Up todate info on epilepsy classification Signs and Symptoms and management Included are also EEG findings

1. 1
BY ORIBA DAN LANGOYA, MBCHB V
& KUSEMERERWA MABLE, MBCHB V
Supervisor: Dr. Kaddu Mark

2. 2
Outline
• Definition
• Etiology
• Classification
• Differential Diagnosis
• Treatment of Epilepsy

3. 3
Definition of Seizures
• Is a paroxysmal event due to abnormal excessive or
synchronous neuronal activity in the brain.
• Seizures are usually unpredictable
• Seizures usually brief ( < 5 minutes) and stop
spontaneously
• Convulsion, ictus, event, spell, attack and fit are used
to refer to seizures.
• Epilepsy is the tendency to have recurrent seizures.

4. Epilepsy
• Epilepsy describes a condition in which a person has
recurrent seizures due to a chronic, underlying process.
• This implies that a person with a single seizure, or recurrent
seizures due to correctable or avoidable circumstances, does
not necessarily have epilepsy.
• Using the def of epilepsy as 2 or more unprovoked seizures,
the incid of epilepsy is ~0.3–0.5% in diff popn throughout,
and the prev of epilepsy has been estimated at 5–30 persons
per 1000.
• Nonepileptic seizures (NES) are sudden changes in behavior
that resemble epileptic seizures but are not associated with
the typical neurophysiological changes that characterize
epileptic seizure

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Etiology of Seizures
• Seizures are either provoked or unprovoked
• Provoked Seizures: Triggered by certain provoking factors in
otherwise healthy brain
• Metabolic abnormalities (hypoglycemia and hyperglycemia,
hyponatremia, hypocalcemia, Hypomagnesium, Non ketotic
hyperglycemia, Uremia, Hypoxia, Hyperthyroidism, Dialysis
disequilibrium syndrome, Porphyria, hypocalcaemia)
• Alcohol withdrawal
• Acute neurological insult (infection, stroke, trauma)
• Illicit drug intoxication and withdrawal
• Prescribed medications that lower seizure threshold
(theophylline, TCA)
• High fever in children
• Unprovoked Seizures: Occur in the setting of persistent brain
pathology

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Etiology of Epilepsy
• Any process that alters the structure (macroscopic or
microscopic) or the function of the brain neurons can
cause epilepsy
• Processes that lead to structural alteration include;
• Congenital malformation
• Degenerative disease
• Infectious disease
• Trauma
• Tumors
• Vascular process
• Inborn errors of metabolism
• In majority of patients, the etiology is proposed but not
found
• In elderly , vascular, degenerative and neoplastic causes
are more common compared to younger adults.

8. CLASSIFICATION OF SEIZURES
The International League against Epilepsy
(ILAE) Commission on Classification and
Terminology, 2005–2009

9. General Principles
• A fundamental principle is that seizures may be
either focal or generalized.
• Focal seizures originate within networks limited to
one cerebral hemisphere.
• Generalized seizures arise within and rapidly
engage networks distributed across both cerebral
hemispheres.
• Focal seizures are usually associated with structural
abnormalities of the brain.
• In contrast, generalized seizures may result from
cellular, biochemical, or structural abnormalities
that have a more widespread distribution.

10. FOCAL SEIZURES
• Arise from a neuronal network either discretely localized
within one cerebral hemisphere or more broadly distributed
but still within the hemisphere.
• They can be described as focal seizures with or without
dyscognitive features.
• Focal seizures can also evolve into generalized seizures.
• Focal Seizures Without Dyscognitive Features
• FS can cause motor, sensory, autonomic, or psychic symptoms
without impairment of cognition.
• Three additional features of focal motor seizures are worth noting.
Ie,
• phenomenon, described by Hughlings Jackson and known as a
“Jacksonian march,
• localized paresis (Todd’s paralysis),
• Epilepsia partialis continua

11. Focal Seizures Without Dyscognitive
Features
• Focal seizures may also manifest as changes in
• somatic sensation (e.g., paresthesias),
• Vision (flashing lights or formed hallucinations),
• Equilibrium (sensation of falling or vertigo)
• Autonomic function (flushing, sweating, piloerection)
• Temporal or frontal cortex may also cause alterations in
hearing, olfaction, or higher cortical function (psychic
symptoms)
• This includes the sensation of unusual, intense odors
(e.g., burning rubber or kerosene) or sounds (crude or
highly complex sounds), or an epigastric sensation that
rises from the stomach or chest to the head

