1

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

10

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

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.

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

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 entryHyperpolarizing of GABA.

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)

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

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)

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

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

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)

20

Investigations

II. Confirmation of epilepsy:Dynamic investigations :

result changes with attacksE.g. EEG

Static investigations : result same between and during attacksE.g. Brain scan

21

Electroencephalography (EEG)

Uses of EEG in epilepsyDiagnostic: support diagnosis, classify seizure, localize focus, quantify

Prognostic: adjust anti-epileptic treatment

22

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.

23

Neuroimaging

Structural neuroimaging

Functional neuroimaging

24

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

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)

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.

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

28

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

30

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.

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.

33

Status Epilepticus

34

Algorithm of patient with Seizures