Neurorehab2 Parkinson's

Front 1

Parkinson's Pathology

Caused by dopaminergic cell death in ___ and ___ that leads to decreased release of dopamine

Back 1

substantia nigra compacta

pedunculopontinue nucleus

Front 2

Parkinson's

Dopaminergic cell death - leads to decreased release of dopamine

results in Disinhibition of:
___ and ___ Tracts

Back 2

vestibulospinal and

reticulospinal tracts

Front 3

Primary motor control problem with PD:
o Execution problems of ___:
 Loss of automaticity, skilled movements
 Loss of ability to activate such movements and continue sequence of movements
 Slowing of more complex movements
 Difficulty initiating movements.

Back 3

Basal Ganglia

Front 4

Parkinson's

o Symptoms become clinically apparent only when ___ of cells are damaged
o For PD, the ability to move is not lost but the ___ is lost.

Back 4

70-80%

activation problem

Front 5

Prognosis of ____
• Progressive, chronic, degenerative disease
• Longitudinal Course of PD:
o ____ onset: often unilateral onset of subtle motor features such as ____ tremor, loss of arm swing, slowing of movement
o Rate of progression varies: eventually symptoms worsen and become bilateral
o Postural instability: marks the beginning of more severe disease, and significantly increases risk of falls.
 Side note: PT level of commitment required: treatment must be individualized and continually adjusted as the disease evolves.

Back 5

Parkinson's

Insidious

resting

Front 6

Modified Hoehn and Yahr Staging
Stage ___

No signs of disease

Back 6

Stage 0

Front 7

Modified Hoehn and Yahr Staging
Stage ___

Unilateral disease

Back 7

Stage 1

Front 8

Modified Hoehn and Yahr Staging
Stage ___

Unilateral plus axial Involvement

Back 8

Stage 1.5

Front 9

Modified Hoehn and Yahr Staging
Stage ___

Bilateral disease, without impairment of balance

Back 9

Stage 2

Front 10

Modified Hoehn and Yahr Staging
Stage ___

Mild bilateral disease, with recovery on pull test

Back 10

Stage 2.5

Front 11

Modified Hoehn and Yahr Staging
Stage ___

Mild to moderate bilateral disease; some postural instability; physically independent

Back 11

Stage 3

Front 12

Modified Hoehn and Yahr Staging
Stage ___

Severe disability; able to walk or stand assisted

Back 12

Stage 4

Front 13

Modified Hoehn and Yahr Staging
Stage ___

Wheelchair bound or bedridden unless aided

Back 13

Stage 5

Front 14

• Screening for PD Early Signs:
o Age-related cell death in ___
o >65 y/o (1 in 100)
o ___ face
o ____ tremor in hand or thumb
o Loss of ___

Back 14

substantia nigra

Masked face

Unilateral tremor

loss of smell

Front 15

Hallmark signs of ___

Tremor - usually resting

Rigidity - hypertonicity, hyperreflexia

Bradykinesia - Difficulty performing repetitive or sequential movements (mvts get smaller and smaller)

Postural Instability

Akinesia: absence of movement associated w/ an inability to initiate movement

Freezing

Impaired balance

Dyskinesia - purposeless writhing movements

o Non-motor signs:
 Autonomic failure: constipation, impotence
 Neuropsychiatric dysfunction: depression, dementia

Back 15

Parkinson's Disease

Front 16

 ___: slowing and reduction of movement
• Involves SMA and 1º motor cortex loops
• Movement execution & stopping movement problems
• Result: Difficulty performing repetitive or sequential movements (mvts get smaller and smaller)

Back 16

Bradykinesia

Front 17

• Bradykinesia and motor instability:
o Disruption of neurotransmitters between ___ and ___
o SMA is essential for:
 Regulating increase in neural drive
 Stopping movement
o Disruption of this circuit could be reason for bradykinesia, dimunition, festinating gait

Back 17

internal globus pallidus

SMA/PMC

Front 18

o ___ is essential for:
 Regulating increase in neural drive
 Stopping movement

Back 18

SMA - supplementary motor area

Front 19

• ____: absence of movement associated w/ an inability to initiate movement
o Striatum prob, so can’t play role in pattern recognition and matching demands of task to motor output
o Result: can’t move in certain environments

Back 19

Akinesia

Front 20

• ____: sudden cessation of movement part way through an action sequence. (same striatum prob)

Back 20

Freezing

Front 21

• ___: Purposeless writhing movements
o Excessive GABA due to long-term levodopa meds
o Result: painful dystonias, embarrassing, interferes with function and roles.

Back 21

Dyskinesia

Front 22

o Non-motor signs of PD:
 ___ failure: constipation, impotence
 Neuropsychiatric dysfunction: depression, dementia

Back 22

Autonomic

Front 23

o ___ Response to PD:
 Reduced activity, mm. weakness (LE), reduced mm length, contractures, deformity, reduced aerobic capacity, imbalance
 Age related changes to sensory: visual, vestibular, proprioceptive
 Preexisting level of dependency: higher rate for falls (institutions vs. community)

Back 23

Adaptive

Front 24

• Simple, discrete movements can be near ___ (b/c they don’t use BG)
• Long, complex action sequence can be much more difficult (b/c uses BG)

Back 24

normal

Front 25

Treatment for Parkinson's
External cues:
o Visual: Stepping exercise. better for ___. Increased step length maintained for 1 mo post.

o Auditory: better for ___
o Proprioceptive

Back 25

bradykinesia

freezing (auditory)

Front 26

• Attentional strategies (to rely on ___ brain)
o Caveats: very difficult to dual task, may not be as effective w/ cognitively-impaired

Back 26

frontal-cortical

Front 27

• ___ Rx:
o Stop. And restart.
o Provide ext. cues.
o Break down complex movement to simple submovements.
o Avoid dual tasking
o Focusing attention.

Back 27

Bradykinesia

Front 28

• ____ Rx:
o Ext. cues: auditory, visual, or proprioceptive
 Auditory: freezing during gait
 Visual: hypokinesia during gait
 Music or rhythmical cues
o Focused attention: avoid dual tasking

Back 28

Akinesia

Front 29

• ___ Rx:
o Talk to MD about meds (levadopa)

Back 29

Dyskinesia

Front 30

• ___ Rx:
o Walking, sit to stand, turning around, turning over and getting out of bed
o Driving, golfing, going to seat in theater

Back 30

Function

Front 31

• ___ Rx:
o Work on absent/delayed reactive balance and miscalculations for proactive balance

Back 31

Balance

Front 32

Pt. ___

o Precue/focus attention when change in environment expected (see crowd ahead, change from tile to carpet)
o Plan route if obstacles ahead, including stops if long distance or expect need to change direction)
o Prepare mentally to recover balance by stepping, teach stepping response
o Prepare for probable events that will disturb balance *bus stops, elevator stops, train starts)
o Adapt environment to diminish changes (stripes on floor at areas that pose difficulty)

Back 32

Education

Front 33

Pathology of ___

• Hyperkinesia, basal ganglia disorder
o Disinhibition/Inadequate inhibition of the thalamus and pedunculopontinue nucleus (“no brakes”)
• Degeneration of the striatum
• Decreased activity in the “output nuclei”
• Results in:
o Inhibition of medial activation tracts --> excessive activity in corticofugal tracts

Back 33

Huntington’s Chorea

Front 34

• Hyperkinesia, basal ganglia disorder
Huntington's Chorea
o Disinhibition/Inadequate inhibition of the ___ and ___ (“no brakes”)

Back 34

thalamus

pedunculopontinue nucleus

Front 35

Huntington's Chorea

Degeneration of the ___

Back 35

striatum

Front 36

Huntington's Chorea

Decreased activity in the "___"

Back 36

"output nuclei"

Front 37

Huntington's Chorea

• Results in:
o Inhibition of medial activation tracts --> ___ activity in corticofugal tracts.

Back 37

excessive

Front 38

____

Reduced movement speed and amplitude; at the extreme, it is known as "hypokinesia," which refers to "poverty" of movement

Back 38

Bradykinesia

Front 39

____

Difficulty initiating movements

Back 39

Akinesia

Front 40

Episodes of ___

Motor blocks/sudden inability to move during the execution of a movement sequence

Back 40

freezing

Front 41

Impaired ___

difficulty maintaining upright stance with narrow BOS in response to a pertubation to the COM or with eyes closed; difficulty maintaining stability in sitting or when transferring from one position to another; can manifest as frequent falling

Back 41

Impaired balance and postural control

Front 42

__

overactivity of muscles; can manifest as dystonia; wriggling/writhing movements; chorea or rarely athetosis

Back 42

Dyskinesia

Front 43

___

Usually resting ___; more rarely postural or action ___

Back 43

tremor

Front 44

___

hypertonicity and hyperreflexia in agonist and antagonist muscle groups in a given limb

Back 44

Rigidity

Front 45

___

Reduced activity, muscle weakness, reduced muscle length, contractures, deformity, reduced aerobic capacity

Back 45

Adaptive responses

Front 46

movement size progressively decreases during sequential actions. This diminution of movement is known as ___ and can be clearly seen in people with gait hypokinesia, in whom the footsteps become shorter and shorter the further they walk. Likewise, the handwriting of people with PD is typically miniaturized and becomes both smaller and slower as a paragraph is written. When a person with PD stops a movement sequence, has a short rest, and begins again, the movement size and speed start at values that are close to normal, then again start to reduce as the new sequence is performed.

Back 46

“motor instability”

Front 47

Bradykinesia in people with PD results from disruption of the neurotransmitters used in the neural projections from the ___ of the basal ganglia (BG) to the motor cortical regions known as the ___ and the primary motor cortex.

Back 47

internal segment of the globus pallidus

supplementary motor area (SMA)

Front 48

The ___ is critical in regulating the increase in neural activity that needs to occur before a movement is executed. It also ensures that a movement is terminated at the appropriate time.

Back 48

SMA

Front 49

Clinical evidence suggests that akinesia and freezing episodes are ___ dependent.

Back 49

context

Front 50

why do some people with PD find it difficult to cease actions such as walking, turning around, or speaking?

Back 50

Because they have sustained discharge in the SMA, rather than the rapid drop in neural activity in the SMA that normally allows movements to be terminated.
Difficulty terminating locomotor actions such as walking, running, or turning during walking is thought to be one of the major factors that predisposes people with PD to slips, trips, and falls.

Front 51

some people with advanced PD who have been receiving levodopa medication for more than 15 to 20 years develop ___, which may be associated with relatively excessive amounts of GABA/enkephalin.

Back 51

dyskinesia

Front 52

___ = purposeless wriggling or writhing movements as well as dystonic posturing of the feet, hands, trunk, and neck. Dyskinesia includes chorea, athetosis, tics, dystonia, and tremor.

Back 52

Dyskinesia

Front 53

___ - refers to excessive and sustained overactivity of a particular muscle group such as the triceps surae or long finger flexors. The overactivity occurs for periods of minutes to hours and frequently recurs over the course of a day, month, or even years.

Back 53

Dystonia

Front 54

A ___ in a person with PD is most easily detected by quickly and unexpectedly pulling the person backward at the shoulders while he or she is standing with his or her feet slightly apart.

Back 54

balance disturbance

Front 55

PD = the ability to move is not lost; rather there is an activation problem. As a result, people with PD appear to be reliant on ___ mechanisms to initiate movement.

Back 55

cortical control

Front 56

External cues may assist people with PD to move more easily because they utilize the intact ___ of the brain rather than the defective BG-SMA circuits to control movement.

Back 56

premotor cortex

Front 57

Walking - The fundamental deficit in gait hypokinesia is a disorder in ____.

Back 57

step length regulation

don't step out far enough

Front 58

• ___
o Usually Asymmetric
o Cardinal Signs: Tremor, Rigidity, Bradykinesia
o Levodopa Responsive
o Later Findings –
 Postural Instability
 Levodopa-unresponsive gait disorder
 Non Motor Features

Back 58

Idiopathic Parkinson’s Disease

Front 59

• ___
o Unlike PD, Lewy Bodies rapidly spread throughout the brain, including the cerebral cortex
o Levodopa Responsive Parkinsonism
o Rapidly Progressive Dementia
o Hallucinations

Back 59

Diffuse Lewy Body Disease

Front 60

• ___
o Early Postural Instability and Falls
o Parkinsonism -Unresponsive to Levodopa
o “Stone Face”
o Dementia
o Ocular Signs

Back 60

Progressive Supranuclear Palsy: PSP

Front 61

• ___
o Asymmetric Parkinsonism with Poor Response to Levodopa
o Apraxia and Alien Limb
o Spasticity, Rigidity, Dystonia
o Gait and Balance Problems
o Dementia always occurs, but may be a late feature

Back 61

Corticobasal Degeneration: CBGB

Front 62

• ___
Cardinal Findings
o Parkinsonism
o Unresponsive to Levodopa
o Autonomic Failure-Low Blood Pressure
o Cerebellar Signs
o Corticospinal Tract Signs-Spasticity
Types
o Striato-Nigral Type
 Parkinsonism First
o Shy-Drager Syndrome
 Autonomic Failure First
o Olivo-ponto-cerebellar Type OPCA
 Ataxia First

Back 62

Multiple Systems Atrophy: MSA

Front 63

• ____
o Haldol and other antipsychotic medications cause symmetric findings that are indistinguishable at times from Idiopathic Parkinson’s Disease
o Reglan is a dopamine blocker and is an important cause of Parkinsonism in elderly patients (Anti-nausea medication)

Back 63

Drug-related Parkinsonism

Front 64

Voluntary Movement:
____ Tract

 Upper motor neurons
 Located in the motor cortex

 Lower motor neurons
 Located in the ____ horn of the
spinal cord

Back 64

Corticospinal

ventral

Front 65

Basal Ganglia and Cerebellum
 Work in harmony with the sensorimotor
cortex to ___ movement.

Back 65

modulate

Front 66

Basal Ganglia & Cerebellum
 These structures do not have direct
connections with ___ motor neurons.

 The basal ganglia and cerebellum
modulate the activity of ___ motor
pathways.

Back 66

lower

descending

Front 67

Basal Ganglia & Cerebellum

 The ___ form motor control
loops with the motor centers on the same
side.

Back 67

basal ganglia

Front 68

Basal Ganglia & Cerebellum

 The ___ interacts with
the contralateral cerebral cortex.

Back 68

cerebellar hemispheres

Front 69

The Basal Ganglia consists of 5
primary motor nuclei:
 Caudate
 ____
 Globus pallidus
 ____
 Substantia nigra

Back 69

Putamen

Subthalamic
nucleus

Front 70

3 Basal Ganglia Nuclei

Back 70

 Caudate
 Putamen
 Globus Pallidus

Front 71

2 Brainstem Nuclei

Back 71

 Substantia Nigra
 Subthalamic Nucleus

Front 72

Language of the
Basal Ganglia

 Caudate
 Putamen
= _____

AFFERENT STRUCTURES:
Receive input from the entire cerebral cortex, thalamus, substantia nigra, and dorsal
raphe nucleus.

Back 72

Striatum

Front 73

Language of
Basal Ganglia

Putamen
Globus pallidus
= ____

Back 73

Lentiform
Nucleus

Front 74

Language of
Basal Ganglia

___ =
Medial (Internus)
Lateral (Externus)

EFFERENT STRUCTURES:
The ___ Internus projects to the Thalamus
and Pons. It is part of the “output nuclei”

Back 74

Globus pallidus

Globus Pallidus

Front 75

Language of Basal Ganglia

__=
Compacta and Reticularis

The ____ Reticularis projects to the
Thalamus and Pons; also part of the “output nuclei”

Back 75

Substantia nigra

Substantia Nigra

Front 76

"Output nuclei"

Back 76

Globus pallidus Internus

Substantia Nigra Reticularis

Front 77

The individual nuclei of the basal ganglia link
together to form a ___.

Back 77

functional unit

Front 78

Two Control Loops
 Input
 Information enters BG system from almost all
areas of the cerebral cortex, expecially from
motor areas and somatosensory cortex.

 Output
 Information from BG projects back to the cortex
via the ____.

Back 78

thalamus

Front 79

Two Control Loops

____

Cortex --> Striatum--> Globus Pallidus-->
Thalamus--> Cortex

Back 79

Input

Front 80

Two Control Loops

____

Cortex --> Striatum --> Substantia Nigra --> Thalamus --> Cortex

Back 80

Output

Front 81

Striatum (caudate + putamen) is processing
center for ___ from cerebral cortex,
thalamus and substantia nigra.

Back 81

input

Front 82

 Globus pallidus and substantia nigra
comprise efferent, ___ portion of BG.

Back 82

output

Front 83

Two Primary loops – Direct & Indirect

Overall ___
EFFECT ON THE
THALAMUS (MOTOR
OUTPUT NUCLEI)

Back 83

INHIBITORY

Front 84

___ loop, or direct loop, ___ the
thalamocortical loop.

In concert, discrete MODULATION is
possible.

Back 84

Input

activates

Front 85

___ loop, or indirect loop, ___ the
thalamocortical system.

In concert, discrete MODULATION is
possible.

Back 85

Output

inhibits

Front 86

Neurotransmitters:

 Glutamate = ___

 GABA = ___

 Dopamine = Can be either

Back 86

Excitatory

Inhibitory

Front 87

Dopamine - neurotransmitter

Can be excitatory ___ or inhibitory (D2),
depending on the ___ subtype
 Very important in Basal Ganglia circuits

Back 87

(D1)

receptor

Front 88

____ tracts
 Includes corticospinal, corticopontine and
corticobulbar descending motor tracts.

Back 88

Corticofugal

Front 89

Disinhibiton:
The basal ganglia “output nuclei” ___ the motor
thalamus and pedunculopontine nucleus

 Inadequate ___ results in hyperkinetic
disorders, i.e.,
 removing inhibition produces excitation.
 “No brakes”

Back 89

inhibit

inhibition

Front 90

loss of activation

Excessive ____ results in hypokinetic
disorders
 cannot excite lower motor neurons!
 “No gas!”

Back 90

inhibition

Front 91

Basal Ganglia Dysfunction

 Inadequate inhibition --> ___

 Excessive inhibition -->hypokinesis

 Depending on the location, lesions or cell death in the
BG can cause either hyper- or hypokinesia.

Back 91

hyperkinesis

Front 92

When there are problems in the
loops of the BG:
 Examples:
 Parkinsons Disease -->Hypokinesia

 Huntingtons Disease --> Hyperkinesia

Back 92

ok

Front 93

Parkinson’s Disease
 Pathology
 Cell death in the ___
(also in ___)
 The cells that die are dopaminergic (i.e. use
dopamine as the primary neurotransmitter)

Back 93

substantia nigra compacta

pedunculopontine nucleus

Front 94

Cell death in the substantia nigra compacta and
pedunculopontine nucleus
 The cells that die are dopaminergic
 Results in:
 ___ of the vestibulospinal and reticulospinal
tracts
 ___ inhibition of the VL thalamus --> ____
activity in corticofugal tracts

Back 94

Disinhibition

Increased

reduced

Front 95

Huntington’s Disease
 Degeneration of the ____
 Decreased activity in the ___
 ___ of the thalamus and
pedunculopontine nucleus
 Results in:
 Inhibition of medial activation tracts -->
excessive activity in corticofugal tracts

Back 95

striatum

“output nuclei”

