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ch 9- neurological conditions and movement Flashcards

1
Q

Signs

A

=objective findings, determined through physical examination
Ex. high bp, eye movement problem

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2
Q

Symptoms

A

=subjective perceptions that a patient describes but may not be documented with a physical examination
Ex. fatigue, dizziness, joint pain

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3
Q

negative sign/symptom

A

loss of normal behaviour
Ex. Paresis

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4
Q

positive sign/symptom

A

release of abnormal begaviour
Ex. exaggerated reflexed

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5
Q

CNS lesions can result in different

A

primary and secondary impairements/effects

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6
Q

Primary impairments
-affects?
-cause?

A

affect neuromuscular, sensory, and/or cognitive systems
–> they are a direct result of the CNS lesions

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7
Q

Secondary impairments

A

can impair movement
–> NOT the direct result of CNS lesions
- they develop because of the original problem

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8
Q

Primary neuromuscular impairments
Examples

A

Weakness, paresis, and paralysis (or plegia)

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9
Q

Muscle strength

A

ability to generate enough force in a muscle to produce a movement

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10
Q

What is the neural component of muscle strength related to? (3 things)

A
  1. the type of motor units required
  2. the number of motor units recruited
  3. the discharge frequency of motor neurons
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11
Q

Muscle weakness

A

the inability to generate normal levels of force

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12
Q

Paralysis (or plegia)

A

total or severe loss of muscle activity

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13
Q

Paresis

A

mild or partial loss of muscle activity

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14
Q

Paralysis or Paresis in terms of motor units

A

decreased voluntary motor unit recruitment
-inability or difficulty recruiting skeletal motor units to generate movement

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15
Q

What are changes in muscle tone are characterized by?

A

the muscle’s resistance to passive stretch

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16
Q

What is the range of muscle tone (from low to high)

A

Flaccidity, Hypotonia, Normal, Spasticity, Rigidity

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17
Q

Flaccidity

A

complete loss of muscle tone

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18
Q

Hypotonia

A

reduction in the stiffness of a muscle to lengthening

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19
Q

Spasticity

A

=increased resistance to passive stretch
-VELOCITY DEPENDENT

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20
Q

How is spasticity velocity-dependent?

A

due to hyperexcitability of the stretch reflex
-increased alpha motor neuron excitability (more readily activated)
-removing supraspinal input= removes tonic inhibition=larger reflexive response
-greater muscle activity and faster velocity

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21
Q

Rigidity

A

=increased resistance to passive movement
-NOT VELOCITY DEPENDENT

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22
Q

velocity-dependent

A

the resistance is related to the speed of the muscle/limb movement

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23
Q

What are 4 categories of coordination problems

A
  1. Activation/sequencing problems
  2. Timing problems
  3. Scaling forces
  4. Involuntary movements
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24
Q

Activation and sequencing problems

A

-changes in muscle synergies (how they work together)
-co-activation of muscles surrounding joints
-difficulty coordinating muscle timing in a limb
-difficulty coordinating different limbs together

