L3 Parkinson's Flashcards
Pathophysiology of PD
-Complex progressive neurodegenerative disease with idiopathic onset
-defined by loss of dopaminergic neurons in substantia nigra pars compact located in midbrain and associated with lewy bodies
-presents as unilateral and then becomes bilateral
-progresses insidiously over 5-15 years
When do symptoms of PD typically emerge?
after a loss of 50-70% of SNpc dopaminergic neurons
loss of dopaminergic in basal ganglia precedes onset of motor symptoms
Lewy bodies
intraneuronal protein aggregates, deposits of a protein called alpha-synuclein
Prevalence/incidence of PD
onset is at 40-70 yo
affects 1% of individuals over 65
higher in males vs femlaes
happens more in the rust belt (s CA, s. TX, PN, FL)
Clinical Diagnosis/Presentation of PD
-Motor Features
-Non-Motor Features
-Late stage non-motor features
Motor Features of PD
Tremors
Bradykinesia
Rigidity
Hypomimia
Hypophonia
Micrographia
Postural stability
Retropulsion
Freezing
Festinating Gait
En bloc turning
Non Motor Features of PD
depression
anxiety
REM sleep behavior disorder
Bradyphrenia
Cognitive Decline
Resting Tremor
-most commonly observed when the limb is relaxed
-asymmetrical and involves mainly the hands and UE, may involve LE and chin
-pill-rolling, looks like like they are rolling their a pill between their fingers
Postural Tremor
-subtype of action tremor
-occurs with holding position against gravity
Bradykinesia and Hypokinesia
slowed and decreased amount of movements
can be caused by increased inhibitory basal ganglia outflow to the thalamus
Rigidity
an increase in resistance to passive movement of a limb
cogweel is seen in PD, which is characterized by ratchet-like interruptions in tone felt as you move the limb passively through ROM. Rigidity with superimposed tremor
Masked faces/hypomimia
decrease in spontaneous blink rate and facial expression
Hypophonia
reduced vocal loudness
Micrographia
writing becomes smaller
Postural Instability
decreased ability to make reflex postural adjustments to maintain balance
Retropulsion
if pulled back slightly, may require several steps to regain balance
Freezing
difficulty initiating movement
Festinating gait
small shuffling steps
En bloc turning
turning with the trunk as one unit instead of with twisting at the torso
REM sleep behavior
slep disorder in which a person physically enacts out their dreams
Bradyphrenia
responses are slowed, appropriate if given enough time
Cognitive Decline
dementia is not an early feature of PD, but estimated to present later in the course of 15-40% of cases
commonly see executive dysfunction
Prognostic Factors for PD
- Those with severe baseline continue to be more impaired later in disease process
- Presentation w/out tremor may be predictor of more rapidly increasing disability
- Older age may be predictor of more rapidly increasing disability
- Cognitive impairment is increased with future disability and motor impairment
Hoehn and Yahr Scale
measures severity of PD’s symtpoms, classifies patients in following stages
stage 1-5
Stages of Hoehn and Yahr Scale
1 = unilateral involvement
1.5 = unilateral and axial involvement
2 = bilateral s/s, no balance impairment
2.5 = mild bilateral disease with recovery on pull test
3 = mild to mod disease physically independent
4 = severe disability, still able to walk or stand assisted
5 = w/c or bedridden
Unified PD Rating Scale
50 Q assessment to rate the motor and non-motor symptoms associated with PD
Part 1 = non-motor experiences of daily living
2 = motor experiences of daily living
3 = motor exam
4 = motor complications
Medical Management of PD
- Cabidopa Levodopa
- Deep Brain Stimulation
Carbidopa-levodopa
-most effective drug for treating PD
-carbidopa is decarboxylase inhibitor that prevents that breakdown of levodopa to dopamine in PNS
Adverse Effects of Carbidopa-Levodopa
GI disturbances
orthostatic hypotension
psychiatric problems
Wearing off of levodopa
decreased effectiveness of therapies at the end of the period doses
Levodopa-induced dyskinesias
excessive movement due to abnormal response to dopamine in the system
Deep Brain Stimulation
-stimulus delivered by implanted stimulation device that can be externally programmed and turned off at any time
-tx is bilateral
-targets subthalamic nucleus in pts with advanced PD
Multiple System Atrophy
more prominent autonomic dysfunction and loss of striatal neurons projecting to the GP and SNpr
associated with atrophy of intermediolateral cell column of SC and makes dopaminergic therapies ineffective
MSA-P and MSA-C are variants
Multiple system atrophy w/predominant parkinsonism (MSA-P)
striatoniagral degeneration
Multople System Atrophy with cerebellar features
olviopontocerebellar atrophy
Progressive supranuclear palsy
most common atypical parkinsonism syndrome, about 5% of patients
degeneration of structures in midbrain-deincephalic junction
presents as early postural instability, dementia, dysarthria, dysphagia, supranuclear gaze palsy
Dementia with Lewy Bodies
presence of intraneuronal alpha synuclein but throughout the neocortex as opposed to in the substantia nigra
presents with prominent psychiatric symptoms, dementia, hallucinations
Freezing of Gait Questionnaire
6 item questionnaire that assesses the severity of freezing unrelated to falls in people with PD
Parkinson’s Fatigue Scale
helps to meausre the presence of fatigue and its impact on daily function
PDQ-39
QOL measure looking at how often they have experienced a variety of emotions or challenges in the last month scoring from never to always on a 5 point scale
Exercise Benefits in PD
-neurogenesis, an increase in dopamine synthesis and release, increased dopamine in striatum
-preservation of dopaminergic cell bodies and terminals associated with improved running distance and speed
-aerobic programs improves gait parameters, WOL, levodopa efficacy
Rigidity Exercise
trunk rotation
reciprocal movements
rhythmic movements
erect alignmnet
large COM movements
increase limits of stability
Rigidity impact on mobility
agonist/antagonist co-cont
flexed trunk
reduced trunk rotation
reduced joint ROM
high axial tone
Bradykinesia impact on mobility
slow small movements
narrow bOS
lack of arm swing
Bradykinesia and Exercise
fast large steps
COM control
large arm swings
Freezing and Mobility
-poor anticipatory postural stability
-abnormal mapping of body and movement
-abnormal visual-spatial maps
-divided attention affects mobility
Freezing and Exercise
-improve weight shifting
-understand role of external cues
-exercise in small spaces
-practice dual tasks
Inflexible Program Selection and Mobility
-poor rolling, STS, turns
-difficult floor transfers
-inability to change strategy quickly
Inflexible Program Selection and Exercise
-plan task in advance
-quick change strategies
-sequencing components of task
Impaired sensory integration and mobility
-inaccurate w/out vision
-imbalance on unstable surface
-poor alignment with environment
Impaired sensory integration and exercise
-kinesthetic awareness
-decrease surface dependence
-flexible orientation
Reduced executive function and attention and mobility
difficulty with dual tasks and sequences of action
Reduced executive function and attention and exercise
practice gait and balance with secondary task and sequences of actions
