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VET 433: Neurology > Seizures > Flashcards

Seizures Flashcards

(69 cards)

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1
Q

pyramidal neurons

A

excitatory neurons in the cerebral cortex

input comes from other neurons to stimulate or inhibit

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2
Q

feedforward inhibition

A

neurons send excitatory signals to inhibitory neurons that block the pyramidal neurons

overall INHIBITORY effect on pyramidal neuron

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3
Q

feedback inhibition

A

the effect of pyramidal neuron stimulation causes feedback inhibition on the same pyramidal neuron

overall INHIBITORY effect on pyramidal neuron

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4
Q

EPSPs (excitatory synaptic potentials)

A

signals generated by surrounding cortical input

EPSPs converge to initiate an action potential

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5
Q

glutamate

A

main EXCITATORY neurotransmitter

fast transmission via ionotropic receptors (Na and Ca ion channels)

slow transmission via metabotropic receptors

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6
Q

GABA

A

major INHIBITORY neuron

GABAa receptors: allows Cl- influx on the post-synaptic membrane

GABAb: mediated by K+ current; located on pre-synaptic membrane

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7
Q

epileptogenesis

A

the process by which a normal brain develops into an epileptic brain

due to genetic abnormalities or acute brain injury

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8
Q

intrinsic properties of seizure pathogenesis

A

focal zone of hyperexcitable neurons caused by a mutation in ion channels, receptors, second messengers, etc

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9
Q

extrinsic properties of seizure pathogenesis

A

changes in extracellular ion concentration, modulation of glial cell function, transmitter metabolism/uptake, invasion of inflammatory cells, network changes

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10
Q

focal epileptic seizures

A

abnormal electrical activity arises in a localized group of neurons

only ONE cortical region is firing abnormally

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11
Q

signs of focal epileptic seizures

A

ictal onset is consistent (signs stay the same in each seizure)

lateralized signs

  • motor: facial twitches, repeated jerking head movements, rhythmic blinking, repeated rhythmic jerks of one extremity
  • autonomic: dilated pupils, hypersalivation, vomiting
  • behavioral: anxiousness, restlessness, abnormal attention seeking, fear
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12
Q

generalized epileptic seizures

A

abnormal electrical activity arises in bilateral hemispheres

MULTIPLE cortical regions are firing abnormally

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13
Q

signs of generalized epileptic seizures

A

tonic, clonic, or tonic-clonic seizures

  • motor: bilateral
  • autonomic: hypersalivation, urination, defecation
  • behavioral: loss of consciousness
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14
Q

myoclonus

A

sudden, brief, involuntary single or multiple contractions of muscle or muscle group of various locations

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15
Q

atonic

A

sudden loss or diminution of muscle tone without preceding myoclonic or tonic event

involves head, trunk, jaw, or limb musculature

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16
Q

automatism

A

a coordinated, repetitive motor activity

usually occurs when cognition is impaired and subject is amnesic afterwards
(resembles involuntary movement)

orofacial: lip. smacking/pursing, chewing, licking, swallowing

pedal: running movements in distal limbs

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17
Q

focal to generalized epileptic seizures

A

abnormal activity arises in bilateral cerebral hemispheres

characterized by tonic, clonic, or tonic-clonic seizures (same as generalized)

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18
Q

what are the stages of seizures

A
  1. prodrome
  2. ictus
  3. post-ictus
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19
Q

prodrome

A

changes in behavior (anxiety, withdrawal, vocalization)

not always apparent
lasts minutes to days

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20
Q

ictus

A

rapid onset of tonic-clonic phases; can begin focally (facial twitches)

tonic: increased muscle tone/extension, loss of consciousness, pupils dilated
clonic: contraction and relaxation, jaw movements, autonomic signs

HIGH energy expenditure phase

lasts seconds to minutes

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21
Q

post-ictus

A

disorientation, aggression, or restlessness following ictus

may be transiently blind or deaf
lasts hours to days

can take up to 2-3 days to become back to normal

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22
Q

idiopathic epilepsy signalment

A

likely a genetic basis

breeds: spaniels, aussies, rotties, border collies, GSDs, dachshunds

age: 1-5 years (dogs), variable in cats

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23
Q

idiopathic epilepsy history

A

seizure episodes reported by owner

may have a NORMAL interictal neurologic exam
- if seizure was a few days ago - should be neuro normal
- if seizure was within 2-3 days - may still be in post-ictus and have deficits

