Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

M2 Neuron Brain Behavior > 9/29 Seizures/Epilepsy - Bhise > Flashcards

9/29 Seizures/Epilepsy - Bhise Flashcards

You may prefer our related Brainscape-certified flashcards:
The Brain flashcards
1
Q

terminology:

ictal

post-ictal

interictal

A

ictal: during a seizure

post-ictal: immediately following seizure

interictal: time between seizures

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Todd’s paresis

A

post-ictal contralateral hemiparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

epileptiform

A

on EEG, discharge with appearance of being potentially epileptogenic (spike or sharp wave)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

seizure

A
  • transiet episode with signs/sx of abnormal excessive synchronous neuronal activity in brain
  • physical manifestations vary based on pattern of network involvement in brain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

mapping old terminology to current terminology

grand mal

petit mal

A

grand mal → generalized

petit mal → focal/partial onset/absent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

seizure classification

two general types

multiple subtypes

A

1. general

  • tonic-clonic
  • tonic: only stiffening
  • clonic: only rhythmic jerking
  • myoclonic: rapid brief jerks
  • atonic/astatic: loss of postural tone
  • absence: brief staring spells

2. focal/partial

  • simple partial: no altered consciousness
  • complex partial: alteration of consciousness
  • secondary generalized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

generalized tonic-clonic convulsion

A

bilateral tonic stiffening of extremeties alternating with clonic jerking

  • impaired consciousness
  • sympathetic sx: tachycardia, mydriasis
  • mild cyanosis at mouth, distal extremities
  • foaming at mouth
  • urinary incontinence
  • lateral tongue biting
  • post-ictal fatigue, weakness, amnesia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

simple partial seizure

A

type of focal/partial seizure

  • manifestation related to brain region involved
  • may be an aura
  • no alteration of awareness
  • may progress into a CPS or GTC seizure
  • post-ictal deficit maybe seen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

complex partial seizure

A

typical presentaiton: staring and alteration of awareness

  • possible gaze deviation, forced head deviation, or unilateral/asymmetric limb involvement
  • possible automatisms
  • might progress into GTC seizure
  • might see post-ictal deficit

often no recal of most of event

EARLIEST manifestation helps localize the source brain region

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

secondary generalized seizure

A

seizure activity beginning in one part of brain that spreads to involve the rest

transition may be slow over minutes OR fast and appear “generalized” at onset

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

symptomatic causes of seizure: categories

A
  1. metabolic-toxic
  2. structural
  3. benign
  4. genetic
  5. abnormal substrate
  6. rare causes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

symptomatic causes

metabolic toxic seizure

A
  • electrolyte imbalance
  • ingestion
  • medication-induced
  • rapid withdrawal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

symptomatic causes

structural

A
  • head trauma
  • stroke
  • anoxia
  • meningitis/encephalitis
  • tumor
  • brain malformation (AVM, cortical dysplasia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

symptomatic causes

benign

A
  • fever(children)
  • post syncopal
  • contact
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

symptomatic causes

abnormal substrate

A
  • autism
  • other genetic disorder
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

symptomatic causes

rare causes

A
  • inflammatory
  • degenerative
  • inborn error of metabolism
17
Q

mechanism of seizure

forces involved

concept of seizure threshold - how?

A

excitation

  • ionic currents: Na, Ca INWARDS
  • nt: glu, asp

inhibition

  • ionic currents: Cl INWARD, K OUTWARD
  • nt: GABA

in seizure, excitation >> inhibition

  • excitability to the extent that a seizure is produced occurs due to reduced seizure threshold

how?

  1. hypersynchronization (synaptic connectivity leading to propagation)
  2. inability to self-terminate (failure of negative feedback or feed-forward loop)
  3. changes in extracellular environment
  4. synapse chanel remodeling → permanency!
18
Q

mechanism of genetic epilepsies

A

genetic epilepsies code for proteins in ion channels

→ ion flow is affected (overexcitable or low inhibition)

19
Q

parts of the brain that are particularly prone to seizing activity

A

cerebral cortex and hippocampus particularly prone to synchronized bursts of activity

  • strong recurrent excitatory connections
  • intrinsically burst-generating neurons
  • ephaptic interactions among closely spaced neurons
  • synaptic plasticity
20
Q

epilepsy

A

disorder of the brain that results in seizures that are:

  1. recurrent
  2. unprovoked
  3. stereotyped
21
Q

seizure etiology

(classification)

A
  1. idiopathic → genetic
  2. symptomatic → structural/metabolic
  3. cryptogenic → unknown
22
Q

idiopathic seizures

A
  • genetic in nature without brain insult
  • probably polygenic inheritance

ex. benign epilepsy with centrotemporal spikes, childhood absence epilepsy

23
Q

symptomatic seizures

A

clear/known brain insult causes seizures

ex. metabolic-toxic, fever, head injury, tumor, meningo-enceph, pre/perinatal ischemic/anoxic injury, neuronal migration defect

24
Q

cryptogenic seizures

A

no evidence of a known brain insult or documented testing abnormality

  • test for: metabolic, radiologic, genetic evals
  • usually see degeneration, progression, regression
  • ex. infantile spasms
25
Q

genetics of seizures

A

most often polygenic and multifactorial

  • single gene can cause epilepsy syndrome
  • single gene can cause multiple syndromes or non-seizure disorders (ex. movement disorders)
  • diff genes (monogenic), may cause a single epilepsy syndrome

typically involve ion channels: Na, Ca, GABA, K

26
Q

localization of seizures and effects seen

  • temporal: medial vs lateral
  • frontal: dorsofrontal, SMA, orbitofrontal
  • parietal
  • occipital
A

temporal

  • medial: staring, automatism, posturing, fear
  • lateral: staring, vertigo, hearing

frontal: brief, bizarre, nocturnal

  • dorsolateral: contralateral vision
  • SMA: fencing posture
  • orbitofrontal: elaborate, sounds, smells

parietal: sensory

occipital: formed visual phenomena

27
Q

EEG

A

measures electrical activity over scalp generated by the cortex

  • captures wakefulness, drowsiness, stage2 sleep
    • epileptiform activity commonly activated in stage2 sleep
28
Q

when would you get an MRI of brain?

A

patients with evidence of focality in seizures

  • looking for underlying structural lesion (encephalomalacia, cortical dysplasia, stroke, tumor, AVM, etc)
29
Q

absence seizures

A
  • multiple events daily (could be > 100 daily)
  • usually 10s or less, triggered by hyperventilation, return to full awareness
    • often unnoticed
    • might have subtle automatisms during seizure
  • can contribute to poor academic performance

EEG: 3 Hz spike and wave

30
Q

Lennox Gastaut

A

starts between infancy-14yo

  • most common in 2-3yr old
  • more in boys

multiple seizure types seen

  • axial tonic
  • atonic
  • atypical absence

cognitive impairment or regression

EEG: slow spike and wave, GPFA seizures

tx: tough to control

31
Q

infantile spasms

when/who?

symptoms?

EEG

tx?

A

onset: 3-18months
* children with trisomy 21 or tuberous sclerosis more susceptible

characteristics

flexor, extensor, or combo events in clusters around sleep-wake transition

West syndrome: combo of spasms, hyparrhythmia, devpt regression

EEG shows hypsarrythmia: chaotic, high ampl, multifocal apikes, electrodecrement

idiopathic, symptomatic, or cryptogenic

tx: ACTH, vigabatrin, steroids, ketogenic diet

32
Q

benign rolandic epilepsy

A

most common type of childhood epilepsy

ages 4-15, most commonly 7yo

symptoms

  • nightime focal onset or rapid secondary generalized seizure
  • speech arrest, drooling, gurgling, facial tonic-clonic activity, facial hemisensory
  • infrequent seizures
  • cognitive problems (often with language)

EEG: bilateral independent centrotemporal spikes

good outcomes! likely to outgrow, so practitioners might choose not to treat

  • if do treat, treat following second seizure
33
Q

Wada test

A
  • injection of anesthetic into R or L internal carotid artery
  • test each hemisphere for memory and language
34
Q

status epilepticus

A

one continuous seizure > 30 min

OR

recurrent seizures without regaining consciousness between seizures for over 30 min

35
Q

acute management of status epilepticus

A
  1. ABCs
  2. IV lorazepam or diazepam
  3. fosphenytoin
  4. phenobarbital or valproic acid
  5. versed drip or pentobarbital coma

M2 Neuron Brain Behavior (53 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions