Adult Neuro Rehab Exam 1

Front 1

Stroke is the __ most common cause of death in the US

Back 1

3rd

Front 2

Modifiable risk factors of stroke:

Back 2

Hypertension
Smoking
Obesity
Elevated serum fibrinogen levels
Diabetes
Sedentary lifestyle
Contraceptives w/ high levels of estrogen
Systolic hypertension
Cardiac disease
Atrial fibrillation
Alcohol abuse

Front 3

Non-modifiable risk factors for stroke:

Back 3

Age (esp. past 75)
Gender (higher in males)
Race (higher for African-Americans and Hispanics)
Heredity

Front 4

Types of stroke:

Back 4

ischemic stroke (88%)
Hemorrhagic strokes (12%

Front 5

Types of ischemic stroke:

Back 5

TIAs (transient ischemic attacks)
Thrombosis
Embolism
Lacunar stroke

Front 6

Types of hemorrhagic strokes

Back 6

Hypertensive
Aneurysm

Front 7

Causes of ischemic stroke:

Back 7

Arterial supply to the brain is blocked.
Caused by narrowing of arteries- atherosclerosis or cholesterol deposition.
Atherosclerosis can lead to thrombotic or embolic strokes.
Caused by blood clots moving from the heart. Often as a result of irregular heart beat (a-fib), heart attack, or abnormalities of heart valves.

Front 8

Hemorrhagic stroke-

Back 8

bleeding from an artery into the brain causing damage to where the blood goes.

Front 9

TIAs-

Back 9

Not really strokes, but precursors of stroke.
Brief, focal loss of function.
Full recovery w/in 24 hours.
Probably due to ischemia.

Front 10

If TIAs are caused by plaques, treatment:

Back 10

include endarterectomy or angioplasty to surgically stop progression.

Front 11

Conservative approaches to treatment of TIAs:

Back 11

monitor blood pressure, blood flow, diet, and exercise.

Front 12

Immediately following stroke comes a medical management period in which health care professionals attempt to:

Back 12

Stop progression of the lesion
Reduce cerebral edema
Decrease risk of hydrocephalus
Treat seizures
Reduce secondary complications

Front 13

Thrombosis causes __% of strokes

Back 13

50

Front 14

Thrombosis develops in...

Back 14

minutes, hours, or days.

Front 15

Thrombosis occurs frequently at...

Back 15

places where arteries branch and where plaques may have narrowed the arteries for years.

Front 16

__% of thrombotic strokes occur during sleep.

Back 16

60

Front 17

People who develop thrombosis often also have:

Back 17

hypertension, diabetes, or vascular disease elswhere

Front 18

Transitional area-

Back 18

Around the area of anoxia, this area has decreased blood flow. Effects here are reversible.

Front 19

Thrombotic and embolic infarctions comprise __% of all strokes.

Back 19

80

Front 20

Signs of stroke:

Back 20

can you raise arms, problems with balance, slurred speach, tongue deviation.

Front 21

Treatment of thrombosis

Back 21

Medication- thrombolytic therapy (urokinase, streptokinase and t-PA) must be given within 6 hours. 90-180 minutes is optimal. Most patients wait 24 hours.

Front 22

If stroke is hemorrhagic, thrombolytics will...

Back 22

often kill them.

Front 23

Anti-coagulant drug uses:

Back 23

may stop strokes in evolution and TIAs.

Front 24

Anti-coagulant drugs include:

Back 24

heparin, warfarin (coumadin), and antiplatelet drugs.
Careful patients don't have an injury when on these drugs b/c it's difficult to stop bleeding.

Front 25

Embolic stroke is the cause of __% of strokes.

Back 25

38

Front 26

Where does an embolus come from?

Back 26

the heart or plaques from any artery.

Front 27

What artery is most involved in embolic stroke?

Back 27

middle cerebral

Front 28

How fast do embolic strokes occur?

Back 28

Rapidly, within seconds or minutes, and without warning. No opportunity for collateral blood supply to develop.
These are more severe strokes.

Front 29

What types of medication may be used for embolic strokes?

Back 29

thrombolytics

Front 30

Focus of primary and secondary treatment of embolic strokes focus on:

Back 30

prevention. Includes anticoagulant therapy for people with heart disease or other conditions causing blood clots.

Front 31

Secondary prevention of embolic strokes include:

Back 31

preventive care after stroke including diet, exercise, and healthy lifestyle.

