MODUL SEIZURE 2015 Student Guidancex

Block
VII
Module
: The Nervous System & Psychiatry

: Seizure
Course Period : Academic Year 2014

2015 4th Semester
Name
Student
Guidanc
e
Faculty of
Medicine
Brawijaya
University 2015
MODUL SEIZURE 2015
STUDENT GUIDANCE
Course Period : 4th Semester
MODULE : NERVOUS SYSTEM &
PSYCHIATRY
SUBMODULE: NERVOUS
SYSTEM TOPIC : SEIZURE
1. SUB-TOPICS
: 1.
Introduction
2.
Neurophysiology of Cerebral
Cortex 3.
Pathophysiology of
Seizure
4.
Differential diagnosis of
Seizure 5.
Investigation in
Epileptic Seizure 6.
Seizure
Management
2. CONTRIBUTORS
1.
Nurul H, Department of Anatomy
Histology 2.
Dian Hasanah,
Department of Physiology
3.
Machlusil Husna, Department of
Neurology 4.
Nurdiana, Department
of Pharmacology
3. COMPETENCY AREA
This module is a part of the elaboration of
1.
The area of competence 2 ie. The Clinical Skill
2.
The area of competence 3 ie. The Scientific-Base of
Medical Sciences . 3.
The area of competence 4 ie. The
Management of Health Problems
4.
The area of competence 7 ie. The Professionalism.
4. COMPETENCY COMPONENT
1.
2.
The Clinical Skill : Neurological examination

The Scientific-Base of Medical Sciences : To apply the concepts and
principle of Biomedical Sciences, Clinical Sciences and Public Health in
appropiate with Primary Health Care.
3.
The area of competence 4 i.e. Management of Health Problems: To

manage the diseases, illness and patients problem as a individual person, a
part of family and community and To prevent diseases and illness
4.
The Professionalism: to have professional attitude
5. CLINICAL COMPETENCE
In a vignette of a patient with seizure, the student be able to:
1.
make a clinical diagnosis of seizure, to make simple aids and

additional investigation requested by student himself ( such as simple
laboratory or EEG).
2.
Make a judgement that an initial treatment is required before being
referred and describe to carry out an initial treatment and immediately
refer to the relevant specialist (emergency cases).
6. LEARNING OBJECTIVES
At the end of the Teaching-Learning Process of this topic, in a vignette of a
patient with a seizure the student should be able to:
1.
Describe the anatomical structure that take
part in seizure 2.
Describe mechanism of seizure
3.
Describe mechanism of epileptogenesis
4.
Describe the definition seizure and epileptic seizure
5.
Describe the classification of seizure and
epileptic seizure 6.
Describe the pathophysiology
of epileptic seizure
7.
Describe the signs and symptoms of epilepsy
8.
Describe the outline a practical approach to diagnosis and initial
management of seizure 9.
Differentiate between true seizure and
psychogenic seizure
10. Demonstrate the neurological examination
of seizure 11. Describe antiepileptic drugs
7. LECTURE DESCRIPTION
This topic is a part of Module of The Nervous System integratedly designed for
medical student of the 4th semester through Teaching-Learning Process in the
7th Block both in Lecture and Small Group Discussion. This part of Module will
facilitate the student to have an understanding and approach to the patient with
seizure.
MODUL SEIZURE 2015 3
MODUL SEIZURE 2015
I.
Introduction
A. Definitions
A seizure (from the Latin sacireto take possession of) is the clinical manifestation
of an abnormal, excessive, hypersynchronous discharge of a population of cortical
neurons. Epilepsy is a disorder of the central nervous system characterized by
recurrent seizures unprovoked by an acute systemic or neurologic insult.
Epileptogenesis is the sequence of events that turns a normal neuronal network
into a hyperexcitablenetwork. Recognizing the distinction between seizures
and epilepsy is essential. Epilepsy may require chronic treatment (with
antiepileptic medication and, in some cases, surgery) whereas therapy for an
isolated seizure is directed toward the underlying cause and may not require
antiepileptic drugs (AEDs). Furthermore, epilepsy often has profound psychosocial
ramifications for the patient, and is thus a diagnosis to be assigned with care.
B. Overview
In order to understand the concepts of seizures, epilepsy and epileptogenesis, we

will first consider some of the basic anatomic and electrophysiologic properties of
the cerebral cortex, and the factors that determine the level of neural activity at
the cellular and cell network level. We will then discuss the physiologic basis of the
electroencephalogram (EEG), routinely used in assessing patients with seizures
and other neurological disorders. Finally, we will address some of the main
features of the abnormal physiological activity that occurs within a seizure
focus, and present a few of the proposed mechanisms that may underlie certain
seizure types.
II. Neurophysiology of the Cerebral

Cortex A. Basic Anatomy of Cortex
The human cerebral cortex consists of 3 to 6 layers of neurons. The

phylogenetically oldest part of the cortex (archipallium) has 3 distinct neuronal
layers, and is exemplified by the hippocampus, which is found in the medial
temporal lobe. The majority of the cortex (neocortex or neopallium) has 6 distinct
cell layers and covers most of the surface of the cerebral hemispheres. A
particularly important cortical structure in the pathophysiology of one of the more
common epilepsy syndromes is the hippocampus. This structure is common in
temporal lobe epilepsy. As seen in the slide, the hippocampus consists of three
major regions: subiculum, hippocampus proper (Ammons horn) and dentate gyrus.
The hippocampus and dentate gyrus have a three layered cortex. The subiculum
is the transition zone from the three to the six layered cortex. Important regions
of the hippocampus proper include CA1, CA 2 , CA3. The cortex includes two
general classes of neurons. The projection, or principal, neurons (e.g.,pyramidal
neurons) are cells that project or send information to neurons located in
distant areas of the brain. Interneurons (e.g., basket cells) are generally
considered to be local-circuit cells which influence the activity of nearby neurons.
Most principal neurons form excitatory synapses on post-synaptic neurons,
while most interneurons form inhibitory synapses on principal cells or other
inhibitory neurons. Recurrent inhibition can occur when a principal neuron forms
synapses on an inhibitory neuron, which in turn forms synapses back on the
principal cells to achieve a negative feedback loop. (illustrates an example of a
type of interneuron-granule cell and its role in a negative feedback loop in the
hippocampus.)
Recent work suggests that some interneurons appear to have rather

extensive axonal projections,rather than the local, confined axonal structures
previously suggested. In some cases, such interneurons may provide a very
strong synchronization or pacer activity to large groups of neurons.
B. Basic Neurophysiology and Neurochemistry Governing

Excitability Given that the basic mechanism of neuronal excitability is the
action potential, a hyperexcitable state can result from increased excitatory
synaptic neurotransmission, decreased inhibitory neurotransmission, an
alteration in voltage-gated ion channels, or an alteration of intra- or extra-cellular
ion concentrations in favor of membrane depolarization. A hyperexcitable state
can also result when several synchronous subthreshold excitatory stimuli occur,
allowing their temporal summation in the post synaptic neurons. Action
potentials occur due to depolarization of the neuronal membrane, with
membrane depolarization propagating down the axon to induce
neurotransmitter release at the axon terminal. The action potential occurs in an allor-none fashion as a result of local changes in membrane potential brought about
by net positive inward ion fluxes. Membrane potential thus varies with activation
of ligand- gated channels, whose conductance is affected by binding to
neurotransmitters; or with activation of voltage-gated channels, whose
conductance is affected by changes in transmembrane potential; or with changes in
intracellular ion compartmentalization.
Neurotransmitters are substances that are released by the presynaptic nerve
terminal at a synapse and subsequently bind to specific postsynaptic receptors for
that ligand. Ligand binding results in channelactivation and passage of ions into
or out of the cells. The major neurotransmitters in the brain areglutamate,
gamma-amino-butyric
acid
(GABA),
acetylcholine
(ACh),
norepinephrine,
dopamine, serotonin,and histamine. Other molecules, such as neuropeptides and
hormones, play modulatory roles that modify neurotransmission over longer time
periods.
The major excitatory neurotransmitter is the amino acid glutamate. There are
several subtypes of glutamate receptors. Glutamate receptors can be found
postsynaptically on excitatory principal cells as well as on inhibitory
interneurons, and have been demonstrated on certain types of glial cells.
The
ionotropic subclasses are the alpha-amino-2,3-dihydro-5-methyl-3-oxo4-isoxazolepropanoic acid (AMPA), kainatereceptors, and N-methyl-D-aspartate
(NMDA); these allow ion infux upon activation by glutamate (Appendix A, Table
1). They are differentiated from one another
by
cation
permeability as
well
as
differential sensitivity to
pharmacological agonists/antagonists. All
ionotropic glutamate receptors are permeable to Na+ and K+, and it is the infux of
Na+ and outfow of K+ through these channels that contribute to membrane
depolarization and generation of the action potential. The NMDA receptor also has
a Ca++ channel that isblocked by Mg++ ions in the resting state, but under
conditions of local membrane depolarization, Mg++ is displaced and the channel
becomes permeable to Ca++; influx of Ca++ tends to further depolarize the cell,
and is thought also to contribute to Ca++ mediated neuronal injury under
conditions of excessive neuronal activation (such as status epilepticus and
ischemia), potentially leading to cell death, a process termed excitotoxicity.
The other major type of glutamate receptor is the metabotropic receptor,
which functions by means of receptor-activated signal transduction involving
membrane-associated G-proteins . There are at least 3 subtypes of
metabotropic receptors, based on differential agonist potency, mechanism of
signal transduction, and pre- versus post-synaptic localization.
Experimental studies using animal epilepsy models have shown that NMDA,
AMPA and kainite agonists induce seizure activity, whereas their antagonists
suppress seizure activity. Metabotropic agonists appear to have variable effects
likely dependent upon their different location and mechanisms of signal
transduction. The major inhibitory neurotransmitter, GABA, interacts with 2 major
subtypes of receptor: GABAA and GABAB receptors. GABAA receptors are
found postsynaptically, while GABAB receptors are found presynaptically, and

