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TLOC, Epilepsy and EEG Flashcards

1
Q

Seizure definition?

A

the clinical manifestation during abnormal excessive excitation and synchronisation of a population of cortical neurons

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2
Q

Epilepsy definition?

A

a tendency to recurrent seizures >24hrs apart which are not provoked by systemic or acute neurologic insults

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3
Q

Describe what an EEG is

A

records cortical electrical activity, usually from the scalp, most important neurophysiological study for diagnosis, prognosis and treatment of epilepsy, electrodes are attached in in the 10/20 system

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4
Q

Which side of EEG is odd numbers and which even?

A

Left - Odd

Right - Even

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5
Q

Describe the 1981 classification of seizures

A

Partial: Simple, complex and secondary generalised

Generalised: absence, myoclonic, atonia, tonic, tonic-clonic

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6
Q

Describe absence seizures

A
  • Brief staring spells with impaired awareness
  • Hypoventilation is a provoking method
  • 3-20 seconds
  • Sudden onset and sudden resolution,
  • Typically in children, normal development and intelligence
  • Typically resolved by 18 years
  • Generalised 3 Hz spike waves discharge
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7
Q

Describe myoclonic seizures

A
  • Brief shock-like jerk of muscles or group of muscles,
  • Not all myoclonus is epileptic e.g. when falling asleep
  • 4-6Hz polycyclic waves (more than one spike)
  • Can be subtle or dramatic
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8
Q

Describe tonic seizures

A
  • Symmetric tonic muscle contraction of extremities with tonic flexion of waist and neck
  • Distinct to tonic-clonic,
  • 2-20 seconds
  • EEG – slow wave, attenuation (stopping) and then rapid waves
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9
Q

Describe atonic seizures

A
  • Sudden loss of muscle tone,
  • Floppy and fall on floor,
  • Milder version just head,
  • Similar EEG to tonic seizures
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10
Q

Describe tonic-clonic seizures

A
  • Association with loss of consciousness and post ictal confusion/lethargy,
  • Stiffening of all muscles (also larynx so can scream), followed by fast low amplitude jerking and then slow high amplitude jerking
  • 30-120 seconds
  • Afterwards patients very confused and not aware of where they are
  • EEG- sharp activity everywhere, a lot of muscle interference
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11
Q

Describe a focal without impaired awareness seizure

A
  • Aura
  • Patient is aware
  • Diverse range as due to where in the brain the seizure is, if in the visual cortex you can get visual aura often large coloured circles, motor = jerking, can be more subtle e.g. temporal = dream like experience
  • The aura will always be the same for the patient
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12
Q

Desribe a focal with impaired awareness seizure

A
  • Arise from one part of brain but patient loses awareness,
  • Manifestations depend on the area affected
  • Autonomisms – semi-purposeful movements
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13
Q

Describe a focal evolving to bilarteral tonic-clonic seizure

A
  • Start in one place e.g. aura etc. and then spread to the whole brain
  • Generalised tonic-clonic phase looks the same as primary tonic-clonic phase
  • Typically 1-3 mins
  • Can have Todd’s paresis – weakness on the opposite side of brain to where the seizure started
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14
Q

What sort of factors can be used to group epilepsy patients into syndromes

A
  • Seizure type
  • Age of onset
  • Natural history/prognosis
  • EEG patterns
  • Aetiology/genetics
  • Response to treatment
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15
Q

Describe temporal lobe epilepsy syndrome

A
  • Onset at any age
  • EEG shows temporal lobe epileptiform discharges
  • Simple partial, complex partial and secondary generalised tonic clonic seizures can all be had
  • May be symptomatic or cryptogenic
  • Inter-ictal EEG shows sharp and slow waves that are abnormal
  • 2 sharp waves pointing to each other – point to focus
  • Can be due to hippocampal sclerosis
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16
Q

Describe juvenile myoclonic epilepsy syndrome

A
  • Juvenile onset
  • Myoclonic seizures, GTCS, and absences
  • Seizures have morning predominance, exacerbated by sleep deprivation and alcohol
  • Idiopathic
  • EEG shows generalised spike or polyspike/wave discharges
  • Often photosensitive (30-40%)
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17
Q

Describe West epilepsy syndrome

A
  • Paediatric syndrome
  • Can be symptomatic or cryptogenic
  • Infantile onset
  • Spasms
  • Hypsarrythmic EEG – sharp waves and slow waves everywhere which are chaotic, followed by attenuation of EEG (flexion of the body and extension of limbs)
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18
Q

What did the 2010 classicifcation of epilepsy seizures introduce?

