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Neuro > Status epilepticus State of Art Review > Flashcards

Status epilepticus State of Art Review Flashcards

1
Q

Epileptic seizure is defined

Status epilepticus (SE) is commonly defined

A
  • hypersynchronous neuronal electrical activity in
  • cerebral cortex
  • manifests as a paroxysmal and transient abnormality of consciousness, motor activity, autonomic function, sensation, or cognition

seizure activity that lasts for more than 5 minutes, or the occurrence of 2 or more seizures without recovery of consciousness

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2
Q

Refractory status epilepticus is defined

Superrefractory status epilepticus is defined as

acute repetitive seizures
aka

A

SE that does not respond to first‐line anticonvulsant therapy

SE continuing or recurring more than 24 hours after initiation of treatment with anesthetic therapy

occurrence of 2 or more distinct seizures within a 24‐hour period
cluster seizures

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3
Q

Status epilepticus has been identified in ____ of dogs presenting to the hospital for seizure activity and was the first manifestation of a seizure disorder in ____ of dogs

A

16.5%

58%

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4
Q

Status epilepticus of longer duration is less

A

responsive to anticonvulsant therapy compared to SE of shorter duration

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5
Q

Seizures result from

any event that disrupts the balance between

A

spontaneous, excessive, hypersynchronous electrical discharge from a group of neurons in cortical tissue

neuronal excitation & inhibition can cause a seizure

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6
Q

proposed that SE develops due to

A

failure of inhibition or excessive stimulation

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7
Q

major inhibitory neurotransmitter is
3 categories:
Binding of GABA to GABA‐A receptors causes

A

GABA
GABA‐A, GABA‐B, and GABA‐Aρ
chloride influx and hyperpolarization of the cell
- GABA‐A agonists - benzodiazepines and barbiturates can terminate seizure activity.

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8
Q

GABA‐B receptor is a G‐protein coupled receptor-

A

ligand binding opens K channels and closes Ca++, which leads to hyperpolarization of the membrane

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9
Q

prolonged seizure activity =

A

diminished inhibitory effects of GABA -receptors become less effective

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10
Q

major excitatory neurotransmitters

2 main types of glutamate receptors are

N‐methyl‐d‐aspartate (NMDA) receptors are what type of receptors:
drugs:

A

glutamate
aspartate
acetylcholine

inotropic -AMPA, NMDA
metabotropic

inotropic glutamate

methadone, ketamine

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11
Q

inotropic NMDA channels cause:

Metabotropic glutamate receptors use:

A

influx of Na & Ca++
= depolarization of membrane and AP generation

second messenger system to increase inward currents of Na & Ca++ = leads to depolarization

Kainite, AMPA, and NMDA agonists shown to stimulate seizure activity

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12
Q

one MoA of drug resistance is overexpression of:

P‐glycoprotein is a multidrug transport protein encoded by the gene:

is found in:

functions as:

It is thought

what causes Pgp upregulation

A

P‐glycoprotein

MDR1

capillary endothelial cells o BBB

ATP‐dependent efflux pump - Ab, immunosuppressive agents, and possibly lipophilic anticonvulsant drugs

thought that overexpression of Pgp enables resistance to anticonvulsant therapy by prohibiting uptake of these medications into the CNS at therapeutic level

NMDA receptors & COX‐2

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13
Q

SE is characterized by:

hippocampal neurons can occur even if the initiating seizure focus is:

Neuronal death is mainly mediated by excitatory neurotoxic effects -

A

neuronal cell necrosis, gliosis, and network

not located in the hippocampus

glutaminergic receptor overstimulation
=cellular calcium influx, which triggers a sequence of events that result in apoptosis or necrosis

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14
Q

MoA cerebral edema:
vasogenic MoA

cytotoxic MoA:

A

Seizure foci have high metabolic demands
= increased blood flow
-this hyperperfusion =disrupt BBB
= vasogenic edema

excessive glutamate = cytotoxic edema

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15
Q

Transient periictal MRI abnormalities are

A

brain MRI signal abnormalities attributable to seizure activity and may totally or partially resolve on follow‐up

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16
Q

Systemic effects of status epilepticus

phase I, or compensated SE:

Phase II, or uncompensated SE:

A

Systemic effects of status epilepticus

  • increase in SNS activity occurs secondary to seizure
  • > catecholamines & cortisol = hypertension, tachycardia, hyperglycemia, hyperthermia, and ptyalism
  • cerebral metabolic demand is high, and cerebral blood flow is increased to maintain oxygen delivery to the brain. -can cause cardiac arrhythmias, acidosis, rhabdomyolysis, hypotension, shock, NCPE

after 30 minutes

  • cerebrovascular autoregulation fails
  • > ICP
  • systemic hypotension and autonomic dysfunction occur, leading to decreased cerebral blood flow
  • body is unable to compensate for the persistently high cerebral metabolic demand
  • hypoglycemia, hyperthermia, hypoxia, respiratory failure, acidosis, hyperkalemia, hyponatremia, and uremia
17
Q

Sudden unexpected death in epilepsy (SUDEP) def.:

source of epileptic deaths

A

defined in human epileptics as “the sudden, unexpected, witnessed or unwitnessed, nontraumatic, and nondrowning death of a patient with epilepsy

  • **with or without evidence of a seizure, excluding documented status epilepticus
  • PM no structural or toxicological cause of death.”

15%

18
Q

MoA:

MORTality in Epilepsy Monitoring Units Study (MORTEMUS) aimed to characterize events:

may be under recognized in vet med

A

unknown
may be due to an abnormality of breathing, CV dysfunction, arousal deficits ( seizure progressive to ascending arousal system in brainstem and depressing it)

=centrally mediated alteration of both respiratory and cardiac functions after generalized tonic‐clonic seizures

all occur post generalized convulsive seizure

  • tachypnea began after a seizure, followed by apnea, bradycardia, and postictal generalized electroencephalogram (EEG)
  • profound flattening of the EEG recording that occurs after seizure activity
  • apnea always occurred before terminal asystole
  • majority of events (14/16) observed occurred at night
19
Q

hereditary basis for epilepsy dogs

term unknown or presumptive unknown epilepsy be used in cats

A

Labrador Retrievers, German Shepherd Dogs, Golden Retrievers, Bernese Mountain Dogs, Belgian Tervurens, Vizslas, Keeshonds, English Springer Spaniels, and Border Collies

20
Q

SE was more frequently associated with

genetic/unknown epilepsy more likely to

___—___% of dogs that presented in SE had no prior documented seizure activity

A

structural‐metabolic epilepsy

cluster but NOT SE

44% - 58% (another study)

21
Q

new classification

A

Genetic: seizures are result of a known or presumed genetic defect.

Structural‐metabolic: structural or metabolic disease that is confirmed to be associated with an increased risk of developing epilepsy.

Unknown: underlying etiology unknown; could be fundamentally genetic or result from an unidentified structural or metabolic disorder.

22
Q

dx. CSE vs NCSE

ppl NCSE defined as:

presents as:

common in:

A

convulsive SE (CSE) or nonconvulsive SE (NCSE).

majority of small animals CSE

defined as EEG evidence of seizure activity without the clinical appearance

2 primary phenotypes

  1. ambulatory patients who present in states of confusion with or without subtle twitches - termed to be in “walking status”
  2. severely impaired level of consciousness that display very subtle, if any, overt motor manifestations of seizure activity. These patients have been referred to as the ictally comatose “subtle status

critically ill patients

23
Q

vet med NCSE

% in humans

how to dx:

A
  • underrec bc not using EEG commonly
  • humans - NCSE in 21% of patients; 25% of these patients had prior seizures

index od suspicion
EEG
should be considered in any patient with a prolonged postictal state

24
Q

cats > 7 yrs

A

3.5 times more likely structural‐metabolic epilepsy vs unknown/idiopathic epilepsy

25
Q

depressed level of consciousness ddx:

A
  1. post-ictal
  2. underlying structural or metabolic
    cytotoxic edema (glutamate overstim NMDA = Ca++ necrosis apotosis)
  3. NCSE, though NCSE can only be confirmed with EEG
  4. AED
26
Q

index of suspicion for structural‐metabolic epilepsy if:

A

persistent, focal, interictal neurological deficits for ≥48 hours following cessation of seizure

27
Q

EEG

A

helpful to discriminate nonepileptic paroxysmal disorders, such as cardiogenic syncope

28
Q

describe Reversible MRI abnormalities have been documented in dogs as a consequence of seizure activity:

lesions will improve or resolve in many patients over a period of

A

represent vasogenic and cytotoxic edema

bilaterally symmetrical T1‐hypointense and T2‐hyperintense lesions with a predilection
temporal
pyriform lobes

may also be observed in the cingulate gyrus and hippocampus

1–18 weeks

Neuro (7 decks)

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