Classification of Seizures
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Classification of Seizures. Why do we need to classify seizures?. Different seizures affect different parts of the brain Different antiepileptic drugs are more effective with different seizures. Classification of Seizures. Partial Seizures - Simple partial - Complex partial

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Why do we need to classify seizures
Why do we need to classify seizures?

  • Different seizures affect different parts of the brain

  • Different antiepileptic drugs are more effective with different seizures

Classification of seizures
Classification of Seizures

  • Partial Seizures

    - Simple partial

    - Complex partial

    - Partial Seizures with Secondary Generalization

  • Generalised Seizures

    - Absence Seizures (Petit Mal)

    - Atypical Absence Seizures

    - Generalized, Tonic-Clonic Seizures (Grand Mal)

    - Atonic Seizures

    - Myoclonic Seizures

  • Unclassified

Partial seizures
Partial Seizures

  • occur within discrete regions of the brain

  • less than 2 minutes

  • If consciousness is fully preserved,

    the seizure is a simple partial seizure

  • If consciousness is impaired,

    the seizure is a complex partial seizure

Partial seizures1
Partial Seizures

Simple Partial

  • cause motor, sensory or autonomic changes

  • precursors to complex partial seizure or tonic-clonic seizure

  • no alteration in consciousness

  • last a few seconds

  • changes in sensory sensation

    - déjà vu, flashbacks

    - somatic sensation (paresthesias)

    - vision (flashing lights or formed hallucinations)

    - equilibrium (sensation of falling or vertigo)

    - autonomic function (flushing, sweating, piloerection)

Partial seizures2
Partial Seizures

Complex Partial

  • One of the most common types of seizures

  • focal seizure activity + transient impairment of the patient's ability to maintain normal contact with the environment

  • frequently begins with aura (simple partial seizure)

  • unable to respond appropriately to visual or verbal commands during the seizure

  • Lasts 2-3 minutes

  • The behavioral arrest is usually accompanied by automatisms

  • post-ictal confusion ranges from seconds up to an hour

Partial seizures3
Partial Seizures

Partial Seizures with Secondary Generalization

  • partial seizures that spread involving both cerebral hemispheres leading to a generalized seizure

  • often difficult to distinguish from a primarily generalized tonic-clonic seizure

Generalized seizures
Generalized Seizures

  • arise from both cerebral hemispheres simultaneously

Generalized seizures1
Generalized Seizures

Absence Seizures (Petit Mal)

  • sudden, brief lapses of consciousness without loss of postural control

  • lasts for only seconds (<10s)

  • no aura

  • no postictal confusion

  • usually accompanied by subtle, bilateral motor signs such as rapid blinking of the eyelids

  • begins in childhood (ages 4 to 8) or early adolescence

Generalized seizures2
Generalized Seizures

Atypical Absence Seizures

  • have features that deviate from both the clinical and EEG features of typical absence seizures

  • usually is of longer duration (>10s)

  • less abrupt in onset and cessation

  • accompanied by more obvious motor signs (tonic, clonic or automatisms)

  • usually associated with diffuse or multifocal structural abnormalities of the brain

Generalized seizures3
Generalized Seizures

Generalized, Tonic-Clonic Seizures (Grand Mal)

  • the main seizure type in approximately 10% of all persons with epilepsy

  • most common seizure type due to metabolic derangements

  • with or without aura

    Tonic phase

  • tonic contraction of muscles

    throughout the body

  • loud moan or cry

  • lasts 10 to 20 s

    Clonic phase

  • superimposition of periods of muscle

    relaxation on the tonic muscle contraction

  • Respirations are impaired, secretions pool

    in the oral cavity, and the patient becomes


Generalized seizures4
Generalized Seizures

Generalized, Tonic-Clonic Seizures (Grand Mal)

  • Contraction of the jaw muscles

  • increased heart rate, BP, and pupillary size

  • Lasts 1-2 minutes

    Postictal phase

  • characterized by unresponsiveness, muscular flaccidity, and excessive salivation that can cause stridorous breathing and partial airway obstruction.

