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Neuro Rehab II > Parkinsons > Flashcards

Parkinsons Flashcards

1
Q

Parkinsons disease most commonly begins at what age?

A

between 55 and 60

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2
Q

Annual incidence of PD (age range > or = 65)

A

160/100,000 (14/100,000 all age groups)

59,000 (estimated # of US cases in 2005, nearest 1000)

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3
Q

Prevalence of PD (age range > or = 65)

A

9.5/1000

349,000

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4
Q

PD:

  1. Ratio of M:F
  2. Age of peak incidence
A
  1. 1.5

2. > or = 70

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5
Q

Meta-analysis of 6 european studies (n=819 PD) published between 1995 and 2004 compared with population-wide statistics from UK:
For the following, answer life expectancy and avg age of death
1. Age at onset 25-39:
2. Age at onset 40-64
3. Age at onset 65+

A
  1. 38; 71
  2. 21; 73
  3. 5; 88
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6
Q

8 patient complaints with PD

A
  1. Tremor
  2. Weakness/slowing down/fatigue
  3. difficulty rolling over in bed, getting up out of chairs
  4. change in handwriting
  5. slow gait, dragging feet
  6. slurred speech
  7. imbalance
  8. muscle pain
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7
Q

Clinical diagnosis of PD requires what 3 things?

A
  1. Tremor (pill-rolling)
  2. Muscular rigidity (cogwheeling)
  3. Slowness and restricted movement - bradykinesia
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8
Q

9 “secondary signs” of PD

A
  1. Decreased arm swing
  2. Shuffling gait/festination
  3. hypomimia
  4. micrographia
  5. sialorrhea
  6. dysarthria, hypophonia, monotonous speech
  7. postural instability
  8. freezing
  9. late onset dementia
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9
Q

Define PD pathologically

A

characterized by the degeneration of dopamine neurons in the substantia nigra, a dark pigmented area located in the brainstem (C Tretiakoff, 1919; doctoral dissertation)

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10
Q

Define PD

  1. biochemically:

2. Clinically:

A
  1. Characterized by >80% depletion of the neurotransmitter dopamin in the striatum (Arvid Carlsson, 1959) Provides rationale for replacement therapy with dopaminergic drugs
  2. characterized by bradykinesia/akinesia, cogwheel rigidity, resting tremor, postural instability/gait disturbance, balance problems.
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11
Q

What are Lewy bodies?

A

Intracytoplasmic hyaline inclusions, alpha-synuclein in core, ubiquitin at rim. associated with parkinsons disease pathology

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12
Q

Familial PD is usually autosomal ________

A

Dominant. except for that on region 1p36 of gene PARK9. Protein ATP 13A2 which is a lysosomal protein

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13
Q

Which genes are associated with Familial PD?

A

Park 1, - Alpha - synuclein; synaptic protein
Park 4, Multiplication of alpha synuclein chromosomal region - excess alpha synuclein protein
Park 8, LRRK2, Dardarin protein phosphorylation
Park 9. ATP 13A2 - lysosomal protein

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14
Q

Young-onset PD has autosomal _____ inheritance

A

recessive, can be AD in PARK2 gene, also familial PD in Park9 gene is AR.

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15
Q

Which genes are associated with young-onset PD

A

Park 2, Parkin, ubiquitin-protein ligase
Park 6 PINK1, mitochondrial stress-induced degeneration
Park 7 - DJ-1; oxidative stress protection.

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16
Q

26% of early-onset PD patient’s carry mutations in one of 3 genes: (with percentages of each)

A

Parkin 6%
GBA (glucocerebrosidase 6$)
LRRK2 3%

Carriers in 2 different genes 1%.

