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NEUROMUSCULAR II (Potter) > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Explain the exiting of nerve roots at vertebrae

A

at C8 the nerve roots exit below
at C1-C7 they exit above
in T spine they exit below corresponding vertebrae

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2
Q

end of the SC is at

A

conus medullarus (L2)

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3
Q

below L2 is the

A

cauda equina

peripherial nerves = potential for regeneration

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4
Q

injury to the spinothalmic tract would result in (contra or ipsi sx)

A

contra

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5
Q

injury to post columns (dorsal columns) would result in (contra or ipsi sx)

A

ipsi

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6
Q

injury to lateral corticospinal tract would result in (contra or ipsi)

A

ipsi

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7
Q

injury to medial corticospinal tract would result in (contra or ipsi sx)

A

ipsi

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8
Q

the spinothalmic tract is aka

A

anterolateral system

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9
Q

the anterolateral system (aka spinothalmic tract) has what functions

A

pain
temp
crude touch

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10
Q

the spinothalmic tract crosses where

A

in SC

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11
Q

the dorsal column functions

A

disc (fine) touch
vibration
proprioception

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12
Q

the dorsal column (aka post column) crosses in the

A

BS

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13
Q

the lateral corticospinal tract functions

A

motor to extremities

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14
Q

the medial corticospinal tract functions

A

motor to trunk

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15
Q

damage to the SC on one side would yield motor damage to the (contra or ipsi side of damage)

A

ipsi side from that level and down

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16
Q

overall, the corticospinal tracts are the ___ pathways

A

motor

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17
Q

overall, the dorsal columns and ant/lateral system are the ___ pathways

A

sensory

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18
Q

C5 motor level

A

elbow flexors

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19
Q

C6 motor level

A

wrist extensors

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20
Q

C7 motor level

A

elbow ext

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21
Q

C8 motor level

A

long finger flexors (FDP)

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22
Q

T1 motor level

A

small finger abd

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23
Q

L2 motor level

A

hip flexors

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24
Q

L3 motor level

A

knee ext

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25
Q

L4 motor level

A

ankle DF

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26
Q

L5 motor level

A

long toe ext (EHL)

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27
Q

S1 motor level

A

PF

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28
Q

C2 sensory location

A

behind ear

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29
Q

C3 sensory location

A

above clavicle

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30
Q

C4 sensory location

A

AC jt

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31
Q

C5 sensory location

A

lateral elbow

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32
Q

C6 sensory location

A

dorsal thumb (at proximal phalanx)

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33
Q

C7 sensory location

A

dorsal middle finger (at proximal phalanx)

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34
Q

C8 sensory location

A

dorsal pinky finger (at proximal phalanx)

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35
Q

T1 sensory location

A

medial elbow

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36
Q

T2 sensory location

A

axilla

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37
Q

T3 sensory location

A

3rd intercostal space (midline of clavicle)

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38
Q

T4 sensory location

A

nipple line

4th intercostal space (midline of clavicle)

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39
Q

T5 sensory location

A

5th intercostal space

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40
Q

T6 sensory location

A

xiphoid process (in midline with clavicle)

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41
Q

T7 sensory location

A

1/4 way btwn xiphoid and umbilicus (higher up)

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42
Q

T8 sensory location

A

1/2 btwn xiphoid and umbilicus

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43
Q

T9 sensory location

A

3/4 way btwn xiphoid and umbilicus

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44
Q

From T3-T12, use what anatomical location as marker

A

all are at midline of clavicle

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45
Q

T10 sensory location

A

at level of umbilicus

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46
Q

T11 sensory location

A

1/2 way btwn umbilicus and ing. lig

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47
Q

T12 sensory location

A

at ing. lig

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48
Q

L1 sensory location

A

btwn T12 and L2’s location

upper middle ant thigh

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49
Q

L2 sensory location

A

middle ant thigh

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50
Q

L3 sensory location

A

medial epicondyle of knee

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51
Q

L4 sensory location

A

medial malleolus

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52
Q

L5 sensory location

A

3rd MCP of toe

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53
Q

S1 sensory location

A

lateral calcaneous

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54
Q

S2 sensory location

A

middle of popliteal fossa

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55
Q

S3 sensory location

A

ischial tub

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56
Q

S4/5 sensory location

A

peri area

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57
Q

which type of SCI is more common

A

traumatic

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58
Q

what vert levels of traumatic SCI are more common and why

A

C5/C6
T12-L1
bc energy takes path of least resistance and these segments are very mobile

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59
Q

explain very basically what occurs with traumatic SCI

A

hemorrhaging
necrosis of gray matter
primary and secondary injury

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60
Q

what spinal level controls the diaphragm

A

C4

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61
Q

what levels (not specific segments but general level) of spine are more and least likely to have SCI, and describe which are more likely to be complete vs incomplete

A

Cervical and Lumbar are more common and are usually incomplete

Thoracic is less common but is often complete (less common bc it lacks mobility and is protected by ribs)

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62
Q

what is the determining factor regarding extent of injury to L spine

A

cauda equina involvement

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63
Q

what injury often accompanies a SCI

A

TBI

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64
Q

4 movement patterns that lead to SCI (MOI)

A

flexion
compression
flexion with rotation
hyperext

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65
Q

flexion SCI cause damage where

A

ant vertebral

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66
Q

2 types of flexion SCI (most common)

A

wedge

ant cord

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67
Q

diving head first on a hard surface would yield in what type of SCI

A

compressive (it’s a straight vertical force)

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68
Q

2 types of compressive SCI

A

burst

teardrop

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69
Q

explain where damage occurs with a flexion with rotation SCI

A

Post to ant forces cause damage to lamina, peduncle, facets fx

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70
Q

this type of SCI is typically seen in older pts. who fall. they can result in complete SCI, but most often result in central Cord syndrome

A

hyperextension

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71
Q

reasons for non traumatic SCI

A 
Tumor
Transverse myelitis
Syringomyelia
Vertebral subluxation
Infection
Vascular malformations
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72
Q

what is transverse myelitis

A

a non traumatic SCI, typically sudden onset, involves a specific spinal cord level, and inflammatory process

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73
Q

what is synringomyelia

A

a non traumatic SCI, a condition that causes an opening somewhere in the spinal cord – effects multiple levels –fills up with fluid

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74
Q

RA at what vert levels can cause a non traumatic SCI

A

C1/C2 – these pts can be subject to vertebral subluxation

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75
Q

explain complete vs incomplete SCI

A

complete: Both motor and sensory function absent below level of injury, including lowest sacral segments
incomplete: Some motor and sensory function preserved below level of injury, including lowest sacral segments

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76
Q

what are the lowest sacral segments, and why are they significant

A

S4 and S5 – control BB
Complete SCI – are incontinent of BandB

In order to be classified as incomplete: S4 and S5 have to be preserved in order to be classified as incomplete

S4/S5 preservation can often be predictors of prognosis

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77
Q

explain zone of partial preservation

A

Term used for patients with COMPLETE SCI who have partial preservation (i.e., sparing) of motor and/or sensory function below level of injury.
Example: Patient with complete C5 tetraplegia who can perform partial DF of his ankle.

However, keep in mind that they are still complete, so S4/5 are still not preserved

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78
Q

paraplegia vs tetraplegia

A

tetra is loss at trunk and all 4 limbs

para is B leg loss

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79
Q

what is ant cord syndrome

A

an Incomplete injury

Loss of motor function, and pain, temperature, and crude touch sensation below level of injury

So the corticospinal tracts and the spinothalmic tracts are damaged but the post column functions are preserved bc post SC is intact

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80
Q

cause of ant cord syndrome

A

often an ant spinal A stroke

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81
Q

what is central cord syndrome

A

an Incomplete injury= UE motor only effected

Typically involves cervical spine
from a fall = hyperextension injury

results in UE weakness with sparing of LE

Sparing of sacral motor and sensory function

central cord =falls = hyper ext

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82
Q

Pts with central cord syndrome would have more trouble with WB/walking or dressing themselves/daily ADL’s