  • Bladder or bowel incontinence may occur

  • Last over minutes to hours

Generalized seizures5
Generalized Seizures

Atonic Seizures

  • sudden loss of muscle tone lasting 1 to 2 s

  • Consciousness is briefly impaired

  • usually no postictal confusion

  • A very brief seizure may cause only a quick head drop or nodding movement, while a longer seizure will cause the patient to collapse

    Myoclonic Seizures

  • sudden and brief muscle contraction that may involve one part of the body or the entire body

  • lasts 1 to 2 s.

  • A normal, common physiologic form of myoclonus is the sudden jerking movement observed just when you are falling asleep (hypnic jerk)

Epilepsy syndromes


Three important syndromes:

  • Juvenile Myoclonic Epilepsy

  • Lennox-Gastaut Syndrome

  • Mesial Temporal Lobe Epilepsy Syndrome

Juvenile myoclonic epilepsy
Juvenile Myoclonic Epilepsy

  • Generalised seizure disorder

  • Unknown cause

  • Appears in early adolescence

2 lennox gastaut syndrome
2. Lennox- Gastaut Syndrome seizures

  • Triad

    • multiple seizure types (generalised tonic-clonic, atonic & atypical absence seizures)

    • an EEG showing slow (<3 Hz) spike-and-wave discharges and a variety of other abnormalities

    • impaired cognitive function

  • CNS disease or dysfunction as a result of: seizures

    • developmental abnormalities

    • perinatal hypoxia/ ischemia

    • trauma

    • infection

  • Nonspecific response of the brain to diffuse neural injury

  • Poor prognosis (due to the underlying CNS disease and the physical and psychological consequences of severe, poorly controlled epilepsy)

3 mesial temporal lobe epilepsy syndrome
3. Mesial Temporal Lobe Epilepsy Syndrome seizures

  • Complex partial seizures

  • Responds well to surgical intervention, refractory to anticonvulsants

  • Distinctive clinical, EEG and pathological features

  • History seizures

    • febrile seizure

    • family history of epilepsy

    • early onset

  • Clinical observation

    • aura

    • behavioral arrest

    • complex automatism

    • unilateral posturing

    • postical disorientation, memory loss, dysphasia

  • Laboratory studies

    • EEG, PET & SPECT changes

    • MRI findings- hippocampal sclerosis

  • Three factors
    Three factors within the CNS

    • Endogenous factors

      • a.k.a. predisposing factors

      • Influence the threshold for having a seizure

      • Presence of differences between individuals in the susceptibility for seizures

      • Examples include:

        • Genetic factors

        • Degree of development

    Three factors cont d
    Three factors (cont’d) within the CNS

    • Epileptogenic factors

      • Conditions that have an extremely high likelihood in resulting in a seizure

      • Initiate epileptogenesis

      • Examples include:

        • Severe penetrating head trauma

        • Stroke

        • Infections

    Three factors cont d1
    Three Factors (cont’d) within the CNS

    • Precipitating factors

      • Speaks for itself

      • Examples include:

        • Intrinsic physiological processes

          • Psychological or physical stress

          • Sleep deprivation

          • Hormonal changes assoc with the menstrual cycle

        • Extrinsic processes

          • Toxic substances

          • Medications

    Three factors summary
    Three Factors (summary) within the CNS

    • Three factors interplay to emphasize the concept behind the many causes of seizures and epilepsy

    • Role in treatment

      • Predisposing  close f/up & aggressive diagnostic evaluation

      • Epileptogenic  estimation of recurrence & duration of therapy

      • Precipitating  removal > drug treatment

    Causes according to age
    Causes According to Age within the CNS

    • In clinical practice, classifying by age is important as it determines:

      • Incidence of seizures or epilepsy

      • Likely aetiologies of seizures or epilepsy

    Neonatal early infancy
    Neonatal & Early Infancy within the CNS

    • Hypoxic-ischemic encephalopathy

    • Trauma

    • CNS infection

    • Congenital CNS abnormalities

    • Metabolic disorders

    • Born to mothers using neurotoxic drugs

    • Hypoglycaemia

    • Hypcalcemia

    • Inborn errors of metabolism

    • Idiopathic/Inherited forms of benign neonatal convulsions

    Late infancy early childhood
    Late Infancy & Early Childhood within the CNS

    • Febrile seizures

      • Peak incidence between 18 to 24 months

      • Generalized tonic-clonic seizure during a febrile illness

      • Usually during first day of illness

      • Two types:

