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Neurology > Seizure Discord > Flashcards

Seizure Discord Flashcards

1
Q

What are seizures?

A

sudden and excessive excitation and synchronization of a population of cortical neurons in the brain that cause a variety of clinical manifestation

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2
Q

epilepsy

A
  • a disease of spontaneous recurrent seizures
  • random firing of cells (abnormal neurons undergo prolonged depolarizations with rapid firing
  • abnormal synchronization
  • altered neuronal microenviornment - imbalance btwn exictatory and inhibitory signals
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3
Q

epoleptogeneisis

A

sequence of events that converts a normal neuronal network into an epileptic network

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4
Q

what is the prevalence of epilepsy?

A
  • prevalence of 1-3% in lifetime
  • third most common neurological disorder (localized- focal or partial; spread to cause a secondary generalized seizure; affect all cortical neurons)
  • highest frequency of ID in children under 5 and adults over 65
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5
Q

Whats an EEG?

A
  • graphical depiction of cortical electrical activity – recorded from the scalp
  • advantage of high temporal resolution but poor spatial resolution of coritcal disorders
  • EEG- important neurophysiological study for diagnosis, prognosis, and treatment of epilepsy
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6
Q

What are EEG abnormalities?

A

Background activity:
* slowing not consitent with behavioral state
* significant asymmetry
Transients abnormalities/discharges:
* spikes
* sharp waves
* spike and slow wave complexes
* may be focal, lateralized, or generalized

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7
Q

What causes epilepsy?

A
  • largely >60% idiopathic (unknown)
  • children: congenital malformations, perinatal injuries or hypoxia, developmental neruologic disorders, metabolic defects, injury, and infection, hormonal imbalance
  • young adults: head trauma, brain tumors, infection, and arteriovenous malformations
  • elderly: cerebrovascular disease, CNS degenerative disease, and brain tumor
  • genetic- increased risk by 2-3x with first degree relative connection
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8
Q

Whats the general model for seizure triggers?

A
  • imbalance of exictatory (glutamate) and inhibitory (GABA) signals
    siezure triggers:
  • EPSPs
  • Na+ influx
  • Ca++ currents
  • paroxysmal depolarization
    control:
  • IPSPs
  • K+ Efflux
  • Cl- influx
  • pumps
  • low pH
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9
Q

What are the mechanisms of generating hyper-excitable networks?

A
  • excitatory axonal “sprouting”
  • loss of inhibitory neurons
  • loss of excitatory neurons “driving” inhibitory neurons
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10
Q

what are extrinsic factors modifying neuronal exictability?

A
  • changes in extracellular ion concentrations
  • remodeling of synapse location or configuration by afferent input
  • modulation of transmitter metabolism or uptake by glial cells
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11
Q

What are the two types of GABA recpetors?

A
  • GABAA: post synaptic, specific recognition sites, ligand-gated Cl- channel
  • GABAB: presynaptic GPCRs, simulate opening of K+ currents causing hyperpolarizatoin
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12
Q

what can decrease synthesis of GABA?

A

changes in astrocytes

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13
Q

What can cause convulsions in experimental animals?

A

glutamate and selective agonsits of NMDA-, kainite- & AMPA- receptors

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14
Q

What receptors are enhanced in patients with temporal lobe epilespy?

A

NMDA receptors

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15
Q

Increase in what is observed druing seizures?

A

Increased glutamate, a major excitatory neurotransmitter, release

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16
Q

What are the two groups of glutamate receptors?

A

Ionotropic- fast synaptic transmission
* NMDA, AMPA, kainite
* Ligand gated Na+/K+ and Ca++ channels

Metabotropic- slow synaptic transmission
* regulation of second messengers- GPCRs (cAMP and inositol)
* Modulation of synaptic activity

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17
Q

What are modulators of glutamate receptors?

A
  • Glycine
  • polyamine sites
  • zinc
  • redox site
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18
Q

What happens when an epileptogenic focus is in a state of partial depolarization?

A
  • high frequent bursts of action potentials
  • hypersynchonization of a neuronal population
  • membranes of these cells have increased ionic permeability– susceptible to activation by stimuli
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19
Q

What does a general model of siezures look like?

A
  • population of pathologically excitable neurons
  • increase in excitatory glutamtergic activity through recurrent connections- spread discharge
  • reduction in activity of normally inhib GABA projections
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20
Q

What is evidential of the pathophysiology of seizures?

A
  • Decreased binding of GABA and benzos
  • decreased Cl- currents in response to GABA
  • decreased glutamate decarboxylase activity– synthesizes GABA
  • interfere with GABA causes seizures
  • increased sensitivity to excitatiry amino acid transmission
  • progressive increase in glutamate release during kindling
  • increased glutamate and aspratate
  • upregulation of NMDA receptors in kindled rats
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21
Q

What can happen in the brain if cortical excitations go unchecked?

A
  • spreads to the adjacent cortex and contralateral cortex (interhemispheric pathways) and to anatomically and functionally related pathways in subcortical nuclei
  • clinical manifestations of seizures begin– signs depned on where in the brain seizure originates
22
Q

What are the 4 classifications of epilepsy?

A
  • focal
  • generalized
  • generalized and focal
  • unknown
23
Q

What are the two types of focal seizures?

A
  • Focal with retained awareness
  • focal impaired awareness
24
Q

What does a focal seizure mean?

A

local onset that can be determined

25
Q

What is a focal seizure with retained awareness?

A
  • focal with minimal spread of abnormal discharge
  • normal consioudness and awareness are maintained
26
Q

What is a focal seizure with impaired awareness?

A
  • local onset, then spreads
  • impaired consciousness
27
Q

How do clinical manifestations of focal seizures vary?

A
  • vary with site of origin
  • degree of spread
  • presence and nature of aura
  • automatisms
  • other motor activity
28
Q

What is the most common focal seizure?

A

temporal lobe epilepsy

29
Q

What are the generalized seizures?

A
  1. generalized tonic-clonic sz
  2. absence sz
  3. clonic and myoclonic sz
  4. tonic/atonic sz
  5. febrile
  6. status epilepticus
30
Q

What is a bilateral tonic-clonic seizure?

A
  • begins focally
  • with or without focal neurological symptoms
  • variable symmetry, intensity and duration of stiffening and jerking phases
  • 1-2 min
  • postictal confusion and somnolence
31
Q

generalized tonic-clonic seizures?

A
  • recruitment of neurons thru cortex
  • convulsions occur in all gneralized tonic-clonic seizures
  • tonic: muscles tense
  • clonic: muscles contract and relax rapidly
32
Q

absence seizures?

A
  • sudden onset and abrupt cessation
  • consiousness altered
  • associated with mild clonic jerking of eyelid or limbs
  • postural tone changes
  • non convulsive
33
Q

myoclonic seizures?

A
  • myoclonic jerking
34
Q

atonic seizures?

A
  • sudden loss in postural tone
  • most often in children
35
Q

febrile seizures?

A
  • fever provoked - usually by age 6
  • possible circulating toxins and immune reactions trigger excitability
  • Interluekin modify excitatory NT function
  • ion channels and currents are temperature dependent
36
Q

status epilepticus?

A
  • more than 5 min of continuous seizure
  • two or more seizures back to back without full recovery btwn them
37
Q

what are triggers for seizures?

A
  • hypoglycemia (low glucose)
  • hypoxia
  • hyponatremia (low Na)
  • low blood calcium
  • hyperthermia
  • pH changes
  • kidney or liver failure
  • hormonal changes/preganancy
38
Q

how does trauma trigger seizures?

A
  • moderate- severe brain injuries can cause pottraumatic epilepsy
  • occur from contusion area
  • increase in exitatory amino acids after brain injury
39
Q

what is the goal of antiepileptic drugs?

A
  • treat symptoms of seizures
  • maximize quality of life by minimizing seizure and ADRs
40
Q

what are three strategies used in treatment?

A
  • increase GABA transmission
  • stabilize membrane, prevent depol by action on ion channel
  • decrease EAA transmission
41
Q

which 8 drugs increase GABA?

A
  1. barbituares
  2. benzos
  3. gabapentin
  4. levetiracetam
  5. tiagabine
  6. topiramate
  7. valproate
  8. vigabatrin
42
Q

what 4 drugs decrease Ca++?

A
  1. ethosuximide
  2. levetiracetam
  3. pregablin
  4. valproate
43
Q

what 6 drugs decrease Na+?

A
  1. carbamazepine
  2. lamotrigine
  3. oxcarbazepine
  4. phenytoin
  5. topiramate
  6. valproate
44
Q

what are characteristics of ideal anti-epileptic drugs?

A
  • suppress seizures NOT causing sedation or CNS toxicity
  • well tolerated/highly effective
  • avoid undesirable side effect on vital organs
  • rapid onset
  • long duration
45
Q

what are general facts about AEDs?

A
  • good oral absorption and bioavailablity
  • metabolized in liver but some excreted unchanged in kidneys
  • more severe CNS sedation
  • best drug chosen my minimal side effects
46
Q

what are 8 side effects of ADEs?

A
  1. sedation (barbituates)
  2. cosmetic (phenytoin)
  3. weight gain (valproic acid, gabapentin)
  4. weight loss (topiramate)
  5. reproductive fucntion (valproic acid)
  6. cognitive (topiramate)
  7. behavioral (felbamate, leviteracetam)
  8. allergic
47
Q

what does a GABAa receptor complex do normally?

A

increase Cl- conductance into cell

48
Q

Which drugs effect sodium channels?

A
  • carbamazepine
  • phenytoin
  • topiramate
  • lamotrigine
  • valproate
  • zonisamide
49
Q

How do ADEs effect sodiums channels?

A
  • prolong inactivation of Na+ channels
  • reduce ability to fire at high frequencies
50
Q

what drugs effect ca2+ channels?

A
  • valproate
  • ethosuximide
51
Q

how do ADEs block Ca2+ channels?

A
  • reduce flow thru T-type Ca2+ channels
  • reduce pacemaker current in generalized absence seizures
52
Q

what are 2 glutamate targets?

A
  • NMDA receptors
  • AMPA receptors

Neurology (6 decks)

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