CVA impairments 1 (more motor)

Question 1

What is the difference between hemiparesis and hemiplegia?

Answer 1

Hemiparesis- mild to moderate weakness on contralateral side

Hemiplegia- severe to profound weakness on contralateral side, also termed “dense hemiplegia” (no active movement observed)

Question 2

Why can ipsilateral weakness be seen in some strokes?

Answer 2

10-25% of CST descends ipsilaterally (ACST), mostly effects proximal muscles

Question 3

What is the difference between primary weakness and secondary weakness?

Answer 3

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

Question 4

In what patterns is post-stroke weakness typically seen?

Answer 4

typically see weakness in a distal > proximal pattern

extensors > flexors
exception: DF > PF

ER > IR

Abductors > Adductors

evertors > invertors

Question 5

In what situations can you see facial weakness?

Answer 5

-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

Question 6

What is motor control?

Answer 6

“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

Question 7

How would you define a motor control impairment?

Answer 7

Inability to produce precise and steady motor output with the paretic limb
Can be misinterpreted as primary weakness

common impairments : apraxia, abnormal synergies

Question 8

What is an abnormal synergy? What are some typical components of these synergies?

Answer 8

A synergy is a failure in isolating joint movement
Brain accidentally groups muscles together

Question 9

Typical pattern seen for UE flexor synergy?

Answer 9

UE flexor synergy: scapular retraction/elevation or hyperextension
shoulder abduction, external rotation
Elbow flexion
Forearm supination
Wrist and finger flexion

Question 10

Typical pattern seen for UE extensor synergy?

Answer 10

Scapular protraction
Shoulder adduction, internal rotation
Elbow extension
Forearm pronation
Wrist and finger flexion

Question 11

Typical pattern seen for LE flexor synergy?

Answer 11

Hip flexion, abduction, external rotation
Knee flexion
ankle dorsiflexion, inversion
toe DF

Question 12

Typical pattern seen for LE extensor synergy?

Answer 12

Hip extension, adduction, internal rotation
Knee extension
ankle plantarflexion, inversion
toe PF

Question 13

What is motor praxis?

Answer 13

ability to plan and execute coordinated movements

Question 14

What is apraxia? What are the different types of apraxia?

Answer 14

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

Question 15

Go study stages of motor recovery

Answer 15

:)

Question 16

What plays a major role in advancement through the stages of motor recovery?

Answer 16

Initial weakness, spasticity, cognitive deficits, and access to rehab

Question 17

Why is it hard to use MMT to assess post-stroke patients? How can we assess if MMT is not indicated?

Answer 17

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)

Question 18

What is the fugl-meyer?

Answer 18

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

Question 19

What is the MDC and MCID for UE and LE portions of the fugl-meyer?

Answer 19

MDC UE: 5.4
MDC LE: 5

MCID UE: 10
MCID LE: 10

Question 20

What is the RiverMead motor assessment?

Answer 20

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

Question 21

What are aerobic capacities like post CVA?

Answer 21

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

Question 22

What are some contributors to reduced endurance in CVA?

Answer 22

-Baseline CV health
-Primary CVA impairments
-Post-stroke deconditioning

Question 23

How does baseline cardiac dysfunction play a role in post-stroke reduced endurance?

Answer 23

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

Question 24

How do primary CVA impairments play a role in reduced endurance post stroke?

Answer 24

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…

Question 25

Why is deconditioning seen after stroke and what does it lead to?

Answer 25

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

Question 26

What are some sub-maximal protocols for graded exercise testing following stroke, but prior to starting exercise?

Answer 26

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.

Question 27

What types of machines/exercises can be used post stroke?

Answer 27

Leg cycle ergometer, semi-recumbent cycle ergometer, UE/LE ergometer, treadmill walking, seated stepper

Question 28

What should you do if you cannot do graded exercise testing post stroke?

Answer 28

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)

Question 29

What outcome measures can be used for endurance?

Answer 29

-6 minute walk
-2-minute walk (acute CVA)

Question 30

What is coordination?

Answer 30

The ability to use different parts of the body to move together smoothly and efficiently

Question 31

What are some critical components of coordination?

Answer 31

Sequencing, grading, timing

Question 32

What is incoordination?

Answer 32

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

Question 33

What are some potential impairment findings during a coordination exam?

Answer 33

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

Question 34

What is ataxia?

Answer 34

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

Question 35

How do we classify ataxia?

Answer 35

By the cause of it and the location (truncal, limb, gait)

Question 36

What are some origins of impairments in coordination?

Answer 36

Cerebellar damage

basal ganglia damage

somatosensory deficit
specifically medial lemniscus pathways/structures

Question 37

What examination findings would you see with cerebellar damage?

Answer 37

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

Question 38

What examination findings would you see with basal ganglia damage?

Answer 38

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

Question 39

What examination findings would you see with dorsal column damage?

Answer 39

-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

Question 40

What are some common post-stroke impairments that can impact coordination?

Answer 40

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

Question 41

What is tone?

Answer 41

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

Question 42

What is the typical progression of tone abnormalities following stroke?

Answer 42

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

Question 43

How do we assess tone? What are the components of it?

Answer 43

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

Question 44

Go study slides 38-43 (different tables on cva impairments 1)

Answer 44

:)