A

Introduces idea of networks:

Focalised – started somewhere in the brain which triggered one localised hemisphere network

Generalised – starts somewhere but rapidly involves bilateral network in both hemispheres

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19
Q

What is the criteria for mild TBI?

A
  • Loss of consciousness <30 min
  • No skull fracture
  • PTA (Post trauma amnesia) <1 day
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20
Q

What is the criteria for moderate TBI?

A
  • LOC >30mins and <24 hours
  • With or without skull fracture
  • PTA >1 <7 days
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21
Q

What are the criteria for severe TBI?

A
  • LOC > 24 hours
  • With contusion, hematoma, or skull
  • PTA > 7 days
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22
Q

What is the classification for immediate seizures following TBI

A

within 24 hrs

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23
Q

What is the classification for early seziures following a TBI?

A

seizure within a week, skull fractures or intracranial bleed increases chance of early seizures, early seizures are an indicator for PTE

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24
Q

What is the classification for late seizures following TBI?

A

afer a week post trauma, diagnosis for PTE

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25
Q

What is a concussive seizure? is it epilepsy?

A

immediately at the trauma, thought to have different causes the tonic-clonic, looks the same but it doesn’t have same post-ictal confusion, doesn’t have an effect on likelihood to have further seizures and is not epilepsy

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26
Q

What is the increase in risk of getting epilepsy post TBI? What about post penetrating injury?

A
  • The increase in risk of getting PTE is small for mild and moderate TBI
  • It is larger for the severe TBI (10% increase in 5 years)
  • Prevalence of epilepsy >50% after penetrating injury
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27
Q

What is an example of PTE latency?

A

• Gage – 1843 accident, 1860 first seizure, shows latent period

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28
Q

How does the chance of getting PTE change over time?

A

• There is often a latent period where no seizures are had, chance of getting PTE is still slowly increasing even 30 years post TBI

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29
Q

What are the 3 stages of processing neuronal repair post TBI?

A

3 stages post damage:
• Ion channel activation, immediate early gene activation
• Neuronal death, neuroinflammation and oxidative stress
• Neuronal loss and neurogenesis, network reorganisation, hippocampal sclerosis

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30
Q

Which stage is thought to be key for epilepogenesis?

A

network reorganisation

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31
Q

Was it found that treatment of early seizures post TBI were sucessful for preventing PTE?

A

Treatment of early seizures – reduce oxidative stress and excitotoxity, to decrease chances of getting PTE. This looks to work at the immediate point but long term no difference between phenytoin treated early seizures and placebo

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32
Q

Which inflammatory mediator is thought to be indicated in epileptogenesis?

A

IL1B

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33
Q

What do studies into IL1B show regarding epilepogenesis?

A
  • Studies into the role of inflammation in PTE
  • Thought that some of the inflammatory mediators contribute to epileptogenesis
  • Higher levels of IL1B in CSF of patients with severe TBI than mild, this is kept raised in patients that develop epilepsy
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34
Q

What are the findings of studies modelling TBI in mice regarding electrophysiological biomarkers?

A
  • Found somato - motor recovery but they develop epilepsy later on
  • Another study looks at electrophysiological markers for epileptogenicity – found markers in rats EEG, but not in human until 2 years (when epilepsy symptoms already), no early marker.
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35
Q

What is the effect of cooling post TBI in mice?

A

lower number of seizures (thought to be because cooling is anti-inflammatory)

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36
Q

Which pathway is thought to be implicated in epileptogenesis?

A

mTOR

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37
Q

What are some of the roles of the mTOR pathway?

A
  • mTor pathway controls cell growth and survival, proliferation and cellular metabolism, synaptic plasticity and neuronal morphology.
  • Neuronal mTOR promotes axonal regeneration in response to CNS injury
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38
Q

What is tuberous sclerosis? Symptoms? What is it caused by?

A

• Tuberous sclerosis – a neurocutaneous syndrome
o Cutaneous features
o Brain abnormalities (cortical tubers, subependymal giant cell astocytomas) and epilepsy
o Caused by mutations in TSC1 and TSC2 (in the middle of the mTOR pathway)

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39
Q

What are the symptoms of PMSE syndromes? What is it?

A

An mTORopathy

o Polyhydramnios
o Megaencephaly
o Symptomatic epilepsy

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40
Q

What is hemi-megaencephaly? What is it caused by?

A

o Unilateral hemispheric enlargement associated with severe seizures
o Somatic mutations found in genes involved in mTOR pathway, such as PIK3CA, AKT3

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41
Q

What is focal cortical dysplasia? What is it caused by?

A

o Common cause of epilepsy,
o Cortical neuron migration not effective
o Somatic mutations have been found in some mTOR pathway genes
o Rare familial cases with germline mutations implicated

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42
Q

What is evidence that mTOR pathway is involved in the development of PTE?

A
  • Its rapidly phosphorylated post brain injury

* Inhibition by rapamycin leads to prevention of development of PTE in mice

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43
Q

What is TLOC?

A

spontaneous loss of consciousness with complete recovery

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44
Q

What are possible causes of TLOC?

A 
Cardiac 
Stroke or TIA 
Seizure disorder 
Vasogvagal 
Orthostatic hypotension 
Medication

Not necessarily epileptic, more cases of cardiac syncope

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45
Q

What are the clinical challenges of TLOC?

A
  • Main witness unconscious – relying collateral history
  • Eyewitness account unreliable but essential
  • Unpredictable
  • Occasionally life threatening
  • Driving restrictions, health and safety
  • Initial diagnosis often inaccurate, delay – person should be seen 4 weeks after first blackout
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46
Q

What is the major risk associated wiht TLOC?

A
  • Can be first symptom of a fatal arrhythmia

* Sudden death is often attributed to cardiac arrhythmias

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47
Q

How mny people die of cardiac arrhythmias in US per annum?

A

350,000

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48
Q

What things to ask about happened before a TLOC attack ?

A
  • Warning – aura, pre-syncopal
  • Provoking features
  • Associated symptoms
  • Which circumstances?
  • Can the attacks be prevented?
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49
Q

What to ask about happened during a TLOC attack (if someone witnessed it)

A
  • Actual LOC
  • Duration
  • Change in complexion
  • Verbal/tactile responsiveness
  • Movement/limb jerking
  • Injuries
  • Pulse
  • (tongue biting and urine incontinence – not good indicators)
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50
Q

What factors to ask about after a TLOC attack?

A
  • Recovery – rapid? Prolongued?
  • Confused or sleepy?
  • The duration
  • How much the patient remembers
  • Frequency of attacks
51
Q

What are the symptoms of vasovagal syncope?

A

o Convulsive movements common
o Lack of post-ictal confusion
o Hearing people around you before you can respond
o Reoccurrence of blackout on regaining upright posture

52
Q

What could cause vasovagal syncope?

A

Posture – lying to standing
Provocation – hot, hyperventilating?
Prodromal – viral illness

53
Q

How much of the population faints per year? How many referrals to Aand E?

A
  • 0.5% of the population faint per annum (women v men)

* 1:200 referrals in A and E

54
Q

Why is ECG important after TLOC?

A

Always do ECG first – heart before brain
Found on ECG that the QT interval is extended – long qt syndrome
Recovery indicates cardiac not epilepsy
Can be fatal

55
Q

What are the causes of cardiac syncope? What is the onset/ duration/recovery of cardiac syncope?

A
  • Temporary but sudden reduction I nblood supply and hence oxygen to the brain as a result of cardiovascular conditions
  • Triggers syncope by vasodilation, hypotension or arrythmia (bradycardia, tachycardia or valvular disease)
  • Onset of syncope is relatively rapid and recovery from LOC is spontaneous, complete and usually prompt
56
Q

What are the characteristics of epilepsy to look for when TLOC occurs?