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17
Q

with regard to PD

  1. younger patients ____ older patients carry a gene mutation
  2. Higher mutation frequencies were seen in: 2
A
  1. younger patients > older patients
  2. Jews (32% vs non-jews 14%)
    those with vs without a family hx of PD (24% vs 15%)
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18
Q

PD etiology (5)

A
  1. Excitotoxins - glutamate
  2. Environmental toxins - MPTP, Rotenone, paraquat
  3. Free Radicals and oxidative stress
  4. Infectious - post-encephalitic parkinsonism, nocardia, other
  5. Genetic - alpha synuclein, parkin, LRRK2, Map theta
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19
Q

Parkinsons testing: (5)

A 
CT/MRI normal/non-specific atrophy
2. eeg, blood, csf studies normal 
3. fluorodopa PET scan 
4. DAT scan
5 no definitive laboratory tests
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20
Q

5 causes of secondary parkinsonism

A
  1. head trauma
  2. post-encephalitic parkinsonism
  3. metabolic disorders (ie hypothyroidism
  4. toxins and industrial exposure - manganese, CO, carbon disulfide
  5. drugs: neuroleptics, LiCo3, antiemetics, reserpine
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21
Q

Differentiate parkinsons disease vs essential tremor

A

PD
Resting tremor
Minimal difficulty with fine movements

ET:
tremor worse with fine movements

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22
Q

Lewy body dementia accounts for ______ of the 7 million cases of dementia in the US

Pathology?

A

Accounts for < or = 20% of the 7 million cases of dementia in the US
*Pathology
Global cortical amyloid burden as assessed by PiB (Pittsburgh Compound B_-PET imaging is high in DLB and AD, but low in PDD, PD and Normal Controls

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23
Q

Lewy body dementia:

  1. Core features (3)
  2. Prognosis
A

Core features
Fluctuating cognition, pronounced variations in attention and alertness (50 - 75 % of patients)
Recurrent visual hallucinations, typically well formed & detailed (80 % of pts)
Spontaneous motor features of parkinsonism (onset of dementia and parkinsonism must occur within ~ 1 year of each other; tremor unusual)
Prognosis
Progressive intellectual and functional deterioration.
Average survival after the time of diagnosis is about 8 years

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24
Q

Multiple systems atrophy:

  1. sex predom?
  2. Incidence? Age?
  3. Prevalence
  4. Mean age of onset
  5. Disease progression; survival rates/percentages
A

Conflicting reports, probably affects both sexes equally
Incidence: 0.6/100,000 (Ages 50-99: 3/100,000)
Prevalence: 1.9 – 4.9/100,000
Mean age of onset = 54
Disease Progression: quicker than PD
80% disabled 5 years after onset of motor symptoms
20% 12-year survival
Mean survival after initial diagnosis is ~ 6 years.
As many as 10% of PD cases that are diagnosed incorrectly are identified as MSA upon autopsy

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25
Q

Criteria for “definite” multiple systems atrophy diagnosis

A

Findings of widespread and abundant CNS α-synuclein – positive glial cytoplasmic inclusions (Pap–p–Lantos inclusions)
Neurodegenerative changes in striatonigral or olivopontocerebellar structures

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26
Q

A definite (pathological) Dx of multiple systems atrophy requires (2)

A
  1. a typical neuropathological lesion pattern: pons, medulla, putamen, cerebellum, SNpc, preganglionic autonomic structures
    deposition of α-synuclein-positive glial cytoplasmic inclusions
  2. MSA: ??? 1° oligodendrogliopathy
    early myelin dysfunction
    progressive synucleinopathy
    associated axonal damage → 2° neurodegeneration
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27
Q

Multiple Systems Atrophy Criteria for the diagnosis of probable MSA:
A sporadic, progressive, adult (>30 y) – onset disease characterized by(3)

A

Autonomic failure involving urinary incontinence (inability to control the release of urine from the bladder, with erectile dysfunction in males) or an orthostatic decrease of blood pressure within 3 min of standing by at least 30 mm Hg systolic or 15 mm Hg diastolic and
Poorly levodopa-responsive parkinsonism (bradykinesia with rigidity, tremor, or postural instability) or
A cerebellar syndrome (gait ataxia with cerebellar dysarthria, limb ataxia, or cerebellar oculomotor dysfunction)

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28
Q

Multiple System Atrophy Additional features of possible MSA-P (9)

A

Babinski sign with hyperreflexia
Stridor
Rapidly progressive parkinsonism
Poor response to levodopa
Postural instability within 3 yrs of motor onset
Gait ataxia, cerebellar dysarthria, limb ataxia, or cerebellar oculomotor dysfunction
Dysphagia within 5 yrs of motor onset
Atrophy on MRI of putamen, middle cerebellar peduncle, pons, or cerebellum
Hypometabolism on FDG-PET in putamen, brainstem, or cerebellum

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29
Q

Multiple System Atrophy Additional features of possible MSA-C (6)

A

Babinski sign with hyperreflexia
Stridor
Parkinsonism (bradykinesia and rigidity)
Atrophy on MRI of putamen, middle cerebellar peduncle, or pons
Hypometabolism on FDG-PET in putamen
Presynaptic nigrostriatal dopaminergic denervation on SPECT or PET

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30
Q

define orofacial dystonia

A

Atypical spontaneous or L-DOPA induced dystonia predominantly affecting orofacial muscles, occasionally resembling risus sardonicus of cephalic tetanus.

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31
Q

define pisa syndrome

A

Subacute axial dystonia with a severe tonic lateral flexion of the trunk, head, and neck (contracted and hypertrophic paravertebral muscles may be present).

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32
Q

define Disproportionate antecollis

A

Chin-on-chest, neck can only with difficulty be passively and forcibly extended to its normal position. Despite severe chronic neck flexion, flexion elsewhere is minor.

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33
Q

define dysarthria

A

Atypical quivering, irregular, severely hypophonic or slurring high-pitched dysarthria, which tends to develop earlier, be more severe and be associated with more marked dysphagia compared to PD.

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34
Q

Multiple Systems Atrophy Red flags “non-supporting features” (7)

A 
Classic pill-rolling rest tremor
Clinically significant neuropathy
Hallucinations not induced by drugs
Onset after age 75 y
Family history of ataxia or parkinsonism
Dementia (on DSM-IV)
White matter lesions suggesting multiple sclerosis
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35
Q

Multiple Systems Atrophy Red flags - supporting features (12)

A 
Orofacial dystonia 
Disproportionate antecollis 
Camptocormia (severe
anterior flexion of the spine) and/ or Pisa syndrome (severe lateral flexion of the spine)
Contractures of hands or feet
Inspiratory sighs 
Severe dysphonia 
Severe dysarthria 
New or increased snoring
Cold hands and feet
Pathologic laughter or crying
Jerky, myoclonic postural/action tremor
36
Q

Multiple Systems Atrophy MRI signal abnormalities (2)

A

A Hyperintense putaminal rim on T2-weighted images
(“Hot cross bun” sign)
B Signal change in the pons on T2-weighted images
(Pontine atrophy)

37
Q

PD/Parkinson’s-Plus syndromesSynucleinopathies

name 4

A

1Parkinson’s disease
2Dementia with Lewy Bodies (DLB)
3Multiple System Atrophy (MSA)
MSA – P: Parkinson predominant (strionigral degeneration)
MSA – C: Cerebellar predominant (Olivopontocerebellar degeneration)
4Pure Autonomic Failure

38
Q

Corticobasilar Degeneration Criteria for the clinical diagnosis (4)

A
  1. Insidious onset and progressive course
  2. No identifiable cause (e.g., tumor or infarction)
  3. Cortical dysfunction as reflected by at least one of the following:
    - Focal/asymmetric ideomotor apraxia
    - Constructional apraxia
    - Alien limb phenomenon
    - Focal or asymmetric myoclonus
    - Cortical sensory loss
    – Apraxia of speech/nonfluent aphasia
    -Visual or sensory hemi-neglect
  4. Extrapyramidal dysfunction
    - Focal or asymmetric appendicular rigidity lacking prominent and sustained levodopa response
    - Focal or asymmetric appendicular dystonia
39
Q

7 types of cortical dysfunction

A

Focal/asymmetric ideomotor apraxia – Constructional apraxia
Alien limb phenomenon – Focal or asymmetric myoclonus
Cortical sensory loss – Apraxia of speech/nonfluent aphasia
Visual or sensory hemi-neglect

