Seizures Flashcards

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1
Q

Provide a brief definition of a seizure

A

Abnormal and uncontrolled electrical activity in the brain causing changes in consciousness, movement and behaviour.

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2
Q

Describe some of the causes of seizures

A

Causes will change the integrity of the cell membrane making it easier for the neurons to depolarise.

  • Hypoxia: failure of Na/K pump = rise in RMP
  • Hypoglycaemia: unable to produce ATP = Na/K failure
  • Head injury: damage to neurons = release of glutamate
  • Toxins/Drugs: hypopolarise the cell = easily excitable
  • Infection
  • Metabolic changes
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3
Q

What are the classifications of seizures?

A

Generalised seizures: widespread seizure activity across both hemispheres of the brain that impairs consciousness
-Tonic clonic: stiffness followed by jerking movements
-Tonic: stiffening of muscles causing full body rigidity
-Atonic: sudden loss of muscle tone through whole body
-Abscence: staring, loss of facial expression and unresponsiveness
-Clonic: regularly repeated jerking movements
-Myoclonic: brief but significant jerking of muscles
Partial seizures seizure activity to one area of the brain with normal conscious state, activity may spread
-Simple partial: numbness, tingling or twitching to one area of the body, deja vu, hallucinations
-Complex partial: display of strange, random or repetitive behaviour (chewing, mumbling, altered awareness)
-Status epilepticus: A continuous seizure lasting >30mins or two or more seizures without regaining consciousness in between.

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4
Q

How do neurons transmit signals?

A

This occurs at the synapse of two neurons.
Inside the axon terminal of the sending neuron are synaptic vesicles, which are filled with a neurotransmitter. As a action potential arrives at the axon terminal it activates voltage-gated Ca2+ channels, causing Ca2+ to rush into the cell. This allows the synaptic vessicles to fuse with the cell membrane, causing release of the neurotransmitter. The neurotransmitter then diffuses across the synaptic cleft and binds to receptors on the post-synaptic cell - leads to either opening or closing of ion channels.

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5
Q

What are the main neurotransmitters?

A
  • Glutamate: is the major excitatory neurotransmitter and works to continue propagation of a signal. This occurs as when it binds to a receptor on the post-synaptic cell it may cause an influx of positive ions such as Na+ = cell becomes closer to threshold for depolarisation. This may need more than one excitatory signal for threshold to be reached.
  • GABA (gamma-aminobutyric acidic): is the major inhibitory neurotransmitter and works to cancel the signal and prevent it from propagating. This inhibitory effect may occur as the binding of GABA to the post-synaptic neuron causes an influx of ions (such as Cl-) that cause the neuron to to hyperpolarise. This makes it harder for the neuron to depolarise and fire an action potential.
  • Others such as dopamine and serotonin play specific roles in certain parts of the brain that aid in particular neuro functions (memory, learning, motor, sensory).
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6
Q

Explain the pathophysiology of seizures

A

Under normal circumstances, excitatory synaptic activity is tightly regulated by inhibitory neurons. Disruption to this process may occur due to things such as trauma, genetic abnormalities, hypoxia etc. which causes hyperexcitability of neurons.
-Too much excitation: increased levels of glutamate, increased entry of Na+ (failure of Na/K pump) = Increased AP propagation
-Too little inhibition: not enough GABA, decreased Cl- enty (causing cell to hyperpolarise) = unopposed AP propogation
How the seizure presents depends on the area of the brain that is affected by the seizure activity.

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7
Q

What are treatment priorities for seizures:

A
  • Airway: insert airway adjunct if possible (OPA, NPA)
  • Breathing: HI-flo 02 ASAP due to high 02 consumption and high risk of hypoxia
  • Midazolam: for generalised seizures, administer ASAP if risk of airway comprimise (aspiration), hypoxia or physical injury. Otherwise administer if activity is >5mins. 100mcg/kg IM max of 10mg and max of 5mg/IM site. Dose repeated once after 5mins
  • BGL: high glucose consumption and often a reversible cause
  • Address cause of seizure - hypoxia, hypoglycaemia, head injury, hypothermia etc.
  • Follow seizure management plan where possible
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8
Q

Describe the pharmacology of midazolam

A

Drug type: Benzodiazepine
Onset: 5-15m Duration: varies Half life: 2.5 hours
Metabolism: Hepatic Excretion: Renal
MOA: Is an allosteric modulator for GABA (increases affinity of GABAa receptors for GABA). This causes normal effects of GABA - hyperpolarises cell by causing an influx of Cl- into post-synaptic neuron. This causes cell RMP to become more negative and makes it more difficult to be stimulated by an AP.
Indications: patients experiencing a generalised seizure >5mins.
Contraindications: known allergy
Side effects: hypotension, respiratory depression (CNS depressent action)

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9
Q

What can ICPs add and when may you call them?

A
  • IV midazolam
  • Can administer kepra (levetiracetam) as an alternative to midaz
  • May be able to address more causes - administer IV medications for paediatrics
  • Call when about to give second dose of midaz.
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10
Q

What are febrile seizures?

A
  • Seizures or convulsions in the setting of high temperature and the absence of CNS infection, inflammation or previous afebrile seizures
  • Usually tonic clonic seizures, last for >15mins and dont reoccur within 24hrs
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11
Q

Why do alcoholics have seizures when they stop drinking?

A

Alcohol use, particularly long-term, causes CNS depressive effects by suppressing the effect of glutamate and increasing the effect of GABA.
Chronic use of alcohol causes the body to upregulate the glutamate receptors to balance out the effect.
When alcohol use is stopped, the levels of GABA in the brain reduce, and neurons are more susceptible to seizure activity due to the increased glutamate receptors.

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