quiz 1: motor Flashcards
PT Diagnosis Vs. Medical Diagnosis
PT Diagnosis: effect of pathology on movement (L sided w R hemiplegia w gait balance)
medical diagnosis: look at pathology (L. sided ischemic stroke)
Why do a neuro eval?
- identify if disease process or impairment is impacting the nervous system
- localize the lesions: recognize patterns and deduce pathology
NAGI model of Disablement
Pathology –> Impairment –> Functional Limitations –> Disability
NAGI Model: Pathology -what is it -give 4 examples: Stroke TBI Parkinsons MS
underlying disease/defect occurs at the cellular level
1. Stroke: impaired blood supply to CNS bc thromboembolsim or bleeding – bld supply lost
- TBI: acute trauma to the brain - damage can be diffuse
- Parkinsons: specific damaged substantia nigra -tremor, rigidity
- MS: autoimmune CNS demyelination (lesions can be anywhere in nervous system)
NAGI Model: Impairment
- what is it
- give 5 examples:
Disruption of motor, sensory, or cognitive process
spasticity, sensory loss, bradykinesia, fatigue, thermosensitivity
NAGI Model: Functional Limitation
Limitation of performance at the level of the whole organism or person
inability to walk, balance, reach, stand, etc.
gait, balance, transfer, bed mobility, ADL, IADL
NAGI Model: Disability
decreased ability/inability to perform social roles
-unable to participate in society as did before
QOL
PT Exam for Impairment
sensory, motor, spasticity, ROM, etc
PT Exam for Functional Limitation
balance, transfers
PT Exam for Disability
QOL measures, self report measures
Lesion localization
- focal
- diffuse
- multifocal
- multifocal and diffuse
based on characteristics of lesion can assume location
- focal: in one spot (specific sx) [parkinsons]
- diffuse: many regions [MS]
- multifocal: many foci [alzheimers in various lobes]
- multifocal and diffuse: TBI (force through frontal lobe and forced to other side of the brain and diffuse in btwm)
coup countrecoup
coup injury is under site of impact
contrecoup is on side opposite impacted area
What makes up CNS
-what if lesion here?
brain, brainstem, spinal cord
lesion here is UMN lesion
What makes up PNS
-what if lesion here?
once nerve exits from the spinal cord
lesion here is LMN lesion
UMN Lesion
motor damage involved in CNS
LMN Lesion
motor damage involved in PNS
if clear that there is UMN damage, what do we know about the sensory system?
nothing, it is motor and not sensory
Dermatomal/Myotomal
if lesion in C1, everything that C1 mediates, motor and sensory, will be involved
myotomal–motor
dermatomal–sensory
C1 Myotomal LMN involvement
anything motorically innervated by C1 is involved
C1 Dermatomal LMN involvement
anything sensorically innervated by C1 will have sensory involvement
Peripheral Myotomal/dermatomal (c1)
only in the myatome or dermatome of that C1
CNS myotomal/dermatomal (c1)
it is not only that myotome or dermatome but everything below that level if it is in the cord itself
Non-myotomal/non-dermatomal
above the cord stroke: it is not a myatome or dermatome pattern but instead it is a diffuse weakness because it is above the cord.
lesion localization:
- CNS
- PNS
CNS: cortical, subcortical, cerebellar, basal ganglia, spinal cord
PNS: anterior horn cell, nerve root, plexus, in peripheral nerve itself
Validity vs Reliability
validity: does test measure what it claims to measure
reliability: repeatable: inter-rater reliability, intra-rater reliability
berg balance scale
test of falls (not of balance) 56= low risk of falls
<42 high risk of falls
Specificity vs Sensitivity
specificity: able to pick up various signs and sx of pathology
Sensitivity - able to rule out other pathologies
motor exam to test?
muscle strength (force output), motor function (tasks), motor control (nervous system with muscle relationship) - motor force and timing
locate the lesion
examine for symmetry, hypertrophy Psuedohypertrophy in duchennes), atrophy
what is muscle tone
normal resting state of muscle, normal tension of muscle, created by ongoing activities of Motor Unit recruitment
Types of Decreased/Increased Tone
Decreased: hypotonia, flaccidity
Increased: hypertonia, spasticity, rigidity
Spasticity
velocity dependent reaction to stretch
- increased “gain” of the stretch reflex
- hallmark of the UMN syndrome
- hyperactive reflex to stretch
- must be CNS (motoric involvement) [not PNS]
MAS 0 1 1+ 2 3 4
Modified Ashworth Scale
0: no increase in tone
1: slightly increased tone/ catch and release/ min resistance at end of ROM
1+: slightly increased tone/ a catch/ minimal resistance throughout the remainder of ROM (less than 1/2)
2: More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved
3: Considerable increase in muscle tone, passive movement difficult
4: Affected part(s) rigid in flexion or extension
exertional spasticity
increased spasticity with exertion
provocative testing
to see if spasticity under any conditions - spasticity is never normal (if a pt with CNS involvement does not show spasticity then rev them up to see what fatigue will do)
Rigidity
- cogwheel
- led pipe
rigidity: non velocity dependent rxn to stretch
- cogwheel: successive catches and releases (parkinsons)
-lead pipe: stiff and not flexible that remains uniform throughout the range of passive movement (alzheimers)
T or F: Spasticity indicates CNS involvement
T
T or F: CNS involvement indicates spasticity
F
flaccidity
minimal or absent muscle tone
minimal or absent muscle contractions to command or reflex
absent or diminished stretch reflex
—-if do a quick stretch no resistance will be felt
What are the causes of flaccidity?
