Brainscape's Knowledge GenomeTM

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


See full index

Boards > Epilepsy and Sleep > Flashcards

Epilepsy and Sleep Flashcards

1
Q

How should the dose of Lamictal be adjusted in pregnancy?

A

increased since pregnancy increases lamictal clearance.

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

what are symptoms of temporal lobe seizures?

A

altered consciousness, atomotisms, deja vu, complex partial seizures, olfactory hallucinations.

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

When a patient has the fencer’s posture during a seizure, where does their seizure usually come from.

A

frontal lobe- supplementary motor cortex.

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

What is proposed mechanism of action of gabapentin and pregabalin?

A

binding to L-type Ca channels, modulate presynaptic neurotransmitter release.

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

How is Gabapentin excreted?

A

renal

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

What are advantages and disadvantages of Gabapentin?

A

Advantage: does not interact with other drugs. Disadvantages: can worsen generalized epilepsy, absorption is non-linear.

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

Which medications can exacerbate myoclonic epilepsy?

A

Lamictal, Carbamazepine, Gabapentin, Pregabalin, Vigabatrin.

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

Which anti-convulsants are hepatic enzyme inducers?

A

Phenytoin, Carbamazepine, Phenobarbital, Primidone, Oxcarbamazepine and Topirimate >200mg/day.

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

Which anti-convulsants are hepatic enzyme inhibitors

A

VPA,

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

at what age does the posterior dominant alpha rhythm develop to the adult frequency?

A

8-10 years

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

which medications can aggravate absence seizures?

A

phenytoin, carbamazepine, gabapentin, lamictal.

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

what is the mechanism of action of Benzodiazepines?

A

GABAa agonists.

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

what is the interaction between oral contraceptives and Lamotrigine?

A

OCP’s containing ethinylestradiol increase Lamotrigine clearance.

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

How is Topirimate metabolized?

A

Excreted in urine.

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

What is the mechanism of action of Lacosamide?

A

inactivation of slow voltage Na channels- leads to decreased membrane hyperexcitability. Also interacts with CRMP2- involved in neuronal differentiation and axon guidance.

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

What is the mechanism of action of Rufinimide?

A

prolongation of inactive state of Na channels.

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

How is Rufininide metabolized?

A

enzymatic hydrolysis of carboxylamide group (NOT via cyp system), elimination in urine.

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

What is inheritance of Aicardi syndrome?

A

X-linked Dominant

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

what is the pathomenumonic eye findings in Aicardi syndrome?

A

chorioretinal lacunae

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

What are the characteristics of Unverricht Lundborg Syndrome?

A

stimulus induced progressive myoclonic epilepsy that is action related, various seizure types, neurologic decline, ataxia and tremor.

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

What gene is involved in Unverricht Lundborg Syndrome and what chromosome is it on?

A

EPM1 on Chr 21q22. Encodes Cytasin B which regulates apoptosis.

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

What are the clinical features of Sialadosis Type I?

A

progresive action myoclonus, pregoressive ataxia, vision loss, cherry red spot. Onset in adolescence or adulthood.

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

What is the enzyme deficiency in Sialadosis Type I?

A

alpha-neuroaminidase.

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

What are the clinical features of Sialadosis Type II?

A

myoclonus, coarse facial features, corneal clouding, hepatomegaly, skeletal dysplasia, learning disability. Onset between birth and 20s.

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

what is the enzyme defect in Sialadosis Type II?

A

N-acetyl neuroaminidase and beta-galactosialidase

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

what is the inheritence of the sialadoses?

A

autosomal recessive.

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

what gene is implicated in sialadoses and what chromosome is it on?

A

Neu1 on Chr6p

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

what are the clinical features of Lafora body disease?

A

onset in adolescence, progressive myoclonic seizures and other seizure types. Ataxia, dysarthria and progressive dementia.

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

what gene is involved in Lafora Body disease and what chromosome is it on?

A

EPM2A on Chr6q.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the pathologic finding in Lafora body disease?

A

PAS positive Lafora body inclusions in skin biopsy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what is the frequency of alpha waves?

A

8-13 Hz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the frequency of beta waves?

A

>13 Hz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the frequency of theta waves?

A

4-7 Hz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what is the frequency of Delta waves?

A

1-4 Hz

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are the main features of N1 sleep

A

loss of posterior alpha rhythm, increased theta, loss of muscle artifact, vertex waves, POSTS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the features of N2 sleep?

A

sleep spindles, K-complexes, vertex waves, POSTS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What are the features of N3 sleep?

A

high amplitude delta, rare spindles, k-comoplexs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the features of REM Sleep?

A

can have some alpha, spontaneous REM, tonic motor activity suppression on EMG, central sawtooth waves.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

what is the AHI in mild OSA?

A

5-15

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the AHI in moderate OSA?

A

15-30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the AHI in severe OSA?

A

>30.

42
Q

what are the non-REM parasomnias?

A

confusional arousals, sleepwalking, night terrors.

43
Q

what stage of sleep do non-REM parasomnias arise from?

A

Stage III (slow wave)

44
Q

what is Klein-Levin Syndrome?

A

recurrent episodes of hypersomnia during which sleep is not refreshing. Can be associated with irritability, aggressiveness, confusion and hypersexuality.

45
Q

what is idiopathic hypersomnia?

A

long term inability to obtain adequate sleep.

46
Q

what is the physiologic basis of narcolepsy?

A

loss of hypocretin neurons in the lateral hypothalamus.

47
Q

what degenerative disease have been associated with REM sleep disorders?

A

alpha-syneuclopathies.

48
Q

what are some treatments of narcolepsy?

A

gamma-hydroxybuterate, triciclyc anti-depressants, SSRIs

49
Q

what are two features of narcolepsy on polysomnography?

A

MSLT

50
Q

what structure is responsible for REM sleep?

A

locus correlius

51
Q

what aspect of narcolepsy are stimulants helpful for?

A

sleep attacks

52
Q

at what age to well formed, synchronous sleep spindles appear?

A

2 years

53
Q

at what gestational age does the EEG consist of primarily trace discontinue?

A

24-28 weeks

54
Q

starting at what gestational age is trace discontinue confined to quiet sleep?

A

32 weeks

55
Q

at what age does trace alternans arise?

A

36 weeks

56
Q

what is activite moyenne? at what gestational age does it arise?

A

continuous low voltage mixed frequency during wakefulenss. 36-40 weeks.

57
Q

at what gestational age does continuous slow wave sleep arise?

A

44 weeks

58
Q

at what gestational age are delta brushes peaking?

A

32-34 weeks

59
Q

at what gestational age do asynchronous sleep spindles arise?

A

44-46 weeks

60
Q

what percentage of the time does the term neonate spend in the waking state?

A

30%

61
Q

what term neonatal sleep state is characterized by decreased muscle tone, irregular respirations and occasional face and body movements. What percentage of time is spent in this state?

A

active sleep, 50-60%

62
Q

what term neonatal sleep state is characterized by muscle tone similar to waking, regular respirations, and little movement. what percentage of the time is spent in this sleep state?

A

quiet sleep, 30-40%

63
Q

What is Bancaud’s phenomenon?

A

failure of one side to abolish alpha rhythm with eye opening. Indicates abnormality on that side.

64
Q

sail waves over the posterior region

A

posterior slowing of youth

65
Q

Episodic theta occurring over the sylvian area

A

temporal transients- seen in normal aging.

66
Q

what EEG pattern is seen in dialysis dementia? Due to the accumulation of what substance?

A

bilateral spike and wave discharges. Aluminum

67
Q

what are the 5 grades of EEG after anoxic injury?

A
  1. reactive alpha with some theta 2. Dominant Theta 3. continuous polymorphic slow delta 4. invariant low amplitude delta without change with stim 5. nearly iso-electric
68
Q

in what type of injury is there reactive alpha most predominant over the posterior head?

A

vascular lesion to ventral pons

69
Q

when do benign epileptiform transients of sleep occur?

A

during drowsiness in adults

70
Q

what EEG finding is circled?

A

Wicket spikes- arc like spikes that occur in trains. Normal variant.

71
Q

what are the blue arrows pointing to?

A

Lambda waves- evoked waves due to shifting saccades when a visual stimulus is presented

72
Q

rolandic alpha that slows with aging and abolishes when you move contralateral arm

A

mu rhythm

73
Q

at what serum concentration does phenytoin reach zero order kinetics?

A

15

74
Q

what class of drugs alters free phenytoin level without changing total level?

A

siacylates

75
Q

addition of what drug can cause immediate phenytoin toxicity?

A

Valproate because it displaces protein bound phenytoin resulting in immediately higher level

76
Q

which wave of auditory evoked brainstem potential corresponds to activation of the distal CN VIII?

A

I

77
Q

what brainstem auditory evoked potential corresponds to activation of the proxiam CN VIII?

A

II

78
Q

what brainstem auditory evoked potential corresponds to activation of the superior olive and trapezoid body?

A

III

79
Q

what brainstem auditory evoked potential corresponds to activation of the upper pons?

A

IV

80
Q

what brainstem auditory evoked potential corresponds to activation of the midbrain?

A

V

81
Q

what wave corresponds to pattern reversal visual evoked potential?

A

p100

82
Q

what corresponds to the N9 wave?

A

Erb’s point after stimulation of median nerve

83
Q

What is the wave at the cerico-medullary junction after stimulation of the median nerve? WHat does it represent?

A

N14. Medial lamniscus

84
Q

what is the wave in contralateral somatosensory cortex after median nerve stimulation?

A

N20

85
Q

what is the wave over the lumbar spinal cord after stimulation of the tibal nerve?

A

N22

86
Q

what is the wave over contralateral somatosensory cortex after stimulation of the tibial nerve?

A

P38

87
Q

what are the two potentially serious side effects of felbamate?

A

hepatic toxicity and aplastic anemia

88
Q

what is the risk of having a baby with major malformations if you are on one anti-convulsant?

A

5-7%

89
Q

in which type of seizure are there well formed visual hallucinations?

A

lateral temporal

90
Q

is motor arest more commen in medial or lateral temporal seizures?

A

mesial

91
Q

which anti-convulsant increases seizures in patients with porphyria?

A

carbamazepine

92
Q

in what disorder is generalized paroxysmal fast activity seen?

A

porencephaly

93
Q

what is the mechanism of action of tetrototoxin?

A

blocks opening of V-gated Na channels

94
Q

which sensory receptors in the skin respond to sustained touch? What sensory fibers do they stimulate?

A

Merckle cells. Type II afferents.

95
Q

which skin sensory receptors resond to descret onset and offset fo touch, but not to sustained touch?

A

Meissner’s corpuscles.

96
Q

what is the resting membrane potential of rods?

A

-40

97
Q

what is the rod cell response to light?

A

hyperpolarization and decrease in tonic release of glutamate.

98
Q

what is the effect of nerve cooling on motor action potentials?

A

slowed conduction velocity and increased distal latency

99
Q

what is the effect of nerve cooling on SNAPs?

A

INCREASED amplitude

100
Q

what is the mechanism of action of the nerve cooling effects?

A

increased time of opening of Na channels, increasing refractory period.

Boards (21 decks)

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