Lecture 12- Motor Examination Flashcards
1
Q
What are the 6 parts of the ICF Model?
A
- Health Condition
- Impaired Body Functions and Structures
- Activity Limitation
- Participation Restrictions
- Environmental Factors
- Personal Factors
2
Q
What is the organization of examination?
A
- Pathophysiology
- Impairements
- Sensory/Perceptual
- Cognitive/Behavioral
- Motor
- Functional Limitations
3
Q
Primary neuromuscular impairements, with time, can often lead to ________ effects.
A
secondary
4
Q
What part of the examination do we most often see secondary sequelae?
A
motor portion
5
Q
Paresis and spasticity are ________ effects of a stroke.
A
primary
6
Q
With time, paresis and spasticity from a stroke can lead to ___________ effects.
A
secondary
7
Q
What is the primary things we are looking for in a motor exam?
A
strength (muscle weakness)
8
Q
Musculoskeletal contributions to strength reflect:
- Length of _________ arm of the muscle
- ______/_______ relationship of the muscle
- Type of muscle fiber
- ___________ area of muscle
- Fiber arrangement
A
- movement
- length/tension
- cross-sectional
9
Q
Neural contributions to strength reflect:
- Number of _________ recruited
- Discharge __________
- Type of motor units recruited
A
- motor units
- frequency
10
Q
What is weakness in the context of neuropathology?
A
- inability to generate force
- inability to recruit or modulate motor neurons
11
Q
Neurologically induced weakness may result from:
- _______ lesion
- Lesion in ________ pathways
- Disruption of impulses from _______ motor neurons
- Peripheral nerve injury
- Synaptic dysfunction at __________
- Damage to muscle tissue
A
- cortical
- descending
- alpha
- NMJ
12
Q
- What is paralysis or plegia?
- What is dense hemiplegia?
A
- total or profound loss of muscle activity
- nothing in muscles involved (even twitch)
13
Q
What is paresis?
A
mild or partial loss of muscle activity
14
Q
Muscle Weakness by Distribution
- What is monoplegia?
- What is hemiplegia?
- What is paraplegia?
- What is tetraplegia?
A
- isolated region that has muscle weakness
- one-sided
- spinal cord injuries, half (lower or upper)
- full body (quad)
15
Q
What are some common observations we will see due to underlying weakness in neurologic pathology?
A
- Postural abnormalities
- Asymmetrical weight bearing
- Abnormal synergies
16
Q
Postural abnormalities can present both at rest and with ________.
A
activity
17
Q
Asymmetrical weight bearing produces big differences in ______ time of gait.
A
stance (weak side less time)
18
Q
What is abnormal synergies?
A
- result of loss of ability to recruit a limited number of muscles that are supposed to control a movement
- muscle weakness can produce mass pattern of movement
19
Q
What are the most common synergies we see and where do we see them?
A
- Flexor synergy - UE
- Extensor synergy - LE
20
Q
What is flexor synergy characterized by?
A
- scapular retraction and elevation
- shoulder abduction and ER
- elbow flexion
- supination
- wrists and finger flexion
21
Q
What is extensor synergy characterized by?
A
- hip extension, adduction, and IR
- knee extension
- ankle PF and inversion
- toe PF
22
Q
Can you have extensor synergies in the UE and flexor synergies in the LE?
A
Yes, just less likely
23
Q
What is muscle tone?
A
muscles resistance to passive stretch
24
Q
Is a certain amount of muscle tone normal?
A
Yes
25
Normal tone is high enough to resist the effects of ______ but low enough to allow our muscles to move freely.
gravity
26
What is hypotonicity?
flaccid muscle (floppy)
27
What is hypertonicity/spasticity?
rigid (stuck)
28
Tone is both _______ and non-________ components.
neural
29
- Neural contributions to muscle tone come from a net balance of ___________ input on motor neurons from corticospinal, rubrospinal, reticulospinal, vestibulospinal tracts.
- Descending info coming from these tracts are _________.
- descending
| - inhibitory
30
Neural contributions to muscle tone also come from the sensitivity of ________ connections.
synaptic
31
Non-neuronal contributions to muscle tone come from connective tissue plasticity and __________ properties of the muscles, tendons and joints
viscoelastic
32
What is the difference between spasticity and hypertonia?
- Both are resistant to movement
| - Spasticity is velocity dependent while hypertonia is not.
33
In ________ we will see the same results whether we move the muscle fast or slowly.
hypertonia
34
Spasticity
- _________ dependent increase in resistance to passive movement
- Sometimes described as _________ phenomenon
- Occurs as a result of damage to _________ tract or other nearby descending paths (ex: corticoreticulospinal)
- Can be associated with ________ (commonly in distal extremities > proximal)
- velocity
- clasp-knife
- pyramidal
- clonus
35
What is clonus?
- quick stretch causing bouncing of muscle
| - more common distal
36
Clonus is indicative of a _____ injury.
UMN
37
What 2 main things happen after acute CNS damage?
- paresis
| - CNS plastic rearrangements
38
What is thought to be the main reason we see muscle overactivity?
CNS plastic rearrangements after acute CNS damage
39
What are the 2 spasticity mechanisms?
- changes in neural contributions
| - results in alterations to threshold of stretch reflex
40
Decrease in descending activity leads to a _________ in inhibitory synaptic input which leads to _______ in tonic excitatory input
- decrease
| - increase
41
What scale is used to assess muscle tone?
Modified Ashworth Scale
42
What is the scale of the Modified Ashworth Scale?
0-4
0= no increase in muscle tone
4= affected part(s) rigid in flexion or extension
43
Does the Modified Ashworth Scale look at hypotonicity?
No, 0 means normal
44
What is another, lesser used scale to assess muscle tone?
Tardieau Scale
45
Different tests performed for the Tardieau Scale.
V1 (PROM)= slow as possible
V2 (spasticity)= speed of limb falling under gravity
V3 (spasticity)= fast as possible
46
Which muscle tone scale accounts for clonus?
Tardieau Scale
47
Hypertonia is _________ independent.
velocity
48
Hypertonia is predominantly seen in flexors or extensors?
flexors
49
What are the 2 main presentations of hypertonia?
- Leadpipe
| - Cogwheel
50
What is leadpipe hypertonia?
constant resistance to movement throughout entire ROM
51
What is cogwheel hypertonia?
alternating episodes of resistance and relaxation
52
Hypertonia can present as ________ at rest. What are the two types?
Posturing
- decorticate
- decerebrate
53
Decorticate posturing is a result of lesions ______ the red nucleus while decerebrate posturing is a result of lesions ______ the red nucleus.
- above
| - below
54
How does decorticate posturing present itself?
- UE flexion
| - LE extension/IR/PF
55
How does decerebrate posturing present itself?
-UE and LE extension
56
We tend to see ________ much more with cortical involvement.
spasticity (pyramidal)
57
We tend to see _______ much more with basal ganglia involvement.
rigidity (extrapyramidal)
58
Brainstem involvement above/below the red nucleus can result in what?
```
above= decorticate posturing
below= decerebrate posturing
```
59
In regards to chronicity, increases in non-neuronal changes results in increased "__________"
stiffness
60
What are some common pathologies with hypertonicity?
- CVA, TBI, MS
| - Parkinsons Disease (rigidity)
61
People with hypotonicity have a _____________ in resistance to lengthening.
reduction
62
How is hypotonicity different from flaccidity?
Flaccidity is a complete loss of muscle tone while hypotonicity isn't a full loss
63
Hypotonicity is a disruption of ________ input from stretch reflex resulting in a lack of cerebellar efference influence resulting in decreased input to _______ motor neurons.
- afferent
| - gamma
64
What are some common pathologies with hypotonicity?
- cerebellar lesions, DS, muscular dystrophies, late stage ALS, post-polio
- ACUTE CNS injuries -> hypertonicity/spasticity once subacute/chronic
65
Functional implications of an INCREASE in muscle tone:
- abnormal posturing
- misalignment
- high risk for injury during prolonged rest (skin breakdown)
- bias with recruitment (increased likelihood of synergistic movement)
- destabilization with changes in position (clonus, increased risk for contractures)
66
Functional implications of a DECREASE in muscle tone:
- fall into gravity
| - high risk for injury during dynamic tasks
67
What is coordination?
- the ability to use different parts of the body together smoothly and efficiently
- affects quality of movement
68
What kind of velocity curve should we see with coordination?
bell shaped velocity curve
69
What are the 3 critical componenets of coordination?
- sequencing
- timing
- grading
70
What is incoordination?
- movements that are awkward, uneven, inaccurate
| - disruption of sequencing, timing, grading
71
Does incoordination cause a lack in the bell-shape velocity curve? Why or why not?
Yes, loss of coupling between synergistic joints and muscles
72
What lesions cause incoordination?
- motor cortex, basal ganglia, cerebellar lesions
| - also tied to proprioceptive lesions
73
What are the 3 terms used to describe the grading/scaling of incoordination?
- dysmetria
- hypermetria
- hypometria
74
What is dysmetria? (C)
-problems judging path to get to a location
75
What is hypermetria?
-overshooting target they are reaching for
76
What is hypometria?
-undershooting target they are reaching for
77
Coordination deficits can cause timing difficulties as well:
- ________ reaction times
- ________ movement times
- Difficulties ___________ movement
- Rebound phenomenon
- Dysdiadochokinesia
- increased
- slowed
- terminating
78
What is rebound phenomenon?
- difficulty checking/halting movement when resistance is moved
- more common in cerebellar lesions
79
What is dysdiadochokinesia?
inability to perform rapid alternating movements
80
Coordination deficits can cause activation and sequencing difficulties as well:
- abnormal _________
- coactivation
- impaired inter-joint ________
- synergies
| - coordination
81
Coactivation may cause contraction of both ________ and _________ during walking.
flexors and extensors
82
What is impaired inter-joint coordination?
- can only move 1 joint at a time
| - may have to elevate shoulders, then flex shoulder, then extend elbow to reach
83
What are the tests we perform to examine coordination deficits?
- finger to nose
- alternating supination/pronation
- hand or foot tapping
- heel to shin
84
All tests performed for coordination look at _____ joint movements and we observe the patients performing them.
-multi
85
What are involuntary movements?
movements we aren't performing on purpose
-dystonia
-tremors
-athetosis
choreiform
86
What is dystonia a disorder of?
basal ganglia
87
Dystonia
- Basal ganglia
- Syndrome dominated by __________ muscle contractions
- Causes twisting, repetitive movements, abnormal postures
- Coactivation ________/_________
- Focal, segmental, hemibody, or generalized/whole
- sustained
| - agonist/antagonist
88
What are tremors?
- Rhythmic, involuntary oscillatory movement of a body part
| - Can be intermittent or constant, sporadic or as a sequelae to disease or injury
89
Where are tremors most often seen?
hands
90
What is the difference between resting tremor and action tremor?
Resting Tremor
-occurs in body part that is not voluntarily activated, relaxed
Action Tremor
-any tremor that is produced by voluntary contraction of a muscle
91
What are the 2 most common subcategories of action tremors?
- postural tremor- person maintains a part of body against gravity (put arms up)
- intential tremor- produced with a purposeful movement (reaching across table or up)
92
Choreiform and Athetosis are both linked to dysfunction of what?
basal ganglia
93
- What is athetosis?
- Does it affect UE or LE more?
- What is it common in?
- slow, writing and twisting movements
- UE>LE
- common in cerebral palsy
94
- What is choreiform?
| - What can cause this?
- involuntary, rapid, irregular and jerky movements
| - seen with Huntington's Disease; side effects of PD medicine
95
Spasticity and hypertonia can lead to loss of ____, contractures
ROM
96
Immobilization of joints can lead to increased _________.
- Increase resistance to stretch, decrease in sarcomeres can lead to ________ in connective tissue.
- Decrease rate of protein synthesis can lead to ________.
-stiffness
- increase
- atrophy
97
When we have ROM issues, we see a change in ______/________ relationship.
- This leads to further weakness
- alters mechanical advantage
length/tension
98
Endurance issues can be both _______ and ________.
primary and secondary
99
Endurance Issues:
- Decrease in central drive to spinal cord motor neurons
- Decrease in activity level/immobility
- Presence of _________
comorbities (Afib, CAD, COPD, DM, etc...)
100
Can neuromuscular impairements cause musculoskeletal pain?
Yes, should always keep an eye out for it.
101
Musculoskeletal Pain Main Reasons:
- ___________ movements resulting in overworking of certain muscles
- Muscle __________ causing abnormal loading through joints
- ____ and alignment issues
- Decreased efficiency of movements leading to increased __________ required to complete tasks
- synergistic
- asymmetries
- ROM
- workload
