Due to sudden repeated spontaneous discharges of groups of CNS neurons



Symptoms depend on CNS area undergoing seizure

Unknown cause (about 50% of cases)



CNS trauma



Tumor



Metabolic/Toxic states (Hypoxia (stroke), Hyperpyrexia, Encephalitis, etc)



Drug-induced (eg. Lithium, Bupropion, Chlorpromazine, Alcohol withdrawal, etc)

Motor activity

Distortions of perceptions (all 5 senses except touch) and memory (deja vu phenomenon).

Behaviour (violence, brief disruptions of conciousness)

Generalized seizures:

Proportions and involvement

Loss of Consciousness



Motor involvement

Motor involvement of generalised seizures:

Tonic activity: Increase in muscle tone.

Clonic activity: Rhythmic muscle contractions.

Atonic activity: Loss of muscle tone

Generalized tonic-clonic movements of the limbs



Tongue biting



Incontinence

Partial seizures:

proportion and involvement:

60% of seizures.

Involve focal cortical areas and so produce a more restricted cluster of symptoms.

May involve motor disturbances and alterations of perceptions or behaviour



Simple partial seizures do not involve loss of consciousness



Complex partial seizures are associated with impairment of consciousness

1. Antiseizure therapy.

2. Classical anticonvulsants.

3. Benzodiazepines.

4. New anticonvulsants.

1. Phenytoin.

2. Valproic acid. (Valproate, Divalproex).

3. Carbamezepine.

Oxcarbazepine (recently introduced Carbamazepine metabolite)

Clonazepam



Diazepam



All benzodiazepines have anticonvulsant activity

New Anticonvulsants

Gabapentin



Topiramate



Lamotrigine

Increase the Inhibitory input to the neuron to suppress firing (Increase GABA action)

 Block electrical activity of the nerve to slow the nerve impulses

 Block Glutamate receptors so wave of excitation cannot spread

Benzodiazepines

Valproate

Phenobarbital

Gabapentin ?

Which drugs Block Na

+ Channel 

electrical activity

Carbamazepine

Phenytoin

Valproate

Lamotrigine

Which drug Block Glutamate

receptors?

Generally the same across all anticonvulsants. 

Dose related and usually transient.

Divided doses.

Administration with meals. 

Start low, go slow. 

maximize effect and reduce toxicity

 Serum levels are especially important for Phenytoin

 Phenytoin levels are not proportional to dose

Sedation, Tremor, Ataxia

 Cognitive and vision impairment

Elevated hepatic enzymes – Generally asymptomatic

 Periodic monitoring of liver function

Valproate and Carbamazepine frequently associated with a transient leukopenia 

 Generally reverses with time or dosage reduction. 

 Aplastic anemia in rare cases 

 Periodic hematology monitoring

Weight gain

 Common with Valproate 

 25% of patients on long-term therapy gain up to 20 kg

Benign skin rashes in 5 – 20% of patients

 Severe and potentially fatal skin hypersensitivity reactions are not uncommon

 Stevens-Johnson syndrome – Mortality rate 5 – 10%

 Toxic Epidermal Necrolysis – Mortality rate 45% 

 Presence of anticonvulsant-induced rash should prompt drug discontinuation

Most anticonvulsants induce the enzymes responsible for metabolizing drugs 

 Increases metabolism of concurrently administered drugs

 Can lead to loss of concurrent drug’s therapeutic effect unless appropriate dosage 

adjustment

Symptoms are an extension of the normal adverse effect profile

 Treatment includes removal of any unabsorbed medication from the 

stomach (gastric lavage or emesis) followed by supportive therapy

Valproate, Carbamazepine, Phenytoin and possibly other anticonvulsants

Pregnancy and breast-feeding

Neural tube defects 

 Folate supplementation initiated before pregnancy for all anticonvulsants

 50% of all pregnancies are unplanned

 Folate supplementation for all women of child-bearing age

 Transient vitamin K deficiency

 Neonatal clotting disorders 

 Supplementation with vitamin K

Phenytoin causes a fetal hydantoin syndrome

 Similar to fetal alcohol syndrome

 Avoid phenytoin in women of child-bearing age if possible