can thereby modulate synaptic release. In the adult brain, GABAA receptors are
permeable to Cl- ions; upon activation Cl-infux hyperpolarizes the membrane and
inhibits action potentials. Therefore, substances which are GABAA receptor
agonists, such as barbiturates and benzodiazepines, are well known to suppress
seizure activity. GABAB receptors are associated with second messenger systems
rather than Cl-
MODUL SEIZURE 2015
channels, and lead to attenuation of transmitter release due to their

presynaptic location. The second messenger systems often result in opening of
K+ channels, leading to a hyperpolarizing current. Certain GABAB agonists,
such as baclofen, have been reported to exacerbate hyperexcitability and
seizures.
Relevant to epilepsy, glutamate and GABA both require active reuptake to be
cleared from the synaptic cleft. Transporters for both glutamate and GABA exist on
both neurons and glia (primarily astrocytes). Interference with transporter
function has also been shown to activate or suppress epileptiform activity in
animal models, depending on which transporter is being blocked.
C. Factors Governing Excitability of Individual Neurons
The complexity of neuronal activity is partly due to various mechanisms

controlling the level of electrical activation in one or more cellular regions. These
mechanisms may act inside the neuron or in the cellular environment, including
other cells (e.g., neighboring neurons, glia, and vascular endothelial cells) as well
as the extracellular space, to modify neuronal excitability. The former may be
termed neuronal or intrinsic, and the latter extra-neuronal or extrinsic.
1. Examples of neuronal (intrinsic) factors include:
The type, number and distribution of voltage- and ligand-gated channels. Such
channels determine the direction, degree, and rate of changes in the
transmembrane potential, which in turn determine whether an action potential
occurs. Voltage-gated sodium channels, for example, form the basis of the rapid
depolarization constituting the action potential. Among ligand-gated channel THE
GABA receptor complex mediates infow of chloride ions which hyperpolarize the
cell, forming the basis of neuronal inhibition, as described previously.
Biochemical modification of receptors. For example, phosphorylation of the
NMDA receptor increases permeability to Ca++, resulting in increased excitability.
Activation of second-messenger systems. Binding of norepinephrine to its
alpha receptor, for example, activates cyclic GMP, in turn activating G-proteins
which open K+ channels, thereby decreasing excitability.
Modulating gene expression, as by RNA editing. For example, editing a single
base pair of mRNA encoding a specific glutamate receptor subunit can change
the ion selectivity of the assembled channel.
2. Examples of extra-neuronal (extrinsic) factors include:
Changes in extracellular ion concentration due to variations in the volume of the
extracellular space. For
example,
decreased
extracellular
volume
leads
to
increased
extracellular
K+concentration,resisting
the outward movement of K+ ions needed to repolarize the cell, thereby
effectively increasing excitability.
Remodeling of synaptic contacts. For example, movement of an afferent axon
terminal closer to the target cell body increases the likelihood that inward ionic
currents at the synapse will bring thetarget neuron to threshold. The coupling
between the pre- and post-synaptic elements can be made more efficient by
shortening of the spine neck. In addition, previous synaptic experience such as a
brief burst of high frequency stimulation (e.g., long-term potentiation-LTP) also
increases the efficacy of such synapses, increasing their excitability.
Modulating transmitter metabolism by glial cells. Excitability increases, for
example, if glial metabolism or uptake of excitatory transmitters such as
glutamate or ACh decreases.
D. How Network Organization Influences Neuronal Excitability
Neurons are connected together in elaborate arrays that provide additional levels
of control of neuronal excitability. An example of a very basic neuronal network is

the well-studied dentate gyrus and hippocampus. In the dentate gyrus, aferent
connections to the network can directly activate
the projection cell (e.g., granule cells). The input can also directly activate
local interneurons (bipolar and basket cells), and these may inhibit projection
cells in the vicinity (feed-forward inhibition). Also, the projection neuron may in
turn activate the interneurons which in turn act on the projection neurons
(feedback inhibition). Thus, changes in the function of one or more cells within
a circuit can significantly affect both neighboring and distant neurons. For
example, sprouting of excitatory axons to make more numerous connections can
increase excitability of the network of connected neurons. Alternatively, loss of
inhibitory neurons will also increase the excitability of the network. Inhibitory
function can also be reduced by a loss of excitatory neurons that activate or
drive the inhibitory neurons.
III. Pathophysiology of Seizures: An Alteration in the Normal

Balance of Inhibition and Excitation
A. Basic Mechanisms of Focal Seizure Initiation and Propagation
The hypersynchronous discharges that occur during a seizure may begin in a very
discrete region of cortex and then spread to neighboring regions. Seizure initiation
is characterized by two concurrent events:
1) high-frequency bursts of action potentials, and 2) hypersynchronization
of a neuronal population. The synchronized bursts from a sufficient number of
neurons result in a so-called spike discharge on the EEG. At the level of single
neurons, epileptiform activity consists of sustained neuronal depolarization
resulting in a burst of action potentials, a plateau-like depolarization
associated with completion of the action potential burst, and then a rapid
repolarization followed by hyperpolarization. This sequence is called the
paroxysmal
depolarizing shift. The bursting activity resulting from the relatively prolonged
depolarization of the neuronal membrane is due to influx of extracellular Ca++,
which leads to the opening of voltage-dependent Na+ channels, infux of Na+,
and generation of repetitive action potentials. The subsequent hyperpolarizing
afterpotential is mediated by GABA receptors and Cl- infux, or by K+ effux,
depending on the cell type.
Seizure propagation, the process by which a partial seizure spreads within the
brain, occurs when there is sufcient activation to recruit surrounding neurons.
This leads to a loss of surround inhibition and spread of seizure activity into
contiguous areas via local cortical connections, and to more distant areas via long
association pathways such as the corpus callosum.
The propagation of bursting activity is normally prevented by intact
hyperpolarization and a region of surrounding inhibition created by inhibitory
neurons. With sufcient activation there is a recruitment of surrounding neurons
via a number of mechanisms. Repetitive discharges lead to:
1) an increase in extracellular
K+, which blunts the extent of hyperpolarizing outward K+ currents, tending
to depolarize neighboringneurons;
2) accumulation of Ca++ in presynaptic terminals, leading to enhanced
neurotransmitter release; and
3) depolarization-induced activation of the NMDA subtype of the excitatory amino
acid receptor, which causes more Ca++ infux and neuronal activation. Of
equal interest, but less well understood, is the process by which seizures
typically end, usually after seconds or minutes, and what underlies the failure
of this spontaneous seizure termination in the life-threatening condition
known as status epilepticus.
MODUL SEIZURE 2015
B. Current Theories as to How Inhibition and Excitation Can Be

Altered at the Network Level
Our understanding of the CNS abnormalities causing patients to have recurrent

seizures remains limited. It is important to understand that seizures and epilepsy
can result from many different pathologic processes that upset the balance
between excitation and inhibition. Epilepsy can result from processes which
disturb extracellular ion homeostasis, alter energy metabolism, change receptor
function, or alter transmitter uptake. Despite major differences in etiology, the
outcome of synchronous bursting of cortical neurons may superficially appear to
have a similar phenotype. Seizure phenotype may be modified more by the
location and function of the neuronal network recruited into the synchronous
bursting than by the underlying pathophysiology. Because of the well organized
and relatively simple circuits within the entorhinal-dentate-hippocampal loop, the
limbic system has been intensively studied in experimental models of epilepsy.
These investigations have led to two theories regarding the cellular network
changes which cause the hippocampus, among the most common sites of origin
of partial seizures, to become hyperexcitable. The first proposes that a selective
loss of interneurons decreases the normal feed-forward and feedback inhibition
of the dentate granule cells, an important group of principal neurons. The other
theory suggests that synaptic reorganization follows injury and creates recurrent
excitatory connections, via axonal sprouting, between neighboring dentate
granule cells. More recently, it has been proposed that the loss, rather than
being of GABAergic inhibitory neurons, is actually of excitatory neurons which
normally stimulate the inhibitory interneurons to, in turn, inhibit the dentate
granule cells. These mechanisms of hyperexcitability of the neuronal network
are not mutually exclusive, could act synergistically, and may coexist in the
human epileptic brain. Seizures may also appear to arise from widespread cortical
areas virtually simultaneously. The mechanisms underlying such generalized
seizures are uncertain. One type of generalized seizure, the absence seizure,
(also called petit mal) is a generalized seizure consisting clinically of a brief staring
spell in conjunction with a characteristic burst of spike-wave complexes on the EEG.
Generalized spikewave discharges in absence seizures may result from aberrations
of oscillatory rhythms that are normally generated during sleep by circuits
connecting the cortex and thalamus. This oscillatory behavior involves an
interaction between GABAB receptors, Ca++ channels and K+ channels located
within the thalamus. Pharmacologic modulation of these receptors and
channels can induce absence seizures, and there is speculation that genetic
forms of absence epilepsy may be associated with mutations of components of
this system.
C. Epileptogenesis: The Transformation of a Normal Network Into a