Front 32

Lacunar strokes-

Back 32

ischemic strokes that occur in smaller arteries in the brain

Front 33

Lacunar strokes occur:

Back 33

occur in smaller penetrating "end" arteries.
Patients make remarkable recoveries.
Frequently occur in people w/ multiple medical diagnoses involving the circulatory system.

Front 34

Completed stroke-

Back 34

deficits persist more than 1 day. Deficits are stable; nothing's changing.

Front 35

Progressive or extending stroke-

Back 35

Ischemic stroke w/ deficits that increase over time b/c of repeated emboli or developing thrombus.

Front 36

Hemorrhagic strokes are caused by...

Back 36

AV malformations or weakness of arterial walls, aneurysms, or head injuries.

Front 37

In hemorrhagic strokes, bleeding in the brain...

Back 37

produces an oval shaped clot that resolves slowly. No longer room for brain.

Front 38

Treatment for hemorrhagic stroke:

Back 38

lowering arterial blood pressure to prevent further bleeding, and surgery to remove the clot and decrease intracranial pressure. May also include bleeding into subarachnoid space.

Front 39

Aneurysm

Back 39

Break bleeding into the brain

Front 40

Which arteries may be involved in stroke?

Back 40

Middle cerebral (A of stroke)
Anterior cerebral
Posterior cerebral

Front 41

Middle cerebral A:

Back 41

80% of strokes.
Contralateral pralysis of upper extremity.
Contralateral sensory loss of upper extremity
(legs less involved)
Hemianopia
Limb-kinetic apraxia (most commonly in L hemisphere.

Front 42

Dominant hemisphere middle cerebral A strokes cause

Back 42

Speech deficit (L side of brain)

Front 43

Non-dominant hemisphere strokes cause:

Back 43

hemi-neglect, unawareness of distance and midline. (R side of brain)

Front 44

Anterior cerebral A strokes cause:

Back 44

(10% of strokes)
Contralateral paralysis (lower more than upper)
Contralateral sensory loss (lower more than upper)
Grasp reflex, sucking reflex
Lack of spontaneous behavior, motor inattention, perseveration, and amnesia.

Front 45

Posterior cerebral A strokes cause:

Back 45

(7% of all)
Cortical blindness of contralateral visual field (can see, but can't process)
Memory deficit
Ataxia
Contralateral hemiparesis (usually due to cerebellar damage)
Involvement of thalamus can result in contralateral sensory loss.

Front 46

Why is blood flow so important?

Back 46

Brain doesn't store oxygen or glucose effectively.
Oxygen consumption increases from the brain stem to the cortex.

Front 47

Why can such a small infarct cause so much damage?

Back 47

Depends on location.

Front 48

Predictors of recovery from stroke:

Back 48

Return of arm movment in first 2 weeks- possibility of arm recovery.
No grip recovery at 24 days correlates with no arm function at 3 months.

Front 49

Spontaneous stroke recovery-

Back 49

Recovery in the majority of stroke patients occurred within the 1st six months.

Front 50

Severity of initial deficit is __ proportional to the prognosis for recovery.

Back 50

Inversely

Front 51

What is responsible for spontaneous stroke recovery (SSR)?

Back 51

1. Functional or adaptive recovery
2. Recovery of post-stroke edema
3. Reperfusion of ischemia
4. Diaschisis
5. CNS reorganization

Front 52

Functional or adaptive recovery-

Back 52

Recovery defined as neurological or functional.

Front 53

Functional recovery-

Back 53

a result of clients learning to do previously learned tasks and becoming independent in areas like self-care, mobility, independent living, social, and vocational skills. Inversely proportional to the degree of damage from the stroke.

Front 54

Recovery of post-stroke edema-

Back 54

Up to 8 weeks.
Secondary edema disrupts neuronal functioning.
Although hemorrhages tend to be associated w/ more damage from edema, recovery is often more dramatic as well.

Front 55

An ischemia insult consists of:

Back 55

An area of infarct (which doesn't resolve) surrounded by an area of moderate blood flow (ischemic penumbra). This area is at risk for ischemia but is still salvageable.

Front 56

Reperfusion-

Back 56

Through drug therapy and time, can allow non-functioning neurons to resume function.

Front 57

Diaschisis-

Back 57

A state of low reactivity that occurs after injury to the brain in areas of the brain previously stimulated by this portion of the brain that is where neuronal connections lie. Recovery of reactivity in these more distal portions of the brain occur after stroke.

Front 58

What occurs during CNS reorganization?

Back 58

synaptogenesis, which may include strengthening current synapses.
Reflection of the demands that we place on our patients. Alter demands by altering task and environment.

Front 59

How is synaptogenesis enhanced?

Back 59

motor learning- practice of new and learned skills.

Front 60

Re-acquiring motor skills requires changes to:

Back 60

undamaged portions of the involved cortex, as well as to the undamaged cortex.

Front 61

Clinical trials support reorganization through:

Back 61

CIT/forced use
Supported body weight treadmill training
Recumbent biking
Extensive early HEP
E-stim
LE weight bearing in a biomechanically correct position.
Avoiding secondary complications.

Front 62

Stroke implications: initial impairments-

Back 62

Motor, sensory, perceptual, cognitive, and communication

Front 63

Stroke implications: secondary impairments/conditions

Back 63

Muscle shortening, contractures, pain, subluxation, DVTs, edema, seizures, bowel and bladder dysfunction, sexual dysfunction, dysphagia, depression, etc.

Front 64

Stroke implications: functional outcomes

Back 64

Performance of day-to-day activities including participation in leisure and vocation, and the psychological and social impact on the person and their families. Not just self care!

Front 65

The first step in establishing hypotheses about the impairments and subsequent dysfunction associated w/ stroke is...

Back 65

understanding cortical function

Front 66

Cerebral cortex is composed of what lobes?

Back 66

frontal, parietal, temporal, occipital

Front 67

What are the functions of the frontal lobe?

Back 67

Motor- Primary motor area, Pre-motor area, Motor association area

Executive cognitive skills- judgment and reasoning

Personality- emotions- Motivation and inhibition/social skills.

Expressive speech- difficulty expressing themselves- expressive aphagia

Front 68

What are the functions of the parietal lobe?

Back 68

Primary sensory areas- receives and processes the sensation of touch

Sensory association areas- analyzes combined info from all senses.

Where you are in space, where you are in relationship to one another.

Front 69

L brain functions of parietal lobe

Back 69

R/L discrimination
Praxis- establishing motor plans

Front 70

R brain functions of parietal lobe

Back 70

Visuospatial orientation- background vs. foreground, distance, height perception, etc.

Front 71

Functions of the temporal lobe?

Back 71

Auditory sensation and memory- the what system

Front 72

L brain functions of the temporal lobe

Back 72

language (receptive aphagia- problems hearing, speaking)
Interpretation

Front 73

R brain functions of the temporal lobe

Back 73

Sounds, rhythm, and music
Visual performance
Affective expression

Front 74

Functions of the occipital lobe

Back 74

synthesis and integration of visual info
Visual memory
Formation of visuospatial relationships.
Visual reception

Front 75

R brain occipital lobe attends to what visual field(s)?

Back 75

L and R

Front 76

L brain occipital lobe attends to what visual field(s)?

Back 76

R only

Front 77

Why does L hemineglect occur?

Back 77

the L side of the temporal occipital lobe only attends to the R visual field so when there is R brain damage, you often lose the L visual field.

Front 78

People w/ ___ hemisphere strokes have more primary deficits that create greater dysfunction and have poorer functional outcomes than people w/ ___ hemisphere damage. Why?

Back 78

R; L; Language, lose a lot more, lose ability to know where you are in space, which affects ability to move in space, etc.

Front 79

L brain dysfunction causes:

Back 79

R hemiparesis
R sensory loss
Aphasia w/ decreased reading and writing
Apraxia/motor planning
L/R confusion
Compulsiveness
Slowness
Depression

Front 80

R brain dysfunction causes:

Back 80

L hemiparesis
L sensory loss
Visuospatial impairment
Poor body scheme
Poor attention
Neglect syndrome
Memory probs for procedures
Time disorientation
Problem solving
Poor awareness
Impulsiveness/safety
Concrete thinking
Emotional lability

Front 81

Steps in clinical decision-making for stroke assessment:

Back 81

1. Initial data collection- Chart review: lesion site, severity, course of stroke and management to date.

2. Acquire info about patient's pre-morbid performance of roles w/in context. Patient and family interview; establish goals

3. Skilled observation of task performance

4. Establish the hypothesis or relationship between performance of tasks and impairments.

5. Determine what additional info you need from others, from specific tests and measures of standardized tests of task performance and/or impairments.

Front 82

Purpose of top down approach to assessment:

Back 82

Determine roles, environemnts and tasks that have meaning.

Prioritize the roles/tasks by their importance to the person

Establish present competency in role/tasks through skilled observation

Observation of functino can help determine underlying impairments/reasons the person cannont perform tasks and provide connection to function.

Front 83

Advantages of top down approach:

Back 83

Streamlines eval

Helps to focus on specific problems

Focuses on how intervention will impact the disability and functional limits

Insures functional outcome

Front 84

Advantages and limits of bottom up approach:

Back 84

Helpful for new therapist for refining observation skills.
Costly
Context
Must infer meaning of impairment to functional limitations and disabilities.

Front 85

When should you use tests of impairments?

Back 85

When they will help you differentiate what the underlying impairments are that are causing functional loss. If it makes a difference to your intervention.

Front 86

Acute care rehab goals are...

Back 86

secondary to medical stability and are short-term and in readiness for more extensive rehab; usually restorative/remedial intervention

Front 87

Acute care detailed evaluation is...

Back 87

rare b/c of time limits and risky resulting in errors in d/c recommendations

Front 88

Acute care assessment should include...

Back 88

should include observation of motor impairment, cognition and language, balance, visual perception and executive function

Front 89

NIH stroke scale is used for...

Back 89

prediction

Front 90

Long term acute care (LTAC) for people w/ strokes when:

Back 90

Continued medically unstable require more than 100 days care which is more than available for SNF. Either medically induced coma or ventilator dependent.

Front 91

Assessment in LTAC

Back 91

Much like acute care w/ emphasis on observation

Front 92

Goals in LTAC

Back 92

Prevent physical and mental deterioration as person becomes medically stable.

Limited rehab goals; ROM, positioning, basic ADLs

Front 93

SNF, TCU (transitional care unit), ECU (extended care unit)

Back 93

100 day extension of hospitalization (Med A SNF).
Cannot withstand rigors of IP rehab.

Front 94

SNF, TCU, ECU goals

Back 94

either to go on to IP or to home w/ continued therapy

Front 95

SNF, TCU, ECU assessment

Back 95

comprehensive to understand all aspects of performance

Front 96

Stroke assessments for SNF include:

Back 96

Minimum data set
Cognitive screening
Functional limitation assessments
ADL assessments

Front 97

Minimum data set-

Back 97

required initial assessment at the time of admission

Front 98

Cognitive screening-

Back 98

Motor learning requires capacity for learning
Mental status exam

Front 99

IP rehab for people w/ strokes include those who are..

Back 99

medically stable and ready for intensive therapy (Med B)

3 hours of therapy daily w/ goal of highest level of performance necessary to go home.

Front 100

IP assessment :

Back 100

Understand all aspects of the person's ability to perform ADLS/IADLS and the impact of stroke on person's wants and needs to resume previous roles.

Preparation to return home and participating in community.

Front 101

Stroke assessments for IP:

Back 101

IRF-PAI at time of admission
FIM (functional independence measure)

Front 102

FIM

Back 102

scaled items from 1-7 in over 6 areas.
Widely used for program evaluation and an individual outcome tool.
Self-care and mobility
Predict caregiver burden

Front 103

Home health for people w/ strokes

Back 103

Next step toward community reintegration
Progress expected to continue w/ assistance of family.
Assessments center around tasks in environment and modification.
Caregiver's role is one of the significant parts of intervention.

Front 104

Stroke assessments for home health

Back 104

OASIS- initial assessment

Stroke Specific QOL scales (SS-QOL)

Other measures that provide quantifiable understanding of the impact of the stroke on person including disability measures.

Front 105

OP for people w/ stroke

Back 105

1860 cap
Maximum independence in all aspects of life- community reentry

Front 106

Assessment in OP

Back 106

Comprehensive assessments centered on activities, responsibilities, and roles- COPM to est goals

Front 107

Analyzing tasks to improve performance in OP includes:

Back 107

Assisting caregiver- functional outcome measures
Work
Community based tasks
Driving

Front 108

COPM-

Back 108

Clients ID things they need and want to do in areas of self care, productivity, and leisure.

Rate importance of the things they want to do on scale of 1-10

Determines a performance over satisfaction measure determined at admission and d/c

Front 109

Generally speaking, as the person becomes less acute and the person is coming to the end of rehab from acute hospitalization to home halth, selection of assessments and intervention should be:

Back 109

top down and disability/compensatory based

Front 110

What are the 3 scenarios when planning intervention?

