to the cortex. They can
spread to other regions of the brain to become generalized with loss of
consciousness. Focal seizures are commonly classified according to their
clinical features into Auras, Motor, Autonomic and Dyscognitive.
- Auras
Auras are subjective and may be sensory or experiential and reflect the
initial seizure discharge. An aura may be an isolated phenomenon or
progress to a focal seizure with objective features (with or without
altered awareness) or to a bilateral convulsion.
- Motor
Motor features involve motor manifestations presenting as an increase
(positive) or decrease (negative) in muscle contraction. Motor features
may be elementary or complex.
- Autonomic
Autonomic features are characterized by autonomic phenomena, which
can involve cardiovascular, gastrointestinal, vasomotor, and
thermoregulatory functions. Examples include palpitations, nausea,
butterflies, hunger, chest pain, urge to urinate or defecate, goose
bumps, sexual sensation, feeling hot or cold, pilo-erection, pallor,
tachycardia or bradycardia/asystole, flushing, pupillary changes and
lacrimation.

- Dyscognitive
Dyscognitive features involve altered awareness or responsiveness.
The degree of contact with the environment may vary and it may
accompany complex motor or experiential sensory features.
2. Generalized seizure
A generalized seizure is conceptualized as originating at some point
within, and rapidly engaging, bilaterally distributed networks. Such bilateral
networks can include cortical and subcortical structures, but do not necessarily

17
include the entire cortex. The clinical presentation includes loss of
consciousness.

Generalised seizures are classified into the following categories:

Convulsive : Tonic – Clonic

Generalised tonic-clonic seizures are the best known type of generalised
seizures. They present with loss of consciousness at the onset. They are
characterised by the following features:

- In the tonic phase, cessation of breathing occurs as all the muscles go

into spasm and may be accompanied by a cry.
- In the clonic phase convulsive movements are marked by alternate
contraction and relaxation of the muscles.
- Tongue biting and/or incontinence of urine/stool may occur.
- On regaining consciousness the patient is confused and may feel tired
or have a headache.

Tonic Seizures
These types of seizures are accompanied by higher frequency of injuries
except when they occur during sleep. They present with:

- Loss of consciousness.
- Sudden stiffening of the extensor muscles and falling if standing.
- Patient fixes the limbs in a strained position.
- Tongue biting may occur
- Tightening of the jaw/clenching of teeth
Clonic Seizures
This is a form of generalized seizures characterised by repeated rhythmic
movements or jerks.

Myoclonic Seizures
These consist of sudden brief muscle contractions that may occur singly or
in cluster affecting any group of muscles unilaterally or bilaterally. These
types of seizures may be repeated many times over a long period.
18
 Typical Absences
These types of generalised seizures mainly affect children in the school
going age between 5 -15 years. They manifest at onset with loss of
consciousness (sometimes incomplete), staring blankly with or without
blinking or lip-smacking lasting for 5- 10 seconds that may be mistaken for
day dreaming. Some clonic movements of the eye lids, eye brows (eyelid
myoclonia), face and mouth may accompany the absence (myoclonic
absence).

- Some may go into spontaneous remission during adolescence.

- They may co-exist with tonic-clonic seizures in the same patient.
Atypical absences
An atypical absence seizure has less abrupt onset and prolonged loss of
consciousness of loss of awareness than typical absence seizures. They are
often associated with other features such as gradual loss of muscle tone of
the head trunk or limbs and subtle myoclonic jerks. Atypical absence
seizures often occur in individual with intellectual impairment. The loss of
awareness may be minimal with patient continuing activity but more
slowly or with mistakes.

5. Diagnosis and Adjunct Examination

Diagnosis is done quickly within 5-10 minutes. The first thing we do is:
Anamnesis
History of epilepsy, history of tumor, seizure history of drugs, alcohol, other
cerebrovascular diseases, and metabolite disorders. Notice the duration of seizures,
seizures (focal, general, tonic / clonic), level of consciousness between seizures,
previous seizure history, family history of seizures, fever, birth history, growth, and
illness.
Physical examination
Complete neurological examination includes the level of vision and hearing
awareness, physiological reflexes and pathology, lateralization, papillary edema
due to increased intracranial effects of tumors, bleeding, etc. The motor system is
paresthesias, hypesthesia, anesthesia.
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Adjunct examination
Laboratory examination of blood, electrolytes, glucose, renal function with
urine analysis and culture, if there is an alleged infection, then performed blood
culture. Imaging of CT Scan and MRI to evaluate structural lesions in the brain.
EEG to know the electrical activity of the brain and done as quickly as possible if
the patient has mental disorders. Lumbar puncture, we may do if there is a
suspected CNS infection or subarachnoid hemorrhage.