        • Simple

        • Complex

    Late childhood
    Late Childhood within the CNS

    • Well-defined epilepsy syndromes

    • Temporal lobe epilepsy

    • Developmental disorders

    • Head trauma

    • CNS infection

    • CNS tumour

    Adolescence early adulthood
    Adolescence & Early Adulthood within the CNS

    • Head trauma

    • CNS infections

    • Brain tumours

    • Congenital CNS abnormalities

    • Illicit drug use

    • Alcohol withdrawal

    Older adults
    Older Adults within the CNS

    • Cerebrovascular disease

    • Trauma

    • CNS tumours

    • Degenerative diseases

    Non age dependant
    Non-age Dependant within the CNS

    • Metabolic disturbances

      • Electrolyte imbalance

      • Renal failure

      • Hepatic failure

    • Endocrine disorders

    • Hematologic disorders

    • Vasculitides

    • Medications & Abused substances

    Partial seizures4
    Partial Seizures within the CNS

    Begins from a discrete region of the cortex which slowly spread to the neighbouring regions.

    Divided into two phases:

    • Seizure initiation phase

    • Seizure propagation phase

    Seizure initiation phase
    Seizure initiation phase within the CNS

    Consists of 2 concurrent events occurring in an aggregate of neurons:

    • High frequency bursts of potentials

      relatively long-lasting depolarization of neuronal membrane, initially initiated by the influx of Ca2+ from the ECF which later cause the opening of voltage-dependent Na+ channels and Na+ influx. This results in generation of repetitive AP. Depending on cell type, either GABA or K+ channels will cause hyperpolarization.

    • Hypersynchronization

      Synchronized burst from sufficient number of neurons will produce spike discharges seen on the ECG.

    Seizure propagating phase
    Seizure propagating phase within the CNS

    Spread of bursting activity normally prevented by 2 mechanism:

    • Intact hyperpolarization

    • inhibitory neurones Region of inhibitory surrounding

      When sufficient neurons are recruited loss of surrounding inhibition propagation of seizure activity into:

    • Contiguous areas thru local cortical connections

    • More distant areas thru long commisural pathways e.g. corpus callosum

    Neuronal excitability
    Neuronal Excitability within the CNS

    Can be affected by various factors:

    • Intrinsic to neuron

      Conductance of ion channels, response characteristics of membrane receptors, cytoplasmic buffering, 2nd messenger systems and protein expression

    • Extrinsic to neuron

      Amount or type of neurotransmitters present at synapse, modulation of receptors by ECF ions and temporal and spatial properties of synaptic and non-synaptic input

    • Non-neuronal cells

      Astrocytes, oligodendrocytes

    Some explainable situations causing seizures
    Some explainable situations causing seizures within the CNS

    • Domoic acid ingestion

      Analogue of glutamate ( main excitatory NT in brain)

    • Penicillin

      Antagonizes the effects of GABA at its recpetors reducing seizure threshold seizures!

    Other precipitating factors of seizures not well understood
    Other precipitating factors of seizures- not well understood within the CNS

    • Sleep deprivation

    • Alcohol withdrawal

    • Fever

    • Hypoxia

    • Infection

    Epileptogenesis within the CNS

    Transformation of normal neuronal network into one which is chronically hyperexcitable.

    Takes months to years between CNS injury and first seizure.

    Pathologic studies of hippocampus of patients with TLE shows that:

    • due to changes in neuronal network loss of neurons contributing to inhibition of neurons

    • Remaining neurons sprout in a way that increases the network excitability

    Initial injury (very focal region) within the CNS

    • local hyperexcitability

    • structural changes over time

    • seizures

    Genetic causes of epilepsy
    Genetic causes of epilepsy within the CNS

    Recent identification of genetic mutations associated with variety of epilepsy syndromes important conceptual advances.

    Found that many inherited idiopathic epilepsies are due to channelopathies (mutations affecting the ion channel fx.)

    Current challenge is to identify multiple susceptibility genes that underlie the more common forms of idiopathic epilepsies.

    Mechanism of action of antiepileptic drugs
    Mechanism Of Action of Antiepileptic drugs within the CNS

    Generally blocks the initiation and spread of seizures.


