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NCS Prep > 9 Parkinson's Disease > Flashcards

9 Parkinson's Disease Flashcards

1
Q

Basal ganglia components

A 
Caudate
Putamen
Globus pallidus (internus and externus)
Subthalamic nucleus
Substantia nigra (pars compacta and pars reticulata)
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2
Q

Striatum

A

Caudate and putamen

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3
Q

Lentiform nucleus

A

Globus pallidus and putamen

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4
Q

Basal ganglia function

A

Regulates movement via control of sequencing, muscle tone, muscle force
Communicates through thalamus to cortex
To lower motor neurons via pedunculopontine nucleus of midbrain

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5
Q

Basal ganglia neurotransmitters

A

GABA (inhibitory)
Glutamate (excitatory)
Dopamine (both)

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6
Q

Function of direct pathway in BG

A

Facilitates movement

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7
Q

Nigrostriatal impact in the direct pathway

A

Dopamine acts as an excitatory NT by binding to D1 receptors, further exciting stratum leading to dis-inhibition of thalamus and increased motor activity

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8
Q

Function of indirect pathway in BG

A

Suppresses unwanted movement

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9
Q

Nigrostriatal impact in the indirect pathway

A

Dopamine acts as an inhibitory NT by binding to D2 receptors, inhibiting striatum leading to reduced inhibition of thalamus and increased motor activity

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10
Q

Parkinson’s disease definition

A

Chronic, progressive CNS disorder that results from death of dopamine-producing cells in substantia nigra

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11
Q

Direct pathway effect in PD

A

Less dopamine results in decreased facilitation of motor output

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12
Q

Indirect pathway effect in PD

A

Less dopamine results in increased inhibition of (decreased) motor output- less output occurs because there is more movement suppression

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13
Q

Cellular mechanisms of PD

A 
Oxidative stress
Accumulation of toxic proteins
Mitochondrial malfunction
Inadequate neurotrophic factors (GDNF)
Inflammatory glia
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14
Q

Environmental/dietary factors in PD

A

Pesticides and herbicides, heavy metals
Smoking, caffeine, possibly alcohol protect
Antioxidants, dairy/milk, iron possible positive association

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15
Q

PD from genetic cause

A

Younger onset, dystonia, early dementia

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16
Q

Cardinal signs of PD

A

Tremor (70%, begins unilaterally)
Rigidity (cogwheel or leadpipe- proximal, extends distal)
Akinesia/bradykinesia
Postural instability

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17
Q

Other motor signs and symptoms of PD

A 
Freezing of gait
Forward flexed posture
Incoordination (gross and fine)
Hypomimia (facial expression)
Dystonia
Dysarthria
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18
Q

Non-motor signs and symptoms of PD

A 
Loss of smell
Sleep disturbances
Mood disorders
Dysautonomia
Constipation
Depression
Dysphagia
Hypophonia
Micrographia
Sialorrhea
Cognitive dysfunction
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19
Q

Dementia with Lewy bodies

A

Misfolded alpha-synuclein proteins (Lewy bodies) are hallmark of PD
Progressive dementia- deficits in attention and executive function
Fluctuating cognition
Visual hallucinations

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20
Q

Primary Parkinsonism

A

85% of all PD cases
Unilateral onset, slow progression
Tremor dominant- more favorable prognosis, relative preservation of mental status, earlier age of onset
Postural instability/ gait disturbance- more rapid progression, severe cog dysfunction, two variants (postural instability with falling and freezing of gait)

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21
Q

Diagnostic criteria for primary Parkinsonism

A

Clinical diagnosis
Presence of at least 2/4 cardinal signs
Positive levodopa response
Other causes ruled out

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22
Q

Types of secondary Parkinsonism

A

Vascular
Drug-induced
Infection
Toxins

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23
Q

Vascular Parkinsonism

A

One or more small strokes
LE and gait more affected
Rest tremor uncommon
Scarce response to levodopa

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24
Q

Drug-induced Parkinsonism

A

From neuroleptic/anti-psychotic meds
Symmetrical presentation
Orolingual dyskinesia, tardive dyskinesia, or akathisia may be present
Ceasing meds can reverse symptoms, can take up to 2 years

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25
Q

Infection-induced Parkinsonism

A

Encephalitis
Influenza
HIV
Meningitis

26
Q

Toxin-induced Parkinsonism

A 
Carbon monoxide
Heavy metals (manganese, copper, lead)
Mercury (tremor)
MPTP
Toluene (paint thinners, adhesives)
27
Q

Parkinson-plus syndromes

A

Progressive supranuclear palsy
Multiple system atrophy
Corticobasalganglionic degeneration

28
Q

Progressive supranuclear palsy

A

Early postural instability and falls
Vertical gaze paresis
Difficulty controlling eyelids (PSP stare)
5.3 year survival

29
Q

Multiple system atrophy

A

PD-symptoms, plus autonomic dysfunction and cerebellar dysfunction
8.5 year survival

30
Q

Corticobasalganglionic degeneration

A 
Focal rigidity
Marked dystonia (usually one arm)
Limb apraxia
Alien hand syndrome
PD-symptoms
6-8 year survival
31
Q

