Movement Disorders - Rothrock Flashcards

1
Q

Which pyramidal tract is involved in motor?

A

corticospinal tract

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2
Q

What are the extrapyramidal motor tracts.

A
Basal ganglia
cerebellar
vestibulospinal
rubrospinal
"Mollaret's Triangle"
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3
Q

Parkinsonism is when ACh levels are far greater than (blank) levels

A

dopamine

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4
Q

Choreoathetosis is when Dopamine levels are far greater than (blank) levels

A

ACh

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5
Q

PD is a loss of dopaminergic neurons in the (blank) tract

A

nigrostriatal

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6
Q

PD leads to a shortage of DA in which circuit?

A

extrapyramidal motor cicrcuit

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7
Q

t/F: parkinsonism is the same thing as PD

A

false

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8
Q

What part of the substantia nigra is the primary victim of PD?

A

pars compacta

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9
Q

Where do the fibers of the pars compacta project?

A

to the corpus striatum which is made up of the caudate and putamen

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10
Q

what is the avg. age of onset of PD?

A

55 years

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11
Q

how does PD affect the sexes?

A

male:female 3:2

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12
Q

what percent of the nigrastriatal neurons are lost before the motor signs of parkinson’s emerge?

A

60-80%

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13
Q

what are the potential causes of PD?

A
  1. idiopathic
  2. genetic
  3. environ. toxins
  4. diet
  5. multiple causes
  6. alpha synuclein lewy bodies
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14
Q

what type of ACh receptors are overactivated in PD?

A

mACh which leads to increased GABA release

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15
Q

What is the acronym for the clincal signs of parkinsonism?

A

Tremor
Rigidity
Akinesia (or bradykinesia)
Postural changes (loss of righting reflex, stooped posture)

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16
Q

What is PD characterized by posturally?

A

stooped posture, EXAGGERATED FLEXION

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17
Q

What are the ancillary features of PD?

A
sialorrhea (drooling)
micrographia
hypophonic speech with decreased inflection
slow thinking
subcortical dementia
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18
Q

Is PD characterized by symmetrical or asymmetrical movement?

A

asymmetrical

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19
Q

what are the drugs that increase DA levels?

A
  1. levodopa
  2. MAO-B inhibitors (rasagiline/Azilect)
  3. COMT inhibitors (entacapone/Comtan aka carbidopa)
  4. DM receptor agonists (Requip)
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20
Q

What is the other treatment option for PD that is not increasing DA levels?

A

anti-ACh

anitmuscarinics (Artane)

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21
Q

what is the most robust therapeutic for PD?

A

levodopa

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22
Q

How does levodopa enter the brain?

A

via the L-amino transporter

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23
Q

Can actual dopamine cross the BBB?

A

noooope

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24
Q

what is the issue with levodopa half life?