Hyperexcitable Network
Clinical observations suggest that certain forms of epilepsy are caused by

particular events. For example, approximately 50% of patients who suffer a
severe head injury will develop a seizure disorder. However, in a significant
number of these patients, the seizures will not become clinically evident for
months or years. This silent period after the initial injury indicates that in some
cases the epileptogenic process involves a gradual transformation of the neural
network over time. Changes occurring during this period could include delayed
necrosis of inhibitory interneurons (or the excitatory interneurons driving
them), or sprouting of axonal collaterals leading to reverberating, or selfreinforcing, circuits. In the future, patients at risk for developing epilepsy due to an
acquired lesion may benefit from treatment with anti-epileptogenic compounds
that could prevent these network changes.
An important experimental model of epileptogenesis is kindling, discovered by

Goddard and coworkers in the 1960s. Daily, subconvulsive stimulation (electrical
or chemical) of certain brain regions such as the hippocampus or amygdala result
in electrical afterdischarges, eventually leading to stimulationinducedclinical
seizures, and in some instances, spontaneous seizures. This change in
excitability is permanent and presumably involves long-lasting biochemical

and/or structural changes in the CNS. A variety of changes have been
measured in kindling models, including alterations in glutamate channel
properties, selective loss of neurons, and axonal reorganization. However, the
exact mechanisms underlying kindling, and its applicability to human
epileptogenesis, remain unknown
IV. Differential diagnosis of epilepsy in adults and children

1. Diferential diagnosis of epilepsy in adults
Epileptic seizures need to be considered in the differential diagnosis of a

range of clinical presentations. These are principally:
Loss of awareness
Generalised convulsive
movements Drop attacks
Transient focal motor attacks
Transient focal sensory attacks
Facial muscle and eye
movements Psychic
experiences
Aggressive or vocal
outbursts
Episodic
phenomena in sleep
Prolonged confusional or fugue states
The principal diferential diagnoses for each presenting clinical scenario
follow with brief explanatory text the key diagnostic features of each diagnosis.
It is not uncommon for a patient to come to medical attention after a dramatic
event, but not to do so after minor episodes. Understanding the occurrence
and nature of minor events is crucial to making an accurate diagnosis. A
checklist of symptoms to specifically enquire for is given in Table 1.
Have there been any spontaneous and otherwise unexplained paroxysmal symptoms?
In
partic ula r:
Sudden
falls
Involuntary jerky movements of limbs whilst
awake Blank spells
Unexplained incontinence of urine with loss of awareness, or in sleep
Odd events occurring in sleep, e.g. fall from bed, jerky
movements, automatisms Episodes of confused behaviour with
impaired awareness, recollection
Possi ble sim ple par tial
sei zure s Epigastric rising
sensation
Dj vu
Premonitio
n Fear
Elation, Depression
De-personalization, derealization
Inability to understand or express language (written
or spoken) Loss of memory, disorientation
Olfactory, gustatory, visual, auditory hallucination
Focal motor or Somatosensory deficit, or positive symptoms (jerking, tingling).
Table 1 Checklist of possible seizure-related symptoms to enquire for when

considering a possible diagnosis of epilepsy
10
MODUL SEIZURE 2015
1.1 Principal diferential

diagnoses 1.1.1 Loss of
awareness
Whatever the cause the patient may have amnesia for both the event and its
exact circumstances. The three main causes are: syncope, epilepsy, and
cardiac arrhythmias. Transient cerebral ischaemia due to vascular abnormalities
is less common. Microsleeps (very short daytime naps) may occur with any
cause of severe sleep deprivation or disruption. Other causes of diagnostic
confusion are much rarer and include: hypoglycaemia or other intermittent
metabolic disorders, structural anomalies of the skull base affecting the
brainstem, or lesions afecting the CSF circulation.
Syncope
Syncope is the commonest cause of episodes of loss of awareness. Simple
faints or vasovagal syncopal attacks can usually be related to identifiable
precipitants. Most often they occur on getting up quickly, or standing for
prolonged periods, particularly if associated with peripheral vasodilation
(e.g. during hot, stufy weather, crowded trains or rooms, or are related to
drug or alcohol use). Frightening, emotional or unpleasant scenes, and
painful stimuli may also be triggers, due to increased vagal activity. There
are various other causes of syncopal attacks, and classification depends
on terminology. Cough and micturition syncope are well recognised.
Changes in intrathoracic pressure (cough syncope), impaired baroreceptors
due to atheroma
of the carotid (carotid sinus syncope), cardiac arrhythmias, or autonomic
disturbances may also lead to cerebral hypoperfusion and fainting. As these
may not be due to vasovagal reflex changes, the typical aura of a vasovagal
syncope may not be present.
Epilepsy
Several types of seizure may present with loss of awareness as the sole
reported feature. These include absences, complex partial, tonic or atonic
seizures. Typical absences involve arrest of activity, reduced or lost
awareness, eyelid blinking or twitching, and sometimes small myoclonic
facial or limb jerks, or brief facial automatisms such as lip smacking or
chewing. Typical absences are usually brief but often occur many times per
day. There may also be isolated myoclonic jerks. Atonic seizures usually
give rise to drop attacks but may appear to cause blank spells if the patient
is sat or laying down and so cannot fall. Complex partial seizures may cause
loss of awareness with few if any other features. Detailed enquiry must
always be made for any associated psychic or motor phenomena that may
raise the possibility of a seizure disorder.
Cardiac disorders
There are often prodromal features similar to simple syncope, as well as
palpitations, chest pain, shortness of breath or other features of
cardiovascular insufficiency. Attacks due to transient complete heart block
are abrupt and short with rapid loss of consciousness. Lack of cardiac
output may be due to short episodes of ventricular tachycardia or
fibrillation. Prolongation of the QT interval may lead to such events.
Attacks may be preceded by palpitations, extreme fatigue or
presyncopal features. Mitral valve prolapse and aortic stenosis may
present with episodic loss of awareness due to fuctuating cardiac output
or
associated
arrhythmias.
Aortic
stenosis
and
hypertrophic
cardiomyopathy is especially prone to present with episodes of sudden

collapse with loss of awareness during exercise.
Microsleeps
Any cause of sleep deprivation may lead to brief day-time naps, sometimes
lasting for only a few seconds. Impaired quality of sleep may also be a
factor. The most important is obstructive sleep apnoea. Narcolepsy can
present with short periods of suddenly falling asleep during the day.
Panic attacks
Panic attacks usually present with feelings of fear and anxiety, associated
with autonomic changes and hyperventilation. This leads to dizziness or
lightheadedness, orofacial and/or peripheral paraesthesia (which may be
asymmetric), carpopedal spasm, twitching of the peripheries, blurred
vision, or nausea. Occasionally these preludes may be forgotten, and
attacks present with loss of awareness. Often, but not always, there is a
clear precipitant, such as a particular situation. None of these features
are consistent, however, and differentiation from epilepsy can be difficult.
Hypoglycaemia
Hypoglycaemic attacks causing loss of consciousness are extremely rare
except in patients with treated diabetes mellitus. Very occasional cases
may be seen due to insulin secreting tumours. In such cases there may be a
history of a missed meal prior to the attack.
Other neurological disorders
If a head injury causes loss of consciousness, there is amnesia. In
accidental head injury, particularly road trafc accidents, it may be difficult
to distinguish amnesia caused by the injury from cases in which there was
a loss of consciousness that caused the accident. Isolated episodes of loss
of awareness may also be caused by abuse of psychotropic drugs or other
substances. Occasionally, structural CNS abnormalities may present with
episodes of loss of awareness.
Non-epileptic attack disorder (NEAD)
Non-epileptic attack disorder, previously known as pseudoseizures
typically gives rise episodes of two broad types:
(a) attacks involving motor
phenomena (b) attacks of lying
motionless.
The latter are often prolonged, continuing for several minutes or sometimes hours.
Such behaviour is very rare in epileptic seizures: there will nearly always be other
positive phenomena in epileptic attacks that last for more than a few minutes. In
addition, attacks are often triggered by external events or stress. Patients with
NEAD often have a history of abnormal illness behaviour. Non-epileptic attack
disorder is much commoner in females than males, and usually commences in
adolescence or early adulthood (see Table 2).
Precipitating
cause When alone
or asleep Onset
Aura
Speec
h
Movement
Injury
Epileptic attack
NEAD
Rare
Common, emotional & stress
related Common
May be reported
Usually short
May be short or over several
minutes Various, usually stereotyped Fear, panic, altered mental
state
Cry, grunt at onset; muttering, words
in automatisms
Semi-voluntary, often
unintelligible Atonic, tonic; if clonic,
Asynchronous failing of limbs;
pelvic synchronoussmall amplitude jerks
thrusting; opisthotonous
Tongue biting, fall; directed violence May bite tongue, cheeks,
l
i
p, hands, Rare
Directed
throw self to ground.
12
MODUL SEIZURE 2015
Consciousness
with
Complete loss in generalized tonic
violence not uncommon

Variable, often inconsistent
clonic; may be incomplete in complexs seizure

type partial
Response to stimulation
None in generalized tonicclonic; may
Often reacts and this may
terminate respond in complex partial and post episode
ictally
Incontinence
Common
Sometimes
Duration
Few minutes
Few minutes, may be
prolonged. Recovery
Depends on seizure type. Few
May be
rapid or very prolonged
minutes and more
prolonged confusion
Table 2 Differentiation of epileptic seizures and non-epileptic attack disorder (NEAD)
1.1.2 Generalised convulsive movements

Epilepsy
A generalised convulsion is generally the most readily diagnosed epileptic
classically, there is a cry, generalised stiffening of body and limbs, followed
by rhythmic jerking of all four limbs, associated with loss of
awareness,eyes staring blankly, tongue biting and urinary incontinence.
The generalized convulsive movements usually last for a minute or so, and
as the attack proceeds the jerking slows in frequency and increases in
amplitude. There is often cyanosis, and afterwards irregular breathing
followed by confusion, headache and sleepiness.
Syncope with secondary jerking movements
People who faint often have small, brief myoclonic twitches of the
extremities. With prolonged cerebral hypoperfusion these may be more
prominent, and be reported as "a convulsion". The myoclonic jerking is
usually irregular and short lived.
Primary cardiac or respiratory abnormalities presenting with secondary
anoxic seizures Episodes of complete heart block may have syncopal
features followed by collapse and secondary anoxic seizures. Usually the
attacks last for less than one minute.
Involuntary movement disorders and other neurological conditions
There is no alteration in consciousness. The best known is paroxysmal
kinesogenic choreoathetosis. Attacks are usually precipitated by sudden
specific movements. They last a few seconds to minutes. Paroxysmal
dystonia presents with attacks lasting for minutes to hours. Patients with
known involuntary movement disorders such as idiopathic torsion
dystonia may show severe acute exacerbations mimicking convulsive
movements. Patients with learning disabilities often have stereotyped or
repetitive movements, which may include head banging or body rocking,
and more subtle movements which may be dificult to diferentiate from
complex partial seizures.
Hyperekplexia
Attacks are characterised by excessive startle, may cause stifening, and
collapse with a sudden jerk of all four limbs. Attacks are provoked by
sudden unexpected stimuli, usually auditory. Hyperekplexia needs to be
distinguished from seizures induced by startle.

