Brainscape's Knowledge GenomeTM

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


See full index

Neurobiology of Adult Brain Disorders > Epilepsy > Flashcards

Epilepsy Flashcards

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

Define seizure

A

the clinical manifestation of an abnormal and excessive synchronization of a population of cortical neurons

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

Define epilepsy

A

a tendency toward recurrent seizures unprovoked by any systemic or acute neurologic insults

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

Define eplieptogenesis

A

sequence of events that converts a normal neuronal network into a hyperexcitable network

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

What are the two main types of seizures?

A

partial, generalized

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

What are the two types of partial seizures?

A

simple partial, complex partial

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

What are the types of generalized seizures?

A

absence, myoclonic, clonic, tonic, tonic-clonic, and atonic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

define partial seizure

A

seizures arising from a focal area of the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

define generalized seizure

A

seizures which involve the entire brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

define a simple partial seizure

A

focal seizures without the loss of consciousness

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

define a complex partial seizure

A

focal seizures with the loss of consciousness

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

What are the two types of epilepsies?

A

idiopathic and symptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define an idiopathic epilepsy

A

arises from an unknown cause thought to have a strong genetic basis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define symptomatic epilepsy

A

epilepsy that arises from a known cause which may include, head injury, brain tumor, stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are some of the in vivo models of epilepsy?

A

numerous genetic models
acquired focal models (lesions, injury)
chemoconvulsant models of seizures (kainic acid)
chemoconvulsant models of status epilepticus (kainic acid)
electrical stimulation
models of epileptogenesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are some in vitro models of epileptiform activity?

A

resected tissue from patients with epilepsy
cell culture models
acute slice models
organotypic slices

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define temporal lobe epilepsy

A

an epilepsy syndrome with seizure arising from the temporal lobe with a high degree of involvement of the hippocampus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the most common form of epilepsy?

A

TLE - temporal lobe epilepsy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Basic mechanism underlying seizures and epilepsy are __ and __ __.

A

feedback
feed-forward inhibition

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are four possible causes of hyperexcitability

A

excitatory post synaptic potentials (EPSPs)
inhibitory post synaptic potentials (IPSPs)
changes in voltage gated ion channels
alteration of local ion concentrations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the major neurotransmitters in the brain?

A

glutamate, GABA, Acetycholine, dopamine, serotonin, histamine, and other modulators (neuropeptides, hormones)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

__ is the brain’s major excitatory neurotransmitter

A

glutamate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the two groups of glutamate receptors and how do they differ?

A

ionotropic - fast synaptic transmission
metabotropic - slow synaptic transmission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the three subtypes of ionotropic glutamate receptors?

A

AMPA, kainate, NMDA
glutamate-gated cation channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the most common types of metabotropic glutamate receptors?

A

g-protein coupled, regulation of secondary messengers (cAMP and phospholipase C)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Metabotropic glutamate receptors modulate __ __

A

synaptic activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What are some modulates of glutamate receptors?

A

glycine, polyamine sites, Zinc, redox site

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What is the major inhibitory neurotransmitter in the CNS?

A

GABA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the two types of GABA receptors? How do they differ?

A

A: post-synaptic, specific recognition sites, linked to Cl- channel
B: presynaptic autoreceptors that reduce transmitter release by decreasing calcium influx, postsynaptic coupled to G-proteins to increase K current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are two cellular mechanisms of seizure generation?

A

excitation - too much
inhibition - too little

30
Q

Describe the excitation cellular mechanism of seizure generation

A

ionic - inward sodium and calcium currents
neurotransmitter - glutamate, aspartate

31
Q

Describe the inhibition cellular mechanism of seizure generation

A

ionic - inward cl, outward K currents
neurotransmitter - GABA

32
Q

What neuronal factors modify neuronal excitability?

A

ion channel type, number and distribution
post-translational modification of channels (phosphorylation)
activation of second-messenger systems that affect channel function (G proteins)
modulation of gene expression of ion channels

33
Q

What are possible inherited types of epilepsy?

A

voltage-gated ion channel mutations
ligand-gated ion channel mutations

34
Q

T/F: different mutations in the same gene can result in radically different types of seizures and epilepsy

A

true

35
Q

What are methods of acquired epilepsy?

A

auto-immune
changes in channel expression after seizure

36
Q

What synaptic factors modify neuronal excitability?

A

alterations in expression of transmitter gated ionotropic channels
post-translational changes in neurotransmitter channels
remodeling of synapse location or configuration
changes in gap junction synaptic function

37
Q

What are some non-synaptic (extrinsic) factors modifying neuronal excitability?

A

changes in extracellular ion concentration
changes in extracellular space
modulation of transmitter metabolism or uptake by glial cells

38
Q

What are four mechanisms for generating hyperexcitable networks?

