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BLOCK NEUROPSYCHIATRY

GROUP 4
2nd Scenario

Group Members :
Olivia Ramadhanty Hariyanto Putri 011611133032
Meiwinda Rizky Nurhidayah 011611133033
Kevin Alvaro Handoko 011611133034
Monitrya Nababan 011611133035
Chronica Elsa Retta Lumban Tobing 011611133036
Baiq Dwi Hadiatul Azni 011611133037
Ratih Dyah Utami 011611133038
Elena Ghentilis Fitri Amelia 011611133039
Yunita Ratri Adhiningsih 011611133040
Kania Alawiyah 011611133040

Tutor:
Lynda Rossyanti, dr., Sp. ParK
TABLE OF CONTENT

Cover ........................................................................................................................ 1
Table of Content ........................................................................................................ 2
Scenario .................................................................................................................... 3
Objective ................................................................................................................... 4
Chapter I ................................................................................................................... 5
1.1 Main Problem ....................................................................................................... 5
1.2 Keywords ............................................................................................................. 5
1.3 Additional Question with Reason and Additional Information .................................... 5
1.4 Early Hypothesis ................................................................................................... 5
1.5 Early Concept Maping ........................................................................................... 6
1.6 Learning Issue I .................................................................................................... 6

Chapter II .................................................................................................................. 7
2.1 Cognitive Strategy ................................................................................................ 7
2.2 Answers of Learning Issue I .................................................................................. 7
2.3 Logic and Critical Analysis with Evidence Based Learning ....................................... 30
2.4 Obstacles ............................................................................................................. 31
2.5 Learning Issue II .................................................................................................. 31

Chapter III ................................................................................................................ 32


3.1 Methods and Steps in Finding Information............................................................... 32
3.2 Answers of Learning Issue II ................................................................................. 32
3.3 Analysis .............................................................................................................. 39
3.4 Final Hypothesis .................................................................................................. 40
3.5 Group Opinions ................................................................................................... 40
3.6 Final Concept Mapping ........................................................................................ 42

References ............................................................................................................... 43
Journal Aprraisal ...................................................................................................... 46

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SCENARIO

A man, 42 years old, was taken to primary health care due to seizure.

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LEARNING OBJECTIVE

After finish this neuropsychiatri block, we hope that the student will be
able to analyze clinical problem of neuropsychiatry syndrome in
accordance to SKDI at simulation case based on the understanding of
neurobehaviour, neuroscience, neurobiology, psychodynamic, and
neuropsychiatry’s history taking and examination skills.

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CHAPTER 1

1.1. Main problem


Seizure

1.2. Keywords
- A Man
- Primary health care
- Seizure

1.3. Additional question


a. Is there a history of diabetes & hypertension in patients and his family? To find out
whether seizures are caused by trigger factors of DM and hypertension (distinguish
epileptic true seizures from non epileptics).
b. What is the body temperature during a patient's febrile seizure in childhood?
(Because the lower temperature that you have during seizures, it will cause
epilepsy).
c. What is the patient's vision and hearing function? Does the patient feel that there is
noise, blurred vision, something strange before the onset of seizures takes place? (To
determine the severity of the seizure, it has disturbed the patient's daily life and
knows whether the patient's seizures are preceded by the aura).
d. Does the patient have a history of taking drugs such as asthma (amynophiline),
analgesics or sleeping pills (phenothiazine)? (To find out if the patient's seizures are
provoked by drugs).
e. Did patients often drink alcohol and drugs before they stopped taking them? (To find
out whether there are effects of drug withdrawal and alcohol on patient seizures
(differentiating epileptic true seizure with non epileptics)).
f. Does the patient have a history of kidney disease? (To find out whether there is a
relationship between kidney disease and patient’s seizures (differentiating epileptic
true seizure with non-epileptic)).
g. What activities do patients do before seizures occur? (To find out the activity of
patients before seizures is quite satisfying or not (distinguishing whether the patient's
seizure is a true seizure or pseudoseizure / psychogenic seizure)).
h. What are the results of meningeal sign examinations on patients? (To find out if the
patient has a brain infection).

1.4. Early Hypothesis


Seizure that occur in patients, can be caused by :
a. True Seizure
- Epilepsy seizure (Unprovoked seizure)
- Acute Symptomatic Seizure (Provoked seizure)

b. Pseudoseizure
- Psychogenic seizure

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- Metabolic disease
- Cardiovascular disease
And also according to ILAE 2017, seizures can be classified into :

1.5. Early Concept Mapping


42th years old man, came with seizure

True Seizure Pseudo Seizure

Epilepsy Provoked Psychogenic Metabolic Cardiac


seizure

1.6. Learning Issues


1. How is the physiology of excitatory and inhibitory neurotransmitters from CNS?
2. What is the pathophysiology of seizures?
3. How is the explanation of true seizure?
a. Epileptic Seizure
b. Non-Epileptic Seizure
4. How is the explanation of pseudo seizure?
a. Psychogenic seizure
b. Metabolic disease
c. Cardiac disease
5. How is the explanation of the classification of seizures according to ILAE 2017?

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CHAPTER 2

2.1. Cognitive Strategy


Cognitive strategy is an organized internal ability that can help students in the
learning process, thinking process, problem solving and decision making (Gagne,
1974). The cognitive strategy applied in this Neuro-Psychiatry Module is based on
metacognition theory, which includes problem solving, decision making, critical
thinking, creative thinking. These skills are not separate but integrated with each other.
So, at the same time when students use their cognitive strategies to solve problems, they
also use their skills to make decisions, think critically, and think creatively.
There are 4 types of cognitive strategies that can be embraced in learning, namely
Chunking, Spatial, Bridging, and Multipurpose. In this Neuro-Psychiatry Module, the
cognitive strategy used is "Spatial". Spatial is a strategy to show the relationship
between things one to another. In this category include "frames" (tables) and "concept
maps" (concept maps). Students are given a scenario that then must be found the
problem, what are the factors that affect, even to the countermeasures and solutions. To
facilitate the completion of the case, students are guided to prepare an appropriate
concept map to be able to answer the initial hypothesis that has also been prepared by
the students. To improve thinking ability, students are also given the opportunity to
conduct field surveys, so they can observe the cases being handled directly.

2.2. Answer of Learning Issues I


2.2.1.How is the physiology of excitatory and inhibitory?
―The nerve cells which are used for the perception of external events will, upon
being excited by the proper stimulus, transmit an action potential down their axons.
When the electrical signal reaches the axon terminal bundle, it interacts with structures
called synaptic knobs. It stimulates an influx of calcium (Ca2+) through voltage-gated
Ca2+ gates. This caused the movement of vescicles toward the membranes of the
synaptic knobs. Inside these vescicles are neurotransmitter chemicals. The
neurotransmitters are manufactured in the cell body and travel down the axon to be
stored in vescicles associated with the synaptic knobs. When a vesicle reaches the cell
membrane of the synaptic knob, it fuses with the cell membrane and releases its
neurotransmitter into the synaptic region. On the postsynaptic neuron are receptors that
will specifically bind these neuotransmitters. The neurotransmitter will either excite or
inhibit the firing of the postsynaptic neuron.‖ (Hyperphysics.phy-astr.gsu.edu, 2018)
There are some neurotransmitter in excitatory and inhibitory. Acetylcholin,
epinephrine, norepinephrine, serotonin, and glutamate are excitatory neurotransmitters.
While GABA and glycine are inhibitory neurotransmitters. All excitatory
neurotransmitter cause an opening of ligan-gated sodium ion channels. As a result,
sodium ions flows in and the cell becomes less negative on the inside. These
neurotransmitter also create a local increase of permeability of sodium ion channel
which lead to local depolarization that’s known as an Excitatory Postsynaptic Potential
(EPSP). Inhibitory neurotransmitters cause an opening of ligand-gated potassium ion
channels which leads to a local hyperpolarization (more negative than normal). This is

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known as a Inhibitory Postsynaptic Potential (IPSP) because it’s going to be LESS
likely to throw off an action potential.

―Reversal potentials and threshold potentials determine postsynaptic excitation


and inhibition. (A) If the reversal potential for a PSP (0 mV) is more positive than
the action potential threshold (-40 mV), the effect of a transmitter is excitatory, and it
generates EPSPs (Excitatory Post Synaptic Potentials) . (B) If the reversal potential for
a PSP is more negative than the action potential threshold, the transmitter is inhibitory
and generate IPSPs ( Inhibitory Post Synaptic Potentials). (C) IPSPs can nonetheless
depolarize the postsynaptic cell if their reversal potential is between the resting
potential and the action potential threshold. (D) The general rule of postsynaptic action
is: If the reversal potential is more positive than threshold, excitation results; inhibition
occurs if the reversal potential is more negative than threshold.‖ (Purves et al., 2018)

2.2.2.How is the pathophysiology of seizure?


Seizures are paroxysmal manifestations of the electrical properties of the cerebral
cortex. A seizure results when a sudden imbalance occurs between the excitatory and
inhibitory forces within the network of cortical neurons in favor of a sudden-onset net
excitation.
The brain is involved in nearly every bodily function, including the higher cortical
functions. If the affected cortical network is in the visual cortex, the clinical
manifestations are visual phenomena. Other affected areas of primary cortex give rise to
sensory, gustatory, or motor manifestations. The psychic phenomenon of déjà-vu occurs
when the temporal lobe is involved.
The pathophysiology of focal-onset seizures differs from the mechanisms
underlying generalized-onset seizures. Overall, cellular excitability is increased, but the
mechanisms of synchronization appear to substantially differ between these 2 types of
seizure and are therefore discussed separately.

Pathophysiology of focal seizures


The electroencephalographic (EEG) hallmark of focal-onset seizures is the focal
interictal epileptiform spike or sharp wave. The cellular neurophysiologic correlate of
an interictal focal epileptiform discharge in single cortical neurons is the paroxysmal
depolarization shift (PDS).

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The PDS is characterized by a prolonged calcium-dependent depolarization that
results in multiple sodium-mediated action potentials during the depolarization phase,
and it is followed by a prominent after-hyperpolarization, which is a hyperpolarized
membrane potential beyond the baseline resting potential. Calcium-dependent
potassium channels mostly mediate the after-hyperpolarization phase. When multiple
neurons fire PDSs in a synchronous manner, the extracellular field recording shows an
interictal spike.
If the number of discharging neurons is more than several million, they can
usually be recorded with scalp EEG electrodes. Calculations show that the interictal
spikes need to spread to about 6 cm2 of cerebral cortex before they can be detected with
scalp electrodes.
Several factors may be associated with the transition from an interictal spike to an
epileptic seizure. The spike has to recruit more neural tissue to become a seizure. When
any of the mechanisms that underlie an acute seizure becomes a permanent alteration,
the person presumably develops a propensity for recurrent seizures (ie, epilepsy).
The following mechanisms (discussed below) may coexist in different
combinations to cause focal-onset seizures:
 Decreased inhibition
 Defective activation of gamma-aminobutyric acid (GABA) neurons
 Increased activation
If the mechanisms leading to a net increased excitability become permanent
alterations, patients may develop pharmacologically intractable focal-onset epilepsy.
Currently available medications were screened using acute models of focal-onset
or generalized-onset convulsions. In clinical use, these agents are most effective at
blocking the propagation of a seizure (ie, spread from the epileptic focus to secondary
generalized tonic-clonic seizures). Further understanding of the mechanisms that
permanently increase network excitability may lead to development of true antiepileptic
drugs that alter the natural history of epilepsy.