Non-epileptic attacks involving prominent motor phenomena are

commoner than those with arrest of activity. Movements are varied but
often involve semi purposeful thrashing of all four limbs, waxing and waning
over many minutes, distractibility or interaction with the environment,
prominent pelvic movements and back arching (Table 2). Non epileptic
attacks may be difficult to differentiate from complex partial seizures of
frontal lobe origin, which can present with very bizarre motor attack
1.1.3 Drop attacks
Any cause of loss of awareness may proceed to a sudden collapse or drop attack.
Epilepsy, syncope and other cardiovascular disorders are the commoner causes of
drop attacks.
Epilepsies
Sudden drop attacks are common in patients with learning disabilities
and secondary generalised epilepsies. The falls may be tonic or atonic.
Cardiovascular
If cerebral hypoperfusion is sufficient to cause sudden collapse there is
usually loss of awareness (see above). Syncope and cardiac abnormality
are rare causes of a presentation with drop attacks.
Movement disorders
Most movement disorders that cause drop attacks have other more
prominent features which make the diagnosis clear (e.g. Parkinson's
disease). Paroxysmal kinesogenic choreoathetosis may cause drop attacks
if there is lower limb involvement.
Brainstem, spinal or lower limb abnormalities
There are usually fixed neurological signs. Tumours of the third ventricle
may present with sudden episodes of collapse. Spinal cord vascular
abnormalities may present with lower limb weakness leading to falls without
impairment of awareness.
Cataplexy
Cataplexy usually occurs in association with narcolepsy, although it may be
the presenting clinical feature. There is no loss of consciousness with
attacks.
Attacks may
be precipitated by
emotion, especially laughter. Often there is only loss of tone in the neck
muscles, with slumping of the head rather than complete falls.
Metabolic disorders
Periodic paralysis due to sudden changes in serum potassium is rare. The
condition may be familial or associated with other endocrine disorders or
drugs. Usually there is a gradual onset, and the attacks last for hours.
Idiopathic drop attacks
These attacks are most common in middle aged females. They take the form
of a sudden fall without loss of consciousness. Characteristically the
patients remember falling and hitting the ground. Recovery is
instantaneous, but injury may occur.
Vertebrobasilar ischaemia
This condition is over diagnosed and probably accounts for very few drop
attacks. Typically, the attacks occur in the elderly, with evidence of vascular
disease and cervical spondylosis.
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The attacks may be precipitated by head turning or neck extension resulting
in distortion of the vertebral arteries and are of sudden onset, with features
of brainstem ischaemia such as diplopia, vertigo, and bilateral facial and limb
sensory and motor deficits
1.1.4 Transient focal motor attacks
The commonest cause of transient focal motor attacks is epilepsy. Tics may
develop in adolescence. Paroxysmal movement
disorders
are
rare,
although unilateral
paroxysmal
kinesogenic
choreoathetosis
may mimic motor seizures. Transient cerebral ischaemia usually presents with
negative phenomena. Tonic spasms of multiple sclerosis are usually seen once
other features of the illness have become apparent, but may be apresenting
feature.
Focal motor seizures
Focal motor seizures may involve jerking and posturing of one extremity,
or reflect the spread of epileptic activity along the primary motor
cortex. There is often associated paraesthesia. There may be localised
transient weakness following the attack for seconds or minutes, sometimes
longer. Seizures arising in many different brain regions may cause
dystonic posturing.
Epilepsia partialis continua is a rare form of epilepsy that often causes
diagnostic confusion. There is very frequent focal motor activity such as
jerking of the hand. This can persist for hours or days, continue into sleep,
and may go on for years. The movements often become slow and
pendulous, with some associated dystonic posturing.
Tics
Tics usually present with stereotyped movements in childhood or
adolescence, sometimes restricted to one particular action (e.g. eye blink)
but may be multiple in nature. Tics may be confused with myoclonic jerks.
They can be suppressed voluntarily, although to do so leads to a rise in
psychological tension and anxiety that is then relieved by the patient
allowing the tics to occur. Repetitive tics and stereotypies are particularly
common in those with intellectual disability.
Transient cerebral ischaemia
Transient ischaemic attacks (TIAs) usually present with negative phenomena,
i.e.
loss
of use
of a limb, hemiplegia or other deficits, although positive phenomena such
as paraesthesiae may occur. Transient ischaemic attacks may last for a few
minutes, but may persist for up to 24 hours. TIAs are not usually
stereotyped or repeated with the frequency of epileptic seizures, and there
are usually associated features to suggest vascular disease.
Tonic spasms of multiple sclerosis
These spasms usually occur in the setting of known multiple sclerosis,
but may be the presenting feature, although other evidence of
multiple sclerosis may be found on examination and investigation. The
spasms may last for several seconds, sometimes longer than one minute.
Paroxysmal movement disorders

Paroxysmal kinesogenic choreoathetosis may present with focal motor
attacks
that
are very similar to epileptic events. Tremor may occur in a variety of
movement disorders and is usually sufficiently persistent to elucidate the
nonepileptic nature, but may be dificult to
distinguish from certain forms of epilepsia partialis continua. Myoclonus

of subcortical origin may be suspected from the distribution of involved
muscles (e.g. spinal myoclonus may be restricted to specific segments,
either unilateral or bilateral). Peripheral nerve entrapment
usually
presents with weakness but occasionally can present with episodic jerks or
twitches.
1.1.5 Transient focal sensory
attacks Somatosensory
attacks
Epileptic seizures involving the primary sensory cortex are less
common than motor seizures, and may cause spreading paraesthesia.
Seizures involving the second sensory areas or mesial frontal cortex may
cause sensory illusions. There are usually other epileptic features due to
involvement of adjacent or related brain structures. Transient sensory
phenomena may also be seen in peripheral nerve compression or other
abnormalities of the ascending sensory pathways, hyperventilation or panic
attacks and in TIAs. TIAs are not usually stereotyped or repeated with the
frequency of epileptic seizures, and there are usually associated features
to suggest vascular disease.
Lesions of sensory pathways cause persistent symptoms, but diagnostic
confusion may arise in the early natural history, when complaints are
intermittent, or if they are posture related. Hyperventilation may be
associated with localised areas of paraesthesia (e.g. one arm).
Intermittent sensory illusions may be experienced in relation to amputated
or anaesthetic limbs. Migrainous episodes may also cause localised areas of
paraesthesia, but usually have the distinction of a gradual evolution of
sensory phenomena, both positive and negative, and associated features of
migraine.
Transient vestibular symptoms
Acute attacks of vertigo may occasionally be due to a seizure in parietal or
temporal lobes. In these cases there are generally associated features that
point to cerebral involvement, such as a focal somatosensory symptoms,
deja vu or disordered perception. Peripheral vestibular disease is a much
more common cause and may give rise to paroxysmal rotational vertigo
and perception of linear motion and there are often also other symptoms of
auditory and vestibular disease such as: deafness, tinnitus, pressure in
the ear and relation to head position.
Visual symptoms
Migraine is a common cause of episodic visual phenomena. The evolution is
usually gradual, over several minutes, with fortification spectra, and
associated photophobia, nausea and headache. Epileptic phenomena are
usually much shorter, evolving over seconds, and the visual hallucinations
are more commonly of coloured blobs, rather than jagged lines.
1.1.6 Facial muscle and eye movements
Changes in facial movements may occur in various neurological conditions
including focal motor seizures, complex partial seizures with automatisms, tics,
dystonias or other
paroxysmal movement disorders, especially drug induced dyskinesias and
hemifacial spasm, as well as psychological disorders.
Partial seizures
Benign rolandic epilepsy usually presents with seizures in childhood affecting the
face, often with unilateral grimacing, hemicorporeal sensory and motor
phenomena, or secondarily generalised seizures occurring in sleep. Focal
motor
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seizures may cause twitching of one side of the face that may be restricted
to specific areas. Eye deviation may be seen with seizures arising in frontal,
parietal or occipital cortex. Complex partial seizures may cause automatisms
with lip smacking, chewing,
swallowing, sniffing or grimacing, with amnesia and impaired awareness. If these
features are due to seizure activity the attacks are usually relatively
infrequent, whereas with dystonia or other movement disorders episodes are
likely to occur many times per day.
Movement disorders
Hemifacial spasm typically presents in the elderly or middle aged with clusters of
attacks that initially involve the eye but subsequently spread to the rest of
that side of the face. Facial weakness may develop that persists between
attacks.
Bruxism may occur either during the day or in sleep, especially in children
with learning disability. Episodes are usually more prolonged than with
the automatisms of complex partial seizures, and there are no associated
features to
suggest an epileptic basis.
As with dystonia and other movement disorders afecting the face there may
be evidence of involvement elsewhere, and attacks are usually more
frequent than is seen with isolated seizures.
Other neurological disorders
Defects of eye movement control are common in patients with a wide range
of neurological disorders. There are usually associated features that
indicate a nonepileptic basis. Bizarre eye movements also occur in
blindness and may be mistaken for epileptic activity. Careful examination is
required to ascertain the precise features of the eye movement disorder,
and in particular any precipitating factors or features of cerebellar or
brainstem disease.
1.1.7 Psychic experiences

