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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
References ............................................................................................................... 43
Journal Aprraisal ...................................................................................................... 46
2
SCENARIO
A man, 42 years old, was taken to primary health care due to seizure.
3
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.
4
CHAPTER 1
1.2. Keywords
- A Man
- Primary health care
- Seizure
b. Pseudoseizure
- Psychogenic seizure
5
- Metabolic disease
- Cardiovascular disease
And also according to ILAE 2017, seizures can be classified into :
6
CHAPTER 2
7
known as a Inhibitory Postsynaptic Potential (IPSP) because it’s going to be LESS
likely to throw off an action potential.
8
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.
9
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.
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
10
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.
11
GABA-B receptors are located in the presynaptic element of an excitatory
projection.
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.
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.
12
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.
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
13
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).
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.
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
14
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.
For further reading, a review by Mastrangelo and Leuzzi addresses how genes
lead to an epileptic phenotype for the early age encephalopathies
15
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.
16
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.
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.
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).
20
Picture 1. The differences between pseudoseizure (PNES) and true seizure (Bhatia, 2004)
Source : http://medind.nic.in/ibv/t04/i7/ibvt04i7p673.pdf
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‖.
23
and electrocardiographic (ECG) recording with multiple scalp and chest
electrodes is required—a situation that is rarely fulfilled.
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).
25
rapid recovery. Atypical types with other symptoms can also
be found
Emotional
A focal non-motor seizure that can have elements such as fear
26
and joy
27
Generalized tonic-clonic
seizure Bilateral convulsion with loss of awareness
heredity
substances
28
and/or falls
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.
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
31
CHAPTER 3
32
(Timofeev et al., 2013)
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%.
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?
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
3.3. 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.
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
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45
JOURNAL APPRAISAL
46
Methods
hierarchy of evidence
Case control study
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).
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
Conclusion : valid
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.
48
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(2018). Excitatory and 2. http://hyperphysi inhibitory excitatory
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pathophysiolo edscape.com/article 1. https://emedicin article pathophys n about applicable
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seizure
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true seizure? umum tonik-klonik is.id/index.php/is n of true the ?
(epileptic seizure) di UGD RSUP m/article/viewFil seizure explanatio
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i1.105
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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-
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4a. How is the 1. Alsaadi, TM and Internet : Health The 1.Valid Informatio 1.Yes Is it 1.Yes
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(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
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3. https://emedicin
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4. http://medind.nic
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Enrico; Manni,
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nonepileptic
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epilepsy-associated,
54
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epilepsy
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346. doi:10.1007/s0
0415-003-1009-
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085740
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Ward, T. (2016).
"Psychogenic
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to Examine the
Evidence". Perspecti
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631. doi:10.1177/17
45691616645540. P
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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
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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
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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
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iers in Cellular
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Lobe Epilepsy Epilepsy: Practice 184509-overview Health epilepsy temporal ?
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the Seizure First Aid | epilepsy/about/first- web manageme about the applicable
management Epilepsy | CDC. aid.htm nt for right ?
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at: with for patients
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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
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available on :
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https://www.emedic
epilepsy ? inehealth.com/epile at_is_epilepsy article epilepsy patient with
psy/article_em.htm# epilepsy
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2. https://www.webmd.c
63
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Someone Has a an-emergency
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available on :
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.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