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Neuro Eval > Parkinson > Flashcards

Parkinson Flashcards

1
Q

motor control issues in PD

A
  • Disorders of Tone (Rigidity)
  • Disturbances of Posture and Balance Function
  • Movement Dysfunction (Akinesia, Bradykinesia)
  • Disorders of Locomotion
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2
Q

major impairments in PD are mostly associated with..

A

initial conditions, preparation, initiation, and execution
- termination problems may arise during walking (festination/hastening)

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3
Q

initial conditions- problems of posture components

A
  • Mobility (shortening of structures on the ventral surface; loss of spinal flexibility especially later in the disease)
  • Force Generation (decreased strength of trunk extensors)
  • Rigidity
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4
Q

is sway significantly increased?

A

no - except in long term disease

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5
Q

problems of posture - use of sensory information

A

May have increased dependence on vision
and decreased adaptive capacity to repeated stimuli in standing
- maybe impairments in proprioceptive regulation

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6
Q

problems of tone: neural factors

A

multiple potential mechanisms for rigidity. One not clearly identified as primary factor over others

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7
Q

problems of tone: musculoskeletal factor

A

Changes in the visco-elastic properties of connective tissue (increased stiffness).

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8
Q

problem of initiation: akinesia

A
  • delay in initiation
  • may occur in the postural component of
    the movement (postural adjustment) and/or in the focal (actual) movement
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9
Q

what largely contributes to problems of akinesia

A

neural factors associated with motor planning in the preparation stage

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10
Q

when is akinesia revealed

A

with increased movement complexity
- but pts with PD can generally use advanced information

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11
Q

APA for stepping in PD

A
  • Most commonly, the APA is reduced in amplitude
  • L-Dopa appears to improve this
  • Deep brain stimulation does not
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12
Q

other common impairments in APA

A

delays, reduced presence (absent-later disease), and/or incomplete or multiple EMG bursts

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13
Q

problems of execution: bradykinesia

A
  • Slowed movement (bradykinesia) and decreased amplitude of movement (hypokinesia) are also common examination
    findings
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14
Q

what has been attributed to problems of generating an adequate motor command? (energizing the muscular system)

A
  • decreased speed and amplitude of simple movements
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15
Q

bradykinesia with a simple elbow movement

A
  • Correct agonist recruited
  • Duration of agonist EMG burst is generally normal
  • decreased size of the initial agonist burst
  • Movement achieved through a
    series of small agonist bursts
  • Timing of subsequent ag/antag
    preserved
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16
Q

what can pts with PD do to the initial agonist burst

A
  • they can modulate it because the larger amplitude movements or those against greater loads result in larger agonist bursts
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17
Q

there is an instability to achieve what?

A

absolute levels of initial agonist activation
- scaling the agonist burst to movement demands

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18
Q

what does PD result in an underestimation of?

A

the size of the impulsive force generated by the initial agonist required to produce the desired movement.

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19
Q

there is some evidence suggesting that patents with PD may be…

A
  • weak in some muscle groups even when there is sufficient time to develop maximal force.
  • Rate of rise of force development (muscle activity) is impaired in PD –> This has been shown to be true despite normal maximal force production capability
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20
Q

brady/hypokinesia in complex movement

A
  • Longer movement times
  • Lack of coordination between phases
  • Acting more sequentially than simultaneously
  • Simple actions replace complex actions
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21
Q

brady/hypokinesia: complex movements conclusion

A
  • Inability to combine and execute a series of motor actions that comprise a complex motor sequence
  • disturbances with triggering internal generated movements (role of SMA)
    (dont do well sitting up on their own)
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22
Q

normal function of BG is probably related to..

A

routine automatic execution of sequences of movements generated in cortical motor areas

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23
Q

problems of reactive control

A
  • Less sequential activity with more co-contraction to platform perturbations.
  • Less adaptive capacity as well
    (pedunculopontine nucleus)
24
Q

experiment on problems of reactive control

A
  • Persons with PD exhibit more sway, lower LE joint torques, and lower step thresholds to perturbations
  • Directional differences when perturbed forward or backward with shorter and more steps when perturbed backward.
  • L dopa helped # of steps but not step length
25
Q

major objective of PT for PD:

A

improve QoL by improving and preserving independence, safety and well-being through
exercise

26
Q

goals of PT for PD

A
  • EMPHASIS ON PHYSICAL ACTIVITY IN THE EARLY PHASE
  • Improve voluntary movements (strength; speed; initiation)
  • Reduce excessive rigidity
  • Avoid complications of immobilization
27
Q

treatment guided by stage of disease… idk if we need to know that

A
28
Q

Treatment ideas that Dr Hanke says you need to commit to memory - truncal stiffness

A

make trunk movements
provide flexibility home program

29
Q

Treatment ideas that Dr Hanke says you need to commit to memory - mis-scaling of movement amplitudes

A

use of large amplitude movements

30
Q

Treatment ideas that Dr Hanke says you need to commit to memory- inability to start

A

mental, verbal, tactile, manual cues

31
Q

Treatment ideas that Dr Hanke says you need to commit to memory - hastening

A

selection of proper cueing frequencies
visual line cueing

32
Q

Treatment ideas that Dr Hanke says you need to commit to memory - problems with simultaneous and sequential movements