Intermittent psychic phenomena can be seen in partial seizures (especially of
temporal lobe origin), migraine, panic attacks, transient cerebral ischaemia, drug
induced fashbacks, or with illusions associated with loss of a sensory modality as
well as psychotic illnesses.
Epilepsy
Partial seizures of temporal lobe origin are especially likely to be
manifest by auras involving psychic phenomena. The most common are
fear, deja vu, memory fashbacks, visual, olfactory or auditory
hallucinations. Other manifestations include altered perception of the
environment with a distancing
from reality or change in size or shape of objects; altered language function;
emotions such as sadness, elation, and sexual arousal.
Psychic experiences may have some relation to past experiences. They are
usually recalled as brief scenes, sometimes strung together. They usually
lack clarity, for example a patient may describe an illusion of someone
standing in front of them who they know, but they cannot name them or
describe them in detail. A rising epigastric sensation may occur alone or in
association with such experiences. Elemental visual phenomena, such as

fashing lights, are more often seen in occipital lobe epilepsy. Altered
thought patterns may be seen in both temporal and frontal lobe seizures.
Migraine
Migrainous psychic phenomena may involve an initial heightening of

awareness. The principal features are usually visual illusions that may be
elemental or complex. They rarely have the same intense emotional
components of temporal lobe illusions or hallucinations. The time course
is usually more prolonged than with partial seizures, and there are
associated features of a pounding headache, photophobia and nausea or
vomiting. There may be recognized precipitants, and there is often a
relevant family history.
Panic attacks
These are usually associated with feelings of fear and anxiety.
Hyperventilation may lead to dizziness and light-headedness. There are
often unpleasant abdominal sensations similar to the epigastric aura of
partial seizures. The evolution, associated increases in heart rate and
respiration, longer time course and history of precipitating factors
generally make the diagnosis clear.
Drug induced fashbacks
These share many of the qualities of psychic temporal lobe seizures. They
are individualised hallucinations usually related to the circumstances of the
drug abuse, often with emotional content of fear or anxiety. A careful
history should be taken for substance abuse, especially LSD and mescaline.
Hallucinations or illusions caused by loss of a primary sense
Hallucinations and illusions of an absent limb are well recognised in
amputees. Similarly, people who lose sight either in the whole or part field
may experience visual hallucinations or illusions in the blind field. Such
phenomena can be elemental or complex and include evolving scenes.
Similar experiences can occur with deafness.
Such experiences due to the loss of a primary sense present particular
diagnostic dificulty when they occur in the setting of a structural lesion
which could result in both phenomena. An occipital infarction, for example,
could cause visual loss and could also give rise to epileptic seizures.
Often the hallucinations due t sensory loss are more prolonged, lasting for
minutes or hours, but can be brief.
Psychotic hallucinations and delusions
Hallucinations and delusions are the hallmark of psychotic illnesses. The
following features would suggest a psychiatric rather than epileptic basis:
complex nature with an evolving or argued theme, auditory nature
involving instructions or third person language, paranoid content or
associated thought disorder. Psychotic episodes are usually more long
lasting than isolated epileptic seizures, although intermittent psychosis
may have a similar time course to nonconvulsive status.
Persistent mood changes may be a helpful guide, but even short temporal
lobe seizures may be followed by mood changes lasting for hours or days.
Furthermore, flurries of epileptic attacks may themselves cause an organic
psychosis lasting for several days. Ruminations and pseudo-hallucinations,
in which the patient retains some insight, may occur in affective disorders.
Non-epileptic attack disorder may be associated with reports of
hallucinations and illusions. These often evolve out of previous
questioning by members of the medical profession. Initially the symptoms
may seem plausible, but should be suspected if they are florid and
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multiple in type (e.g. auditory, olfactory and visual at different times) with
evolving stories or patterns of expression.
1.1.8 Aggressive or vocal outbursts

These are rarely epileptic in nature if they occur in isolation. They are especially
common in adults and children with learning disabilities. In this setting there is
organic brain disease which could lower the overall seizure threshold. Most cases
do not have their basis in epilepsy.
A not infrequent forensic issue is the occurrence of violent, or other, crimes
in patients with epilepsy, it which it is a defence claim that the crime was
committed in a state of automatism. Certain features are strong evidence against
an epileptic basis to the attack.
Absence of a prior history of epilepsy with
automatisms Premeditation and evidence of
planning or preparation
Directed violence
Evidence of complicated and organized activity during
the episode
Recall of events during the episode
Witness accounts not indicative of a disturbance of
consciousness
Subsequent attempts at escape or
concealment of evidence.
1.1.9 Episodic phenomena in sleep
Attacks occurring during sleep present particular diagnostic difficulties because they are
often poorly witnessed, and the patient may have little, if any, recall of the event
or the preceding circumstances.
Normal physiological movements
Whole body jerks commonly occur in normal subjects on falling asleep.
Fragmentary physiological myoclonus usually involves the peripheries or
the face, and occurs during stages 1 and 2 and REM sleep. Periodic
movements of sleep may be an age related phenomenon, being seen in
less than 1% of young adults, but occurring with increasing frequency
during middle and old age such that they are present in perhaps half the
elderly population. Typically these movements occur at regular intervals of
10-60 seconds and may occur in clusters over many minutes.
Frontal lobe epilepsy
Frontal lobe seizures may display specific sleep related
characteristics causing diagnostic confusion. Such attacks are
often frequent, brief, bizarre and maybe
restricted to sleep. Attacks may include apnoea, dystonic, myoclonic,
or choreiform movements that may be unilateral or bilateral, and some
retention of awareness. The attacks are scattered throughout the night,
and usually arise from non-REM sleep. Frequency is highly variable, but
some patients have more than 20 attacks in a night. An important clue to
the diagnosis is the occurrence of
additional secondary generalised seizures and seizures occurring in wakefulness.
Other epilepsies
Seizures arising in other brain regions may present with nocturnal attacks.
Patients may be aroused by an aura, although often this is not recalled
when attacks arise from sleep. Complex automatisms, in which patients
get out of bed and wander around may cause confusion with
parasomnias. With nocturnal seizures of any type the partner is frequently
awoken by particular components, such as vocalisation and does not

witness the onset. Generalised tonic-clonic seizures not uncommonly
occur on or shortly after
awakening.
Pathological fragmentary myoclonus
Excessive fragmentary myoclonus persisting into sleep stages 3 and 4 may
be seen with any cause of disrupted nocturnal sleep.
Restless leg syndrome
The restless leg syndrome is characterised by an urge to move the legs,
especially in the evening when lying or sitting. It may be associated with
various unpleasant paraesthesiae. All patients with restless legs have
periodic movements of sleep. These may be severe and can also occur
during. In addition there may be a variety of brief daytime dyskinesias.
Non REM parasomnias
These involve night terrors or sleep walking. They usually present in
childhood or adolescence, and are often familial. The attacks arise from slow
wave sleep, typically at least thirty minutes, but not more than four hours,
after going to sleep and the timing is often stereotyped. Attacks may be
spaced out by months or years and rarely occur more than once per week,
and usually no more than one attack occurs in a single night. They are more
likely after stressful events, or when sleeping in a strange bed.
Night terrors involve intense autonomic features (sweating, fushing,
palpitations) and a look of fear. Patients may recall a frightening scene
or experience, but do not usually recount a vivid dream prior to the
attacks. They may be difficult to arouse, and confused for several minutes.
Vocalisations are common. Sleep walking may involve getting out of bed
and performing complex tasks. Sometimes it is possible to lead the
patient back to bed without awakening. They may respond if spoken to,
but their speech is usually slow or monosyllabic. Brief, abortive episodes
are commoner, involving sitting up in bed with fidgeting and shuffling
(mimicking a complex partial seizure). Non-REM parasomnias may cause
self injury but rarely directed aggression. They are associated with enuresis.
REM parasomnias
REM parasomnias usually occur in middle age or the elderly, and show a
marked male predominance. They more often occur in the later portion
of sleep. During REM sleep patients may have an increase in the
frequency or severity of fragmentary myoclonus, thrash about, call out,
display directed violence, or appear to enact vivid dreams. Attacks may
last from seconds to minutes. If awoken patients may recall part of
these dreams. Although REM sleep behavior disorders may occur in healthy
elderly subjects they are also seen in association with drugs (e.g. tricyclics)
or alcohol, or central nervous system diseases such as multisystem atrophy.
The possibility of REM sleep disorders needs to be considered both at initial
presentation, and also in patients known to have central nervous system
disorders.
Sleep apnoea
Patients with sleep apnoea usually present with day-time hypersomnolence.
However, the apnoeic episodes may cause episodic grunting, flailing about
or other restless activity that appears to mimic nocturnal epilepsy.
Occasionally the resultant hypoxia leads itself to secondary seizures.
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Other movements in sleep
Nocturnal body rocking may occur in patients with learning disability, or
following head injuries. In patients with many different forms of day-time
dyskinesias, similar movements may occasionally occur during overnight
sleep, usually in the setting of brief arousals.
1.1.10 Prolonged confusional or fugue states

