9/29 Seizures/Epilepsy - Bhise Flashcards

(35 cards)

1
Q

terminology:

ictal

post-ictal

interictal

A

ictal: during a seizure

post-ictal: immediately following seizure

interictal: time between seizures

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2
Q

Todd’s paresis

A

post-ictal contralateral hemiparesis

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3
Q

epileptiform

A

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

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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
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5
Q

mapping old terminology to current terminology

grand mal

petit mal

A

grand mal → generalized

petit mal → focal/partial onset/absent

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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
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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
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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
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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

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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

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11
Q

symptomatic causes of seizure: categories

A
  1. metabolic-toxic
  2. structural
  3. benign
  4. genetic
  5. abnormal substrate
  6. rare causes
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12
Q

symptomatic causes

metabolic toxic seizure

A
  • electrolyte imbalance
  • ingestion
  • medication-induced
  • rapid withdrawal
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13
Q

symptomatic causes

structural

A
  • head trauma
  • stroke
  • anoxia
  • meningitis/encephalitis
  • tumor
  • brain malformation (AVM, cortical dysplasia)
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14
Q

symptomatic causes

benign

A
  • fever(children)
  • post syncopal
  • contact
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15
Q

symptomatic causes

abnormal substrate

A
  • autism
  • other genetic disorder
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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
genetics of seizures
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
localization of seizures and effects seen * temporal: medial vs lateral * frontal: dorsofrontal, SMA, orbitofrontal * parietal * occipital
**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
EEG
measures electrical activity over scalp generated by the cortex * captures wakefulness, drowsiness, stage2 sleep * epileptiform activity commonly activated in stage2 sleep
28
when would you get an MRI of brain?
patients with evidence of focality in seizures * looking for underlying structural lesion (encephalomalacia, cortical dysplasia, stroke, tumor, AVM, etc)
29
absence seizures
* 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
Lennox Gastaut
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
infantile spasms when/who? symptoms? EEG tx?
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
benign rolandic epilepsy
**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
Wada test
* injection of anesthetic into R or L internal carotid artery * test each hemisphere for memory and language
34
status epilepticus
one continuous seizure \> 30 min OR recurrent seizures without regaining consciousness between seizures for over 30 min
35
acute management of status epilepticus
1. ABCs 2. IV lorazepam or diazepam 3. fosphenytoin 4. phenobarbital or valproic acid 5. versed drip or pentobarbital coma