A. Decreased inhibition
The release of GABA from the interneuron terminal inhibits the postsynaptic
neuron by means of 2 mechanisms: (1) direct induction of an inhibitory
postsynaptic potential (IPSP), which a GABA-A chloride current typically
mediates, and (2) indirect inhibition of the release of excitatory neurotransmitter
in the presynaptic afferent projection, typically with a GABA-B potassium
current. Alterations or mutations in the different chloride or potassium channel
subunits or in the molecules that regulate their function may affect the seizure
threshold or the propensity for recurrent seizures.

Mechanisms leading to decreased inhibition include the following:


 Defective GABA-A inhibition
 Defective GABA-B inhibition
 Defective activation of GABA neurons
 Defective intracellular buffering of calcium

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Normal GABA-A inhibitory function
GABA is the main inhibitory neurotransmitter in the brain, and it binds primarily
to 2 major classes of receptors: GABA-A and GABA-B. GABA-A receptors are
coupled to chloride (negative anion) channels, and they are one of the main targets
modulated by the anticonvulsant agents that are currently in clinical use.

The reversal potential of chloride is about negative 70 mV. The contribution of


chloride channels during resting potential in neurons is minimal, because the
typical resting potential is near -70 mV, and thus there is no significant
electromotive force for net chloride flux. However, chloride currents become
more important at more depolarized membrane potentials.

These channels make it difficult to achieve the threshold membrane potential


necessary for an action potential. The influence of chloride currents on the
neuronal membrane potential increases as the neuron becomes more depolarized
by the summation of the excitatory postsynaptic potentials (EPSPs). In this
manner, the chloride currents become another force that must be overcome to fire
an action potential, decreasing excitability.

Properties of the chloride channels associated with the GABA-A receptor are
often clinically modulated by using benzodiazepines (eg, diazepam, lorazepam,
clonazepam), barbiturates (eg, phenobarbital, pentobarbital), or topiramate.
Benzodiazepines increase the frequency of openings of chloride channels, whereas
barbiturates increase the duration of openings of these channels. Topiramate also
increases the frequency of channel openings, but it binds to a site different from
the benzodiazepine-receptor site.

Alterations in the normal state of the chloride channels may increase the
membrane permeability and conductance of chloride ions. In the end, the behavior
of all individual chloride channels sum up to form a large chloride-mediated
hyperpolarizing current that counterbalances the depolarizing currents created by
the summation of EPSPs induced by activation of the excitatory input.

The EPSPs are the main form of communication between neurons, and the release
of the excitatory amino acid glutamate from the presynaptic element mediates
EPSPs. Three main receptors mediate the effect of glutamate in the postsynaptic
neuron: N -methyl-D-aspartic acid (NMDA), alpha-amino-3-hydroxy-5-methyl-4-
isoxazole propionic acid (AMPA)/kainate, and metabotropic. These are coupled
by means of different mechanisms to several depolarizing channels.

IPSPs temper the effects of EPSPs. IPSPs are mediated mainly by the release of
GABA in the synaptic cleft with postsynaptic activation of GABA-A receptors.All
channels in the nervous system are subject to modulation by several mechanisms,
such as phosphorylation and, possibly, a change in the tridimensional

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conformation of a protein in the channel. The chloride channel has several
phosphorylation sites, one of which topiramate appears to modulate.
Phosphorylation of this channel induces a change in normal electrophysiologic
behavior, with an increased frequency of channel openings but for only certain
chloride channels.

Each channel has a multimeric structure with several subunits of different types.
Chloride channels are no exception; they have a pentameric structure. The
subunits are made up of molecularly related but different proteins.

The heterogeneity of electrophysiologic responses of different GABA-A receptors


results from different combinations of the subunits. In mammals, at least 6 alpha
subunits and 3 beta and gamma subunits exist for the GABA-A receptor complex.
A complete GABA-A receptor complex (which, in this case, is the chloride
channel itself) is formed from 1 gamma, 2 alpha, and 2 beta subunits. The number
of possible combinations of the known subunits is almost 1000, but in practice,
only about 20 of these combinations have been found in the normal mammalian
brain.

Defective GABA-A inhibition


Some epilepsies may involve mutations or lack of expression of the different
GABA-A receptor complex subunits, the molecules that govern their assembly, or
the molecules that modulate their electrical properties. For example, hippocampal
pyramidal neurons may not be able to assemble alpha 5 beta 3 gamma 3 receptors
because of deletion of chromosome 15 (ie, Angelman syndrome).

Changes in the distribution of subunits of the GABA-A receptor complex have


been demonstrated in several animal models of focal-onset epilepsy, such as the
electrical-kindling, chemical-kindling, and pilocarpine models. In the pilocarpine
model, decreased concentrations of mRNA for the alpha 5 subunit of the surviving
interneurons were observed in the CA1 region of the rat hippocampus.

Defective GABA-B inhibition


The GABA-B receptor is coupled to potassium channels, forming a current that
has a relatively long duration of action compared with the chloride current evoked
by activation of the GABA-A receptor. Because of the long duration of action,
alterations in the GABA-B receptor are thought to possibly play a major role in
the transition between the interictal abnormality and an ictal event (ie, focal-onset
seizure). The molecular structure of the GABA-B receptor complex consists of 2
subunits with 7 transmembrane domains each.

G proteins, a second messenger system, mediate coupling to the potassium


channel, explaining the latency and long duration of the response. In many cases,

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GABA-B receptors are located in the presynaptic element of an excitatory
projection.

Defective activation of GABA neurons


GABA neurons are activated by means of feedforward and feedback projections
from excitatory neurons. These 2 types of inhibition in a neuronal network are
defined on the basis of the time of activation of the GABAergic neuron relative to
that of the principal neuronal output of the network, as seen with the hippocampal
pyramidal CA1 cell.

In feedforward inhibition, GABAergic cells receive a collateral projection from


the main afferent projection that activates the CA1 neurons, namely, the Schaffer
collateral axons from the CA3 pyramidal neurons. This feedforward projection
activates the soma of GABAergic neurons before or simultaneously with
activation of the apical dendrites of the CA1 pyramidal neurons.

Activation of the GABAergic neurons results in an IPSP that inhibits the soma or
axon hillock of the CA1 pyramidal neurons almost simultaneously with the
passive propagation of the excitatory potential (ie, EPSP) from the apical
dendrites to the axon hillock. The feedforward projection thus primes the
inhibitory system in a manner that allows it to inhibit, in a timely fashion, the
pyramidal cell's depolarization and firing of an action potential.

Feedback inhibition is another system that allows GABAergic cells to control


repetitive firing in principal neurons, such as pyramidal cells, and to inhibit the
surrounding pyramidal cells. Recurrent collaterals from the pyramidal neurons
activate the GABAergic neurons after the pyramidal neurons fire an action
potential.

Experimental evidence has indicated that some other kind of interneuron may be a
gate between the principal neurons and the GABAergic neurons. In the dentate
gyrus, the mossy cells of the hilar polymorphic region appear to gate inhibitory
tone and activate GABAergic neurons. The mossy cells receive both feedback and
feedforward activation, which they convey to the GABAergic neurons.

In certain circumstances, the mossy cells appear highly vulnerable to seizure-


related neuronal loss. After some of the mossy cells are lost, activation of
GABAergic neurons is impaired. Synaptic reorganization is a form of brain
plasticity induced by neuronal loss, perhaps triggered by the loss of the synaptic
connections of the dying neuron, a process called deafferentation. Formation of
new sprouted circuits includes excitatory and inhibitory cells, and both forms of
sprouting have been demonstrated in many animal models of focal-onset epilepsy
and in humans with intractable temporal-lobe epilepsy.

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Most of the initial attempts of hippocampal sprouting are likely to be attempts to
restore inhibition. As the epilepsy progresses, however, the overwhelming number
of sprouted synaptic contacts occurs with excitatory targets, creating recurrent
excitatory circuitries that permanently alter the balance between excitatory and
inhibitory tone in the hippocampal network.

Defective intracellular buffering of calcium


In rodents, recurrent seizures induced by a variety of methods result in a pattern of
interneuron loss in the hilar polymorphic region, with striking loss of the neurons
that lack the calcium-binding proteins parvalbumin and calbindin. In rat
hippocampal sections, these interneurons demonstrate a progressive inability to
maintain a hyperpolarized resting membrane potential; eventually, the
interneurons die.

In an experiment, researchers used microelectrodes containing the calcium


chelator BAPTA and demonstrated reversal of the deterioration in the membrane
potential as the calcium chelator was allowed to diffuse in the
interneuron. [9] These findings showed the critical role of adequate concentrations
of calcium-binding proteins for neuronal survival in settings with sustained rises
of intracellular calcium, such as in status epilepticus and other brain insults. This
mechanism may contribute to medical intractability in some epilepsy patients.

The vulnerability of interneurons to hypoxia and other insults also correlates to the
relative presence of these calcium-binding proteins. The premature loss of
interneurons alters inhibitory control over the local neuronal network in favor of
net excitation. This effect may explain, for example, why 2 patients who have a
similar event (ie, simple febrile convulsion) may have remarkably dissimilar
outcomes; that is, one may have completely normal development, and the other
may have intractable focal-onset epilepsy after a few years.

B. Increased activation
Mechanisms leading to increased excitation include the following:
 Increased activation of NMDA receptors
 Increased synchrony between neurons due to ephaptic interactions
 Increased synchrony and/or activation due to recurrent excitatory collaterals

Increased activation of NMDA receptors


Glutamate is the major excitatory neurotransmitter in the brain. The release of
glutamate causes an EPSP in the postsynaptic neuron by activating the
glutaminergic receptors AMPA/kainate and NMDA and the metabotropic
receptor. Fast neurotransmission is achieved with the activation of the first 2 types
of receptors. The metabotropic receptor alters cellular excitability by means of a
second-messenger system with later onset but a prolonged duration. The major
functional difference between the 2 fast receptors is that the AMPA/kainate

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receptor opens channels that primarily allow the passage of monovalent cations
(ie, sodium and potassium), whereas the NMDA type is coupled to channels that
also allow passage of divalent cations (ie, calcium).

Calcium is a catalyst for many intracellular reactions that lead to changes in


phosphorylation and gene expression. Thus, it is in itself a second-messenger
system. NMDA receptors are generally assumed to be associated with learning
and memory. The activation of NMDA receptors is increased in several animal
models of epilepsy, such as kindling, kainic acid, pilocarpine, and other focal-
onset epilepsy models.

Some patients with epilepsy may have an inherited predisposition for fast or long-
lasting activation of NMDA channels that alters their seizure threshold. Other
possible alterations include the ability of intracellular proteins to buffer calcium,
increasing the vulnerability of neurons to any kind of injury that otherwise would
not result in neuronal death.

Increased synchrony between neurons caused by ephaptic interactions


Electrical fields created by synchronous activation of pyramidal neurons in
laminar structures, such as the hippocampus, may increase further the excitability
of neighboring neurons by nonsynaptic (ie, ephaptic) interactions. Changes in
extracellular ionic concentrations of potassium and calcium are another possible
nonsynaptic interaction, as is increased coupling of neurons due to permanent
increases in the functional availability of gap junctions. This last may be a
mechanism that predisposes to seizures or status epilepticus.

Increased synchrony and/or activation from recurrent excitatory collaterals


Neuropathologic studies of patients with intractable focal-onset epilepsy have
revealed frequent abnormalities in the limbic system, particularly in the
hippocampal formation. A common lesion is hippocampal sclerosis, which
consists of a pattern of gliosis and neuronal loss primarily affecting the hilar
polymorphic region and the CA1 pyramidal region. These changes are associated
with relative sparing of the CA2 pyramidal region and an intermediate severity of
the lesion in the CA3 pyramidal region and dentate granule neurons.

Prominent hippocampal sclerosis is found in about two thirds of patients with


intractable temporal-lobe epilepsy. Animal models of status epilepticus have
reproduced this pattern of injury; however, animals with more than 100 brief
convulsions induced by kindling seizures had a similar pattern, suggesting that
repeated temporal lobe seizures may contribute to the development of
hippocampal sclerosis.

Subtler and apparently more common than overt hippocampal sclerosis is mossy-
fiber sprouting. The mossy fibers are the axons of the dentate granule neurons, and

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they typically project into the hilar polymorphic region and toward the CA3
pyramidal neurons. As the neurons in the hilar polymorphic region are
progressively lost, their synaptic projections to the dentate granule neurons
degenerate.

Denervation resulting from loss of the hilar projection induces sprouting of the
neighboring mossy fiber axons. The net consequence of this phenomenon is the
formation of recurrent excitatory collaterals, which increase the net excitatory
drive of dentate granule neurons.

Recurrent excitatory collaterals have been demonstrated in human temporal lobe


epilepsy and in all animal models of intractable focal-onset epilepsy. The effect of
mossy-fiber sprouting on the hippocampal circuitry has been confirmed in
computerized models of the epileptic hippocampus. Other neural pathways in the
hippocampus, such as the projection from CA1 to the subiculum, have been
shown to also remodel in the epileptic brain.

For further reading, a review by Mastrangelo and Leuzzi addresses how genes
lead to an epileptic phenotype for the early age encephalopathies

Pathophysiology of generalized seizures


The best-understood example of the pathophysiologic mechanisms of generalized
seizures is the thalamocortical interaction that may underlie typical absence seizures.
The thalamocortical circuit has normal oscillatory rhythms, with periods of relatively
increased excitation and periods of relatively increased inhibition. It generates the
oscillations observed in sleep spindles. The thalamocortical circuitry includes the
pyramidal neurons of the neocortex, the thalamic relay neurons, and the neurons in the
nucleus reticularis of the thalamus (NRT).
Altered thalamocortical rhythms may result in primary generalized-onset seizures.
The thalamic relay neurons receive ascending inputs from the spinal cord and project to
the neocortical pyramidal neurons. Cholinergic pathways from the forebrain and the
ascending serotonergic, noradrenergic, and cholinergic brainstem pathways prominently
regulate this circuitry.
The thalamic relay neurons can have oscillations in the resting membrane
potential, which increases the probability of synchronous activation of the neocortical
pyramidal neuron during depolarization and which significantly lowers the probability
of neocortical activation during relative hyperpolarization. The key to these oscillations
is the transient low-threshold calcium channel, also known as T-calcium current.
In animal studies, inhibitory inputs from the NRT control the activity of thalamic
relay neurons. NRT neurons are inhibitory and contain GABA as their main
neurotransmitter. They regulate the activation of the T-calcium channels in thalamic
relay neurons, because those channels must be de-inactivated to open transitorily.

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T-calcium channels have 3 functional states: open, closed, and inactivated.
Calcium enters the cells when the T-calcium channels are open. Immediately after
closing, the channel cannot open again until it reaches a state of inactivation.
The thalamic relay neurons have GABA-B receptors in the cell body and receive
tonic activation by GABA released from the NRT projection to the thalamic relay
neuron. The result is a hyperpolarization that switches the T-calcium channels away
from the inactive state into the closed state, which is ready for activation when needed.
The switch to closed state permits the synchronous opening of a large population of the
T-calcium channels every 100 milliseconds or so, creating the oscillations observed in
the EEG recordings from the cerebral cortex.
Findings in several animal models of absence seizures, such as lethargic mice,
have demonstrated that GABA-B receptor antagonists suppress absence seizures,
whereas GABA-B agonists worsen these seizures. Anticonvulsants that prevent absence
seizures, such as valproic acid and ethosuximide, suppress the T-calcium current,
blocking its channels.
A clinical problem is that some anticonvulsants that increase GABA levels (eg,
tiagabine, vigabatrin) are associated with an exacerbation of absence seizures. An
increased GABA level is thought to increase the degree of synchronization of the
thalamocortical circuit and to enlarge the pool of T-calcium channels available for
activation.

2.2.3.How is the explanation of true seizures?


a. Epilepsy (Unprovoked Seizures)
Epilepsy is a common medical and social disorder or group of disorders with
unique characteristics. Epilepsy is usually defined as a tendency to recurrent
seizures. The word ―epilepsy‖ is derived from Latin and Greek words for
―seizure‖ or ―to seize upon‖. This implies that epilepsy is an ancient disorder;
indeed, in all civilizations it can be traced as far back as medical records exist. In
fact, epilepsy is a disorder that can occur in all mammalian species, probably more
frequently as brains have become more complex. Epilepsy is also remarkably
uniformly distributed around the world. There are no racial, geographical or social
class boundaries. It occurs in both sexes, at all ages, especially in childhood,
adolescence and increasingly in ageing populations.

Idiopathic and genetically determinedepilepsies


The idiopathic (or primary) generalized epilepsies are the most common of the
genetically determined epilepsies. The precise mode of inheritance for most of
these conditions is currently unknown. Other inherited conditions in which
seizures are the sole clinical manifestation include the idiopathic partial epilepsies
(e.g. benign rolandic epilepsy). In addition to these conditions with seizures as the
main clinical expression, there are many rare inherited disorders that present as
neurological or systemic illnesses including seizures. The most common of these
disorders are tuberous sclerosis and neurofibromatosis. Trisomy 21 (Down’s
syndrome) may be accompanied by seizures, particularly in later life.

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Symptomatic epilepsies
Common causes of symptomatic epilepsies include head trauma, birth trauma,
cerebrovascular disorders, cerebral anoxia, brain infections, cortical
malformations and brain tumours. 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. Head trauma is
an important cause of symptomatic epilepsy and may account for up to 10% of all
cases of epilepsy. The likelihood of developing epilepsy after head trauma
depends on the severity of the injury and the presence of complicating factors,
including prolonged loss of consciousness, post-traumatic amnesia, intracranial
bleeding, missile penetration, or depressed skull fracture. It is unusual for epilepsy
to develop unless one of these factors is present. Seizures occurring immediately
after the injury do not usually presage the development of chronic epilepsy.

Cryptogenic epilepsies
Currently up to 40% of patients have no identifiable cause for their seizures. This
proportion is rapidly decreasing as advances in neuroimaging, particularly
magnetic resonance imaging (MRI), are made. The term cryptogenic epilepsy is
sometimes used interchangeably with idiopathic epilepsy. This should be avoided,
and the term idiopathic epilepsy reserved for those inherited conditions in which
seizures occur as the only manifestation of the disorder.

Progressive epilepsies
The progressive myoclonic epilepsies are a group of disorders characterized by
the development of myoclonic and other seizures in association with other clinical
inherited degenerative brain disorders and inborn errors of metabolism. These
include adrenoleukodystrophy, Alpers’ disease and Tay-Sachs disease.
Phenylketonuria, porphyria and neuronal ceroid-lipofuscinosis may also cause
seizures. Epilepsy may sometimes complicate degenerative brain conditions such
as Alzheimer’s disease, Huntington’s chorea, striatonigral degeneration and
Creutzfeld-Jakob disease; as many as 20% of patients with Alzheimer’s disease
may develop seizures. Involvement of the central nervous system eventually
occurs in the majority of people developing AIDS. It may take the form of
opportunistic infection or neoplastic lesions. An encephalopathy that seems to be
caused by HIV itself has also been recognized. Intracranial tumours, either
primary or metastatic, may result in epilepsy. Tumours are responsible for about a
fifth of seizures starting between the ages of 30 and 50 years, and about 10% of
seizures starting after the age of 50 years.

b. Acute Symptomatic Seizures (Provoked Seizures)


Provoked seizures are single seizures, a similar type of abnormal electrical
activity in the brain that can be caused by ;
a. trauma,

17
b. low blood sugar (hypoglycemia<36 mg/dl )
c. low blood sodium (hyponatremia),
d. high fever,
e. febrile convulsionin early childhood
f. Sleep deprivation
g. Metabolic Encephalopathy
h. CNS infection ;like encephalitis, meningtitis, CNS TB Infection, and
neurocystisercosis.
CNS Tuberculosis Infection :In tuberculous meningitis, seizure can occur
because of encephalopathy, tuberculoma, or infarction. Seizure can be the
presenting feature in 10–20% patients with CNS tuberculosis. The seizure in
CNS tuberculosis may be generalized in 58%, focal in 38%, and tonic in 4%
patients. Seizures are commoner in children than in adults (74% vs 14%). Half
the patients presenting with acute symptomatic seizures may have seizures as
sequelae.
i. Alcohol or drug abuse
Alcohol withdrawal seizures are common and are diagnosed on the basis of
the patient’s drinking history as reported by friends or relatives. The majority
(90%) of alcohol withdrawal seizures occur within 48 h of withdrawal. These
usually occur singly or in brief clusters. The great majority of alcohol
withdrawal seizures are generalized; a focal onset suggests an intracranial
structural lesion. If seizures occur after 48 h, other possibilities such as head
injury should be considered. The diagnostic yield of CT scan after the first
alcohol-related seizure is high because of the presence of structural lesions;
however, for recurrent alcohol-related seizures, CT is not indicated. Change in
type and frequency of seizure after 48 h of drinking necessitates imaging.
EEG is usually normal in alcohol-related seizure and any abnormality
should suggest an alternative diagnosis.
j. Pharmacological agents

Seizures that are caused by problems like these are called "provoked" seizures,
and they do not usually occur again once the problem is remedied. People with
provoked seizures are not said to have epilepsy.As an example, if patient is in

18
hypoglycemic condition, when the serum glucose is under thirty-six milligrams
per deciliter, then seizure is not epilepsy.

Tests and procedures


Depending on the circumstances of seizure, age, and individual situation,
healthcare provider may order one or more tests, including:
 Blood tests may be done to check for problems (such as low or high blood
sugar) that may have caused your seizure, and to check for markers in the
blood that could point to the type of seizure you had.
 Lumbar puncture (spinal tap) may be done after a seizure to check for signs of
infection. This is usually done in an emergency room, if the individual does
not seem to be recovering normally from the seizure, or if the person has a
fever or other signs of brain infection.During this test, a needle is inserted into
the space surrounding the spinal cord and a fluid sample is taken. The sample
is checked for bacteria or other signs of signs of infection, such as an
abundance of white blood cells.
 Electroencephalography (EEG) may be done to check for abnormal electrical
activity in the brain. During this test, electrode pads are placed on your scalp.
The clinician may try to induce an abnormality in the EEG by having the EEG
technician use flashing lights or ask you to hyperventilate. Both of these
maneuvers may produce abnormalities in your brain waves, which could be
helpful in determining your diagnosis.
 Brain imaging studies, such as MRI or CT scans, may be done to check for
tumors, strokes, or other structural problems in the brain. However, these tests
are often normal in people with epilepsy.

2.2.4.What are Pseudo-seizures ?


a. Psychogenic Non EpilepticSeizures
Psychogenic non epileptic seizures are the example of paroxysmal non epileptic
episodes that are resemble and misdiagnosed as epileptic seizures (Benbadis,
2018). PNES do not result from abnormal cortical discharges, rather they are
somatic manifestations of psychological distress (Alsaadi and Marquez, 2005).
Most people with PNES (75%) are women, with onset in the late teens to early
twenties being typical (Mellers, 2004).

The common precipitant factors of PNES are often related to family (parental
discord, separation, death, chronic illness in a parent, overprotection or neglect,
financial problems, alcoholism in father etc.) or school (pressure of performance,
forthcoming exams, peer pressure, abuse or any recent change in school, class or
friends) (Bhatia, 2004). Besides, there are also many kinds of psychiatric or
personality disorder, such as borderline personality (Galimberti et. al, 2003), post
concussional syndrome, post traumatic neurosis, somatization disorder,
conversion disorder, and drug abuse (Margono, 2018). Other risk factors for

19
PNES include having a diagnosis of epilepsy, having recently had a head injury or
recently undergone neurosurgery (Wilshire and Ward, 2016).

