1. EPILEPSY AND
SEIZURE
DISORDERS
PRESENTERS: LUYIMBAZI IVAN
NANSUBUGA CAROL
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2. Introduction-Seizures
 Seizures- paroxysmal events due to
abnormal excessive or hypersynchronous
neuronal activity in the brain cortex.
 The clinical characteristics of a seizure are
the result of the area of the brain that is
abnormally stimulated
 5-10% of the population will have at least
one seizure in their lifetime
 Highest incidence is in childhood and late
adulthood.
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3. Seizure terms
 Ictal= seizure
 Post-ictal= confusion following seizure
 Aura= abnormal sensation preceding loc
 Automatisms= nonsensical involuntary
movements
 Tonic=contraction producing extension
and arching
 Clonic= alternating muscle contraction-
relaxation
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4. Etiology
 CNS
 Head trauma
 Seizure in 1 week of
injury not predictive
of epilepsy
 Stroke
 Mass (tumor/abscess)
 Meningitis/encephalitis
 Congenital
malformations/ cortical
dysplasias
 Idiopathic
 Systemic
 Hypo/hyperglycemia
 Hypo/hypernatremia
 Hypocalcemia
 Uremia
 Hepatic encephalopathy
 Hypoxia
 Hyperthermia
 Drug overdose or
withdrawal
 EtOH withdrawal sz
occurs within 48h
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5. CLASSIFICATION
Focal seizures originate
within network limited to
one cerebral
hemisphere
Generalized seizures- arise
within and rapidly
engage networks across
both cerebral
hemispheres, result from
biochemical or structural
abnormalities
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6. FOCAL SEIZURES
a) Focal seizures without cognitive impairment
 Motor symptoms Involves motor strip,
Manifested by abnormal movement of an
extremity,
 Somatosensory symptoms Involves sensory
strip, temporal(hearing and smell) or
occipital(visual) lobe
 Autonomic symptoms involves temporal
lobe (tachycardia, pallor, flushing,
sweating)
 Psychic symptoms Involve frontal or
temporal lobe (limbic system): affective
disturbances, cognitive deficits,
hallucinations
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7. FOCAL SEIZURES…….
b) Focal seizures with cognitive impairment
Typically frontal or temporal lobe onset
Often stereotyped for the individual patient
Average duration 1-3 minutes
Onset can be followed by impaired
consciousness
Many times will progress to a generalized
seizure
Frequently seen in adult onset epilepsy
Automatisms: coordinated involuntary
movements, typically orobuccolingual or
non-purposeful hand movements
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8. Generalised Seizures
Typical Absence seizure
 Characterized by brief sudden loss of
consciousness without loss of postural control
 Lasts secs, consciousness returns suddenly,
No post ictal confusion
 Genetically determined, onset at 4-8yrs,
 Main seizure type in 15-20% of children with
epilepsy.
 Can occur hundreds of times in a day but
child unaware, 1st clues;- day dreaming,
decline in school performance
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9. Generalised Seizures
Atypical Absence Seizure
Longer duration of loss of
consciousness,
Less abrupt onset and
cessation
More obvious focal signs
Less responsive to drugs
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10. Generalised Tonic Clonic Seizures
 Main seizure in 10% of people with
epilepsy
 Commonly results from metabolic
derangements
 Usually abrupt onset, no auras,
 Tonic phase
 Clonic phase
 Post-ictal phase
 Post-ictal confusion can last hours-days
especially in alcoholics
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11. Generalised Seizures
Atonic seizures
 Sudden losses of postural muscle tone, lasts
1-2 secs,
 Consciousness briefly impaired, No post ictal
confusion.
Myoclonic Seizure
 Sudden brief muscle contraction involving
one part or entire body
 A normal physiological form- Is sudden jerk
while falling asleep.
 Caused by cortical dysfunction.
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12. Classification
 Pseudoseizures
 Non-epileptic seizures
 May be manifestation of conversion disorder,
factitious disorder or malingering
 Features that may distinguish from epileptic seizures
 Pre-attack preparation, absence of post-ictal
confusion
 “Disorganized” movements, pelvic thrusting,
thrashing
 Bilateral convulsions without loss of
consciousness
 Violent or goal-directed behavior, obscene
language,
 Video EEG may help to diagnose
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13. Seizure Mechanisms
 Involves 2 phases-initiation and
propagation
 Initiation involves 2 concurrent events-
high frequency bursts of Action
potential, hypersynchronisation
 Ca2+ influx depolarising neuronal mem
 Opening of Na+ channels, Na entry
 Hyperpolarizing of GABA.
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14. Mechanisms of Anti Epileptic Drugs
 Antiepileptic drugs appear to act primarily by blocking the initiation or spread of
seizures. The mechanisms include;
 inhibition of Na+-dependent action potentials (e.g., phenytoin, carbamazepine,
lamotrigine, topiramate, zonisamide),
 inhibition of voltage-gated Ca2+ channels (phenytoin, gabapentin, pregabalin)
 attenuation of glutamate activity (lamotrigine, topiramate, felbamate)
 potentiation of GABA receptor function (benzodiazepines and barbiturates)
 increase in the availability of GABA (valproic acid, gabapentin, tiagabine)
 modulation of release of synaptic vesicles (levetiracetam).
 act by inhibiting T-type Ca2+ channels in thalamic neurons.( valproic -absence
seizures)
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15. Epilepsy
 Epilepsy- Is a clinical condition in which they are recurrent(2 or
more) un provoked seizures.
