Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHTY314 > Week Two > Flashcards

Week Two Flashcards

0
Q

What are some things to assess in the objective assessment - dragon slide

A

Vision
Cranial nerves
Sensation
Muscle length and joint ROM - we are involved in this
Muscle tone - we are involved in this
Motor control/recovery/functional activities
Co-ordination
Balance
Gait
Perceptual/cognitive function
Cover these in Ax, important as it contributes to our diagnosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

What is important we gain from the subjective assessment - dragon slide

A 
Establish rapport
HPC
PMH
SHx
Communication 
Orientation 
Helps us to workout what makes them tick
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What to note in the analysis

A

What, why, how?
Your assessment needs to be careful and thorough
Need to be able to interpret the results - interpret the degree inch iChat the impairment may affect them - mod, mild, severe
Start distally with Ax and work proximally
- if they have sensation distally they’ll have it proximally due to global distribution of nerves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Intervention

A

Chose and be able to rationalise the treatment
Have a preparatory activity (warm-up)
Ensure the activity meets the chosen goal
Prepare a progression of that activity (or make it easier)
Hands on
Treat them and teach them exercises
Work on improving their impairments - e.g. Strength deficit = work on strength

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the three levels of goals

A

Preparation goal
Nearly meeting the goal
Meeting the goal
We need to be able to make them easier if required

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do we need to determine in order to see if it’s an UMNL or LMNL

A

Type of bone
What side
Flaccidity occurs initially in UMNL as well - it’s the transitional period, due to lack of signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Signs of a LMNL

A 
Reduced or absent tone - flaccidity 
Reduced or absent tendon reflexes
Inability to activate muscle/muscle weakness
Resultant disuse atrophy 
Affected by altered sensation 
Often associated with autonomic changes

Flaccidity - always
Inability to contract the muscles
Altered sensation as it’s a peripheral nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

UMNL signs

A

Negative signs - was there but not anymore

  • flaccidity (initial/transient)
  • weakness
  • loss of dexterity
  • fatiguability

Positive - wasn’t there but is now

  • spasticity and clonus
  • spastic dystonia
  • flexor and extensor ‘spasms’
  • spastic co-contraction
  • exaggerated DTRs
  • associated reactions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 7 primary neurological impairments

A 
Motor
Sensory 
Coordination
Speech 
Vision
Cognitive 
Perceptual
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the 6 secondary neurological impairments

A

Decreased muscle length/contracture
Decreased cardio-pulmonary function/fitness/endurance
Sensory changes and potential for pressure lesions
Learned non-use (resulting in disuse and atrophy)
Adaptive motor behaviour
Psycho-social changes (including depression)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the five factors that impact motor control and movement

A 
The individual
The task demands
The environment 
Perception 
Cognition
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is motor control

A

The ability to regulate or direct the mechanisms essential to movement
Good motor control - accomplishes the desired task and the most efficient matter

Poor motor control - inefficient, inaccurate movement that may not accomplish the desired task

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Assessment of motor control/performance/activity/recovery

A 
Loss of motor control 
Weakness
Abnormal tone
Loss of coordination 
Loss of dexterity
NB: all motor output is affected by loss of sensation/proprioception
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

How is motor control assessed

A

Observation of quality of movement/functional activities

Brunnstrom stages of control (joint out of synergy - interaction or cooperation) asses how many joint are out of synergy

CIMM - Chedoke-McMaster Impairment Inventory - used for multiple impairments (Gowland motor recovery scale)

MAS - motor assessment scale

Fugl-Meter assessment of sensoriomotor recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is motor control affected following a CNS lesion

A

General UMN weakness - clinically referred to as loss of voluntary control of muscles
Slowness to initiate and complete a movement
Loss of dexterity/coordination
Inability to fractionate movement (ability to make a specific movement at a single joint without also making other joints move) e.g. Lack of selective movement

NB: a spastic muscle is a weak muscle, use altered strength tests initially

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the seven stages of motor recovery - dragon slide

A
  1. Flaccid paralysis - no volitional movement
  2. Spasticity emerging, some resistance to PM, no vol mvt but synergistic mvt can be elicited
  3. Marked spasticity, attempted vol mvt produces synergistic mvt only
  4. Spasticity decreasing, synergistic mvt still present but capable of mvt of at least 1 joint out of pattern
  5. Spasticity only elicited at end of ROM or with rapid mvt, relative independence from synergies
  6. Isolated joint movement now freely performed, synergies only elicited with rapid complex mvts
  7. Normal movement - strength, timing, endurance and coordination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are mass patterns and what are the reasons