Patients with PNES usually conscious, do not have regular pattern of


movement/stereotype of seizure (tonic-clonic), and do not experience
incontinence, cyanosis, bitten tongue when the seizures occur (Margono, 2018).
The differences between pseudoseizure (PNES) and true seizure can be seen in
picture below (Bhatia, 2004) :

20
Picture 1. The differences between pseudoseizure (PNES) and true seizure (Bhatia, 2004)
Source : http://medind.nic.in/ibv/t04/i7/ibvt04i7p673.pdf

Benbadis (2018) mention that the differential diagnosis of PNES are:


 Absence Seizures
 Ambulatory Electroencephalography (EEG)
 Brainstem Gliomas
 Complex Partial Seizures
 Dizziness, Vertigo, and Imbalance
 Driving and Neurological Disease
 EEG Seizure Monitoring
 Emergent Management of Myasthenia Gravis
 EpilepsiaPartialis Continua
 Epileptiform Discharges
 First Adult Seizure
 Focal EEG Waveform Abnormalities
 Frontal Lobe Epilepsy
 Intellectual Disability
 Juvenile Myoclonic Epilepsy
 Pediatric First Seizure
 Pediatric Status Epilepticus

Aside from history taking and physical examination, we can confirm whether
seizures in patient are PNES or true seizure through additional examinations. The
most definitive test to distinguish epilepsy from PNES is long term video-EEG
monitoring, with the aim of capturing one or two episodes on both video recording
and EEG simultaneously or by attempt to trigger an episode (Asano et. al, 2005).
In areas where EEG video monitoring is not available, clinicians can used a staged
approach for diagnosis developed by the task force of the International League

21
Against Epilepsy (LaFrance et. al, 2013). The task force proposed the following
four categories of certainty for PNES diagnosis:
 Documented PNES – confirmed by clinical history plus EEG video
monitoring
 Clinically established PNES – defined by clinical history, clinician witness,
and EEG recording of habitual events without video
 Probable PNES – determined by clinical history, clinician witness of video or
live events, and a normal EEG
 Possible PNES – relies on patient’s self-report of clinical events and a normal
EEG

b. Syncope
Syncope is a temporary loss of consciousness usually related to insufficient blood
flow to the brain. It's also called fainting or "passing out. It most often occurs
when blood pressure is too low (hypotension) and the heart doesn't pump enough
oxygen to the brain. It can be benign or a symptom of an underlying medical
condition. Many non life-threatening factors, such as overheating, dehydration,
heavy sweating, exhaustion or the pooling of blood in the legs due to sudden
changes in body position, can trigger syncope. (American Heart Association,
2017). The Syncope itself is a symptom, defined as a transient, self limited loss of
consciousness with a relatively rapid onset and usually leading to falling; the
subsequent recovery is spontaneous, complete, and usually prompt. The
underlying mechanism is a transient global cerebral hypoperfusion. It is
sometimes characterized by symptoms that mimic an epileptic seizure such as
confusion muscle twitching, shaking, convulsions and physical collapse.

Seizure is, according to the same document, synonymous with an epileptic fit,
which is the manifestation of a paroxysmal discharge of abnormal rhythms in
some part of the brain, and ―Epilepsy is then defined as a condition in which
seizures recurre, usually spontaneously‖. A Seizure is a sudden, involuntary
change in behavior, muscle control, consciousness, and/or sensation. A seizure is
often accompanied by an abnormal electrical discharge in the brain. Symptoms of
a seizure can range from sudden, violent shaking and total loss of consciousness to
staring into space, altered vision, and difficult speech. Approximately 10 percent
of the population will experience a single seizure in their lifetime.

So, it can be said that syncope is not seizures at all although syncope can result in
movements or behaviors that mimic seizures. The difference is, an epileptic
seizure produces a brief disturbance in the normal electrical functions of the brain,
while syncope is caused by a reduction in blood flow carrying oxygen to the brain.
A seizure can sometimes accompany a syncope episode and syncope can
sometimes accompany a seizure.

22
There are clinically important relations between cardiovascular causes of syncope
and seizure disorders (fig 11).). Involuntary movements, often referred to as
myoclonic jerks, may accompany syncope due to cardiovascular causes and create
a differential diagnostic problem against seizure with important therapeutic and
prognostic implications. These implications are basically: the underlying disease
may not receive proper treatment, and some cardiac causes of syncope carry a
considerable mortality risk; bradycardias might be aggravated by some (ion
channel active) antiepileptic drugs (AEDs); and a diagnosis of epilepsy may also
lead to significant psychosocial consequences. Put slightly differently: ―Hardly
anyone with epilepsy will come to any harm from a delay in diagnosis whereas a
false positive diagnosis is gravely damaging‖.

Therefore seizure-like or convulsive syncope from the cardiovascular perspective


has been chosen as the topic for this article. ―Convulsive syncope‖ is not a
recommended term by the ESC task force, ― …because it carries the risk of
increasing confusion between syncope and epilepsy‖. Unfortunately, there is no
simple term to denote syncope accompanied by ―myoclonic jerks‖ or ―jerking
movements‖, which are preferred; therefore, for linguistic reasons and because it
is used in some of the references, ―convulsive syncope‖ is used in this article,
which focuses on cardiovascular or cardiogenic syncope.

Involuntary movements, often referred to as myoclonic jerks, may accompany


syncope due to cardiovascular causes and create a differential diagnostic problem
against seizure with important therapeutic and prognostic implications.
Myoclonus or myoclonic jerks (sometimes tonic spasms) is probably the most
misleading symptom in the differential diagnosis between syncope and seizure
disorders. It is frequently part of spontaneous or provoked syncope related to
vasovagal reaction.The diagnosis thus requires that the episodes are spontaneous
or unprovoked and recurrent.In order to differentiate between syncope and
seizure, videotelemetry with simultaneous electroencephalographic (EEG)

23
and electrocardiographic (ECG) recording with multiple scalp and chest
electrodes is required—a situation that is rarely fulfilled.

c. Miokardial / Atrial Fibrilation


Since some cardiovascular arrhythmias, such as asystole or VT, may cause loss of
consciousness complicated by abnormal movements due to generalised cerebral
hypoxia, leading to the initial impression of seizure, cardiac issues should be
systematically considered in patients with a diagnosis of epilepsy remaining
uncertain. Moreover, even under the supervision of board-certified cardiologists
or electrophysiologists, artefacts on electrocardiograms could be misinterpreted as
ventricular tachycardia and cause inappropriate resuscitation, cardioversion or
device implantation. Artefacts are defined as ECG abnormalities that may be due
to sources other than the electrical activity of the heart. By far, body tremor is the
most common cause, resulting in electrocardiographic artefact in clinical practice,
and could be misdiagnosed as VT. In addition to the tremors, other factors such as
clonic jerking, loose leads, etc. may play a role. Incorrect interpretation of these
artefacts can lead to unnecessary and potentially harmful procedures, such
cardioversion or drugs, invasive electrophysiological testing, or implantation of
cardioverter defibrillators. However, there has been no electrocardiographic
algorithm effectively differentiating pseudo-VT.

2.2.5.What is ILAE classification of seizure?


Classification of seizure

Figure 1. Basic operational classification of seizure types.

24
Figure 2. Expanded operational classification of seizure types.
Figure 1 shows the basic updated seizure classification, whereas Figure 2 presents
an expanded version that covers the most common or most important types of seizures
in greater detail, although not every seizure type can be represented in a classification,
and in clinical practice a detailed description of the symptoms observed remains
essential.
Some relevant terminology is explained in the attached glossary (table 1).

Table 1. Glossary of terms.

A sudden interruption of activities accompanied by a blank


Absence stare with occasional

deviation of the eyes lasting a few seconds to half a minute


with subsequent

25
rapid recovery. Atypical types with other symptoms can also
be found

Sudden loss of muscle tone lasting a few seconds which can


Atonic affect the head,

body, arms and legs

Coordinated motor, actively accompanied usually by impaired


Automatism awareness and

often followed by amnesia

Symmetrical or asymmetrical jerking of the same group of


Clonic muscles

Relating to thinking, language, memory, and other similar


Cognitive functions

Comorbidities Conditions associated with or causing the epilepsy

Emotional
A focal non-motor seizure that can have elements such as fear

26
and joy

A chronic disorder of the brain characterised by an enduring


Epilepsy disposition

towards recurrent unprovoked seizures. The diagnosis requires


at least 2

seizures occurring greater than 24 hours apart or one seizure


with a relevant

abnormal electroencephalographic pattern or brain scan


suggesting a high

probability of a second seizure (Fisher et al., 2014)

Starting with one cerebral hemisphere, either in a specific


Focal place in the brain or

more widely distributed

Originating at some point, but rapidly spreading across both


Generalized sides of the brain

27
Generalized tonic-clonic
seizure Bilateral convulsion with loss of awareness

That part of biological science that is concerned with the study


Genetics of variation and

heredity

Hyperkinetic Agitated thrashing or leg pedalling movements

No known or suspected cause other than possible hereditary


Idiopathic predisposition

Produced by the processes in body cells that build up or break


Metabolic down natural

substances

Motor Involving movement of muscles in any way

Sudden, brief contractions of muscles resulting in dropping or


Myoclonic spilling things

28
and/or falls

Transient symptoms and/or signs due to abnormal excessive or


Seizure simultaneous

neuronal activity of a population of neuronal cells in the brain

Sudden flexion and/or extension of trunk muscles which can


Spasm include grimacing,

head nodding, and eye movements

Characteristic seizures associated with abnormal


Syndrome investigations that occur

together in a recognisable pattern

An increase in muscle contraction, lasting from a few seconds


Tonic to some minutes

Focal onset seizures may be accompanied by continued awareness, depending on


the site of onset and extent and speed of the spread of the abnormal electrical activity.
Often, however, the individual will lose aware-ness at some stage during the focal
seizure, which is now referred to as a ―focal impaired awareness‖ seizure. Arrest of

29
movement or loss of memory for events occurring during the seizure can also be part of
the seizure pattern. People with atonic or myoclonic seizures and epileptic spasms will
usually retain aware-ness, or loss of awareness will be so brief as to be hard to detect.
Cognitive seizures refer to problems during the seizure such as impaired speech,
hallucinations, illusions, or feelings of déjà-vu. Emotional seizures can manifest as
anxiety, fear, joy or any other emotion. An absence is atypical when it differs from the
usual fast onset and EEG pattern of a 3-4 per second generalized spike-wave pattern. If
seizure patterns are not clearly recognisable, the episodes will remain unclassified.

Structure
Common seizures can be divided into motor spasms and no seizures. Other types
include myoclonic, atonic, tonic or combination that can allow certain patterns to be
recognized, which leads to the diagnosis of epilepsy syndrome. Unknown origin
seizures can be considered "not classified" with or without other features, such as
motor, nocturnal, tonic-clonic, epileptic seizures (which can be called "infantile
spasms" in children less than one year of age), and behavior catch. However, focal
onset is often evident with the déjà-vu aura, strange taste or smell, or a rising sensation
in the abdomen, followed by loss of consciousness, slapping lips, and rubbing hands.
The term "aura" has been maintained because, if it appears on its own, conscious
seizures focus. Seizures that are not witnessed or that occur during sleep often occur. If
they are rare, it is not possible to ascertain the type of seizure, or even to determine
whether the episode has a focus or general onset.

