constraints on motor control Flashcards
(133 cards)
1
Q
Apraxia
A
inability to carry out an intended movement even thought sensation, movement ability, and coordination are all capable of functioning properly
2
Q
apraxia is considered
A
primary perceptual impairment
3
Q
apraxia is associated with damage to what side of the brain
A
left
4
Q
pt. with spatial relation disorders will have difficulty with
A
perceiving relationships b/w
- self w/ other objects
- other objects and self
multiple objects
(position in space)
5
Q
Body image and body scheme disorders are described as
A
decreased awareness of body parts, their relationship to each other, and the environment
6
Q
an example of body image/ body scheme disorders is
A
unilateral neglect
7
Q
unilateral neglect
A
an inability to perceive and respond to stimuli on one side of the body
8
Q
perception
A
is making sensory information meaningful
9
Q
what is an example of perception with the body
A
verticality
10
Q
what is the difference b/w visual vertical and postural vertical
A
postural vertical is somatosensory information determined without visual input
11
Q
patient with vestibular deficits may have difficulty with
A
- gaze stabilization
- posture
- balance
12
Q
where can vestibular damage occur
A
in the cortex or the periphery
13
Q
patients with visual deficits may have difficulty with
A
- depth perception
- visual fields
- acuity
- oculomotor control
14
Q
list the locations of somatosensory lesion
A
- dorsal column/medial lemniscus
- anterolateral lesion
- somatosensory cortex lesion
15
Q
dorsal column/medial lemniscus lesion
A
loss of
- discriminative touch
- light touch
- kinesthesia
16
Q
anterolateral lesion
A
loss of
- pain
- temperature
- coarse touch
- kinesthesia
17
Q
somatosensory cortex lesion
A
loss of
- proprioception
- two point discrimination
- sterognosis
- touch localization
18
Q
sterognosis
A
is being able to identify an object based on the perception of its structure
19
Q
list primary neuromuscular impairments
A
- paresis
- spasticity
20
Q
paresis
A
weakness from loss of cortical drive
21
Q
what is a constraint
A
anything that constrict, restrain, restrict, limit the individual
22
Q
constraints w/n the individual are known as
A
impairments
23
Q
Primary Cognitive System Impairments
A
- arousal/level of consciousness
- attention
- orientation
- memory
24
Q
how does level of consciousness/arousal correlate to movement
A
- must be alert enough to respond to environmental stimuli
25
how does attention correlate to movement
- inability to focus on task affects motor learning
26
selective attention
ones ability to attend to something w/o becoming distracted
27
orientation impairments can be described as
lack of situational awareness
28
what do most people lose orientation to ?
place and time
29
memory impairments
decreased ability to process, store, and retrieve info
30
what should you do when treating patients with a decreased response time
slow down, lots of pauses, and give them time to process what you are saying
31
Primary Neuromuscular impairments affecting the motor system
- mm weakness
- coordination problems
- involuntary movements
- abnormalities of mm tone
- abnormal synergies
32
synergy
pattern of movement
33
mm weakness
inability to generate adequate level of force
34
paralysis/plegia
total/severe loss of mm activity
35
primary mm weakness is a result of
lesions in descending motor paths --> inability to recruit and or modulate motor neurons
36
Neural aspects of force production
- # of motor units recruited
- type of motor unis recruited
- frequency of discharge
37
musculoskeletal aspects of force production
prolonged paresis or disuse can cause secondary changes to muscle tissue such as atrophy
38
describe the difference b/w weakness in UMN lesion and weakness in ortho patients
in a neuro pt. the capacity to generate force in an isolated mm does not predict the mm ability to work with other mm like it does for ortho pt.
39
describe an example of positioning affecting mm
STNR (head and arms go together, lower body does the opposite
40
in neuro pt. weakness may be
in the delivery or lack of delivery to the mm not in the mm directly
41
why is MMT not the best test for neuro pt.
b/c MMT test mm ability to function in isolation
| - neuro pt. are unable to isolate the mm
42
how does change in body positon influence change in reflex, tone, and synergies in an abnormal pt.
a pt. may have anti-gravity movement in one position but not in the other.