- Normal
- LMN lesion
- muscle damage
- component of spinal or cortical shock
Can flaccidity be due to CNS involvement?
flaccidity can be do to CNS involvement = cortical spinal shock (stroke, SCI)
nervous system shuts down and get flaccidity below the level of the lesion for hours to months
rehab: work on rom dont let a contracture on involved side
Diaschisis
shock
- can be cortical or spinal (following cortical spinal injury)
- period of flaccidity immediately following lesion, can last hours to months
- unable to prognose until shock is resolved
Upper Motor Neuron Syndrome-dx
TRIAD of symptoms following CNS lesions comprised of
- spasticity
- hyperreflexia
- pathological reflexes (clonus, babinksi)
Upper motor neuron syndrome (UMNS) is the motor control changes that can occur in skeletal muscle after an upper motor neuron lesion.
Lower Motor Neuron Syndrome
- flaccidity
- hyporeflexia/arreflexia
- occasional fasiculations (muscle twitch)
AROM Test
(see notes)
Spasticity Eval
prom slowly to assess range limits then do quickly
may need to provacative testing by repeating
Deep Tendon Reflex
- –monosynaptic stretch reflex
- –stimulus quick stretch of tendon with reflex hammer
- -response: muscle contraction: visible motion with palpable or observational contraction
DTR Technique
- locate and expose tendon
- tendon should be on relative stretch
- strike sharply with hammer at a 90 degree angle to the tendon
- use Jendrassik manouvre to reinforce (interlock fingers)
- alternate: strike muscle belly
C5
biceps (musculocutaneous)
C6
brachiradialis (radial)
C7
triceps (radial)
L3, L4
Quadriceps (femoral)
S1,S2
achilles tendon (tibial)
DTR Grades 0 1+ 2+ 3+ 4+ 5+
which have clonus?
0-ABSENT-no visible contraction
1+ hyporeflexia: slight contraction, need reinfocement
2+ normal slight muscle contraction w/ jt movement
3+ hyperreflexia: brisk contraction with mod jt movement
4+ abnormal hyperreflexia: strong contraction w/ 1-3 beats of clonus
5+ abnormal hyperreflexia: sustained clonus
UMN
CVA TBI SCI MS CP Brain Tumor ALS
but not in parkinsons, no spasticity in parkinsons, have rigidity
Babinski
what indicates UMN?
what indicates LMN?
plantar response
blunt probe down across sole of foot from heel to toe
- negative: toe flexion an adduction, angle plantarflexion
- positive sign: toes fan an extend, ankle dorsiflexion - indicates UMN
- equivocal response: toes go up and down
- no response: LMN lesion
- triple flexion response: ankle dorsiflexion, knee flexion, hip flexion (so flexion x 3)
Clonus
what indicates UMN?
what indicates LMN?
rhythmic beating of jt in response to sustained stretch-bring ankle from plantarflexion to full dorsiflexion and hold at end range.
normal: 1-1.5 beats
abnormal: 2-5 beats or sustained more than 5 beats (UMN)
absent: LMN or normal and just toned
MAS 0
0: no increase in tone
MAS 1
1: slightly increased tone/ catch and release/ min resistance at end of ROM
MAS 1+
1+: slightly increased tone/ a catch/ minimal resistance throughout the remainder of ROM (less than 1/2)
MAS 2
2: More marked increase in muscle tone through most of the ROM, but affected part(s) easily moved
MAS 3
3: Considerable increase in muscle tone, passive movement difficult
MAS 4
4: Affected part(s) rigid in flexion or extension
DTR 0
0-ABSENT-no visible contraction
DTR 1+
1+ hyporeflexia: slight contraction, need reinfocement
DTR 2+
2+ normal slight muscle contraction w/ jt movement
DTR 3+
3+ hyperreflexia: brisk contraction with mod jt movement
DTR 4+
4+ abnormal hyperreflexia: strong contraction w/ 1-3 beats of clonus
