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CNS Module: Exam 2 > Parkinson's > Flashcards

Parkinson's Flashcards

1
Q

What are the motor complications associated with Parkinson’s?

A
  • decreased ability to perform ADL’s (activities of daily living)
  • increased risk for falls and fractures
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2
Q

What are the NON-motor complications associated with Parkinson’s?

A
  • cognitive impairment/dementia
  • apathy, depression and/or psychosis affect QoL
  • swallowing, GI, speech difficulties
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3
Q

What are thought to be the causes of Parkinson’s?

A
  • head trauma
  • genetic
  • environmental (exposure to pesticides, well water?)
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4
Q

why is DA deficiency important?

A

DA deficiency is responsible for the core motor features
- neuronal injury/loss of substantia nigra pars compacta (MAJOR source of DA projections to basal ganglia)

  1. prion-like pattern spread of misfolded proteins from peripheral tissue to brainstem (early premotor and non-motor sx)
  2. motor symptoms present
  3. cortical regions! = late onset dementia
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5
Q

What mechanisms cause PD?

A
  • mitochondrial dysfunction
  • oxidative stress
  • neuroinflammation
  • faulty protein degradation
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6
Q

Bradykinesia definition

A

slowness of movement

  • gait
  • facial expressions
  • ask them to snap, stand/sit
  • tremor
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7
Q

Parkinsonism diagnosis:

A

Bradykinesia + (tremor OR rigidity)

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8
Q

Parkinson’s diagnosis:

A
  • clinical exam
  • MRI (to rule out hydrocephalus, diffuse vascular disease or mass/lesions if UNUSUAL presentations)
  • SPECT (single-photon emission computed tomography): nuclear imaging scan that integrates computed tomography and a radioactive tracer
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9
Q

Parkinsonism vs Parkinson’s

A

ParkinsonISM:

  • secondary to neurodegenerative disorders
  • Drugs (metoclopramide, FGA & SGA)

PD:
- idiopathic (unknown cause)

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10
Q

What are the symptoms of PD?

A
  • stooped posture
  • masked face
  • back rigidity
  • forward tilt of trunk
  • flexed elbows and wrists
  • hand tremor
  • reduced arm swing
  • tremors in the legs
  • slightly flexed hip and knees
  • shuffling/short stepped gait
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11
Q

What features support diagnosis of Parkinson’s?

A
  • unilateral onset of tremor, bradykinesia, rigidity
  • persistent asymmetry of motor signs
  • falls (later in progression)
  • significant loss of smell
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12
Q

What features exclude diagnosis?

A
  • essential tremor (postural & kinetic vs resting)
  • symmetry of motor signs at onset
  • falls at presentation or EARLY
  • strokes with stepwise progression of parkinsonian feature
  • head injuries
  • encephalitis
  • neuroleptic tx at onset of sx
  • sustained remission
  • early/severe autonomic involvement, disturbances of memory, language, and praxis
  • cerebral tumor
  • supernuclear gaze palsy
  • negative response to lots of levodopa
  • MPTP exposure
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13
Q

How do PD patients typically respond to levodopa?

A

excellent response
> 10 yr response

(severe levodopa induced chorea)

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14
Q

What are the motor related S&S?

A

T remor
R igidity
A kinesia/bradykinesia
P ostural instability

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15
Q

What are the NON-motor related S&S?

A
  • malaise
  • easily fatigued
  • subtle personality changes
  • sleep disorder
  • constipation
  • pn
  • depression
  • dementia
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16
Q

What does a tremor of PD look like?

A

slow frequency; AT REST

  • inhibited during movement & sleep
  • aggravated by emotional stress
  • pill rolling quality
  • look at upper & lower extremeties @ rest
  • have pt reach out hands, tremor would reemerge after several seconds delay
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17
Q

Rigidity defintion:

A

resistance to efforts by the clinician to elicit passive joint movement
- may be any part of the body & related to stiffness/pn

  • examine for rigidity & ask about stiffness/pn
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18
Q

Bradykinesia definition:

A

generalized slowness of movements & repetitive movement fatigue
- may be decr. facial expression, difficulty with fine motor tasks, speaking softer, difficulty turning/getting out of bed/chair/car, shortened or dragging steps

  • observe sitting/walking
  • pt complains of: weakness, sluggishness, tiredness
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19
Q

Surgical intervention?

A
  • ablative surgery
  • pallidotomy (posterolateral part of the globus pallidus interna – contralateral dopamine)
  • thalamotomy (ventral intermediate nucleus – contralateral intractable tremor)
  • deep brain stimulation
  • –> thalamic stimulation (ventral intermediate nucleus)
  • –> pallidal stimulation
  • –> subthalamic stimulation (best at decr. contralateral bradykinesia & tremor)
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20
Q

Non-pharm options

A
  • PT
  • OT
  • Speech
  • Psychology

generally VERY beneficial

  • exercise may help improve motor function
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21
Q

What meds do we use in early disease?

A

MAO-B (selegiline, rasagiline, safinamide)
Amantadine
Anticholinergics (cogentin, artane)
DA agonists (requip, mirapex, neupro)

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22
Q

When do we avoid anticholinergics?

A

patients > 70 yo

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23
Q

When do we want to use DA agonists?

A

< 65 yo

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24
Q

Selegiline

A

early stages of PD or adjunct to L-dopa (delay levo by 9 mo)

  • improves wearing off
  • DI: meperidine, DM, sympathomimetic amines, SSRI

(MAO-Bi)

25
What are MAO-Bi known for?
worsening dyskinesias
26
Rasagaline
- mono or adjunct to levo - improves wearing off * treat motor complication of random-off CI: cyclobenzaprine, mirtazapine, St. John's wort, meperidine, methadone, tramadol, DM, sympathomimetic amines
27
Safinamide
adjunct tx of wearing off (without worsening dyskinesias) - no dietary restriction of tyramine CI: MAOi, opioids, DM, SNRI, TCA, Cyclobenzaprine, methylphenidate, amphetamines, St. Johns wort
28
Amantadine
EARLY PD * benefit w/i a couple of days improve dyskinesias & may alleviate tremor! CAUTION: geriatric SE: livedo reticularis (reddish mottling of skin), ankle edema, hallucinations (+) decr. severity of dopa induced dyskinesias (antiglutamatergic) (-) tolerance may develop, cognitive SE, withdrawal potential
29
Anticholinergics
(benztropine, trihexyphenidyl) - tremor = not relieved by agonist or l-dopa - combo c other meds for PD - improve bladder dysfunction (female) & drooling * not in pt > 70 yo
30
Anticholinergic AE
- forgetfulness/ decr. ST memory - hallucinations, psychosis - dry mouth - blurred vision - constipation - trouble with urination (worsens BPH)
31
What do we use in mod-severe disease?
1. DA agonists 2. Levodopa/carbidopa 3. Combo tx
32
Peripheral AE of DA agonists
- N/V | - ortho HoTN
33
Central AE of DA agonists
- motor changes - dyskinesias - psychiatric disturbances - pedal edema - pleuropulmonary (ergots)
34
Are DA agonists or L-dopa more likely to cause dyskinesias?
L-dopa
35
DA agonists
(+) antiparkinsonian effects, decr. risk for l-dopa related motor complications (-) neuropsych SE, erythromelagia, pedal edema, sedative SE * 4-6 wks before you can see improvements
36
L-dopa counseling points
- avoid giving WM to improve absorption in severe disease AE: - dopaminergic - peripheral (usually controlled by adding carbidopa) - central * at least 3 days bw dose adjustments - 2-3 wks for therapeutic response (quicker than DA agonists)
37
L-dopa advantages & disadvantages
(+) best anti-parkinsonian drug, works with most pts, maybe improve mortality? (-) SE, dyskinesias/dystonias, motor changes, neuropsych sx, sedation
38
Initial tx: levodopa/carbidopa 1. age 2. funct 3. AE
1. all pt 2. sustained tx benefits 3. dyskinesias/ motor fluctuations
39
Initial tx: DA agonists 1. age 2. funct 3. AE
1. immediate tx response NOT needed (< 65 yo) 2. decr. risk of dyskineasias/motor complications 3. incr. risk for impulse control disorder
40
What agents are adjunct tx?
- COMTi - apomorphine - istradflylline (adenosine a2 blocker)
41
Catachol-O-methyl-transferase (COMT)
- extend levodopa effect = decrease "off" time | - may incr. dyskinesias --> DECR. L-dopa dose
42
COMTi AE
- diarrhea - central & peripheral DA SE - liver toxicity (tolcapone)
43
COMT (+) & (-)
(+) decr. "off" time, enhanced motor responses in pts with L-dopa motor fluctuation, improved ADL scores if stable L-dopa responders * better if at onset of L-dopa tx (-) DA SE (dyskinesias), discoloration of urine, - tolcapone: explosive diarrhea, liver tox
44
Apomorphine
- acute, intermittent tx of hypomobility "off" episodes CI: 5HT3 & COMTi AE: - severe N/V (coadmin w/ trimethobenzamide) - angina - cardiac arrest - HoTN & ortho HoTN - MI - syncope
45
Istradeflylline
- for "off" periods as adjunct to carbi/levo special dosing for: - smoking > 20 cig/d = 40 mg - on CYP3A4i = 20 mg - CYP3A4 inD = DO NOT USE
46
Istradeflylline AE:
- dyskinesias - dizziness - constipation - N - hallucinations - insomnia
47
What happens with DA excess?
- dyskinesias - hallucinations - delusions
48
What happens with DA deficiency?
worsening PD symptoms
49
What do we do abt: Random off?
sx unrelated to med dosing time 1. entacapone and rasagiline 2. pergolide, pramipexole, ropinirole, tolcapone 3. apomorphine, cabergoline, selegiline
50
What do we do abt: wearing off?
sx @ the end of dosing interval (plasma levels decr.) - incr. dose frequency - CR carb/levo - DA agonist - selegiline, rasagiline - COMTi - amantadine
51
What do we do abt: dyskinesias?
involuntary movements during PEAK plasma levels - amantadine - smaller/ more frequent doses
52
What do we do abt: dystonias?
sustained muscle contractions/ abnorm postures (distal lower extremeties) - HS SR carbido/levod - DA agonists - baclofen - botulinum toxin
53
What can we use for depression in PD pts?
- SSRI, SNRI, bupropion - TCADs (amitriptyline, nortriptyline, desimpramine) * caution c worse cognition, ortho HoTN --> fall risk (pramipexole with motor & mood sx are targeted
54
What can we use for psychosis with PD?
- Quetiapine - Pimavanserin - Clozapine
55
What about PD + mild cognitive impairment?
- atomoxetine
56
What about dementia + PD?
- donepezil | - rivastigmine
57
What if pt experiences ortho HoTN?
1. incr. fluids + Na consumption, elevate head of bed, compression stockings (non-pharm) 2. fludrocortisone 3. midodrine
58
What is Sialorrhea? How do we treat?
excess drooling 1. glycopyrrolate/scopolamine transderm 2. botulinum tox 3. atropine drops

CNS Module: Exam 2 (8 decks)

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