Exam 1 Flashcards
Explain the exiting of nerve roots at vertebrae
at C8 the nerve roots exit below
at C1-C7 they exit above
in T spine they exit below corresponding vertebrae
end of the SC is at
conus medullarus (L2)
below L2 is the
cauda equina
peripherial nerves = potential for regeneration
injury to the spinothalmic tract would result in (contra or ipsi sx)
contra
injury to post columns (dorsal columns) would result in (contra or ipsi sx)
ipsi
injury to lateral corticospinal tract would result in (contra or ipsi)
ipsi
injury to medial corticospinal tract would result in (contra or ipsi sx)
ipsi
the spinothalmic tract is aka
anterolateral system
the anterolateral system (aka spinothalmic tract) has what functions
pain
temp
crude touch
the spinothalmic tract crosses where
in SC
the dorsal column functions
disc (fine) touch
vibration
proprioception
the dorsal column (aka post column) crosses in the
BS
the lateral corticospinal tract functions
motor to extremities
the medial corticospinal tract functions
motor to trunk
damage to the SC on one side would yield motor damage to the (contra or ipsi side of damage)
ipsi side from that level and down
overall, the corticospinal tracts are the ___ pathways
motor
overall, the dorsal columns and ant/lateral system are the ___ pathways
sensory
C5 motor level
elbow flexors
C6 motor level
wrist extensors
C7 motor level
elbow ext
C8 motor level
long finger flexors (FDP)
T1 motor level
small finger abd
L2 motor level
hip flexors
L3 motor level
knee ext
L4 motor level
ankle DF
L5 motor level
long toe ext (EHL)
S1 motor level
PF
C2 sensory location
behind ear
C3 sensory location
above clavicle
C4 sensory location
AC jt
C5 sensory location
lateral elbow
C6 sensory location
dorsal thumb (at proximal phalanx)
C7 sensory location
dorsal middle finger (at proximal phalanx)
C8 sensory location
dorsal pinky finger (at proximal phalanx)
T1 sensory location
medial elbow
T2 sensory location
axilla
T3 sensory location
3rd intercostal space (midline of clavicle)
T4 sensory location
nipple line
4th intercostal space (midline of clavicle)
T5 sensory location
5th intercostal space
T6 sensory location
xiphoid process (in midline with clavicle)
T7 sensory location
1/4 way btwn xiphoid and umbilicus (higher up)
T8 sensory location
1/2 btwn xiphoid and umbilicus
T9 sensory location
3/4 way btwn xiphoid and umbilicus
From T3-T12, use what anatomical location as marker
all are at midline of clavicle
T10 sensory location
at level of umbilicus
T11 sensory location
1/2 way btwn umbilicus and ing. lig
T12 sensory location
at ing. lig
L1 sensory location
btwn T12 and L2’s location
upper middle ant thigh
L2 sensory location
middle ant thigh
L3 sensory location
medial epicondyle of knee
L4 sensory location
medial malleolus
L5 sensory location
3rd MCP of toe
S1 sensory location
lateral calcaneous
S2 sensory location
middle of popliteal fossa
S3 sensory location
ischial tub
S4/5 sensory location
peri area
which type of SCI is more common
traumatic
what vert levels of traumatic SCI are more common and why
C5/C6
T12-L1
bc energy takes path of least resistance and these segments are very mobile
explain very basically what occurs with traumatic SCI
hemorrhaging
necrosis of gray matter
primary and secondary injury
what spinal level controls the diaphragm
C4
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
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)
what is the determining factor regarding extent of injury to L spine
cauda equina involvement
what injury often accompanies a SCI
TBI
4 movement patterns that lead to SCI (MOI)
flexion
compression
flexion with rotation
hyperext
flexion SCI cause damage where
ant vertebral
2 types of flexion SCI (most common)
wedge
ant cord
diving head first on a hard surface would yield in what type of SCI
compressive (it’s a straight vertical force)
2 types of compressive SCI
burst
teardrop
explain where damage occurs with a flexion with rotation SCI
Post to ant forces cause damage to lamina, peduncle, facets fx
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
hyperextension
reasons for non traumatic SCI
Tumor Transverse myelitis Syringomyelia Vertebral subluxation Infection Vascular malformations
what is transverse myelitis
a non traumatic SCI, typically sudden onset, involves a specific spinal cord level, and inflammatory process
what is synringomyelia
a non traumatic SCI, a condition that causes an opening somewhere in the spinal cord – effects multiple levels –fills up with fluid
RA at what vert levels can cause a non traumatic SCI
C1/C2 – these pts can be subject to vertebral subluxation
explain complete vs incomplete SCI
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
what are the lowest sacral segments, and why are they significant
