Seizures Flashcards
(84 cards)
1
Q
Pathogenisis of seizures
A
Abnormal electrophysiolgical ctivity (cellular dysfunction)
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
3
Q
Localization of seizures
A
Some common focal origins but also diffuse types
4
Q
Temporal profile of seizures
A
Transient (except status epliepticus)
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)
6
Q
What can be a clue to focal origin
A
Aura
7
Q
Scalp electrodes detect synaptic potentials in cortex
A
EEG
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
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
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
11
Q
What is the arrangement of electrodes
A
Standardized arrangement
12
Q
Beta wave on EEG
A
Wake state: eyes open, active
13
Q
Alpha EEG
A
Wake state, eyes closed, relaxed
14
Q
Theta EEG
A
Drowsy/sleep
15
Q
Delta EEG
A
Sleep
16
Q
What is a normal EEG
A
Beta or alpha waves
Goes from frontal lobe down to occipital
17
Q
Gerenalized (diffuse/bilateral) seizures
A
Sudden and widespread cortical origin ( no neuroanatomical focus)
18
Q
What are the two different types of generalized (diffuse/bilateral) seizures
A
Tonic clonic (grand mal) Absence (petit mal)
19
Q
Tonic clonic seizures
A
- grand mal
- consciousness interrupted
- convulsive
- too much firing, sometimes disoriented afterwards
20
Q
Absence seizures
A
- generalized (bilateral/diffuse)
- petit mal
- consciousness interrupted (unaware during seizure)
- mostly blank stare
- can show some subtle muscle contractions
21
Q
Partial (focal) seizures
A
Cortical origin in one lobe or part of a lobe *neuroanatomical focus)
22
Q
What subgroup of seizures has a neuranatomical focus
A
Partial (focaL)
23
Q
What are the two different types of partial (focal) seizures
A
Simple focal
Complex focal
24
Q
Simple focal seizure
A
- partical (focal) seizure
- consciousness maintained (aware during seizures)
- common origin sites are motor and sensory regions (parahippocampus region)
25
Complex focal seizure
- partial (focal) type of seizure
- consciousness interrupted (unaware during seizure)
- common origin: temporal lobe
- spreads and beceoms generalized
26
What is the most common origin of complex focal seizures
Temporal lobe
27
Neural mechanism of tonic clonic seizures
Simultaneous "burst-firing" and synchronization of cortical neurons across cerebral cortex
28
Temporal profile of tonic clonic seizures
Sudden onset, renascent course (minutes)
29
Initial stage of tonic clonic seizures
Tonic
| -stiffening, bilateral extension, often arched back
30
Second stage of tonic clonic seizures
Clonic
- rhythmic
- conclusive felxion/extension or 'shaking'
- chewing or biting motions
31
Consciousness in tonic clonic seizures
Loss of consciousness and initial post-vital phase
32
What do tonic clonic seizure EEGs lack
Beta and alpha waves
33
Pre-ictal waves for clonic tonic
Alpha and beta
34
Post-ictal waves
Hypoactivity, then recovery into alpha and beta
35
Neural mechanism of absence seizures
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
Temporal profile of absence seizures
Sudden onset, transient course (seconds), but can be many times throughout the day
37
Presentation of absence seizures
- 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
What is the pattern of the EEG on someone with absence seizures
Spike and wave pattern
39
What normally sustains the conscious state
Thalamocortical projections of the reticular activating system
40
Current hypothesis on absence seizures
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
What is critical to cortical functions and the wake/conscious state
Thalamocortical-thalamic loops, rhythmic activity in these loops
-intralaminar nucleus on the thalamus
42
What is the reticular activating system (RAS) important for q
In the thalamus. Critical for maintain wake state/consciousness, brainstem projections 'relay' through central thalamus to cortex
43
Absence seizures are a disruption at what level
Thalamic level
44
What are the two nuclei that are responsible for maintinaing wake and conscious state
Centromedian nucleus and intralaminar nuclei
45
What synapses in the centromedian and intralaminar nucleus
Projections from the midbrain and pons
46
Neural mechanisms for simple focal seizures
Synchronized burst firing starts in one specific cerebral lobe or isolated part of one cerebral lobe.
47
Fock of the simple focal seizures include
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
Temporal profile of focal simple seizures
Sudden onset, transient course (seconds)
49
Presentation of focal simple seizures
- 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
What is a focal complex seizure
Temporal lobe origin with secondary generalization
51
Neural mechanism of focal complex seizures
-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
Who could be a candidate for severing the splenium of the corpus callosum or removal of cortical tissue?
Someone with complex focal seizures
53
Temporal profile of someone with focal complex seizures
Sudden onset, transient course (minutes). The initial simple seizures can last only seconds before spreading (generalization)
54
Presentation of complex focal seizure
- 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
Status epilepticus
Sustained seizure activity
| Chronic sustained loss of consciousness in status epilepticus
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Status epileptics vs coma
Accounts for as much as 20% of coma cases, mistaken for comas
57
Sustained, constunous seizure activity
Status epilepticus
58
Presentation of status epilepticus
-convulsive motor signs can be noticeable more or very subtle muscle twitching, undetectable motor signs
59
What is status epilepticus detected by
EEG and is clearly different from coma. Coma shows absence of seizure activity
60
What is status epilepticus treated with
Anti-convulsants
61
How do you diagnose seizures
-you have to find the root of the cause, there is something causing the seizures, they don't just happen
62
What are some things that could cause seizures
Fever, infection, hemorrhagic stroke, tumor
Anything that irritate intact tissue
63
Epilepsy
Have had mroe than one seizure: recurrence is a key criteria for epilepsy. Must be more than 24 hours
64
How do you classify seizure types
By EEG
65
What is different in epilepsy EEGs vs non-epilepsy seizure EEGs
Epilepsy specific patterns in the waveforms that are absent in the non epilepsy seizures.
66
What is another trait of epilepsy
Exclusion of an anatomical lesion or growing mass
67
Hallmark waveform features in seizures
Sharp wave
Spike
Spike and wave
68
Stimulus-induced seizure activity: normal vs epileptic response
-strobescope-induced burst-firing activity in occipital cortex remains limited to occipital lobe in normal subjects, but spreads anteriorly in epileptic subject
69
Underlying neurobiological causes of seizures
- 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
Kindling phenomenon
How repeated episodes of high frequency stimulation of neurons can induce a delayed state of hyper-excitability and seizure like activity.
71
Anti seizure meds
- GABA(A) receptor agonists
- GABA re-uptake transporter inhibitors
- Voltage gates Ca++ channel blockers
- voltage-gates Na+ channel blockers
- sodium valproate (valproic acid)
72
What is the most common anti seizure med
GABA (A) receptor agonists
73
What is the major inhibitory NT in the CNS
GABA
74
Where is GABA found in the brain
Everywhere
75
Functional significance in GABA
- involved in virtually all functions
| - GABA receptors are targeted by many Rx classes for many purposes
76
Clinical significance of GABA
- deficiency leads to pathological increase in neuronal excitability
- GABA dysfunction may be key factor in seizures
77
What is GABA synthesized from
Glutamate by glutamic acid decarboxylase (GAD)
78
How is GABA transported from the cytoplasm
Into synaptic vesicle
79
How is GABA cleared from synaptic cleft.
By plasma membrane transporters
80
How is GABA metabolized (degraded)
By mitochondrial enzymes
81
GABA (A)
Inhibitory and ionotropic
| -ionotropic makes it very powerful acting
82
GABA(B)
Metabotropic
| -can be excitatory or inhibitory
83
Chloride and GABA
GABA(A) binds the chloride channels and allows Cl to get into the cell, this hyperpolarizes the cell
84
GABA(A) receptor target for multiple Rx
Benzodiazepines
- GABA(A) agonists
- anti-convulsants
- anti anxiety
- sedative/hypnotic
- coma inducing
- lethal injection
Also Rohypnol (date rape drug) and GHB