12. An EEG shows the first 10 seconds of FS discharge, with 5-Hz rhythmic theta
activity in channels recorded in the right temporal scalp

13. Focal Seizures with Dyscognitive Features
• May also be accompanied by a transient impairment of the
patient’s ability to maintain normal contact with the
environment.
• Inability to respond appropriately to visual or verbal
commands during the seizure and has impaired recollection or
awareness of the ictal phase
• Seizures frequently begin with an aura (i.e., a focal seizure
without cognitive disturbance)
• The start of the ictal phase is often a sudden behavioural &
marks the onset of the period of impaired awareness.
• The behavioral arrest is usually accompanied by automatisms,
which are involuntary, automatic behaviors that have a wide
range of manifestations.
• Eg. chewing, lip smacking, swallowing, or “picking” movements of
the hands

14. Interictal EEG in localization-related epilepsy.

15. • Patient is typically confused following seizure, &
transition to full recovery of consciousness may
range from seconds up to an hour.
• Exams immediately following the seizure may show
an anterograde amnesia or, in cases involving the
dominant hemisphere, a postictal aphasia.
• The range of potential clinical behaviors linked to
focal seizures is so broad
• Detailed EEG is required.

16. EVOLUTION OF FOCAL SEIZURES TO
GENERALIZED SEIZURES
• FS can spread to involve both cerebral hemispheres and
produce a GS, usually of the tonic-clonic.
• Observed frequently following FS arising from a focus
in the frontal lobe
• Often difficult to distinguish from a primary
generalized-onset tonic-clonic seizure.
• The focal onset is not clinically evident and may be
established only through careful EEG analysis.
• Distinguishing btn these 2 entities is extremely
important,
• Because there may be substantial differences in the evaluation
and treatment of epilepsies associated with focal versus
generalized seizures

17. GENERALIZED SEIZURES
• GS are thought to arise at some point in the brain
but immediately and rapidly engage neuronal
networks in both cerebral hemispheres
• Several types of GS have features that place them
in distinctive categories and facilitate clinical
diagnosis.
Typical Absence Seizures
Atypical Absence Seizures
Generalized, Tonic-Clonic Seizures
Atonic Seizures
Myoclonic Seizures

18. Typical Absence Seizures
• TAS are xterized by sudden, brief lapses of
consciousness without loss of postural control.
• Typically lasts for only seconds, consciousness returns
as suddenly as it was lost, and there is no postictal
confusion.
• Absence seizures are usually accompanied by subtle,
bilateral motor signs such as rapid blinking of the
eyelids, chewing movements, or small-amplitude,
Clonic movements of the hands
• TAS are associated with a group of genetically
determined epilepsies with onset usually in childhood
(ages 4–8 years)
• or early adolescence and are the main seizure type in
15–20% of children with epilepsy.

19. TAS Cont.
• The seizures can occur hundreds of times per day, but the child
may be unaware of or unable to convey their existence.
• Often subtle, pay attention to often unexplained “daydreaming”
and a decline in school performance recognized by a teacher
• The EEG hallmark of typical absence seizures is a generalized,
symmetric, 3-Hz spike-and-wave discharge that begins and ends
suddenly, superimposed on a normal EEG background.
• Periods of spike-and-wave discharges lasting more than a few
seconds usually correlate with clinical signs.
• Hyperventilation tends to provoke these electrographic discharges
and even the seizures themselves

20. Absence seizure. The 3-Hz spike and wave pattern of absence epilepsy

21. Atypical Absence Seizures
• Deviate both clinically & electrophysiologically from
typical absence seizures.
• Eg.
1. The lapse of consciousness is usually of longer duration
and less abrupt in onset and cessation,
2. The seizure is accompanied by more obvious motor signs
that may include focal or lateralizing features
3. The EEG shows a generalized, slow spike-and wave
pattern with a frequency of ≤2.5 per second, as well as
other abnormal activity.
4. Usually associated with diffuse or multifocal structural
abnormalities of the brain
5. The seizures are less responsive to anticonvulsants

22. Generalized, Tonic-Clonic Seizures
o Generalized-onset tonic-clonic seizures are the main seizure type
in ~10% of all persons with epilepsy.
o They are also the most common seizure type resulting from
metabolic derangements
o The seizure usually begins abruptly without warning.
o The initial phase of the seizure is usually tonic contraction of
muscles throughout the body.
o Tonic contraction of the muscles of expiration
o and the larynx at the onset will produce a loud moan or “ictal cry.”
o Respirations are impaired, secretions pool in the oropharynx, and
cyanosis develops.
o Contraction of the jaw muscles may cause biting of the tongue.

23. Generalized, Tonic-Clonic Seizures
• Enhancement of sympathetic tone leads to increases in HR, BP,
and pupillary size.
• After 10–20 s, the tonic phase of the seizure typically evolves
into the clonic phase.
• Produced by the superimposition of periods of muscle
relaxation on the tonic muscle contraction.
• The periods of relaxation progressively increase until
• The end of the ictal phase, which usually lasts no more than 1
min
• The postictal phase is characterized by unresponsiveness,
muscular flaccidity
• Patients gradually regain consciousness over minutes to hours.

24. Generalized, Tonic-Clonic Seizures
• Patients subsequently complain of headache, fatigue, &
muscle ache.
• The EEG during the tonic phase of the seizure shows a
progressive increase in generalized low-voltage fast activity,
followed by generalized high-amplitude, polyspike
discharges.
• In the clonic phase, the high-amplitude activity is typically
interrupted by slow waves to create a spike-and-wave pattern.
• The postictal EEG shows diffuse slowing that gradually
recovers as the patient awakens
• There are a number of variants, pure tonic & Pure clonic
seizure
• Usually associated with specific epileptic syndromes having
mixed seizure phenotypes, such as the Lennox-Gastaut
syndrome (discussed below).

25. Atonic Seizures
• Characterized by sudden loss of postural muscle tone
lasting 1–2 s.
• Consciousness is briefly impaired, but there is usually
no postictal confusion.
• A very brief seizure may cause only a quick head drop
or nodding movement, whereas a longer seizure will
cause the patient to collapse.
• The EEG shows brief, generalized spike-and-wave
discharges followed immediately by diffuse slow waves
that correlate with the loss of muscle tone.
• Similar to pure tonic seizures, atonic seizures are
usually seen in association with known epilepsy
syndromes.

26. Myoclonic Seizures
• Sudden and brief muscle contraction that may involve
one part of the body or the entire body.
• Physiological form is the sudden jerking movement
observed while falling asleep
• Pathologic myoclonus is most commonly seen in
association with metabolic disorders, degenerative CNS
diseases, or anoxic brain injury.
• Myoclonic seizures are considered to be true epileptic
events because they are caused by cortical (versus
subcortical or spinal) dysfunction.
• The EEG may show bilaterally synchronous spike-and-
wave discharges synchronized with the myoclonus
• Myoclonic seizures usually coexist with other forms of
generalized seizures but are the predominant feature of
juvenile myoclonic epilepsy

27. CURRENTLY UNCLASSIFIABLE SEIZURES
• Not all seizure types can be designated as focal or
generalized
• Epileptic spasms are such an example.
• These are xterized by a briefly sustained flexion or extension of
predominantly proximal muscles, including truncal muscles.
• EEG in these usually shows hypsarrhythmias, which
consist:
• Of diffuse, giant slow waves with a chaotic background of
irregular, multifocal spikes and sharp waves.
• Epileptic spasms occur predominantly in infants and
likely result from differences in neuronal function
and connectivity in the immature versus mature
CNS

28. EPILEPSY SYNDROMES
• Are disorders in which epilepsy is a predominant feature,
and
• There is sufficient evidence (e.g., through clinical, EEG,
Radiologic, or genetic observations) to suggest a common
underlying mechanism.
1. JUVENILE MYOCLONIC EPILEPSY
• Is a generalized seizure disorder of unknown cause that
appears in early adolescence.
• Usually xterized by bilateral myoclonic jerks that may be
single or repetitive.
• Seizures are most frequent in the morning after awakening and can
be provoked by sleep deprivation.
• Consciousness is preserved
• Many patients also experience GTCS, and up to one-third have
absence seizures.
• Respond well to appropriate anticonvulsant medication. There is
often a family history of epilepsy, and genetic linkage

