• Epileptic seizures – many causes, but all characterised by excessive neuronal activity, commonly followed by redcued activity
• Epilepsy is a sx, not a dis
• Common – 1/200 have epilepsy and taking anti-epileptic drugs, 1/50 lifetime incidence of at least 1 seizure
• Clinical manifestations of the seizure – depend on the spatial and temporal distbn of the excessive neuronal activity
• Sub-clinical bursts of abnormal neuronal activity also occur; detected by EEG as sharp waves or spikes (aka epileptiform activity)
• Clinical seizures – abrupt onset, self-limited, last usu <1-2 mins
• Prolonged or frequent seizures w/o full recovery betw attackes → status epilepticus
• Prolonged partial or generalised seizures may produce permanent cerebral damage
• Seizures freq occur for no apparent reason but may be triggered by hormonal factors such as menstrual cycle or stimuli such as fatigue, flashing lights or hyperventilation

Causes of Epilepsy

1. Intrinsic cerebral disturbance
a. Basic predisposition to seizures, often inherited, not assoc w demonstrable dis of brain → idiopathic epilepsy (generalised seizures)
b. Structural lesion (esp cortex) – trauma, tumors, infarct, infection, cortical dysgenesis, AV malformation, scar, hippocampal sclerosis
2. Systemic metabolic disturbance – hypoxia, hypocalcaemia, hypogly, hyponatremia, uraemia (RF), fever (children), drug use (phenothiazines, antidepressants) or withdrawal (ETOH, bnezos, barbiturates)

Idiopathic epilepsy – no underlying structural brain dis
Symptomatic epilepsy – underlying brain dis present
Cryptogenic epilepsy - presumed underlying brain dis

Differential Dx

• Syncope
• Pseudoseizures (psychogenic)
• TIAs (vertebrobasilar circ (impaired consciousness)
• ICA (sensory)

Clinical Features of Epilepsy

Classification of Seizures

1. Generalised seizures
a. Generalised convulsion (tonic/clonic, grand mal)
i. Initial stiffening (tonic phase; pt falls like a tree); up to 30s, assoc w respiratory arrest + cyanosis
ii. Limb jerking (clonic phase); may be tongue biting or urinary incontinence
iii. May be a post-ictal phase with brief coma, followed by confused state and sometimes headache
iv. May be followed by sleep
b. Absence seizure (petit mal)
i. Onset in childhood (3-10y age)
ii. Brief lapses of awareness, assoc w clonic mvments (esp eyelid flickering)
iii. No aura or post-ictal drowsiness
iv. May be precipitated by hyperventilation
v. Typical EEG abnormality – generalised 3-4Hz spike and wave abnormality
vi. 80% remit <30y
vii. 30-50% also have tonic-clonic seizures
c. Atonic seizure (epileptic drop attacks)
d. Tonic seizures (Ø clonic jerks)
e. Bilateral myoclonic jerks (not always epileptic, not always benign)
2. Partial seizures (focal seizures)
A. Simple partial seizures (consciousness retained) – tumors, AV malformation, strokes, abscesses
a. Focal motor seizures (twitching/jerkign)
i. Arise in motor cortex
ii. May be followed by temporary hemiparesis (todd’s paresis) – temporary metabolic exhaustion
iii. Types –
1. Localised (foot, head, mouth)
2. Jacksonian march
3. Versive (head turning)
4. Benign rolandic (see later)
5. May see focal motor status epilepticus (epilepsia partialis continua) with ongoing motor activity and no alteration in LOC
b. Focal sensory
i. Somatosensory (localised or Jacksonian march)
ii. Visual (uniformed spots or lights)
iii. Auditory (uniformed sounds)
c. Benign Rolandic Epilepsy
B. Complex partial seizures (pt loses awareness of their surroundings)
a. Temporal lobe seizures (see below)
b. Frontal lobe epilepsy
c. Parietal lobe epilepsy
d. Occipital lobe epilepsy

Epileptic Syndromes

1. Characterised by partial seizures (see above)
a. Temporal lobe epilepsy – simple partial or complex partial seizures characterised by
i. Develop from childhood onwards
ii. Aura (noticed by pt)
1. visceral (nausea, epigastric rising sensation)
2. hallucinations (olfactory, gustatory, auditory, formed visual)
3. psychosensory (dreamy state, déjà vu, jamais vu, fear, exhilaration)
4. if seizure stops here, no alteration of awarness → simple partial seizure)
iii. Benign with motionless stare (noticed by observer) → oro-alimentary (lip smacking, chewing) + motor (fumbling, picking at clothes, walking, undressing) automatisms common
iv. Dystonic posturing sometimes – if unilateral; seizure usu in contralateral hemisphere
v. Note – if pt unable to communicate or understand, seizure may arise in left (dominant) hemisphere; but if seizure arises in non-dominant temporal lobe, may still be able to communicate
vi. Usu marked post-ictal confusion
vii. May progress to generalised seizure
viii. Common causes – hippocampal sclerosis, tumors (gliomas, benign tumors), angiomas, infections, trauma
b. Frontal lobe epilepsy – 20-30% of partial seizures
i. Often v short, freq at night, often occurring in clusters
ii. Usu no aura, consciounsness preserved, no post-ictal confusion
iii. Often bizarre – prominent vocalisation, violent dramatic mvments
iv. Discharge spreads rapidly, often generalise, status epilepticus common
c. Benign rolandic epilepsy (Benign childhood epilepsy with centrotemporal spikes)
i. Primary partial epilepsy (idiopathic)
ii. Differs from both TLE and FLE as not assoc w underlying structural brain dis
iii. Develops at ~10y age
iv. Seizures occur at night
v. Typical feats – incl unilateral paraesthesia of tongue and face, clonic mvments of tongue and face, speech arrest and preservation of consciousness
vi. May progress to 2ndry generalisation
vii. Children otherwise normal; seizures stop at puberty; child may have only one seizure ever
viii. EEG – freq centrotemporal spikes (arise in centre and temporal parts of brain)
2. Characterised by generalised seizures (see above)
a. Idiopathic (primary) generalised epilepsy (centrencephalic epilepsy)
i. Combinations of absence, tonic/clonic and myoclonic seizures
ii. Onset in c/hood, early adult life (major genetic component)
iii. Pt otherwise normal, normal devt, normal neuroimaging
iv. Tonic-clonic seizure occur with idiopathic generalised epilepsy AND with a partial seizure that becomes generalised - do not assume a tonic-clonic seizure is due to generalised idiopathic epilepsy unless there is a convincing hx of myoclonic jerks or a characteristic 3-4 hz spike and wave pattern on EEG
b. Absence epilepsy
i. Onset usu 3-10y
ii. Characterised by recurrent absence seizures where the pt stares and is momentarily unresponsive, Øaura, Øconfusion
iii. 30-50% also have tonic-clonic seizures, 80% remit <30y
iv. Atypical absences – clinically similar but slower onset/recovery
1. Seen with underlying brain dis eg Lennox gastaut syndr
2. 1-2 Hz spike on EEG
3. Frequently sig intellectual impairment
c. Juvenile myoclonic epilepsy
i. Myoclonic = single isolated jerks
ii. Common (5% of all epileptics)
iii. Onset during teens, lifelong tendency to seizures (usu anti-epileptic therapy for life)
iv. Frequent myoclonic jerks esp in first hr after waking from sleep (helps clinch the dx)
v. Infrequent tonic-clonic seizures, often preceded by clusters of myoclonic jerks (esp in first few mins after waking)
vi. 30-40% have absence seizures as well (but not usu clinically apparent)
vii. Sxs aggravated by sleep deprivation and alcohol
3. Others
a. Symptomatic/Cryptogenic epilepsy – in diffuse/multifocal brain dis, often many seizures types (atonic-tonic, myoclonic jerks, atypical absences); these seizures may look like those seen in idiopathic generalised epilepsy or absence epilepsy, but they are due to underlying structural brain dis
b. Febrile seizures (.38.5’C) – 3% of children 6mo-5y; ↑ incidence if f.hx
i. Most are simple (brief, symmetrical tonic-clonic convulsion);
ii. ~20% are complex; duration >15mins, recurrent during single febrile episode, focal or lateralising feats
iii. ~5% develop epilepsy; ↑ risk if complex seizures
iv. Prognosis benign when short duration symmetrical tonic-clonic convulsions
v. Seizures that are asymmetrical or last >15 mins, prognosis more sinister
Most impt localising feat of an epileptic attack is the v first sx – often called the aura

Diagnosis of Epilepsy

1. EEG
• Spontaneous and evoked brain activity recorded from the scalp → key tool
• Dx – EEG provides the only interictal sign (sens ~50% but rate of detection ↑ w repeated studies), specificity 98% (ie 2% false positive rate);
• Classfication – useful in distinguishing absence from complex partial seizures
• Etiology – detection of assoc EEG abnormalilties may suggest cause of seizures (eg focal EEG changes suggest underlying structural lesion and indicate need for brain imaging)
• Limited role for detecting structural brain dis (CT/MRI better)

• Obtain when suspicion of focal onset epilepsy
• Identify structural lesion – eg hippocampal sclerosis, neuronal migration d/o etc
• Not reqd in a person you suspect has primary generalised epilepsy based on the clinical feats → obtain EEG instead
• If EEG shows evidence of a generalised epileptic syndr, brain imaging not reqd
• If EEG shows focal abnormalities, neuro imaging reqd
• MRI superior to CT
• CT may be used in emergency screening situation

