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Module 202 > T1S1 seizures and epilepsy > Flashcards

T1S1 seizures and epilepsy Flashcards

1
Q

epilepsy definition

A

recurring, unprovoked seizures

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2
Q

acute symptomatic seizures can be triggered by -

A

stoke, alcohol withdrawal, metabolic disturbance

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3
Q

seizure types

A

generalised onset- electrical discharges appear to start over the whole brain at the same time

focal onset- electrical discharge appears to start in one cortical region and then may remain localized or spread over the whole brain (secondary generalized)

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4
Q

seizure classifications

A
  • tonic clonic seizures
  • absences
  • tonic seizures
  • atonic seizures
  • myoclonic seizures
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5
Q

idiopathic generalised seizures

A
  • onset in childhood and adolescence
  • usually no focal symptoms or signs
  • polygenic cause
  • generalised discharges on eeg
  • may be photosensitive
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6
Q

juvenile myoclonic epilepsy

A
  • commonest form of generalised epilepsy
  • lifelong usually
  • early morning myoclonic jerks
  • photosensitive/ sleep deprived triggers
  • generalised tonic clonic seizures, without warning
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7
Q

tonic clonic seizures

A

no warning (injury risk)

  1. tonic phase
    - continuous muscle spasm, fall, cyanosis, tongue biting, inconcinence
  2. clonic phase
    - rhythmic jerks which slow down and get larger in amplitude as attack ends
  3. post seizure phase
    - coma, drowsiness, confusion, headache
    - muscle ache
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8
Q

abences

A
  • abrupt
  • 5-20 secs
  • multiple times a day, can lead to learning difficulties
  • unresponsive, amnesia
  • rapid recovery
  • eyelid flickering

3hz spike and wave on eeg

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9
Q

focal onset seizures

A

simple partial seizure (SPS)- patient aware- aura (warning)

complex partial seizure (CPS)

  • aura with level of reduced awareness (warning)
  • can be secondary generalised ie patient may experience CPS or SPS before tonic clonic seizure

aura is knowing its about to happen- may be altered smell, fear, deja vu, epigastric rising sensation

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10
Q

secondary tonic clonic seizures

A
  • aura
  • cant abort attack
  • 1-3 mins before falling
  • then tonic clonic seizure
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11
Q

most seizures are in the - lobe

A 
temporal (70%)
symptoms:
- hallucination of taste, speech, smell, visuals
- epigastric rising sensation
- pallor/flushing/hr changes
- lip smacking/chewing motions
- dystonic posturing (limbs rise)

If words are formed during attack, it is in non dominant hemisphere

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12
Q

frontal lobe seizures

A

10-30 secs

  • rapid recovery
  • frequent but usually nocturnal
  • eyes and head forced to contralateral side
  • thrashing motor activity
  • eeg often normal
  • automatisms, distonic posturing
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13
Q

parietal lobe seizures

A
  • positive sensory symptoms
  • tingling, pain
  • distortion of body shape/image
  • jacksonian march of +ve sensory symptoms
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14
Q

occipital lobe seizures

A
  • visual hallucinations (balls of coloured or flashing lights)
  • 25% blackout or whiteout
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15
Q

epileptogenesis

A
  • the process by which parts of a normal brain are converted to a hyperexcitable brain
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16
Q

epileptic seizure def

A
  • an explosion of synchronous activity by lots of neurons at once that has a tendancy to spread throughout the cerebral cortex causing an electrical brainstorm
  • this causes a brief change in behaviour
17
Q

why is the brain prone to seizure activity

A
  • action potentials rely on positive feedback so are inherently unstable
  • a single neuron can fire a train of action potentials simultaneously without external stimulation (intrinsic excitability)

thus a network of connected excitatory neurons is potentially explosive; stimulation of any one can lead to a chain reaction due to the progressive spread of activity over a large area

to avoid this we have inhibitory synpases

EPILEPSY REPRESENTS A FAILURE OF INHIBITORY REGULATION, EITHER FOCALLY OR GENERALLY

18
Q

channelopathies

A
  1. Na+ inactivation is too slow
    - eg generalised epilepsy with febrile seizures
    - action potential repolarisation impaired
  2. reduction in the number of functional k+ channels
    - eg benign familial neonatal convulsions
    - action potential repolarisation impaired
19
Q

eeg

A
  • electroencephalogram
  • highest synchronous activity when the brain is at rest
  • when stimulated the brain becomes dyssynchronous
  • hyperexcitation of seizure leads to synchronous eeg activity
20
Q

origin and spread of focal to generalized seizures

A
  • focal (1000 neurons)
  • caused by paroxysmal depolarising shift

spread to other brain regions along normal neuronal pathways

secondary generalization: when activity spreads to thalamus (tonic clonic)

primary generalized seizures reach the cerebral cortex via normal neuronal pathways from the thalamus

see pic s8 x

21
Q

antiepileptic drugs (AEB) general

A
  • do not prevent development of epilepsy
  • prevent spread of the excitation across the lobes
  • control the symptom (seizure) rather than the cause
22
Q

how do AEDs prevent generalisation

A

causes of increase excitation:

  • increased membrane permeability
  • increased efficiency of excitatory synaptic transmission (glutamate)
  • decrease efficiency of inhibitory synaptic transmission (GABA)

treatments may be aimed at opposing these actions, eg na channel blockers and gaba enhancers

23
Q

na channel blockers

A
  • block repetitive neuron firing
  • normal neuronal functioning is not impaired
    phenytoin, lamotrigine, zonisamide, lacosomide
24
Q

carbamazine, oxcarbazepine and eslicarbazepine

A
  • competitively inhibit voltage gates Na channel by binding to receptor in its inactive state, prolonging the period between successive firings
25
Q

perampanel

A
  • non competitive blockade of AMPA glutamate receptor
  • reduce generalisation

ie reduces efficacy of excitatory synaptic transmission

26
Q

2 ways of reducing excitation manipulating glutamate

A
  1. Reducing efficiency of excitatory synaptic transmission

2. controlling transmitter release

27
Q

controlling glutamate release

A
  • calcium channels are voltage gated and require high ap to let calcium in
  • ca signals neurotransmitter release
28
Q

increase efficacy of inhibitory synaptic transmission

A

GABA

  • hyperpolarisation blocks burst firing (See s15 drugs)
29
Q

levetiracetam

A
  • modulates neurotransmitter release

- keeps patients alert but may have side effects of agitation or mood lowering

30
Q

what makes ideal AED

A
  • good efficacy, easy and rapid to titrate
  • no interactions
  • no cognitive side effects
  • no drowsiness
  • cost
  • different routes of administration
31
Q

established vs modern AEDs

A

established:

  • single mode of action
  • less selective effects
  • more cognitive/sedative effects
  • more interractions
  • cheap
  • narrow therapeutic range

modern:

  • broad spectrum
  • more selective action
  • less sedation
  • less long term toxicity
  • 10x more spen
32
Q

matching drug to patient:

A

primary generalised epilepsy:

  • sodium valproate, lamotrigine first line
  • broad spectrum AEDs

focal onset epilepsy
- carbamazepine, lamotrigine first line
-

33
Q

some drugs exacerbate —-

A

generalized seizure types eg

  • phenytoin
  • carbamazepine
34
Q

side effects

A

benzodiazepines- drowsiness, hyperactivity, personality change, cognitive impairment

phenytoin- ataxia, diplopia, cerebellar atrophy

sodium valparoate- sedation, tremor, nausea, vomiting, hair thinning, weight gain

most give birth defects

also very variable results on different people

Module 202 (49 decks)

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