29. LENNOX-GASTAUT SYNDROME
• Occurs in children and is defined by the following
triad:
1. Multiple seizure types (including GTCS, atonic, and
atypical absence seizures);
2. An EEG showing slow (<3 Hz) spike-and-wave
discharges & a variety of other abnormalities;
3. Impaired cognitive function in most but not all cases.
• LGS is assoc with CNS disease or dysfunction from a
variety of causes, including de-novo mutations
• Developmental abnormalities, perinatal hypoxia/ischemia,
trauma, infection, and other acquired lesions.
• The multifactorial nature of this syndrome, nonspecific
response of the brain to diffuse neural injury.
• Poor prognosis due to the underlying CNS disease

30. MESIAL TEMPORAL LOBE EPILEPSY
SYNDROME
o MTLE is the most common syndrome associated with focal
seizures with dyscognitive features.
o An epilepsy syndrome with distinctive clinical,
electroencephalographic, and pathologic features
o High resolution MRI can detect the xteristic hippocampal
sclerosis that appears to be essential in the pathophysiology
of MTLE
o Recognition of this syndrome is esp important because it
tends to be refractory to tx with anticonvulsants but responds
well to surgical intervention.

31. DIAGNOSIS
Laboratory screening – the following are necessary in
evaluation of a first seizure
Serum electrolytes, glucose, magnesium, calcium, CBC, RFTs,
LFTs, TFTs and toxicology screen
Prolactin – prolactin concentration rises shortly generalized
tonic clonic seizures. Sample is drawn 10 to 20 minutes after the
event and compared with the baseline drawn atleast six hours
before.
Lumbar puncture – Incase of suspected infectious process or
metastatic cancer. It may be misleading since prolonged seizures
may result in pleocytosis.
Electroencephalogram
Neuroimaging- MRI and CT scan.
50% of patients regardless of age have normal neuroimaging
studies.

33. MANAGEMENT
Goals for treatment
• Controlling seizures,
• Avoiding treatment side effects
• Maintaining or restoring quality of life
The optimal treatment plan is derived following ,
• Accurate diagnosis of the patient's seizure type(s)
• Objective measure of the intensity and frequency of the seizures
• Awareness of medication side effects,
• Evaluation of disease-related psychosocial problems
Antiepileptic drugs (AEDs)
Patients should have knowledge about available AEDs including
their mechanisms of action, pharmacokinetics, drug-drug
interactions, and adverse effects.

34. Differential Dx of seizures

35. Management cont’d
Treatment depends on the type/class of seizures e.g. partial
or generalized seizures
When to start AEDs
• Immediate antiepileptic drug (AED) therapy is usually not
necessary in individuals after a single seizure, particularly if a
first seizure is provoked by factors that resolve.
• AED therapy should be started in patients who are at
significant risk for recurrent seizures, such as those with
remote symptomatic seizures.
• AED treatment is generally started after two or more
unprovoked seizures, because the recurrence proves that the
patient has a substantially increased risk for repeated seizures,
well above 50 percent.
• AED therapy is not necessarily life-long.

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Treatment of Established Epilepsy
1) First Line
Approved Anti-Epileptic Drugs (AEDs)
2) Second Line (intractable epilepsy)
Epilepsy Surgery
Vagus Nerve Stimulation Therapy
Experimental Therapy
oAEDs
oImplanted Devices

37. Selection of AED

38. STATUS EPILEPTICUS
• Series of seizures occur without the patient
regaining awareness between attacks over a period
of 30 min.
• Mostly it refers to recurrent tonic clonic seizures
(major status).
• It’s a life-threatening medical emergency.
• Partial motor status is clinically obvious.
• It’s precipitated by abrupt withdrawal of
anticonvulsant drugs, the presence of a major
structural lesion or acute metabolic disturbance.

39. ETIOLOGY
Some of the more common predisposing factors include:
• Antiepileptic drug noncompliance or discontinuation
• Withdrawal syndromes
• Acute structural injury (e.g. , brain tumor or cerebral metastasis,
stroke, head trauma, subarachnoid Remote or longstanding
structural injury
• Metabolic abnormalities
• Chronic epilepsy; status epilepticus may represent part of a
patient's underlying epileptic syndrome
• Mortality rates for adults with first episode is about 20%.
Mortality rate for patients with cerebral anoxia is about 69 to
81%.
• Mortality is due to metabolic stress of repeated convulsions

41. The End
DAN & MABLE,
MBchB V