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Neuro PT > Lecture 4 > Flashcards

Lecture 4 Flashcards

Experience-Based Neuroplasticity and Motor Learning

1
Q

what are some principles of neuroplasticity?

A
  • use it or lose it
  • use it and improve
  • specificity
  • reps
  • intensity
  • sailence
  • time since onset (the most neuroplasticity in 1st year 3-6 months)
  • age
  • transference
  • interference
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2
Q

FULL community ambulaiton is m/s

A

1.4 m/s

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3
Q

grading of functional tasks for LE and UE

A

slides 4 and 5 - read

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4
Q

what’s the importance of errors and variability in practice?

A

task and environemtn variability is more like real life (enhanced errors during locomotor training enhanced walking ability)

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5
Q

what’s something to be aware of with error / variability during practice?

A

patient must be able to learn/adapt to the error/variability

don’t reach “too much” (learned helplessness, demoralization, result of failing)

want them to be motivated NOT to fail

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6
Q

plasticity coninutes during ____ because it includes downsizing of dendrites/spines of unecessary input and facilitates storage and consolidaiton of earlier day’s learning

A

sleep

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7
Q

depression on neuroplasticity

A

- reduced hippocampus size
- neuronal loss
- less neurogenesis
- deficits in concentration/memory

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8
Q

stress on neuroplasticity

A
  • mild stress enhances learning/memory
  • chronic/high stress leads to neuronal loss in the hipocampus
  • deficits in concentration/memory
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9
Q

regular ex in mid to late life decreases risk of?

A

dementia

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10
Q

aerobic ex improves

A

cognition
neurogenesis
increase dendrtic spine density
angiogenesis
long term potentiaiton

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11
Q

98% of patients with a stroke independently walked at 6 months IF:

A
  • independent sitting balance first 3 days
  • LE strength of at least 1/5 in hip flexors, knee extensors, and ankle DF in first 3 days
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12
Q

27% of patients post stroke walked if criteria ?
10% walked if criteria?

A
  • unmet at 3 days
  • unmet at 9 days

note: a longer time of no movement is less chance of walking recovery

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13
Q

upon admission to inpatient rehab:
BBS and FIM-L scores
predicts 20x more likely to achieve household ambulaiton by dc

A

BBS - <20
FIM-L 1 or 2

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14
Q

What is UE functional recovery predictor post stroke?

A

AROM of shldr and middle finger predicted 71% variance in UE Function at **3 months **

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15
Q

a very early rehabilitation trial (AVERT) results

A

sig diff in:
- time in PT
- time to first mobilizaiton
- cost of care at 3 months
- function:
- modified rankin at 3,12 months and ability to walk unassisted at 3,6 months

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16
Q

what happened to individuals who participated in the Standing Feedback Trainer (SFT) versus normal treatment?

A

their center of pressure (lateral) was more towards midline in SFT group.

note: SFT did not necessarily improve their gait but it significantly improved standing balance

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17
Q

unlimited household ambulaiton is

A

0.27 m/s

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18
Q

limited community ambulation is?

A

0.58 m/s

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19
Q

unlimted community ambulation is

A

0.80 m/s

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20
Q

how many m/s needed to cross a commercial street?

A

2 m/s

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21
Q

community ambulation for adults without stroke is at least ?

A

1.2 m/sec

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22
Q

“Normal 64 y/o able to ambulate with a speed of 1.07 m/s while chronic stroke survivors of similar age walked at __m/s”

A

0.8 m/s

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23
Q

supported treadmill ambulation - benefits

A
  • enhance walking for patients that find it hard bc of gravity, posture instability, balance
  • enhances motor learning by giving reps
  • PT can challenge the patient more
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24
Q

what is the ESSENTIAL neuroanatomy of walking?

A
  • mm and periph nerves
  • SC Pattern generator
  • VL AND MV SC pathways
  • medullary reticular formation
  • mesencephalic locomotor region
  • subthalamic “ “
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25
Q

what are intrinsic circuits located in the ventral and intermediate gray matter that produces and repeats a functional behavior

for walking, it switches between flexor and extensors

A

Spinal cord CPG - essential neuroanatomy

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26
Q

what are the general properties of central pattern generators (CPG)?

A
  • involved in intra/interl limb mvmt
  • can react appropriately to sensory input
  • ability to recover, learn
27
Q

the decision to walk is made in which center?

A

medial medullary reticular formation

28
Q

this area is the final integrative center for locomotion before the cord
“Driving center” for locomotin in animals
decision to walk made here
source of pathway that decends in V-L cord to provide tonic drive to CPG in SC
involved in inter-limb coordination via feedback loops that detect symmetry or asymmetry of limb movement

A

medial medullary reticular formaiton

29
Q

why PTs can influence gait at the level of the medial medullary reticular formation?

A

supported treatmill forces limbs to move symmetrically and that feedback will go to the medial medullary RF. the RF will now be more trained for CPG’s.

note: gait speed is important bc it will control level of feedback going to cerebellum via stretch mm receptors

30
Q

the mesencephalic locomotor region may help

A

modulate speed of walking
- “exploraotry locomotion”

31
Q

subthalamic locomotor region is responsible for

A

spontaneous goal-directed locomotin

32
Q

important (but not ESSENTIAL) neuroanatomy

A
  • sensation
  • Dorsal lateral pathways
  • pontomedullary locomotor strip
  • cerebellum
  • red nucleus
  • lateral vestibular nuclei
  • substantia nigra
  • GP, Internal segment
  • nucleus accumbens
  • limbic cortex
33
Q

the important but not essential regins interact with the essential regions to control locomotion indirectly by?

A
  • timing of swing vs stance phase of gait
  • detecting sensory gains during walking
  • coordinaiton
  • motivation to walk*
34
Q

____is the top of the dierarchy, where you can identify the motivation to walk. it also explains why “fear” shuts down the system
(test q)

A

hippocampus

35
Q

what are the accessory regions?

A

motor cerebral cortex
pyramidal tract

36
Q

what might the cerebral cortex participate in?

A

it may influence initiation, timing, transitioning from stance to swing, and the precise positionnig of the foot

Note: cortex might interfere with walking if attention is required for a task

37
Q

what are 3 KEY sensory inputs operate the CPG?

A
  1. stretch of hip flexors (longer stride**)
  2. unwieghitng fo tricpes surae (gives leg premission to take step)
  3. WB to facilitate extensor tone in stance limb (muscle receptors in triceps surae, pressure receptor in foot and joint receptors)
38
Q

what happens during mid stance to heel-off?

A

hip extension triggers swing of the limb via activation of the velocity and amplitude dependent muscle spindles

PT should stretch ilioposoas to let the hip swing

39
Q

keu spinal cord segments on hip flexors

A

L 2,3,4

40
Q

If the hip is kept from extending, walking

A

STOPS

41
Q

controling and avoiding with gait training

A

control:
- afferent input associated with the hip flexor stretch and triceps surae

avoid:
- working on static posture if walking is the goal

42
Q

lokomat paramets can progress patient by:

A
  • increasing speed
  • increasing time
  • decrease BWS
  • decrease guidance forces

note: can adust R/L sides, cadence, hipr aknd knee angles of ROM

43
Q

lokomat VS manually asisted: key differences

A

speed: manually assisted can achieve higher speed > lokomat
intervention: need 2-4 ppl for manual assist rather than lokomat (1 person)
level of assist: manually assisted is more specific than lokomat

44
Q

things to keep in mind on treadmill

A
  • little footwear as possible
  • fast as possible on TM
  • symmetrical limbs
  • hips achieve hip extension in late stance
  • arms swinging is ideal
45
Q

case study: person with chronic CVA

A
  • added AFO by the 4th session increased the total min / session
45
Q

what is CIMT?

A

constraint induced movement therapy - forcing to use the the affected limb

46
Q

develpment of learned non-use
look at table in slide 43

A
47
Q

T/F with learned non-use, use-dependent or treatment-induced cortical reorganization can occur with appropriate and aggressive treatment. the brian can reorganize and relearn to use the affected limb, reversing non-use

A

True

48
Q

cortical mapping done by TMS or fMRI has shown ____ in the muscle output area size in the affected hemisphere

A

increases

49
Q

what are the requirements for cortical reorganization to occur?

A

massed practice (hours / day and successive days)
high motivation drive and concentration

50
Q

increased arm use of the affected limb comes form

A
  • overcoming non-use
  • use depending cortical reorganizaiton
51
Q

Candidates for CIMT?

A
  • raise arm to atleast 45 deg
  • extend elbow 20 deg when shldr flexed 90 degrees
    **ability to extend wrist 10-20 degrees, slightly extend at least 2 fingers
  • ability to understand and follow directions **

there’s more, read on slide 47

52
Q

what are components of CIMT protocol?

A
  • repetitive, task-orientent training
  • adherence-enhancing behavioral strategies
  • contrainging use less affected
53
Q

repetitve, task oriented practice

A

shaping (starts with gross shoulder mvmt and finger tips then gradually reaching the goal)
task practice

54
Q

adherence-enhaincing behavrioal strategies

A
  • sign a behavioral contract
  • home diary
  • home skill assignemn
  • daily adminstration of motor activity log
  • home practice
55
Q

contraining use of LESS involved side using

A

mitt
note: document wearing time and always reminding the pt to use more involved side

56
Q

what were significant changes in the UE study (unilateral treat vs bilateral) and nonsignificatnt?

A

significant:
- fugl meyer
- grooved pegboard
- TMS activation sites significant changes 3 months later

not sig: motor activity log

57
Q

EXCITE Trial significant changes

A
  • wolf funciton
  • motor activity log
  • SIS
  • Improvements maintained for 12-24 months
58
Q

Lang C presnetaiton at IV step conference results showed

SLIDE 60

A
  • more is NOT better
  • no consistent dose response relationship
  • 90% reported sig change
  • none changed UE usage at home
  • small but sig performance measures for all but the 200 rep group
59
Q

balance training follwing acute-onset CNS injury

slides 60-64

A
  • strong evidence NOT perform sitting/balance aiming for improved postural stability or WB symmetry for people post stroke
  • NOT perform sitting/standing balance training with vibration for ppl post stroke
  • dynamic/static nonwalking balance ex paired with virutal reality is strongly encouraged
60
Q

T/F evidence is stroke to use BWS TM training following acute onset CNS injury (stroke, iSCI, TBI)

A

false

61
Q

robotic assisted wlaking training following acute on set CNS injury

A

not use for ppl post stroke or iSCI

62
Q

CPG of AFOs and FES post stroke

A
  • very strong evidence AFO and FES improves gt speed, mobility and dynamic balance
  • QOL, endurance, mm activation
    note: AFO may cause more compensaiton than FES but one isn’t superior from the other
  • NOT used to diminish PF spasticiy
63
Q
A

Neuro PT (8 decks)

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