Disinhibition

Front 96

*Not all circuits in BG are motor
circuits.
 Recent evidence suggests BG involved in:
 Cognitive and Emotion processing
 ___ implications

Back 96

Motor Learning

Front 97

Parkinson’s Disease
 A Disorder of the Basal Ganglia
 Caused by cell death in the Substantia Nigra
that leads to decreased release of the
neurotransmitter dopamine
 Symptoms become clinically apparent only
when ___% of cells are damaged
 Etiology not well-understood

Back 97

70-80%

Front 98

Epidemiology of PD
 500,000 to 1 million patients in US
 40,000 to 60,000 new cases/year
Lang & Lozano. N Engl J Med. 1998;339:1044-1053.
Olanow & Koller. Neurology. 1998;50(suppl 3):S1-S57.
Tuite & Ebbitt. Semin Neurol. 2001;21:9-14.
 Average age of onset is 60 years
 Affects up to 0.3% of general population,
but 1% to 3% of those older than 65 years
 Prevalence increasing as the population
___

Back 98

ages

Front 99

PD Is Largely a Disease of ___

Only 5% to 10% of
patients have symptoms
before age ___
(“young-onset PD” or
YOPD)

Back 99

Older
Adults

40

Front 100

Longitudinal Course of PD
 ___ Onset
 often ___ onset of subtle motor features such as resting tremor, loss of
arm swing, or slowing of movement

 Rate of progression varies
 eventually symptoms worsen and become bilateral

 Postural ___
 marks the beginning of more severe disease, and significantly increases risk
of falls

***Level of Commitment required from Therapist:
Treatment must be individualized and continually adjusted as the disease
evolves.

Back 100

Insidious

unilateral

instability

Front 101

Screening for PD – Early signs
 Age-related cell death in substantia nigra
 >___ y.o. (1 in 100)
 Masked face
 Unilateral ___ in hand or thumb
 Loss of ___

Back 101

65

tremor

smell

Front 102

Hallmark Signs of ___
 Hallmark Signs are:
 Tremor – Rigidity – Bradykinesia - Postural
Instability

 Non-Motor Signs:
 ___ failure (constipation, impotence)
 Neuropsychiatric dysfunction (depression,
dementia)

Back 102

PD

Autonomic

Front 103

Skilled Movement
 Intentional movements are initiated by the cerebral
cortex (premotor & motor areas)
 Basal ganglia and Cerebellum “shape” the final
descending signal (via the ___) on the
descending ___ and corticospinal motor
pathways.
 Both the BG and CB have an essential and distinct
role in the organization of normal motor output.
 Both the BG and the CB play an important role in
___ processes.

Back 103

Thalamus

corticobulbar

motor learning

Front 104

Motor Control roles of ____:
 Execution of a motor plan
 Feedforward motor control
 Scaling of movement
 “Braking” or “Gating” Switches in behavioral set
 Central Set Switching
 Initiation of movement? (controversial)

Back 104

Basal Ganglia

Front 105

BG may be the 2nd step in
“initiation of movement”
 Traditionally has been held responsible for
motor planning function of “initiation”
 More recent research implicates it as
“___” the movement
 Equivalent studies when looking at f MRI and
activating patterns

Back 105

executing

Front 106

Basal ganglia are active before EMG
activity of prime movers of a task.

____ “set”
 Ability to initiate and carry out smoothly and in proper
sequence a set of movements that comprise a defined
response.

Back 106

Response

Front 107

Basal ganglia are active before EMG
activity of prime movers of a task.

____ “set” (Central set)
 Preparation of the body prior to a task to meet the needs
of the environment.
 Initiation of movement, changing from one movement to
another, choosing the correct movement

Back 107

Activating

Front 108

How do these execution problems
present in individuals with PD?
 Loss of ___, skilled movements
 Loss of ability to activate such movements
and continue sequence of movements
 Slowing of more complex movements
 Difficulty initiating movements

Back 108

automaticity

Front 109

clinical presentation

___:
 Absence of movement associated with an
inability to initiate movement

Back 109

Akinesia

Front 110

clinical presentation

___:
 Sudden cessation of movement parthway
through an action sequence.

Back 110

Freezing

Front 111

Akinesia and Freezing –
Context dependent
 ___ implicated (in animal studies) recognizing
patterns of input about the environment from the
cortex.
 This information is used for planning and executing
intelligent behavior.
 When the striatum is defective, motor performance
will not recognize or match the task demand.

Back 111

Striatum

Front 112

Bypassing the BG with external
cues
 Increase reliance on ___ areas of the
brain
 Use External cues and Attentional strategies to
activate these areas
 The BG is “off the hook”
*Caveats:
– very difficult to dual task using this strategy.
- may not be effective with cognitively-impaired

Back 112

frontal-cortical

Front 113

External cues
 Can be visual, auditory, proprioceptive

 During Gait (Nieuwboer, 2008)
 Evidence is ___ for clinical effectiveness
 ___ seem better for freezing
 ___ seem better for bradykinesia

Back 113

weak

Auditory

Visual

Front 114

Visual Cues
 Example of Stepping
Exercises. Patient with
gait freezing develops a
motor program of
stepping by using visual
cues.

Back 114

picture of pt. walking over multiple boards spaced out on the floor, so he takes big steps

Front 115

Effects of long-term gait training using visual
cues in an Individual with PD.
Sidaway et al, PTJ, Vol 86, #2, 2006
 Case study A – B design
 78 y.o.w. with 12 year history of PD (H&Y 3)
 Methods:
 Uncued walking for 4 weeks, 30 mins, 3X week
 Cue walking for 4 weeks, visual
 Results:
 No improvements after uncued walking
 Improvements after cued walking and were maintained at
1 month post

Back 115

ok

Front 116

Standardized Assessment of
Freezing
 Freezing of Gait Questionnaire
 Giladi et al, Construction of freezing of gait
questionnaire for patients with Parkinsonism.
Parkinsonism & Related Disorders 6 (2000), 165-
170.

Back 116

ok

Front 117

___:
Slowing and Reduction of Movement

Back 117

Bradykinesia

Front 118

Motor ___:
Diminution of movement
 Movement size progressively decreases
during sequential actions
 Footsteps, handwriting, alternating movements

Back 118

instability

Front 119

Bradykinesia and Motor Instability
 Disruption of neurotransmitters between internal
globus pallidus and ___.

 ___ is essential for:
 regulating increase in neural drive;
 ___ movement


 Disruption of this circuit could be reason for
bradykinesia, dimunition, ____ gait

Back 119

SMA/PMC

SMA

Stopping

festinating

Front 120

Impaired ___
 Pathology?
 Connections between GB and brainstem?
 Decreased scaling of responses?

 Consequences?
 Absent or delayed reactive balance
 Miscalculations for proactive balance

Back 120

Balance

Front 121

Pharmacotherapy of PD
Levodopa versus ___

Back 121

Dopamine Agonists

Front 122

Remember:
You are treating two patients in one.
 Two phases of medication:
 “On Phase”
 Normal  Hyperkinesia
 “Off Phase”
 Bradykinesia  Akinesia

Back 122

ok

Front 123

Levodopa/carbidopa (___)

Back 123

Sinemet®

Front 124

___ agonists
 Bromocriptine (Parlodel®)
 Pergolide (Permax®)
 Ropinirole (Requip®)
 Pramipexole (Mirapex®)
 Apomorphine (Apokyn®)

Back 124

Dopamine

Front 125

___: Advantages
 Most potent anti-parkinsonian drug
 Immediate therapeutic benefits (within 1
week)
 Easily titrated
 May reduce mortality
 Lower cost of generic forms

Back 125

Levodopa

Front 126

Levodopa: Disadvantages
 ___ on disease course
 No effect on nondopaminergic symptoms
 Dysautonomia, cognitive disturbances,
postural instability
 May aggravate ___ dysfunction
 Motor fluctuations and ___ develop
over time

Back 126

No effect

autonomic

dyskinesia

Front 127

____: Long-Term Concerns
 Motor fluctuations
 Up to 50% of patients after 5 years of
treatment
 70% or more of patients after 15 years of
treatment
 End-of-dose “wearing off” phenomenon
 Unpredictable “on-off” fluctuations
 Dyskinesia

Back 127

Levodopa

Front 128

Benefits of Early Use
of ___

 Reduced risk of ___ compared with levodopa therapy

 Antiparkinsonian effects comparable with
levodopa in early stages of disease

 Levodopa can be added later as needed

Back 128

Dopamine Agonists

dyskinesia

Front 129

___ Adverse Effects
 Nausea/vomiting
 Sedation
 Insomnia
 Orthostatic hypotension
 Hallucinations
 Dyskinesia in more advanced disease
 Leg edema
 Uninhibited Behaviors

Back 129

Dopamine Agonist

Front 130

What does the ___ do?
• Gatekeeper for programs coming down from the
cortex
– Movement “memory”
• Movement initiation
• Execution of automatic, complex movement
• Force generation
• Spatial memory and relationships
“Plays a major role in allowing people to execute
well-learned skilled movements quickly and
smoothly.” Morris, 2000

Back 130

basal ganglia

Front 131

As a result,
people with PD appear to be reliant
on ___ control mechanisms to
initiate movement.