Back 110

1. Remediate/correct impairments that may correct the disability or functional limitation- restorative/remedial intervention design
2. Remediate/correct the disability or functional limitation itself by using existing streangths- can be restorative and compensatory
3. Compensator/adaptive approach- using alternative methods to overcome the disability or functional limitation

Front 111

UE impairments after stroke:

Back 111

Pain
Contractures
Superimposed ortho conditions
Learned non-use
Loss of biomechanical alignment
Weakness
Tone

Front 112

What UE impairments cause:

Back 112

Inability to WB during ADLs and mobility.
Inability to move objects across a surface or from one surface to another using grasp.
Inability to reach and manipulate, including poor arm trajectory between point A and B and shaping of the hand for coordinated tasks.

Front 113

Who will recover arm function?

Back 113

Grades 3 or above on active finger extension scale on day seven after stroke predicts good recovery.
Presence of an initial shoulder shrug 11 days after predicted good hand movement and function 1-3 months after.
Shoulder abduction at 11 days predicted good hand movement at 1 month.
Synergistic hand movement 11 days predicted good hand function after 1-3 months.
AROM shoulder flexion and middle finger flexion after 3 weeks.

Front 114

What does it take to move the arm to drink from a water bottle?

Back 114

Visually locate object- eye-hand coordination to see and calculate distances involved.
Must have adequate reach and grasp.
Must manipulate object- form grip, grasp, and release.
Sufficient cognition to generate a plan, execute plan, maintain intention throughout plan.

Front 115

Assessing visual regard:

Back 115

1. Can patient locate and maintain eye gaze on a fixed or moving target in the central or peripheral field. (Eyes move, head still)
2. Can the patient locate then stabilize on a target in the far periphery (eyes on target while head moves)
3. Eye-head-trunk movements to find objects in far periphery.
4. Does patient complain of blurriness, dizziness, double vision?

Front 116

People w/ stroke may have what problems w/ visual regard?

Back 116

A visual field cut
Visual neglect
Breaking visual fixation- lack of flexibility/adaptability to change
Slowed reaction time

Front 117

UE m weakness is a problem that starts...

Back 117

proximally

Front 118

GH dysfuction following stroke... The Shoulder Rules:

Back 118

Position of thoracic spine
Position of scapula on thorax
Function of rotator cuff

Front 119

Typical thoracic spine position of patients:

Back 119

Thoracic flexion w/ lateral flexion toward weak side.

Front 120

What contributes to thoracic spine position in patients?

Back 120

Weak pelvis acted on by gravity causing PPT.
Lumbar flexion may be as mild as WB behind ischial tuberosities.
W/ poor pelvic stability, thoracic flexion occurs causing elongation in back extensors and shortening of rectus abdominis.

Front 121

MM that become shortened w/ overall kyphosis and side bending:

Back 121

rectus abdominis, obliques.
IO tends to become tight so they rotate down toward the side and have lateral flexion

Front 122

MM that become elongated and weak w/ spinal flexion and lateral flexion

Back 122

Lat dorsi
Glut max
Back extensors

Front 123

If lose visual regard, will you regain arm function?

Back 123

no

Front 124

B/c the thoracic spine is in a position of kyphosis and side bending toward the involved side, the scapula...

Back 124

follows the curve of the thorax.
Exacerbated by weight of the arm causes scapular downward rotation.

Front 125

Weakness in serratus anterior causes the scapula to...

Back 125

wing and tip.

Front 126

B/c thoracic spine and serratus weakness...

Back 126

glenoid tips down and places humerus at risk for s/l

Front 127

Downward scapular rotation (w/ winging and tipping) causes...

Back 127

Disorientation of glenoid fossa. Instead of facing up, out, and forward at about a 60 degree angle, it faces downward resulting in decreased static stability.

Front 128

What becomes stretched and weak w/ downwardly rotated scapula and what does it cause?

Back 128

SA and LT leading to problems initiating upward rotation.

Front 129

What becomes short w/ downwardly rotated scapula and what does it cause?

Back 129

Levator scapulae and rhomboids; shortening leads to further elevation and downward rotation

Front 130

transcurrir

Back 130

to pass away

Front 131

Loss of compressive muscle force that compresses head of humerus into glenoid is caused by loss of...

Back 131

whole cuff

Front 132

Inability to initiate abduction caused by loss of...

Back 132

supraspinatus

Front 133

Inability to glide humerual head downward caused by loss of...

Back 133

infraspinatus, teres minor, subscapularis.

Front 134

Inability to ER the humerus to avoid impingement caused by loss of...

Back 134

infraspinatus and teres minor

Front 135

General arm weakness w/ loss of cuff strength can cause:

Back 135

Inferior s/l- initially held together by capsule and ligaments until they become stretched.
Lead person to position arm in protective position of IR stretching IT mm. Pecs, teres major and lats get tight.
Further stretching of cuff.
Initiation of GH movement w/ deltoid which causes impingement.