2.3. Logic and Critical Analysis With Evidence Based Learning


The main problem in the scenario given is a 42 years-old middle-class married
man, named Mr. S, a furniture company worker, lives in KedungSroko, high school
graduated, in a conscious state come to a primary health centre with a recent history of
seizure. From anamnesis, our group finds that a year ago, the patient also has the same
seizure, and it has happened three times. The seizures type and duration are similar to
what has happened just now. The patient describes the seizure begun with a stiff left
arm and started to jerk his left arm and then all of his body also start to jerk. The patient
describes that the seizure last between one to two minutes. Before the seizure, patient
felt well and did not feel any aura. During his seizure, the patient could not respond to
questions and bit his tongue. After the seizure, patient is in a conscious state but
disorientated. And the patient remembers that he felt stiffness on his left arm then, he
wet himself, a sign of bladder incontinence. This patient told that he did not have fever,
so it is not a sign of infection. The patient previously has not sought any help from any
doctor. Mr. S has never taken any drug regarding his seizures. He also said that he has
sleep deprivation which is more likely to be the trigger for the seizure. Hence, our group
conclude that the patient had a focal seizure to generalized seizure.
Through the anamnesis, the patient did not have any history of seizure within his
family or relatives. But, he had a history of a road accident roughly two years ago,
which results to head trauma. He has a habit of speeding using motorcycle which
explains the insult on the head. At that time, he went through a decreasing

30
consciousness state for five hours. We also knew from the anamnesis that Mr. S has the
history of febrile seizure from 18 months to 5 years old. The frequency of this seizure is
three times in five minutes. Stiffness throughout his body and jerky movement are
found during Mr. S’s past seizures. So, we conclude that during his childhood, he
suffers from a simple Febrile Convulsion.
From the physical examination, we found that the vital sign of this patient are
GCS 456, consciousness level: compos mentis, general situation is good. The blood
pressure of this patient is 180/80 mmHg. His heart rate is 90 times/minute with the axial
temperature of 36.7oC and respiratory rate 20 times/minute. His body weight is 70 kg
and his height is 167 cm. Then, we tried to examine his head. We did not find any sign
of anemia, icterus, cyanosis, and dyspnea. But we found that there are surgical scars in
the right temporal area which reaffirm the habit that he has of speeding the motorcycle.
The insult to this particular area explains the brain damage that occur on the right-side
area results in the seizure, which manifest on his left extremity area first. We also did
not find any meningeal sign. Next, we examined his thoracal-abdominal area and the
inspection, percussion, palpation, and auscultation on this area are on the normal cutoff.
Next, we examined the extremity area, the inspection examination is in the normal
cutoff. The arm motoric strength of this patient is 5/5 and the leg 5/5, which are normal.
The cerebellar sign of this patient is normal. The physiological reflex of this patient is
+2, which also indicates that this patient is normal in this examination. This patient did
not manifest any pathological sign. The sensory examination is also normal. The cranial
nerves examination is also normal. Lastly, we found that the psychological examination
is also normal.

2.4. Obstacles
1. The patient data from anamnesis, physical examination, and additional examination
have not been able to determine directly the illness
2. lack of knowledge regarding several differential diagnoses proposed
3. There are some similarity between the differential diagnoses that we find it hard to
differentiate

2.5. Learning Issues 2


1. How is the epileptogenesis on this patient?
2. What is Temporal Lobe Epilepsy ?
3. How does the management of epilepsy ?
4. How is the referral procedure for epilepsy patients?
5. How to educate patients with epilepsy?

31
CHAPTER 3

3.1. Method and Steps in Finding Information


Our group focuses on finding information from reliable sources such as NCBI,
textbooks, and a few other reliable sources besides blogs and websites. We do finding
information from November, 29th to December, 6th .
Steps on finding information :
1. Determine answerable question for the learning issue
2. Find the specific keywords
3. Focus more on reliable page such as WHO, NCBI articles, textbooks, and reliable
websites e.g. .gov, ,org to find the answer to learning issues
4. Search for a relatable, valid, and applicable articles
5. Make conclusions or summaries from the articles/journals
6. Answer the learning issues
7. Make the references.

3.2. Answering Learning Issues 2


3.2.1.How is the epileptogenesis on this patient?
―Epileptogenesis is the process whereby a normal brain becomes progressively
epileptic because of precipitating injury or risk factors such as TBI, stroke, brain
infections or prolonged seizures. Epilepsy development can be described in three
stages: (1) the initial injury (epileptogenic event); (2) the latent period (silent period
with no seizure activity); and (3) chronic period with spontaneous recurrent seizures.
Although the precise
mechanisms underlying
spatial and temporal events
remain unclear,
epileptogenesis may
involve an interaction of
acute and delayed
anatomic, molecular, and
physiological events that
are both complex and
multifaceted. The initial
precipitating factor
activates diverse signaling
events, such as
inflammation, oxidation,
apoptosis, neurogenesis
and synaptic plasticity,
which eventually lead to
structural and functional
changes in neurons. These changes are eventually manifested as abnormal
hyperexcitability and spontaneous seizures‖ (Clossen and Reddy, 2017).

32
(Timofeev et al., 2013)

3.2.2.What is Temporal Lobe Epilepsy ?


 Definition
Temporal lobe epilepsy is the most common form of focal (partial) or location
related epilepsy. It accounts for approximately 60% of all people living with
epilepsy. There are two types of TLE. One involves the medial or internal structures
of the temporal lobe; while the second, called neocortical temporal lobe epilepsy,
involves the outer portion of the temporal lobe. The most common version of these
two is medial temporal lobe epilepsy.
 Medial temporal lobe epilepsy often begins within a structure of the brain called
the hippocampus or its surrounding structures. It accounts for almost 80% of all
temporal lobe seizures.
 Medial temporal lobe epilepsy is also considered a syndrome, which means that
a lot of different conditions can result in medial temporal lobe epilepsy.
Individuals who have medial temporal lobe epilepsy have seizures by definition
of temporal lobe origin.
 There are a lot of different older names for the seizures that occur in TLE,
including, "psychomotor seizures," "limbic seizures," "temporal lobe seizures,"
"complex partial," and "simple partial." The modern name for these seizures is
"focal onset," which is then characterized by whether the person stays aware or
has impaired awareness.
 While medial temporal lobe epilepsy is a very common form of epilepsy, it is
also frequently resistant to medications and associated with a particular finding
on an MRI (magnetic resonance imaging). This finding is called hippocampal
sclerosis (sclerosis means hardening) and it makes this a challenge to treat both
medically and oftentimes surgical therapy is the best option for these
individuals.

 Etiology
Medial temporal lobe epilepsy usually begins at the end of a first or second
decade in most people, following either a seizure with fever or an early injury to the

33
brain. In women, hormonal influences during their menstrual cycle and ovulation
may lead to reports of increased seizures during their menstrual cycle.

 Characteristic
 Seizures in TLE include focal aware (simple partial) seizures, such as auras, and
focal impaired awareness (complex partial) seizures.
 The most common auras are déjà-vu experiences or some gastrointestinal upset.
Feelings of fear, panic, anxiety, or a rising epigastric sensation or butterflies
with nausea are also other ways in which auras present in medial temporal lobe
epilepsy. Some people also report a sense of unusual smell; this may raise a
possibility of a hippocampal abnormality or a tumor in that area.
 Focal impaired awareness (complex partial) seizures can be associated with a
fixed stare, impaired consciousness, fumbling with their fingers, or lip-smacking
movements that last 30 to 60 seconds. There can be a posture change in an arm
that also can help identify the location in the brain of these seizures. Some
people also speak gibberish or lose their ability to speak in a sensible manner.
Some individuals report difficulty with the language, particularly if the seizures
are coming from the dominant temporal lobe. Some people may have a
generalized tonic-clonic jerking and this can lead to weakness after the seizure
has stopped.
 Some individuals can also have prolonged seizures and in some rare
situations, status epilepticus may occur.

 Differential Diagnosis
 Panic Disorder
This may be associated with autonomic phenomena and anxiety similar to those
observed in the simple partial (focal aware) phase of a temporal lobe seizure.
However, unlike temporal lobe epilepsy, which lasts seconds to 2 minutes, panic
attacks last several minutes (usually >10 min).
 Migraine Headache
Migraine headache is another paroxsymal neurologic disorder that sometimes
can be mistaken for seizures (and vice versa), as it also has an aura and can
produce various neurologic signs and symptoms if complex or complicated.
Interestingly, two seizure medications are FDA-approved to prevent migraines:
divalproic acid and topiramate.
 Excessive daytime somnolence
This may be due to a sleep-related breathing disorder or narcolepsy. It causes
episodes of loss of time due to falling asleep frequently.
 Non epileptic syndrome
Approximately 10–30% of patients with psychogenic seizures also have
epileptic seizures. The diagnosis of psychogenic seizure needs to be made after a
thorough evaluation as some seizures that are atypical may be true seizures. The
importance of diagnosing non epileptic seizures is important as psychogenic

34
seizures do not respond to antiepileptic events and require psychiatric
intervention.
 Frontal lobe epilepsy
Frontal lobe complex partial seizures (focal impaired awareness seizures) have
certain distinct characteristics. They appear in clusters of many brief seizures
with rapid onset and ending and minimal, if any, postictal state. Prominent
features include bizarre behavioral changes such as vocalizations and complex
motor and sexual automatisms. However, distinguishing frontal lobe complex
partial seizures from those of the temporal lobe based solely on clinical features
may be difficult; EEG is invaluable for localization.
 Absence Epilepsy
Generalized absence seizures have an abrupt onset with no aura, usually last less
than 30 seconds, and have no postictal state. EEG in absence shows generalized,
bilaterally synchronous spike-and-wave discharges and photosensitivity.
Complex partial seizures usually are preceded by a distinct aura, last longer than
a minute, and have a period of postictal confusion. EEG shows focal spikes in
complex partial seizures

 Physical Examination
 Computed Tomography Scanning
CT scanning of the head is often obtained in the emergency department, as it is
ubiquitous and is adequate for assessing blood and large lesions, but the
resolution is not that of MRI.
 Magnetic Resonance Imaging
As mentioned, MRI is the neuroimaging modality of choice for patients with
temporal lobe epilepsy. Most brain MRI scans do not include coronal images,
but for temporal lobe epilepsy this sequence is more informative than are the
axial and sagittal cuts. All patients with newly diagnosed temporal lobe epilepsy
should have a high-resolution MRI scan with at least a 1.5-Tesla MRI, although
the availability of a stronger magnet like 3-Tesla is increasing resolution.
High-resolution MRI shows hippocampal atrophy in many patients with
temporal lobe epilepsy by visual analysis alone, and, although volumetric
studies can be performed, they are labor intensive. Hippocampal atrophy is
bilateral in 10–15% of cases. An increase in the T2-weighted signal intensity in
the hippocampus may be seen on fluid-attenuated inversion recovery (FLAIR)
MRI; this finding is also consistent with hippocampal sclerosis.
 Positron Emission Tomography
PET with 18-fluorodeoxyglucose (PET-FDG) is a useful tool for interictal
seizure localization in surgical candidates when the MRI result is normal. PET-
FDG scans usually are performed as an adjunctive measure to delineate the
epileptogenic zone. Interictal deficits include reduced glucose metabolism in the
medial and lateral temporal lobe. PET scans can be fused with either CT or MRI
and are useful in the presurgical evaluation. Ictal PET scan recordings are rare,