Back 131

cortical

Front 132

Morris’ Model for PT with PD
• Based on the assumption that normal
movement can be obtained by teaching
patients strategies to bypass the BG
pathology.
• Tx Strategy:
– Use of external cues
– Attentional strategies
– Avoid ___ learning requirements

Back 132

novel

Front 133

Morris’ Model for PT with PD:
Key Components
• Task Analysis and Task-Specific
training.
• Effects of ____ on movement
• Caretaker needs
• Effects of ___, co-morbidities,
secondary deficits due to decreased
mobility

Back 133

medications

aging

Front 134

Characteristics of Movement
during tasks in those with PD
• Simple, discrete movements can be
near-normal (don’t use BG)
• A long, complex action sequence can
be much more difficulty (uses BG)
• Tx Strategy:
– Break down complex movements
– Use ___ cue to initiate movement
– Avoid ___ tasking
– ___ Rehearsal

Back 134

rhythmical

dual

Mental

Front 135

Key elements of the model for training people w/ PD (Morris)

1. Movement ____
2. ___ impairment
3. Task analysis and task-specific training
4. Environment
5. Medication
6. ___/concurrent pathologies
7. ___ adaptive changes
8. Need of patient and ___

Back 135

1. disorders
2. Cognitive
6. Aging
7. Secondary
8. caregivers

Front 136

What is bradykinesia?
• Slowness of movement
– Hypokinesia – poverty of movement
• Pathology?
– Involves ___ and primary motor cortex loops
– Movement execution, stopping movement
• Consequences?
– Difficulty performing repetitive or sequential
movements
• Movement gets smaller and smaller and smaller and smalle

Back 136

SMA

Front 137

What can we do for ____?
• Stop. And re-start.
• Provide external cues.
• Break down a complex movement into
simple submovements.
• Avoid dual tasking.
• Focusing attention.

Back 137

bradykinesia

Front 138

What is akinesia?
• Absence of movement – “freezing”
• Pathology?
– ___ plays role in pattern recognition and
matching demands of task to motor output.
• Consequences?
– Freezing in certain environments

Back 138

Striatum

Front 139

What can we do for ___?
• External cues – auditory, visual, or
proprioceptive
– Auditory -->freezing during gait
– Visual --> hypokinesia during gait
– Music or rhythmical cues
– Why do external cues work?
• Focused attention – avoid dual tasking
– Why does focused attention work?

Back 139

akinesia

Front 140

What is dyskinesia?
• Purposeless writhing movements
• Pathology?
– Excessive ___ due to long-term ___
• Consequences?
– Painful dystonias, embarrassing, interferes with
function and roles

Back 140

GABA

levodopa
meds

Front 141

Impaired ___
• Pathology?
– Connections between GB and brainstem?
• Consequences?
– Absent or delayed reactive balance
– Miscalculations for proactive balance

Back 141

Balance

Front 142

The General Population
• For people age 65 and older,
falls are the leading cause of
injury death.

1 out of 3 adults 65 or older falls
each year.
Incidence of Falls
y
• 1 out of 2 adults over the age of 80
falls annually.

Back 142

ok

Front 143

incidence of falls in PD

distribution of fracture location in Parkinson's

Back 143

hip and pelvis

skull

hand and wrist

Front 144

The most serious fall injury is hip fracture:
- at least one half of all older adults
Hip fracture in general population:
Mortality and Disability
hospitalized for hip fracture never
regain their former level of function;
- 25% die within one year.

Back 144

ok

Front 145

Hip Fractures
• 5% of falls in those 65 or older result in
fractures (Wilkins, 1999)
– 1-2% result in hip fractures
• __% of falls in those with PD result in
fractures! (Wielinski, 2005)
– 35% result in hip or pelvic fractures

Back 145

11%
PD, more fractures, more hip/pelvic fractures, bad!

Front 146

Falling Risk Factors in PD
Robinson et al, 2005
• Age
• Stage or severity of disease
• Orthostatic hypotension
• Polypharmacy
• Side Effects of PD meds:
– dyskinesias, hallucinations, sleep disorders, urinary urgency
• Depression, anxiety, fear of falling
• Polypharmacy
• Sleep disturbances
• Balance and gait disturbances
• Impaired arm swing during giat
• Inability to rise from a chair
• Cognitive Impairments
• Bradykinesia, Rigidity and Freezing

Back 146

ok

Front 147

Of the 38% of individuals who fall,
13% fall more than 1x/week
– Koller et al., 1989

Back 147

PD falls often

Front 148

____ Risk Factors to identify
those with PD for Recurrent Falls
Dennison et al, 2007
1. Leg agility or lower leg coordination
2. Rising from a chair without using arms
3. Quality of gait
4. Tandem walking
5. Motor planning of hands and/or feet
6. Fear of falling
7. Freezing of gait
8. Posture
9. Postural stability
10.Dyskinesia
11.Orthostatic Hypotension

Back 148

Modifiable

Front 149

Orthostatic Hypotension
• 10-30% prevalence in “normal’ older adults
• ___% in those with PD, due to ___.
– Senard JM et al, 1997

• ___ often implicated
– Cardiovascular drugs
– Parkinson drugs
• OH Can be ____ of underlying disease process
Screen:
• 20 mm Hg or more or diastolic blood pressure of 10
mm Hg or more within 3 minutes of quiet standing
after being supine for 2 minutes.

