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Disorders of the Nervous System > Epliepsy > Flashcards

Epliepsy Flashcards

1
Q

what is the epidemiology of epilepsy

A

75 million worldwide
3rd most common neurological disease
0.7% incidence in UK

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2
Q

what is the definition of epilepsy and seizure

A

epilepsy = tendency to have recurrent seizures
seizure = episodes of altered consciousness

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3
Q

what is ictogenesis

A

the development of a seizure
brain state transition

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4
Q

what is epileptogenesis

A

the development of epilepsy

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5
Q

what does interictal mean

A

between seizures

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6
Q

what does paroxysmal mean

A

sudden, violent outburst

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7
Q

how do people die of epilepsy

A

rare occasions where the seizure doesnt stop
if the brain is locked in a persistent epileptic state, it becomes a neurological emergency -> increase of 50% mortality even with medical care

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8
Q

what is SUDEP in epilepsy

A

sudden unexpected death in epilepsy
someone with epilepsy goes to sleep alone, in morning they are dead
telemetry units show when people have seizure it is common to stop breathing briefly, and seizure can also affect cardiac, respiratory and brain systems

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9
Q

what is epilepsy incidence distribution associated with

A

socioeconomic factors
driving, reduced employment opportunities
14% are unemployed
epilepsy is a drive for downward social mobility
people also get judged

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10
Q

outline interictal activity ( between seizures)

A

transient abnormal focal neural discharges seen on EEG
basis for most diagnoses
- not in hope of catching seizure but to assess whether brain is ‘twitchy’
evidence of hyperexcitability

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11
Q

outline interictal cognitive deficits

A

Kleen et al.
epileptic rat trained to chose between 2 levers depening on where light comes on
the longer the pause the more rat gets door wrong
performance declines with time
but if rat has epilepsy, performance remains good
if they have a discharge at time when they choose door, performance drops

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12
Q

what are co-morbidites associated with epilepsy

A

excess mortality
memory deficits
schizophrenia - 7 fold increase, common pathophysiologies
depression, stress, anxiety
downward social movement

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13
Q

outline the causes of epilepsy

A

genetic - dont have full penetrance,
brain injury - trauma, stroke
brain infection - HPV = calcified lesions in brain associated with HPV infection in utero, evidence is strong, measles - since MMR vaccine in 70s, temporal lobe epilepsy has dropped
brain tumours
drugs (alcohol)

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14
Q

are there currently any anti-epileptogenic drugs

A

no

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15
Q

what are some causes of seizures

A

drugs (alcohol)
electrical stimulation (ECT)
sensory triggers - flashing lights, - rare
metabolic imbalance - pH (can stop seizure by making someone acidotic e.g breathing in and out of paper bag)
hormonal state - menstrual cycle, cluster patterns
brain state - transitions, absence seizure discharges dont happen during sleep, some happen only during sleep
temperature, fatigue, stress

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16
Q

what is the spotlight of attention

A

at any given moment, only a small proportion of nerve cells are active
most information coming into the brain is suppressed e.g like out clothes
brain processes things serially not in parallel

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17
Q

what is an absence seizure

A

blank out
stare into space for a few seconds

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18
Q

what did Liu et al show through compromised computation

A

absence seizures likely compromise brain function by blocking flow of activity through thalamus and also interictal events
recently suggested these discharges also alter intellectual performance

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19
Q

what are the cells like during a seizure

A

all cells active at the same time, only one possible combination of doing that, then they are all turned off, so seizure represents catastrophic reduction in number of possible ways brain can work

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20
Q

when does the maximal number of possibilities exist in neurones

A

when half the neurons are active
these are called ‘ensembles’

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21
Q

what do optical illusions do in terms of neuronal ensembles

A

brain flips from one ensemble to another

22
Q

outline brain associations

A

good for leaping and thinking about one thing to make a connection with another - like if they look similar
this is the essence of invention

23
Q

outline pattern completion

A

comes from the way the brain is wired
arises from recurrent connections
when two cells are coactive their connection strengthens

24
Q

what are synchronising influences to the cortex

A

sensory input
glia
intrinsic bursting

25
Q

what causes synchronised activity in the cortex

A

LTP/LTD - basis for memory
binding problem
signal transfer - requires a lot of input, info passes through quickly - can fail?

