Test 3: Spasticity Flashcards
what is muscle tone
resistance of muscle to passive stretch/elongation
amount of tension at rest
normal muscle tone
high enough to counter gravity but low enough to allow freedom of movement
balanced/isolated for smooth/coordinated movement
signs of UMN lesion
hypertonicity
clonus
babinski
abnormal synergy
LMN syndrome signs
peripheral nerves
reduced or absent reflexes
neurogenic atrophy, not disuse
hypotonia/flaccidity
describe hypotonia
decreased/absent tone
diminished/absent stretch reflex
neurogenic muscle atrophy
finding with LMN
how might acute UMN lesions present
can initially produce hypotonia due to spinal or cerebral shock
after shock period is over, UMN show UMN signs and development of spasticity
characteristics of hypertonia
increased tone
resistance to passive movement NOT dependent on velocity
can be with or without spasticity
what falls into the category of hypertonia
spasticity
rigidity
dystonia
decorticate and decerebrate rigidity
what is spasticity
increased, involuntary, VELOCITY DEPENDENT muscle tone
resistance to passive and active movement
faster the passive movement, the stronger the resistance
can occur as primary condition (i.e. degenerative) or secondary to stroke, TBI, SCI, inflammatory conditions like MS, etc
spasticity originates from injury to what
descending motor pathways (pyramidal tracts)
brain stem (medial/lateral vestibulospinal tracts, dorsal reticulosponal tract
results in lack of inhibition of spinal reflexes causing them to be hyperexcitable
can spastic muscle be manual muscle tested
no
describe the synergy patterns associated with synergy
appears when spasticity is present
primitive movements that dominate reflexes and voluntary effory
interferes with coordinated voluntary movements and functional tasks
Flexor synergy pattern of UE
scapular retraction and elevation
shoulder abduction and ER
elbow flexion
forearm supination
wrist and finger flexion
LE flexor synergy pattern
hip flexion, abduction, and ER
knee flexion
ankle DF and inversion
toe DF
UE extensor synergy pattern
scapular protraction
shoulder adduction and IR
elbow ext
forearm pronation
wrist and finger flexion
LE extensor synergy pattern
hip extension, adduction, and IR
knee extension
ankle PF and inversion
toe PF
dystonia is commonly seen from
lesion to basal ganglia
characteristics of dystonia
involuntary and sustained muscle contractions
can be twisting, writhing, and repetitive movements
cocontraction of agonist and antagonist
increased tone
can affect only 1 body part (focal dystonia) or multiple (segmental)
diseases that result in dystonia
primary idiopathic dystonia (hereditary)
wilson’s disease
parkinson’s disease with long term L-dopa therapy
what is dyskinesia
general term used for describing abnormal involuntary writhing movements of a body part including face, UEs, and LEs
can be smooth fluid involuntary writhing movements or rapid jerky type
can present like tics
can be a side effect of meds
common types of dyskinesia
athetosis
chorea
dystonia
parkinson’s disease
tardive dyskinesia
myoclonus
describe athetosis
most common with cerebral palsy
due to damage to basal ganglia
involuntary writhing slow/continuous
more twisting observed
affects face, mouth, trunk, and limbs
less jerky than chorea
can let go of hand after grabbing
describe dystonia
involuntary and sustained muscle contractions
can be twisting/writhing/repetitive
involves cocontraction of agonist and antagonist
cant let go of hand of they grab it
describe chorea
involuntary, rapid, abrupt twisting
writhing movements that may appear to jump form one extremity to another
characteristics of rigidity
stiffness
resistacne to movement that is independent of velocity of movement
associated with lesions of basal ganglia
seen in parkinsons
result of excessive supraspinal drive on alpha motor neurons; not related to spinal reflex mechanisms
leadpipe rigidity
constant increase in muscle tone and stiffness of affected muscles
cogwheel rigidity
rigidity with tremor resulting in rachet like jerkiness when the extremity is moved
seen in UE at elbow and wrist
what is decorticate rigidity
severe injury to cortex (higher corticospinal tract lesion)
UEs posture into shoulder IR/add, elbow flex, wrist flex, and fisted hands
LEs extended with severe PF contractures
long term impact = severe ROM contractures
what is decerenrate rigidity
indicates injury at brain stem with poor outcomes
UEs posture in shoulder IR with full ext at elbow, flexion at wrist and fisted hand
LEs posture in ext with severe PF contracture
what is opisthotonos
strong sustained muscle contraction of extensors of neck and trunk
rigid, hyperextended posture
describe the re-emergence of primitive reflexes
often reemerge in neuro insult/disease
primitive reflexes fire rostrally to drive development of cortex
as cortex matures sufficiently it fires back to inhibit prim. reflexes
insult ot brain causes cortex to fail allowing these reflexes to reemerge
always want to check for them!
