Week 2 Flashcards
Primary neuromuscular impairments after CVA
- damage to descending cortical drive
- type 1 increase, type 2 decrease - loss of force production
- loss of motor units and asynchronous/abnormal motor unit firing
Secondary muscular impairments after CVA
- increased fatigue
- delayed reaction times
- prolonged movement times
- disuse muscular atrophy
- length-tension changes
A set of internal processes associated with feedback or practice leading to relatively permanent changes in the capability for motor skill
motor learning
The reappearance of motor patterns present prior to CNS injury performed in the same manner as prior to injury
motor recovery
Sequential Motor Recovery Stages Following Stroke
Stage 1 – flaccidity and no movement of limbs
Stage 2 – minimal voluntary movement responses and spasticity begins
Stage 3 – voluntary control of movement synergies and increased spasticity (can be severe)
Stage 4 – movement combos that don’t follow the paths of either synergy and spasticity begins to decline
Stage 5 – difficult movement combos are learned, and synergies lose their dominance
Stage 6 – disappearance of spasticity and individual joint movements are possible with coordination
Fugl-Meyer Assessment MDC and MCID
MDC - 5.4 UE and 5 LE
MCID - 10 UE/LE
Rivermead Motor Assessment MCID
3 points
dysmetria
inability to judge distance or ROM
Dyssynergia
fragmented movement patterns
- Movements occur in sequence of component parts rather than a single & coordinated smooth output
- jerkiness, have to break down complex movements to individual movements
Asynergia
loss of ability to associate muscles together for complex movements
Rebound phenomenon
inability to rapidly and sufficiently halt movement of a body part after a strong isometric force
Typical patterns of spasticity in scapula
retraction, downward rotation
Typical patterns of spasticity in shoulder
adduction and IR, depression
Typical patterns of spasticity in elbow
flexion
Typical patterns of spasticity in forearm
pronation
Typical patterns of spasticity in wrist
flexion, adduction
Typical patterns of spasticity in hand
finger flexion, clenched fist thumb, adducted in palm
Typical patterns of spasticity in pelvis
retraction (hip hiking)
Typical patterns of spasticity in hip
adduction, IR, Extension
Typical patterns of spasticity in Knee
flexion and extension
Typical patterns of spasticity in foot and ankle
PF, INversion, Equinovarus, toes claw, toes curl
Typical patterns of spasticity in hip and knee
flexion, sacral sitting
Typical patterns of spasticity in trunk
lateral flexion w/ concavity, rotation
Typical patterns of spasticity in posture forward (prolonged sitting posture)
excessive forward flexion and forward head
Acute endurance recommendations
< 11-12 RPE (3-4 mRPE)
Resting HR + 10-20bpm
walking, ADLs, standing activities
IP/Outpatient Rehab endurance recommendations
RPE 11–14 (3-5/6 mRPE)
40%–70% VO2 reserve or HR reserve; 55%–80% HRmax
20-60min/session, 3-5x/week
+adequate warm-up and cool-down
large muscle groups
General slowing of cognitive & motor processes
lethargy
Dulled or blunted sensitivity, difficult to arouse
obtundation
State of semi-consciousness, only arouses with intense stimulation
stupor
Unconsciousness
coma
What are the cutoff scores for the Glasgow Coma Scale (GCS) and what do they tell you?
scores 3-15
< 8 severe
9-12 moderate
13-15 mild
measures level of consciousness
R hemisphere lesion behavior
- difficulty perceiving emotions
- difficulty w/ expression of negative emotions
- irritability, confusion
- impulsive, quick movements
- poor judgement
- rigidity of thought
- poor insight/absent awareness of impairments
- high safety risk
L hemisphere lesion behavior
- difficulty w/ expression of positive emotions
- slow, anxious, cautious
- disorganized and distracted when attempting to complete a task
- compulsive behavior
- aware of impairments
- need extra coaxing to participate
- high safety risk
R hemisphere lesion perceptual deficits
- body scheme impairments - unilateral neglext, Pusher’s syndrome, anosognosia (unaware of condition/think they are fine), somatagnosia, R-L discrimination
- difficulties w/ spatial relationships - hand eye coordination, figure-ground, position in space
- agnosias - visual, auditory, sensory
L hemisphere lesion perceptual deficits
- apraxia - ideational and ideomotor
Where is the lesion for most patient’s with Pusher’s syndrome? Which side do they push to?