    • Inhibition of Na+ dependent AP in a frequency dependent manner

    • Inhibition of voltage gated Ca2+ channels

    • Decrease in glutamate release

    • Potentiation of GABA receptor function

    • Increasing the availability of GABA

    • Inhibition of T-type Ca2+ channels in thalamic neurons

      There are no ‘ anti-epileptogenic’ drugs available which helps prevent emergence of seizure formation following injuries

    Adult case 1

    Adult Case 1 within the CNS

    Personal details

    • Patient Initials: NS

    • Registration Number: HPD 31667

    • Age: 39 years old

    • Race: Indian

    • Gender: Female

    • Occupation: Caterer

    • Date of Admission: 26th April 2009

    • Date of Clerking: 28th April 2009

    Chief complaint
    CHIEF COMPLAINT within the CNS

    Presented with 3 episodes of seizures 1 day before admission.

    History of presenting illness

    3 epsiodes of seizure 1 day before admission

    2 hr interval between episodes

    Each episode lasts 20 seconds

    No aura or premonition before the attacks

    1st episode was while daughter was massaging

    • During the seizure: within the CNS

    • Loss of consciousness

    • Muscles tense and body becomes stiff

    • Followed by jerky movements of arms and legs

    • Patient bit her lips but not her tongue

    • Eyes roll upwards

    • No frothing, drooling of saliva or urinary incontinence

    • Temporary amnesia

    • After seizures she has: within the CNS

    • Headache

    • Fatigue

    • Body ache

    • Vomiting

    • Fever

    • Drowsiness

    • Regains memory a few hours after attacks

    • She would fall asleep for 2 to 3 hrs after each attack

    First seizure 17 y.o. within the CNS

    Married at the age of 16 y.o.

    1st episode before the birth of her first child.

    Previously 1 / year

    Lately more frequent

    Usually > 1 fit per episode

    She had 3 episodes of seizures in 2008.

    On anti-epileptic drugs (?) from onset within the CNS

    She took them regularly

    Stopped 4 years ago as the doctor was worried about side effects

    Frequency of attacks have increased

    Weight loss from 86kg to 63kg in past 4 years

    Currently complains of loss of sleep and loss of appetite

    Newly diagnosed diabetic. Diagnosed on admission within the CNS

    Glucose level = 9.5 mmol/L

    Also a pre-hypertensive

    Has leg swelling and slow healing leg ulcers since 3 yrs ago.

    Family history
    FAMILY HISTORY within the CNS

    Father – Deceased. Had Type 2 DM and cardiovascular disease.

    Mother – Deceased. Intestinal cancer.

    Grandmother – 89 years old. Asthmatic

    Father and uncle had epilepsy.

    Married and has 4 children. All are healthy. None has epilepsy.

    Social and personal history

    Works as a caterer.

    Works hard and for long hours.

    Believes work-related stress and tiredness may be the precipitating factor for her seizure attacks.

    Physical examination
    Physical Examination within the CNS

    General : Patient was conscious, alert and communicative. She was lying supine on bed. She was in no obvious, respiratory distress, no obvious pain, no gadgets attached

    Hands: No clubbing, no peripheral cyanosis, no delayed capillary refill, no koilonychia, no leukonychia, no splinter haemorrhages, no Janeway nodes or Osler’s lesions, no thenar and hypothenar muscle wasting

    Vital signs:

    Temperature- 37degrees,

    Blood pressure- 125/80 mmHg,

    Heart rate- 72 beats permin

    Respiratory rate- 15 breaths permin

    Physical examination1
    Physical Examination within the CNS

    Arms: No scratch matchs, no purpura, no ecchymosis, no bruises,no muscle wasting

    Eyes: No jaundice, no pallor, no xanthelasma, no corneal archus

    Mouth: Good oral hygiene, no leukoplakia, no angular stomatitis, no central cyanosis, Lips swollen due to biting during seizure episode.

    Neck: No obvious swelling, no sinus discharge, JVP- 3cm, normal

    Physical examination2
    Physical Examination within the CNS

    Cardiovascular: Size and shape of chest is normal. No scars, no visible pulsation.

    Upon palpation, apex beat cannot be located, no parasternal or apex heave, no palpable thrills.