35
and EEG should be obtained during PET scan to determine if the the study is
incterictal or ictal.
 Single-Photon Emission Computed Tomography
SPECT scanning is also an adjunctive imaging modality useful only for surgical
candidates; the accuracy of seizure localization is about 80–90%. Ictal SPECT
scans done with hexamethylpropyleneamine oxime (HMPAO) show
hyperperfusion in the region of seizure onset. The characteristic pattern is
hyperperfusion of the medial and lateral temporal lobe. This requires ictal
injection within 30 seconds of seizure onset. The ictal SPECT scan subtracted
from the interictal scan (SISCOM) can be very useful in the pre durgical
evaluation. Interictal SPECT testing is less sensitive than are PET-FDG and ictal
SPECT scanning and is not used routinely for localization of the epileptogenic
zone.
 Magnetic Resonance Spectroscopy
Magnetic resonance spectroscopy (MRS) may be clinically useful in selected
patients with possible neoplastic process. It has great research applications.
 Electroencephalography
Electroencephalography should be performed in all patients with suspected
temporal lobe epilepsy. We can see some abnormalities, such as : Interictal
abnormalities, consisting of spike/sharp and slow complexes, usually are located
in the anterior temporal region (F7/F8 and T3/T4 electrodes) or basal temporal
electrodes (most commonly T1/T2 and in research settings, T9/T10 and
F9/F10). During video-EEG monitoring, sphenoidal electrodes can be useful. A
patient with temporal lobe epilepsy can have a normal EEG. The yield of the
EEG can be increased on a repeat study with prolonged recordings, and, in
certain patients, activation with sleep deprivation can be useful.
Video-EEG telemetry is used as part of the pre surgical evaluation. It also is
used if the diagnosis of temporal lobe epilepsy is suspected but still in question
and in patients suspected of having psychogenic seizures. Intracranial EEG with
placement of intracranial subdural electrodes is done only if the patient is a
surgical candidate and MRI and other non-invasive EEG data are not
sufficiently localizing.
 Magnetoencephalography
Another complementary method to assess cerebral physiologic activity similar
to EEG is magnetoencephalography (MEG), which measures the magnetic fields
generated by the epileptic spikes. The main use of MEG is the co-registration
with the MRI to give magnetic source imaging (MSI) in 3-dimensional space.
The spikes that are analyzed for MSI are interictal spikes and this is not as
informative as ictal EEG recordings in surgical evaluations.
 Prognosis
In comparison with the general population, morbidity and mortality are
increased in persons with temporal lobe epilepsy, due to increased accidents from
the episodes of consciousness loss. Mortality also results from sudden unexpected

36
death in epilepsy (SUDEP). Patients with refractory temporal lobe epilepsy,
especially those with secondarily generalized tonic clonic seizures, have a risk of
sudden death that is 50 times greater than that in the general population. The
presence of a seizure-free state 2 years after anterior temporal lobectomy is
predictive of long-term seizure-free outcome for the patient.
About 47–60% of patients become seizure free with medical treatment. After 3
first-line antiepileptic drugs (AEDs) have failed, the chance for seizure freedom is
5–10%. The ILAE now has a formal definition of medically intractable/drug-
resistant epilepsy, which defined as after a patient has had an adequate trial with 2
antiepileptic drugs and is still having seizures. Surgery in well-selected patients with
refractory temporal lobe epilepsy yields a seizure-free outcome rate of 70–80%.

3.2.3.How does the management of epilepsy ?


 What to do during the seizure:
 Stay calm.
 Help the person lie down, and place something soft under the head and neck.
 Keep the person (especially the head) away from sharp or hard objects such as
the corner of a table.
 Time how long the seizures lasts, especially the stiffening and jerking
movements.
 Turn the person onto one side with the head and mouth angled toward
the ground. This helps saliva or fluids to drain out of the mouth. It also
prevents the tongue from blocking the airway.
 Loosen all tight clothing. For example, undo top shirt buttons, belts, and skirt or
pant buttons. Remove any eyeglasses or tight neck chains.
 Do not try to take out contact lenses. You could easily scratch someone’s eye by
trying to remove the small lens during a seizure.
 Do not hold the person down; you may injure the person or get injured yourself.
 Do not put anything in the person's mouth. The tongue cannot be
swallowed during a seizure, yet you could get hurt. The muscles for chewing are
very strong, so a finger can be bitten, or, an object can be bitten off and
cause choking.
 Keep onlookers away. One or two people can give first aid. It can be
embarrassing for the person to awaken to a crowd of people.

 What to do after the seizure:


 Do not try to restrain the person. He or she may be confused and become
agitated or fight against the restraints.
 Try to keep the person in a safe place. Walking around may be okay, but keep
them away from a street, stairs, or other dangerous places.
 Do not give pills, fluids, or food until the person is fully alert.
 Stay with the person until he or she is fully alert and oriented. Be careful. The
person may say they are fine, but still be quite confused.

37
 Have witnesses tell the person who had a seizure what happened and how long it
lasted. Writing this down is best.
 Give reassurance and support!
 Check to see if a person is aware after the seizure.
 Ask a series of questions that require more than a yes or no answer.
 Such as "What is your address?" and "What is the date?

3.2.4.How is the referral procedure for epilepsy patients?


 Referral System
The referral system is a system of administering health services that carries out
the delegation of authority and responsibility for cases that occur vertically, both
vertically in the sense of one health service facility to another health facility, or
horizontally in the meaning of the same strata of health service facilities.

 Procedures for Implementing a Referral System


 Patients who will be referred must have spoken and deserve to be referred. The
answer is patients from one experience:
 The results of the physical examination can be ascertained that they cannot be
overcome.
 The results of the physical examination by medical examination were not able to
be overcome.
 Requires a more complete medical examination, but the examination must
reflect the patient concerned.
 Services used for better health care.

 Standard procedure for patients


 Clinical Procedure
1. Perform anamesa, physical examination and medical examination to
determine the main diagnosis and differential diagnosis.
2. Say a pre-referral case according to the case
3. Decide on the service unit for referral purposes
4. For patients who must be accompanied by medical / paramedic staff who are
competent in their field and know the patient's condition
5. Patient members with a mobile health center or ambulance vehicle, so that
staff and patients can wait until there is certainty that patients are coming
and outpatient.

 Administrative Procedure
1. Done after the patient has been given pre-referral measures
2. Make a patient record of medical records
3. Giving informed consent (approval / rejection of reference)

38
4. Make a referral letter for the first 2 copies of the patient sent to the referral
with the patient concerned. The second sheet is stored as an archive. Record
the location of the patient in the patient registration book.
5. Means of transportation and as much as possible establish communication
with the place of reference.
6. Patient delivery after integrated administration

3.2.5.How to educate patients with epilepsy ?


 Education for the patients with epilepsy
1. Physician should tell the patients and their family about general knowledge of
epilepsy, prognoses of epilepsy, and the possibility of recurrence seizures
2. Physician should ask the family to do these steps when seizures occur :
 Cushion the person's head.
 Loosen any tight neckwear.
 Turn the person on his or her side.
 Do not hold the person down or restrain the person.
 Do not place anything in the mouth or try to pry the teeth apart. The person
is not in danger of swallowing his or her tongue.
 Observe seizure characteristics-length, type of movements, direction of head
or eye turning. These characteristics may help the doctor diagnose the type
of seizure.
3. Patients should take anticonvulsant medication regularly to prevent seizure.
(Huff, 2017)

 Education for first aid for epilepsy patients :


Seizure first aid is a matter of taking precautions
 Keep other people out of the way.
 Clear hard or sharp objects away from the person.
 Don't try to hold her down or stop the movements.
 Place her on her side, to help keep her airway clear.
 Look at your watch at the start of the seizure, to time its length.
 Don't put anything in her mouth. Contrary to a popular myth, you can't swallow
your tongue during a seizure. But if you put an object in her mouth, she could
damage her teeth or bite you. (Pathak, 2018)

3.3. Analysis
From the history of the patient's, data were obtained both from the identity, history
of the current illness, past medical history, and other supporting information to make
the diagnosis. The first thing to know is the type of seizure experienced by the patient,
whether it is a true seizure or psychogenic seizure. A history of unconsciousness during
seizures was found, history of tongue biting, history of aura and duration of seizures for
1-2 minutes leading to true seizure. No data was found to support the patient's

39
psychogenic seizure. This can also be seen from the results of psychological
examinations within normal limits.
After knowing the patient has a true seizure, then it is determined whether the
patient has epilepsy or non-epilepsy. In determining this, it can be seen whether seizures
are provoked by a condition or not. If there are underlying conditions, such as severe
hypoglycemia or sleep deprivation, the patient's condition is not epilepsy. Information
that supports that patients can experience provoked seizure is due to the history of sleep
deprivation. However, there is no data on how long sleep deprivation experienced by
patients so we still have to think of other options, namely unprovoked seizure or
epilepsy.
The results of the patient's history found that there was a history of head trauma
due to a traffic accident and confirmed by physical examination that a suture scar was
found in the right temporal lobe. Because there is a suspicion of a brain abnormality,
additional examinations are carried out in the form of CT Scan and EEG. There were no
abnormalities in the CT scan results, but the EEG results showed a sharp wave in the
right temporal lobe. The EEG picture can convince us that there is an abnormality in the
right temporal lobe of the patient and can also be seen from the patient's data that the
seizures start from the left arm and then spread throughout the body.
The patient's disease course can be explained as follows: (1) the patient has an
accident 2 years ago and unconscious, this event can be called Initial Epileptogenic
Trigger, (2) then enters the latent period for one year, (3) Emergence of Chronic
Epilepsy occurs. Assessment for Emergenge of Chronic Epilepsy or referred as
Epilepsy can use ILAE criteria. This patient met the criteria for epilepsy because he had
at least 2 seizures without provocation (patients had 3 seizures in the past year), where
the distance between seizures was more than 24 hours.
After carrying out a series of history, physical examination, and other supporting
informations, the conclusion of the diagnosis can be drawn that the patient experiences
Temporal Lobe Epilepsy. Furthermore, patients will be referred to a neurologist,
because the competence of general practitioners in dealing with epilepsy is 3A.
Competence 3A means the doctor must be able to diagnose, provide initial
management, and then refer.

3.4. Final Hypothesis


Based on the data we collected and the discussions we had conducted, we
concluded that patients were suspected of Temporal Lobe Epilepsy due to several
medical history that we have mentioned in the previous section, and based on the
supporting examination.

3.5. Group’s Opinion


In the first meeting on Wednesday, November 28th 2018, we were given a case in
scenario. There is a man named Mr. S, 42 years old, came to the primary health care
with a seizure. First of all, we thought that it could be a true seizure, which can be
divided as epileptic and non epileptic seizure or just a pseudo seizure, which can be
classified as psychogenic seizure, atrial fibrillation or syncope.

40
Then, we ask informations about this patient to our tutor, dr. Linda. From
anamnesis, we got some informations such as : The seizures that he experienced is
began from the left arm that felt stiff, then he began to snap his left arm and finally it
spread to the entire body. The seizures occur for 1-2 minutes. His general condition is
good and conscious, but during his seizures, he was unconscious and unresponsive to
questions. Before the onset of seizure, he was sleeping. He also mentioned that during
seizures, he squeezed the tongue and there was incontinence. He also said that he felt
uncomfortable in his epigastrium, which we called as aura. Two years ago, he suffered
head trauma in a traffic accident and he drop his consciousness for 5 hours. One year
ago, he also had seizures three times where the characteristics were same as now. When
he was little, he had febrile seizures which lasts in his 18 month until 5 years old. After
that, patients also feel less sleep these days.
From physical examination, we got information that he has a stitch marks in his
head, specifically in the right temporal lobe. His GCS is 456 and he is compos mentis.
His meningeal sign is negative. Other physical examination of the patient is in normal
limits. The patient didn’t have a history of heart disease, hypertension or diabetes so we
began to think that this was not a syncope or atrial fibrillation. The patient didn’ have a
history of psychological disorders or the patient did not have psychological related
problems, so we began to rule out psychological seizures as a cause of the seizure. We
began to think of a connection between trauma to the right head of the patient with
complaints of patient seizures starting from the left arm, because most abnormalities in
the brain are contralateral to peripheral abnormalities. After that, we determine the
learning issue as our material in increasing knowledge related to patient complaints.
At the second meeting, which is an online tutorial or e-forum on Friday,
November 30, 2018, we submit our learning issue answers and also add some answers
of the additional questions that we submit to PBL. After that, our tutor, dr. Linda, give
us some data of additional examination, such as CT scan and EEG. The CT scan was
normal, but in EEG, we found a sharp wave in the right temporal region. This
information actually makes us to think that the seizures that patients experience right
now are related to head trauma due to the accident that the patient experienced two
years ago, moreover with one year ago the patient had experienced three times seizures,
which characterictics are similar aa seizure that he experience right now.
In the third meeting on December 5th, 2018, we conclude a final hypothesos and
make the final mind map. In this meeting, we argue that seizure that he have was
included in unprovoked type, because there are no things that can provoke patients to
seizures, such as severe hypoglycemia conditions because patients do not have a history
of diabetes and do not take anti-diabetic drugs that can risk hypoglycemia if not
balanced with adequate food consumption. So we assume that patients have temporal
lobe epilepsy, due to unprovoked seizures and occurring in more than 1x, where the
distance between seizures is more than 24 hours.

41
3.6. Final Mind Map

42
REFERENCES

Alsaadi, TM and Marquez, AV (2005). Psychogenic Nonepileptic Seizures. Am Fam


Physician. 72(5):849-856. [Online] available at :
https://www.aafp.org/afp/2005/0901/p849.html. Retrieved on November 29, 2018

Asano, E; Pawlak, C; Shah, A; Shah, J; Luat, AF; Ahn-Ewing, J; Chugani, HT (2005). "The
diagnostic value of initial video-EEG monitoring in children--review of 1000
cases". Epilepsy Res. 66 (1–3): 129–
35. doi:10.1016/j.eplepsyres.2005.07.012. PMID 16157474

Benbadis, SR (2018). Psychogenic Nonepileptic Seizures. [Online] available at :


https://emedicine.medscape.com/article/1184694-differential. Retrieved on November
29, 2018

Bergfeldt, L. (2003). DIFFERENTIAL DIAGNOSIS OF CARDIOGENIC SYNCOPE AND


SEIZURE DISORDERS. Heart, 89(3), pp.353-358.

Bhatia, MS (2004). Review Article : Pseudoseizures. Indian Pediatrics. 41:673-679. [Online]


available at : http://medind.nic.in/ibv/t04/i7/ibvt04i7p673.pdf. Retrieved on
November 29, 2018

Cdc.gov. (2018). Seizure First Aid | Epilepsy | CDC. [online] Available at:
https://www.cdc.gov/epilepsy/about/first-aid.htm [Accessed 6 Dec. 2018].

Clossen, B. and Reddy, D. (2017). Novel therapeutic approaches for disease-modification of


epileptogenesis for curing epilepsy. Biochimica et BiophysicaActa (BBA) - Molecular
Basis of Disease, 1863(6), pp.1519-1538.

Emedicine.medscape.com. (2018). Temporal Lobe Epilepsy: Practice Essentials,


Background, Etiology. [online] Available at:
https://emedicine.medscape.com/article/1184509-overview [Accessed 6 Dec. 2018].

Epilepsy Foundation. (2018). Temporal Lobe Epilepsy (TLE). [online] Available at:
https://www.epilepsy.com/learn/professionals/about-epilepsy-seizures/symptomatic-
and-probably-symptomatic-focal-epilepsies-0 [Accessed 6 Dec. 2018].

Galimberti, Carlo Andrea; Ratti, Maria Teresa; Murelli, Rosanna; Marchioni, Enrico; Manni,
Raffaele; Tartara, Amelia (2003). "Patients with psychogenic nonepileptic seizures,
alone or epilepsy-associated, share a psychological profile distinct from that of
epilepsy patients". Journal of Neurology. 250 (3): 338–346. doi:10.1007/s00415-003-
1009-0. PMID 12638026

https://emedicine.medscape.com/article/1184846-overview

43
https://www.medicinenet.com/script/main/art.asp?articlekey=5442
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3098518/#!po=61.3636
https://www.uptodate.com/contents/seizures-in-adults-beyond-the-basics
https://www.webmd.com/epilepsy/guide/understanding-seizures-and-epilepsy#1

Huff, JS. (2017). Epilepsy. [online] available on :


https://www.emedicinehealth.com/epilepsy/article_em.htm#what_is_epilepsy.
Retrieved on : December 5th 2018

Hyperphysics.phy-astr.gsu.edu. (2018). Chemical Neurotransmitters. [online] Available at:


http://hyperphysics.phy-astr.gsu.edu/hbase/Biology/neurtran.html [Accessed 30 Nov.
2018].

Karabulut, O., Ozeke, O., Erbay, I., Ekici, E., Cay, S., Ozcan, F., Topaloglu, S. and Aras, D.
(2018). Pseudoseizure with Pseudo-ventricular Tachycardia. European Journal of
Arrhythmia & Electrophysiology, 04(01), p.28

LaFrance WC; Baker GA; Duncan R; Goldstein LH; Reuber M (2013). Minimum
requirements for the diagnosis of psychogenic nonepileptic seizures: a staged
approach: a report from the International League Against Epilepsy Nonepileptic
Seizures Task Force. Epilepsia. 54(11):2005-18

Margono, HM (2018). Psychogenic seizures

Mellers, JD (2005). "The approach to patients with "non-epileptic seizures"". Postgraduate


Medical Journal. 81 (958): 498–
504. doi:10.1136/pgmj.2004.029785. PMC 1743326. PMID 16085740

M.J. Brodie, et al..2018, The 2017 ILAE classification of seizure types and the epilepsies:
what do people with epilepsy and their caregivers need to know?, Epileptic Disord,
Vol. 20, No. 2, doi:10.1684/epd.2018.0957

Pathak N. (2018). What to Do When Someone Has a Seizure. [online] available on :


https://www.webmd.com/epilepsy/epilepsy-seizure-what-to-do-in-an-emergency.
Retrieved on December 6th 2018

Purves, D., Augustine, G., Fitzpatrick, D., Katz, L., LaMantia, A., McNamara, J. and
Williams, S. (2018). Excitatory and Inhibitory Postsynaptic Potentials. [online]
Ncbi.nlm.nih.gov. Available at: https://www.ncbi.nlm.nih.gov/books/NBK11117/
[Accessed 30 Nov. 2018].

Timofeev, I., Sejnowski, T., Bazhenov, M., Chauvette, S. and Grand, L. (2013). Age
dependency of trauma-induced neocortical epileptogenesis. Frontiers in Cellular
Neuroscience, 7.

44
Wilshire, C. E.; Ward, T. (2016). "Psychogenic Explanations of Physical Illness: Time to
Examine the Evidence". Perspectives on Psychological Science. 11 (5): 606–
631. doi:10.1177/1745691616645540. PMID 27694458

www.heart.org. (2018). Syncope (Fainting). [online] Available at:


https://www.heart.org/en/health-topics/arrhythmia/symptoms-diagnosis--monitoring-
of-arrhythmia/syncope-fainting [Accessed 2 Dec. 2018].

45
JOURNAL APPRAISAL

Title of paper : The diagnostic value of initial video-EEG monitoring in children—Review of


1000 cases

1. The Completeness of the Paper’s Format Apprasisal

The Item of Appraisal Exist / nonsexist (mention the pages)

■ Title Exist on page 129

■ Abstract and or Summary Exist on page 129

■ Introduction, background Exist on page 130

■ Method Exist on page 130

■ Result Exist on page 130

■ Discussion Exist on page 133

■ acknowledgement Exist on page 134

■ Reference Exist on page 135

Conclusion : The Format is complete

2. Validity of the research Appraisal


 Purpose : This study to group patients with seizure categories based on
ILAE and video-EEG

46
 Methods

Appraisal Item Finding on page..

Design Retrospective review

hierarchy of evidence
Case control study

Sample The ages of patients ranged from 1 month to 17


years (median age: 7 years)

sample size 1000 children patients with epileptic disorders


consist of 523 boys and 477 girls

eligibility criteria Patients with epileptic disorders with length stay


was 1.5 days (range :1-10 days)

sampling frame According to the age, the patients were classified into
three groups as follows; 416 children belonged to
‘Preschool Group’ (0.1–5.9 years), 399 ‘School-age
Group’ (6.0–11.9 years), and 185 ‘Adolescence Group’
(12.0–17.9 years).

method to collect data Make observation by look assessed the applicability of


the International League Against Epilepsy (ILAE) in
children whose video-EEG monitoring confirmed that
the habitual events were epileptic

measurement and or assessment Longer monitoring was associated with higher rate of a
study classified as ‘useful-epileptic’ in all age groups
(Chi square test: p < 0.001). In addition, longer
monitoring was associated with lower rate of a study
classified as ‘inconclusive’ in adolescences (p < 0.001)

47
Instrument Used Video-EEG monitoring protocol

Randomization Not available

Intervention Not available

analysis method This study is carried out by observation on 1000

children with suspected seizure disorders


demonstrated that these outcomes occurred with
approximately one-fourth of the population in each
category

Compatibility between design and the purpose of the research : compatible

Compatibility of measurement method and the instrument used : compatible

Conclusion : valid

3. Research IMPORTANCE Appraisal

This journal define the case control study that shows The diagnostic value of initial video-EEG
monitoring in children—Review of 1000 cases. Literatures used in this journal support the
purpose of making this journal.

How the importance of this study for your case?

Important / Not important

48
Validity Importance Applicability
Question Source Searching method Info type Foundatio Foundatio Foundatio
Result Result Result
n n n
1. How is the 1. Purves, D., Augustine, Internet : Book The 1. Valid Informatio 1.Yes Is it 1.Yes
Physiology of G., Fitzpatrick, D., 1. https://www.ncbi Physiology 2. n about 2.Yes applicable 2.Yes
excitatory and Katz, L., LaMantia, A., .nlm.nih.gov/boo of Invalid the ?
inhibitory? McNamara, J. and ks/NBK11117/ excitatory Physiology
Williams, S. and of
(2018). Excitatory and 2. http://hyperphysi inhibitory excitatory
Inhibitory cs.phy- and
Postsynaptic astr.gsu.edu/hbas inhibitory
Potentials. [online] e/Biology/neurtra
Ncbi.nlm.nih.gov. n.html
Available at:
https://www.ncbi.nlm
.nih.gov/books/NBK1
1117/

2. Hyperphysics.phy-
astr.gsu.edu.

49
(2018). Chemical
Neurotransmitters.
[online] Available at:
http://hyperphysics.p
hy-
astr.gsu.edu/hbase/Bi
ology/neurtran.html

2. How is the 1. https://emedicine.m Internet : Internet The 1.Valid Informatio 1.Yes Is it 1.Yes
pathophysiolo edscape.com/article 1. https://emedicin article pathophys n about applicable
gy of seizure? /1184846-overview e.medscape.com/ iology of the ?
article/1184846- seizure pathophys
overview iology of
seizure
3a. How is the 1. Kristanto A. 2017. Internet : Internet The 1.Valid Understan 1.Yes Is it 1.Yes
explanation of Epilepsi bangkitan 1. https://isainsmed article explanatio ding the applicable
true seizure? umum tonik-klonik is.id/index.php/is n of true the ?
(epileptic seizure) di UGD RSUP m/article/viewFil seizure explanatio
Sanglah Denpasar- e/105/131 (epileptic n of true
Bali. Intisari Sains seizure) seizure

