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Block 8 Week 5 > Rockroth: Movement Disorders > Flashcards

Rockroth: Movement Disorders Flashcards

1
Q

PD is a progressive neurodegenerative disorder associated with the loss of (blank) neurons contributing to the nigrostriatal tract. Degeneration of neurons within the (blank) leads to a shortage of dopamine in this extrapyramidal motor circuit

A

dopaminergic; substantia nigra

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2
Q

Which neurons are the primary victims of PD-related degeneration?

A

the dopaminergic neurons in the PARS COMPACTA of the substantia nigra

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3
Q

Mean age of onset of Parkinsons?

Who gets it, males or females?

A

55 years; 3:2 male:female

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4
Q

About what percentage of dopaminergic neurons are lost before motor signs of the disease emerge?

A

60-80%

**you have to lose lots of your motor neurons before you reach this threshold level

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5
Q

What causes Parkinson’s disease?

A

We don’t know!!
genetics, epigenetics, environmental toxins, diet, multiple causes??
lewy bodies of alpha-synuclein

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6
Q

In PD, the loss of dopamine results in a relative excess of (blank) activity via mACh receptors

A

cholinergic

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7
Q

Clinical manifestations of Parkinson’s disease?

A

TRAP!

Tremor (course resting tremor, “pill rolling”)

Rigidity (increase in muscle tone, “cogwheeling”)

Akinesia (inability to initiate movement) or bradykinesia (slowness of movement), masked facies (reptilian stare), short, shuffling steps

Postural changes (imbalance, loss of righting reflexes), stooped posture

Other: drool, trouble writing, low melody of speech

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8
Q

Parkinson’s is a disease characterized by asymmetry of (blank).

A

motor signs

dopamine vs ACh

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9
Q

What are some drugs that increase dopamine levels?

A

Drugs that increase dopamine:

levodopa combined with carbidopa (prevents peripheral breakdown of L-DOPA)
amantadine
MAO-B inhibitors
COMT inhibitors

dopamine agonists: ropinirole

anti-cholinergics

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10
Q

Why do you combine levodopa with carbidopa?

A

carbidopa is a DOPA decarboxylase inhibitor that doesn’t cross the BBB - it increases the effective concentration of levodopa getting to the brain by preventing its breakdown

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11
Q

How is levodopa different from dopamine?

A

it can cross the BBB via an L-amino acid transporter

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12
Q

What is one downside to the use of L-dopa?

A

it’s short-acting, so it wears off and causes an end-of-dose effect

**works for 2-3 hours, and then the pt returns to previous state of bradykinesia, etc

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13
Q

What is the on-off effect that can occur with patients treated with levodopa?

A

terrible parkinsonism which fluctuates with periods of hyperkinesia

**causes a roller-coaster effect, may be corrected with more continuous dopamine receptor stimulation

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14
Q

Side effects of levodopa?

A

nausea and vomiting
orthostatic hypotension
hallucinations and distorted thinking
dyskinesias (involuntary movements)

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15
Q

What is amantadine? How is it believed to work?

A

used to treat Parkinson’s disease; believed to promote release of dopamine from substantia nigra

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16
Q

One downside to amantadine? Side effects of amantadine?

A

tachyphylaxis: its benefit wears off easily;
restlessness, insomnia, agitation
hallucinations and confusion
livedo reticularis (discoloration of extremities)

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17
Q

How do MAO-B inhibitors increase dopamine levels?

A

inhibit dopamine metabolism to keep more around

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18
Q

When are MAO-B inhibitors used?

A

often used mono-therapeutically for early/mild PD;

in combo with levodopa/carbidopa for advanced PD

19
Q

Give an example of an MAO-B inhibitor

A

rasagiline (Azilect)

20
Q

Side effects of MAO-B inhibitors?

A

confusion, hallucinations
can enhance dopaminergic side effects when taken with levodopa
5HT syndrome

21
Q

When are COMT inhibitors used? How do they work?