40
Q

Corticobasilar Degeneration Features Differentiating CBD vs. nonCBD (signs 4 & symptoms 3)

A

Symptoms:
Limb stiffness
Clenched hand

Signs:
Bradykinesia	
Dystonia	
Fisted hand	
Postural instability
Limb tremor
41
Q

Corticobasilar Degeneration Reported MRI Findings 2

A
  1. Asymmetric frontoparietal cortical atrophy

2. Asymmetric atrophy of the cerebral peduncles

42
Q

Progressive Supranuclear Palsy NINDS-SPSP Criteria

Clinical features: 4

A

Gradually progressive
≥ age 40 at onset
No evidence for competing diagnostic illness
Vertical gaze palsy or slowing of vertical saccades + postural instability/falls in 1st year

43
Q

Progressive Supranuclear Palsy NINDS-SPSP Criteria

Prognosis (3)

A

Progressive intellectual and functional deterioration.
Average survival after the time of diagnosis is about 5 years
~ 30% ten-year survival rate

44
Q

Progressive Supranuclear Palsy Pathology (4)

A

1 Deposits of hyperphosphorylated MAPτ
2 Human CNS τ
- Exists as 6 isoforms; three contain 3 microtubule binding repeats (3R), 4 contain a 4th (4R).
- ↑ Presence of 4R τ isoforms in PSP
3PSP vs. AD
- PSP τ: present as straight filaments within globose PSP tangles in neurons and glia (tufted astrocytes)
- AD τ: paired helical filaments in neurofibrillary tangles
4Glial cell pathology rarely seen in other tauopathies

45
Q

Progressive Supranuclear Palsy MRI signal abnormalities:

A

penguin sign: marked atrophy of midbrain tegmentum. The shapes of midbrain tegmentum (bird’s head) and pons (bird’s body) on midsagittal MR images look like a lateral view of a standing penguin with a small head and big body
Recall: Patient with MSA-P → marked atrophy of pons.

46
Q

PD/Parkinson’s-Plus syndromesTauopathies: (3)

A

1 Alzheimer’s Disease
2 Frontotemporal dementias (Pick’s Disease)
3 Tauopathies with predominant Parkinsonism
- Corticobasilar degeneration
- Progressive Supranuclear Palsy (6/105)
- Frontotemporal dementia and parkinsonism linked to Chr 17 (MAPτ mutation with neuronal τ inclusions); but also Chr 17 progranulin mutation with ubiquitin (+ TDP-43) inclusions.

47
Q

4 drug therapies for parkinsons disease

A

L-Dopa/Carbi-Dopa
Dopaminergic agonists
Cholinergic antagonists
Metabolic inhibitors

48
Q

4 surgical therapies for parkinsons disease

A

(Thalamotomy)
(Pallidotomy)
Brain stimulation (DBS)
In vivo gene therapy

49
Q

10 potential neuroprotective agents

A 
Caffeine
Coenzyme Q10
Creatine
Estrogen
GM-1 ganglioside
Minocycline
Nicotine
GPI-1485
Rasagiline
Selegiline
Ropinirole
Pramipexole
50
Q

Name 4 direct dopamine agonists

A

Bromocriptine

Rotigotine

Pramipexole

Ropinerole

51
Q

4 MOA of dopamin agonists

A

Directly stimulate dopamine receptors

Independent of dopamine production

No free radical generation

Monotherapy or adjunctive therapy

52
Q

6 adverse effects of direct dopamine agonists

A 
Nausea
Vomiting
Postural hypotension
Hallucinations
Somnolence
Impulse Control
Hypersexuality
Gambling
Spending/shopping
53
Q

3 positives of levodopa

A

Works for almost all patients with Parkinson’s Disease
Improvement of disability and possibly mortality
Most effect on bradykinesia and rigidity, less effect on tremor and postural instability

54
Q

Carbidopa:

  1. combined with:
  2. Prevents peripheral conversion of:
  3. Total of _______ dose is usually required to inhibit peripheral decarboxylase activity.
A

Combined in fixed ratios with levodopa

Prevents the peripheral conversion of levodopa

Total of 75 mg/day is usually required to inhibit peripheral decarboxylase activity

55
Q

Levodopa/carbidopa:

3 pharmokinetic considerations

A

1 high-protein diets cause decreased absorption
2 fluctuation of amount of DA at the receptor sites
3 IR half-life 60-90 minutes

56
Q

6 acute adverse effects of carbidopa/levodopa

A 
nausea/vomiting
orthostatic hypotension
hallucinations 
cardiac arrhythmias
confusion
agitation
57
Q

what is “wearing off’ effect of Carbidopa/levodopa

A

as dopamine neurons decrease, the medication is less effective. At this point, the effec lasts a couple of hours. Calls for PEG-J tube continuous administration

58
Q

what is “on-off” phenomenon?

Dyskinesia appears when?

A

Refers to the switch in parkinsons disease between mobility and immobility in levodopa treated patients, which occurs as an end-of-dose or “wearing off” worsening of motor function or, much less commonly, as sudden and unpredictible fluctuations. Motor complications occur in 50% of PD patients who have received Levodopa for 5-10 years and constitute a major cause of disability in advanced PD.

59
Q

5 limitations to controlled release levodopa/carbidopa

A 
Fewer daily doses
Less plasma fluctuations
Delay to effect
Cannot crush; can divide
No measurable effect on “freezing”
60
Q

2 factors with COMT inhibitors
Works by:
benefit?

A

Prevents breakdown of dopamine

More levodopa available to cross blood brain barrier

61
Q

Name the two COMT inhibitors.

limitations?

A
  1. Tolcapone
    - severely restricted due to hepatotoxicity
    - must sign consent form
    - mainly peripheral, slight central effect
  2. Entacapone
    - increased AUC, increased t1/2; no change in Cmax, or tmax of levodopa
    - Dosing
    - One tablet with each levodopa/carbidopa dose; max 8/day
    - Does not cross blood brain barrier
    - Must use with levodopa/carbidopa
62
Q

Adverse effects of entacapone (5)

A 
Dyskinesias
Nausea
Hallucinations/vivid dreams
Diarrhea
Urine discoloration - orange
63
Q

Amantadine
Mechonism of action (4)
Dosing:

A 
Mechanism of Action
- Enhances dopamine release
- Blocks reuptake
- Stimulates DA receptors
- Blocks Glu receptors
Dosing
- 100 mg 1 po bid-tid
- caution in renal dysfunction
64
Q

two uses for amantadine in PD

A

Treatment of early Parkinson’s disease

Treatment of levodopa-induced dyskinesias

65
Q

6 adverse effects of amantadine

A 
dizziness
nausea
nightmares
insomnia
anxiety
livedo reticularis - skin rash
66
Q

1 Name two anticholinergic meds used in PD.
2 Most useful for:
3. best with which patients? Avoid with which patients?

A
  1. Trihexyphenidyl, Benztropine
  2. Most useful for tremor
    3 Best when used with younger patients
    Avoid in demented patients
67
Q

two indications for use of anticholinergics in parkinsons disease

A

Early Parkinson’s disease with tremor as main symptom

Later Parkinson’s disease with all symptoms except tremor under good control

68
Q

Initial dosing of trihexyphenidyl and bentropine:

Adverse effects: (5)

A 
Initial dosing
trihexyphenidyl 0.5 mg 1 po bid
benztropine 0.5 mg 1 po bid
Adverse effects
dry month
urinary retention
dry eyes
constipation
confusion
69
Q

What is neat about deep brain stimulators?

When would you place in the thalamus?