A

Gravity driven movements

Evolutionary reasons
Gravity - fundamental sensory input
Anti-gravity extensors activity in order to ambulate
Flexor pattern in UL - motivation to ambulate, such as source food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Upper limb mass pattern

A

Flexion

  • scap retraction
  • shoulder IR and adduction
  • elbow flexion
  • wrist and finger flexion
  • forearm supination
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Lower limb mass pattern

A

Extension

  • hip extension, adduction and IR
  • knee extension
  • ankle PF and inversion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is muscle tone

A

A state of readiness of skeletal muscle so that the muscular system is in a state of arousal prepared forte task demands placed on it

Resistance to lengthening of a muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What factors determine tone

A

Level of excitability
Intrinsic muscle stiffness
Level of sensitivity of reflexes

NB: patients where we only see spasticity and not flaccidity- spinal cord injury patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is flaccidity

A

Complete loss of muscle tone
DTRs are absent
No muscle contraction
Floppy and hypermobile/unstable

Nothing at all - complete loss of motor tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What is hypotonia

A 
Reduction in muscle stiffness 
Weakness 
Poor muscular co-contraction 
Poor trunk control
Decreased stability

In cerebellar lesions and Down syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is spasticity

A

Motor disorder characterised by a velocity-dependent increase in stretch reflex
Exaggerated tendon jerks, resulting from hyper-excitability
Neural and non-neural contributions
Purely related to disinhibition reflex arc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are some neural contributions to spasticity

A

Disordered inhibition
Reflex hyper-excitability
Unmasked proprioceptive phenomena - e.g. Babinski (flex toes is negative (older), extend toes is positive (baby)). Regression to primary reflex so MUST be an UMNL
Unwanted co-contraction

25
Q

What are some non-neural contributions to spasticity

A

Increased stiffness - due to altered ratio of muscle to connective tissue
Altered thixotrophy - increased viscosity
Adaptive shortening

26
Q

How is muscle tone assessed

A

Observation at rest
Palpation
Slow passive mvt to determine stiffness and length - gives an idea of ROM and what the mvt feels like
Resistance to rapid passive mvt - note catch and release phenomenon of hyper-reflexia
Brisk or exaggerated DTRs
Associated reactions - walking with an arm flexed up

Clonus - severe spasticity, continuous re-eliciting of catch/release effect, non-fatiguable - if you keep the joint at an angle it will continue without fatigue

27
Q

R1 and R2 of Tardieu Scale

A 
R1 = fast movement 
R2 = slow movement
28
Q

What is a clinical picture of hypertonia

A

Hyperactive stretch reflexes - hyper-reflexia and/or clonus
Dystonia - sustained abnormal muscle contraction leading to abnormal positioning of limbs
Inappropriate synergist recruitment
Stereotypical movement synergies
Associated movements

People with high tone sometimes only have small movements/noise

29
Q

Abnormal tone related to cortical dysfunction

A

Hypotonia (usually transient)
Hypertonia
Clonus

30
Q

Abnormal tone related to basal ganglia dysfunction

A 
Athetosis - writhing mvts 
Chorea
Dystonia
Myoclonus 
Hemiballismus
31
Q

Abnormal tone related to cerebellar dysfunction

A

Hypotonia

NB: most cerebral palsy children have basal ganglia issues

32
Q

Objective findings in vision

A 
Field
Acuity 
Eye tracking
Neglect/inattention
Hemianopia - loss of vision 
Homonymous - both sides in the same part
33
Q

When is an optic nerve lesion common and why

A

Multiple sclerosis due to demyelination of optic nerve

34
Q

How can the pituitary gland contribute to vision impairments

A

The optic kiasm is the structure just above the pituitary gland, pituitary gland can squeeze down into optic kiasm and cause loss of vision (hemianopia)

35
Q

Assessment of sensation in objective Ax

A

Light touch
Pinprick
Proprioception - position sense and motion sense
Stereognosis - mental perfection of depth
2 point discrimination - easier on hand than back
Inattention/neglect

36
Q

What’s the difference between sensory neglect and sensory inattention

A

Neglect - it’s not your arm
Inattention - can’t deal with perceptual information from both sides at the same time, only senses unaffected side. However when done separately they can

37
Q

Things to note when assessing muscle length/ROM

A

Be very mindful of the shoulder
Patterns/synergies
Secondary impairments

Be aware of instability and damage to flaccid joints such as the shoulder
If they score a 1 or 2 on the Oxford scale, look at motor recovery scale

38
Q

Assessing co-ordination in objective Ax

A 
Ataxia 
Pendular reflexes 
Rebound phenomenon 
Dysmetria 
Dyssynergia
Dysdiodokokinesia 
Dexterity

DANISH

  • Dysdiodokokinesia
  • Ataxia
  • Nystagmus
  • Intention tremor/dysmetria
  • Stuttering/dysarthria
  • Hypotonia
39
Q

Assessing balance in objective Ax

A

Ability to achieve anti-gravity posture
Alignment (COG over BOS)
Ability to make anticipatory adjustments
Ability to make compensatory adjustments
Ability to make protective responses

40
Q

What does high level function involve

A 
Balance
Coordination
Speed 
Dexterity 
Endurance 
Power 
Ability to multi-task

Concussion affects these systems
Need to give them appropriate exercises to get them back to this level

41
Q

Issues involved with perception/cognition

A 
Pusher syndrome 
Attention 
Insight 
Intellectual function 
Memory
Emotional liability
Language 
Visual perception 
Spatial perception
Praxis 
Executive function
42
Q

What’s the difference between quality and quantity measurements

A

Quantitative - provides us with a numbers that is useful for baselines, comparative signs and detecting change (improvement or decline)

Qualitative - details necessary to drive treatment and reasons why change hasn’t occurred

43
Q

What are some limitations of outcome measures

A

Document change but don’t really say why the change has occurred
Measure the ability e.g. Balance, but don’t say why the balance is impaired
Need to do something else to get qualitative information

44
Q

Describe the mechanisms that result in increased tone

A

Damage to the brain
Flaccidity due to nervous system in shock - peripheral pathways still in shock
Overexcited neurons disordered synergies, inhibition - too much nervous activity
Ability for some mvt, but no voluntary mvt
Recovery of some vol mvt into available synergies
Constant moving isolated joints - motor recovery scale

45
Q

Defund spasticity and describe the neurophysiological mechanisms that cause it

A

Motor disorder characterised by velocity dependent stretch reflex. Neural contributions include: disordered inhibition, hyper-excitability, unmasked proprioceptive phenomena, hyper-excitability, unmaked proprioceptive phenomena, un-wanted co-contraction

46
Q

Explain the difference between spasticity and stiffness

A

Stiffness is non-neural, spasticity is neural
Stiffness - difficulties moving the joint due to unwanted cross linking
Spasticity - due to unwanted co-contraction

47
Q

If their proximal instability is worse than their distal instability what part of the cerebellum have they injuried

A

Vermis

48
Q

Outline factors you would note when assessing motor control

A

Timing
Strength
Co-ordination
Endurance

49
Q

Compare the three scales

A

Fugl-Meyer, MAS and CMII

50
Q

What are the factors that contribute to increased tone

A

Non-neural - shortening of muscle length, stiffened
Neural - motor neuron lesions, UMNL- brain derived inhibition
Rigid co-contraction, spasticity/hyper-reflexia, contracture
NB: child has flexor spasticity rather than extensor due to flexion from crawling

51
Q

Methods for assessing tone

A

Observation
Rapid and slow PROM
Tardieu scale - measuring spasticity
Modified Ashworth’s scale - measure of stiffness, for Pt’s with Parkinson’s, cannot be used with patients with spasticity

52
Q

Motor assessment scale

A

For hemiplegic patients

53
Q

What is Brown’s sequar syndrome

A

Motor loss same side
Sensory loss opposite side

Such as that with a unilateral T10 spinal injury

54
Q

What is the Ritchie Articular index

A
  1. Pain with movement early
  2. Pain in mid range
  3. Pain free movement
55
Q

What does a resting tremor occur

A

With basal ganglia issues
Goes away on intended movement
Not a cerebellar injury

56
Q

What are the signs of a cerebellar dysfunction

A

Dysmetria/intention tremor - inability to do smooth co-ordinated mvts
Ataxia
DDK - inability to do rapid changing mvts
Rebound phenomena
Dexterity - no fine coordinated mvts
Truncal ataxia
DTRs

57
Q

Rebound phenomena test

A

Resist elbow/joint mvt then let go, will straighten out as the body has decided there’s no resistance anymore

58
Q

Tests for DDK

A

Rapid supination/pronation

Toe tapping with knees bent up

59
Q

Tests for dysmetria

A

Thumb to finger tip - reverse and forward 3 times

Heel-shin - heel to medial malleolus and slide up to the knee

60
Q

Tests for dexterity

A

Heel to knee

Finger tap - thumb to all fingers

PHTY314 (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions