CVA impairments 1 (more motor) Flashcards
What is the difference between hemiparesis and hemiplegia?
Hemiparesis- mild to moderate weakness on contralateral side
Hemiplegia- severe to profound weakness on contralateral side, also termed “dense hemiplegia” (no active movement observed)
Why can ipsilateral weakness be seen in some strokes?
10-25% of CST descends ipsilaterally (ACST), mostly effects proximal muscles
What is the difference between primary weakness and secondary weakness?
Primary weakness is due to neuromuscular impairments directly related to the nervous system injury
ex include: damage to descending cortical drive, increased type 1 fibers, decreased type 2 fibers leads to slowing and loss of muscle force production, loss of motor units and asynchronous firing
Secondary weakness comes as a snowball effect of the primary weakness (musculoskeletal impairments)
ex: increased fatigue, decreased reaction times, prolonged movement times, disuse atrophy, length-tension changes
In what patterns is post-stroke weakness typically seen?
typically see weakness in a distal > proximal pattern
extensors > flexors
exception: DF > PF
ER > IR
Abductors > Adductors
evertors > invertors
In what situations can you see facial weakness?
-MCA stroke where face lies in homunculus
-Damage to corticobulbar tracts limiting descending drive to facial nerve
-Facial nuclei damage in brainstem
Only lower face will be weak, forehead will be spared due to bilateral innervation
What is motor control?
“The process of initiating, directing, and grading purposeful voluntary movement”
PLAN PROGRAM EXECUTE
Ability to regulate or direct mechanisms essential to movement
Creates movements that require minimal cognitive load
It is a very integrated process and is commonly involved after stroke
How would you define a motor control impairment?
Inability to produce precise and steady motor output with the paretic limb
Can be misinterpreted as primary weakness
common impairments : apraxia, abnormal synergies
What is an abnormal synergy? What are some typical components of these synergies?
A synergy is a failure in isolating joint movement
Brain accidentally groups muscles together
Typical pattern seen for UE flexor synergy?
UE flexor synergy: scapular retraction/elevation or hyperextension
shoulder abduction, external rotation
Elbow flexion
Forearm supination
Wrist and finger flexion
Typical pattern seen for UE extensor synergy?
Scapular protraction
Shoulder adduction, internal rotation
Elbow extension
Forearm pronation
Wrist and finger flexion
Typical pattern seen for LE flexor synergy?
Hip flexion, abduction, external rotation
Knee flexion
ankle dorsiflexion, inversion
toe DF
Typical pattern seen for LE extensor synergy?
Hip extension, adduction, internal rotation
Knee extension
ankle plantarflexion, inversion
toe PF
What is motor praxis?
ability to plan and execute coordinated movements
What is apraxia? What are the different types of apraxia?
Apraxia: Inability to plan and execute purposeful movements that cannot be accounted for by any other reason
Lesions:
Premotor frontal cortex (either side)
Left inferior parietal lobe
Corpus callosum
Ideomotor Apraxia
Inability to produce movement on command, but able to move automatically
Conceptualization of task remains intact
Ideational Apraxia
Inability to produce movement both on command or automatically
Complete breakdown of conceptualization of task
Go study stages of motor recovery
:)
What plays a major role in advancement through the stages of motor recovery?
Initial weakness, spasticity, cognitive deficits, and access to rehab
Why is it hard to use MMT to assess post-stroke patients? How can we assess if MMT is not indicated?
It is often difficult for post CVA patients to isolate certain movements that are required for MMT
Instead, we should examine and document strength through observation of functional movement
Have to explain more, documentation is usually more involved
(patient is able to demonstrate 50% of desired Active hip flexion during swing phase)
What is the fugl-meyer?
an outcome assessment that measures sensorimotor function: includes motor function, balance, sensory function, ROM, joint pain
Looking at patient’s impairments
great validity but pretty lengthy
What is the MDC and MCID for UE and LE portions of the fugl-meyer?
MDC UE: 5.4
MDC LE: 5
MCID UE: 10
MCID LE: 10
What is the RiverMead motor assessment?
performance based motor recovery assessment that has 3 sections
gross motor (bed transfers, mobility)
leg and trunk (rolling, bridging, standing)
Arm (shoulder protraction, reaching, grip,
considering how weakness or lack of control is affecting someone’s ability to move
if you get to item you can’t do, test is done
What are aerobic capacities like post CVA?
Patients after CVA are terribly deconditioned
-Increased energy requirements
-VO2 levels double with household chores
-Up to 3x normal VO2 levels with ambulation on level ground
This can lead to fatigue, mobility limitations, pain, emotional reactions, sleep disturbances, social isolation
They use more of their glass of milk for smaller, typically lower energy tasks
What are some contributors to reduced endurance in CVA?
-Baseline CV health
-Primary CVA impairments
-Post-stroke deconditioning
How does baseline cardiac dysfunction play a role in post-stroke reduced endurance?
Many patients have baseline cardiovascular dysfunction & reduced physical activity
Up to 80% have HTN
20-40% of patients have silent cardiac ischemia
↓ cardiac output, widespread atherosclerosis, cardiac decompensation, rhythmic disorders are common pre-morbid findings in the post-stroke population
↓ aerobic capacity Means patients are behind the gun before they even had a stroke
How do primary CVA impairments play a role in reduced endurance post stroke?
A multitude of stroke-related impairments increase energy expenditure with even simple, low-intensity tasks
Weakness
1o and 2o
Impaired motor control
Cognitive and perceptual deficits
Balance
Pain
Fatigue
Etc…
Why is deconditioning seen after stroke and what does it lead to?
Result of acute illness, bedrest, limited activity levels
Leads to further impairments across multiple systems, leading to reduction of mobility efficiency and effectiveness
Neurological:
Degradation of neural circuits due to loss of active engagement
Cardiovascular:
↓ cardiac output, HRmax
↑ resting and exercise BP
Pulmonary:
↓ lung volume, pulmonary perfusion and vital capacity, altered chest wall excursion
↓ Respiratory lung output accompanied by ↑ oxygen demands of new movement patterns worsened fatigue and endurance
Musculoskeletal:
↓ muscle mass, bone mass, flexibility
Behavioral:
Depression, anxiety, fear
What are some sub-maximal protocols for graded exercise testing following stroke, but prior to starting exercise?
Peak HR 120 bpm or 70% age-predicted HRmax
BP <250/115 mmHg
AHA and ASA recommend doing graded exercise testing with ekg monitoring prior to starting an exercise program.
What types of machines/exercises can be used post stroke?
Leg cycle ergometer, semi-recumbent cycle ergometer, UE/LE ergometer, treadmill walking, seated stepper
What should you do if you cannot do graded exercise testing post stroke?
If unable to do graded exercise testing:
Light-to-moderate exercise recommended while monitoring patient response
↑ training frequency, duration, or both to compensate for reduced intensity
Close monitoring of HR, BP
Borg Rate of Perceived Exertion (RPE) or modified version (pictured)
What outcome measures can be used for endurance?
-6 minute walk
-2-minute walk (acute CVA)
What is coordination?
The ability to use different parts of the body to move together smoothly and efficiently
What are some critical components of coordination?
Sequencing, grading, timing
What is incoordination?
Movements that are awkward, uneven, and inaccurate
Disruption of sequencing, grading, and timing
Found with motor cortex, basal ganglia, cerebellar lesions
Also tied to proprioceptive loss
What are some potential impairment findings during a coordination exam?
Dysdiadochokinesia: impaired ability to perform rapid alternating movements
Dysmetria: inability to judge distance or range of movement
Hypometria, Hypermetria
Dyssynergia: fragmented movement patterns
Movements occur in sequence of component parts rather than a single & coordinated smooth output
Asynergia: loss of ability to associate muscles together for complex movements
More severe form of dyssynergia
Rebound Phenomenon: inability to rapidly and sufficiently halt movement of a body part after a strong isometric force
Tremor: unintentional, oscillatory movement
Resting, Intentional
What is ataxia?
Uncoordinated movements that manifest when voluntary movements are attempted
Umbrella term, official word for incoordination
results in difficulty with fluidity, timing, accuracy, and speed of movements
How do we classify ataxia?
By the cause of it and the location (truncal, limb, gait)
What are some origins of impairments in coordination?
Cerebellar damage
basal ganglia damage
somatosensory deficit
specifically medial lemniscus pathways/structures
What examination findings would you see with cerebellar damage?
Ipsilateral damage:
-Trunk, limb, and/or gait ataxia
-Dysmetria, dysynergia, dysdiadochokinesia
-Balance deficits
-oculomotor deficits
-lack of check reflexes
-May see mild hypotonia
-Intentional tremor
-Slurred speech (dysarthria)
-Significant difficulties with motor learning
What examination findings would you see with basal ganglia damage?
Contralateral damage:
-Can see trunk, limb, or gait ataxia -Dysmetria, dysynergia, dysdiadochokinesia -Balance deficits -Spasticity (if non-CVA pathology, may see rigidity) -Resting and intentional tremor -difficulty initiating movements -Slowed movements, smaller movements -Considerable strength deficits
What examination findings would you see with dorsal column damage?
-Can see trunk, limb, or gait ataxia
-Dysmetria, dysynergia, dysdiadochokinesia
-Balance deficits
-Abnormal sensory exam (specific proprioception)
-Unlikely to see tremor
hard to have coordination if you don’t know where limb is in space
What are some common post-stroke impairments that can impact coordination?
Weakness
Motor control
Sensory loss
Cognition and communication deficits
Vision (diplopia)
very many things that can affect coordination that has nothing to do with coordination
What is tone?
Tone is characterized by a muscle’s resistance to passive stretch
some muscle tone is what we need
will see spasticity if Corticospinal tract involved
What is the typical progression of tone abnormalities following stroke?
Acute UMN injuries may show temporary hypotonia due to cerebral or spinal shock (CNS acutely shuts down to protect itself)
Then in the subacute phase> chronic UMN injuries : development of spasticity
How do we assess tone? What are the components of it?
Through the modified ashworth scale:
0: No increase in muscle tone
1: slight increase in muscle tone, manifested by a catch and release or by minimal resistance at the end of the range when affected parts are moved in flexion or extension
1+: Slight increase in muscle tone, manifested by a catch, followed by minimal resistance throughout the remainder (less than half of range of motion)
2: more marked increase in muscle tone throughout most of the ROM, but affected parts are easily moved
3: considerable increase in muscle tone, passive movement difficult
4: Affected part(s) rigid in flexion or extension
Go study slides 38-43 (different tables on cva impairments 1)
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