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Neuro Rehab 2 > Parkinsons - 1a/b PD > Flashcards

Parkinsons - 1a/b PD Flashcards

1
Q

what nuclei is the basal ganglia composed of

A

3 nuclei at base of cerebral cortex
- caudate nucleus
- putamen
- globus pallidus

2 brainstem (midbrain) nuclei
- substantia nigra
- subthalamic nucleus

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2
Q

what is the normal function of the basal ganglia

A

initiation and continuation/fluidity of mvmt as well as inhibition of undesired mvmts

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3
Q

how does the basal ganglia influence and control mvmts

A

controls the production of mvmt
- timely running of complex mvmt patterns via direct and indirect loops in the cerebrum

“on off” switch for selected motor programs
- communication to cortex to either initiate and continue or inhibit mvmts

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4
Q

is parkinsons considered a mvmt or motor disorder and why

A

mvmt disorder

extrapyramidal system disorder, no pathology in motor corticospinal tracts bc no direct connections to alpha or gamma motor neurons

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5
Q

what does the basal ganglia communicate with

A

communicates w motor cortex via thalamus along indirect and direct loops

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6
Q

what are the 2 loops that compose the basal ganglia’s corticothalamic loops

A

direct
indirect

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7
Q

what is the pathway of the basal ganglia’s direct loop

A

cortex -> putamen -> globus pallidus -> thalamus

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8
Q

what is the pathway of the basal ganglia’s indirect loop

A

cortex -> putamen -> globus pallidus -> subthalamic nucleus -> thalamus

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9
Q

describe how the basal ganglia’s corticothalamic loops works

A

cortex determines voluntary mvmt needed
-> BG selects & presents motor programs to motor cortex via thalamus
- appropriate motor program facilitated by direct pathway/loop
- competing motor programs inhibited by indirect pathway/loop

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10
Q

direct vs indirect pathway functions

A

direct pathway
- voluntary mvmt produced

indirect pathway
- suppress unwanted mvmts

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11
Q

what are the 3 neurotransmitters associated w the BG and what is the main one

A

**dopamine **
acetylcholine (ACh)
gamma-aminobutyric acid (GABBA)

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12
Q

where is dopamine produced

A

substantia nigra

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13
Q

what are dopamines functions & impact on BG

A

excitatory to neurons in direct loop
inhibitory to neurons in indirect

has greatest impacts on pathways out of neurotransmitters

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14
Q

where is ACh found

A

caudate and putamen

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15
Q

what is the function of ACh & impact on BG

A

inhibitory to action of dopamine
- changes BG’s pathways indirectly

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16
Q

what is GABBA’s function & impact on BG

A

overall inhibitory neuro transmitter found throughout brain
- changes BG’s pathwq]ays indirectly

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17
Q

what is the neuropathology of PD

A

degenerative neurologic condition bc of progressive death of dopamine-producing cells in substantia nigra
-> alterations of neural activity or signaling in corticothalamic loops (both indirect and direct loops)

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18
Q

how does the neuropathology of PD impact the direct loops’s function

A

impaired function produces:
- bradykinesia (slow mvmts)
- akinesia (paucity/loss of mvmt)

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19
Q

how does the neuropathology of PD impact the indirect loops’s function

A

impaired function produces:
- tremors (resting tremors)
- chorea (unwanted, extraneous mvmts)

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20
Q

what are 3 possible etiologies of PD and what is the most common

A

idiopathic* - majority
neurotoxins
genetic factors

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21
Q

what are some examples of idiopathic etiologic factors (5)

A
  1. proteinopathy
    - failure of construction of protein cells that lead to dysfunction
  2. mitochondrial dysfunction
    -> interferes w cellular energy produciton
  3. oxidative stress
    - accumulation of free radicals and other toxins -> excitoxicity
  4. excitotoxicity
  5. inflammatory markers
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22
Q

what is hard to differentiate w idiopathic etiologic factors and why

A

hard to know if idiopathic etiologies are causes or s/sx of PD

by time dx, substantial loss of cells in substantia nigra already

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23
Q

what are 3 ex of neurotoxin etiologies

A

pesticides
heavy metals - factories, water/air
agent orange - vietnam war

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24
Q

what are genetic factors as an etiology linked to

A

linked to earlier onset, more rapid progression of motor sx and cog changes

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25
Q

how does a genetic predisposition impact the risk of developing PD

A

many people w a genetic predisposition don’t have PD

likely that an exposure to an environmental factor triggers the dz

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26
Q

parkinsons vs parkinsonisms vs PPS

A

parkinsons = idiopathic

parkinsonisms = can attribute sx to another cause

PPS = distinct health conditions that have overlapping parkinsons features, but have distinct hallmarks/features that can be determined as a different health condition when doing a differential dx

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27
Q

what are common parkinsonisms (6)

A

head trauma (ie boxing)
toxins, pesticides, metabolic d/o
antipsych, antidep, and HTN meds
viral infections, tumors
alzheimer’s dz
normal pressure hydrocephalus

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28
Q

how can head trauma lead to a parkinsonism

A

damage nuclei

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29
Q

how can hydrocephalus lead to a parkinsonism

A

compress basal ganglia
-> interfere w communication loops
—> cause sx similar to parkinsons

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30
Q

what are 4 parkinson-plus syndromes

A

multiple system atrophy (MSA)
progressive supranuclear palsy (PSP)
corticobasal ganglionic degen (CBD)
dementia w lewy body (DLB)

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31
Q

what is the single largest risk factor for PD

A

age

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32
Q

what is the epidemiology for PD

A

2nd most common neurodegen d/o
fastest growing neuro condition worldwide

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33
Q

what is the average age of onset for PD

A

50-60yo

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34
Q

at what age is considered early onset PD

A

<40yo

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35
Q

at what age is considered juvenile onset PD

A

<21yo

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36
Q

what are common characteristics of the onset of PD

A

unilateral and asymmetrical

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37
Q

what are the hallmarks of PD and what is the significance of these

A

bradykinesia
tremor
rigidity

2 out of 3 required for dx

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38
Q

what is the significance of seeing postural instability in PD

A

later manifestation not required for a dx, but also a hallmark of PD

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39
Q

s/sx of PD (4 hallmarks + 3)

A

hypokinesia
akinesia
bradykinesia
tremor
postural instability
rigidity
dyskinesia

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40
Q

what type of dx is PD

A

clinical dx

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41
Q

when is dyskinesia seen

A

secondary to gold standard meds for PD

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42
Q

what is hypokinesia and what are 4 ways this can manifest

A

reduced amplitude of mvmt

  1. lack of arm swing and trunk rotation in gait
  2. lack of facial expression (“masked faces”)
  3. micrographia - small handwriting
  4. hypokinetic dysarthria & dysphagia
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43
Q

what is akinesia and how does this commonly manifest

A

freezing episodes, lack of mvmt

common in gait “fog”
- can’t turn on mvmt or initiate

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44
Q

what is bradykinesia and what are 2 ways this can manifest

A

slow mvmts and delayed reaction times

  1. difficulty performing simultaneous or sequential mvmts
  2. difficulty w transitional mvmt, direction changes
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45
Q

resting tremors: where can this be seen, aggravating and relieving factors

A

extremities, trunk, jaw, tongue
- pill rolling hand tremor is common
- unilateral initially

worsen w stress
stop when moving and sleep

46
Q

dyskinesia: what is it, when is this commonly seen, what can this result in

A

random and purposeless mvmts affecting limbs, trunk, face, or tongue

side effect of PD med (levodopa)

result in: ms pain, embarrassment, self-limiting behaviors

47
Q

what is posturography

A

sequence of activation is intact but speed and amplitude of firing is impaired

48
Q

what are 3 common characteristics of postural instability and what can postural instability lead to

A
  1. ineffective responses to external perturbations
  2. posturography
  3. dec anticipatory/feed forward postural adjustments

leads to inc episodes of falling

49
Q

what is are good tests to assess postural instability

A

push test
pull test - give post perturbation at shoulder girdle (abnormal >2steps to regain balance)

50
Q

what is rigidity and what are 2 phenotypes

A

inc resistance to passive elongation in agonist and antagonists

  1. cogwheel - tremor superimposed on rigidity, catch and release
  2. lead pipe - sustained resistance
51
Q

what ms are affected by rigidity and how

A

prox ms often affected first
- forward flex/kyphotic posture
asymmetrical early in dz process

52
Q

what secondary things can rigidity lead to

A

inc energy demands and leads to fatigue
secondary adaptive ms shortening and disuse weakness

53
Q

what are 2 common gait d/o are seen in PD

A

festinating gait
freezing of gait (FOG)

54
Q

what is a festinating gait and when might this patient have difficulty

A

progressive inc in speed and shortening of stride
- inc cadence, dec in step length
loss of heel toe progression -> shuffles

dec ability to step over obstacles or walk on uneven surfaces

55
Q

what is freezing of gait (FOG) and when is this especially a problem for pts

A

gait ignition failure, akinetic gait

obstacle clearance and negotiating doorways are especially problematic

56
Q

what are some common non-motor sx (7)

A

attentional and cog deficits
sensory impairments
sleep disturbances
mental health issues
autonomic dysfunction
anosmia & sialorrhea
fatigue and CV issues