A

more trouble with daily ADL’s dt UE weakness

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83
Q

one main cause of Brown Sequard syndrome

A

a hemi sectioning like a stabbing

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84
Q

What is Brown Sequard Syndrome

A

an incomplete SCI

Ipsilateral loss of proprioception, deep and discriminatory touch, vibration, & motor function
Contralateral loss of pain, temp, and crude touch

contra loss of spinothalmic tract
ipsi loss of dorsal column and corticospinal tracts

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85
Q

what is post cord syndrome

A

loss of post/dorsal column function below level of injury

often d/t stroke of post spinal A

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86
Q

what % of SCI occur after the original accident d/t improper mvmt/care

A

About 25% of SCIs occur after original insult

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87
Q

within the first 24 hours of a SCI, what is critical to watch for

A

Hypotension & neurogenic shock – disruption in sympathetic NS
hypotension and brady cardia

More common in higher level SCI

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88
Q

pts with SCI should be treated at what type of facility

A

level 1 trauma center

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89
Q

main med used after a SCI

A

Methelprednisone (steroid to decrease inflammation) is main med for SCI immediately

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90
Q

primary vs secondary injury of SC

A

Primary- Due to the insult, local deformation of cord
Irreversable

Secondary-Shortly after initial trauma, first few hours
Ischemia, axonal degeneration, inflammation
May be reversable

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91
Q

traumatic vs non traumatic SCI, what title of health care provider is most important for each

A

traumatic- orthopedist

non traumatic - neurologist

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92
Q

soft tissue image type

A

MRI

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93
Q

Multi-slice or spiral/helical image type

A

CT

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94
Q

what is ASIA

A

American Spinal Cord Association (ASIA index).

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95
Q

Mainstay of stabalization devices for C spine cord injury bc it provides the best stabilization

A

halo

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96
Q

how long do pts have to wear halo, what is main con

A

12 wks

very top heavy

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97
Q

when is cspine traction used over a halo, what is a con

A

Used when medical problems don’t allow use of other devices

they are on bedrest

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98
Q

when are cervical spine orthosis used (ex: a menerva brace)

A

Often used for cervical spine injuries that do not result in neuro deficits

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99
Q

cons of cspine orthosis

A

Often used for cervical spine injuries that do not result in neuro deficits

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100
Q

thoracolumbar braces are worn how long

A

up to 3 months

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101
Q

thoracolumbar surgical Rods that attach to lamina above and below injury level, these limit motion and are very stable
Avoid high torque forces

A

Harrington rods

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102
Q

special considerations of cspine pre-stabalization (precautions)

special considerations for thoracolumbar spine

A

Cervical: No neck ROM
shoulder flex and abd to 90 degrees only
ER may be limited

Thoracolumbar: No hip flex past 90degrees, SLR may be limited to 30

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103
Q

why is full elbow ext so important for pts with SCI

A

bc they spend a lot of time in long seated position and they need elbow ext to keep them from falling over

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104
Q

what is needed to be able to sit in long seated

A

Full shoulder extension and ER
Full elbow extension
Hamstrings to 110

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105
Q

during transfers for pts with SCI, what motion is needed to occur when knee is flexed

A

DF

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106
Q

what motions are required for SCI pts with ADLS

A

tight long finger flexors (especially for pts who have lost motor function to hands/wrists)
full hip ER

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107
Q

explain muscle tone for pts with a SCI

A 
Initially flaccid (spinal shock= edema); 
gradual increase in tone (like stroke)
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108
Q

what are the 10 main complications (listed in the ppt) for pts with SCI

A 
px
decub ulcers
ectopic bone
postural hypotension
autonomic dysreflexia
mental health
resp issues
DVTs
contractures
osteoperosis
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109
Q

what is autonomic dysreflexia

A

Pathology of autonomic N.S. at injury levels above T6
Trigger: noxious stimulus below level of injury
Results in HTN, HA, profuse sweating
Can cause stroke, blindness, death

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110
Q

what is neurological level

A

Lowest segment where there is normal sensation (2) and

antigravity motor function (≥ 3)

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111
Q

why is 3/5 against gravity important for asia scoring

A

functional is against gravity

112
Q

what is sensory level for asia

A

lowest level that is a 2

113
Q

explain scoring options for asia sensory

A 
Scoring
0 = absent
1 = altered
2 = normal
(1 can be too much or too little)
114
Q

which classification of asia is complete injury (no sensory or motor below a certain level, and lack of S4/S5)

A

Asia a

115
Q

explain Asia B classification

A

sensory incomplete

Sensory preserved below neurological level and includes
AND
no motor preserved below levels below motor level on either side

(essentially means they have some sensation but no motor below the level)

116
Q

explain asia C

A

motor incomplete
Motor preserved below neurological level
> half of muscles ≤ 3/5

117
Q

explain asia D

A

ASIA D = motor incomplete
Motor preserved below neurological level
> half of muscles ≥ 3/5

118
Q

what is asia E

A

normal

119
Q

what asia classifications have poorer prognosis

A

A and B bc lack of motor

120
Q

what is different about Tspine levels for asia

A

you cannot classify motor like C spine, whatever sensory level is..is what your motor level is

if sensory level is a Tspine, motor is automatically that level

121
Q

complete vs incomplete SCI (how to tx differently)

A

complete - aim for compensation

incomplete - aim for remediation

122
Q

which asias will we almost always tx with compensatory txs

A

A and B

123
Q

why strengthen muscles that are 5/5 for SCI pts

A

bc we need to work on strength for the new compensatory movements they will be doing

124
Q

prerequisites for function

A 
strength
ROM
balance
endurance
psycho abilitys
125
Q

how might spacticity be a good thing

A

typically only in incomplete pts

it can help tighten a limb for function (WB, transfers)

126
Q

___ practice is good for teaching new transfers for SCI pts

A

part

127
Q

what is a CV precaution of SCI pts

A

ortho HTN (long seated is good for them )

128
Q

3 main strategies used by pts with SCI for function

A

Muscle substitution
Momentum
Head-hips relationship

129
Q

explain muscle substitution

A

Used when a muscle normally producing the movement is weak or absent
Patient learns to use an alternate muscle to perform the movement by having the alternate muscle pull in a different way

130
Q

if triceps are weak, how could you muscle substitute

A

ER shoulder and supinate

131
Q

why would we not want to overstretch the long finger flexors

A

they need tenodesis

132
Q

serratus level is

A

C6

133
Q

which muscle is important to stretch for pts who cannot stand

A

soleus

134
Q

what levels are more likely to have resp issues with a SCI

A

C4 and above

135
Q

what is dysthesia and where is it seen

A 
SCI pts
abnormal sensations (often a burning type of px)
136
Q

% of SCI pts with chronic px

A

70

137
Q

atrophy of muscles = loss of circulation and tissue preservation = skinny bony areas is an issue bc of

A

decubs forming for SCI pts

138
Q

biophosphonate drugs tx

A 
heterotopic ossifications (ectopic bone)
vigerous ROM and trauma causes bone where it shouldn't be (occurs in bigger jts mainly)
139
Q

sx of ectopic bone are

A

similar to infection/inflammation

hot, red, lack of ROM

140
Q

what 2 issues are causes for postural hypoTN in SCI pts

A

Venous pooling and lack of SNS function

141
Q

autonomic dysreflexia is a(n)

A

medical emergency

extreme HA and HTN

142
Q

explain autonomic dysreflexia sx and outcomes if not handled properly

A

Results in extreme HTN and head ache, profuse sweating

Can cause stroke, blindness, coma, and death

143
Q

how to avoid autonomic dysreflexia

A

monitor BP, sit up (45 degrees), remove noxious stimulus, inform nurse/MD

144
Q

why do pts with KAFOs still require a wc

A

they typically use wcs for community transport bc KAFO’s are not really functional and they also require hands to be on crutches (so its really not functional)

145
Q

which asia classification has more potential for motor return

A

ASIA D

146
Q

PT focus for SCI pts should be

A

mobility/transfer training

147
Q

Asia C pts best ambulatory training would be

A

BWS

148
Q

KAFOs are for which Asia classifications

A

A

B

149
Q

why do we use BWS

A

it allows us to trial and error in a safe way

keeps us and pts safe

150
Q

summary of articles about amb training for SCI pts

A

overground was best
conventional over treadmill
robotics not so great bc pt isn’t having to correct self

151
Q

what muscles would help a SCI pt to stand/pivot transfer if the muscle was spastic

A

quads (min to mod spasticity)

152
Q

type of transfer for asia b

A

sensory incomplete (motor is complete)

these pts will do scoot bc they don’t have the motor to stand

153
Q

type of transfers for asia c

A

motor incomplete (half the muscles are less than 3/5)

these pts will do scoot pivot bc they wouldn’t be strong enough for stand (especially early)

154
Q

type of transfers for asia d

A

motor incomplete (muscle grade of 3 or more in half the muscles below the level)

these pts. Could use both – but can do stand.

155
Q

a pt with C6 tetra, how would they lock their wc brakes or handle arm rests

A

tenodesis

156
Q

when thinking prognosis of future function, if the neuro level is L2 or below what is significant to remember

A

L2 and below is peripheral = can possibly regenerate

157
Q

trunk control segment (approx)

A

T6

158
Q

what time frame is typically the predictor of future function of a SCI pt

A

at 6 months

what that have at that time is typically what they will have

159
Q

time frame for incomplete injuries, when does MOSTrecovery occur

A

½ - ⅔ of the 1-year motor recovery occurs in first 2 months (like cortical lesions)

biggest recoveries are first 2 months
6 months is usually prognostic marker

160
Q

most significant functional and motor predictor of prognosis for a SCI

A

severity

161
Q

5 main predictors for prognosis for SCI

A 
severity
age
level of injury
complete/incomplete
MOI- lower energy = better outcome
162
Q

explain how level of injury differs for SCI pts (cspine vs tspine)

A

Cervical SCI: more incapacitating (overall) than thoracic

Thoracic SCI: less potential for recovery than cervical (T spine have less chance to transition to incomplete from complete)

1 level in tspine isn’t as significant as 1 in cspine

163
Q

time frame LTG for SCI

A

1-2 yrs

164
Q

tetra or high tspine injuries stay in rehab how long

A

5-8 wks rehab

165
Q

paras stay in rehab how long

A

3-4 wks

166
Q

functional goals for SCI C1-3

A 
Respirator dependent
will need full-time attendant
Can talk, chew, swallow
Can sip, blow
Can use sip-and-puff w/c
167
Q

what is still intact with a C1-C3 injury

A

face/neck muscles

cranial nerves

168
Q

functionality of C4

A

power wc dependent
bed mobility and transfers are dependent
pt will be able to verbalize and direct the care giver to perform transfers
May not be able to breath on own all time
They can power a WC
They can shoulder shrug

169
Q

muscles innervated by C4

A

Upper trapezius,
Diaphragm
Cspine paraspinal muscles

Neck flexion, extension, rotation; scapular elevation; inspiration

170
Q

muscles innervated by C5

A

Elbow flexors, supinators (Deltoid, biceps, RC, brachialis, brachioradialis, rhomboids)

171
Q

functionality C5 level

A 
grooming with adaptive equp.
manual wc propulsion for house only
Bed mobility with some asst.
Cannot grasp reg spoon or fork
Part time care attendant
Low endurance
172
Q

other than the wrist extensors, what muscles are innervated by C6

A

Lat. dorsi
Serratus
Pecs (clavicular)

173
Q

functionality C6

A 
Eat w/ adapted utensils
Dress almost Ind–big benchmark
I bed mob/transfer w/ sliding board
I pressure relief- benchmark
Good cough – still impaired
Drive w/ hand controls- benchmark
I manual w/c (friction rim)
May use power w/c
Assist w/ self-ROM
174
Q

what muscle is key for bed mobility

A

serratus - C6

175
Q

functionality of C8-T1

A

all UE functional
can pop wheely
can drive with hand controls
can eat without adaptive devices

176
Q

T4-T6 muscles

A

MOST intercostals
upper back
mid trunk
resp is better but still no forced cough

177
Q

level to bend and pick something up off the floor (trunk control)

A

T4-T6

178
Q

what level is FULL intercostal function

A

T9-T12
best resp function
good core

179
Q

level of first potential for ambulation (with KAFO) SCI

A

T9-T12

180
Q

L2-L4 functionality

A

can amb with KAFO

quads, hip flexors, adductors (all some function)

181
Q

muscle needed to hip hike with KAFOs on

A

quadratus

182
Q

muscles innervated L4-L5

A 
Low back
Quads
Medial hams
Tib ant and post
Toe ext
183
Q

our main goals for an acute pt in ICU with GBS

A

positioning for prevention, PROM, (education to staff and family for both), assist in pulmonary hygiene

184
Q

PT dx for GBS

A

force production deficit with expectation of recovery down the road

185
Q

possible PT dx for SCI

A

Monitored Mobility, Sensory Detection Deficit, LE Paresis with Flaccidity

186
Q

biggest diff btwn GBS and MS

A

with GBS there is a chance of remyelination bc its a PNS issue not CNS

187
Q

most GBS pts have good prognosis for recovery with residual weakness where

A

distal extremeties

188
Q

GBS pts have absent

A

DTRs

189
Q

Most common cause of acute, flaccid paralysis in developed countries ___

Most common motor neuron disease___

A

flaccid paralysis- GBS

motor neuron disease - ALS

190
Q

does GBS have geographic distribution like MS

A

no

191
Q

who has GBS more, men or women

A

men

192
Q

why is there a slight peak in incidence of GBS at certain times in life….and when are they

A

Slight peak in late adolescence & early adulthood, and elderly = decreased immune sx causes some form of infections (at these age ranges we are more prone to infections)

193
Q

trigger for GBS

A

Triggered by a preceding bacterial OR viral infection in 60-70% of patients (resp or GI) 1-3 weeks prior

Bacterial = C jejuni Gastroenteritis is most common

194
Q

explain pathophysiology of what occurs with GBS (why does body attack itself)

A

When pple get c jenuni, the body’s immune sx kicks in and attack the ganglioside thinking that the gangliosides on peripheral axons are bad and an autoimmune response occurs

195
Q

bugs that cause GBS

A

cytomegalovirus
haemophilis influenza
c jejuni

196
Q

after the GBS pt has had a virus/bacterial inf, what occurs next

A

Gradual symmetrical ascending paralysis over days - 4 weeks with paresthesias and numbness (starts with involving feet and hands and travels to trunk)

197
Q

once the ascending paralysis occurs and travels to trunk (with GBS), what happens next

A

a plateau of about 2 weeks

198
Q

what happens after the plataeu with GBS

A

Gradual resolution of paralysis (weeks to months) (onset paralysis is distal to proximal, resolution is proximal to distal)

199
Q

GBS is predominantly (motor or sensory)

A

motor sx

200
Q

dx of GBS is done how

A

nerve conduction study (EMG)

lumbar puncture (protein build up bc myelin is made of protein)

Antigangioside antibodies

201
Q

most common form of GBS

A

Acute inflammatory demyelinating polyneuropathy

202
Q

cells that get demylenated with GBS (type)

A

schwann cells on myelin

203
Q

sx of acute inflammatory demyeliating polyneuropathy

A

LEs involved before UEs
Will involve distal and proximal muscles (inc. Cr. N)
Can involve sensory nerves (esp. deep sensation)
DTRs typically absent
Proximal pain/aching
Variable autonomic involvement (abnormal cardiac/resp response to exercise)
Can end up on a vent

204
Q

mortality rate is high in what phase of GBS

A

acute, infl, demy. poly

205
Q

CV issues with GBS (acute setting)

A

Autonomic dysfunction
Hypotension occurs in 10% of severely affected patients; treated by IV fluids
Hypertension: short-acting hypotensive agents
DVT prevention

206
Q

O2 sat of ___ is goal for GBS

A

88

under 88 there is potential for issues

207
Q

other than O2 sats, what are the parameters for other vitals to know whether or not to terminate PT with GBS pt

A

HR 40-130 bpm
RR 5-40 breaths / min
Systolic BP > 200 mm Hg

208
Q

2 main medical ways GBS is tx

A 
plasmaphoresis
immunoglobulins (preferred)
209
Q

effects wear off after ____ weeks for immunoglobulin tx of GBS

A

6

pts usually are improved at this time though

210
Q

bc of fatigue, what must we do during tx for GBS pts

A

modify and alter our plan always

prioritize

211
Q

what are key tests to perform on a GBS pt day 1

A

mobility
balance
strength
VS

212
Q

bc overdoing it can cause further weakness in neuro pts, how to monitor overuse with therex

A

Px, stiffness, prolonged weakness are signs of them over doing it
If you wake up tomorrow morn and are still tired, we over did the ex

Its a good idea to educate pts that these side effects might occur
Its not unusual for pts with GBS to have mild cramping aches and pxs but then it goes away

213
Q

GBS and ALS guidelines for resistance training

A

≥ 3/5: against gravity with resistance as tolerated

≤ 3-/5: gravity neutral or into gravity, with assistance prn

214
Q

PT focus for GBS should be on

A

LE and trunk strengthening

215
Q

most strength gains for GBS happen when

A

first 6 months

216
Q

(-) correlations between strength recovery slope and;:

  • Plateau stage duration
  • Acute stage duration

GBS, what does this mean

A

The longer the pt is in the plateue or acute stage, the slower their progress goes

217
Q

its common for tingling in distal ext to occur up to ___ months with GBS

A

6

218
Q

what do a good % of GBS pts need at 1 year for amb

A

B AFOs - feet are distal so the return last

219
Q

substitutions for C5

A

shoulder elevation

220
Q

substitutions for C6

A

supination

221
Q

substitutions for C8

A

wrist ext

222
Q

PT dx for ALS

A

force production deficit

223
Q

length pts with ALS are in an in pt rehab setting is typically

A

2-3 wks

224
Q

most common motor disease

A

ALS

225
Q

incidence of ALS

A

Incidence more common in males

226
Q

3 variants of ALS

A

Classical sporadic- insidious onset for no reason
Pacific- occurs in Guam
Familial

227
Q

etiology of ALS is

A

unknown

there are theories about possible triggers though

228
Q

theories about triggers for ALS

A

Environmental trigger-Likely role in the pacific variant
May be diet-related
Trauma- athletics
Physical and emotional stress

229
Q

ave age at onset for ALS

A

60

230
Q

3 ways ALS begins at onset (which is most common)

A

Upper limb
Lower limb- usually 1 first***
Bulbar- impairments with bulbar involvement effect cranial nerves (speech and swallowing issues)

231
Q

which of the types of ALS onsets has poorest outcome

A

bulbar - resp issues (CN and swallow)

232
Q

2 factors that have shown to be associated with less rapid onset of ALS

A

Younger age at onset

Males w/ hand involvement at onset

233
Q

drug that extends survival by at least 3 mos for ALS

A

Riluzole

234
Q

life expectancy ALS

A

3-5 yrs post dx

235
Q

only ___% of pts dx with ALS live more than 3 yrs post dx

A

50

236
Q

GBS is an issue with ____ neurons, while ALS is an issue with

A

GBS is lower motor neurons (peripherial)

ALS is a mix of upper and lower

237
Q

in summary, explain progression of ALS

A

if there is deg of neurons LMN then LMN sx will occur, as disease progresses (legs first then travels up) towards brain then they can get involvement at higher levels, so the sx will later reflect UMN signs

Eventually it can reach fronto-temporal cortex effecting memory, cognition behavior (prob solving issues)

238
Q

what are the sx related to the UMN issues with ALS

A

Spasticity
Hyperreflexia
Loss of dexterity & speed
Pathological reflexes

239
Q

what are the sx related to LMN issues with ALS

A

Weakness & atrophy

Hyporeflexia

Fasciculations- abnormal oversensitive axons that depolarizes = twitching

Muscle cramps

240
Q

bulbar sx with ALS

A

suck/gag reflexes
resp issues
speech

241
Q

a general psychological prob with ALS

A

pts don’t always have time to grieve one loss before disease continues to progress

242
Q

leading cause of death for ALS

A

resp failure

243
Q

what is predictor of mortality for ALS

A

pulmonary function

FVC

244
Q

sx of resp muscle weakness (ALS)

A 
May or may not include dyspnea (bc no exercise)
Orthopnea
Sleep disturbance
Daytime hypersomnolence
Morning headaches
Abnormal breathing patterns
245
Q

what is typically spared with ALS pts

A

BB are continent, but ability to transfer and hygiene care are often dependent

246
Q

OM for ALS

A

AFRS
ALS function rating scale (self reported)
0-4 scale (4 normal)
(takes into acct multiple aspects: ADLs, motor, speech)

247
Q

what are unrealistic goals for ALS

A

prevent strength loss

increase strength

248
Q

why is stretching and positioning so important for ALS

A

bc spacticity causes px and these txs can help better than the meds can (meds cause more weakness)

249
Q

strengthening guidlines ALS

A

don’t do res ex for muscles less than 3/5

only do res/strengtening for pts early dx

250
Q

Emotional impact of the diagnosis
Denial and other emotional responses
Uncertain future: inevitable loss

What stages of ALS

A

Early

1 and 2

251
Q

Multiple losses experienced
Great need to make decisions
May be reluctant to use compensatory strategies

what stages of ALS

A

mid

3-4

252
Q

Confronted w/ terminal aspects of disease
Worries about family and loved ones
Decisions regarding life-saving measures

what stages of ALS

A

late

5-6

253
Q

total exercise time for ALS should be

A 
Total = 30 -45 min
10-15 min at a time
do 2-3 bouts throughout the day 
mod only-no max
only in early stages
254
Q

why is exercise so beneficial early in ALS

A

decreases spacticity and increases QOL

255
Q

what are measures to take before the step of a ventilator for pts with ALS

A

Non-invasive positive pressure (mask or canula)
Can prolong survival time without ventilation
Helps maintain FVC values
Improves respiratory symptoms, QOL, and cognition
Shown to improve exercise capacity

256
Q

only method to provide indefinite life prolonging support to ALS pts

A

trach

257
Q

type of care team appropriate for ALS pts

A

palliative

258
Q

4 aspects of palliative care

A

Communication
Symptom control
Rehabilitation
Terminal care

259
Q

3 aspects of tx for ALS pts

A

remediation, prevention, compensation

260
Q

what stages of ALS should we focus on remediation

A

1 and 2

261
Q

what stage of ALS should we focus on prevention

A

all

262
Q

what stages of ALS should we focus on compensation

A

2 on

263
Q

what are examples of remediation in regards to tx of ALS

A

conditioning
maintaining strength
maintaining leisure activities

264
Q

examples of prevention in regards to tx of ALS

A

decub prevention

airway clearance

265
Q

beginning to show signs of weakness is usually what ALS stage

A

2

266
Q

mod to max weakness in some areas

ambulation beginning to be impaired is what ALS stage

A

3

267
Q

Severe leg weakness; mild arm weakness
Use of wheelchair for locomotion; may be able to use arms for ADLs

describes what stage of ALS

A

4

268
Q

max assist with most ADLs
Progressive weakness; decreased endurance
Wheelchair use; lift may be necessary; need for assistance w/ ADLs and mobility

what stage of ALS

A

5

269
Q

what is the focus of stage 6 of ALS

they are total dependent

A

comfort

peace

270
Q

specific group of muscles min. weak
independent in ADLs

what stage of ALS

A

1

271
Q

why is Tspine the least likely area in spine for a SCI

A

it lacks mobility and is protected by ribs

272
Q

of the pathologies, which pts will have absent DTRs

A

GBS

273
Q

what level is upper traps

A

C4- they can shoulder shrug

274
Q

ALS is a ____ disease while GBS is a ___ disease

A

ALS- Upper and lower motor neuron

GBS - demylinating paralysis of LMN

275
Q

level pt can pop a wc wheely

A

C8-T1

276
Q

Type of SCI MOI that causes ant cord syndrome

A

Flexion

277
Q

bulbar has to do with what disease

A

ALS

NEUROMUSCULAR II (Potter) (3 decks)

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