Management of Epilepsy

1. General Principles
a. Safety – during seizures (move objects away, recovery position, no objects in their mouth)
b. Avoiding risky activities – eg scuba diving, mountain climbing, ?swimming, fires, bar heaters, microwave preferred, back elements on stove turn pot handles inward, always pour hot water away, don’t lock bathroom doors, shower>bath, ladders, scaffolding
c. Avoidance of precipitating factors eg sleep deprivation, alcohol
d. Education and support
2. Principles of Drug Therapy
a. Do not treat after just one seizure
b. Use correct drug for correct type of epilepsy
c. Start with 1 drug incr until pt seizure free or side effects intolerable; if unsuccessful change to another drug (overlap for 6 wks)
d. If 2 individual drugs fail – consider a combination; choose 1 for baseline and try various 2nd drugs (do not continue if no obvious benefit)
e. If this fails, be prepared to reconsider the dx (eg pseudoseizures)
f. Serum levels useful for checking compliance, unusual metabolism and suspecte toxicity; but therapeutic levels should only be used a guide
3. Pregnancy
a. Risks of uncontrolled tonic-clonic seizures greater than the risk of adverse effects
b. Teratogenicity – 2-6% risk, may be >10% on polytherapy; greatest on valproate where increased risk of spina bifida + cardiac and skeletal abnormalities
c. Folic acid before conception may reduce valproate-induced neural tube defects
d. Note – enzyme-inducing anti-epileptic drugs reduce efficacy of OCP
e. ?lamotrigine may be less teratogenic than valproate and may be considered 1st line therapy in women of childbearing potential
4. Driving
a. Must stop for 1 y unless seizure was due to unusual provocative factors unlikely to recur; may be reduced to 6 m on neurologist recommendation
b. Must stop for 6 months when drug therapy changed or reduced; if a seizure occurs, pt may drive 6 months after resuming prior therapy that worked
c. Any hx of epilepsy → permanent ban from passenger service vehicles, aambulances, vehicle recovery and heavy vehicles (only 1 yr if clearly provoked)
d. A doctor is obliged to inform a pt the LTSA rules and must inform LTSA if they suspect/knows the person continues to drive against advice
5. Prognosis
a. 40% of those seen in hosp w 1st seizure have recurrence <2y (most within 6 months)
b. 70% who have 2 seizures have a third seizure
c. ↑ risk w structural lesions or if there are epileptiform discharges on EEG

Status Epilepticus

Prolonged or freq seizures w/o consciousness betw attacks
1. Medical emergency – risk to life and permanent cerebreal damage
2. General – search for causes early on, maintain ABCs
3. IV anticonvulsants necessary, but only if pt is in true status (not recovered)
4. Use only one drug at a time

Anti-epileptic Drugs

Generalised seizures (tonic-clonic)
1. Valproate, carbamazepine or lamotrigine
2. Phenytoni or clobazam (2nd line)
3. Topiramate (3rd line)

Generalised seizures (absence seizures)
1. Sodium valproate or ethosuximde (children only)
2. Clobazam or clonazepam (2nd line)
3. Lamotrigine (3rd line)
4. NOT carbamazepine

Juvenile myoclonic epilepsy
1. Valproate
2. Clobazam or lamotrigine
3. Topiramate

Partial seizures (complex or simple)
1. Carbazamepine, Sodium valproate or Lamotrigine
2. Phenytoin or clobazam (2nd line)
3. Topiramate (3rd line)

Carbamazepine (Tegretol)
• Indications – tonic-clonic seizures, partial (simple or complex) seizures
• Ineffective for absence seizures and juvenile myoclonic epilepsy
• Dosage – start slowly (eg 100 mg nocte), ↑ dose by 100 mg every few days; give bd, usual therapeutic dose 600-1600 mg/day
• Adverse effects – rash, sedation, other cogv s.effs, hyponatremi, cardiac conduction defects, neutropenia (usu benign), liver dis
• Toxic doses → ataxia, deplopia, nystagmus
• Interactions – induces metabolism of other drugs including oral or injected contraceptives and warfarin

Sodium Valproate (Epilim)
• Broad spectrum of activity
• Dosage – usual maintenance dose in adults 800-3000 mg/day taken in 2 doses; start with 200-400 mg bd; gradually ↑ dose according to clinical response; can be induced faster than carbazamepine
• Adverse effects – nausea, weight gain, hair loss, hand tremor, LF, thrombocytopenia, pancreatitis
• Teratogenicity – neural tube defects (spina bifida); ↓ risk by taking folic acid
• Interactions – inhibits metabolism of lamotrigine

Phenytoin (Dilantin)
• Indications – tonic-clonic seizures, partial seizures, ineffective against absence seizures
• Dose – usual maintenance dose 300mg/day as single dose, metabolism is saturable so marked changes in bld levels can be produced by sml changes in dose; loading dose (either 1000mg PO or 18mg/kg IV); alternatively can be started at usual maintenance dose but therapeutic levels may not be achieved for 2-3wks
• Adv effects – cosmetic (hirsuitism, coarsening of facial feats), sedation and cogv s.effs, peripheral neuropathy, cerebellar ataxia after chr use, osteomalacia
• Toxic dose – can cause ataxia and nystagmus

Lamotrigine (Lamictal)
• Broad spectrum of activity and better tolerated than older epileptic drugs
• Indications- tonic-clinic, absence and partial seizures
• Dose – start low dose (12.5 mg/day); ↑ dose gradually every wk to achieve maintenance dose 100-400 mg/day
• Interactions – metabolism inhibited by valproate, lamotrigine dose must be lowered if these drugs used together, also interacts w carbazamepine
• Adv effects – skin rash soon after tx begins, usu well tolerated

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