Back 149

49%

ANS dysfunction

Medications

earliest sign

PD lots of OH, pass out and fall

Front 150

Medications --> Polypharmacy
• Use of ___ medications
• Major offenders on their own:
– Psychotropic meds
• Antidepressants, sedatives, antipsychotic
– Class 1a antiarrythmic meds
– Digoxin
– Diuretics
• Leipzeig, 1999
• Side Effects of Sinemet
– Orthostatic Hypotension, GI problems, breathing,
confusion, hallucinations, depression, sleepiness
Screen all medications (Rx and OTC).

Back 150

3 or more

Front 151

Cognitive Impairment
• Almost ___ the risk for falling.
• Affects approximately 15% of general population
who are >65 years old
• Risk increases with advancing age:
• 65- 74 y.o. 3%
74-84 y.o. 18%
>85 y.o. 47%
Screens:
• Folstein Mini-Mental Exam

Back 151

doubles

Front 152

___ Weakness
• Identified as most potent risk factor in recent
meta-analysis of RCTs in general population.
• Increase odds of falling by more than 4X
• Rubenstein & Josephson, 2006
Screen:
• Sit to Stand Test
– Rise from chair with arms crossed as many times
as you can in 30 seconds.
• 13 times or more: low risk of falls
• 9 to 12 times: moderate risk
• 8 or less times: high risk

Back 152

Leg

Front 153

“Therefore, the greater the ___, the faster subjects with PD performed
the STS (sit to stand test).

For controls, the greater the knee strength, the faster they performed
the STS.” Inkster, 2003

Back 153

hip strength

Front 154

Gait and Balance Disorders
• Affect 20-50% who are >65 years old.
• Increases risk by 3X
• Use of assistive device increases 2.6X
– Rubenstein & Josephson, 2006
• Affects ___% of those with PD in mid to
late stages of the disease

Back 154

100%

Front 155

Functional Reach Test
Behrman, Light, Flynn & Thigpen, 2002
• 43 subjects with PD
• Identified fallers versus non-fallers

Back 155

least distance reached in cm = PD + falls

middle: PD - falls

farthest distance reached = controls

Criterion for falls risk: reach < 25.4 cm (Duncan et al., 1992) - pretty crappy, lots of false negatives (reached greater than 25.4, but still had falls!)

False negatives are an issue in
the PD population.
“In order to decrease the number of false
negatives, and accurately screen more
persons with PD at risk for falls, we
believe the cut-off scores for these
should be reconsidered.”

Front 156

Reactive Balance:
Coactivation
Overcorrection
Presence of hip
Control Subject Subject with PD
strategy activation

Back 156

Increased magnitude of response
• Coactivation (braking)
• No adaptation

Front 157

Postural response test
(Pastor et al., 1996)
If clinician pull backwards on patient at shoulders, typical
response is lack of a posterior stepping response and a
rigid fall backwards into clinician’s arms.
• Patient in stance with feet 10 cm apart.
• “I am going to tap you off balance, and I won’t let you
fall.”
0 Stays upright without taking a step
1 Takes one step backwards but remains steady
2 Takes more than one step backwards, followed by the need
to be caught
3 Takes several steps backwards, followed by the need to be
caught
4 Falls backwards without attempting to step

Back 157

ok

Front 158

Patient Education

Precue/focus attention when change in ___ expected (i.e. see crowd ahead, change from tile to carpet)

Back 158

environment

Front 159

patient education

plan route if obstacles ahead, including stops if a long distance or expect you will need to change direction

prepare mentally to recover balance by stepping; teach stepping response

prepare for probable events that will disturb balance (bus stops, elevator stops, train starts)

Adapt environment to diminish changes - ___ on floor at areas that pose difficulty

Back 159

stripes

Front 160

Inherent to PD, associated with cognitive disorders

Difficulty performing ___ tasks at once (turn and
talk; Bond et al., 2000)
• Impairment in problem-solving and
planning. May increase incidence of behavior
that is high-risk for persons with PD

Back 160

2

Front 161

Falls Efficacy Scale (by ____)

Measures a person’s confidence in doing Falling
ADL without falling.
On a scale of 1 to 10 with 10 meaning NOT confident or sure at all, 5
being FAIRLY confident/sure, and 1 being COMPLETELY confident/sure,
how confident/sure are you that you can do each of the following without
falling?

____ has a strong correlation with
1) frailty: person self-limits activities and 2) incidence of falls.

Back 161

Tinetti

Self-efficacy

Front 162

• Age-related changes
Sensory impairments:
visual, vestibular,
proprioceptive
• Weakness; inability to stand up from a chair without
using one’s arms to push off (LE strength)
Non-PD
Related
• Gender: Females have greater frequency of
falls than males.
• Muscle tightness / inflexibility
• Decreased fitness levels
• Pre-existing level of dependency: higher rate for falls
– institutions vs. community

Back 162

ok

Front 163

Data from Mangione (1999)

For an 85 year old to remain living
independently, one needs a minimum
aerobic capacity of:

• __ ml 02/kg/min for men
• 15 ml 02/kg/min for women

Back 163

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