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207 > ch 9- neurological conditions and movement > Flashcards

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
Q

Timing problems

A

-slower reaction time and movement time
-problems ending a movement

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26
Q

Scaling forces

A

=inappropriate scaling of forces (inappropriate muscle activity for a movement)

27
Q

Scaling forces: Dysmetria

A

= problems with judging distance of range of movement
Ex. seen with cerebellar damage

28
Q

Involuntary movements

A

-Dystonia
-Associated movements
-Themor
-Choreiform movements
-Athetoid movements

29
Q

Dystonia

A

sustained contractions (from co-contraction of antagonist and agonist muscles)

30
Q

Associated movements

A

unintentional movement of one limb during voluntary movement of a different limb

31
Q

Themor

A

oscillatory movement of a body part

32
Q

Choreiform movement

A

rapid, irregular and jerky movements

33
Q

Athetoid movements

A

slow, writhing, and twisting movements

34
Q

Primary sensory impairments

A

-reduced cutaneous sensation
-impaired proprioception
-vestibular and visual problems
-sensory integration deficits (can be tested with SOT )

35
Q

Secondary musculoskeletal impairments (examples)

A

-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
Q

Neurorehabilitation

A

to make it possible or easier to move which allows for more exercise, improved strength, ROM, and neuroplasticity

37
Q

Eye disease examples (2)

A
  1. Macular Degeneration:
    -loss of central vision
  2. Glaucoma
    -loss of peripheral vision
38
Q

Lifestyle effects of eye diseases

A

increase fall risk, restrict activities of daily living, and reduces quality of life

39
Q

Signs and symptoms of visual impairment

A

-visual field loss
-decreased visual acuity
-reduced contrast sensitivity
-reduced motion sensitivity
-problems with dark adaptation

40
Q

Rehabilitation options for people with eye disease

A

-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
Q

Cerebrovascular accident is commonly referred to

A

stroke

42
Q

Why do strokes occur? result?

A

restricted blood supply to the brain (from a blockage)
-causes cell damage and impaired neurological function
-sensory, motor, cognitive and language decline

43
Q

Motor deficits of stroke are characterized by

A

paralysis (hemiplegia) or weakness (hemiparesis) on the side of the body OPPOSITE of the lesion in the brain

44
Q

Stroke impairments: changes in muscle properties

A

decrease in fast-twitch fibres, number of motor units and ability to recruit motor units

45
Q

Stroke impairments

A

-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
Q

Stroke rehabilitation: Upper limb

A

-arm and hand exercises
-CIMT (constraint-induced movement therapy)
-robot assisted therapy
-rTMS (repetitive transcranial magnetic stimulation)

47
Q

Stroke rehabilitation: Lower limb

A

-agility exercise
-exoskeletons
-bodyweight supported treadmill training

48
Q

CIMT for stroke rehab: rationale

A

-Unilateral sensory/motor loss –> “learned non-use” of the limb
-CIMT improves muscle strength, motor performance, functional ability, and brain performance

49
Q

What is CIMT? (How does it work)

A

=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
Q

4 ways to classify stroke

A
  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
Q

spinal cord injury (SCI) and stroke rehab: Exoskeletons
Why?

A

-partial body weight support
-greater mobility for patient
-increase step count (would otherwise use a wheelchair)

52
Q

Body weight supported treadmill (BWST): How can it initiate walking?

A

-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
Q

BWST: Why?

A

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
Q

BWST: positive feedback w GTOs

A

GTOs in extensor muscles may provide feedback to CPGs to maintain/increase activity in extensor muscles

55
Q

Describe the experiment that proves voluntary control over walking can be recovered after SCI
(study in rats can be translated to humans)

A

-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
Q

Parkinsons definition

A

a slow, progressive hypokinetic (movement disorder that gets worse over time and decreases movement)

57
Q

Why is movement decreased over time?

A

-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
Q

When do signs and symptoms of Parkinson’s disease appear?

A

after 80% of the neurons in the substantia nigra of the basal ganglia die

59
Q

4 main characteristics of Parkinson’s disease

A
  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
Q

resting tremor often involves

A

rhythmic, alternating opposotion of the forefinger and thumb in a stereotypic “pill-rolling” motion

61
Q

Bradykinesia (slowness of movement) and the concept of “movement vigor”

A

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
Q

Rigidity is defined as

A

an increased resistance to passive movement (NOT velocity dependent like spasticity is)
Types: cogwheel (ratchety) or lead pipe (smooth)

63
Q

Poor balance (postural instability) and impaired gait

A

-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
Q

speed-accuracy trade-off:
Parkinson’s disease vs. controls

A

-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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