A
  • Description of an aura – patients struggle to explain, try really hard
  • Prolonged post ictal confusion is likely epilepsy
  • Short attacks – very brief
  • Head turning or posturing of body
  • Stiffening of body and myoclonic jerking (not oscillation)
  • Abnormal behaviour of which patients do not remember
  • Severe tongue bite
57
Q

What are characteristics of NEAD?

A
  • More common than epilepsy
  • Gradual onset, undulating motor activity with pauses
  • Sinusoidal and synchronous arm and leg movements
  • Prolonged atonia, rhythmic pelvic movements, side to side head movements
  • Post ictal crying, high anxiety in carers
  • Prolonged attack with unexpectedly sudden recovery
58
Q

How do you distinguish NEAD?

A
  • Unusually frequent, drug-unresponsive seizures
  • History of multiple unexplained symptoms, multiple surgical procedures
  • History of personality disorder, alcohol abuse, self-harm, parasuicide, childhood abuse, psychiatric treatment
59
Q

What indication may cause you to be concerned about NEAD due to trauma or abuse?

A

Particularly violent, prolonged movements

60
Q

What are some of the risks of misdiagnosing NEAD?

A

• Inappropriate treatment
o Risk of adverse effects of anti-epileptic drugs including teratogenicity
• Ineffective treatment when there is an effective treatment
• Reinforcement of abnormal illness behaviour
o Evolution of functional symptoms
o Incapacity
o Some employers give financial allowance due to epilepsy diagnosis – then lose that because the diagnosis is reversed

61
Q

What are the indicators that TLOC could be due to heart block?

A

Heart block – p waves independent to QRS complex on ECG
Rapid recovery
She can recall the episodes

62
Q

What would cause a TIA diagnosis post TLOC to be changed to epilepsy ?

A

Multiple stereotyped attacks post-diagnosis

63
Q

What is the alpha rhythm?

A

Normal EEG rhythm seen when eyes closed in occipital region

64
Q

Which factors can cause variable EEGs?

A

Age, artefacts, level of consciousness, drugs and cerebral pathology

65
Q

what are some common causes of EEG artefact and variability?

A
  • Alpha rhythm – at back of head with eyes closed is normal
  • Child EEG – can look chaotic normally
  • Chewing artefact
  • Muscle tension artefact
  • In sleep its normal to have sharp waves at the vertex
  • Anaesthetised patient – flattened EEG in the middle
  • Drugs – antidepressants can cause variable EEG
  • Cerebral palsy – damage at birth can cause abnormal EEGs but not have seizures
66
Q

What are the uses of EEG in epilepsy?

A
  • Diagnosis
  • Classification
  • Identification of syndromes
  • Management of Status Epilepticus
  • Work- up for epilepsy surgery
67
Q

How can EEG assist the diagnosis of epilepsy?

A
  • Clinical history should make the diagnosis and EEG just refines diagnosis
  • Inter-ictal EEG does not exclude epilepsy or prove epilepsy (there are many abnormalities that are asymptomatic and also normal EEGs for those with epilepsy)
  • Therefore the EEG is to be used alongside the degree of clinical suspicion
68
Q

Why is EEG not useful to make a diagnosis of epilepsy?

A
  • Inter-ictal EEG does not exclude epilepsy or prove epilepsy (there are many abnormalities that are asymptomatic and also normal EEGs for those with epilepsy)
  • Specificity of EEG – of those who have never had a clinical seizures in healthy adults 0.5-4% of have abnormal EEG. In population coming to clinics people are not healthy e.g. other cerebral disease such as cerebrovascular, migraine, cerebral palsy, Alzheimers
69
Q

What are some features of an interictal EEG in epilepsy?

A

Non-specific slow waves
Spike and wave
Focal slow waves

70
Q

What are the characteristics of Lennox Gastaut epilepsy syndrome? What is the treatment available?

A 
ONset childhood 
Persists to adulthood
Characteristic interictal EEG of spike and slow wave 
Ictal EEG - runs of spikes
Cannabis treatment
71
Q

When is EEG most commonly used for management of status epilepticus?