A

short; end-of-dose effect is common; peak-dose effect leads to hyperkinesia

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25
What enzyme converts levodopa to Da?
L-amino acid decarboxylase (DOPA decarboxylase)
26
Where in the body is DOPA decarboxylase found?
peripheral tissue and in the brain!
27
Because of the presence of DOPA decarb'ase in the periphery, what do we give with L-DOPA and why?
carbidopa, a DOPA decarb'ase inhibitor that DOES NOT CROSS THE BBB to increase effective dose of L-DOPA reaching the brain
28
what are the SE of levodopa?
N/V orthostatic hypotension hallucinations and distorted thinking dyskinesias, fixed dystonias, choreoathetosis
29
Amantadine promotes DA release from the...
substantia nigra
30
In what severity of PD do you use amantadine?
early/mild cases of PD
31
which DA increasing drug shows tachyphylaxis?
Amantadine; effects are short lived
32
What are the SE of amantadine?
restlessness, insomnia, agitation hallucinations and confusion livedo reticularis (lacy purple skin discoloration)
33
How do MAO-B inhibitors work?
inhibit DA metabolism; good for early/mild PD; use with levodopa/carbidopa for adv. PD
34
What are the SE of MAO-B inhibitors?
confusion, hallucinations Enhance DA SE (GI distress, dyskinesia) when taken with levodopa Serotonin syndrome in pts taking SSRIs
35
T/F: COMT is only found in the brain
false; found in brain and peripheral tissues
36
What is the action of COMT?
converts levodopa to 3-O-methyldopa which competes with levodopa for transport into the brain
37
T/F: COMT inhibitors can be used as monotherapy
false; used as adjunctive with levodopa
38
Where do the COMT inhibitors work?
in the periphery so the levodopa can make it to the brain
39
What are the SE of COMT inhibitors?
N/V Urine discoloration (orange, red, brown, or black) sleep disturbance
40
DA receptor agonists activate which DA receptor?
D2 receptors
41
What is the plus of using a DA receptor agonist over levodopa?
provider a smoother and more continuous receptor activation and rarely cause dyskinesia
42
T/f: D2 agonists require functional DA neurons
false; that's why they are good in adv. PD where there are few DA neurons!!
43
T/F: D2 agonists can be used as monotherapy
true; in early cases of PD
44
what's the plus for using D2 agonists with levodopa?
decrease the "off" period and decreases the dose requirement
45
What are the side effects of D2 receptor agonists?
``` Dizziness and hallucinations Impulse control disorders Hypotension Insomnia Nausea ```
46
What completely unrelated dz are D2 agonists also indicated for?
restless leg lol
47
which D2 agonist is a ergot alkaloid?
Parlodel
48
Which D2 receptor agonist is used to treat neuroleptic malignant syndrome?
Parlodel
49
What are the clinical signs of NMS?
rigidity, tremulousness, fever, autonomic instability (BP), agitation>delirium>coma
50
plasma (blank) is elevated due to rhabdomyolysis from NMS
plasma CPK
51
T/F: NMS progresses rapidly and requires aggressive tx
true
52
What causes NMS?
typical antipsychotics like butyrophenones, phenothiazines, and promethazine ALSO atypical antipsychotics
53
mACh receptor agonists may improve tremor in early PD but have little effect on (blank and blank)
rigidity and bradykinesia
54
What are the side effects of mACh receptor agonists?
dry mouth urinary retention confusion and memory impairment (think opposite of SLUDGE syndrome)
55
what is the treatment strategy for PD in pts younger than 65?
1. more emphasis on long-term considerations 2. start with D2 agonist 3. add levodopa/carbidopa when agonist no longer sufficient
56
What is the treatment strategy for older pts with PD?
1. emphasis on providing symptomatic relief w/ few SE | 2. use levodopa/carbidopa
57
T/F: pts that only have mild tremor can go on anti-mACh monotherapy
true
58
deep brain stimulation targets which two brain structures?
subthalamic nucleus and globus pallidus internus
59
what is the target Sx for deep brain stim?
tremor; DBS less likely to help balance and gait excessive off time DA-responsiveness Sig. dyskinesia with current meds
60
t/F: initial trial of levodopa/carbidopa can be used to help confirm a PD Dx
true
61
What drugs are the preferable initial rx?
D2 agonist and MAO-B inhibitors; especially in younger pts
62
T/f: COMT inhibitors can be used in monotherapy
false; use w/ levodopa
63
What are the signs of Progressive supranuclear palsy?
``` impaired eye movements (vertical) -- doll's eye axial rigidity mild, slowly progressing dementia dysphagia refractory to PD meds ```
64
Describe a physiologic tremor
Action tremor: | symmetric, high freq/low ampl; may involve speech; worse w/ fatigue, caffeine, exposure to cold; better w/ alcohol
65
Describe an essential tremor
may involve the head; autosomal dom inheritance
66
describe the parkinsonian resting tremor?
asymmetric, low freq/high amplitude; tends to spare speech and head