Summary
Summary Seizures and epilepsy
- Module
- Year 3 Semester 2 (MPHARM)
- Institution
- The University Of Manchester (UOM)
summary of anticonvulsants in therapy for epilepsy and seizures
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Seizures+EpilepsyCauses of seizures
1. Imbalance between excitatory and inhibitory postsynaptic potential
Excitatory: glutamate
Inhibitory: GABA
More excitatory postsynaptic potential causes seizures
2. Alterations in ion channel function
Mutations in genes encoding ion channels
Particularly Na+ and K+ channels
Changes in ion function affects the spread of electrical signals
Increased Na+ and Ca2+ causes seizures
3. Paroxysmal depolarization
Sudden shift in the electrical charge across a neuron’s membrane
Towards a more positive state
Increasing the chance of depolarization
Threshold is easier to reach
Causing increased action potentials and electrical activity
How do we treat seizures?
Anticonvulsants: antiseizure medication
4 types of anticonvulsants
Na+ channel inhibitors (category 1 e.g., valproate, phenytoin and carbamazepine)
Ca2+ channel inhibitors (e.g., gabapentin and pregabalin)
Enhanced GABA mediated inhibition (valproate, BZDs, levetiracetam)
Glutamate receptor inhibitors (e.g., lamotrigine)
MOA Na+ channel inhibitors
Blocks voltage gated sodium ion channels
Prevents depolarization of the neuron
Reducing the chance of an action potential forming
Reducing the likelihood of abnormal electrical activity associated with seizures
Stabilising them in the inactive state.
During a seizure there can be an increased influx of sodium ions.
MOA of Ca2+ channel inhibitors
During a seizure there can be an excessive influx of calcium ions into the neuron
Causing an increased release of neurotransmitter across the synapse
Causing increased firing of action potentials at the postsynaptic neuron
Blocking calcium ion channels, you reduce the entry of calcium ions into the neuron
Helps modulate the neurotransmitter release and stabilise neuronal membranes
MOA GABA enhanced mediated inhibitors work?
GABA is the major inhibitory neurotransmitter in the brain.
It binds to GABA-A receptors on neurons
Leading to an influx of chloride ions and hyperpolarization of the neuron.
Hyperpolarization inhibits neurons from firing.
Modulating the imbalance of inhibitory and excitatory potentials
, MOA glutamate receptor inhibitors?
act on the glutamatergic system in the brain
glutamate is the primary excitatory neurotransmitter in the CNS
It acts by blocking NMDA receptors
o these are inotropic glutamate receptors
o So by inhibiting these you reduce excessive excitatory neurotransmission.
o This channel is blocked by magnesium ions.
They can also modulate AMPA receptors whicha re another glutamate receptor.
o Depending on the specific drug they can enhance or inhibit AMPA receptor
function.
ANKI TO UPLOAD:
What is sudep?
sudden unexpected death in epilepsy
unknown cause but likely complication from epilepsy
How do we diagnose epilepsy?
- establish paroxysmal event was actually a seizure and not something else
- epilepsy is spontaneous and recurrent
- good history and a witness is useful
- diagnosis should be made by a specialist
- no single diagnostic tool
- not one type of epilepsy
- blood test: infection cause
- ECG: cardiac cause
- Legal or illicit drug use
- Many common drugs lower threshold? Taking any
- Overdose on any drugs
- Description of the attack
Other causes of seizures that’s not epilepsy
- Head injury
- Infection
- Biochemical imbalance e.g. hyponatraemia
- Migraines
- Syncope (faining can cause limb shaking)
- Encephalitis (can get seizures but if you treat it then they will go)
- Non-epileptic attack disorder
Types of seizure
- Focal seizure: partial seizures, from an area in the brain
o Either retained: patient knows whats going on
o Or impaired: unconscious
- Tonic clonic
o Tonic: sudden stuffness of legs, diaphragm and arms
o Clonic: twitching or jerking
- Absence: brief lapses of consciousness, like staring into space, common in children
- Myoclonic: brief shock like jerks, limb jerming
- Atonic: sudden loss of strength, person may fall
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