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Neuro DRx > 04a: MS and Movement > Flashcards

04a: MS and Movement Flashcards

1
Q

MS is a disease of (X) cells, causing (central/peripheral) de-myelination.

A

X = oligodendrocytes

Central only! (doesn’t affect Schwann cells)

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2
Q

Role of (X) supplementation and deficiency has been found to play a role in MS.

A

X = vitamin D

Vit D supplementation prevents and slows the progression of the
disease, while deficiency worsens the disease

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3
Q

Migration studies support the view that there is (X) trigger is in the pathogenesis of MS.

A

X = environmental (low risk in Japan and almost no cases in Inuit populations)

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4
Q

List the 4 MS phenotypes and star the one seen most commonly at onset of MS in patient.

A
  1. Pure relapsing-remitting (RRMS)* (85%)
  2. Secondary-progressive (SPMS)
  3. Primary-progressive (PPMS; 10%)
  4. Progressive relapsing (PRMS; 5%)
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5
Q

(X) phenotype of MS develops in many patients that initially had pure relapsing-remitting (RRMS).

A

X = secondary-progressive (SPMS)

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6
Q

What’s characterized as benign MS?

A

No progression for 15 y

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7
Q

What’s Clinically Isolated Syndrome (CIS)?

A

One neurological episode

or “relapse” of MS

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8
Q

List three clinical symptoms of visual pathways seen in MS relapse.

A
  1. Diplopia (INO or CN 3, 4, 6 issue)
  2. Optic neuritis (painful movement, vision affected)
  3. Nystagmus
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9
Q

MS clinical symptom: Localized SC inflammation that involves the full thickness of the cord and produces symptoms related to the sensory/motor innervation at that level.

A

Transverse myelitis

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10
Q

MS diagnosis is based on either (X) or (Y).

A 
X = Multiple white matter lesions separated in time and space (relapsing disease)
Y = Progressive disease from onset with typical clinical findings
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11
Q

McDonald criteria for (X) findings in (Y) disease.

A 
X = dissemination in time and space of lesions
Y = MS
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12
Q

MS: list the ways that MRI lesions meet McDonal criteria for “disseminated in time”

A
  1. Both enhancing and non-enhancing lesions in same MRI OR

2. Appearance of new lesions after initial MRI

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13
Q

MS: list the ways that MRI lesions meet McDonal criteria for “disseminated in space”

A

At least one T2 lesion in 2 out of the 4 typical locations for MS

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14
Q

List the four typical locations for lesions in MS.

A
  1. Periventricular
  2. Juxtacortical
  3. Infratentorial
  4. SC
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15
Q

T/F: There are no definitive laboratory test or MRI features for MS.

A

True - other diseases can mimic MS (consider alternative diagnoses, even after making MS diagnosis)

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16
Q

Progressive MS diagnosis: (X) year(s) of disease progression plus 2/3 of which criteria?

A

X = 1

  1. Lesions disseminated in space in brain
  2. Lesions disseminated in space in SC
  3. Oligoclonal bands in in CSF
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17
Q

Neuromyelitis Optica (NMO) was initially thought to be part of (X) disease, but is now considered distinct. What are the symptoms?

A

X = MS

Optic neuritis and transverse myelitis

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18
Q

T/F: Neuromyelitis Optica has better prognosis than MS.

A

False

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19
Q

(X) Ab in (serum/CSF) is seen in 80% of patients with Neuromyelitis Optica (NMO)

A

X = Aquaporin-4

Serum or CSF

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20
Q

List some clinical symptoms that can act as hints for Neuromyelitis Optica.

A
  1. Poor visual recovery
  2. Bilateral optical neuritis
  3. Transverse myelitis
  4. Hiccups, N/V (area postrema affected)
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21
Q

List two “injectable” disease-modifying drugs for MS that have been around for over 20 y. These are administered via which route?

A
  1. IFN-beta (IM, SC)

2. Glatiramer acetate (SC)

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22
Q

What is the mechanism of the disease-modifying drugs for MS (IFN-beta, Glatiramer acetate).

A

Th1 (bad) to Th2 (good) shift

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23
Q

List some oral disease-modifying drugs for MS.

A
  1. Fingolimod
  2. Teriflunomide
  3. Dimethyl Fumarate
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24
Q

MS medication: Fingolimod MOA

A

Sphingosine R blocker (inhibits T cell migration from lymph nodes)

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25
Q

(X) drug improves walking speed in 30-40% of patients with MS.

A

X = Dalfampridine

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26
Q

Tremor that improves with EtOH.

A

Essential tremor

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27
Q

Most common movement disorder.

A

Essential tremor

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28
Q

Essential tremor (present/absent) at rest and (present/absent) during action. Family Hx positive in (X)% of patients.

A

Absent; present

X = 50 (AD)

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29
Q

Essential tremor has been correlated to activity in (X) parts of brain.

A

X = sensorimotor area and cerebellum

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30
Q

Essential tremor: more (symmetric/asymmetric) than the tremor of PD. (X) key PD symptoms are not seen in this tremor.

A

Symmetric;

X = bradykinesia and rigidity

31
Q

Essential tremor: usually involves (upper/lower) limbs in addition to:

A

Upper

Head (no-no) and voice

32
Q

Essential tremor: which two meds mainly used (solo or in combo).

A
  1. Primidone (old antiepileptic)

2. Propranolol

33
Q

The target for the treatment of essential tremor with Deep Brain Stimulation is the (X).

A

X = ventrointermediate

nucleus (VIM) of the thalamus

34
Q

Parkinsonism comprised of which constellation of signs on PE?

A
  1. Rigidity
  2. Bradykinesia (slow mvmt)
  3. Gait abnormalities/postural instability
  4. Tremor
35
Q

Difference between Parkinsonism and PD.

A

PD is Parkinsonism with no known cause

36
Q

Parkinsonism can have which etiologies?

A
  1. Drug/med or toxic cause
  2. Vascular
  3. Post-traumatic
  4. NPH (Normal P hydrocephalus)
37
Q

Mean survival in PD after onset is (X) years and most common causes are:

A

X = 20+

pulmonary infection/aspiration, and complications of falls

38
Q

PD: CT/MRI show (X) abnormalities and SPET/PET show (symmetric/asymmetric) (Y) abnormalities.

A

X = no
Asymmetric
Y = decrease dopamine levels

39
Q

DaTscan used to detect:

A

Dopamine transporters

(DaT) in the brain

40
Q

Risk Factors for PD:

A
  1. Age
  2. Genetics
  3. Environmental (toxic products, well water, repeated head injury)
41
Q

Alien hand syndrome can occur in (X), which is one of the (Y) Syndromes.

A 
X = Corticobasal degeneration
Y = Parkinson Plus
42
Q

Corticobasal degeneration has (symmetric/asymmetric) onset with (slow/rapid) clinical course and (X) changes on CT/MRI.

A

Asymmetric;
Rapid (5-10y)
X = contralateral atrophy

43
Q

Corticobasal degeneration: PET may show (increased/decreased) contralateral fluorodopa uptake in (X) parts of brain.

A

Decrease

X = basal ganglia and association cortices

44
Q

T/F: Parkinson Plus Syndromes respond to PD drugs.

A

False

45
Q

T/F: Parkinson Plus Syndrome pathology involves Tau protein

A

True

46
Q

Parkinson plus syndrome with gait disturbance and frequent falls:

A

Progressive Supranuclear Palsy (PSP)

47
Q

T/F: Neuro manifestations of Wilson’s includes tremor.

A

True - wing-beating

48
Q

Wilson’s: (high/low) ceruloplasmin, and (high/low) urinary copper levels.

A

Low; high

49
Q

Slit lamp examination revealing Kayser-Fleischer rings is indicative of (X) disease.

A

X = Wilson’s

50
Q

MRI in Wilson’s often shows abnormal (T1/T2) signaling in (X) part of brain.

A

T2

X = basal ganglia

51
Q

Medical therapies for Wilson’s include:

A
  1. Reducing copper
    in the diet
  2. Rx with zinc, penicillamine, or trientene
  3. Liver transplant
52
Q

Huntington’s: (X) inheritence with gene on chromosome (Y). What’s the trinucleotide repeat sequence?

A 
X = AD
Y = 4

CAG

53
Q

Huntington’s: Imaging studies reveal …

A

Atrophy of caudate and putamen

54
Q

Which meds can be used to treat Huntington’s chorea?

A
  1. Dopamine antagonists (haloperidol, risperidone, olanzapine)
  2. Benzos may help
  3. Tetrabenazine (suppresses chorea)
55
Q

What’s ataxia?

A

Lack of coordination while performing voluntary movements (may appear as
clumsiness, inaccuracy, or instability)

56
Q

Ataxia usually caused by damage to the (X).

A

X = cerebellum (inputs/outputs)

57
Q

Rx for ataxia:

A

Treat underlying cause; supportive therapy

58
Q

Rx for myoclonus

A

Removing the offending agent, and considering treatment

with an antiepileptic (valproate), or a benzodiazepine

59
Q

Cornerstone of symptomatic

management of PD that replaces (X) (pre/post)-synaptically.

A

Carbidopa/levadopa
X = DA
Pre-synaptically

60
Q

PD treatment: DA receptor (agonist/antagonist) that acts directly on (pre/post)-synaptic receptors.

A

Pramipexole

Agonst; post-synaptic

61
Q

(X) PD drug is COMT, aka (Y), (stimulator/inhibitor) that increases amount of (Z) available

A

X = entocapone
Y = Catechol O-methyl transferase
Inhibitor
Z = levodopa

62
Q

(X) PD drug is MOA-B (stimulator/inhibitor) that increases amount of (Y) available

A

X = Rasalagine
Inhibitor
Y = dopamine

63
Q

Carbidopa is added to levodopa to:

A

decrease the

nausea

64
Q

Levodopa side effects:

A

N/V, dyskinesias (late side effect)

65
Q

(Levodopa/Pramipexole) does not compete with protein in food and can be taken at any time.

A

Pramipexole (DA agonist)

66
Q

Pramipexole side effects:

A

Drowsiness (sleep attacks);

Others: HA, confusion, compulsions, hallucinations and paranoia

67
Q

Entacapone should be used in combo with (X) to be effective.

A

X = levodopa

since it’s a COMT inhibitor

68
Q

Side effects of Entacapone:

A

Diarrhea, abdominal pain, urine discoloration, liver function changes

69
Q

Side effects of Rasaligine:

A

HA, nausea, HT arthralgia, dyskinesias, hallucinations

70
Q

(X) drug was introduced as an antiviral agent and reported

useful in PD in 1969. What’s its MOA?

A

X = amantadine
DA reuptake blockade
activity, anticholinergic action and blockade of NMDA receptors

71
Q

Side effects of amantadine:

A

Confusion, hallucinations

72
Q

Anticholinergic drug occasionally (now rarely) used for the treatment of PD:

A

Trihexyphenidyl HCl

73
Q

Writing or dancing movements that patients may experience after they have been on dopaminergic medications for 5+ years

A

Dyskinesias (considered “ON” behavior and may not troublesome to patient)

Neuro DRx (10 decks)

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