Epileptic seizures usually last for seconds or minutes. After generalised
convulsions (or less often complex partial seizures) there may be confusion lasting
for many minutes, but rarely more than an hour. Such episodes only present
diagnostic difficulty if the initial seizure is unwitnessed or forgotten.
Nevertheless, epileptic states can last for longer periods of time, as can other
types of cerebral disorder and the diferential diagnosis of prolonged epileptic
confusional
states
(non-convulsive
status)
should
include:
acute
encephalopathy, nonconvulsive status epilepticus, transient global amnesia,
intermittent psychosis, hysterical fugue (NEAD).
Acute encephalopathy
Virtually any severe metabolic disturbance may cause an acute
encephalopathy (e.g. diabetic ketoacidosis, hypoglycaemia, respiratory,
renal or hepatic failure, drug ingestion, hyperpyrexia, sepsis). Transient
metabolic disturbances are most often seen in treated diabetes mellitus
due to insulin induced hypoglycaemia. Occasionally metabolic disorders
may present with exacerbations with symptomatology lasting for hours or
days that give the appearance of an episodic condition. These include:
porphyria and urea cycle enzyme defects. Acute neurological conditions
also need to be considered, particularly: encephalitis, meningitis, other
intracranial infection, head injury, cerebral infarction or haemorrhage.
Drug abuse may cause isolated episodes or recurrent bouts, related to
intoxications.
Nonconvulsive status epilepticus
Patients with complex partial seizures, typical or atypical absences may
present with prolonged confusional states due to complex partial
epilepticus or absence status. Such attacks may be the first manifestation
of the seizure disorder, or occur in the setting of known epilepsy.
Intermittent psychosis
Although usually more sustained, psychiatric disorders may present with
episodes of delusions, hallucinations or apparent confusion, lasting for hours
or days.
Transient global amnesia
These episodes typically commence acutely, and last for minutes or hours
and
involve both retrograde and anterograde amnesia. Patients may perform
complexactivities, but afterwards have no recall of them. There is a lack
of other neurological features to the attacks, and consciousness appears
to be preserved. The attacks may involve bilateral medial temporal
dysfunction which in some patients may be on the basis of ischaemia,
whilst some may have an epileptic basis.
Hysterical fugue
A fugue state may arise without an organic physical cause, as a conversion
symptom. These episodes may be brief or very prolonged, lasting for days or
even weeks. If seen at the time of an episode inconsistencies are often
found on examination of the mental state. In some
cases, the question of malingering arises, most commonly in a situation

in which the person's state prevents questioning by Law Officers. The
diagnosis is more difcult to identify if the patient is only seen
subsequently. The matching of witness accounts and the apparent sequence
of events is essential, but it may remain difficult to come to a firm
conclusion. In this situation, there is sometimes a forensic aspect, typically
when the person concerned is alleged to have committed a crime and they
profess to have no memory of the events. A checklist of possible seizurerelated symptoms to enquire for when considering a possible diagnosis of
epilepsy can be found in Table 1.
2. Diferential diagnosis of epilepsy in children
There are a range of possibilities in the differential diagnosis when considering

the child with a funny turn. The considerations will vary depending on certain
key features of the event, as well as the age of the child. The history is key to any
diagnosis, and is likely to be far more useful than any investigation that can be
requested. Always seek the initial event a trigger or warning, however young
the child. There may be a typical behavior prior to any event or a slightly older
child may be able to relate a feeling prior to or during the event. A description of
each change in the child should be sought, and the evidence of loss or not of
awareness. Other important aspects of the history are medications taken,
developmental history and past medical history but information from these will
only be supplementary to the history of the events themselves. There are a
number of possibilities within the differential diagnosis of epilepsy in childhood;
however a lack of awareness of such alternatives remains the major reason for
error and the premature, possible misdiagnosis, of epilepsy. The following is a
classification of possibilities, although not exhaustive.
Syncope & related disorders

Disorders of orthostatic
control
Respiratory
syncope
Cardiac
syncope
Brainstem
syncope
Other
Neurological
Behavioural/psychia
Refex syncope
Refex & expiratory apnoeic syncope
Fainting lark
Upper airway
obstruction Arrhythmias
Complete heart
block Wolf
parkinson white
Brugada
syndrome Tumour
Brain stem herniation or
compression Hyperekplexia
Anoxic epileptic seizures
tric
T
i
c
s
M
y
o
c
l
o
n
u
s
P
a
r
oxysmal dystonia
Sandifers syndrome
Paroxysmal
dyskinesias
Cataplexy
Benign paroxysmal
vertigo/torticollis Migraine
Alternating
hemiplegia Eye
movement disorders
Overflow movements
Daydreams
Dissociative states
Self gratification
behaviour
Hyperventilation
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Panic/anxiety
Non epileptic attack
disorder Fabricated attacks
Pseudosyncope
Stereotypies/ritualistic
behavior
Parasomnias
Table 3 Classification of possibilities in childhood

epilepsy
Sleep myoclonus
Headbanging
Confusional
arousal
REM sleep disorder/night terrors
2.1 The child under the age of 12 months

In a child of this age it may be incredibly difcult to determine the true nature of an
event
when taking the history for the first time. There is likely to be considerable
anxiety on the part of carers, and if there is any doubt, referral is advised
Is the event related to any particular activity?
For example, feeding may suggest reflux, history of medication ingestion may
suggest dystonic reaction, sleep may suggest benign sleep myoclonus.
What is the major motor component?
Is the major motor component apparent hypertonia, hypotonia
or dystonia? Is this movement repetitive or sustained?
Either repetitive short duration over short period or with greater duration
between. Repetitive jerks may imply seizures, although only from sleep may be
sleep myoclonus. Repetitive spasms will be stereotyped, in clusters. Sudden
sustained hypertonia may give a clue to hyperekplexia or brainstem syncope
Are semi-purposeful movements seen at any time? This may give a clue as to the state
of awareness
What parts of the body are involved in the movements? For example, whole
body, eyes vs limb, all limbs vs single/multiple
Is there a behaviour
change? Does the child stare
unresponsively?
Is eye movement seen in association with this? Can they be distracted?
Is the child distressed?
If so intermittently or continuously? Distress may suggest awareness, particularly
in between spasms during clusters
Is there apparent fear?
Of course that may be manifest by distress, and therefore an apparent awareness of
what is happening
Is the event characterised by other

phenomena? Is there a colour change?
Pallor or cyanosis may be seen in cardiac arrythmias;
cyanotic attacks are commonly associated with reflux. Flushing
may be seen with repetitive movement in self gratification
behavior
Is there a change in breathing pattern?
Deep/stertorous breathing with loss of awareness may be seen
in generalised seizures, compared with retained awareness in self
gratification behaviours.
Can the event be interrupted?
If so, then the event is probably a partial seizure or NEAD. If the
event cannot be interrupted, then possibly a generalised seizure.
2.2 In the toddler (aged 1 to 3 years)

Sleep or waking state; parasomnias are very common at
this age and in some instances mimic seizures. Night
terrors usually occur at a specific time each night, and
during which the child may appear unreachable.
Confusional arousals may also cause alarm as the child is
inaccessible
Adverse/noxious events; if the event is always triggered
by this consider breath holding/reflex anoxic seizures
Fever; as in febrile seizures
Movement as in paroxysmal dyskinesias
Feeding as in Sandifers syndrome
Excitement as in overflow movements
Note stereotypic movements/ritualistic behaviours may be
seen in children with developmental delay/communication
disorders at any time, but xcitement/stress or boredom
Emotion as in cataplexy
- Is a fall the major component of the event?
- Is the major motor component apparent hypertonia, hypotonia or dystonia?
o Hypertonia consider reflex/epiratory syncope, tonic/tonic
clonic seizure, hyperekplexia
o Hypotonia consider syncope, cataplexy, akinetic drop
attack although the latter unlikely to occur in the absence of
other seizure types
o Dystonia consider dyskinesia, benign paroxysmal torticollis (BPT)
o Unsteadiness consider benign paroxysmal vertigo (BPV),
intermittent ataxia
Is this movement repetitive or sustained?
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Either repetitive short duration over short period or with

greater duration between. Repetitive jerks may imply
seizures.
Although
repetitive
short
movements
predominantly of the face may be tics
- Are semi-purposeful movements seen at
any time? - This may give a clue as to the
state of awareness
- What parts of the body are involved in the movements?
- For example, whole body, eyes vs limb, all limbs vs single/multiple
o
Is there a behaviour change?

- Does the child stare unresponsively?
o Is eye movement seen in association with this? Can they
be distracted? Is the child distressed?
o If so intermittently or
continuously? -Is there apparent fear?
o Of course that may be manifest by distress, and therefore
an apparent awareness of what is happening.
Is the event characterised by other
phenomena? - Is there a colour change?
o Pallor or cyanosis may be seen in cardiac arrythmias;
cyanotic attacks are commonly associated with expiratory
apnoeic (breath holding) attacks. Flushing may be seen
with self gratification behaviour.
- Is there a change in breathing pattern?
o Either an increase or decrease may give a clue
to the above. - Can the event be interrupted?
2.3 In the older child (aged 3 to 12 years)
- Sleep or waking state; parasomnias are very common at this
age and in some instances mimic seizures.
- Movement as in paroxysmal
dyskinesias - Excitement as in
overflow movements
- Note stereotypic movements/ritualistic behaviours may be seen
in children with developmental delay/communication disorders
at any time, but particularly excitement/stress or boredom.
- Emotion as in cataplexy
- Is a fall the major component of the event?
- Is the major motor component apparent hypertonia, hypotonia or dystonia?
o Hypertonia consider reflex/epiratory syncope, tonic/tonic
clonic seizure, hyperekplexia
o Hypotonia consider syncope, cataplexy, akinetic drop
attack although the latter unlikely to occur in the absence of
other seizure types
o Dystonia consider dyskinesia
o Unsteadiness consider intermittent ataxia
-
Is this movement repetitive or sustained?

o
Either repetitive short duration over short period or with

greater duration between. Repetitive jerks may imply
seizures.
Although
repetitive
predominantly of the face may be tics
short
movements
Are semi-purposeful movements seen at any time?

o This may give a clue as to the state of awareness although
older child likely to be able to relay information about event
What parts of the body are involved in the movements?
o For example, whole body, eyes vs limb, all limbs vs single/multiple
Is there a behaviour change?