R hemisphere centered in area of posterolateral thalamus
- Tendency to push strongly towards the paretic side with nonaffected limbs
Additional symptoms w/ R hemispheric pusher’ syndrome
- left hemiplegia
- High association with left spatial and sensory neglect
Additional symptoms w/ L hemispheric pusher’ syndrome
- right hemiplegia
- high association w/ aphasia
clinical observations seen for vision post stroke
- head turn or tilt during tasks
- avoidance of near tasks
- One eye appears to go in, out, up, or down
- vision shifts from eye to eye as indicated by head tilting
- closes or covers one eye/squints (double vision)
- bumps into walls/objects when moving (field cut)
- misjudge distance
- difficulty finding things
What are common visual dysfunction presentations seen post stroke?
- refractive errors - near/farsightedness, astigmatism, blurry vision - CN 2 nuclei and associated CNS areas
- impaired accommodation - CN 2 and visual tract/visual cortex
- visual field loss - CN 2 and visual tract/visual cortex
- impaired pursuits and saccades - cerebellum
- diplopia - cerebellum
- ptosis - CN 2-6 and associated CNS areas
- ocular motility disturbance - CN 2-6 and associated CNS areas
blood supply for retina and extra-cranial optic nerve
ophthalmic artery
blood supply for intracranial optic nerve and optic chiasm
anterior cerebral
anterior comminicating
superior hypophyseal
blood supply for optic tract
posterior communicating and anterior choroidal arteries
blood supply for optic radiation
middle cerebral artery and posterior cerbral artery
blood supply for lateral geniculate nucleus
anterior and posterior choroidal arteries
What would VOR look like if stroke occurred in Pons?
- loss of abducens nucleus
When looking R, L eye doesn’t abduct
When looking L, R eye doesn’t abduct
What would VOR look like if stroke occurred in Midbrain?
- loss of oculomotor nucleus
When looking R, R eye wouldn’t adduct
When looking L, L eye wouldn’t adduct
What are different ways (in general) that sensory dysfunction can present post stroke?
cortical lesions - specific localized areas of dysfunction
thalamic lesions - diffuse involvement
Hypo/hyperesthesia
decreased/increased sensitivity to sensory stimuli
Paresthesia
abnormal sensation such as numbness, prickling, or tingling
Dysesthesia
touch sensation experienced as pain
allodynia
pain produced by non-noxious stimuls
analgesia
complete loss of pain sensitivity
hyperalgesia
increased sensitivity to pain
atopognosia
inability to localize sensation
What are the 3 most common predictors of falls for acute and subacute stroke survivors
- functional impairment
- cognitive deficits
- impaired balance
primary blood supply for primary visual cortex
posterior cerebral artery
What are the functional implications of hypotonia?
Reduced ability to resist pull of gravity Increased stress on joints Reduced postural control Clumsy or incoordinated movements Impaired balance Reduced power Increased fatiguability
What are the functional implications of spasticity?
- contractures
- skin breakdown
- pain
- abnormal posture
- abnormal movement patterns
- impaired balance
As a PT, when is it appropriate to advocate to the interdisciplinary team that your patient might be appropriate for anti-spasticity medical management?
- tone is interfering w/ function
- pain consideration
- presence of clonus/risk of skin breakdown
What are the post stroke strengthening recommendations put out by the AHA/ASA?
- 1-3 sets of 10-15 reps
- 8-10 exercises involving major muscle
- 50-80% of 1 rep max
- 2-3 days/week
- resistance gradually increased over time as tolerated
What stroke is pseudobulbar affect correlated with?
Correlated with inferior frontal and inferior parietal lobe damage (R or L)
Where might the lesion be if a patient has apraxia?
- premotor frontal cortex
- left inferior parietal lobe
- corpus collosum
What plays a significant role in a patient’s progression through the 6 stages of motor recovery?
- initial weakness
- presence of spasticity
- cognitive deficits
- access to rehab
potential exam findings for cerebellum CVA outside of ataxia, dysmetria, and balance
IPSILATERAL
- oculomotor deficits
- lack of check reflex
- mild hypotonia
- intentional tremor
- slurred speech
- significant difficulties w/ motor learning
potential exam findings for basal ganglia CVA outside of ataxia, dysmetria, and balance
CONTRALATERAL
- spasticity
- resting and intentional tremor
- difficulty initiating movements
- slowed/smaller movements
- considerable strength deficits
potential exam findings for dorsal column CVA outside of ataxia, dysmetria, and balance
CONTRALATERAL
- abnormal sensory exam - proprioception
- no tremor
What is most closely associated w/ depression post CVA?
fatigue - lack of physical and mental energy
What are indications for immediate cessation of exercise?
1 - lightheadedness
2 - dizziness
3 - chest heaviness, pain or tightness; angina
4 - heart palpitations or irregular heart beat
5 - sudden SOB not due to increased activity
6 - volitional fatigue and exhaustion