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Block 8 week 5 > Movement Disorders-Rothrock > Flashcards

Movement Disorders-Rothrock Flashcards

1
Q

What motor systems are pyramidal?

A

corticospinal tract

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2
Q

What motor systems are extrapyramidal?

A
  • basal ganglia
  • cerebellar
  • vestibulospinal
  • rubrospinal
  • “mollaret’s triangle”
  • etc
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3
Q

When you have more acetycholine than dopamine then what is the disorder?

A

Parkinsonism

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4
Q

When you have more dopamine than acetylcholine what is the disorder?

A

Choreoathetosis

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5
Q

(blank) is the occurrence of involuntary movements in a combination of chorea (irregular migrating contractions) and athetosis (twisting and writhing). It is caused by many different diseases and agents.

A

Choreoathetosis

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6
Q

PD is a progressive neurodegenerative disorder associated with the loss of dopaminergic neurons contributing to the (blank) tract.

A

nigrostriatal

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7
Q

Degeneration of neurons within the substanti nigra (SN) leads to shortage of dopamine in the (blank) motor circuit

A

extrapyramidal

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8
Q

Is parkinsonism synonymous with parkinson’s disease?

A

no

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9
Q

The dopaminergic neurons within the (blank) of the substantia nigra (which project to the corpus striatum= caudate and putamen) are the primary victims of PD-related degeneration.

A

pars compacta

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10
Q

What is the mean age of onset of Parkinson’s?
Who does it affect more, males or females?
What is the incidence?
What is the prevalence?

A

55 years (17-85)
Male: female (3:2)
20/100,000
187/100,000

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11
Q

In Parkinson’s, approx (blank) percent of dopaminergic nigrastriatal neurons are lost before the motor signs of the disease emerge

A

60-80%

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12
Q

What are the causes of Parkinson’s disease?

A
  • Idiopathic
  • Genetic mutations or variations/epigenetics
  • environmental toxins (pesticides)
  • diet
  • multiple, interesecting causes
  • Lewy bodies> alpha synuclein
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13
Q

In PD, the loss of dopamine results in relative excess of (blank) activity

A

cholinergic activity

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14
Q

The (blank) system is a monosynaptic tract (axons travel from the motor cotex-> posterior limb of the internal capsule-> decussates in the pyramids of the medulla-> down the spinal cord and synapses in anterior horn)

A

pyramidal

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15
Q

The inferior olive sends a fasciculus to the inferior olive via the (blank)

A

central tegmental tract

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16
Q

What causes palato-myoclonus?

A

lesions in the central tegmental tract due to MS

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17
Q

(blank) is the only movement symptoms that does not disappear with sleep

A

Palato-myoclonus

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18
Q

What class of drug induces parkinsons?

A

Anti-psychotics (haloperidol)

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19
Q

What is the acronym for the clinical manifestations of PD?

A

TRAP

  • tremor
  • rigidity
  • akinesia
  • postural changes
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20
Q

What is the tremor like in PD?

A

(3-6 per sec) - observed in resting distal muscles; pill rolling motion
i.e resting tremor

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21
Q

What is the rigidity like in PD?

A

an increase in muscle tone (ie, increased resistance to passive movement at a joint); the resistance can be either smooth (lead-pipe) or jerky (“cogwheeling”)

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22
Q

What is the akinesia like in PD?

A

(inability to initiate movement)/bradykinesia (slowness of movement)>poverty of facial expression (decreased blinking>”reptilian stare”); short, shuffling steps; “freezing” of movement (esp gait initiation)

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23
Q

What is the postural change like in PD?

A

imbalance and loss of righting reflexes (thus falls); stooped posture (PD is a disease characterized by exaggerated flexion.)

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24
Q

PD is a disease charactered by exaggerated (blanK)

A

flexion

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25
Q

What are some other features of PD?

A
  • sialorrhea (hypersalivation);
  • micrographia (small handwriting);
  • speech: hypophonic (soft speech),
  • decreased inflection, “rushed”;
  • slow thinking; “subcortical” dementia
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26
Q

With the exception of the variant characterized chiefly by axial rigiity, Parkinson’s is a disease characerized by (blank) of motor signs

A

asymmetry

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27
Q

What are drugs that increase dopamine for tx of parkinsons?

A
  • Levodopa (L-dopa) + Carbidopa
  • amantadine
  • MAO-B inhibitors
  • COMT inhibitors
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28
Q

What are the MAO-B inhibitors for parkinsons?

A

Rasagiline

Azilect (works better in CNS)

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29
Q

What are the COMT inhibitors?