Features strongly suggestive of the symptomatic epilepsy diagnosis include:5

1. Generally short seizures.
2. Complex partial seizures arising from the frontal lobe, often with minimal or no
postictal confusion.
3. Rapid secondary generalization (more common in seizures of frontal than of
temporal lobe epilepsy).
4. Prominent motor manifestations which are tonic or postural.
5. Complex gestural automatisms frequent at onset.
6. Frequent falling when the discharge is bilateral. A number of seizure types are
described below; however, multiple frontal areas may be involved rapidly and
specific seizure types may not be discernible.

6. Patophysiology
Seizure Initiation And Prolongation

Why seizures start and stop is unknown, although it is likely that seizure
initiation is caused by an imbalance between excitatory and inhibitory
neurotransmission, leading to the initiation of abnormal neural impulses. The seizure
threshold in the immature brain appears to be lower than in the mature brain, but
the mechanisms that underlie this susceptibility remain unclear. Excitatory synapses
mature earlier than inhibitory synapses and this, coupled with an increase in the
susceptibility of excitatory neurotransmitter receptors, increases the likelihood
6
that an excitation– inhibition imbalance may occur.

20
 There are other important differences between the immature and adult
brain. Stimulation of GABAA receptors in the immature brain results in
depolarisation rather than hyperpolarisation, as occurs in the adult brain. The
immature cerebral cortex has a high synaptic density at around 2 months of age
6
and this may contribute to the development of hypersynchrony of neural groups.

The excitatory amino acid neurotransmitter glutamate increases at the site

of the seizure focus at the beginning of seizure activity in adults with temporal
lobe epilepsy when measured by in vivo intracerebral microdialysis It is believed
that the same may happen at the onset of generalised seizures. Inhibitory
neurotransmitters such as GABA later increase at the seizure focus and redress the
balance between excitation and inhibition. GABA also increases in the substantia
nigra pars reticulata, an area that can modulate a cortical inhibitory response in
adult rats, but not in immature rats. Other mechanisms of inhibitory receptor
modulation, such as adenosine receptor agonism, may also contribute to seizure
termination.

Mechanisms By Which Glutamate Causes Cell Death

Excess extracellular glutamate may result in cell death by causing

necrosis, gene determined cell death, or both. The primary receptor involved in
cytotoxicity related to glutamate is the NMDA receptor, although other glutamate
receptors may be involved. The NMDA receptor is an ionotropic receptor.
Binding of glutamate and glycine or D-serine to appropriate sites on the receptor
results in an influx of calcium through the ionophore. High intracellular
calcium concentrations result in the activation of a large number of calcium
6
dependent processes such as those described in the following.

 Activation of protein kinase C. This enzyme is moved from the cytosol to

the cell wall, resulting in destruction of the wall.
 Nitric oxide and free radical formation. Calcium stimulates constitutive
nitric oxide synthase, causing an increase in intracellular nitric oxide.
Nitric oxide can inhibit mitochondrial respiration directly or indirectly by
forming peroxynitrite free radicals, which are cytotoxic.
21
  Activation of phospholipase A2. This en- zyme breaks down membrane
lipids with the release of arachidonic acid and other fatty acids. One
consequence of this membrane destruction can be cell death.
 Activation of protease calpain I. The mechanism by which this enzyme
causes cell death is unclear, but calpain I inhibitors are partially
neuroprotective

7. Therapy

Antiepileptic Drug Treatment

Drug treatment is similar to that for any other type of focal seizure.
Of the older drugs, carbamazepine or phenytoin monotherapy is the most
appropriate. Carbamazepine is superior for controlling focal seizures in more than
70% of patients (10% of the patients develop idiosyncratic reactions). Phenytoin is
as effective as carbamazepine, but its use is falling dramatically in developed
countries, mainly because of chronic toxicity. Phenobarbitone and primidone are
less efficacious and have been practically eliminated from use, mainly because of
their adverse effects on cognition. Clobazam, though often highly beneficial in
selective cases, is rarely used as continuous AED treatment. Clobazam is, however,
worth trying in patients who do not respond or those who develop side effects, such
allergic reactions to other drugs. Valproate, though a superior drug for generalised
epilepsies, is inferior in focal epilepsies with significant concerns in the treatment
of women.

Stroke

2.1 Definition
Stroke is a collection of symptoms characterized by the development of
clinical manifestations of cerebral function disorders either focal or global (for the
patient in a coma), which happens quickly and more than 24 hours or ended up with
death without being discovered other causes than vascular disorders. This definition
includes stroke due to cerebral infarction (ischemic stroke), nontraumatic

22
intracerebral hemorrhage, intraventricular hemorrhage and some cases of
subarachnoid hemorrhage.1

2.2 Epidemiology
The increasing age of life expectancy will tend to increase the risk of
vascular disease (coronary heart disease, stroke and peripheral artery disease). Data
in Indonesia showed the tendency of an increase in stroke cases both in terms of
mortality, incidence, and disability. The mortality rate based on age is: 15.9% (age
45-55 years) and 26.8% (age 55-64 years) and 23.5% (age 65 years). The incidence
of stroke amounted to 51.6 / 100,000 population

2.3 Etiology and Classification

Stroke can occur because of some pathological circumstance, such as
emboli, trombus, ruptur of blood vessels, change in the blood vessels permeability,
increasing the viscocity, or because there is a change in the quality of blood flowto
the brain blood vessels. That pathological condition assosiated with stroke
classification. Stroke is classified into two types of major categories, non-
hemorrhagic stroke and hemorrhagic stroke. Non hemorrhagic stroke more
commonly known as ischemic stroke, which is a common occurrence of all types of
stroke. From the overall incidence of stroke, 80% to 85% is the incidence of
ischemic stroke. Ischemic cerebrovascular disease is basically due to the occlusion
of blood vessels of the brain that cause the cessation of the oxygen and glucose
supply. This stroke is categorized into two groups, namely thrombus occlusion and
embolic occlusion.3,4,5

Table 1. Major classification of stroke5

Ischemia-infarct cerebrum (80-85%) Intracranial hemorrhage (15-20%)

Thrombus occlusion Intraserebral hemorrhage

Lakunar Subaraknoid hemorrhage
Embolic occlusion Intraventrikuler hemorrhage
Cardiogenic
Artery to artery

23
Ischemic stroke

Ischemic stroke can occur with or without infarct. It is the most common
stroke. Stroke is caused by obstruction in one or more arteries located in the
cerebrum, which led to the cessation of the supply of oxygen and glucose.4,5
The obstruction that occur can be a clot (thrombus) that are present in the
brain blood vessels as wll as inherited from the distal organ blood vessels
(embolism) which causes blockage in the brain vascularization. The most common
cause of thrombosis in the form of atherosclerosis that is cause stenosis or
narrowing of the blood vessels. While the most common of embolic stroke is an
embolus coming from large blood vessels or heart.5
The brain gets blood from the heart, blood containing oxygen and nutrients
to the brain. The amount of blood flow to the brain in normal circumstances usually
about 50-60 ml / 100 g of brain tissue / min, mean the brain needs 20% of the blood
pumped from the heart. If the clogged arteries, brain cells (neurons) can not
generate enough energy and the brain stops working.7,8
When the blood flow to the brain stops within 6 seconds will occur neuron
metabolic disorders, if more than 30 seconds EEG picture will be horizontally,
within 2 minutes there will be termination of brain activity, within 5 minutes began
to brain damage and more than 9 minutes, humans will die. Ischemic brain occurs
when blood flow to the brain is reduced to 25-30 ml / 100 grams of brain tissue
perminute.1

2.4 Risk Factors

According to the American Heart Association (AHA), the risk factors of
stroke are divided into two, that are not modifiable risks factors and modifiable
risk factors. Not modifable risk factors include: age, sex, low birth weight, race or
ethnicity, and genetic factors. Modifiable risk factors include: hypertension,
smoking, diabetes, nutritional imbalance, lack of physical activity, alcohol
consumption, and drug abuse. incidence of stroke can occur with one or more risk
factors (multifactor).3,6

Table 3. Stroke risk factors3,6

24
Not Modifable Modifable
1. Age 1. Stroke history 10. Smoking
2. Gender 2. Hypertension 11. Alcohol
3. Genetik 3. Heart disease 12. Drug abuse
4. Ethnic 4. Diabetes melitus 13. Hyperhomosisteinemia
5. Carotic stenosis 14. Antibody anti fosfolipid
6. TIA15. Hyperurisemia 15. Hyperurisemia
7. Hypercholesterolemia 16. Elevation of hematocrit
8. Oral contraception 17. Elevation of fibrinogen
9. Obesity

2.5 Clinical Manifestation

The differences in clinical manifestation between infarction stroke and
hemorrhage stroke showed in Table 4

Tabel 4. Difference of clinical manifestation between infarction and haemorrhage

stroke5,7
Symptom or Infarction Intracerebral haemorrhage
examination
Prodormal sign TIA (+) 50% TIA (-)
Doing activity/resting Rest, right after Often while doing physical
wake up activity
Headache and vomit Rarely Often or severe
Lost of consciousness at Rarely Often
onset
Hypertension moderate/ Moderate-severe
normotension
Meningeal sign No Yes
High intracranial pressure Rarely Subhialiod bleeding
symptom
Bloody LCS No Yes
Head CT Scan Hypodensity area Intracranial mass with
hyperdensity area
Angiography Stricture appearance aneurism, AVM, massa
intrahemisfer or vasospasme

1. Gajah Mada Algorithm7

1. Lost of consciousness
Acute stroke 2. Headache
3. Pathology reflex
25
All criteria or two of the three
Lost of consciousness (+), headache (-), pathology reflex (-) Haemorrhage
stroke
Lost of consciousness (-),headache(+),pathology reflex (-)
Lost of consciousness (-),headache(-),pathology reflex (+) infarction
Lost of consciousness (-),headache (-),pathology reflex (-) infarction

2. Siriraj Stroke Score (SSS)7

SSS = 2.5 C + 2 V + 2 H + 0.1 DBP - 3A – 12

C = Consciousness (composmentis = 0, somnolen = 1, sopor/koma = 2)

V = Vomit (none = 0, yes = 1)
H = Headache (none = 0, yes = 1)
DBP = Diastolic blood pressure
A = Ateroma (none = 0, one or more: DM, Angina, vaskular disease = 1)
SSS DIAGNOSE
>1 Hemorrhagic stroke
<-1 Infarction stroke
-1 to 1 Uncertain

2.6 Management
Stroke patients should be handled by a multidisciplinary team.Management
stroke be done by improving the general state of the patient, treat the risk factors,
and prevent complications.2,4,9
2.6.1 Hyperacute stadium
Action at this stadium is done at the Emergency Room, the aim is to prevent
the widespread of brain tissue damaging. At this stage, patients were given oxygen
2 L / min and crystalloid/colloid fluid, avoid administration of dextrose. Brain CT
scan examination, electrocardiography, chest X-ray, complete peripheral blood and
platelet count, prothrombin time / INR, APTT, blood glucose, blood chemistry

26
(including electrolytes), and if hypoxia, do the blood gas analysis. Other actions in
the Emergency Room are providing mental support to patients and provide an
explanation to the family to remain calm.10

2.6.2 Acute stadium

Ischemic stroke
General treatment:
Place the patient’s head in 30opositions, head an chest in a field, change the
sleep position every 2 hours. Mobilization began gradually when hemodynamically
stable. Furthermore, free the airway, give oxygen 1-2 liters / min. If necessary,
intubation. Fever overcome with compresses and antipyretic, then look for the
cause, when the bladder is full, emptied (preferably with intermittent catheters).10
Fluid nutrition with 1500-2000 isotonic cristalloid or colloid and electrolyte
as needed, avoid fluids containing glucose or isotonic saline.Nutrition orally only if
swallowing function well, if there is swallowing disorders or decreased
consciousness, nasogastric tube is recommended.1
If there is seizure, give diazepam 5-20 mg iv slowly for 3 minutes, the
maximum dosage is 100 mg per day, followed by oral administration of
anticonvulsants such as phenytoin, carbamazepine. If the seizure appeared after 2
weeks, given orally long-term anticonvulsant.10
If there is an increased of intracranial pressure, bolus mannitol were given
an of 0.25 to 1 g / kg per 30 minutes intravenously, and if rebound phenomenon
suspected, or general condition deteriorated, followed by 0,25g / kg per 30 minutes
every 6 hours for 3-5 days. Monitoring of the osmolarity should be performed
(<320 mmol), alternatively can be administered hypertonic solutions (NaCl 3%) or
furosemid.10
Special treatment:
The goal is to reperfusion by administration of antiplatelet agent such as
aspirin and anticoagulant, or with trombolytic rt-PA (combinant tissue
Plasminogen Activator), and neuroprotective agent, such as citicoline or
piracetam.Oral administration of aspirin with initial dose 325 mg within 24-48
hours after the onset is recommended.10,11