57
Q

what might be one of the earliest signs of PD

A

anosmia

sleep disturbances also may be seen before mvmt sx

58
Q

what are some attentional and cognitive deficits (4)

A
  1. inability to shift attention, dual tasks
  2. inability to quickly access “working memory” & manipulating memory
  3. difficulty w visuospatial perception and discrimination, learning
  4. subcortical dementia**
59
Q

what sensory impairments are seen (3)

A

paresthesia
pain
proprioception/kinesthesia

60
Q

what sleep disturbances are seen in PD (4)

A

REM sleep behavior d/o
insomnia
daytime sleepiness
nocturia

61
Q

what autonomic dysfunction is seen in PD (4)

A

thermoregulation, sweating
seborrhea
GI disorders, constipation, UI
OH, altered HR and BP

62
Q

what mental health issues have a high co-morbid rate

A

anxiety and depression

63
Q

what is sialorrhea and why is this commonly seen w PD

A

drooling
- lack of ms activity needed for swallowing and needed for secretions management

64
Q

how can PD impact CV function

A

inc trunk tone & rigidity
- > develop flex kyphotic posture –> dec vital capacity -> inc difficulty swallowing –> aspiration -> bronchopneumonia

fatigue and dec CV can lead to multifactorial and secondary impairments

65
Q

what is the significance of secondary impairments to PT

A

secondary impairments are where PT really need to intervene bc can perpetuate health problems

66
Q

what are prodromal symptoms

A

non-motor sx that may precede motor sx by up to 2 decades

67
Q

at what point is there finally an onset of motor sx

A

when 50% or more of dopaminergic neurons have died

68
Q

what are the most common prodromal sx (4)

A

autonomic changes (orthostasis)
anosmia or phantom smells
sleep disturbances
constipation

69
Q

what are the common complaints that lead to people seeking out an MD (2) and what is the significance when these pts usually get referred to PT

A

stiffness in one hand/limb
shoulder/back pain

PTs have to be aware of & perform additional tests
- ask about common non-motor prodromal signs

70
Q

if a PT suspects a person has parkinsons, what should our referral be

A

back to MD
neurologist or preferably a mvmt disorder clinic
- these lead to best outcomes

71
Q

what is the process for diagnosing PD

A

clinical dx based on 2/3 hallmarks
- no definitive dx tests

must exclude parkinsonisms and parkinson-plus syndromes in differential dx

72
Q

what is a DaTSCAN, what is a positive, and what are its 2 main limitations

A

nuclear medicine study

(+) = dec and asymmetrical uptake of pre-synaptic dopamine transporters

doesn’t differentiate PD from parkinsonisms
antidepressant meds may confound results

73
Q

what and how can neuroimaging be utilized in PD

A

MRI/CT scans
- show cell death in SN in late stages only (usually dark -> get lighter as die off)

fMRI
- detect low levels of activity in BG early stages
- but not widely available, mostly used in research centers

74
Q

what are the 2 main clinical subgroups/phenotypes of PD

A
  1. postural instability and gait disorder (PIGD)
  2. tremor dominate (TD)
75
Q

PIGD vs TD phenotypes

A

PIGD
- more rapid rate of progression
- neurobehavioral sx & depression

TD
- less bradykinesia & postural control deficits
- typically more benign course, esp if younger age at onset

76
Q

what is the typical clinical course of PD

A

onset of motor sx usually unilateral and asymmetrical

progressive condition - tends to then affect all limbs

77
Q

what is the common cause of death in PD and why is this significant

A

CV dz, pneumonia

significance of secondary intervention and aerobic activity

78
Q

how does levodopa therapy impact the clinical course of PD and when does it stop being effective

A

can prolong lifespan
doesn’t cure dz or stop progression
- masks sx

doesn’t have same effectiveness once native dopamine depleted

79
Q

what is the gold standard for pharmacological management of PD

A

levodopa/carbidopa (Sinemet)

80
Q

how does levodopa work

A

dopamine precursor is converted after crossing BBB

alleviates bradykinesia & rigidity
- but not tremor

81
Q

what are 2 major difficulties of levodopa therapy

A
  1. therapeutic window and dosing is problematic
    - difficult to determine when person should start therapy
    - will dec effectiveness after 10-15yrs
    - want to optimize mvmt as long as possible
  2. difficult to get pts to stay compliant and take right doses at right time
82
Q

how long optimal benefit of levodopa last

A

wears off after 4-6yrs
- will dec effectiveness after 10-15yrs

83
Q

what are side effects of levodopa and what is the major one to remember (10)

A

**dyskinesia
dystonia
visual hallucinations
delusions
paranoia
depression
hypotension
dizziness
arrhythmias
insomnia

84
Q

what are 4 types of pharmacologic management

A

levodopa (Sinemet)
dopamine agonist
anticholinergic
neuroprotective agents

85
Q

how do dopamine agonists work

A

meds to mimic dopamine
- bind to and activate striatal dopamine receptors

alleviates rigidity and bradykinesia, motor fluctuations

86
Q

why might a pt be on both a dopamine agonist and sinemet

A

can be used to reduce the Sinemet dose

87
Q

what are the side effects of dopamine agonists and what is the major one

A

same SE as levodopa

impulse control disorder
- risky behaviors like gambling, overtly sexual

88
Q

what are anticholinergics used for

A

managing tremors, dystonia, sialorrhea

89
Q

what is the danger of taking anticholinergic meds at wrong times

A

linked to cog impacts of dz you see

90
Q

what are adverse effects of anticholinergics (4)

A

blurred vision
dry mouth
dizziness
urinary retention

91
Q

what are 4 signs of anticholinergic toxicity and what should be done if suspected

A

impaired memory
confusion
hallucinations
delusions

emergency management is needed

92
Q

how do neuroprotective agents work

A

MAO B inhibitors
prevent degradation of native dopamine

93
Q

when/why are neuroprotective agents typically used

A

early treatment and/or later to reduce levels of levodopa needed

94
Q

what are adverse effects of neuroprotective agents (5)

A

nausea
orthostasis
confusion
hallucinations
insomnia

95
Q

when/why is a dose response trial used (3)

A
  1. determines response to med
  2. assist in dx process (no response in PPS)
  3. ensure pt isn’t over or under medicated
96
Q

what is the PT’s role in a dose response trial

A

work w neurologist and do battery of tests
- doc response of specific mvmt disorder to meds

97
Q

what are the 2 main options for surgical management

A

neuroablation (lesioning)
deep brain stim (DBS)

98
Q

what is the goal of a neuroablation (lesioning) and how does this work

A

permanently blocking signals from BG

thermacoagulation and neural tissue death achieved by transmitting high frequency radiowaves stereotacticallly thru small electrode
- targeting globus pallidus (palidotomy) or parts of thalamus (thalamotomy) most frequently

99
Q

what sx is neuro ablation effective in treating

A

reducing tremor, bradykinesia, rigidity

100
Q

pros/cons of neuroablation vs deep brain stim

A

neuroablation
- not highly invasive
- permanent

deep brain stim
- reversible
- higher cost
- risk of infection

101
Q

what is the goal of deep brain stim and how does it work

A

“jam” abnormal signals from BG loops

microelectrode implanted in BG
delivers high frequency electrical discharge via impulse generator implanted under clavicle
creates depolarizing block to jam signals

102
Q

what are 2 contraindications for DBS

A

cog impairments
- have to interrogate it
- go for follow ups

parkinsonisms
- not as effective

103
Q

what are the 2 growing areas of research searching for a cure to PD

A

stem cells
exercise

104
Q

how does stem cell regeneration med research work as a cure for PD

A

extract cells from adult thru cartilage in nose or bone marrow in iliac crest
- process in lab and bring back to pluripotent state
- can be implanted in areas where there are deficiencies, loss of native cells

= differentiate into midbrain dopaminergic neurons

105
Q

what are 4 considerations of stem cell regen

A

immunogenicity
proliferation
timing in dz progression
measuring effects & outcomes

106
Q

what are limitations in stem cell research

A

having trouble getting them to start producing dopamine
- also problems w getting them to stop proliferating and reproducing once implanted -> become tumors

107
Q

what benefits does exercise may have for PD

A

modify disease & slow progression
- may also dec risk of developing PD

108
Q

what type of exercise does research suggest may slow PD progression

A

early intense, large amplitude aerobic activity that includes complex/whole body mvmt
- LSVT Loud

109
Q

how can exercise dec risk of PD

A

exercising mod intense aerobic 3-4x/wk and get GDNF production which has neuroprotective effects

110
Q

what is the key for utilizing exercise to slow PD progression

A

early referral to quickly start exercise

111
Q

what is thought to be the mechanism that exercise uses to slow PD progression

A

activates release of neurotrophic factors and promotes angiogenesis

neuroprotective mechanisms d/t PA (read the following over)
- inc production of superoxide dimutase, endothelial nitric oxide synthase, brain-derived neurotrophic factor, nerve growth factor, insulin-like growth factor, vascular endothelial growth factor, and reduction in production of free radicals

limits alteration in dopaminergic neurons in SN and contributes to optimal functioning in BG

Neuro Rehab 2 (48 decks)

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