A

non-convulsive status

72
Q

Why is EEG needed to treat non convulsive status?

A

• Non-convulsive status – people withdrawn and almost catatonic, EEG may be only way to give diagnosis to allow treatment, EEG very spiking and generalised

73
Q

Why is EEG important for assessment for epilepsy surgery?

A
  • Chosen patients who have good evidence for the focus of the epilepsy – MRI abnormality and EEG concur
  • EEG to ensure exactly where the seizures are starting
74
Q

What are the best focal epicentres for epilepsy surgery?

A
  • Temporal or frontal lobe focal epilepsy normally good options for surgery
  • Medial temporal lobe is the best place
75
Q

How effective is epilepsy surgery if chosen for correctly

A

80% seizure free

76
Q

What are the 5 common abuses of EEG?

A
  • Monitoring of progress – pointless, just ask patient
  • Anti-convulsant withdrawal in adults – no evidence in adults
  • Diagnosis in presence of intracerebral disease
  • Diagnosis where history is of syncope
  • Driving – only for HGV
77
Q

What percent of epilepsy is drug resistant?

A

1/3rd

78
Q

What are some potential consequences of epilepsy?

A 
Stigma 
Social isolation 
Bullying 
Treated differently 
Depression and anxiety - Higher incidence in major depressive order, anxiety, suicidal ideation in epileptic people than general population
Lifestyle adaptations 
Driving restrictions 
Employment 
Financial 
Loss of role 
Loss of independence 
Contraception/pregnancy 
SUDEP
79
Q

What are the qualifying factors to being able to have epilepsy surgery?

A

Must have tried 2 drugs up to the fully tolerated level
For at least 2 years
Patient or carer must say quality of life is too poor
Video EEG with dropped medication to find focus
High quality MRI which backs up EEG focus (very occasionally fMRI)
Psychological assessment
Often can map the brain using electrodes and freezing areas of the brain whilst the patient is awake to test if normal functioning is able without the proposed area for removal

80
Q

What are some of the risks of epilepsy surgery?

A 
Death 
Paralysis 
Infection 
Memory problems 
Stroke
Worsening of epilepsy
81
Q

What are the outcomes of epilepsy surgery (resection) ?

A

70-80% are seizure free - right patient, right surgery and right timing needed to get this level of success
After 10 years some begin to have seizures again
Keep on AED for next 2 years at least, and then slowly wean off if patient is keen

82
Q

What is corpus callosotomy?

A

Removal of the anterior 2/3rds of the corpus callosum

83
Q

What is corpus callosotomy suitable for?

A

tonic or atonic seizures that result in drop attacks
Lennox Gastaut syndrome - often can’t find the focal point of these
Infantile hemiplegia with a functional hand
Where there is a rapid bilateral spread of synchronisation of activity on EEG

Very dehabilitating conditions - disconnecting two sides of the brain will have side effects of discoordination and RL disconnection

84
Q

What is the outcome of corpus callosotomy?

A

70-80% experience significant reduction of drop attacks

Very few are seizure free

85
Q

What is done now if patients have seizures reoccuring after corpus callosotomy?

A

Now just disconnect all commissures (anterior, posterior and corpus callosum)

86
Q

What is vagus nerve stimulation?

A

Left side of the vagus nerve is stimulated (right controls heart)
Stimulation all the time - thought to interrupt abnormal electrical stimulation to brain
Stimulates the NA pathways - increases the threshold of stimulation that results in seizure (epileptic patients have a much lower threshold than normal people)

87
Q

What is the outcome of VNS for epilepsy?

A

70-75% patients has reduced frequency and intensity (recover faster) of seizures

88
Q

What are the problems with vagus nerve stimulation?

A

Wound infection - antibiotics not enough
Hoarse voice
Can take up to 2 years to be effective

89
Q

What is the benefit of VNS if you have tachycardia before a seizure?

A

40% of patients have a significant tachycardia before seizure:
Now the device can detect this and give an extra impulse to prevent seizure

90
Q

What is multiple subpial transection?

A

AIms to stop the sideways spread and movement of electrical discharge
Use a paperclip style wire to make vertical incisions to prevent the sideways spread of epileptiform activity

91
Q

What is multiple sub-pial transection used for?

A

Used for areas such as motor control of the hand/larynx where removal isn’t an option:
Brocca’s area
Sensory cortex
Motor cortex

92
Q

What is the outcome of multiple subpial transection

A

1/3rd permanent good relief, in general they just make it a bit better
16% long term seizure free

93
Q

Why is mspt not particularly effective in the long term?

A

Nerves reconnect

94
Q

What is deep brain stimulation?

A

Stimulating the centromedian thalamic nucleus, anterior thalamic nucleus, cerebellar cortex (epilepsy is only supratentorium), hippocampus etc. to try and desynchronise by blocking discharge with electrical stimulation of a different frequency

95
Q

What epilepsies is DBS usually used for?

A

Stimulation for movement disorders and often multiple focal sources of epilepsy

96
Q

What is the outcome of DBS?

A

15-30% see a reduction in seizure frequency after short term (1-3 months).

97
Q

What is the ketogenic diet?

A

High fat, low carbohydrate diet

98
Q

How does the ketogenic diet work?

A

Induces ketosis - excessive ketones which cross BBB and produce antiepileptic effect
Alongside drugs

99
Q

Who is the ketogenic diet normally successful for?

A

Generally for children and often specifically for Lennox-Gastaut syndrome
Can have success - particularly in disabled people as peg feed is easily able to calculate exactly and deliver

100
Q

What are the side effects of the ketogenic diet?

A 
Kidney stones 
High cholesterol levels 
Dehydration 
Constipation 
Slowed growth or weight gain 
Bone fractures
101
Q

If you reduce seizure frequency do you reduce risk of SUDEP

A

No. If you don’t completely stop the seizures the risk of SUDEP doesn’t change, even if the seizures reduce a lot. Mainly trying to increase quality of life.

102
Q

Definition of staus epileptius

A

‘A seizure that lasts more than 30 mins OR multiple seizures without recovery’

103
Q

How does duration of seizure effect the outcome?

A

• The longer seizures last, the less likely to stop spontaneously

104
Q

when do seizures become self-sustaining and likely to cause brain damage?

A

15-30 mins

105
Q

What are the three types of SE?

A
  • Generalised status epilepticus
  • Focal with altered awareness status epilepticus – can go on for hours/day, difficult to spot
  • Epilepsia partiala continua – uncommon, continuous focal status
106
Q

What is the incidence, lifetime risk, mortality and chance of severe neurological/cognitive morbidity with generalised SE?

A
  • Incidence – 10-41/100 000
  • Lifetime risk if have epilepsy is 10%
  • Often first presentation of epilepsy in 50% of adults
  • Mortality 9-60%
  • Severe neurological/ cognitive morbidity – 11-16%
107
Q

What are features of convulsive status epilepticus?

A
  • Convulsions associated with rhythmic jerking
  • Tonic-clonic movements
  • Mental status impairment
  • Focal neurological deficit – arm or leg that’s not moving at all e.g.
108
Q

What are features of non-convulsive status epilepticus?

A

• Seizures activity on EEG without clinical findings of GCSE
o Wandering confused, automatisms
o Acutely unwell, obtunded +/- motor abnormalities
• Negative symptoms
o Anorexia, aphasia, amnesia, catatonic, coma, confusion
• Positive symptoms
o Agitiation, automatisms, blinking, laughter, nausea, nystagmus, psychosis

109
Q

Describe the changes that occurs at synapses as you reach SE?

A

• Normally have balance of excitatory glutamate from pre-synaptic terminal and AMPA/NMDA receptors with inhibitory GABA and GABA receptors
• Longer seizure:
o More AMPA and NMDA receptors and more glutamate
o Depletion of GABA and GABA receptors
o Most treatments target the GABA receptors so the longer the seizure the more difficult to respond

110
Q

What are some causes of SE?