what is ANTR
asymmetric tonic neck reflex
- extension of UE and LE on the side the head rotates to
- flexion of UE and LE opposite of the side the head is turned to
assessment for ANTR
severe brain injury clients have high tone everywhere
ANTR may not be obvious visually
palpate for change in mm tone with head RT to identify the reflex
Intervention for ANTR
head position matters and is critical to reduce muscle tone that results from this reflex
what is SNTR
symmetric tonic neck reflex
neck ext = UE ext and LE flex
neck flex = UE flex and LE ext
assessment of STNR
move head into flexion and then to extension while palpate for change in muscle tone at elbow
intervention of STNR
head position to neutral which may require good posture control and positioning of trunk and pelvis
what is tonic labyrinthine
linked to vestibular system development and important precursor to development of posture reflexes
2 components:
- FWD TLR
- BWD TLR
assess how use of tilt-n-space influences this reflex
i.e. like babies; lay down supine and they extend, flex one part and they flex everything/curl into a ball
bermuda triangle of spasticity
posturing/rigidity
TLR
STNR
passive motion testing to examine muscle tone
ask pt to relax
move extremity in all directions
repeat specific motions with increased velocity
**the first quick motion/stretch will cause highest level of spasticity so pay attention
clonus = quick stretch; + spasmodic contraction of agonist; describe beats and if sustained
0 on MAS
no increase in tonw
1 on MAS
slight increase in tone
with catch and release or minimal resistance at end of ROM when affected part moving in flexion/ext
1+ on MAS
slight increase in muscle tone, manifested as a catch
followed by minimal resistance through remainder (less than half) of ROM
2 on MAS
marked increase in muscle tone throughout most ROM but affected parts still easily moved
3 on MAS
considerable increase in tone
passive movement difficult
4 on MAS
affected parts rigid in flexion or extension
what to document with tone abnormalities
what segment involved
what type of abnormal mm tone is present
spasticity? which mm groups and MAS score
asymmetric or symmetric?
how is segment postured?
obligatory synergy pattern present with active movement?
what is the impact of abnormal tone on movement/posture/function
outcomes of unmanaged spasticity
contractires
spinal deviation/scoliosis
wounds
inability to access active movement
possible effects of structural spinal deformity
impacts organ systems
impairs breathing
increases skin breakdown risk
wounds possible from PF/supinated feet
heel ulcers
5th Met head ulcers
lateral malleolus ulcers
flexion of toes may result in what ulcer
PIP ulcer
postural deviations/scoliosis may result in ulcers where
IT ulcers
GT ulcers
PT interventions for abnormal tone
Wbing
prolonged stretch
static splint
synamic splint
serial casting
modalities
positioning
benefits pf proper positioning
manages primitive reflexes
manage deviations
LE extensor tone and magic hip angle
reduce destructive hip position
goal for dynamic splinting
low load prolonged stretch
goal is to increase time in splint and tolerance for increasing resistance for gaining ROM
modalities for abnormal tone
goal = change motor neuron excitability
cryotherapy
heat*
US*
NMES
dry needling
etc
what might you work on for spasticity management for a complex client
manage primitive reflexes
manage psoture deviations
LE extensor tone and magic hip angle
reduce destructive hip position
12-24 hour posture management
what is magic hip flexion angle
reduces extensor tone
flex both hips together to find this angle
needed in WC seating intervention
