TLOC, Epilepsy and EEG Flashcards
(124 cards)
1
Q
Seizure definition?
A
the clinical manifestation during abnormal excessive excitation and synchronisation of a population of cortical neurons
2
Q
Epilepsy definition?
A
a tendency to recurrent seizures >24hrs apart which are not provoked by systemic or acute neurologic insults
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
4
Q
Which side of EEG is odd numbers and which even?
A
Left - Odd
Right - Even
5
Q
Describe the 1981 classification of seizures
A
Partial: Simple, complex and secondary generalised
Generalised: absence, myoclonic, atonia, tonic, tonic-clonic
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
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
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
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
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
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
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
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
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
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
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%)
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)
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
19
Q
What is the criteria for mild TBI?
A
- Loss of consciousness <30 min
- No skull fracture
- PTA (Post trauma amnesia) <1 day
20
Q
What is the criteria for moderate TBI?
A
- LOC >30mins and <24 hours
- With or without skull fracture
- PTA >1 <7 days
21
Q
What are the criteria for severe TBI?
A
- LOC > 24 hours
- With contusion, hematoma, or skull
- PTA > 7 days
22
Q
What is the classification for immediate seizures following TBI
A
within 24 hrs
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
24
Q
What is the classification for late seizures following TBI?
A
afer a week post trauma, diagnosis for PTE
25
What is a concussive seizure? is it epilepsy?
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
26
What is the increase in risk of getting epilepsy post TBI? What about post penetrating injury?
* 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
27
What is an example of PTE latency?
• Gage – 1843 accident, 1860 first seizure, shows latent period
28
How does the chance of getting PTE change over time?
• There is often a latent period where no seizures are had, chance of getting PTE is still slowly increasing even 30 years post TBI
29
What are the 3 stages of processing neuronal repair post TBI?
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
30
Which stage is thought to be key for epilepogenesis?
network reorganisation
31
Was it found that treatment of early seizures post TBI were sucessful for preventing PTE?
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
32
Which inflammatory mediator is thought to be indicated in epileptogenesis?
IL1B
33
What do studies into IL1B show regarding epilepogenesis?
* 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
34
What are the findings of studies modelling TBI in mice regarding electrophysiological biomarkers?
* 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.
35
What is the effect of cooling post TBI in mice?
lower number of seizures (thought to be because cooling is anti-inflammatory)
36
Which pathway is thought to be implicated in epileptogenesis?
mTOR
37
What are some of the roles of the mTOR pathway?
* 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
38
What is tuberous sclerosis? Symptoms? What is it caused by?
• 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)
39
What are the symptoms of PMSE syndromes? What is it?
An mTORopathy
o Polyhydramnios
o Megaencephaly
o Symptomatic epilepsy
40
What is hemi-megaencephaly? What is it caused by?
o Unilateral hemispheric enlargement associated with severe seizures
o Somatic mutations found in genes involved in mTOR pathway, such as PIK3CA, AKT3
41
What is focal cortical dysplasia? What is it caused by?
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
42
What is evidence that mTOR pathway is involved in the development of PTE?
* Its rapidly phosphorylated post brain injury
| * Inhibition by rapamycin leads to prevention of development of PTE in mice
43
What is TLOC?
spontaneous loss of consciousness with complete recovery
44
What are possible causes of TLOC?
```
Cardiac
Stroke or TIA
Seizure disorder
Vasogvagal
Orthostatic hypotension
Medication
```
Not necessarily epileptic, more cases of cardiac syncope
45
What are the clinical challenges of TLOC?
* 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
46
What is the major risk associated wiht TLOC?
* Can be first symptom of a fatal arrhythmia
| * Sudden death is often attributed to cardiac arrhythmias
47
How mny people die of cardiac arrhythmias in US per annum?
350,000
48
What things to ask about happened before a TLOC attack ?
* Warning – aura, pre-syncopal
* Provoking features
* Associated symptoms
* Which circumstances?
* Can the attacks be prevented?
49
What to ask about happened during a TLOC attack (if someone witnessed it)
* Actual LOC
* Duration
* Change in complexion
* Verbal/tactile responsiveness
* Movement/limb jerking
* Injuries
* Pulse
* (tongue biting and urine incontinence – not good indicators)
50
What factors to ask about after a TLOC attack?
* Recovery – rapid? Prolongued?
* Confused or sleepy?
* The duration
* How much the patient remembers
* Frequency of attacks
51
What are the symptoms of vasovagal syncope?
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
What could cause vasovagal syncope?
Posture – lying to standing
Provocation – hot, hyperventilating?
Prodromal – viral illness
53
How much of the population faints per year? How many referrals to Aand E?
* 0.5% of the population faint per annum (women v men)
| * 1:200 referrals in A and E
54
Why is ECG important after TLOC?
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
What are the causes of cardiac syncope? What is the onset/ duration/recovery of cardiac syncope?
* 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
What are the characteristics of epilepsy to look for when TLOC occurs?
* 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
What are characteristics of NEAD?
* 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
How do you distinguish NEAD?
* 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
What indication may cause you to be concerned about NEAD due to trauma or abuse?
Particularly violent, prolonged movements
60
What are some of the risks of misdiagnosing NEAD?
• 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
What are the indicators that TLOC could be due to heart block?
Heart block – p waves independent to QRS complex on ECG
Rapid recovery
She can recall the episodes
62
What would cause a TIA diagnosis post TLOC to be changed to epilepsy ?
Multiple stereotyped attacks post-diagnosis
63
What is the alpha rhythm?
Normal EEG rhythm seen when eyes closed in occipital region
64
Which factors can cause variable EEGs?
Age, artefacts, level of consciousness, drugs and cerebral pathology
65
what are some common causes of EEG artefact and variability?
