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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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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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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