26
Q

what is meant by ‘up’ states?

A

working memory

27
Q

what is recurrent connectivity in the cortex

A

memory completion
attractor dynamics
positive feedback at cellular level

28
Q

why do we have persistent short term activity in the brain

A

basis of short term memory, brain is in semi persistent activity, has ability to flip, happens in recurrent connective networks, crucial for pattern completion

28
Q

what is normal neuronal function kept in check by

A

neuronal inhibition
if all inhibition is removed - disinhibition = single cells may trigger epileptiform events

29
Q

what did the brain slide study show about single neurones

A

they can initate synchronised population discharge in the hippocampus
the study blocked all synaptic inhibition, quickly saw large discharges, every single nerve cell discharged at that moment
shows the entire network is activated in these field events
with 3 iterations, entrained entire network to be activated from single cell

30
Q

how can we see activity in nerve cells

A

Ca2+ network imaging
dying Ca2+ as it enters active cells

31
Q

outline the spatial profile of a seizure

A

core territory where seemingly every neuron is active, this projects forward huge glutaminergic activity onyo this territory - leads to rapid recruitment of interneurons in this territory, then rapid feedforward restraint of pyramidal activity
people describe auras before seizure - preferential activation of inhibitory neurons, there is discrepancy between activation of e/i - protective firing

32
Q

what is the next spatial profile of seizure after ictal

A

penumbral

33
Q

what is the balance between excitation and inhibition

A

either no activity or epileptiform activity - all a balance

34
Q

is the brain defined by balances?

A

not by balances but by TIPPING POINTS

35
Q

how does the all or nothing response come about

A

through positive feedback mechanism, paired up with negative feedback mechanisms pushing it back to normal
the threshold is the LEAST STABLE POINT
happens because of Na+ channels - depolarising , as more open, more posiitve feedback

36
Q

what is an attractor state

A

whenever we have an ‘aha’ moment or memory suddenly pops into out head , if Na channels didnt close automatically, neurons would get stuck in this attractor
energy sink, systems converge toward these states from multiple starting points
means brain heads towards certain stable patterns of activity

37
Q

how do attractor states show the epileptic brain is different to normal brain?

A

has pathological state that is a little bit easier to enter as it has a reduced protective barrier

38
Q

what are bifurcations

A

transitions between ictal and interictal states

39
Q

what happens immediately prior to seizure onset

A

all or nothing switch

40
Q

outline what Graham et al. found about what happens before seizure onset

A

optogenetics - nerve cells fire when iron channels open and ions move across membrane - energy helf there by big ion gradients
bacterial proteins expressed in nerve cell illuminates tissue using light
stimulated pyramidal cells and recorded output
all or nothing allows brain to leap from one state to another
mediated by Ca2+ channels too - depolarising

41
Q

what is the basic mechanism of antiepileptic drugs

A

suppress excitation
enhance inhibition

42
Q

what does AED Phenytoin do

A

stabilises inactive state of Na channels

43
Q

what do benzos and barbiturates do as AEDs

A

benzo = e.g diazepam, elongates opening time of GABAA channels
barb = increased GABAA current

44
Q

what does Ethosuximide do

A

target voltage-dependant Ca2+ channels for treatment of absence seizures

45
Q

outline the success of antiepileptic drugs

A

half of peoples seizures were controlled on 1st drug
1/6th on second drug
1/3 rd remained refractory to medication (epilepsy maintained)

46
Q

what are other treatment options for epilepsy?

A

neurosurgical resection - only if drugs dont work, identifiable focus of pathology,, irreversible
brain stimulation - now use of optogenetics, with no irreversible damage - want to find out when to stimulate to stop a seizure onset
gene therapy - genes can trigger inhibitory potassium channel, more then cell reduces excitability, epileptic seizure triggers gene expression to make more K+ channels - dampen down cells in seizure

47
Q

what are tipping points created by

A

multiple synergistic positive feedback mechanisms

48
Q

what is a seizure?

A

brain state, usually reverses, without ostensible long term damage
typically very intense (hypersynchronous) network activation
typically profound neuronal suppression post-ictally

49
Q

how are auras defined

A

the ‘right’ processing at the ‘wrong’ time

Disorders of the Nervous System (19 decks)

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