 Provoked seizures
 Seizures induced by somatic disorders originating outside the
brain
 E.g. fever, infection, syncope, head trauma, hypoxia, toxins, cardiac
arrhythmias
 Status epilepticus
 Continuous convulsion lasting longer than 30
minutes OR occurrence of serial convulsions
between which there is no return of
consciousness
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16. Mechanism of
epileptogenesis
Refers to transformation of a normal
neuronal network into one that is
chronically hyperexcitable.
CNS injuries (trauma,stroke,infections)
initiate a process that gradually lowers
the seizure threshold in the affected
region.
It can also be mediated by
developmentally regulated events(in
genetic & idiopathic epilepsy)
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17. Epilepsy in Uganda
 Epilepsy is the most common neurological condition
 Prevalence is 2-5 persons/100 people
 High predominance in areas endemic with onchocerciasis(15-
20 cases/1000 people) in Kabalore and Nebbi districts
 Etiology is birth trauma, accidents and untreated malaria.
 60 % of mental illness is a result of epilepsy; poorly managed
disease
Study done by Epilepsy support Association of
Uganda
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18. Diagnosis in epilepsy
 Aims:
 Differentiate between events mimicking epileptic
seizures
 E.g. syncope, vertigo, migraine, psychogenic non-
epileptic seizures (PNES)
 Confirm the diagnosis of seizure (or possibly
associated syndrome) and the underlying etiology
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19. Investigations
 I. Exclusion of differentials:
 urinalysis
 Hematological: CBC
 Biochemical: U&Es, Calcium, glucose,
ABGs
 Radiological: CXR, CT head
 Toxicological: screen
 Microbiological: Lumbar Puncture
(Always used with justification)
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20. Investigations
II. Confirmation of epilepsy:
Dynamic investigations :
result changes with attacks
E.g. EEG
Static investigations : result
same between and during
attacks
E.g. Brain scan
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21. Electroencephalography
(EEG)
Uses of EEG in epilepsy
Diagnostic: support
diagnosis, classify seizure,
localize focus, quantify
Prognostic: adjust anti-
epileptic treatment
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22. EEG
Normal EEG doesn’t rule out
epilepsy
Always abnormal in a GTC
Use of video EEG telemetry to
detect seizure activity on 24hrs
Interictal EEG maybe normal 60%
of times in known epileptics
Can classsify seizure disorders.
MRI recommended to r/o structural
lesions.
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23. Neuroimaging
Structural neuroimaging
Functional neuroimaging
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24. Structural Neuroimaging
 Who should have a structural
neuroimaging?
Status epilepticus
Develop seizures when > 20 years
old
Focal epilepsy (unless typical of
benign focal epilepsy syndrome)
Refractory epilepsy
Evidence of neurocutaneous
syndrome
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25. Structural Neuroimaging
 Modalities available:
 Magnetic Resonance Imaging (MRI)
 Computerized Tomography (CT)
 What sort of structural scan?
 MRI better than CT
 CT usually adequate if to exclude large tumor
 MRI not involve ionizing radiation
I.e. not affect fetus in pregnant
women (but nevertheless
avoided if possible)
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26. Functional Neuroimaging
 Principles in diagnosis of epilepsy:
When a region of brain
generates seizure, its regional
blood flow, metabolic rate and
glucose utilization increase.
After seizure, there is a decline to
below the level of other brain
regions throughout the inter-ictal
period.
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27. Functional Neuroimaging
 Modalities available:
 Positron Emission Tomography (PET)
 Single Photon Emission Computerized
Tomography (SPECT)
 Functional Magnetic Resonance
Imaging (fMRI)
 Mostly used in:
 Planning epilepsy surgery
 Identifying epileptogenic region
 Localizing brain function
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28. Treatment of epilepsy
 Emergency treatment and long term
seizure control
 Rx underlying condition
 Avoid precipitating factors; alcohol,
lack of sleep, lights
 Prevent recurrence with drugs
 Address psychological and social issues
Note; advised to continue AEDs for 1yr
after removal of structural lesion
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29. Anticonvulsants
Cabamazepine
Phenytoin
Valproic acid
Tonic-clonic and focal
Ethosuximide
Valproic acid
Clonazepam
Absence seizures
Valproic acid
Clonazepam
Myoclonic seizures
Diazepam
Lorazepam
Short term
control
Phenytoin
Phenobarbital
Prolonged
therapy
Status Epilepticus
Drugs used in seizure disorders
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31. Epilepsy - Treatment
The treatment target is seizure-
freedom and improvement in
quality of life!
Basic rules for drug treatment:
Drug treatment should be simple,
preferably using one
anticonvulsant (monotherapy).
“Start low, increase slow“.
 Add-on therapy is necessary in
some patients.
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32. Treatment withdrawal
 If patient is seizure-free for three years,
withdrawal of pharmacotherapy should
be considered.
 Withdrawal should be carried out only if
patient is satisfied that a further attack
would not ruin employment etc. (e.g.
driving license).
 It should be performed very carefully and
slowly! 20% of pts will suffer a further sz
within 2 yrs.
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33. Status Epilepticus
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34. Algorithm of patient with Seizures
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