epilepsy and seizure disorders
TRANSCRIPT
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EPILEPSY AND SEIZURE DISORDERS
PRESENTERS: LUYIMBAZI IVAN
NANSUBUGA CAROL
2Introduction-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.
3Seizure 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
4Etiology
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
5CLASSIFICATION
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
6FOCAL 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
7FOCAL SEIZURES…….b) Focal seizures with cognitive impairment
Typically frontal or temporal lobe onsetOften stereotyped for the individual patientAverage duration 1-3 minutesOnset can be followed by impaired
consciousnessMany times will progress to a generalized
seizureFrequently seen in adult onset epilepsy Automatisms: coordinated involuntary
movements, typically orobuccolingual or non-purposeful hand movements
8Generalised 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
9Generalised Seizures
Atypical Absence SeizureLonger duration of loss of consciousness,
Less abrupt onset and cessation
More obvious focal signsLess responsive to drugs
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Generalised Tonic Clonic Seizures
Main seizure in 10% of people with epilepsy
Commonly results from metabolic derangements
Usually abrupt onset, no auras, Tonic phaseClonic phasePost-ictal phasePost-ictal confusion can last hours-
days especially in alcoholics
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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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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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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 entryHyperpolarizing of GABA.
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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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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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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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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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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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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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Investigations
II. Confirmation of epilepsy:Dynamic investigations :
result changes with attacksE.g. EEG
Static investigations : result same between and during attacksE.g. Brain scan
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Electroencephalography (EEG)
Uses of EEG in epilepsyDiagnostic: support diagnosis, classify seizure, localize focus, quantify
Prognostic: adjust anti-epileptic treatment
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EEGNormal EEG doesn’t rule out
epilepsyAlways abnormal in a GTCUse of video EEG telemetry to
detect seizure activity on 24hrsInterictal EEG maybe normal 60%
of times in known epilepticsCan classsify seizure disorders.MRI recommended to r/o
structural lesions.
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Neuroimaging
Structural neuroimaging
Functional neuroimaging
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Structural Neuroimaging
Who should have a structural neuroimaging?Status epilepticus Develop seizures when > 20
years oldFocal epilepsy (unless typical of
benign focal epilepsy syndrome)
Refractory epilepsyEvidence of neurocutaneous
syndrome
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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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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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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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Treatment of epilepsy
Emergency treatment and long term seizure control
Rx underlying conditionAvoid precipitating factors; alcohol,
lack of sleep, lightsPrevent recurrence with drugsAddress psychological and social
issues
Note; advised to continue AEDs for 1yr after removal of structural lesion
29Anticonvulsants
CabamazepinePhenytoin
Valproic acid
Tonic-clonic and focal
EthosuximideValproic acidClonazepam
Absence seizures
Valproic acidClonazepam
Myoclonic seizures
DiazepamLorazepam
Short term control
PhenytoinPhenobarbital
Prolonged therapy
Status Epilepticus
Drugs used in seizure disorders
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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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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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Status Epilepticus
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Algorithm of patient with Seizures