Modified Hoehn and Yahr Scale

A

0- no disease
1- unilateral
1.5- unilateral and axial
2- bilateral, no balance impairment
2.5- mild bilateral disease with recovery on pull test
3- balance impairment. mild-mod disease. independent.
4- severe disability, but can stand and walk unassisted
5- needs wheelchair or bedridden unless assisted

32
Q

MDS-UPDRS Motor

A

Items 0-4 (normal to severe impairment)

Speech, facial expression, tremor, rigidity, coordination, transfers, posture, gait, postural stability, bradykinesia

33
Q

Sinemet facts

A

Levodopa- precursor to dopamine that can cross blood-brain barrier
Carbidopa- prevents levodopa from converting in periphery
Side effects- nausea, drowsiness, orthostatic hypotension, dyskinesia, motor fluctuations, hallucinations
Protein can slow absorption

34
Q

On-off times effect

A

Dyskinesia- at peak dose

Off- no symptom management between doses

35
Q

Other PD meds

A 
Dopamine agonists
COMT inhibitors
MAO type-B inhibitors
Anticholinergics
Amantadine
36
Q

Dopamine agonists

A

Initial or adjunct therapy- delay or reduce motor fluctuations and dyskinesia
Longer half-life than Sinemet but not as effective
Mirapex, Requip, Neupro

37
Q

COMT inhibitors

A

Prevent peripheral degradation of levodopa
May decrease “off” time or dosage
Comtan, Tasmar

38
Q

MAO type-B inhibitors

A

Block breakdown of dopamine in brain

Selegiline, Rasagiline

39
Q

Anticholinergics

A

Inhibit dopamine reuptake in striatum
Mainly for tremors and rigidity
Artane, Cogentin

40
Q

Amantadine

A

Dopamine agonist and dopamine reuptake inhibitor
Often used to treat dyskinesia
Symmetrel, Kemadrin

41
Q

Symptoms unresponsive to meds

A

Postural instability
Freezing
Mental changes
ANS dysfunction

42
Q

Deep brain stimulation

A

Electrodes in brain connected to implantable pulse generator in chest
Minimize “off” times and dyskinesia, lower dosage of meds
Results no better than “on” time
For idiopathic PD only
Intact cog function, good dopamine response

43
Q

Target sites for DBS

A

Thalamus- reduces tremor, no other symptoms
Globus pallidus internus or subthalamic nucleus- reduces tremor, rigidity, bradykinesia, dyskinesia

STN DBS- better ADLs in “off” times, greater med reduction

44
Q

Dopamine’s effect on limbic functions

A

Low- depression, apathy, anhedonia, anxiety

High- euphoria/ mania, impulsivity, pleasure-seeking/risk-taking behavior

45
Q

Depression in PD

A

Most common psychiatric symptom in PD- 40%

Depressed mood, diminished interest/pleasure, fatigue, sleep changes, poor concentration, change in appetite

46
Q

Exercise effects in PD

A

May delay or prevent PD in healthy individuals

May slow disease progression and motor deterioration in early PD

47
Q

High-intensity exercise for PD

A

More normal corticomotor excitability

Lengthened cortical silent period (more normal corticomotor excitability)

48
Q

Forced use cycling effects

A

Improvement in UPDRS-motor, bimanual dexterity, rigidity, bradykinesia
Greater reliance on feedforward vs feedback processes- shifts central motor control processes
Forced exercise has similar effects on symptoms as meds do

49
Q

Individual vs group treatment for PD

A

Individual- best for balance and function improvements

Group- best for gait

50
Q

Treadmill training for PD

A

Improved gait parameters
Improved balance and motor performance
Improved QOL
Reduced fatigue

51
Q

Boxing for PD

A

Improved balance, gait, disability, QOL

Mild-mod PD

52
Q

Dancing for PD

A

Tango slightly superior
Partnered dancers more compliant
Mild-mod PD

53
Q

Tai chi for PD

A

Improve postural stability, reduce falls, improve motor function, improve QOL
Inconsistent effects on gait

54
Q

Dual-task training for PD

A

Best for mild-mod PD

Improves gait and balance in dual task, and in single-task gait

55
Q

How strategies work

A

Bypass basal ganglia via cortical, cerebellar, or brainstem pathways to normalize movement
Shifts to explicit learning vs implicit

56
Q

BESTest

A 
36-item balance assessment
Biomechanical constraints, stability constraints
Anticipatory postural adjustments
Reactive postural responses
Sensory orientation
Stability in gait
Score 0-3 (severe to normal)
Max score 108, converted to percentage
Cut-off <69% for fall risk
57
Q

Mini-BESTest

A 
14-item scale
0-2 (severe to normal)
Max 28
Use AD lowers each item by 1 point
Score of 0 if needs assistance
<23/28 is fall risk
58
Q

Freezing of gait questionnaire

A

6-item, to be given during “on” state
0 (no symptoms) to 4 (most severe)
Total 0-24 (high score is severe freezing)
Based on past week or overall presence of FOG throughout day

59
Q

Parkinson’s disease questionnaire-39

A

Self-report, QOL
Experience over past month
Mobility, ADLs, emotional well-being, stigma, cognition, communication, bodily discomfort
0 (never) to 4 (always)

60
Q

Treatment of freezing of gait

A

Improve weight shifting
External cueing
Exercise in small spaces
Dual task training

61
Q

Trail-making test involves

A

Attention shifting

NCS Prep (19 decks)

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