- Does the child stare unresponsively?
o Is eye movement seen in association with this? Can they be
distracted by touch rather than voice alone? The most
common cause of blank spells remains
daydreaming.
Typical
absence
seizures occur
relatively frequently,at any time and are of short
duration (5-10 seconds)
- Is there apparent fear?
- Is there aggressive/destructive behaviour?
o
True rage attacks in isolation are rarely, if ever
epileptiform in origin. Typically they are seen in children
with learning dificulties, but are not unseen in children
with very specific learning problems that have not yet been
recognised. The children may become aggressive and
destructive, have little, if any recollection of the event
- Is the event characterised by other
phenomena? - Is there a colour change?
o Pallor or cyanosis may be seen in cardiac arrythmias. Pallor
is likely to be seen in association with any syncope.
Flushing may be seen with self gratification behavior
- Is there a change in breathing pattern?
o Either an increase or decrease may give a clue
to the above - Is there visual symptomatology?
o Visual disturbance, if so at what stage of the event may
suggest primary or secondary phenomenon. What is the
character of such (repeated) stereotyped colours or
formed object likely to be seizure; late distorted vision?
secondary.
- Are there sensory symptoms?
o If so, then maybe partial seizure, or paraesthesias due
to other causes Is there vocalisation?
o Audible words or nonsense? At what stage of the
event? Directed speech/vocal outbursts are unlikely to be
epileptic.
- Can the event be interrupted?
o If so unlikely to be a seizure.
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V. INVESTIGATIONS IN EPILEPTIC SEIZURE
Information should be provided to children, young people and adults

and families and/or carers as appropriate on the reasons for tests,
their results and meaning, the requirements of specific investigations,
and the logistics of obtaining them. All investigations for children
should be performed in a child-centred environment.
Electroencephalogram (EEG)
Children, young people and adults requiring an EEG should have the
test performed soon after it has been requested. An EEG should be
performed only to support a diagnosis of epilepsy in adults in whom
the clinical history suggests that the seizure is likely to be epileptic in
origin. The EEG should not be used to exclude a diagnosis of epilepsy
in a child, young person or adult in whom the clinical presentation
supports a diagnosis of a non-epileptic event. An EEG may be used to
help determine seizure type and epilepsy syndrome in children, young
people and adults in whom epilepsy is suspected. This enables them
to be given the correct prognosis. For children, young people and
adults in whom epilepsy is suspected, but who present diagnostic
difficulties, specialist investigations should be available.
Neuroimaging
Neuroimaging should be used to identify structural abnormalities that
cause certain epilepsies. MRI should be the imaging investigation of
choice in children, young people and adults with epilepsy. MRI is
particularly important in those: who develop epilepsy before the age of
2 years or in adulthood who have any suggestion of a focal onset on
history, examination or EEG (unless clear evidence of benign focal
epilepsy) in whom seizures continue in spite of first-line medication.
Children, young people and adults requiring MRI should have the test
performed soon. Neuroimaging should not be routinely requested
when a diagnosis of idiopathic generalised epilepsy has been
made. CT should be used to identify underlying gross pathology if MRI is

not available or is contraindicated, and for children or young people in
whom a general anaesthetic or sedation would be required for MRI but
not CT. In an acute situation, CT may be used to determine whether a
seizure has been caused by an acute neurological lesion or illness.
Other tests
In adults, appropriate blood tests (for example, plasma electrolytes,
glucose, calcium) to identify potential causes and/or to identify any
significant co- morbidity should be considered. In children and young
people, other investigations, including blood and urine biochemistry,
should be undertaken at the discretion of the specialist to exclude other
diagnoses, and to determine an underlying cause of the epilepsy.
Neuropsychological assessment
Neuropsychological assessment should be considered in children,
young people and adults in whom it is important to evaluate
learning
disabilities
and
cognitive dysfunction,
particularly
in
regard
to
language
and
memory.
Referral
for
a
neuropsychological assessment is indicated:
when a child, young
person or adult with epilepsy is having educational or occupational
difficulties
when an MRI has identified abnormalities in cognitively
important brain regions when a child, young person or adult complains
of memory or other cognitive deficits and/or cognitive decline.
VI. GENERAL PRINCIPLES OF MEDICAL MANAGEMENT

Aims of treatment
The primary goal of treatment is to ensure the best possible quality of life that is
compatible with the nature of the patients seizure disorder and with any associated
mental or physical disabilities. To achieve this general goal, various objectives need
to be addressed whenever relevant or feasible.
General Treatment Management
1. Complete seizure control
If exception is made for the control of ongoing seizures and status
epilepticus, the treatment of epilepsy is primarily prophylactic (e.g.
aimed at preventing seizure recurrence). In general terms, therefore,
the primary objective of treatment should be complete seizure control
where this is feasible. This, however, should not be achieved at all costs.
Antiepileptic drugs can produce severe adverse effects, particularly when
they are administered at high dosages or in combination, and the
situation should never arise where a patient is made to suffer more from
the adverse effects of treatment than from the symptoms of the disease.
Whenever complete seizure freedom proves to be a non-realistic goal,
optimal treatment should result from the best compromise between the
desire to minimize seizure frequency and the need to maintain adverse
effects within acceptable limits.
2. Reduction of seizure severity
Although most outcome studies in epilepsy have focused on seizure
frequency, seizure severity, particularly with respect to occurrence

of potentially injurious ictal manifestations, is by itself an important
determinant of quality of life. In patients whose seizures cannot be
controlled completely, it makes sense to aim at suppressing
preferentially those seizures which are most dis- abling. Assessing the
most dis- abling
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seizure types can require assistance from an external observer, but

the patients perceptions are more important. A seizure component
that may appear trivial or negligible to an observer may be perceived
as very distressing by the patient.
3. Avoidance of adverse efects
The prescription of antiepileptic medication entails a significant risk of
adverse effects. While many patients with recently diagnosed epilepsy
can be controlled at low dosages, which produce only modest
detectable toxicity, patients with severe epilepsies may have to pay a
significant price in terms of adverse effects to avoid or minimize seizure
recurrence.
4. Suppression of subclinical epileptic activity
Antiepileptic drug therapy should be aimed primarily at suppressing
the clinical manifestations of seizures, and normalization of the
electroencephalogram (EEG) generally is neither a major nor an
attainable objective, nor in some cases even desirable. In certain
situations, however, suppression of epileptiform EEG abnormalities is a
justifiable therapeutic goal. This is the case when there is a close
correlate between clinical seizures and EEG paroxysms, and the
seizures are not easily quantifiable clinically, as in childhood absence
epilepsy or some photosensitive epilepsies. The EEG may also be
important in guiding treatment in infants and children with severe
epileptiform EEG abnormalities co-existing with brain dysfunction.
5. Reduction of seizure-related mortality nd morbidity
In some cases where seizures are triggered by a treatable cause,
such as a brain tumour, removal of the latter is essential to reduce any
related morbidity and mortality. In recent years, however, evidence
has accumulated that seizures per se are also associated with an
increased mortality, partly in relation to accidents which may occur
during a seizure and partly in relation to the risk of sudden
unexpected death in epilepsy (SUDEP).
6. Addressing co-morbidities
Many
symptomatic
epilepsies
are
aetiologically
related
to
malformative, vascular, neoplastic, degenerative, infammatory or metabolic disorders which affect the central nervous system, and appropriate
management of these conditions must be part of the comprehensive
care of these patients.
Neuropsychiatric disorders are also relatively common in patients
with epilepsy . Although these co-morbidities have been traditionally
regarded as a consequence of the physical and psychosocial limitations
associated with seizures, and the adverse effects of antiepileptic drugs,
there is increasing evidence that other factors are also involved. In
particular, pre-existing depression or a history of suicide attempt
have been identified as separate risk factors for incident unprovoked
seizures.
Many
physicians
treating
epilepsy
do
not
routinely
screen
for
psychiatric disorders, which is regrettable because these co- morbidities

may impact on quality of life more than epilepsy and seizures
themselves, and therefore need to be identified and treated as
appropriate. In a recent study from the USA, the severity of depressive
symptoms and the adverse effects of drugs in patients with epilepsy
correlated independently with subjec- tive health status, and these
factors explained 72% of the variance
7. Avoidance of adverse drug interactions