A

only in combo with levodopa/carbidopa;
these are catechol-o-methyltransferase inhibitors, they convert levodopa to 3-O-methyldopa which competes w levodopa to access the brain

22
Q

Give an example of a COMT inhibitor?

A

entacapone

**acts at peripheral sites

23
Q

Side effects of COMT inhibitors?

A

nausea/diarrhea
urine discoloration (bright red/orange)
sleep disturbances

24
Q

If you have too much ACh around relative to dopamine, what do you get?

A

parkinsonism

**not to be confused w Parkinson’s disease; Parkinson’s is a cause of parkinsonism

25
Q

If you have too much dopamine around relative to ACh, what do you get?

A

choreoathetosis

26
Q

What things can cause parkinsonism?

A

dopamine inhibitors (antipsychotics)

27
Q

provide more smooth and continuous DM receptor activation than levodopa and rarely cause dyskinesias
do not require functional DM neurons to produce their effects and are therefore sometimes helpful as adjuncts in advanced cases of PD in which few DM neurons remain
used as monotherapy in the early stages of PD

A

dopamine agonists

28
Q

What is one dopamine receptor agonist we should know about?

A

Pramipexole (Mirapex)

**also indicated for treatment of restless leg syndrome

29
Q

Side effects of D2 agonists like Pramipexole?

A 
dizziness and hallucinations
impulse control disorders
hypotension
insomnia
nausea
30
Q

Another D2 agonist that is an ergot alkaloid; rarely used for PD, but used for neuroleptic malignant syndrome

A

bromocriptine

31
Q

What is this?
rigidity, tremulousness, fever, autonomic instability (BP), agitation>delirium>coma
plasma CPK markedly elevated due to rhabdomyolysis
rapidly progressive/manage aggressively
usually caused by “typical” antipsychotic drug

A

neuroleptic malignant syndrome

**use dopamine agonist like bromocriptine

32
Q

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

typically used as adjunctive Rx in combination with levodopa and other drugs that augment DM activity; also frequently used in

A

anticholinergics

33
Q

What are some anticholinergics used in PD?

A

trihexyphenidyl

benztropine mesylate

34
Q

How will your treatment strategy change for younger vs older patients with parkinsonism?

A

in younger pts (less than 65yo), more emphasis on long-term considerations bc they have more life to live! start with a dopamine agonist +/ MAOI, only add levodopa when motor symptoms are no longer in control

in older pts with cognitive impairment, emphasis on decreasing symptoms! start with levodopa/carbidopa

35
Q

What to use for pts who have a disability due only to mild tremor?

A

anticholinergic monotherapy

36
Q

Targeting the subthalamic nucleus (STN) and globus pallidus internus (GPi)
Complimentary to pharmacologic management

A

deep brain stimulation

**this is done in addition to medication, not used alone

37
Q

What type of parkinson’s patient makes a good candidate for deep brain stimulation?

A

tremor is the main symptom, less likely to help balance/gait
excessive “off time”
dopamine-responsive
significant dyskinesia w current med regimen

38
Q

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

A

younger

39
Q

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

A

monotherapy

40
Q

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

A

deep brain stimulation

41
Q

This is a variant of Parkinson’s that looks a lot like it! It’s Parkinson’s disease “in extension,” because they have extension posture. They have impaired eye movements esp vertical gaze, axial rigidity, dysphagia, and typically don’t respond to PD meds

A

Progressive supranuclear palsy

42
Q

Different types of action tremors?

A

physiologic tremor
***symmetric, high freq/low ampl; may involve speech; worse w/ fatigue, caffeine, exposure to cold; better w/ alcohol

essential tremor
**may involve head, central tremor, autosomal dominant pattern

benign familial tremor
**family history of essential tremor

cerebellar intention tremor
**as you get toward the target of the action, the tremor increases!

43
Q

Type of resting tremor

A

parkinsonian

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

Block 8 Week 5 (13 decks)

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