27
 It is well established that anticoagulant therapy represents the optimal
management modality for the prevention of cardiogenic cerebral embolism.
However, it is important to determine the level of risk for a particular patient as
well as to assess the relative degree of safety for long-term anticoagulant therapy.
Unfortunately, the end point for treatment failure is stroke, which can be a
devastating determinant.11
Warfarin, with a targeted INR of 2.0 to 3.0, is associated with an overall risk
reduction of 68% in patients with atrial fibrillation, but this mode of therapy should
be restricted primarily to patients with moderate to high risk of embolic events.11
Oral anticoagulation is not superior to antiplatelet therapy for secondary
stroke prevention except when there is an embolic source, such as underlying atrial
fibrillation. Whether antiplatelet therapy or anticoagulation should be used for
medical management of complex atherosclerotic aortic plaques, a potential source
of embolic stroke, remains controversial.11,

2.6.3 Chronic Stadium

Medical measures may include cognitive therapy, behavior, swallowing,
speech therapy, and bladder training (including physical therapy). Given the long
course of the disease, it takes a special intensive treatment of post-stroke in the
hospital with the goal of independence of the patient, understand, comprehend and
implement primary and secondary prevention programs.10
Subacute phase treatment:10
- Continuing the appropriate treatment of acute conditions before
- The management of complications
- Restoration / rehabilitation (as needed of patients), which is physiotherapy,
speech therapy, cognitive therapy, and occupational therapy
- Secondary Prevention
- Family education and discharge planning

2.8.1 Prognosis
Stroke can cause a variety of morbidity, mortality, and recurrence in the
future. Deaths due to stroke was 41.4% from 100,000 population. In 2010, stroke

28
accounted for 7% of all causes of mortality in men and 10% of all causes of death
among women. Recurrence of stroke increases with the time. The possibility of
recurrent stroke within five years was 26.4% and in ten years was 39.2%.3,6,11

29
 THE BASIC OF DIAGNOSE

1. Basic clinical diagnosis

According to history taking, a man 59 years old admitted to the hospital on
October, 12th 2018 with seizure on his all over body most on left extremities
suddenly 8 hours before admission. The seizure occured 9 times, the duration every
seizure under 5 minutes and the space time between of them were 30 minutes with
consciousness condition. Before seizure, the patient had nausea because of
unpleasent smells, did not complain headache and fever. While seizure occured, the
patient felt unconsciousness, stiffness most on left extremities, After the seizure, the
patient was conscious. but didn’t recognize his family for few minutes. His left
extremities became heavier. Then patient’s speak became slurred. This seizure is
the first complaint. He was diagnosed by stroke on February 2018 with the same
characteristized by weakness on left extremities.
From physical examination we’re found paresis of cranial nerve VII central
sinistra, Parese nerve XII sinistra, and hemiparesis on left extremities. It is
consistent with the WHO definition that clinical symptoms of stroke is cerebral
disorders, either focal or global attack in 24 hours.
This is in accordance with the epilepsy that defined as a chronic brain disorder
characterized by repetitive unprovoked seizures more than two times or in more
than 24 hours less than 6 months. Symptomatic epilepsy that defined as caused by
abnormalities or lesions of the central nervous system such as head trauma, nervous
system infection (CNS), congenital abnormalities, splitting lesions, cerebral
circulatory disturbances, toxic (alcohol, drug), metabolic, or neurodegenerative
disorders.

2. Basic topical diagnosis

Carotid system had been considered in this patient because there are left
central CN.VII paresis and hemiparese sinistra. Hemiparese caused by lesion on the
brain. The lesion come from obstruction in cerebral arteries, in this case, anterior
cerebral artery. From the physical examination there is left hemiparesis, so the

30
lesion is on the right hemisphere because a lesion in one side of carotid system will
lead to contralateral neurological deficit.
Frontal lobe epilepsies may start at any age and both sexes are equally
affected. They are probably rare, accounting for about 1–2% of all epilepsies,
though they are second in prevalence, after temporal lobe epilepsies, in
neurosurgical series. In head CT Scan we can also find broad cerebral infarction in
the right hemisphere region frontoparietal and atrophy cerebri to support the
diagnose as symptomatic epilepsy.

