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PT III > Parkinson's and Movement Disorders > Flashcards

Parkinson's and Movement Disorders Flashcards

1
Q

What are the classical symptoms of parkinson’s disease?

A

Asymmetrical bradykinesia

Hypokinesia

rigidity (cog-wheel)

tremor (pill rolling)

gait (shuffle)

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2
Q

What are the non-motor sx of parkinsons disease?

A

Constipation

REM sleep disturbances

PLMS/RLS

hyposmia

Depression/anxiety

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3
Q

What are the non-dopamine related sx of parkinson’s disease?

A

Posture disturbances

dec autonomic function

speech changes

cognitive changes

Pain

seborrhoea

weight loss

fatigue

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4
Q

What is an essential tremor?

A

Neurological cause of action tremor different from parkinsons

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5
Q

Describe the pathophysiology of parkinson’s disease?

A

Dopamine depletion from basal ganglia –> disrupt connection to thalamus and motor cortex –> parkinsonians signs

DA depletion in substantia nigra and nigrostriatal pathway –> inc inhibition of thalamus, reduced excitatory input into motor cortex –> bradykinesia and other parkinsonian signs

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6
Q

What is the role of the nigrostriatal pathway?

A

Nigrostriatal pathway = coordination of movement

hypokinesia of intentional movement and resting tremor

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7
Q

What is the role of the mesocortic pathway?

A

attention, cognition

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8
Q

What is the role of the mesolimbic pathway?

A

pleasure response

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9
Q

What is the role of the tuberoinfundibular pathway?

A

sexual dysfunction

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10
Q

Does parkinsons disease have more DA or ACH?

A

Hypokinetic state has more ACH and less dopamine

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11
Q

What are the five cardinal symptoms of parkinson’s disease?

A

Tremor - pill rolling

Rigidity - almost all patients

Bradykinesia - slowness in performing voluntary movement, reduced facial movement

hypokinesia - reduced ability to initiate movement/freezing

Postural instability/gait disorder - stooped flexed posture

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12
Q

What are the dopamine prodrugs used in parkinsons?

A

Levodopa (+carbidopa or benserazide)

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13
Q

When is parkinson’s therapy started?

A

When symptoms/functional disability becomes a problem for the patient

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14
Q

What is the first line therapy for parkinsons disease?

A

Levodopa (+carbidopa or benserazide) = choice in older people

Can start with dopamine agonist in younger patients w/ significant motor disability

Use anticholinergics if tremor predominates

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15
Q

How is levodopa used in parkinsons disease?

A

Used as first line - improves bradykinesia and rigidity

Need 75mg/day of benserazide or carbidopa to adequately inhibit peripheral dopamine production

Start low, gradual inc

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16
Q

What is a common ADR of levodopa and how is it treated?

A

Nausea - treat with domperidone (be mindful of QT prolongation)

17
Q

What happens in levodopa is dosed too high or too low?

A

Too high = pt becomes dyskinetic - involuntary, writhing movement

Too low = akinetic - no movement/ can’t move muscles on own

18
Q

What is the levodopa end dose effect?

A

When the pattern between the on (w/ dopamine) period becomes unpredictable with the pt experiencing off (when there is no dopamine) when they should be in an on period

19
Q

How does the action of levodopa differ during advanced PD compared to early PD?

A

Advanced - inadequate symptom control, short duration of clinical result followed by an ON period where dyskinesia returns

Early - Sx control food, smooth and extended durations of movement, low dyskinesia

20
Q

List some strategies that can be used to overcome the end of dose effect

A

Combine levodopa and dopamine agonist

Use modified release levo

Smaller more frequent doses of levodopa

adjust dietary protein

switch to dopamine agonists

Use COMT inhibitors (entacapone)

use rasagiline or selegiline

21
Q

What is dyskinesia?

A

Difficulty performing voluntary movement

22
Q

What is dystonia?

A

Involuntary muscle contractions - slow repetitive movements or abnormal posture

23
Q

What are motor fluctuations?

A

Rapid (sometimes unpredictable) fluctuations of akinetic (off) and on (normal of dyskinetic) state

24
Q

What is the role of dopamine agonists in parkinsons disease?

A

Less effective than levodopa as initial therapy - delay onset of dyskinesia and motor fluctations

improve bradykinesia and rigidity

Higher incidence of = confusion, impulse control disorders, hallucinations

25
Q

What are the ergot derivative dopamine agonists? Why are they worse/better?

A

Bromocriptine, cabergoline, pergolide

High doses needed –> inc ADRs
- can cause respiratory or cardiac valve fibrosis

26
Q

What are the non-ergot derivative dopamine agonists? Why are they worse/better?

A

Pramipexole - MR

Rotigotine - transdermal patch

Apomorphine - highly emetic, subcut

27
Q

How is entacapone used in parkinsons disease?

A

Prolongs clinical response to levodopa - used as adjunct to levodopa in patients with motor fluctuations

Pushed dyskinesia a bit more

28
Q

What are the MAO-B inhibitors used in parkinsons disease and what are their roles?

A

Inhibit the metabolism - breakdown - of dopamine

Selegiline (adjunct) - reduces off time in advanced disease

Rasagiline (mono or adjunct) - theoretical risk of MOA-food interactions

29
Q

What is the role of anticholinergics in parkinsons disease? (name some drugs)

A

Used as adjunctive tx when tremor is troublesome - poor efficacy

anticholinergic ADRs = dry mouth, constipation, urinary retention, hallucinations, cog impair, confusion

Benzhexol, benztropine, biperiden

30
Q

How is nausea treated in parkinsons?

A

Worse at initiation and inc dosage

Used = domperidone 10mg tds

AVOID = metoclopramide, prochlorperazine, and other centrally acting dopamine-blocking antiemetics

31
Q

List the CNS effects of Parkinsons disease

A

Hallucinations - secondary to meds (reduce dose)
- occasional + retained insight - don’t treat
- Troublesome = tx w/ antipsychotics - clozapine or quetiapine

Sleep disturbances

Depression - SSRI tx - no quetiapine

Cognitive impairment

Dementia

32
Q

How is orthostatic hypotension treated in parkinsons disease?

A

Defined by drop of 20 mmHg systolic on postural change

Tx: add salt to diet, fludrocortisone
- may add domperidone - QT interval prolongation

33
Q

What are the huntington’s disease symptom triad?

A

Personality changes = impulsive, aggressive

Cognitive decline

chorea = involuntary, irregular movements - dance like

34
Q

How is huntington’s disease treated? (chorea)

A

Tetrabenazine - depleted dopamine and MOA

Antidopaminergic drugs - atypical antipsychotics

Riluzole - antiglutaminergic + neuroprotective

Nabilone

Tx depression - SSRI

35
Q

How is mild restless leg syndrome treated?

A

Its not

36
Q

How is troublesome restless less syndrome treated?

A

Low dose dopamine agonist

Levodopa/ pramipexole/ ropinirole

ADRs = rebound legs, can worsen sx or make it syndrome occur earlier in the day

PT III (6 decks)

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