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Neuro Block 7 > Seizures > Flashcards

Seizures Flashcards

1
Q

Pathogenisis of seizures

A

Abnormal electrophysiolgical ctivity (cellular dysfunction)

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2
Q

Distribution of seizures

A

Focal or diffuse
Focal: seizures starts at 1 site, often spreads, can become diffuse
Diffuse: seizure activity starts with a diffuse distribution

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3
Q

Localization of seizures

A

Some common focal origins but also diffuse types

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4
Q

Temporal profile of seizures

A

Transient (except status epliepticus)

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5
Q

Clinical presentation of seizures

A
  • hyperactivity or hypoactivity of cortical neurons
  • convulsive (involuntary) motor movements
  • stereotypies: repetitive movements
  • loss of consciousness, with ot without later awareness of loss
  • aura: sometimes preceded by sensory hallucinations (blue to focal origin)
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6
Q

What can be a clue to focal origin

A

Aura

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7
Q

Scalp electrodes detect synaptic potentials in cortex

A

EEG

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8
Q

What does EEG detect

A

A population of neurons as generated by the excitatory or inhibitory post synaptic response of pyramidal neurons to excitatory or inhibitory input form DENDRITES

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9
Q

Positive signal in EEG

A

The EPSP occurring near the cell body generates inward electrical current (into the cell) and outward current (out of cell) near the cortical surface

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10
Q

Negative signal one EEG

A

The EPSP occurring near the tip of the dendrite generates inward electrical current (into the cell) and outward current (out of cell) near the cell body

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11
Q

What is the arrangement of electrodes

A

Standardized arrangement

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12
Q

Beta wave on EEG

A

Wake state: eyes open, active

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13
Q

Alpha EEG

A

Wake state, eyes closed, relaxed

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14
Q

Theta EEG

A

Drowsy/sleep

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15
Q

Delta EEG

A

Sleep

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16
Q

What is a normal EEG

A

Beta or alpha waves

Goes from frontal lobe down to occipital

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17
Q

Gerenalized (diffuse/bilateral) seizures

A

Sudden and widespread cortical origin ( no neuroanatomical focus)

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18
Q

What are the two different types of generalized (diffuse/bilateral) seizures

A 
Tonic clonic (grand mal)
Absence (petit mal)
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19
Q

Tonic clonic seizures

A
  • grand mal
  • consciousness interrupted
  • convulsive
  • too much firing, sometimes disoriented afterwards
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20
Q

Absence seizures

A
  • generalized (bilateral/diffuse)
  • petit mal
  • consciousness interrupted (unaware during seizure)
  • mostly blank stare
  • can show some subtle muscle contractions
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21
Q

Partial (focal) seizures

A

Cortical origin in one lobe or part of a lobe *neuroanatomical focus)

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22
Q

What subgroup of seizures has a neuranatomical focus

A

Partial (focaL)

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23
Q

What are the two different types of partial (focal) seizures

A

Simple focal

Complex focal

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24
Q

Simple focal seizure

A
  • partical (focal) seizure
  • consciousness maintained (aware during seizures)
  • common origin sites are motor and sensory regions (parahippocampus region)
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25
Q

Complex focal seizure

A
  • partial (focal) type of seizure
  • consciousness interrupted (unaware during seizure)
  • common origin: temporal lobe
  • spreads and beceoms generalized
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26
Q

What is the most common origin of complex focal seizures

A

Temporal lobe

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27
Q

Neural mechanism of tonic clonic seizures

A

Simultaneous “burst-firing” and synchronization of cortical neurons across cerebral cortex

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28
Q

Temporal profile of tonic clonic seizures

A

Sudden onset, renascent course (minutes)

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29
Q

Initial stage of tonic clonic seizures

A

Tonic

-stiffening, bilateral extension, often arched back

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30
Q

Second stage of tonic clonic seizures

A

Clonic

  • rhythmic
  • conclusive felxion/extension or ‘shaking’
  • chewing or biting motions
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31
Q