3. Basic etiological diagnosis

Basic etiological diagnose of this patient leads to symptomatic epilepsy
caused by non haemmorrhage stroke because on this patient there is focal seizures,
characterized by recurrent epileptic seizures due to intermittent brain function
disorder that occurs due to an old infarct on right frontal lobes and left as cicatrix
that conducted into partial abnormal discharge of paradoxical neurons due to
various etiologies. This patient had weakness of left extremities, without loss of
consciousness and severe headache. It is also supported by Siriraj Score and Gadjah
mada Stroke Algorithm. The patient also had history of uncontrolled hypertension
since 7 months ago.

4. Basic differential diagnosis

The consideration of the idiopathic epilepsy as differential diagnose,
because one of the etiology of epilepsy is idiopathic. Idiopathic epilepsy is a
functional disorder on brain also known as hereditary epilepsy. Manifestasion on
idiopathic was generalized seizure, we but in patient we only find focal seizure,
repeated in short duration. Idiopathic known as hereditary and there is no gross
neuroanatomy/neuropathology.

5. Basic workup
a. Haematology : to find the risk factor for stroke, exclude other cause of
symptoms, assess condition of patient, and consideration therapy

31
 b. Head CT-scan : to know the final pathology diagnose from the location and
the wide of the lesion.
c. EEG : to show the type and location of the activity in the brain
during a seizure for the evaluation of brain disorders.

6. Basic final diagnosis

The final diagnosis of this patient is symptomatic epilepsy. This diagnose is
considered by anamnesis, physical examination, and workup examination. From
anamnesis we found focal repeating seizure in short duration, sudden weakness of
left extremity, occurred when he in resting, speech difficulties. He had history of
uncontrolled hypertension since 7 months ago. From physical examination we’re
found paresis of cranial nerve VII central sinistra and hemiparesis on left
extremities. From MMSE, this patient has no abnormality on cognitive function.
From head CT-Scan we can see there is broad cerebral infarction in the right
hemisphere region frontoparietal dextra and atrophy cerebri. This etiological case is
symptomatic, caused by central nervous system abnormalities (CNS). The type of
patient’s epilepsy is partial complex seizure because there was an aura and loss of
consciousness when seizure came. This case shows that the patient had seizure
from his lesion on central nervous system (lesion strtuctural). On February 2018,
The patient was diagnosed with stroke. Which mean there are big possibility that
clinical’s view of this patient comes from his past illness history.

7. Basic treatment
I. Airway Management to maintain an adequate airway
II. Bed rest to head position elevated 20-300 is to maintain the adequate
circulation to the brain.
III. Pharmacology
a. The aim of IVFD (30ml/kgbb/day) NaCl 0,9% 20 dpm is to maintain the
euvolemic condition.
b. The aim of Phenytoin 3 x100 ml Normal Saline 20 ml iv to prevent any
seizure
c. The aim of Diazepam 10 mg iv prn to manage seizure

32
d. The aim of amlodipine 1 x 10 mg to maintain his blood pressure
e. The aim of injection citicoline 3 x 500 mg iv is as the neuroprotector
f. The aim of Aspirin 2x80 mg p.o is to releave thrombocyte, platelet
aggregation and adhesion by suppressing A2-Thromboxane
g. The aim of Ranitidine Inj. 2 x 50 mg per IV as the gastricprotector.

33
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Tatalaksana Epilepsi. Kelompok Studi Epilepsi Perhimpunan Dokter
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14, 19-23
2. European Stroke Organisation Guidelines for The Management of Post
Stroke Seizure and Epilepsy. European Stroke Journal. 2017:2(2):103-105
3. World Health Organization (WHO). Epilepsy. 2018. Diunduh pada :
www.who.int/news-room/fact-sheets/detail/epilepsy
4. Zelano J. Poststroke Epilepsy: Update and Future Direction.
NCBI.2016;9(5):424-435.
5. Silverman IE, Restrepo L, Mathews GC. Post Stroke Sezuires. Jama
Neurology. 2002;59(2):195-201.
6. Pande SD.Post Stroke Seizure. Do The Locations, Types and Managements
of Stroke Matter.Epilepsia Open. 2018;3(3):392-98
7. Myint PK, Staufenberg EFA, Sabanathan K. Post Stroke Seizure and Post
Stroke Epilepsy. NCBI. Postgrad Med J. 2006; 82(971):568-572.
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2004;35:1769-75
9. Ministry of Health. Kenya National Guidelines For The Management of
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content/uploads/2016/03/Epilepsy-Guidelines-2016.pdf
10. Rumantir CU. Gangguan Peredaran Darah Otak. Pekanbaru: SMF Saraf
RSUD Arifin Achmad/FK UNRI. Pekanbaru. 2007.
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