Patients receiving therapy with a combination of drugs are at risk for
adverse
drug interactions, at either the pharmacokinetic or
pharmacodynamic level. Drug interactions are not restricted to those
resulting from combinations of antiepileptic drugs, but also involve
medications taken for other indications . Physicians should be aware of
this, and should take all necessary steps to minimize any adverse
consequences.
8. Avoidance of obstruction to patients life
Therapeutic outcome may be influenced by the patients ability to
identify and avoid situations which could affect susceptibility to
seizures, such as excessive sleep deprivation, or in some photosensitive epilepsies exposure to intermittent flashing lights or certain
video games. While these risk factors need to be discussed and
appropriate counselling given, it is equally important to avoid undue
restrictions on the patients lifestyle. For example, alcohol abuse should
be actively discouraged, but there is no reason to prohibit one glass of
beer or wine at meal times. In general, patients should be encouraged
to live a normal life, while avoid- ing extreme deviations from what
would be considered a regular lifestyle.
Prescription of medication should also be aimed at minimizing
interference with daily activities. Antiepileptic drugs which can be given
once or twice daily are less likely to obstruct daily rou- tines and to
cause psychosocial embarrassment, and they are associated with a
better compliance. For drugs which can be given once or twice daily but
do not have a long half-life, a twice-daily schedule may be preferable
because it minimizes the adverse consequences of missing one dose. In
general, once-daily dosing does not entail better compliance than twicedaily dosing, but it may have psychological advantages, particularly in
patients who are seizure free and perceive each act of pill-taking as the
only unpleasant reminder of their disease.
9. Prevention of epileptogenesis
Experiments in animal models suggest that some antiepileptic drugs
not only exert a symptomatic effect by raising seizure threshold, but
might also antagonize epileptogenic processes, i.e. the mechanisms
through which an epileptic condition becomes established. The
suggestion has been made that recurrent clinical seizures may also lead
to irreversible neuroanatomical changes which may render the disease
more difficult to control, but evidence for this is controversial. If
uncontrolled seizure activity leads to the chronicization of the disorder, a
case could be made for early and aggressive treatment, and for
preferential use of drugs which putatively antagonize epileptogenic
processes. Available studies, however, suggest that in most epilepsy
syndromes antiepileptic drugs exert merely a symptomatic effect and
do not affect the natural course of the disease .
When should treatment be started?
Antiepileptic drugs (AEDs) are the mainstay of the treatment of epilepsy,
and although their number has expanded exponentially, current
principles governing drug therapy are in many ways similar to those

established a century ago. Because AED therapy is typically maintained
for several years and often for life, particularlyinadults,a decision to
initiate treatment has far-reaching consequences and needs to be
based on careful risk-benefit analyses.
The predicted efficacy of AEDs has to be weighed against potential adverse effects,
while
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at the same time considering the risks associated with withholding of

treatment. These risks should be assessed in the broadest sense,
taking into account the patients perspective in relation not only to
the risk of further seizures but also the risk of seizure-related
morbidity and mortality, as well as AED toxicity. Ideally, assessment of
the potential benefits of treatment should involve an understanding
of the natural course of untreated epilepsy and its consequences.
The risk of recurrence after a first unprovoked seizure has been
analysed in several studies.A meta-analysis12 from 1991 concluded that
the average risk of having a further seizure was 46%, but variation
across studies was substantial. The risk of subsequent seizures was
much higher after a second seizure (more than 70%), even in a cohort
in which most patients were on treatment after their second seizure.On
the basis of this increased risk, there has been a consensus that
treatment is indicated after at least two unprovoked seizures.
From a practical viewpoint, a key finding is that the risk of recurrence
after a first seizure varies considerably in relation to the patients
characteristics. In individuals with risk factors (eg, epileptiform
electroencephalogram [EEG] discharges, an abnormal neurological
examination, or other evidence of a structural CNS abnormality
presumed to be responsible for the seizure), the risk of recurrence after
a first seizure might be similar to the average risk after two seizures.12
This has been taken into account in the newly proposed International
League Against Epilepsy (ILAE) definition of epilepsy as a disorder of
the brain characterized by an enduring predisposition to generate
epileptic seizures14 and requiring occurrence of at least one
unprovoked seizure,
The key to optimum epilepsy management is to adapt treatment
decisions to the characteristics of the individual. In general, AED
monotherapy is indicated after two seizures, but in high-risk patients
initiation of treatment after one seizure might be justifiable. AED
choice is determined by seizure type, adverse-efect profile, and patientspecific features, including age, sex (with special reference to
childbearing potential), and comorbidities. Dose titration and dosing
regimens also need to be carefully individualised.
Failure to
achieve seizure freedom
should prompt diagnostic reassessment
and early consideration of the feasibility of epilepsy surgery. Combination
therapy can be beneficial in patients who did not respond to two or
three sequential monotherapies, although in some cases earlier
institution of polytherapy might be justified. Seizure freedom is always
the ultimate goal, but it should not be pursued at all costs and
overtreatment should be carefully avoided. In patients who do achieve
seizure control, discontinuation of AEDs after at least 24 years of
seizure freedom should be considered, after careful assessment of
potential benefits versus the risk of relapse and related implications.
9. MODULE TASK
Find out your answers to the following tasks by yourself after discuss it
with your group or after reading the suggested references below.
1. What are the anatomical structures that take part
in seizure ? 2. Explain the mechanism of seizure in

hyperglycemia !
3. Explain the mechanism of epileptogenesis !
4. What is the definition of seizure and epileptic seizure ?
5. Describe the classification of seizure and
epileptic seizure ! 6. Describe the pathophysiology
of epileptic seizure !
7. Describe the signs and symptoms of

epilepsy ! 8. How to manage a first time
seizure ?
9. How to differentiate between true seizure and
psychogenic seizure ? 10. What are indications to perform
brain imaging in seizure?
11. Which AED is most appropriate for general epileptic seizure?
12. Make schematic algorithm to differentiate symptoms of
seizure in children! 13. Make schematic algorithm to differentiate
symptoms of seizure in adult !
10. TEACHING-LEARNING PROCESS

1. Each student should work the tasks in a Student-Worksheet
(hand written in A4-size book) prior to Small Group Discussion
(home work).
2. The Student Worksheet will be collected before Small Group Discussion .
3. Student should discuss the tasks in Small Group Discussion. The
conclusion of the discussion will be collected at the end of the
discussion.
4. The facilitators make notes on things the student discuss which
need to clarify at the end of each session or in lecture to achieve
the learning objectives and collect the report of discussion.
11. THE ASSESSMENT
1. The Formative Evaluation will be assessed through
Observation Sheets elaborating the Learning Skill and
Content Mastery
2. The Summative Evaluation will be assesed together with the
other modules in Middle Semester Test and or End Semester Test
scheduled.
12. REFERENCES
American Epilepsy Society. Basic Mechanism of Seizures and Epilepsy. 2009.

Care of the Patient with Seizures. 2nd ed. AANN Clinical Practice Guideline Series. 2009
Engel J, et al (eds). Epilepsy : Global Issue for The Practicing Neurologist. New
York : Demos Medical Publishing. 2005
Diagnosis and Management of Epilepsy in Adults. Scottish Intercollegiate
Guidelines Network. 2003
Stafstrom CE. Hyperglycemia Lowers Seizure Threshold. Epilepsy Curr., 2003; 3(4): 148149.
Grant C and Warlow C. Focal epilepsy in diabetic non-ketotic hyperglycaemia. BMJ, 1985;
290:
12041205.
Perucca E, Tomson T, The pharmacological treatment of epilepsy in adults. Lancet Neurol
2011;
10: 44656
THE EPILEPSIES : The Diagnosis And Management of Epilepsy in Adult and
Children In Primary and Secondary Care. NICE Clinical Guidline.2012
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Block

: The Nervous System & Psychiatry

Course Period : Academic Year 2014

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The Clinical Skill : Neurological examination

The area of competence 4 i.e. Management of Health Problems: To

make a clinical diagnosis of seizure, to make simple aids and

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In order to understand the concepts of seizures, epilepsy and epileptogenesis, we

II. Neurophysiology of the Cerebral

The human cerebral cortex consists of 3 to 6 layers of neurons. The

Recent work suggests that some interneurons appear to have rather

B. Basic Neurophysiology and Neurochemistry Governing

found postsynaptically, while GABAB receptors are found presynaptically, and

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channels, and lead to attenuation of transmitter release due to their

C. Factors Governing Excitability of Individual Neurons

The complexity of neuronal activity is partly due to various mechanisms

D. How Network Organization Influences Neuronal Excitability

of control of neuronal excitability. An example of a very basic neuronal network is

III. Pathophysiology of Seizures: An Alteration in the Normal

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B. Current Theories as to How Inhibition and Excitation Can Be

Our understanding of the CNS abnormalities causing patients to have recurrent

C. Epileptogenesis: The Transformation of a Normal Network Into a

Clinical observations suggest that certain forms of epilepsy are caused by

An important experimental model of epileptogenesis is kindling, discovered by

excitability is permanent and presumably involves long-lasting biochemical

IV. Differential diagnosis of epilepsy in adults and children

Epileptic seizures need to be considered in the differential diagnosis of a

Table 1 Checklist of possible seizure-related symptoms to enquire for when

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1.1 Principal diferential

cardiomyopathy is especially prone to present with episodes of sudden

throw self to ground.

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Complete loss in generalized tonic

violence not uncommon

clonic; may be incomplete in complexs seizure

Table 2 Differentiation of epileptic seizures and non-epileptic attack disorder (NEAD)

1.1.2 Generalised convulsive movements

distinguished from seizures induced by startle.

Non-epileptic attacks involving prominent motor phenomena are

1.1.3 Drop attacks

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1.1.4 Transient focal motor attacks

Paroxysmal movement disorders

distinguish from certain forms of epilepsia partialis continua. Myoclonus

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1.1.7 Psychic experiences

association with such experiences. Elemental visual phenomena, such as

Migrainous psychic phenomena may involve an initial heightening of

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1.1.8 Aggressive or vocal outbursts

parasomnias. With nocturnal seizures of any type the partner is frequently

awoken by particular components, such as vocalisation and does not