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
explain zone of partial preservation
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
paraplegia vs tetraplegia
tetra is loss at trunk and all 4 limbs
para is B leg loss
what is ant cord syndrome
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
cause of ant cord syndrome
often an ant spinal A stroke
what is central cord syndrome
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
Pts with central cord syndrome would have more trouble with WB/walking or dressing themselves/daily ADL’s
more trouble with daily ADL’s dt UE weakness
one main cause of Brown Sequard syndrome
a hemi sectioning like a stabbing
What is Brown Sequard Syndrome
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
what is post cord syndrome
loss of post/dorsal column function below level of injury
often d/t stroke of post spinal A
what % of SCI occur after the original accident d/t improper mvmt/care
About 25% of SCIs occur after original insult
within the first 24 hours of a SCI, what is critical to watch for
Hypotension & neurogenic shock – disruption in sympathetic NS
hypotension and brady cardia
More common in higher level SCI
pts with SCI should be treated at what type of facility
level 1 trauma center
main med used after a SCI
Methelprednisone (steroid to decrease inflammation) is main med for SCI immediately
primary vs secondary injury of SC
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
traumatic vs non traumatic SCI, what title of health care provider is most important for each
traumatic- orthopedist
non traumatic - neurologist
soft tissue image type
MRI
Multi-slice or spiral/helical image type
CT
what is ASIA
American Spinal Cord Association (ASIA index).
Mainstay of stabalization devices for C spine cord injury bc it provides the best stabilization
halo
how long do pts have to wear halo, what is main con
12 wks
very top heavy
when is cspine traction used over a halo, what is a con
Used when medical problems don’t allow use of other devices
they are on bedrest
when are cervical spine orthosis used (ex: a menerva brace)
Often used for cervical spine injuries that do not result in neuro deficits
cons of cspine orthosis
Often used for cervical spine injuries that do not result in neuro deficits
thoracolumbar braces are worn how long
up to 3 months
thoracolumbar surgical Rods that attach to lamina above and below injury level, these limit motion and are very stable
Avoid high torque forces
Harrington rods
special considerations of cspine pre-stabalization (precautions)
special considerations for thoracolumbar spine
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
why is full elbow ext so important for pts with SCI
bc they spend a lot of time in long seated position and they need elbow ext to keep them from falling over
what is needed to be able to sit in long seated
Full shoulder extension and ER
Full elbow extension
Hamstrings to 110
during transfers for pts with SCI, what motion is needed to occur when knee is flexed
DF
what motions are required for SCI pts with ADLS
tight long finger flexors (especially for pts who have lost motor function to hands/wrists)
full hip ER
explain muscle tone for pts with a SCI
Initially flaccid (spinal shock= edema); gradual increase in tone (like stroke)
what are the 10 main complications (listed in the ppt) for pts with SCI
px decub ulcers ectopic bone postural hypotension autonomic dysreflexia mental health resp issues DVTs contractures osteoperosis
what is autonomic dysreflexia
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
what is neurological level
Lowest segment where there is normal sensation (2) and
antigravity motor function (≥ 3)
why is 3/5 against gravity important for asia scoring
functional is against gravity
what is sensory level for asia
lowest level that is a 2
explain scoring options for asia sensory
Scoring 0 = absent 1 = altered 2 = normal (1 can be too much or too little)
which classification of asia is complete injury (no sensory or motor below a certain level, and lack of S4/S5)
Asia a
explain Asia B classification
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)
explain asia C
motor incomplete
Motor preserved below neurological level
> half of muscles ≤ 3/5
explain asia D
ASIA D = motor incomplete
Motor preserved below neurological level
> half of muscles ≥ 3/5
what is asia E
normal
what asia classifications have poorer prognosis
A and B bc lack of motor
what is different about Tspine levels for asia
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
complete vs incomplete SCI (how to tx differently)
complete - aim for compensation
incomplete - aim for remediation
which asias will we almost always tx with compensatory txs
A and B
why strengthen muscles that are 5/5 for SCI pts