A

Excitatory axonal ‘sprouting’
loss of inhibitory neurons
loss of excitatory neurons ‘driving’ inhibitory neurons
change in neuronal firing properties (channelopathies)

39
Q

EEG’s are graphical depictions of __ __ __, usually recording from the __

A

cortical electrical activity; scalp

40
Q

What is the advantage and disadvantage of an EEG?

A

Advantage of high temporal resolution but poor spatial resolution of cortical disorders

41
Q

What is the most important neurophysiological study for the diagnosis, prognosis, and treatment of epilepsy?

A

EEG

42
Q

Describe the physiological basis of the EEG; __ dipole generated by __ __ __ at __ __ of __ __

A

extracellular
excitatory post-synaptic potential
apical dendrite
pyramidal cell

43
Q

Describe the physiological basis of the EEG; electrical field generated by __ oriented __ __ in __ (layer _) and detected by __ __

A

similarly
pyramidal cells
cortex
5
scalp electrode

44
Q

What are four clinical applications of an EEG?

A

seizures/ epilepsy
sleep
altered consciousness
focal and diffuse disturbances in cerebral functioning

45
Q

Describe seizure initiation of focal seizure generation

A

burst of action potentials, i.e. paroxysmal depolarizing shift
hypersynchronization of neighboring cells

46
Q

Describe propagation of focal seizure generation

A

activation of nearby neurons
loss of surrounding inhibition

47
Q

Intracellular and extracellular events of the __ __ __ underlying the __ __ __ detected by surface EEG

A

paroxysmal depolarizing shift
intererictal epileptiform spike

48
Q

What are causes of acquired epilepsy?

A

severe head injury
cerebral hemorrhage
brain tumor
CNS infection
early life febrile seizures

49
Q

What are the three stages of development of acquired epilepsy?

A

acute
latent
chronic

50
Q

Describe the development of acquired epilepsy

A

insult to CNS
epileptogenesis
epilepsy

51
Q

Define the kindling model of delayed epileptogenesis

A

repeated subconvulsive stimuli resulting in electrical afterdischarges

52
Q

Describe the kindling model of delayed epileptogenesis

A

eventually lead to stimulation-induced clinical seizures
in some cases, lead to spontaneous seizures (epilepsy)
applicability to human epilepsy uncertain

53
Q

Describe the hippocampus implication of epileptogenesis

A

seizures lead to neuronal injury leads to rewiring of neuronal networks leads to increased excitability leads to enhanced susceptibility to further seizures leads to seizures (cyclic)

54
Q

Newborn granule cells in rodent epilepsy models contribute to three distinct anatomical alterations in the epileptic brain, name them

A

mossy fiber sprouting
ectopic granule cell migration
hilar basal dendrite sprouting

55
Q

T/F: hippocampal circuit changes with hippocampal sclerosis

A

true

56
Q

What does neuronal ‘birthdating’ with BrdU reveal?

A

increased generation of new neurons in the hippocampal dentate gyrus during epileptogenesis

57
Q

T/F: new neurons generated during epileptogenesis integrate normally

A

false, integrate abnormally

58
Q

__ granule cells are also seen in human __ __ __ and is associated with __ __ __ dispersion

A

ectopic
temporal lobe epilepsy
granule cell layer

59
Q

Ectopic cells contribute to __ __ __

A

mossy fiber sproutin

60
Q

T/F: Ectopic cells have normal physiology

A

false, abnormal physiology

61
Q

Basal dendrites receive __ __ __

A

excitatory MF input

62
Q

__, __, and __ granule cells underlie __ neuronal integration in rodent TLE models. __ cells are comparatively __

A

juvenile, immature, and newborn
aberrant
mature; normal

63
Q

Abnormally interconnected __ __ impair the __ __

A

granule cells
dentate gate

64
Q

What is hypothesized to impair the dentate gate?

A

formation of recurrent excitatory connections in the epileptic dentate gyrus

65
Q

Newborn granule cells sprout __ __ __ that result in __ integration into __ circuitry

A

mossy fibers axons
aberrant
hippocampal

66
Q

Newborn granule cells sprout __ __ __ that recieve mossy fiber synapses in the __, further altering the __ activity

A

hilar basal dendrites
hilus
hippocampal

67
Q

Newborn granule cells migrate into the __, resulting in __ granule cell layer morphology

A

hilus, abnormal

68
Q

Seizures appear to represent an __ state for the brain wherein slight disruptions in normal brain circuitry or physiology arising from many different situations can result in a __ __ __

A

attractor; final common pathway

69
Q

Known causes of epilepsy are __ and __ and can range from __ modificationations of __ __ to __ of __ brain regions

A

genetic; acquired
single channels
reorganization; whole

70
Q

Currently, the study of epileptogenesis in the __ of rodents are the most common

A

hippocampus

71
Q

__ __ epileptogenesis presents a special case because of the lifelong neurogenesis in this region

A

hippocampal-derived

72
Q
A

Neurobiology of Adult Brain Disorders (10 decks)

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