Seizures and Epilepsy Flashcards
(47 cards)
1
Q
What is Epilepsy?
A
- chronic condition of recurrent seizures
that can also vary from brief and nearly
undetectable symptoms to periods of
vigorous shaking and convulsions - not a single disease
- affects 0.5-1% of the population
- 2 or more unprovoked seizures
separated by 24 hours or 1 with a
likelihood of reccurrence eg brain
structure abnormality
2
Q
What is a seizure?
A
- temporary disruptions of brain
function causes by uncontrolled
synchronous, paroxysmal excessive
neuronal activity manifesting as a
stereotypes disturbance of
consciousness, behaviour, emotion,
motor function or sensation - usually lasting seconds to minutes
= abnormal excessive firing of the brain
3
Q
Unprovoked Seizures are
A
caused by an unknown and reversible medical cause
4
Q
Seizures: Features:
A
- abnormal firing of the brain
- focal seizures = localised
- can become generalised = both
hemispheres - if greater than 5 mins = status
epilepticus - medical emergency, mortality is 10-
15%
5
Q
Focal vs Generalised Seizures:
A
insert table
6
Q
What is it called when a seizure lasts longer than 5 mins?
A
Status epilepticus
7
Q
What does a seizure look like?
A
- not always convulsion
- prodrome: feeling, sensations,
changes in behaviour hours or days
before event - preictal/aura: immediately prior (not
always present) - icta: actual event
- post-ictal: drowsy, confused, psychotic,
bitten tongue, lost continence
8
Q
Seizure: History of Events:
A
- diurnal pattern
- if more than one seizure:
- max seizure free period?
- seizure frequency?
- hospitalisations?
- falls and injuries - pre-natal and post-natal development?
- history of febrile seizures
- history of CNS (lesions, infections?)
- history of brain trauma specifically
associated with penetrating injuries - family history of epilepsy
- social history: education, employment,
driving status, drug and alcohol use
9
Q
Seizures: Aetiology:
A
- antenatal: infection, trauma, hypoxia
- genetic
- electrolyte disturbances
- infections
- drugs/meds
- tumours
- trauma
- congenital disorders
- neurodegenerative disorders
Adult: stroke, tumour, trauma, infection
Child: genetic/metabolic disorders,
trauma, infection
9
Q
Seizure symptoms are related to the
A
location of abnormal firing
10
Q
Seizure: Acute Symptomatic Management:
A
- treat the underlying cause:
- blood tests
- lumbar puncture
- imaging
- benzodiazepines: can not be used
prophylactically due to side effects,
tolerance and dependance
(used if going toward status epilepticus - antiseizure/ anti-convulsants
medication if there is a
high risk of recurrence/previous
history of seizures
11
Q
Which lobe has most abnormal firing?
A
temporal lobe
area of most neurogenesis
12
Q
Provoked Seizures and Recurrence:
A
- provoked immediate (toxin,
medication, metabolic) = recurrence is
low in absence of provoking factor - acute symptomatic (close to time of a
brain insult) = recurrence is 80% less
likely than a remote symptomatic
seizure
13
Q
Unprovoked Seizures:
- remote symptomatic
- associated with
A
- remote symptomatic (pre-existing
brain injury) - associated with an epileptic syndrome
- unidentified
14
Q
Seizure Differential Diagnosis:
A
insert table
15
Q
What does EEG record?
A
- result of many excitatory and
inhibitory post synaptic potentials
(large group of neurons active at the
same time) at the level of the cortex - depends on the timing and orientation
of neurons
16
Q
The Eye and the EEG:
A
- eye is electrically charged, positive
cornea and negative retina - eyes roll up when eye is closed
- repetitive blinking can look like a
seizure as rhythmic movement - same as eating
17
Q
EEG Utility For Seizures:
A
- epileptic seizures will have
epileptiform discharges on the EEG
during and event - changes on EEG can also be seen
between seizures = inter-ictal
epileptiform discharges - the sooner an EEG can be obtained
after a seizure, the more likely it will
detect an IED within 72hrs - IED can be reduced by levetiracetam,
valproate and acutely by diazepam
18
Q
What does inter-ictal epileptiform discharges firing refer to?
A
abnormal firing of neurons picked up on EEG between seizures
19
Q
Normal EEG rules out epilepsy.
True or False?
A
False
a normal EEG during an event means the event was not epileptic
but a normal EEG after the event just means that abnormalities was not picked up
20
Q
What is the probability of recurrence in the next ten years after two unprovoked seizures?
A
60%
21
Q
A single seizure vs multiple in 24 hours confers no higher risk of recurrence.
True or False?
A
True
22
Q
Seizures: Acute Treatment:
A
- most self-terminate within minutes
- if a seizure continues then initially
treated with benzodiazepine (quick
acting) - longer a seizure persists the harder it
is to control (internalisation of GABA
receptors)
23
Q
The likelihood of having a second seizure after a first seizure is highest within the first two years.
True or False?
A
True
24
When is neuronal death, injury and alteration to networks believed to occur in regards to seizures?
After a seizure that lasts 30 minutes
declared status epilepticus after 5 minutes
25
Seizure Precautions:
- avoid sleep deprivation, alcohol,
infection
- avoid unsupervised activities that pose
danger with sudden loss of
consciousness: baths, swimming,
working at heights, heavy machinery
- driving
- neuropsychiatric co-morbidities
26
What are the different phases of status epilepticus?
insert slide
27
SUDEP is
sudden unexplained death of epilepsy
28
SUDEP Features:
- 2-18% of all deaths in epileptic patients
- higher in children
- unknown reason -> multifactorial
- increases with severity of epilepsy
- 10 fold higher risk in generalised
seizures
- higher in poorly controlled epilepsy
29
Treating Seizures:
- goal: complete seizure freedom with
no side effects (tolerability)
- around 50-60% of patients become
seizure-free on a single drug
- current drug therapy is effective in 70-
80% of patients
- 30-40% patients may not respond to
medication (refractory)
- rule out seizure imitators
- evaluate possibility of surgically
remediable syndromes
- diet
- devices (vagal nerve stimulator)
30
Most antiepileptics with known mechanisms of action work by (3):
- blocking excitation
- increasing inhibition
- prevent repetitive firing
31
How does diazepam work as an anticonvulsant?
enhancing GABA action (absence seizures can be exacerbated by this mechanism of action)
32
How does carbamezpine work as an anti-convulsant?
iincreases inhibition by inhibiting Na+ channel function
stop Na+ channel from working, prevent influx of Na+, hence prevents firing of action potential
33
How does Gabapentin work as an anti-convulsant?
- increasing inhibition
- inhibition of Ca2+ channel
34
How does sodium valproate work as ana anti-convulsant?
inhibits excessive excitation
- enhancing GABA action?
- inhibiting Na+ channel function **
- inhibiting Ca2+ channel function
35
Which of the following anticonvulsants are broad spectrum?
- carbamazepine
- phenytoin
- gabapentin
- diazepam
- levetiracetam
- sodium valproate
- diazepam
- levetiracetam
- sodium valproate
36
Which of the following anticonvulsants are narrow spectrum?
- carbamazepine
- phenytoin
- gabapentin
- diazepam
- levetiracetam
- sodium valproate
- carbamazepine
- phenytoin
- gabapentin
37
Broad Spectrum Anti-convulsants:
insert table
38
Narrow Spectrum Anti-Convulsants:
insert table
39
compare the IV and subcutaneous route of administration for drugs
IV = rapid, but doesnt last as long
Subcutaneous = slowly, but lingers
40
Steady state:
- steady state is reached in 5 half-lives (5
doses)
- steady state wanted for antiseizure
medication
- give a high loading dose when
therapeutic range needs to be reached
quickly
- get the trough level for monitoring but
do not hold drug if half life is short
41
Complex pharmacokinetics: Phenytoin:
- phenytoin is 90% protein bound
- alterations in protein will impact the
free concentration
- phenytoin is metabolised in the liver
- inter-individual difference in level of
saturation
- rate of elimination is therefore altered
when metabolism is saturated
42
Core Drug: Diazepam (anticonvulsant): Metabolism Considerations:
CP450
43
Core Drug: Vaproate:
- highly protein bound will compete with
phenytoin
- metabolised by the liver, excreted in
urine
- dose dependent teratogenicity
44
Core Drug: Carbamazepine: Metabolism Considerationa:
- metabolised into carbamazepine
epoxide
- potent inducer of CYP450
(autoinduction)
- interactions with lamotrigine, lithium,
phenytoin, valproate
- steady state reached in 20 days due to
autoinduction
45
Drug-Resistant Epilepsy:
- failure of two tolerated and
appropriately chosen anti-seizure
meds
- 30-40% ppl
- surgery
- neurostimulator devices
- ketogenic diet
46
Remission of Epilepsy:
- 10 years seizure free with the last 5
years of antiepileptic drugs
- seizure recurrence rate after drug
discontinuation = 35%
- 3% may not regain seizure control
- most recurrence occurs within 1 year
of discontinuation
- short durations of active disease,
longer seizure free periods, ease of
controlling seizures increases
likelihood of success