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25
Timing problems
-slower reaction time and movement time -problems ending a movement
26
Scaling forces
=inappropriate scaling of forces (inappropriate muscle activity for a movement)
27
Scaling forces: Dysmetria
= problems with judging distance of range of movement Ex. seen with cerebellar damage
28
Involuntary movements
-Dystonia -Associated movements -Themor -Choreiform movements -Athetoid movements
29
Dystonia
sustained contractions (from co-contraction of antagonist and agonist muscles)
30
Associated movements
unintentional movement of one limb during voluntary movement of a different limb
31
Themor
oscillatory movement of a body part
32
Choreiform movement
rapid, irregular and jerky movements
33
Athetoid movements
slow, writhing, and twisting movements
34
Primary sensory impairments
-reduced cutaneous sensation -impaired proprioception -vestibular and visual problems -sensory integration deficits (can be tested with SOT )
35
Secondary musculoskeletal impairments (examples)
-muscle atrophy -changes in muscle fibre type -contractures (a permanent shortening of the muscle, puts limbs/joints into strange positions) -degenerative joint disease (deterioration of the cartilage tissues in a joint that leads to pain)
36
Neurorehabilitation
to make it possible or easier to move which allows for more exercise, improved strength, ROM, and neuroplasticity
37
Eye disease examples (2)
1. Macular Degeneration: -loss of central vision 2. Glaucoma -loss of peripheral vision
38
Lifestyle effects of eye diseases
increase fall risk, restrict activities of daily living, and reduces quality of life
39
Signs and symptoms of visual impairment
-visual field loss -decreased visual acuity -reduced contrast sensitivity -reduced motion sensitivity -problems with dark adaptation
40
Rehabilitation options for people with eye disease
-Optical aids (spectacles, magnifying glasses) -Orientation and mobility training= teaching people to use their remaining vision effectively -Gaze training= teaching people where/when to look to guide movement -Exercise (to prevent falls) -Augmented vision systems= devices that enhance vision in different ways
41
Cerebrovascular accident is commonly referred to
stroke
42
Why do strokes occur? result?
restricted blood supply to the brain (from a blockage) -causes cell damage and impaired neurological function -sensory, motor, cognitive and language decline
43
Motor deficits of stroke are characterized by
paralysis (hemiplegia) or weakness (hemiparesis) on the side of the body OPPOSITE of the lesion in the brain
44
Stroke impairments: changes in muscle properties
decrease in fast-twitch fibres, number of motor units and ability to recruit motor units
45
Stroke impairments
-Changes in muscle properties -Slower motor conduction velocity to paralysis muscles -Standing balance issues: reduced strength of ankle muscle response -Increased fall risk -difficulty walking
46
Stroke rehabilitation: Upper limb
-arm and hand exercises -CIMT (constraint-induced movement therapy) -robot assisted therapy -rTMS (repetitive transcranial magnetic stimulation)
47
Stroke rehabilitation: Lower limb
-agility exercise -exoskeletons -bodyweight supported treadmill training
48
CIMT for stroke rehab: rationale
-Unilateral sensory/motor loss --> "learned non-use" of the limb -CIMT improves muscle strength, motor performance, functional ability, and brain performance
49
What is CIMT? (How does it work)
=Constraint-induced movement thereapy Unaffected hand is secured to a splint and placed in a sling for most of the day Example= worn for 2 weeks, rehab 6 hours/day for the paralysis (paretic) arm and hand
50
4 ways to classify stroke
1. Complete= no funtion below the level of injury, both sides of body is affected 2. Incomplete= some functioning below the primary level of injury, may be able to move one limb more than the other 3. Paraplegia= loss of sensation and movement in legs and part or all of trunk 4. Quadriplegia= paralysis of all four limbs
51
spinal cord injury (SCI) and stroke rehab: Exoskeletons Why?
-partial body weight support -greater mobility for patient -increase step count (would otherwise use a wheelchair)
52
Body weight supported treadmill (BWST): How can it initiate walking?
-people w SCIs may still have functioning CPGs that can produce walking behaviour; need to be stimulated with sensory feedback --> moving the treadmill belt causes hip extension, hip proprioception will trigger CPG to initiate swing phase
53
BWST: Why?
Standing unsupported is hard for someone with a SCI so using a BWST is a way to develop muscles over time with reduced load and increase walking function
54
BWST: positive feedback w GTOs
GTOs in extensor muscles may provide feedback to CPGs to maintain/increase activity in extensor muscles
55
Describe the experiment that proves voluntary control over walking can be recovered after SCI (study in rats can be translated to humans)
-they received lateral hemi-sections (damages half of the spinal cord) -two groups: training on normal treadmill and training on robotic postural interface treadmill like BWST -voluntary steps after a few weeks -all rats could initiate full weight-bearing walking with the hindlimbs -only rats that used the robotic postural interface could initiate walking overground
56
Parkinsons definition
a slow, progressive hypokinetic (movement disorder that gets worse over time and decreases movement)
57
Why is movement decreased over time?
-Certain neurons in the substantia nigra (of the basal ganglia) die or become impaired -These neurons normally produce dopamine which allows for smooth, coordinated movement
58
When do signs and symptoms of Parkinson's disease appear?
after 80% of the neurons in the substantia nigra of the basal ganglia die
59
4 main characteristics of Parkinson's disease
1. Resting tremor of a limb 2. Slowness of movement (bradykinesia) 3. Rigidity of limbs of trunk 4. Poor balance (postural instability) and impaired gait
60
resting tremor often involves
rhythmic, alternating opposotion of the forefinger and thumb in a stereotypic "pill-rolling" motion
61
Bradykinesia (slowness of movement) and the concept of "movement vigor"
bradykinesia represents an implicit decision to not move fast because of a shift in the cost/benefit ratio of the energy expenditure needed to move at a normal speed
62
Rigidity is defined as
an increased resistance to passive movement (NOT velocity dependent like spasticity is) Types: cogwheel (ratchety) or lead pipe (smooth)
63
Poor balance (postural instability) and impaired gait
-unstable when perturbed -turning "en bloc"= turning with a rigid neck and trunk; many small steps needed to accomplish the turn -shuffling gait= short, shuffling steps -decreased arm swing when walking -gait freezing (gait akinesia); inability to move the feet, can't initiate walking
64
speed-accuracy trade-off: Parkinson's disease vs. controls
-no difference between groups for accuracy -Parkinson's patients= reluctant to move fast but accuracy was not compromised (therefore issue with movement vigor)

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