A

four leads on probe, can program them to create different fields. Most commonly placed in GBI.
Thalamus: essential tremor

70
Q

Discuss the three different lead placements with deep brain stimulator:

A

1 Vim
Thalamic stimulation will only treat tremor (PD or ET)
Utilize this placement if the patient has disabling tremor and milder bradykinesia or rigidity

2 STN
Will treat all of the motor symptoms of PD
More difficult to program

3 GPI
Will treat all of the motor symptoms of PD
Location of choice to treat dystonia

71
Q

Parkinsons disease “non-motor” manifestations:

  1. Peripheral nervous system: 2
  2. spinal cord 2
  3. Brainstem: 3
  4. Basal ganglia: 3
  5. Cortical: 3
A

1 Peripheral Nervous System → Pain, constipation
2 Spinal Cord → Orthostatic hypotension, urological disturbances
3 Brainstem → Anxiety, depression, sleep disorders
Basal Ganglia → Impulse control disorders, apathy, restlessness
Cortical → Cognitive, psychiatric disorders, anosmia

72
Q

Pain in parkinsons disease:

  1. ____ is an early and sometimes initial sign
  2. ____ and ____ pain not uncommon in PD patients, most common in lower extremity.

If you have early am dystonia:
If you have dystonia/dyskinesia:
If you have dystolia period

A

shoulder pain is an early and sometimes initial symptom
dystonic and cramping pain not uncommon in PD patients, most common in lower extremity
Early AM dystonia → dopamine deficit
dystonia/dyskinesia → late effect of PD + levodopa tx
dystonia → potential side effect of STN DBS programm

73
Q

two types of GI disturbance in PD

Treatment?

A
  1. nausea often associated with initiation of levodopa and peripheral metabolism to dopamine
    prolonged transit time, constipation, paralytic ileus may result from loss of vagal neurons, changes in myenteric plexus.
  2. adequate hydration, high fiber, PEG. psyllium, bisacodyl
    lubiprostone (intestinal ClC-2 activator; ↑ intestinal fluid secretion) linaclotide (14 aa guanylate cyclase-C agonist → ↑cGMP → increased secretion of Cl- and HCO3- into the intestinal lumen) Both FDA-approved for Irritable Bowel Synd, chronic constipation
74
Q

3 treatments of orthostatic hypotension as it is related to PD

A 
related to disease & medication 
1. treat with ↑fluids, salt
2midodrine 
  ≤ 10 mg tid
t ½ of active metabolite = 3-4h 
3 fludricortison (≤ 0.1 mg q day) 
4 L-DOPS /droxidopa (initial dose: 100mg tid)

L-threo-dihydroxyphenylserine → norepinephrine
FDA-approved 18 Feb 2014 for PD, MSA, pure autonomic failure, DBH deficiency

75
Q

6 types of urological dysfunction in parkinsons disease

A 
nocturia most common complaint (>60%)
storage symptoms in 57 – 83%
voiding symptoms in 17 – 27%
urgency 33 – 54%, frequency 16 – 36%. 
neurogenic detrussor overactivity in 45 – 93% of patients
nocturnal polyuria
remember:  Multiple Systems Atrophy
76
Q

3 ways to treat urological dysfunction in PD

A

treat if UTI
storage symptoms may respond to anticholinergics (oxybutynin, tolterodine, trospium)
voiding symptoms may be caused by anticholinergics, bladder outflow obstruction (CMG) (try α-blocker [terazosin, doxazosin, tamsulosin, and alfuzosin] and/or 5-α-reductase inhibitors [dutasteride, finasteride]; intermittent self-catheterization)

77
Q
  1. prevalence of depression in PD is ____%
  2. ____% of PD patients may suffer from major depressive disorder
  3. Major contributors: (2)
  4. Treatment
A

Prevalence of depression in PD ~ 40%
published rates vary from 7 to 76%
~17% of PD patients may suffer major depressive disorder
The major contributors
depletion of brain catecholamines and serotonin
dysregulation of fronto-subcortical connections that regulate mood
Treatment: tricyclics, SSRIs, SNRIs

78
Q

Parkinson’s DiseaseBrainstem/Sleep Disorders - describe two

A

Nighttime awakenings:
< total sleep time, < sleep efficiency, > frequent awakenings
dopaminergic treatment strongest predictor
Excessive daytime sleepiness (EDS)
associated with PD neuropathology & anti-PD medications
“sleep attacks” initially described with DAs; similar with all dopaminergic therapies
Modafinil (200-400mg/day) may be effective; not FDA approved

79
Q

PD patient’s with brainstem/sleep disorders may have _______.

  1. Patients appear to _____ when in rem sleep. Cause?
  2. ____% of those with probable RBD develop ____ in less than 4 years
  3. RBD affects _____% of patients with synucleopathies.
A

REM Behavior Disorder (RBD)
people with RBD appear to act out their dreams when in REM sleep
~ 34% of those with probable RBD developed MCI or PD ≤ 4 yrs of entering a Mayo Clinic study (2.2X those with normal REM sleep)
RBD affects 30-90% of patients with synucleopathies
a non-dopaminergic lesion of the system controlling REM sleep atonia has been implicated (subceruleus-ceruleus complex ?)
no randomized, double-blind, placebo controlled study has been reported for RBD; clonazepam (0.5-2 mg HS) appears effective, well tolerated .

80
Q 
discuss with regard to PD: 
Hypersexuality: 
Punding: 
Addictive behaviors: 
Associated with:
A

Hypersexuality, pathological gambling, compulsive shopping, binge eating
Punding: compulsion to perform repetitive mechanical tasks, such as sorting, collecting, or assembling and disassembling common items
Addictive behaviors: excessive use/abuse of anti-PD meds
Associated with increasing dopaminergic therapy
but > 15% of ~100 newly diagnosed PD patients screened + for ≥ 1 ICD

81
Q

Parkinson’s DiseaseImpulse control disorder: treatment (3)

A

Reduction or withdrawal of dopaminergic therapy, particularly DAs: (pramipexole, rotigotine, ropinirole)
± DBS surgery as means to reduce dopaminergic therapy
Other suggestions: SSRIs, quetiapine, valproate, naltrexone, topirimate, donepezil, clozapine

82
Q
  1. __% of patients with end-stage PD have dementia
  2. Loss of _____ function? (2)
  3. Similar to findings in ___ dementia.
  4. Treatment (2)
A

> 80% dementia in end-stage PD
Executive dysfunction and visual-spatial problems
affects information processing
distractablity, passivity, slow-thinking
Similar findings in Lewy body dementia (LBD)
Cholinergic neuronal loss, ChAT depletion early in PDD/LBD
Treatment:
cholinesterase inhibitors (rivastigmine, donepezil)
NMDA receptor antagonists (memantine)

83
Q

Psychosis is associated with ____% of PD patients. Assoicated with: ___ prognosis.
Accompanied by: 2
Treatment:

A

Prevalence up to 60%; associated with poorer prognosis
Hallucinations usually visual; typically begins ~ 10 yrs after dx with retained insight
Hallucinations > 2 yrs strong predictor of dementia, NH placement, death.
Delusions may occur in younger patients
Treatment with quetiapine, clozapine

84
Q

Sexual affects of PD in men and women:

Can get a true increase in libido when?

A

Associated illnesses, medications, motor symptoms, depression, anxiety and worsening PD contribute
Erectile dysfunction in 54 – 79% of men
sildenafil 50 – 100 mg in PD patients
Women report difficulties with arousal (~88%), reaching orgasm (~75%)
A true increase in libido may occur as an adverse reaction to treatment with DAs, levodopa

85
Q

List the 5 changes with vision in PD

A
  1. Impaired visual function
    Visual acuity, contrast sensitivity (disease severity: UPDRS III)
    Color/motion perception
    Visualspatial deficit
    ? Retinal dopamine loss
  2. Visual Hallucinations
    illusions (~25%)
    feelings of presence and passage (? Correlates with RBD, EDS)
    complex visual hallucinations (~40%, > association with PDD)
  3. Diplopia and difficulty reading
    disease severity → motility abnormalities, surface irritation
    excessive daytime somnolence (EDS)
  4. Impairments of ocular and eyelid motility
    abnormal saccades
    reduced spontaneous blink
    blepharospasm (advanced PD)
    apraxia of eyelid opening (advanced PD)
  5. Ocular surface irritation
    dry eyes (up to 2/3 of patients)
    blepharitis (up to 75%; PD + age)

Neuro Rehab II (6 decks)

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