    Upon auscultation: Heart sounds rapid. Normal S1S2 sounds were heard, no murmurs, no additional sounds

    Respiratory: No tracheal deviation, equal chest expansion on both sides, equal vibration on both sides, equal resonance on both sides, normal vesicular breath sounds heard, no bronchial or additional breath sounds,

    Physical examination3
    Physical Examination within the CNS

    Gastrointestinal: Not remarkable

    Musculoskeletal: No obvious muscle wasting.Restricted movement of the right leg due to pain. Left leg normal.

    Lower limbs:

    Inspection: Not remarkable

    Palpation: Not remarkable

    Physical examination4
    Physical Examination within the CNS

    • CNS:

    • All Cranial Nerves are intact

    • Upper limbs and lower limbs:

    • Tone- no hyper or hypotonia

    • Power -5/5

      - All reflexes are normal

    • No ankle or knee clonus

    • No Babinski reflex

    • No sensory loss- sensory examinations normal

    Provisional diagnosis

    Epileptic seizure secondary to hyperglycaemia

    Differential diagnosis
    Differential diagnosis within the CNS

    • Idiopathic

    • Metabolic- hyper or hyponatrimia, hyper or hypocalcaemia

      -Alcoholic or benzodiazepine withdrawal

      -Psychoactive drugs (e.g., hallucinogens, cocaine)


    Full Blood Count

    Renal profile
    Renal Profile within the CNS

    Liver function tests
    Liver Function Tests within the CNS

    Investigations within the CNS

    Plasma Calcium levels (2.61 mmol/l)

    High plasma glucose level. (24.6 mmol/l)

    Fasting glucose level was 9.5 mmol/l

    Has high cholesterol level (6.49 mmol/l)

    High LDL levels (5.0 mmol/L)

    Liver function tests and her renal function tests were normal

    Plan of management

    IV diazepam

    Her random blood glucose was monitored

    she is put on a diabetic diet.

    Adult case 2

    ADULT CASE 2 within the CNS

    Personal details1

    Patient Initials: TS

    Registration Number: HTJ 403161

    Sex: Male

    Age: 30 years old

    Date of admission: 22nd April

    Date of Clerking: 22nd April

    Chief complaint1
    CHIEF COMPLAINT within the CNS

    Admitted to hospital for an episode of generalized tonic-clonic seizures

    History of presenting illness1

    Admitted to hospital at 3.15 am for generalized tonic-clonic seizures. Seizures lasted for 2 minutes.

    Jerking of upper and lower limbs and drooling of saliva during attack.

    No urinary or fecal incontinence

    Patient was sleeping during attack.

    Seizures believed to have been brought upon by stress and headache.

    Had headache the previous evening

    First attack since February of 2008. within the CNS

    h/o of MVA in 1997

    First episode shortly after MVA

    Diagnosed with epilepsy by doctor in Sungai Buloh.

    h/o of multiple admission for seizures.

    >2 episodes per year

    Previously on meds (white pill with white line???). Stopped 2 years ago.

    No fever. within the CNS

    SOB x 2/7

    Cough- productive yellowish sputum

    Sore throat

    No nausea/vomiting

    Past medical history

    MVA in 1997

    Admitted to Sungai Buloh hospital and then transferred to GHKL

    Coma for 3 weeks

    No fractures. No neurosurgery done

    Spent a further 2 weeks in the wards

    Had first seizure attack shortly after discharge

    Between 1997 and 2007, pt had around 15 seizures

    Stopped meds 2yrs ago

    Allergic to med (pink coloured tablet???) – develop rashes within the CNS

    No known allergy to food

    Family history1
    FAMILY HISTORY within the CNS


    4th of 8 siblings.

    No hx of epilepsy

    No family hx of DM, HPT, asthma.

    Mother: Deceased, cancer

    Father: Deceased. Was an alcoholic

    Younger brother: Deceased due to dengue

    Social history
    SOCIAL HISTORY within the CNS

    Works in a motor workshop

    Smokes around 20 sticks of cigarette per day but has reduced to 10 per day. Smoking since 19 years old.

    Social alcohol drinker. Stopped drinking 3 years ago.

    Physical examination5

    BP: 107/71 mmHg

    Pulse rate: 61 beats/min

    T: 37⁰C

    Cranial Nerve examination: All normal

    No loss of limb sensations

    No upper limb weakness.

    Lower limb weakness due to Phenytoin

    On/off cramps of both legs

    No diplopia. within the CNS

    No nystagmus

    Gait: Normal

    Babinski reflex: Negative

    Funduscopy: Normal

    Lungs: Clear within the CNS

    CVS: S1/S2 heard. No additional heart sounds.

    P/A: Soft, non-tender, not distended

    Provisional diagnosis1
    Provisional diagnosis within the CNS

    • Epilepsy secondary to head injury sustained in an MVA

    Differential diagnosis1
    Differential Diagnosis within the CNS

    • Structural brain damage due to MVA

    • Tumours

    • Metabolic disorders

    • Hyper/ hyponatremia

    • Hypo/hyperglycaemia


    Full Blood Count

    Renal profile1
    Renal Profile within the CNS

    Liver function tests1
    Liver Function Tests within the CNS

    Plasma Fasting Blood Sugar – 4.5 mmol/L within the CNS

    Sputum FEME

    - pM cell < 25

    - pM organisms (gram +ve cocci +++)

    pM organisms (gram –ve bacilli +)

    Coagulation Profile: within the CNS

    - Prothrombin time : 13.0s

    - INR : 1.08 (low) [2.0 – 2.5]

    - aPTT : 34.7 s

    Thyroid Function Test

    - Plasma free T4 : 17.5 pmol/L

    - Plasma TSH : 0.92 mU/L

    Vitamin B12 – 307 pmol/L

    EEG done in seven years ago after the first episode. within the CNS

    No abnormalities found.

    Paediatric case

    Paediatric Case within the CNS

    Personal details2

    Patient’s Initials: SD

    Age: 1 year old

    Registration Number: HTJ 401311

    Date of Admission: 16th April 2009

    Date of Clerking: 17th April 2009

    Chief complaint2
    CHIEF COMPLAINT within the CNS

    Present with fever, rhinitis and convulsions on the day of admission

    History of presenting illness collateral history from grandmother
    HISTORY OF PRESENTING ILLNESS within the CNS(collateral history from grandmother)

    Fever and rhinitis in the morning on the day of admission.

    Relieved by anti-pyretic syrup

    Convulsions in the evening.

    Lasted only 5 minutes

    First episode

    Jerky movements of arms and legs. within the CNS

    Rolling up of eyeballs

    Drooling of saliva

    No fecal or urinary incontinence

    No poor feeding, vomiting, irritability, lethargy, drowsiness, loss of consciousness

    No nausea/vomiting within the CNS

    No diarrhoea

    No photophobia

    No cough

    No sore throat

    Temperature – 38.5⁰C



    Past medical history1

    No hospitalization / surgery

    No previous episode of epilepsy

    Birth history
    BIRTH HISTORY within the CNS

    BW 2.9kg, full term baby.

    Spontaneous vaginal delivery

    No complications

    Follows immunisation programme

    Last immunisation was for OPV, HiB, DPT, Hepatitis B. Due for MMR vaccination this year.

    Current milestone development
    Current milestone development: within the CNS

    • She is able to:

    • Imitates what others are doing

    • Jabbers and make sounds that are like words

    • Takes a few steps

    • Understands simple sentences and instructions and responds to them

    Family history2
    FAMILY HISTORY within the CNS

    • Cousin had febrile convulsions when he was 5 years old

    • No family history of epilepsy

    Physical examination6

    Vital signs:

    -Temperature: 38⁰C

    -Pulse 163/min

    -BP: 95/75

    Physical findings

    -No significant systemic findings

    -No tonsilitis/pharyngitis

    Differential diagnosis2
    Differential diagnosis within the CNS

    • Meningitis/ encephalitis –poor feeding, vomiting, irritability,lethrgy, drowsiness, loss of consciousness, photophobia

      Brudzinski’s sign-flexion of the neck with the child supine causes flexion of the knees and hips

      Kernig’s sign-with the child lying supine and with the hips and knees flexed, there is back pain on extension of the knee

    • Cerebral malaria

    • tumour



    Renal profile2
    Renal Profile within the CNS

    DIAGNOSIS within the CNS

    Febrile convulsions secondary to upper respiratory tract infection.


    Treatment within the CNS

    First aid
    First aid within the CNS

    Generalized Tonic Clonic

    Don’t do anything!

    Remove any objects around the area that might hurt the patient

    Administer diazepam if available within the CNS

    Call ambulance if seizure is more than 5 minutes, multiple episode within a short time and if the patient is hurt

    Recovery Position

    Epilepsy within the CNS


    No Seizures, No Side Effects

    • Drug choice depend on type of seizure within the CNS

    • Introduce drug and gradually increase dosage

      • Till either no more seizure or presence of side effects

    • Second drug can be added – first drug gradually withdrawn

    • Treatment with two drugs possible

      • Often leads to toxicity

    • Monitoring within the CNS

      • Serum levels of drugs

      • should be measured after treatment is initiated, dosage is changed, or another drug is added to the therapeutic regimen and when seizures are poorly controlled

    Discontinuation of therapy within the CNS

    Should be considered only if seizure free more than 3 years

    Slowly tapered down

    If recur, resume previous drug dosages

    Patient education
    Patient Education within the CNS

    Most patients can achieve complete control of seizures.

    Most people lead a normal

    Side Effects of drug therapy

    Discourage risky activities

    Avoid precipitating factors eg. Alcohol, fatigue etc

    • Driving within the CNS

      • Seizure free for 2 years with medical review every 5 years

    • Sports

      • scuba diving, hang-gliding, parachuting, rock climbing, car racing and swimming alone

    • Employment

      • heavy machinery, dangerous surroundings, heights or deep water

    Febrile convulsion
    Febrile Convulsion within the CNS

    Control fever

    First aid measures

    Rectal diazepam

    History taking

    History Taking within the CNS

    Presenting complaint

    Racing heart within the CNS

    Tingling sensations


    Generalised stiffening


    Ringing noises


    Sudden loss of vision

    Presenting Complaint

    • Sudden fall

    • Jerking limbs

    • Blank stare

    • Urinary incontinence

    • Funny smell

    • Feeling of fear

    • Facial flushing

    • Seeing coloured spots

    • vomiting

    History of present illness
    History of Present illness within the CNS

    • Description of seizure (generalized/ focal)‏

    • Pre-ictal symptoms (alterations of mood, memory, perception, complex hallucination, visceral sensation)‏

    • Post-ictal activity (confused, disorientated, drowsy, headache, retrograde amnesia)‏

    • Duration & frequency

    • Fever?

    • Evidence of progressive intracranial lesions(headache, vomiting, focal neurological symptoms, behavioral changes)

    Precipitating factors
    Precipitating Factors? within the CNS

    • Sleep deprivation

    • alcohol(withdrawal)

    • Recreational drugs

    • Physical & mental exhaustion

    • Flashing light

    • Intercurrent infections & metabolic disturbances

    • Uncommonly: loud noise, music, reading, hot baths

    Risk factors
    Risk Factors? within the CNS

    • Early childhood problems (developmental delay, head injury, CNS infection)‏

    • FH of seizure & cerebral palsy

    • Medical disorders

    Fits in children
    Fits in children within the CNS

    Investigation of suspected epilepsy
    Investigation of suspected epilepsy within the CNS

    • Epileptic nature of attacks?

    • Ambulatory EEG / videotelemetry

    • Type of epilepsy?

    • Standard EEG / sleep EEG

    • Structural lesion?

    • CT / MRI

    • Metabolic disorder?

    • BUSE, LFT, RP, blood glucose, serum calcium & magnesium

    Cont. within the CNS

    • Inflammatory or infective disorder?

    • FBC, ESR, CRP

    • Chest X-ray

    • Serology test for syphilis, HIV, collagen disease

    • CSF examination

    • Indications for brain imaging in epilepsy

    • Epilepsy starts after aged 20

    • Seizures have focal features clinically

    • EEG shows a focal seizure source

    • Control of seizures is difficult or deteriorates

    EEG within the CNS

    Psychosocial aspects of epilepsy

    Children teenagers


    • School phobia – prejudice

      • - overprotective

  • inform school

  • All teachers need to be knowledgeable

  • Discrimination

  • Do not restrict activities, just caution with climbing and swimming.

  • difficulties in learning - lack of concentration,

    • - memory problems

  • behaviour problems - by the epilepsy itself,

  • - changes of medications,

  • - over-protection (spoiling),

  • - or poor acceptance

  • Plan ahead for management

  • DRIVING within the CNS

    • should not drive.

    • in U.S.; crash rate among people with epilepsy lower than crash rate of teenage male drivers.