Consciousness in tonic clonic seizures

A

Loss of consciousness and initial post-vital phase

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32
Q

What do tonic clonic seizure EEGs lack

A

Beta and alpha waves

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33
Q

Pre-ictal waves for clonic tonic

A

Alpha and beta

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34
Q

Post-ictal waves

A

Hypoactivity, then recovery into alpha and beta

35
Q

Neural mechanism of absence seizures

A

Bilateral suppression of the thalamocortical projections of the reticular activating system, a system that normall sustains the conscious state. Possibly involves excessive inhibition of the centromedian and intralaminar nuclei by surrounding reticular thalamic nucleus

36
Q

Temporal profile of absence seizures

A

Sudden onset, transient course (seconds), but can be many times throughout the day

37
Q

Presentation of absence seizures

A
  • typically in children and adolescents
  • blank store with eyes open
  • sometimes muscle contractions in face or hands
  • loss of consciousness during seizure with rapid return to full awareness and normal cognitive function, but often unaware of lapse in consciousness
38
Q

What is the pattern of the EEG on someone with absence seizures

A

Spike and wave pattern

39
Q

What normally sustains the conscious state

A

Thalamocortical projections of the reticular activating system

40
Q

Current hypothesis on absence seizures

A

There is a feedback loop that promotes conscious state between the thalamocortical neuron and corticothalamic neuron (+ signals) and an inhibitory interneuron between the two. There is a problem with the interneuron.

Cortical feedback to reticular thalamic nucleus activates inhibitory internuerons which in turn inhibit thalamocortical projection neurons. The reticular thalamic nucleus neuron can also inhibit ascending input to the thalamus from the sensory system and the reticular activating system from the brainstem. This can also get inhibited

41
Q

What is critical to cortical functions and the wake/conscious state

A

Thalamocortical-thalamic loops, rhythmic activity in these loops
-intralaminar nucleus on the thalamus

42
Q

What is the reticular activating system (RAS) important for q

A

In the thalamus. Critical for maintain wake state/consciousness, brainstem projections ‘relay’ through central thalamus to cortex

43
Q

Absence seizures are a disruption at what level

A

Thalamic level

44
Q

What are the two nuclei that are responsible for maintinaing wake and conscious state

A

Centromedian nucleus and intralaminar nuclei

45
Q

What synapses in the centromedian and intralaminar nucleus

A

Projections from the midbrain and pons

46
Q

Neural mechanisms for simple focal seizures

A

Synchronized burst firing starts in one specific cerebral lobe or isolated part of one cerebral lobe.

47
Q

Fock of the simple focal seizures include

A

Primary motor cortex (involuntary movements)
Primarily somatosensory cortex (sensory loss or parenthesia)
Primary visual cortex (flashes of light, darkness)
Occipitotemproal gyri (object/face hallucinations)
Superior temporal gyrus (tinnitus)

48
Q

Temporal profile of focal simple seizures

A

Sudden onset, transient course (seconds)

49
Q

Presentation of focal simple seizures

A
  • sometimes follows “jacksonian March”: spread along precentral gyrus from the medial surface toward the lateral sulcus. So from ankle, up the leg, torso, arm, face, tongue, larynx
  • can be followed by weakness during post-ictal stage=”todds paralysis” can last from 30 minutes to >24 hours
50
Q

What is a focal complex seizure

A

Temporal lobe origin with secondary generalization

51
Q

Neural mechanism of focal complex seizures

A

-burst firing starts in temporal lobe (often medially in hippocampus and dentate gyrus) as a simple focal seizure but then spreads through rest of temporal love and to rest of the brain (other lobes, opposite hemisphere). Possibly due to impaired function of inhibitory internuerons, whihc allows Burst firing to start. Process becomes neurotoxic to pyramidal neuron at origin site. Possible a developmental disorder

52
Q

Who could be a candidate for severing the splenium of the corpus callosum or removal of cortical tissue?

