Seizure Fundamentals

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OUR CASE

Sharon’s seizure appeared to stop after 2 minutes but she remained drowsy and had not regained full consciousness before she had another tonic-clonic seizure, which also lasted 1 minute before stopping and she’s drowsy again.

She has now been in the resus bay for 6 minutes.

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Is this convulsive status epilepticus?

What is the actual definition of status epilepticus?


Yes.

Prolonged or rapidly recurring convulsions lasting more than 5 min

> Previously, the definition was 30 minutes of continuous seizure activity. 

> In the 1970s, an experiment was conducted in which bicuculline was injected into paralysed and ventilated baboos. Bicuculline is a competitive antagonist of GABA-A receptors. The neurons of these animals demonstrated ischaemic change after just 30 minutes of continuous seizures. 

> Generally a seizure lasting more than 5 minutes is more likely to become prolonged and be associated with adverse outcome.

> Hence a seizure lasting more than FIVE minutes is now used as the definition and used as a threshold for commencing treatment.

> The longer you wait to treat a seizure, the harder it becomes to stop, partially because the benzodiazepine receptors are reduced by seizure activity

PATHOPHYSIOLOGY

A seizure occurs when neurons are synchronously active for a period of time. These activated neurons send electrical signals (which involves ion flow) from neuron to neuron.

Neurotransmitters control this ion flow. Neurotransmitters bind to receptors and can either cause ion channels to open (i.e. excitatory neurotransmitters) or close (inhibitory neurotransmitters)

The temporarily impaired electrical discharges that occur during a seizure can occur from too much excitation or too little inhibition

> Too much excitation: the main excitatory neurotransmitter is glutamate, and the primary receptor for glutamate is NMDA. When glutamate binds to the NMDA receptor, calcium channels are opened, causing the cell to send electrical signals.

> Too little inhibition: the main inhibitory neurotransmitter is GABA which binds to GABA receptors, causing chloride channels to open which inhibits the electrical signal.

When activated neurons fire simultaneously and repeatedly, this can manifest as the outward signs and symptoms we are familiar with, such as abnormal movements and loss of consciousness, or as inward symptoms that are only perceived by the individual as an aura, e.g. fears, strange smells. These manifestations depend on the region of the brain and which neurons are affected.

The pathophysiology of status epilepticus specifically is not completely understood. Like seizures, it involves an imbalance of neurotransmitters causing too much excitation or too little inhibition.

A seizure is thought to progress to status when there is an increase in glutamate release and thus increase in calcium, causing decreased GABA receptors and increased excitatory NMDA and AMPA receptors. This perpetuates the imbalance in excess excitation and reduced inhibition.

2017 ILAE REFERENCE

OVERVIEW VIDEO

WITH PERMISION

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How would you describe this to someone else over the phone?

Ignore the EEG for the purposes of this exercise.


There is a gentleman in a chair having what appears to be a generalised tonic-clonic seizure.

 

He makes unusual sounds, then has obviously increased tone throughout his whole body. He then develops rhythmic jerking movements in all limbs and trunk.

 

He then becomes unconscious and flaccid.

 

He has an uneven breathing pattern but was not cyanosed.

 

There was no sign of incontinence or evidence of tongue biting.

 

I don’t know if he had a preceding aura.”

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