    • In Malaysia, must be seizure-free for at least 2 years

      • If seizures are not in control, then advice not to drive.

      • Make sure that patients are honest to you about their seizures.


    EMPLOYMENT within the CNS

    • discrimination – fear, ignorance, cant work

    • should tell at least 2 colleagues

    • jobs that are not suitable:-

      • Pilots

      • Jobs where you have to handle firearms

      • Driving heavy machinery

      • Politicians, Fire brigade, Ambulance attendant/driver, Baby Sitter

      • Certain sports e.g. professional boxing, race car driver.


    • discuss feeling openly with one another.

    • Support – from spouse, children, relatives, friends

    • interpersonal relationship;

      • natural to worry of rejection

      • help partners understand condition

    • they have normal sexual feelings and normal sex lives.

      • Family planning

      • anticonvulsants impair full effectiveness of OCPs

      • Increased risks of problems during pregnancy due to seizures and medications


    • should be more careful about the safety of children;

      • Feed or diaper the baby on low surface

      • Use a wrist 'leash' or harness when you walk with a toddler.

      • Explain to children about epilepsy

      • Some parents may think that it is their fault- counselors.

    OTHERS within the CNS

    • Depression – common co-morbidity

    • Anxiety and panic disorders

    • Avoidance behaviours – may occur because of concern about embarrassing behaviours during seizures.

    • Other disturbances like sleep disorders, suicidal ideation, and mania must be carefully evaluated

    • Psychotic symptoms may occur ictally (confusion, hallucinations, delusions), and are more frequently associated with partial status epilepticus or absence status.

    Quiz on epilepsy

    QUIZ ON EPILEPSY within the CNS

    These are characterized by the site of the abnormal activity, e.g. pure sensory, motor, or psychic phenomena. But are associated with an impairment of consciousness

    Complex partial seizures

    These begin with features of simple or complex seizures, which then become generalized with tonic-clonic episodes. The initial partial element may be so shortlived that it may be only evident on the EEG.

    Secondary generalized seizures

    Usual onset in childhood. Characterized by loss of consciousness but maintained posture (stops talking an stares into space for seconds), blinking or rolling up of eyes with other repetitive motor actions. No post-ictal phase.

    Absence seizures

    Adolescence onset. Involuntary jerking, particularly in the morning. They are associated with impairment of consciousness.

    Myoclonic seizures

    These are characterized by the site of the abnormal activity, e.g. pure sensory, motor, or psychic phenomena. They are not associated with impairment of consciousness.

    Simple partial seizures

    Vague symptoms before an attack (e.g dizziness, irritability), loss of consciousness. Tonic phase characterized by repetitive jerks, faecal or urinary incontinence, tongue biting. After a seizure, there is often impaired consciousness, lethargy, confusion, headache, back pain and stiffness.

    Tonic-clonic (grand mal) seizures

    A 20 y.o female student presents in the neurology outpatient department with a three-month history of ‘funny turns’ lasting 2-3 minutes. Each is preceded by an ‘odd sensation’, and is followed by a feeling of ‘vacancy’. She has no recollection of these events, but has been told about them by her friends, who say she becomes vacant and unresponsive, with grinding of her teeth and contortion of her face.

    What is the likely cause of her turns
    What is the likely cause of her ‘turns’? outpatient department with a three-month history of ‘funny turns’ lasting 2-3 minutes. Each is preceded by an ‘odd sensation’, and is followed by a feeling of ‘vacancy’. She has no recollection of these events, but has been told about them by her friends, who say she becomes vacant and unresponsive, with grinding of her teeth and contortion of her face.

    Epilepsy- absence seizure

    List the investigations you would perform
    List the investigations you would perform. outpatient department with a three-month history of ‘funny turns’ lasting 2-3 minutes. Each is preceded by an ‘odd sensation’, and is followed by a feeling of ‘vacancy’. She has no recollection of these events, but has been told about them by her friends, who say she becomes vacant and unresponsive, with grinding of her teeth and contortion of her face.

    RP, LFT, glucose level

    Blood level of Calcium, Phosphate, Magnesium


    Serum & urine alcohol and toxin screens

    Blood levels of medication

    Imaging: CT brain

    Lumbar puncture (if CT shows no increased ICP)