A 
Entacapone
Comtan (analogous to carbidopa)
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30
Q

What are the DM receptor agonists used to treat parkinsons?

A

Ropinirole

Requip

31
Q

What are the anticholinergics (antimuscarinics) used to treat parkinsons?

A

trihexyphenidyl

artane

32
Q

What drug has the most robust therapeutic effect for parkinson treatment and what is it effective for?

A

Levodopa (L-dopa)

-ameliorates all the clinical features of PD

33
Q

How does L-dopa get into the brain? What are its downfalls?

A

via an L-amino acid transporter

-it goes in waves so you have a peak amount causing hyperkinesia and then it will fall back down to normal levels etc.

34
Q

Levodopa is converted to DM by the enzyme (blank) which is present in peripheral tissues as well as the brain. What do you have to give with levodopa so that it wont be converted to dopaine in the periphery? how does it work? Whats the ratio of carbidopa to levodopa?

A

aromatic L-amino acid decarboxylase
Carbidopa, it is a decarboxylase inhibitor and cannot cross the BBB so L-dopa will not convert to dopamine until it crosses BBB
1: 10 (carbidopa: levodopa)

35
Q

What are side effects of levodopa?

A
  • Nausea and vomiting
  • Orthostatic hypotension (tends to diminish over time)
  • Hallucinations and distorted thinking
  • Dyskinesias (involuntary movements):
  • fixed dystonias (typically ankle inversion)
  • choreoathetosis (typically a late-developing effect and dose-related)
36
Q

How does amantadine work?
What is it used for?
What are the side effects?
What are downfalls of it?

A
  • promotes early release of DA from substantia nigra
  • early/mild cases of PD and as an adjunct to levodopa

SEs:
restlessness, insomnia, agitation
hallucinations and confusion
livedo reticularis

Can cause tachyphylaxis and its benefits tend to be short-lived

37
Q

(blank) is a common skin finding consisting of a mottled reticulated vascular pattern that appears as a lace-like purplish discoloration of the skin. The discoloration is caused by swelling of the venules owing to obstruction of capillaries by thrombi

A

livedo reticularis

38
Q

What is the MOA of MAO-B inhibitors?
How do you give it and what is it used for?
The use of these may require reduction in what?
What is an example of this?

A

inhibit metabolism of dopamine within the brain;
used as monotherapy for early/mild PD and as adjunctive Rx with levodopa/carbidopa for advanced PD;
their use may require reduction in levodopa dose

Rasagiline (azilect)

39
Q

What are the SEs of MAO-B inhibitors?

A

Confusion, hallucinations
Can enhance dopaminergic side effects (GI distress; dyskinesias) when taken with levodopa
Serotonin syndrome in patients taking SSRIs and other drugs that increase 5-HT levels

40
Q

How does Catechol-O-methytransferase (COMT) inhibitors work?’

A

COMT, an enzyme found in both the brain and in peripheral tissues, converts levodopa to 3-O-methyldopa, which competes with levodopa for transport into the brain
These drug inhibit this so that levodopa wont have any competition.

41
Q

How do you give COMT inhibitors?

A

Used as adjunctive Rx with levodopa/carbidopa; may require reduction in levodopa dose

42
Q

What is an example of a COMT and where does it work?

A

entacapone (comtain)

acts predominantly at peripheral sites (a formulation combining levodopa, carbidopa and entacopone is available)

43
Q

What are SEs of COMT?

A

Nausea and diarrhea
Urine discoloration (orange, red, brown or black)
Sleep disturbances

44
Q

Why are DM receptor agonists awesome?

A

they provide more smooth and continuous DM receptor activation than levodopa and rarely causes dyskinesias
AND
dont require funcitonal DM neurons to work so is still effective when few DM neurons remain

45
Q

What is used as monotherapy in the early stages of PD (reserved for younger individuals who are cognitively intact) and thus delay the need for levodopa?

A

DM receptor agonists

46
Q

DM receptor agonists lack sufficient efficacy to control signs and symptoms by themselves in more advanced disease but can decrease the (blank) when using levodopa and decrease the (blank) requirement

A

“off” period (remember l-dopa levels fluctuate in the brain so D2 agonists will help out when the L-dopa levels are low)
levodopa dosage

47
Q

What is a common D2 agonist?
What are the side effects?
What is it also indicated for?
What are some less common D2 agonists?

A

Pramipexole (Mirapex)

Dizziness and hallucinations
Impulse control disorders 
Hypotension 
Insomnia 
Nausea

Restless leg syndrome

Other agents: ropinirole (Requip), rotigotine (Neupro patch)

48
Q

What is bromocriptine (parlodel)?