* 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
What are the uses of EEG in epilepsy?
* Diagnosis
* Classification
* Identification of syndromes
* Management of Status Epilepticus
* Work- up for epilepsy surgery
67
How can EEG assist the diagnosis of epilepsy?
* 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
Why is EEG not useful to make a diagnosis of epilepsy?
* 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
What are some features of an interictal EEG in epilepsy?
Non-specific slow waves
Spike and wave
Focal slow waves
70
What are the characteristics of Lennox Gastaut epilepsy syndrome? What is the treatment available?
```
ONset childhood
Persists to adulthood
Characteristic interictal EEG of spike and slow wave
Ictal EEG - runs of spikes
Cannabis treatment
```
71
When is EEG most commonly used for management of status epilepticus?
non-convulsive status
72
Why is EEG needed to treat non convulsive status?
• 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
Why is EEG important for assessment for epilepsy surgery?
* 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
What are the best focal epicentres for epilepsy surgery?
* Temporal or frontal lobe focal epilepsy normally good options for surgery
* Medial temporal lobe is the best place
75
How effective is epilepsy surgery if chosen for correctly
80% seizure free
76
What are the 5 common abuses of EEG?
* 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
What percent of epilepsy is drug resistant?
1/3rd
78
What are some potential consequences of epilepsy?
```
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
What are the qualifying factors to being able to have epilepsy surgery?
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
What are some of the risks of epilepsy surgery?
```
Death
Paralysis
Infection
Memory problems
Stroke
Worsening of epilepsy
```
81
What are the outcomes of epilepsy surgery (resection) ?
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
What is corpus callosotomy?
Removal of the anterior 2/3rds of the corpus callosum
83
What is corpus callosotomy suitable for?
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
What is the outcome of corpus callosotomy?
70-80% experience significant reduction of drop attacks
| Very few are seizure free
85
What is done now if patients have seizures reoccuring after corpus callosotomy?
Now just disconnect all commissures (anterior, posterior and corpus callosum)
86
What is vagus nerve stimulation?
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
What is the outcome of VNS for epilepsy?
70-75% patients has reduced frequency and intensity (recover faster) of seizures
88
What are the problems with vagus nerve stimulation?
Wound infection - antibiotics not enough
Hoarse voice
Can take up to 2 years to be effective
89
What is the benefit of VNS if you have tachycardia before a seizure?
40% of patients have a significant tachycardia before seizure:
Now the device can detect this and give an extra impulse to prevent seizure
90
What is multiple subpial transection?
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
What is multiple sub-pial transection used for?
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
What is the outcome of multiple subpial transection
1/3rd permanent good relief, in general they just make it a bit better
16% long term seizure free
93
Why is mspt not particularly effective in the long term?
Nerves reconnect
94
What is deep brain stimulation?
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
What epilepsies is DBS usually used for?
Stimulation for movement disorders and often multiple focal sources of epilepsy
96
What is the outcome of DBS?
15-30% see a reduction in seizure frequency after short term (1-3 months).
97
What is the ketogenic diet?
High fat, low carbohydrate diet
98
How does the ketogenic diet work?
Induces ketosis - excessive ketones which cross BBB and produce antiepileptic effect
Alongside drugs
99
Who is the ketogenic diet normally successful for?
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
What are the side effects of the ketogenic diet?
```
Kidney stones
High cholesterol levels
Dehydration
Constipation
Slowed growth or weight gain
Bone fractures
```
101
If you reduce seizure frequency do you reduce risk of SUDEP
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
Definition of staus epileptius
‘A seizure that lasts more than 30 mins OR multiple seizures without recovery’
103
How does duration of seizure effect the outcome?
• The longer seizures last, the less likely to stop spontaneously
104
when do seizures become self-sustaining and likely to cause brain damage?
15-30 mins
105
What are the three types of SE?
* 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
What is the incidence, lifetime risk, mortality and chance of severe neurological/cognitive morbidity with generalised SE?
* 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
What are features of convulsive status epilepticus?
* 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
What are features of non-convulsive status epilepticus?
• 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
Describe the changes that occurs at synapses as you reach SE?
• 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
What are some causes of SE?
```
• 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
What general symptoms occur with ongoing seizures?
```
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
What is the initial management of SE?
```
o Recovery position
o Keep safe (move furniture)
o Nothing in mouth
o Oxygen
o Monitoring
o 999 – if over 5 mins
```
113
What is the management of SE at 1st stage?
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
What is the management of SE at 2nd stage?
• 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
What is the treatment of SE at third stage?
• 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
What is treatment of SE at 4th stage?
• 4th stage 30-90 minutes: refractory status
| o ICU – anaesthesia
117
What are the pros and cons of using ICU as a treatment for SE?
```
o Anaesthesia pros
Powerful AED affects
Protect airway
Can get scans
o Anaesthesia cons
Immobility – pressure sores, DVT, pneumonia, muscle weakness & nerve damage
Organ dysfunction – GI tract, immune system (hospital acquired infections)
Pneumonia
Psychological impacts – PTSD
```
118
How can you tell if status epilepticus has stopped?
• 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
What are the drugs used to treat SE?
• 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
Why is phenytoin not used anymore?
* 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
What is some ongoing treatment following SE?
```
• 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
What is refractory SE defined as?
‘Seizures that continue despite 2 appropriate AEDS at appropriate dose’
123
What are some predictors of refractory SE?
```
o Encephalitis
o Hyponatraemia
o Longer duration
o More seizure activity
o Epilepsy
o NICU stay
```
124
What are future research venues for SE?
* Continuous EEG monitoring – expensive
* Cheap, easy EEG
* Autoimmune epilepsies antibody driven