A 
•	Acute
o	Stroke 
o	Metabolic abnormalities 
o	Hypoxia e.g. cardiac arrest 
o	Systemic infection 
o	Anoxia 
o	Trauma
o	Drug overdose
o	CNS infection 
o	CNS haemorrhage 
•	Chronic 
o	Low concentration of anti-epileptic drug in epilepsy – low mortality rate as can just give epileptic drug back 
o	Remote symptomatic e.g. tumour, stroke 
o	Alcohol misuse – lowers seizure threshold 
o	Tumour 
o	Idiopathic
111
Q

What general symptoms occur with ongoing seizures?

A 
o	Increased CO 
o	Increased blood pressure, sugar and lactate
•	Decompensation
o	Cardiorespiratory collapse 
o	Electrolyte imbalance 
o	Rhabdomyolysis – affects kidney 
o	Hyperthermia
o	Major organ failure 
o	Cerebral oedema
112
Q

What is the initial management of SE?

A 
o	Recovery position 
o	Keep safe (move furniture) 
o	Nothing in mouth 
o	Oxygen 
o	Monitoring 
o	999 – if over 5 mins
113
Q

What is the management of SE at 1st stage?

A

o Secure airway
o High flow oxygen (breathing)
o Cardiac and respiratory function
o Obtain intravenous access in a large vein
o Check blood glucose levels – check not hypo which is easily treatable

114
Q

What is the management of SE at 2nd stage?

A

• 2nd stage: 0-30 minutes
o Treat seizure
 Consider possibility of NEAD/pregnancy
 Emergency AED therapy
 Emergency investigation – metabolic status and glucose
 Treat severe acidosis

115
Q

What is the treatment of SE at third stage?

A

• 3rd stage: 0-60 minutes (established status)
o Seizures that don’t resolve quickly suggest something is fuelling them
o Consider the cause
o Treatment depends on cause e.g. if NEAD then AEDs won’t work

116
Q

What is treatment of SE at 4th stage?

A

• 4th stage 30-90 minutes: refractory status

o ICU – anaesthesia

117
Q

What are the pros and cons of using ICU as a treatment for SE?

A 
o	Anaesthesia pros
	Powerful AED affects 
	Protect airway 
	Can get scans 
o	Anaesthesia cons 
	Immobility – pressure sores, DVT, pneumonia, muscle weakness &amp; nerve damage 
	Organ dysfunction – GI tract, immune system (hospital acquired infections) 
	Pneumonia 
	Psychological impacts – PTSD
118
Q

How can you tell if status epilepticus has stopped?

A

• Anaesthesia induction requires paralysing – needed to ventilated and give anaesthesia
o After long seizures movement diminishes anyway
• EEG – really only way to find out
o Can see ongoing seizure activity
o Can suggest other causes – e.g. encephalitis, non-epileptic attack

119
Q

What are the drugs used to treat SE?

A

• First line – Benzodiazepines e.g lorazepam, diazepam, midazolam
o GABA receptor targets
o Slows all neurotransmission including consciousness and breathing
o Can last a while and accumulate
o Slow to work
o Can be given IV, buccal, oral, im
o Evidence that they work though – grade A/B evidence
o Paramedics have them
• If that doesn’t work: Valproate or levetiracetam IV (Used to be phenytoin)
• If that doesn’t work: anaesthesia

Evidence is not clear – clinical trials on SE is very difficult to set up

120
Q

Why is phenytoin not used anymore?

A
  • Works as an AED BUT
  • Burns skin badly if IV not in properly – need surgery
  • Cause cardiac arrhythmias
  • Can cause arteries to constrict to hand, fingers can fall off
121
Q

What is some ongoing treatment following SE?

A 
•	Review/continue regular AEDs 
o	Risk of recurrent seizures after status 41% 
o	Get drug history 
o	Drug levels – urine 
o	NG feed and drugs 
o	Consider NEAD/maintaining factors
122
Q

What is refractory SE defined as?

A

‘Seizures that continue despite 2 appropriate AEDS at appropriate dose’

123
Q

What are some predictors of refractory SE?

A 
o	Encephalitis 
o	Hyponatraemia 
o	Longer duration 
o	More seizure activity 
o	Epilepsy 
o	NICU stay
124
Q

What are future research venues for SE?

A
  • Continuous EEG monitoring – expensive
  • Cheap, easy EEG
  • Autoimmune epilepsies antibody driven

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