Seizures Flashcards

1
Q

seizures

A

transient alteration of behaviour due to abnormally excessive + synchronous neuronal activity
abnormal neuronal firing

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2
Q

epilepsy

A

disorder of brain function characterized by periodic and unpredictable occurrence of seizures
symptomatic: known cause
unsymptomatic: no known cause - genetic?

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3
Q

normal neuronal firing

A

neurons fire asynchronously → spread of electrical activity controlled by refractory period + surround inhibition

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4
Q

action potential

A

cell membrane at rest = -70mV
concentration gradietn generates membrane potential
reach threshold = Na+ influx
reversal of potential = K+ efflux
reduction of potential → hyperpolarization - refractory period

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5
Q

surround inhibition

A

mechanism that focuses neuronal activity in CNS
overlapping primary afferents - central is closest to point of stimulation = strongest
primary afferents synapse onto inhibitory interneurons - synapse onto surrounding afferents
a neuron activating strongly inhibits its neighbours

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6
Q

Mechanism of Seizures

A

initiation, propagation, termination

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7
Q

initiation

A

high frequency bursts of action potentials
hypersynchronization of a neuronal population
sustained neuronal depolarization → burst of action potentials driven by Ca2+ influx through NMDA receptors
action potential releases glutamate which binds to AMPA and fires to dislodge Mg2+ from NMDA = amplification of excitatory effect

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8
Q

propagation

A

normally prevented by hyperpolarization and surround inhibition but overcome by sufficient activation
increased extracellular K+ blunts hyperpolarization
Ca2+ accumulation in presynaptic terminals = increased NT release
depolarization activates NMDA receptor to increase Ca2+ influz and increase neuronal activation

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9
Q

termination

A

seizures gradually resolve spontaneously
loss of ion gradients
depletion of ATP
depletion of NT
activation of inhibition (GABA)

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10
Q

status epilepticus

A

a seizure that lasts more than 5 minutes
life threatening
over excitation - neuronal death

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11
Q

postictal period

A

5-30 minutes after seizure
drowsiness, confusion, depression/anxiety
increased inhibition response to excitation

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12
Q

classes

A

where they initiate + how widely they propagate

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13
Q

focal seizures

A

localized + don’t propagate far
simple: retain consciousness
complex: lose consciousness
jerking activity, automatisms
can become generalized

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14
Q

generalized seizures

A

propagation across entire brain
loss of consciousness (complex) + without warning
tonic-clonic: sustained contraction of muscles followed by alternating contraction and relaxation
myoclonic: bried shock like contraction of muscles

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15
Q

non-convulsive seizures

A

absence seizure: abrupt onset of impaired consciousness - lose consciousness but don’t fall
atonic seizures: sudden loss of muscle strength - fall but don’t lose consciousness

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16
Q

anti-seizure drugs

A

used chronically to treat epilepsy
block ionic conductance, block neurotransmitter release, inhibit/activate postsynaptic membrane

17
Q

enhance inhibitory neurotransmission

A

affect GABA

18
Q

benzodiazepines

A

positive allosteric modulator of GABA-A receptors
increase frequency GABA-A opens (increases GABA potency)
no effect in absence of GABA

19
Q

barbiturates

A

positive allosteric modulator of GABA-A receptors
increase duration GABA-A is open for (increases GABA efficacy)
in absence of GABA, acts as agonist

20
Q

vigabatrin

A

inhibits GAMA aminotransaminase

21
Q

tiagabine

A

inhibits GABA transporter = longer action of NT

22
Q

diminish excitatory neurotransmission

A

limits excitation of neurons

23
Q

carbamazepine

A

blocks voltage-gated Na+ channels by causing conformational change of inactivation gate

24
Q

gabapentin

A

inhibits voltage-gated Ca2+ channels by binding to alpha2 subunit

25
Q

perampanel

A

non-competitive antagonist at AMPA receptor
blocks excitation
narrow therapeutic window