bc we need to work on strength for the new compensatory movements they will be doing
prerequisites for function
strength ROM balance endurance psycho abilitys
how might spacticity be a good thing
typically only in incomplete pts
it can help tighten a limb for function (WB, transfers)
___ practice is good for teaching new transfers for SCI pts
part
what is a CV precaution of SCI pts
ortho HTN (long seated is good for them )
3 main strategies used by pts with SCI for function
Muscle substitution
Momentum
Head-hips relationship
explain muscle substitution
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
if triceps are weak, how could you muscle substitute
ER shoulder and supinate
why would we not want to overstretch the long finger flexors
they need tenodesis
serratus level is
C6
which muscle is important to stretch for pts who cannot stand
soleus
what levels are more likely to have resp issues with a SCI
C4 and above
what is dysthesia and where is it seen
SCI pts abnormal sensations (often a burning type of px)
% of SCI pts with chronic px
70
atrophy of muscles = loss of circulation and tissue preservation = skinny bony areas is an issue bc of
decubs forming for SCI pts
biophosphonate drugs tx
heterotopic ossifications (ectopic bone) vigerous ROM and trauma causes bone where it shouldn't be (occurs in bigger jts mainly)
sx of ectopic bone are
similar to infection/inflammation
hot, red, lack of ROM
what 2 issues are causes for postural hypoTN in SCI pts
Venous pooling and lack of SNS function
autonomic dysreflexia is a(n)
medical emergency
extreme HA and HTN
explain autonomic dysreflexia sx and outcomes if not handled properly
Results in extreme HTN and head ache, profuse sweating
Can cause stroke, blindness, coma, and death
how to avoid autonomic dysreflexia
monitor BP, sit up (45 degrees), remove noxious stimulus, inform nurse/MD
why do pts with KAFOs still require a wc
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)
which asia classification has more potential for motor return
ASIA D
PT focus for SCI pts should be
mobility/transfer training
Asia C pts best ambulatory training would be
BWS
KAFOs are for which Asia classifications
A
B
why do we use BWS
it allows us to trial and error in a safe way
keeps us and pts safe
summary of articles about amb training for SCI pts
overground was best
conventional over treadmill
robotics not so great bc pt isn’t having to correct self
what muscles would help a SCI pt to stand/pivot transfer if the muscle was spastic
quads (min to mod spasticity)
type of transfer for asia b
sensory incomplete (motor is complete)
these pts will do scoot bc they don’t have the motor to stand
type of transfers for asia c
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)
type of transfers for asia d
motor incomplete (muscle grade of 3 or more in half the muscles below the level)
these pts. Could use both – but can do stand.
a pt with C6 tetra, how would they lock their wc brakes or handle arm rests
tenodesis
when thinking prognosis of future function, if the neuro level is L2 or below what is significant to remember
L2 and below is peripheral = can possibly regenerate
trunk control segment (approx)
T6
what time frame is typically the predictor of future function of a SCI pt
at 6 months
what that have at that time is typically what they will have
time frame for incomplete injuries, when does MOSTrecovery occur
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
most significant functional and motor predictor of prognosis for a SCI
severity
5 main predictors for prognosis for SCI
severity age level of injury complete/incomplete MOI- lower energy = better outcome
explain how level of injury differs for SCI pts (cspine vs tspine)
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
time frame LTG for SCI
1-2 yrs
tetra or high tspine injuries stay in rehab how long
5-8 wks rehab
paras stay in rehab how long
3-4 wks
functional goals for SCI C1-3
Respirator dependent will need full-time attendant Can talk, chew, swallow Can sip, blow Can use sip-and-puff w/c
what is still intact with a C1-C3 injury
face/neck muscles
cranial nerves
functionality of C4
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
muscles innervated by C4
Upper trapezius,
Diaphragm
Cspine paraspinal muscles
Neck flexion, extension, rotation; scapular elevation; inspiration
muscles innervated by C5
Elbow flexors, supinators (Deltoid, biceps, RC, brachialis, brachioradialis, rhomboids)
functionality C5 level
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
other than the wrist extensors, what muscles are innervated by C6
Lat. dorsi
Serratus
Pecs (clavicular)
functionality C6
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
what muscle is key for bed mobility
serratus - C6