A

Someone with complex focal seizures

53
Q

Temporal profile of someone with focal complex seizures

A

Sudden onset, transient course (minutes). The initial simple seizures can last only seconds before spreading (generalization)

54
Q

Presentation of complex focal seizure

A
  • typically features a pre-ictal aura
  • if the initial origin of the simple focal seizure activity is found, neurosurgical resection is a last resort treatment
55
Q

Status epilepticus

A

Sustained seizure activity

Chronic sustained loss of consciousness in status epilepticus

56
Q

Status epileptics vs coma

A

Accounts for as much as 20% of coma cases, mistaken for comas

57
Q

Sustained, constunous seizure activity

A

Status epilepticus

58
Q

Presentation of status epilepticus

A

-convulsive motor signs can be noticeable more or very subtle muscle twitching, undetectable motor signs

59
Q

What is status epilepticus detected by

A

EEG and is clearly different from coma. Coma shows absence of seizure activity

60
Q

What is status epilepticus treated with

A

Anti-convulsants

61
Q

How do you diagnose seizures

A

-you have to find the root of the cause, there is something causing the seizures, they don’t just happen

62
Q

What are some things that could cause seizures

A

Fever, infection, hemorrhagic stroke, tumor

Anything that irritate intact tissue

63
Q

Epilepsy

A

Have had mroe than one seizure: recurrence is a key criteria for epilepsy. Must be more than 24 hours

64
Q

How do you classify seizure types

A

By EEG

65
Q

What is different in epilepsy EEGs vs non-epilepsy seizure EEGs

A

Epilepsy specific patterns in the waveforms that are absent in the non epilepsy seizures.

66
Q

What is another trait of epilepsy

A

Exclusion of an anatomical lesion or growing mass

67
Q

Hallmark waveform features in seizures

A

Sharp wave
Spike
Spike and wave

68
Q

Stimulus-induced seizure activity: normal vs epileptic response

A

-strobescope-induced burst-firing activity in occipital cortex remains limited to occipital lobe in normal subjects, but spreads anteriorly in epileptic subject

69
Q

Underlying neurobiological causes of seizures

A
  • Various dysfunctions related to GABA, the major inhibitor NT of the CNS: GABA synthesis, dysfunction or reduced number of GABAergic inhibitory internuerons, GABA receptors, synaptic re-uptake transporters
  • dysfunctional Ca++, Cl-, or K+ channels
  • genetic mutations
70
Q

Kindling phenomenon

A

How repeated episodes of high frequency stimulation of neurons can induce a delayed state of hyper-excitability and seizure like activity.

71
Q

Anti seizure meds

A
  • GABA(A) receptor agonists
  • GABA re-uptake transporter inhibitors
  • Voltage gates Ca++ channel blockers
  • voltage-gates Na+ channel blockers
  • sodium valproate (valproic acid)
72
Q

What is the most common anti seizure med

A

GABA (A) receptor agonists

73
Q

What is the major inhibitory NT in the CNS

A

GABA

74
Q

Where is GABA found in the brain

A

Everywhere

75
Q

Functional significance in GABA

A
  • involved in virtually all functions

- GABA receptors are targeted by many Rx classes for many purposes

76
Q

Clinical significance of GABA

A
  • deficiency leads to pathological increase in neuronal excitability
  • GABA dysfunction may be key factor in seizures
77
Q

What is GABA synthesized from

A

Glutamate by glutamic acid decarboxylase (GAD)

78
Q

How is GABA transported from the cytoplasm

A

Into synaptic vesicle

79
Q

How is GABA cleared from synaptic cleft.

A

By plasma membrane transporters

80
Q

How is GABA metabolized (degraded)

A

By mitochondrial enzymes

81
Q

GABA (A)

A

Inhibitory and ionotropic

-ionotropic makes it very powerful acting

82
Q

GABA(B)

A

Metabotropic

-can be excitatory or inhibitory

83
Q

Chloride and GABA

A

GABA(A) binds the chloride channels and allows Cl to get into the cell, this hyperpolarizes the cell

84
Q

GABA(A) receptor target for multiple Rx

A

Benzodiazepines

  • GABA(A) agonists
  • anti-convulsants
  • anti anxiety
  • sedative/hypnotic
  • coma inducing
  • lethal injection

Also Rohypnol (date rape drug) and GHB

Neuro Block 7 (10 decks)

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