A

training with simple sequences

33
Q

treating problems of initial conditions - tone/rigidity

A
  • Functional axial rotation
  • Stretching
  • Extension
  • Aerobic/forced exertion exercises
34
Q

treating delayed in initiation

A
  • Problem: Altered preparation (= delayed onset EMG)
  • When postural component: Proactive balance training and/or Instruct in necessary PA’s
  • When the voluntary movement component: Imitation, Imagination, Cueing
35
Q

Treating execution problems - bradykinesia –> decreased amplitude and speed

A
  • make big ballistic, high force, large amplitude movements
  • exaggerate movements
36
Q

execution problems - AROM, strengthening

A
  • For those who can perform resistance exercise, forced exertion (eg, LE exercise bike) is a good approach.
  • Strengthening helps if they are in a strengthening program. It doesn’t reverse the disease –> Mixed results on falls and function
37
Q

treating multi-segmental movement problems

A
  • Re-conceptualize the task –cognitive movement strategy (now called strategies for complex movement sequences)
  • verbal cues at sticking points; provide key verbal cues; (clock turn, arch)
38
Q

cognitive movement strategies

A
  • Make explicit what is normally automatic
  • Conscious performance of actions in which complex (automatic) activities are transformed to several separate elements that must be
    executed in a set order, and which consist of relatively simple movement components.
  • Compensation for impaired motor planning of complex movement plans through cues and attention.
39
Q

complex movement sequences

A
  • Set and agreed upon with patient and based on individual needs.
  • Perform each component of the movement sequence individually with attention.
  • Identify most difficult component and practice repeatedly
  • Rehearse mentally and physically
  • Repetition
40
Q

treating balance problems

A
  • follow balance progression
  • BOS, Sensory input, challenges to COM
41
Q

biggest bang for your buck

A
  • Aerobic exercise on motor symptoms and gait endurance (LTV)
  • Treadmill training on gait speed
  • Strength training on gait endurance
  • Balance and gait training on balance (BBS) and gait (speed)
  • CMS training on functional mobility
  • Nordic walking, dance, martial arts on motor symptoms to varying degrees
  • Exergaming on functional mobility (TUG) and balance (BBS)
42
Q

what outcome is missing

A

participation

43
Q

observation of the parkinsonism gait

A

Slow, shuffling steps, flexed posture, little trunk and UE motion, foot flat (general poverty of movement)

44
Q

delayed gait initiation- 3 separate problems

A
    1. an absence of a clear and fully expressed postural adjustment
    1. classic “bradykinetic” responses from postural agonists;
    1. relatively normal postural synergy interacting with abnormal standing posture
45
Q

delayed gait initiation is because of

A
  • Impaired capacity by the nervous system to integrate and sequence postural and subsequent locomotor synergies.
  • Alterations in the postural
    component of gait initiation
46
Q

treating delayed gait initiation

A
  • Object visualization/imagination –> Stepping over tape, cane, someone’s foot, an imagined shoe box
  • Make explicit what is normally automatic –> Shift then take a big step
  • Use instruction and manual contacts in lateral and A/P directions within a functional context
47
Q

short, shuffling or freezing of gait

A
  • Altered descending input
  • Disturbance in rhythm formation
48
Q

festination/hastening

A

Possibly two types:
- one associated with FOG considered a core locomotor rhythm problem
- other being related to poor posture (flexed) and insufficient steps to control the forward momentum associated with the flexed posture.

49
Q

festination- locomotor component

A

shortening of steps –> progressive increase of stepping cadence –> freezing of gait
- treatment: external cueing

50
Q

festination- balance component

A

forward learning of the trunk –> small (balance corrective) steps –> fall
- treatment: address posture/balance

51
Q

treating progression problems: auditory pacing

A
  • metronome, wrist/ankle metronome, hand clapping, finger snapping, music in general, singing
  • Auditory rhythmic cues improve walking speed, stride length, step frequency (from -10% up to 10% above natural frequency FOR THOSE WITHOUT FREEZING)
52
Q

treating progression problems: rhythmic auditory pacing

A
  • Click tone embedded in music: typically matched to self-selected cadence.
  • May act as an external timekeeper to which the step cadence becomes entrained.
  • Improved stride length during rhythmic gait facilitation may be due in part to the modulatory effect of RAS on muscle activity (triceps surae)
53
Q

treating progression - visual markings

A
  • lines on floor perpendicular to the line of
    progression, effects on GRFs
  • produces an emotional arousal at a
    behavioral level: is each line a sub-goal?
  • visual stimulation may promote access to
    other pathways (eg, via cerebellum)
54
Q

other ways to treat progression

A
  • Treadmill training
  • Consider effect of assistive device
  • Thinking about taking big steps
  • Nordic walking
  • Cueing big steps; lifting knees up high
  • Choosing a point of reference for
    the patient to walk towards
55
Q

adaptability: inability to adapt the gait pattern

A
  • Difficulty changing speed and direction.
  • Breakdown of complex actions / interaction between cortical and subcortical structures.
  • Environmental surroundings may hinder or facilitate locomotion.
  • Strategies which are used for gait stability problems work for adaptability issues and vice versa
56
Q

treatment for adaptability

A
  • explicit use of range of speeds –> especially on treadmill
  • must work overground –> different environments
  • provide and OFFER CUES to get through areas where change in speed or direction is needed
57
Q

summary

A

Promote physical activity
Big movement
External cueing
Cognitive movement strategies
Warm up exercises for ROM/Rigidity

Neuro Eval (18 decks)

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