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24
Q

structural epilepsy

A

epileptic seizures provoked by intracranial/cerebral pathology

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25
structural epilepsy signalment and history
age: <1 to >5 years (dogs), variable in cats history: seizures, mentation changes, altered behavior, loss of learned responses
26
structural epilepsy presentation
normal neurological exam - if abnormal - indicates signs of cerebral disease
27
syncope
NOT A SEIZURE can mimic an epileptic event caused by CV abnormalities does not usually have tonic-clonic contractions appears as falling to the ground and going limp
28
characteristics of seizures
1. abrupt onset and spontaneous cessation 2. cannot be interrupted 3. tonic-clonic movement 4. altered mentation 5. autonomic signs - salivation, urination, defecation, mydriasis 6. post ictal obtundation 7. present of intracranial/cerebral pathology
29
what is the definitive diagnostic for seizures
electroencephalogram (EEG) must be reading during the time of the abnormal brain activity - can do sedated or ambulatory
30
indications for using EEG
- age of epileptic seizure <6 months or >6 years - interictal neurologic abnormalities - status epilepticus or cluster seizures - idiopathic epilepsy not responding to medical management
31
AED therapy indications
1. identifiable structural lesions OR prior history of encephalopathy or trauma 2. acute, repetitive seizures - >or= 3 generalized seizures in 24 hours - status epilepticus 3. >or= 2 seizures in 6 months 4. prolonged, severe, or unusual post-ictal periods
32
what is the goal of AED therapy
reduce the frequency and severity of seizures want to have a >50% reduction
33
what drugs are AEDs
1. potassium bromide 2. levetiracetam (keppra) 3. phenobarbital 4. zonisamide
34
phenobarbital MOA
increases neuron responsivity to GABA by activating GABAa channels has an anti-glutamate effect by inhibiting Ca channels
35
how is phenobarbital metabolized
hepatic - induces CYP450 and ALP normal to see high ALP on serum chemistries
36
time to reach steady state of phenobarbital
takes 10-14 days to reach steady state
37
phenobarbital dosages
dogs: 3-5 mg/kg BID cats: 1-2 mg/kg BID
38
adverse effects of phenobarbital
PU, PD, PP sedation ataxia weight gain elevated ALP pseudohypothyroid
39
contraindications for phenobarbital
liver disease concurrent CYP450 inhibiting drugs
40
MOA of KBr
Br ion acts like a Cl ion and passes through Cl channels on post-synaptic GABAa receptors to hyperpolarize the membrane
41
how is KBr metabolized
renal
42
how long does it take KBr to reach steady state
very long - takes 3-4 months
43
dosage for KBr
20-35 mg/kg SID
44
adverse effects of KBr
PU, PD, PP sedation ataxia weight gain GI upset hyperreactivity bromism
45
contraindications for KBr
NOT for use in cats renal disease pancreatitis dogs that require rapid control of seizures
46
zonisamide MOA
sulfonamide derivative blocks Ca and Na channels on pre-synaptic side to reduce the amount of glutamate released into the synaptic cleft also binds Cl channels on GABAa receptors
47
how long does it take zonisamide to reach steady state
5-7 days
48
dosage for zonisamide
dogs: 5 mg/kg BID if concurrent phenobarbital: 10 mg/kg due to CYP450 induction
49
adverse effects of zonisamide
sedation, ataxia, GI upset, KCS, polyarthropathy, decreased T4
50
contraindications for zonisamide
pre-existing KCS
51
keppra MOA
binds synaptic vesicular protein that carries glutamate in order to prevent it from binding to pre-synaptic membrane for release
52
metabolism of Keppra
minimal hepatic metabolism mostly excreted in urine
53
time to reach steady state for Keppra
fast - reaches within 24 hours
54
dosage for keppra
20 mg/kg QID
55
adverse effects of keppra
well tolerated, very few adverse effects
56
efficacy of keppra
poor when given alone exception: feline audiogenic reflex seizures
57
status epilepticus
ictus lasting > 5 minutes OR >2 minutes without regaining consciousness requires IMMEDIATE intervention (causes primary brain injury --> neuronal cell death)
58
phase 1 SE
compensated SE increase in autonomic activity --> elevated catecholamines + steroids --> hypertension, tachycardia, hyperglycemia, hyperthermia, ptylatism causes arrhythmias, poor renal perfusion, rhabdomyolysis
59
phase 2 SE
uncompensated SE ~30 minutes following continuous ictus --> cerebrovascular autoregulation fails - causes increased ICP --> hypotension, hypoglycemia, hypoxia --> resp. failure, metabolic acidosis, hyponatremia, hyperkalemia RISK OF SUDDEN DEATH
60
cluster seizures
> or = 3 generalized seizures in 24 hours
61
when is it considered failure to regain consciousness
still unconscious 1-2 hours after ictus
62
goal of emergency seizure management
terminate and prevent future seizure activity, manage complications and underlying conditions causing the seizures
63
steps of emergency seizure management
1. benzodiazepienes 2. stabilize SE 3. long acting AEDs 4. diagnostics 5. monitoring
64
benzodiazepiene administration
midazolam: 0.2-0.5 mg/kg IV or IN diazepam: 0.5 mg/kg IV or 1-2 mg/kg per rectum
65
steps for stabilizing SE
- IV access - obtain BW: lytes, glucose, calcium - flow by O2 - BP (manage high ICP) - temperature (manage hyperthermia) if seizures do not stop after benzo administration --> repeat dose
66
when do you use long acting AEDs
once the benzodiazepienes have stopped the seizures
67
what AEDs are used in emergency situations
phenobarbital - takes longer to reach steady state; high risk of doing loading dose levetiracetam (keppra)
68
monitoring after emergency seizure management
24 hr monitoring q4 monitor pupil size and reactivity, posture, EEG general: temp, hydration, oxygenation, ventilation, HR, BP, recumbent care, bladder management
69
what are negative prognostic indicators for seizures
inflammatory brain disease loss of seizure control after 6 hr hospitalization development of partial SE

VET 433: Neurology (12 decks)

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