Brainscape's Knowledge GenomeTM

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


See full index

Neurology > Neuropathy and myopathy > Flashcards

Neuropathy and myopathy Flashcards

1
Q

Diseases in the anterior horn lead to LMN or UMN disease?

A

LMN

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

What is the classic disease of the anterior horn?

A

Polio

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

UMN and LMN s/sx = what disease?

A

ALS

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

Which has hyperactive, and which hypoactive reflexes: UMN and LMN lesions

A 
UMN = hyperactive
LMN = hypoactive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the MOA of botulinum toxin?

A

Cleavage of SNARE proteins prevents the release of vesicles containing ACh

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

What is bulbar weakness?

A

The bulb is part of the lower pons, so dysarthria and dysphagia

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

Which has greater proximal and which has greater distal weakness: myopathy vs neuropathy?

A

Neuropathy = greater distal weakness

Myopathy = greater proximal weakness

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

Stocking glove distribution of sensation loss is usually a LMN or UMN lesion?

A

LMN

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

What defines acute vs chronic weakness of neuromuscular disorders?

A 
Acute = days-weeks
Chronic = months to years
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Anterior horn cell damage = what type of deficit?

A

Motor only–no sensory

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

How do you differentiate between demyelination and cell body nerve problems?

A

Demyelination can have relapses, while cell body lesions do not.

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

UMN lesions what is the diagnostic modality that is especially helpful?

A

MRIs

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

LMN lesions what is the diagnostic modality that is especially helpful?

A

Nerve conduction test

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

Fasciculations is a hallmark of UMN or LMN lesions?

A

LMN

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

What is the amyotrophic part ALS?

A

symptoms of weakness, atrophy, and fasciculations

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

What is the lateral sclerosis part of ALS?

A

UMN in the DC/ML pathway, producing s/sx of hyperactive DTRs, clonus, and babinski signs

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

Which has a better prognosis: the lateral sclerosis or the amyotrophic form of ALS?

A

Lateral sclerosis

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

What is the mean age of onset of ALS?

A

58 years

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

What is the incidence of ALS?

A

1/100,000

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

What is the prognosis with ALS?

A

Variable–Respiratory involvement is much worse than limb involvement

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

Bulbar involvement with ALS leads to what?

A

Flaccid dysarthria, tongue atrophy, fasciculations

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

True or false: for the most part, ALS spares cognition, EOMs, and sphincters

A

True

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

How does ALS usually present initially?

A

Single limb issue

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

What are fasciculations, generally?

A

“Worm-like” movement beneath the skin of a patient that does not move a limb

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

How do you diagnose ALS?

A

-Clinical diagnosis is correct more than 95% of the time

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

What are the antibodies that can be tested for in multi-focal motor neuropathy?

A

Anti-GM1 antibodies

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

Which usually has eye findings: MG or ALS?

A

MG

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

How often are fasciculations in people in general (without ALS)? How do you differentiate this with ALS?

A

70%

No weakness/atrophy

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

What is the diagnostic criteria for ALS?

A

UMN and LMN signs with sensattion spared in:
-bulbar region and 2 spinal regions
OR
-three spinal regions

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

What is the cause of ALS?

A

Unknown–can be familial, but usually sporadic

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

What is the symptomatic treatment for ALS?

A

PT/OT

Orthotics

32
Q

What is the MOA of Riluzole in treating ALS?

A

Glutamate antagonist

33
Q

What are the usual causes of mononeuropathies?

A

Single nerve damaged, leading to deficits in a single nerve distribution

34
Q

What is mononeuritis multiplex?

A

When two or more (typically just a few, but sometimes many) separate nerves in disparate areas of the body are affected it is called “mononeuritis multiplex,”

35
Q

What is allodynia?

A

Neuropathic pain following nonpainful stimuli

36
Q

What is dysesthesia?

A

Unpleasant sensation that is either spontaneous or evoked by pressure, movement, or touching

37
Q

What is hyperalgesia?

A

heightened pain sensation provoked by painful stimulus

38
Q

What are paresthesias?

A

Irritating spontaneous sensation

39
Q

What are the motor signs of peripheral neuropathies?

A

Distal weakness and foot drop

40
Q

What are the sensory findings with peripheral neuropathies?

A

Loss of vibratory, position, and/or pin

41
Q

What are reflexes like with peripheral neuropathies?

A

Hypoactive to absent

42
Q

What is the role of EMG in diagnosing peripheral neuropathies?

A

Helpful in distinguishing axonal vs demyelinating neuropathy

43
Q

What is the most common type of neuropathy?

A

DM neuropathy

44
Q

What is toxic neuropathies?

A

Uremia induced neuropathy, or extrinsic toxins of neuropathy

45
Q

What are the two major extrinsic toxins that can cause neuropathies?

A

EtOH

Chemotherapy

46
Q

What are the two major immune mediated neuropathies?

A

AIDP-(acute inflammatory demyelinating polyneuropathy) = GB

CIDP (Chronic Inflammatory Demyelinating Polyneuropathy)

47
Q

What is Charcot-Marie-Tooth disease (hereditary motor sensory neuropathy)?

A

AD disease caused by mutations that cause defects in neuronal proteins involved in the production and function of peripheral nerves

48
Q

What are the classic foot findings of CMT disease?

A

Pes cavus and hammer toe

49
Q

What is the expressivity of CMT?

A

Variable

50
Q

What is the frequency of CMT?

A

1/2500

51
Q

What is the most common inherited neurological disorder?

A

HSMN (CMT)

52
Q

What is the mode of inheritance of CMT?

A

AD

53
Q

What is the usual presentation of CMT?

A

Slow, progressive distal weakness; difficulty walking

54
Q

What is a steppage gait?

A

Bring the knees high to clear the anterior tibialis

55
Q

What are the two types of CMT? What are the EMG findings of each?

A

Demyelinating (slow NCV)

Axonal (normal NCV)

56
Q

How do you definitely diagnose CMT?

A

Genetic testing

57
Q

GB is a motor or sensory neuropathy?

A

Motor–sensation is intact

58
Q

What is the classic CSF finding of GB?

A

Albuminocytological dissociation (no WBC increase, but marked protein)

59
Q

What are the two viruses that can cause GB?

A

CMV

EBV

60
Q

What are the two bacteria that predispose to GB?

A
  • Campylobacter jejuni

- Mycoplasma pneumoniae

61
Q

What are the usual s/sx of GB?

A

Difficulty walking

62
Q

What fraction of GB syndrome patients develop respiratory issues?

A

1/3

63
Q

What is the Fisher syndrome variant of GB syndrome?

A

Starts with ophthalmoplegia, ataxia, and loss of DTRs

64
Q

What is the time course of GB disease?

A

50% reach nadir in 2 weeks, with slow recovery over months

65
Q

What percent of patients who develop GB have residual symptoms?

A

15-20%

66
Q

Suspected GB syndrome, but with marked pleocytosis = ?

A

HIV

67
Q

Presence of fibrillations with GB implies a shorter or longer course?

A

Longer

68
Q

What is the treatment for GB syndrome?

A

Plasma exchange or IVIG

69
Q

Which usually has more pronounced atrophy: LMN lesions or UMN lesions?

A

LMN

70
Q

The cell body of a LMN is located where?

A

ventral horn of the spine cord

71
Q

What is the MOA of tetanus toxin?

A

Cleaves synaptobrevin, leading to blocked release of GABA and glycince across the synaptic cleft

72
Q

True or false: the tongue is never affected with ALS

A

False–can have hypoglossal nerve involvement, leading to atrophy of the tongue

73
Q

Which nerves are more myelinated:DC/ML nerves, or spinothalamic tract nerves?

A

DC/ML

74
Q

Inverted champagne bottle appearance of the leg = which disease?

A

CMT

75
Q

What is the difference between GB and CIDP?

A

progression over 2 months suggests CIDP?

Neurology (23 decks)

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