functionality of C8-T1
all UE functional
can pop wheely
can drive with hand controls
can eat without adaptive devices
T4-T6 muscles
MOST intercostals
upper back
mid trunk
resp is better but still no forced cough
level to bend and pick something up off the floor (trunk control)
T4-T6
what level is FULL intercostal function
T9-T12
best resp function
good core
level of first potential for ambulation (with KAFO) SCI
T9-T12
L2-L4 functionality
can amb with KAFO
quads, hip flexors, adductors (all some function)
muscle needed to hip hike with KAFOs on
quadratus
muscles innervated L4-L5
Low back Quads Medial hams Tib ant and post Toe ext
our main goals for an acute pt in ICU with GBS
positioning for prevention, PROM, (education to staff and family for both), assist in pulmonary hygiene
PT dx for GBS
force production deficit with expectation of recovery down the road
possible PT dx for SCI
Monitored Mobility, Sensory Detection Deficit, LE Paresis with Flaccidity
biggest diff btwn GBS and MS
with GBS there is a chance of remyelination bc its a PNS issue not CNS
most GBS pts have good prognosis for recovery with residual weakness where
distal extremeties
GBS pts have absent
DTRs
Most common cause of acute, flaccid paralysis in developed countries ___
Most common motor neuron disease___
flaccid paralysis- GBS
motor neuron disease - ALS
does GBS have geographic distribution like MS
no
who has GBS more, men or women
men
why is there a slight peak in incidence of GBS at certain times in life….and when are they
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)
trigger for GBS
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
explain pathophysiology of what occurs with GBS (why does body attack itself)
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
bugs that cause GBS
cytomegalovirus
haemophilis influenza
c jejuni
after the GBS pt has had a virus/bacterial inf, what occurs next
Gradual symmetrical ascending paralysis over days - 4 weeks with paresthesias and numbness (starts with involving feet and hands and travels to trunk)
once the ascending paralysis occurs and travels to trunk (with GBS), what happens next
a plateau of about 2 weeks
what happens after the plataeu with GBS
Gradual resolution of paralysis (weeks to months) (onset paralysis is distal to proximal, resolution is proximal to distal)
GBS is predominantly (motor or sensory)
motor sx
dx of GBS is done how
nerve conduction study (EMG)
lumbar puncture (protein build up bc myelin is made of protein)
Antigangioside antibodies
most common form of GBS
Acute inflammatory demyelinating polyneuropathy
cells that get demylenated with GBS (type)
schwann cells on myelin
sx of acute inflammatory demyeliating polyneuropathy
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
mortality rate is high in what phase of GBS
acute, infl, demy. poly
CV issues with GBS (acute setting)
Autonomic dysfunction
Hypotension occurs in 10% of severely affected patients; treated by IV fluids
Hypertension: short-acting hypotensive agents
DVT prevention
O2 sat of ___ is goal for GBS
88
under 88 there is potential for issues
other than O2 sats, what are the parameters for other vitals to know whether or not to terminate PT with GBS pt
HR 40-130 bpm
RR 5-40 breaths / min
Systolic BP > 200 mm Hg
2 main medical ways GBS is tx
plasmaphoresis immunoglobulins (preferred)
effects wear off after ____ weeks for immunoglobulin tx of GBS
6
pts usually are improved at this time though
bc of fatigue, what must we do during tx for GBS pts
modify and alter our plan always
prioritize
what are key tests to perform on a GBS pt day 1
mobility
balance
strength
VS
bc overdoing it can cause further weakness in neuro pts, how to monitor overuse with therex
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
GBS and ALS guidelines for resistance training
≥ 3/5: against gravity with resistance as tolerated
≤ 3-/5: gravity neutral or into gravity, with assistance prn
PT focus for GBS should be on
LE and trunk strengthening
most strength gains for GBS happen when
first 6 months
(-) correlations between strength recovery slope and;:
- Plateau stage duration
- Acute stage duration
GBS, what does this mean
The longer the pt is in the plateue or acute stage, the slower their progress goes
its common for tingling in distal ext to occur up to ___ months with GBS
6
what do a good % of GBS pts need at 1 year for amb
B AFOs - feet are distal so the return last
substitutions for C5
shoulder elevation
substitutions for C6
supination
substitutions for C8
wrist ext
PT dx for ALS
force production deficit
length pts with ALS are in an in pt rehab setting is typically
2-3 wks
most common motor disease
ALS
incidence of ALS
Incidence more common in males
3 variants of ALS
Classical sporadic- insidious onset for no reason
Pacific- occurs in Guam
Familial
etiology of ALS is
unknown
there are theories about possible triggers though
theories about triggers for ALS
Environmental trigger-Likely role in the pacific variant
May be diet-related
Trauma- athletics
Physical and emotional stress
ave age at onset for ALS
60
3 ways ALS begins at onset (which is most common)
Upper limb
Lower limb- usually 1 first***
Bulbar- impairments with bulbar involvement effect cranial nerves (speech and swallowing issues)
which of the types of ALS onsets has poorest outcome
bulbar - resp issues (CN and swallow)
2 factors that have shown to be associated with less rapid onset of ALS
Younger age at onset
Males w/ hand involvement at onset
drug that extends survival by at least 3 mos for ALS
Riluzole
life expectancy ALS
3-5 yrs post dx
only ___% of pts dx with ALS live more than 3 yrs post dx
50
GBS is an issue with ____ neurons, while ALS is an issue with
GBS is lower motor neurons (peripherial)
ALS is a mix of upper and lower
in summary, explain progression of ALS
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)
what are the sx related to the UMN issues with ALS
Spasticity
Hyperreflexia
Loss of dexterity & speed
Pathological reflexes
what are the sx related to LMN issues with ALS
Weakness & atrophy
Hyporeflexia
Fasciculations- abnormal oversensitive axons that depolarizes = twitching
Muscle cramps
bulbar sx with ALS
suck/gag reflexes
resp issues
speech
a general psychological prob with ALS
pts don’t always have time to grieve one loss before disease continues to progress
leading cause of death for ALS
resp failure
what is predictor of mortality for ALS
pulmonary function
FVC
sx of resp muscle weakness (ALS)
May or may not include dyspnea (bc no exercise) Orthopnea Sleep disturbance Daytime hypersomnolence Morning headaches Abnormal breathing patterns
what is typically spared with ALS pts
BB are continent, but ability to transfer and hygiene care are often dependent
OM for ALS
AFRS
ALS function rating scale (self reported)
0-4 scale (4 normal)
(takes into acct multiple aspects: ADLs, motor, speech)
what are unrealistic goals for ALS
prevent strength loss
increase strength
why is stretching and positioning so important for ALS
bc spacticity causes px and these txs can help better than the meds can (meds cause more weakness)
strengthening guidlines ALS
don’t do res ex for muscles less than 3/5
only do res/strengtening for pts early dx
Emotional impact of the diagnosis
Denial and other emotional responses
Uncertain future: inevitable loss
What stages of ALS
Early
1 and 2
Multiple losses experienced
Great need to make decisions
May be reluctant to use compensatory strategies
what stages of ALS
mid
3-4
Confronted w/ terminal aspects of disease
Worries about family and loved ones
Decisions regarding life-saving measures
what stages of ALS
late
5-6
total exercise time for ALS should be
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
why is exercise so beneficial early in ALS
decreases spacticity and increases QOL
what are measures to take before the step of a ventilator for pts with ALS
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
only method to provide indefinite life prolonging support to ALS pts
trach
type of care team appropriate for ALS pts
palliative
4 aspects of palliative care
Communication
Symptom control
Rehabilitation
Terminal care
3 aspects of tx for ALS pts
remediation, prevention, compensation
what stages of ALS should we focus on remediation
1 and 2
what stage of ALS should we focus on prevention
all
what stages of ALS should we focus on compensation
2 on
what are examples of remediation in regards to tx of ALS
conditioning
maintaining strength
maintaining leisure activities
examples of prevention in regards to tx of ALS
decub prevention
airway clearance
beginning to show signs of weakness is usually what ALS stage
2
mod to max weakness in some areas
ambulation beginning to be impaired is what ALS stage
3
Severe leg weakness; mild arm weakness
Use of wheelchair for locomotion; may be able to use arms for ADLs
describes what stage of ALS
4
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
5
what is the focus of stage 6 of ALS
they are total dependent
comfort
peace
specific group of muscles min. weak
independent in ADLs
what stage of ALS
1
why is Tspine the least likely area in spine for a SCI
it lacks mobility and is protected by ribs
of the pathologies, which pts will have absent DTRs
GBS
what level is upper traps
C4- they can shoulder shrug
ALS is a ____ disease while GBS is a ___ disease
ALS- Upper and lower motor neuron
GBS - demylinating paralysis of LMN
level pt can pop a wc wheely
C8-T1
Type of SCI MOI that causes ant cord syndrome
Flexion
bulbar has to do with what disease
ALS