What is it used for?

A

a D2 agonist that is an ergot alkaloid

-neuroleptic malignant syndrome

49
Q

What is NMS?

A

Rigidity, fever, tremors, autonomic instability, agitation, delirium, coma.
Rhabdomyolysis and CPK increase
-caused by “typical” antipysychotic drugs (promethazine) and “atypical” antipsychotics (risperidone)

50
Q

What are some typical antipsychotic drugs that can cause NMS?

A

butyrophenones, phenothiazines (including promethazine)

51
Q

What are some other ways you can cause NMS?

A

risperidone, metoclopramide, Lithium and decrease in levadopa dose

52
Q

(blank) may improve tremor in early PD but have little effect on rigidity and bradykinesis (thus most useful when tremor is the major clinical feature)

A

Anticholinergics (mACH receptor antagonists)

***in past used to treat parkinsonism caused by DM receptor ANTagonists)

53
Q

How do you use anticholinergics?

A

-used as adjunctive Rx in combo with levodopa and other drugs that augment DM activity

54
Q

What are some anticholinergics used to treat parkinsons?

A 
trihexyphenidyl (Artane) 
benztropine mesylate (Cogentin)
55
Q

What are the side effects of anticholinergics?

A

Dry mouth
Urinary retention
Confusion and memory impairment

56
Q

How do you treat patients less than 65 years old?

A

long term tx-> start with DM agonist +/- MAO inhibitor
THEN
add levodopa/carbidopa when the agonist no longer provides good control of motor symptoms.

(you do this because they are more likely to develop motor fluctations and dyskinesias because they will have a longer life expectancy)

57
Q

How do you treat older patients with cognitive impairment (older than 65)?

A

– emphasis on providing adequate symptomatic relief with as few adverse effects as possible; use levodopa/carbidopa

58
Q

How do you treat a patient who has a disability due only to mild tremor?

A

monoRx with an anticholinergic

59
Q

What does DBS do?

A

targets the subthalamic nucleus (STN) and globu pallidus internus (GPi)
-> work complimentary to pharmacologic managment

60
Q

What is the main “target” symptom/sign for DBS and why?

What are good reasons to prescribe DBS?

A

tremor
because DBS doesnt really help other symptosm
-excessive “off” time
-dopamine-responsive
-significant dyskinesia with current med regiment

61
Q

T or F
An initial trial of carbidopa/levodopa can be helpful to confirm diagnosis and also to assess responsiveness to this drug.

A

T

62
Q

Dopamine agonists and MAO-B inhibitors may be preferable as initial Rx, particularly in (blank) patients

A

younger patients.

63
Q

(blank) are complimentary to l-dopa and are not useful as monotherapy agents.

A

COMT inhibitors

64
Q

In more advanced patients who are reaching their limit with meds, consider whether they may be good candidates for (blank).

What can also help?

A

DBS.

Physical therapy

65
Q

What seems like parkinsons but is not and has these characteristics:

  • “Parkinson’s in extension”
  • impaired eye movements (esp vertical gaze i.e cant look down) but “doll” easily (blink when trying to look down)
  • axial rigidity
  • mild, slowly progressive dementia
  • dysphagia
  • typically refractory to PD meds
  • fall very easily
A

Progressive Supranuclear Palsy

66
Q

What are the four types of tremors?

A
  • Physiologic tremor
  • Essential tremor
  • Benign familial tremor
  • cerebellar “intention” tremor/rubral tremor
67
Q

What is the only resting tremor?

A

parkinsonian

68
Q

What tremor is this:
symmetric, high freq/low ampl; may involve speech; worse with fatigue, caffeine, exposure to cold; better w/ alcohol. All people normally have this;

A

Physiologic tremor

69
Q

What tremor is this:
symmetric, high freq/low ampl; may involve speech; worse with fatigue, caffeine, exposure to cold; better w/ alcohol
may involve head and can have an autosomal dominant pattern of inheritance and is a central tremor

A

essential tremor

70
Q

What is this:

is an essential (central) tremor that runs in families and can involve the head

A

benign familial tremor

71
Q

What tremor is this:

asymmetric, low freq/high amplitude; tends to spare speech and head

A

parkinsonian

72
Q

Is a physiologic tremor normal?

A

yes everyone has it

73
Q

What is the worst intetion tremor?

A

a rubral tremor

74
Q

is characterized by coarse slow tremor which is present at rest, at posture and with intention. This tremor is associated with conditions which affect the red nucleus in the midbrain, classically unusual strokes.

A

A rubral tremor

Block 8 week 5 (9 decks)

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