50
Medis 8(1): 69-73. (epileptic
doi:10.15562/ism.v8 seizure)
i1.105
3b. How is the 1. https://www.ncbi.nl Internet : Internet The 1.Valid Understan 1.Yes Is it 1.Yes
explanation of m.nih.gov/pmc/articl 1. https://www.ncbi. article, explanatio 2.Valid ding the 2.Yes applicable 2.Yes
true seizure? es/PMC3098518/#!p nlm.nih.gov/pmc/ health n of true 3.Valid the 3.Yes ? 3.Yes
(non epileptic o=61.3636 articles/PMC3098 web seizure explanatio
seizure) 518/#!po=61.3636 (non n of true
2. https://www.webmd epileptic seizure
.com/epilepsy/guide/ 2. https://www.web seizure) (non
understanding- md.com/epilepsy/ epileptic
seizures-and- guide/understandi seizure)
epilepsy#1 ng-seizures-and-
epilepsy#1
3. https://www.uptodat
e.com/contents/seiz 3. https://www.upto
ures-in-adults- date.com/content
beyond-the-basics s/seizures-in-
adults-beyond-
the-basics

51
4a. How is the 1. Alsaadi, TM and Internet : Health The 1.Valid Informatio 1.Yes Is it 1.Yes
explanation of Marquez, AV (2005). 1. https://www.aaf web, explanatio 2. Valid n about 2. Yes applicable 2. Yes
Pseudoseizure? Psychogenic p.org/afp/2005/0 internet n of 3. Valid is the 3. Yes ? 3. Yes
(Psychogenic Nonepileptic 901/p849.html article, Pseudosei 4. Valid explanatio 4. Yes 4. Yes
non epileptic Seizures. Am Fam internet zure 5. Valid n of 5. Yes 5. Yes
seizure)
Physician. 72(5):849- 2. https://www.ncbi journal (Psychoge 6. Valid Pseudosei 6. Yes 6. Yes
.nlm.nih.gov/pub
856. [Online] nic non 7. Valid zure 7. Yes 7. Yes
med/16157474
available at : epileptic 8. Valid (Psychoge 8. Yes 8. Yes
3. https://emedicin
https://www.aafp.or seizure) nic non
e.medscape.com/
g/afp/2005/0901/p8 epileptic
article/1184694-
49.html seizure)
differential

2. Asano, E; Pawlak, C;
4. http://medind.nic
Shah, A; Shah, J;
.in/ibv/t04/i7/ibv
Luat, AF; Ahn-Ewing,
t04i7p673.pdf
J; Chugani, HT
(2005). "The
diagnostic value of 5. https://www.ncbi
initial video-EEG .nlm.nih.gov/pub
monitoring in med/12638026

52
children--review of
1000 6. https://www.ncbi
cases". Epilepsy .nlm.nih.gov/pub
Res. 66 (1–3): 129– med/24111933
35. doi:10.1016/j.epl
epsyres.2005.07.012 7. https://www.ncbi
. PMID 16157474 .nlm.nih.gov/pmc
/articles/PMC174
3. Benbadis, SR (2018). 3326/
Psychogenic
Nonepileptic
8. https://www.ncbi
Seizures. [Online]
.nlm.nih.gov/pub
available at :
med/27694458
https://emedicine.m
edscape.com/article
/1184694-
differential.

4. Bhatia, MS (2004).
Review Article :

53
Pseudoseizures.
Indian Pediatrics.
41:673-679. [Online]
available at :
http://medind.nic.in
/ibv/t04/i7/ibvt04i7
p673.pdf.

5. Galimberti, Carlo
Andrea; Ratti, Maria
Teresa; Murelli,
Rosanna; Marchioni,
Enrico; Manni,
Raffaele; Tartara,
Amelia (2003).
"Patients with
psychogenic
nonepileptic
seizures, alone or
epilepsy-associated,

54
share a
psychological profile
distinct from that of
epilepsy
patients". Journal of
Neurology. 250 (3):
338–
346. doi:10.1007/s0
0415-003-1009-
0. PMID 12638026

6. LaFrance WC;
Baker GA; Duncan R;
Goldstein LH;
Reuber M (2013).
Minimum
requirements for
the diagnosis of
psychogenic
nonepileptic

55
seizures: a staged
approach: a report
from the
International League
Against Epilepsy
Nonepileptic
Seizures Task Force.
Epilepsia.
54(11):2005-18

7. Mellers, JD
(2005). "The
approach to patients
with "non-epileptic
seizures"". Postgrad
uate Medical
Journal. 81 (958):
498–
504. doi:10.1136/pg
mj.2004.029785. PM

56
C 1743326. PMID 16
085740

8. Wilshire, C. E.;
Ward, T. (2016).
"Psychogenic
Explanations of
Physical Illness: Time
to Examine the
Evidence". Perspecti
ves on Psychological
Science. 11 (5): 606–
631. doi:10.1177/17
45691616645540. P
MID 27694458

4b. How is the 1. Bergfeldt, L. (2003). Internet : Health The 1.Valid Informatio 1.Yes Is it 1.Yes
explanation of Differential 1. https://www.ncbi web, explanatio 2.Valid n about is 2.Yes applicable 2.Yes
Pseudoseizure? Diagnosis Of .nlm.nih.gov/pmc internet n of the ?
(Syncope) Cardiogenic /articles/PMC176 article Pseudosei explanatio

57
Syncope And 7616/ zure n of
Seizure (Syncope) Pseudosei
Disorders. Heart, 2. https://www.hea zure
89(3), pp.353-358. rt.org/en/health- (Syncope)
2. www.heart.org. topics/arrhythmi
(2018). Syncope
a/symptoms-
(Fainting). [online]
diagnosis--
Available at:
monitoring-of-
https://www.heart.or
arrhythmia/synco
g/en/health-
pe-fainting
topics/arrhythmia/sy
mptoms-diagnosis--
monitoring-of-
arrhythmia/syncope-
fainting

4c. How is the 1. Karabulut, O., Ozeke, Internet : Internet The 1.Valid Informatio 1.Yes Is it 1.Yes
explanation of O., Erbay, I., Ekici, E., 1. https://www.tou article explanatio n about applicable
Pseudoseizure Cay, S., Ozcan, F., chcardio.com/arti n of the ?
? ( Topaloglu, S. and Aras, cles/pseudoseizur Pseudosei explanatio
arrhytmia/ VT) D. (2018). e-pseudo- zure ( n of

58
Pseudoseizurewith ventricular- arrhytmia/ Pseudosei
Pseudo- tachycardia VT) zure (
ventricularTachycardia. arrhytmia/
EuropeanJournalofArrh VT)
ythmia&Electrophysiolo
gy, 04(01), p.28.
5. What is ILAE 1. Internet : Health ILAE 1.Valid Informatio 1.Yes Is it 1.Yes
classification https://www.medicine 1. https://www.me web, classificati 2.Valid n about 2.Yes applicable 2.Yes
and definition net.com/script/main/ar dicinenet.com/sc internet on and ILAE ?
of seizure? t.asp?articlekey=5442 ript/main/art.asp article definition classificati
?articlekey=5442 of seizure on and
2. M.J. Brodie, et al..2018, definition
The 2017 ILAE 2. https://www.ncbi of seizure
classification of seizure .nlm.nih.gov/pub
types and the med/29620013
epilepsies: what do
people with epilepsy
and their caregivers
need to know?,
Epileptic Disord, Vol.

59
20, No. 2,
doi:10.1684/epd.2018.
0957

The references that were provided above has been appraised accordingly. The references that did not qualify as a valid, important, or applicable were not
used to formulate answers for the questions. These questions were formulated during the first meeting, and were answered and discussed during the
second meeting. Due to the extensive research needed to answer question one, we decided to answer it the next forum to ensure focused and detailed
information.

*Any invalid, unimportant, or non-applicable sources were not used to formulate answers

60
Validity Importance Applicability
Question Source Searching method Info type Foundatio
Foundation Result Foundation Result Result
n
1. What is 1. Timofeev, I., 1. https://www.ncbi.nlm. Health Epileptogen 1.Valid Information 1. Yes Is it 1. Yes
Sejnowski, T., nih.gov/pubmed/2406
Epileptogenesi website esis in 2.Valid about 2.Yes applicable 2. Yes
Bazhenov, M.,
s? Chauvette, S. and 5884 patients epileptogene ?
Grand, L. (2013). Age
with sis in patients
dependency of
trauma-induced 2. https://www.sciencedi epilepsy with epilepsy
neocortical rect.com/science/articl
epileptogenesis. Front
e/pii/S092544391730
iers in Cellular
Neuroscience, 7. 0431

2. Clossen, B. and
Reddy, D. (2017).
Novel therapeutic
approaches for
disease-modification
of epileptogenesis for
curing
epilepsy. Biochimica
et Biophysica Acta
(BBA) - Molecular
Basis of Disease,
1863(6), pp.1519-
1538.

61
2. What is 1. Emedicine.medscape. 1. https://emedicine.me Internet Temporal 1.Valid Information 1.Yes Is it 1.Yes
com.
Temporal dscape.com/article/1 article, lobe 2.Valid about 2.Yes applicable 2.Yes
(2018). Temporal Lobe
Lobe Epilepsy Epilepsy: Practice 184509-overview Health epilepsy temporal ?
Essentials,
? web lobe epilepsy
Background, Etiology.
[online] Available at: 2. https://www.epilepsy
https://emedicine.me .com/learn/professio
dscape.com/article/1 nals/about-epilepsy-
184509-overview seizures/symptomatic
-and-probably-
2. Epilepsy Foundation. symptomatic-focal-
(2018). Temporal Lobe epilepsies-0
Epilepsy (TLE).
[online] Available at:
https://www.epilepsy
.com/learn/profession
als/about-epilepsy-
seizures/symptomatic
-and-probably-
symptomatic-focal-
epilepsies-0
3. How does 1. Cdc.gov. (2018). 1. https://www.cdc.gov/ Health The right 1.Valid Information 1. Yes Is it 1. Yes
the Seizure First Aid | epilepsy/about/first- web manageme about the applicable
management Epilepsy | CDC. aid.htm nt for right ?
of epilepsy? [online] Available patients management
at: with for patients

62
https://www.cdc.g epilepsy with epilepsy
ov/epilepsy/about/
first-aid.htm
4. How does the 1. Buana, KR., 1. http://eprints.undip.a Disertati The way to 1. Information 1. Yes Is it 1. Yes
referral system Muslimin. 2015. c.id/44813/ on referral Invalid about the applicable
for epilepsy SISTEM RUJUKAN system for way to ?
patients? PENYAKIT KULIT epilepsy referral
DAN KELAMIN DI patients system for
PUSAT KESEHATAN epilepsy
MASYARAKAT, patients
MMM, Vol. 4 No. 3
Agustus 2015 : 218-
228
5. How to 1. Huff, JS. (2017). 1. https://www.emedici Health Education 1.Valid Information 1. Yes Is it 1. Yes
educate Epilepsy. [online] nehealth.com/epileps web, for patient 2.Valid about 2.Yes applicable 2.Yes
available on :
patients with y/article_em.htm#wh internet with education for ?
https://www.emedic
epilepsy ? inehealth.com/epile at_is_epilepsy article epilepsy patient with
psy/article_em.htm# epilepsy
what_is_epilepsy.
2. https://www.webmd.c

2. Pathak N. (2018). om/epilepsy/epilepsy-

63
What to Do When seizure-what-to-do-in-
Someone Has a an-emergency
Seizure. [online]
available on :
https://www.webmd
.com/epilepsy/epilep
sy-seizure-what-to-
do-in-an-emergency

The references that were provided above has been appraised accordingly. The references that did not qualify as a valid, important, or applicable were not
usedto formulate answers for the questions. These questions were formulated during the second meeting, and were answered and discussed during the
third meeting.

*Any invalid, unimportant, or non-applicable sources were not used to formulate answer

64

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