lecture 46 Flashcards

yang - pathophysiology of seizure disorders

1
Q

what is the definition of a seizure?

A

paroxysmal disorder of the CNS characterized by abnormal cerebral neuronal discharge with or without loss of consciousness

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2
Q

what is a paroxysm?

A

sudden attack or outburst

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3
Q

what is a convulsion?

A

specific seizure type where the attack is manifested by involuntary muscle contractions

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4
Q

what is epilepsy?

A

repeated seizures due to damage, irritation, and/or chemical imbalance in the brain which leads to a sudden, excessive, synchronous electrical discharge

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5
Q

what is synchronized hyperexcitability?

A

basis of a seizure
disordered, synchronous, and rhythmic firing of a population of brain neurons

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6
Q

how does cell ischemia result from seizures?

A

during a seizure the brain uses more energy than it can manufacture
prolonged seizures result in cell ischemia

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7
Q

what are three types of seizures?

A

focal onset
generalized onset
unknown onset

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8
Q

what are the classifications that focal onset seizures can take?

A

aware | impaired awareness
motor onset | non-motor onset

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9
Q

what can focal onset progress to?

A

focal to bilateral tonic-clonic

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10
Q

what can generalized onset be classified into?

A

motor –> either tonic clonic or other motor
non-motor –> absence seizures

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11
Q

what can unknown onset be classified into?

A

motor –> either tonic clonic or other motor
non-motor
unclassified

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12
Q

what is basis of focal onset seizures?

A

only part of the brain affect – focally in the cortical region (ie temporal lobe)
frequently progress to generalized seizures (focal to bilateral)
makes up 60% of seizures

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13
Q

what is the basis of generalized onset seizures?

A

most are presumed to be genetic

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14
Q

what genes may indicate infantile epilepsy?

A

GARBRA 1/2/3
GARBRG 2
SCN1A/B
SCN 2A
SCN8A

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15
Q

how does a focal seizure transition into generalized?

A

seizure activity spreads from a focus in one part of the brain then progresses to a secondary generalized seizures via projections to the thalamus

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16
Q

what is the pathophysiology of primary generalized seizures?

A

propagate via diffuse interconnections between the thalamus and cortex (no discrete focus)
earliest clinical signs show involvement of both brain hemispheres

17
Q

what appears on an EEG for focal/generalized seizures?

A

focal –> focal sharp waves over right temporal area
generalized –> show involvement of both hemispheres

18
Q

what is the aware type of focal seizures?

A

previously refered to as simple partial
no loss of consciousness with limited convulsions and limited sensory disturbances
subjective experiences like auras also occur

19
Q

what is the impaired awareness of focal?

A

previously referred to as complex partial
clouding of consciousness with repetitive motor behaviors (known as automatism for which pt has no memory)
aura is common
postictal state due to impaired awareness

20
Q

what is a postictal state?

A

occurs during impaired awareness focal
experience confusion, disorientation, and anterograde amnesia

21
Q

what is absence typical type of generalized seizures?

A

petit-mal
brief loss of consciousness but no convulsions, aura, or postictal period
may not realize it after the seizures

22
Q

what is the absence atypical type of generalized seizures?

A

slower onset than typical and more difficult to control than typical

23
Q

what is another name for a generalized tonic-clonic seizure?

A

grand mal
most dramatic of all epileptic seizures

24
Q

what is the main focus of each phase of grand mal seizures?

A

first: tonic - no aura
second: clonic - jerking
stuporous - after jerking

25
Q

what characteristic is common when a focus seizure turns into a focal to bilaterial tonic-clonic seizure?

A

brief aura

26
Q

what is the therapeutic goal of status epilepticus?

A

bring seizures under control within 60 minutes

27
Q

when should drug therapy be withdrawal?

A

in pts who have been clinically free of seizures for 2-5 years

28
Q

what is SUDEP?

A

sudden unexpected death in epilepsy

29
Q

what is paroxysmal depolarizing shift (PDS)?

A

a large depolarization that triggers a burst of action potential

30
Q

how does depolarization occur in the PDS?

A

activation of AMPA and NDMA channels by the excitatory Nt glutamate and voltage-gated calcium channel leading to an influx of cation (Ca2+ ions)

31
Q

how does hyperpolarization occur in PDS?

A

involves the activation of GABA receptors (influx of chloride ions) and voltage and calcium-dependent K+ channels, leading to an efflux of K+

32
Q

how does GABA influence the tonic phase?

A

GABA-mediated inhibition disappears and glutamate-mediated AMPA and NMDA receptor activity increases. (via the influx of cation ions)

33
Q

how GABA influence the clonic phase?

A

GABA-mediate inhibition (Via the influx of Cl- ions) gradually returns –> period of oscillation

34
Q

what can trigger status epilepticus?

A

withdrawal from AEDs, especially sudden d/c

35
Q

what are drugs that aggravate or increase the risk of seizures?

A

alcohol
theophylline
CNS stimulants
bupropion
OC
withdrawal from depressants
Clozapine