43
tone vs. synergy
- tone is observed in a resting state
| - synergy is observed during movement
44
coordination impairment is a classic disorder involving what brain structures
- Basal ganglia
| - cerebellum
45
coordination
sequencing, timing, grading of activation of multiple mm groups
46
incoordination
movements that are awkward, uneven, or inaccurate
47
incoordination is associated with lesions in the
- motor cortex
- basal ganglia
- cerebellum
- proprioceptive system
48
incoordination is influenced by
peripheral factors (change in mm, tendons, fatigue)
49
automatic postural reactions of the LE for normal sequencing
ankle --> knees--> hip --> trunk
50
co activation causes the body to become
rigid
51
sequencing problems include
- activation of mm/ groups in wrong sequence
- activation of mm/groups inappropriate for the action
- co-activation
- impaired inter-joint coordination
52
impaired inter- joint coordination
movement decomposition or movement at one joint at a time
53
inter joint coordination impairments is associated with damage to what part of the brain
cerebellum
54
timing problems
problems initiating movement
- increase reaction time
- delayed movement time
55
timing problems can occur in what kinds of pt.
- CVA
- TBI
- PD
56
timing problems may be a result of
- inadequate force generation (weakness)
- decreased rate of force generation (power)
- cognitive factors
- altered sensory input/perception
decreased
- ROM
- motivation
- postural control
57
slowed movement time may be seen in pt. with
- CVA
- PD
- CP
- cerebellar damage
58
problems terminating a movement is seen in pt. with
cerebellar lesions
59
problems terminating movement may be due to
- inability to stop mm contraction/ control force production
- cognition
- sensory deficit
- poor posture
- pt. with preservation problems
60
dysmetria
inability to scale force, problem judging distance or range
61
dysmetria is a classic _____ impairment
cerebellar
62
hypometria is seen with
BG lesions- PD
63
hypermetria is seen with
cerebellar lesions
64
dysarthria
motor disorder of speech production
65
intention tremor is seen with
CB damage
66
resting tremor is seen with
PD pt.
67
check reflex
they can not terminate the motion
68
rebound phenomenon see in
cerebellar pt.
69
dysdiadochokinesia
difficulty with RAM - rapidly alternating movement
70
dystonia
involuntary, sustained mm contractions; twisting and repetitive movements, and abnormal postures
71
dystonia is associated with
BG disease progression
| - high dosage of antiparkinsonian medication
72
associated movement
unintentional movement of one limb during voluntary movement of another
73
tremor
rhythmical, involuntary oscillatory movement of a body part
74
choreiform movement
involuntary, abrupt, rapid, irregular, jerky movement
75
choreiform movement is associated with
huntingtons - BG lesions
76
athetoid movement
slow, involuntary writhing and twisting
77
is spasticity and tone the same thing?
it is not the same thing but they co occur in pt. with UMN, cortical lesions of the corticospinal tract
78
spasticity in short
hyper-reflexia
79
spasticity
is velocity dependent stretch reflexes
80
spasticity is a result of
hyper excitability of tonic stretch reflexes
81
disinhibiton of spinal reflex
loss of cortical drive or direct damage to
- dorsal reticulo
- rebro
- vestibule
...spinal tracts
82
damage to the cortico-reticular fibers after supra-tentorial lesion produces
spasticity
83
what do mm spindles tell us
how much stretch the mm is experiencing
84
damage to corticospinal tract causes
flexor withdrawal reflex
85
what is the compensation for decreased cortical drive
increase in stretch reflex gain so a small drive signal produces a larger mm response
86
when is spasticity seen
it is not seen immediately after cortical lesion, develops over several weeks after neural damage
87
spasticity is seen to be
a sign of neuro plasticity of the brain adapting to a loss of descending control
88
what are the effects of spasticity on motor control
- loss of reciprocal inhibition
- increased sensitivity of motor neurons
- increased post action potential depression
89
How are stretch reflexes tested (spasticity)
- passive
| - examiner provides a quick stretch stimulus
90
how does spasticity affect volitional movement
if a pt. moves too quickly, they can unintentionally trigger the antagonist inducing spasticity
91
what is an example of spasticity affecting volitional movement
rapid weight loading on a spastic ankle can cause clonus
92
how can patients with spasticity affecting their volitional movement counteract this
move slower
93
what is the problem with anti-spasticity medication
they are not selective
- inters w/ agonist and antagonist ability to contract
- reduce motor learning
94
what patients can benefit from anti-spasticity medication
- pt. whose function is severely restricted
| - pt. whom increasing strength/motor learning is not a primary goal
95
abnormal tone (hypertonia)
tonic ongoing contraction of mm or mm groups at REST
| - motor over-activity
96
what is the difference b/w hypertonia and spasticity
hypertonia has nothing do with velocity (doesn't require any mm stretch)
97
what causes hypertonia
damage to corticospinal tract and damage/decreased cortical drive to BG
98
hypertonia is sensitive to
mm stretch and length
99
how can you temporarily decrease hypertonia
sustained stretch, prolonged lengthening
100
how does prolonged stretch decrease tone
sustained stretch is inhibitory action
101
flaccidity
too little tone at rest
102
how does tone fluctuate
- position of limb and body
- effort, pain
- temperature
- stress
103
how is tone tested
- limb is passive
| - examiner provides a slow stimulus
104
what are we looking for when we test for tone
resistance to slow, even passive movement
105
how does tone affect volitional movement
- easier for pt. to move mm concentrically, difficulty w/ eccentric movement or relaxation
- difficult to move in opposite direction of hypertonic mm
106
why is it difficult to move in the opposite direction of hypertonic movement
- failure of reciprocal inhibition
| - tonic drive to antagonist may exceed drive to agonist
107
for a pt. with high tone which mm contraction is easier
concentric mm contraction
108
what happens if you can reduce the effort need in a pt. with high tone
pt can perform the motion little better but may still compensate
109
abnormal synergies
characterized by mass movement and inability to isolate or fractionate joint motion from one another
110
abnormal synergies are common in
patients with UMN lesion
111
what causes abnormal synergies
abnormal co-activation of all mm in a normal synergistic group
112
how are abnormal synergies tested
- limb is ACTIVE
examiner request pt. do volitionally move the limb -- in a synergy
- out of synergy
113
associated reactions
involuntary motion in one part of the body with volitional movement of another part of the body
114
associated reaction is AKA
overflow phenomenon
115
can associated reactions occur bilaterally?
yes
- if hemiplegic, movement is abnormally synergistic
116
how do we test for associated reactions
observation
- request effortful, resisted movement on the non-hemiplegic side
- works with if pt. attention is elsewhere
117
rigidity occurs at what level
the level of basal ganglia
118
normal tone
readiness to move
119
describe the order of the tone figure
flaccidity > hypotonia> normal> hypertonia
120
hypertonicity on the tone scale
increased resistance to passive movement
121
hypertonicity is seen
later during recovery in Stroke, TBI pt.
122
hypotonia on the tone scale
decreased resistance to passive movment
123
hypotonia is seen in what kinds of pt.
- down syndrome
| - spinocerebellar lesions
124
hypotonia is seen
earlier during recovery in stroke, TBI pt.
125
flaccidity on the tone scale
complete loss of tone, no resistance to movement
126
flaccidity is seen in what kind of pt.
- neural shock
| - peripheral n. injury
127
flaccidity is seen
in the acute phase of pt. with stroke, TBI
128
what is a DTR
quick stretch of mm spindle
129
describe the order of the hyper-reflexia figure
absent > hypo-reflexia > normal > hyper reflexia (true spasticity)
130
describe the order of the abnormal synergies figure (brunnstromm)
no voluntary motion > volitional movement weak w/ incomplete synergies > synergistic movement only, full synergies possible > some out of synergy motion possible > independence from synergies> normal
131
task demands
- stability
- transitions
- mobility
- manipulation
- concurrent tasks (divided attention)
132
environment demands
- surface
- visual
- closed/open
- predictable/variable
- stationary/in motion
- distractions
133
the difficulty of an activity depends on what
- individual abilities and constraints
- demands of task
- the support or challenge provided by the environment