Front 136

How do you measure inferior s/l?

Back 136

1-3 finger measure of s/l

Front 137

What becomes impinged w/ improper GH joint mechanics (roll up and glide up by delt)?

Back 137

Supraspinatus tendon
Long head of biceps
Subacromial bursa

Front 138

What position are the thorax and scapula in patients w/ anterior s/l?

Back 138

same, but have been positioned in or prefer extension of the GH joint (elbow behind acromion).

Front 139

Positioning in GH extension causes...

Back 139

anterior sheer on anterior portion of GH joint. The proximal portion of humerus begins to s/l anteriorly.

Front 140

Anterior s/l places pressure on what muscle?

Back 140

Short head of biceps causing bicipital tendinitis.

Front 141

Patients w/ stroke will often have lots of tone in biceps and be in what position, causing what condition?

Back 141

flexion and supination w/ short head of biceps tendinitis

Front 142

Superior s/l is common or rare?

Back 142

rare

Front 143

Superior s/l caused when:

Back 143

patients have weakness in portions of cuff that glide humeral head downward (ITS).
Arm positioned on surface that's too high.
Continue to activate deltoid w/o initial abduction or downward glide.

Front 144

In superior s/l, where does humeral head become lodged?

Back 144

into the glenoid fossa continually

Front 145

What happens when patients are positioned in forced WB w/o activation of scapular or rotator cuff mm?

Back 145

Eventually, coracohumeral ligament can tear or become lax so the humerus becomes permanently lodged slightly superior and posterior to coracoid process of scapula.

Front 146

If WB on involved arm, be sure...

Back 146

Trunk mm are active to avoid superior s/l

Front 147

Inferior GH ligament may become stretched or torn allowing...

Back 147

greater movement of humerus superiorly.
Superior impingement leads to PAIN.

Front 148

Patients w/ superior impingement usually require:

Back 148

joint mobilization in order to obtain joint play in inferior direction followed by retraining ITS to cause downward glide w/ overhead elevation.

Front 149

To minimize muscle weakness, the goal is:

Back 149

work proximal to distal in every session. Don't wait for proximal control before addressing distal function. These two areas are controlled by different areas in the brain and both need stimulation.

Front 150

What type of strength training should be used post-stroke?

Back 150

progressive resistance strength training

Front 151

How do you minimize faulty biomechanics to prevent ortho injury and pain?

Back 151

Minimize muscle weakness. Taping, verbal/tactile cues

Front 152

What type of activites should be used to increase power exerted by mm?

Back 152

Functional activity that is meaningful and relevant.
Forced use of rolling walker significantly increases UE strength and functional outcomes.

Front 153

When should neuromuscular stimulation be used in the UE?

Back 153

For reduction of s/l and promotion of early muscle return.

Front 154

What improves neural plasticity?

Back 154

Peripheral sensory stimulation alone and paired w/ motor cortical stimulation.

Front 155

Forcing patients to use unaffected side enhanced...

Back 155

motor movement of involved side (crossed synapses), as well as forcing use of the scapula and shoulder to get better distal control.

Front 156

If pain is a problem, can achieve pain relief through...

Back 156

TENS

Front 157

What tasks can be used to evaluate reach?

Back 157

Observe during functional tasks.
Tasks that require different end hand positions such as pointing, grasping, swiping.
Tasks in the central and periphery and require contralateral/ipsilateral reach
Bilateral/unilateral reach
High and low accuracy demands

Front 158

Problems w/ reaching (transportation):

Back 158

Delayed movement timing for stable and moving objects.
Disruptions in interjoint coordination (shoulder, elbow, wrist, finger).
Either undrshooting (too slow) or overshooting (too fast) the object.
Abnormal motor activation (using biceps instead of triceps).
Sensory issues affecting reach

Front 159

Intervention for reaching (transportation phase)

Back 159

Very fast/slow tasks.
Work on accuracy
Practice grasp they think they need before they reach.
Things may be more/less difficult based on height, shape, weight, etc.
Work on functional tasks that force patients to alter tasks, heights reached, shape hand needs to make, and distance.
Ask patients to reach in ipsilateral, midline, and contralateral directions.

Front 160

Problems w/ reaching (hand shaping):

Back 160

Absence of anticipatory hand shaping
Inappropriate closing to late or too soon
Inability to alter hand shape
Larger or smaller pre-grip formation
Inaccurate recognition of object and it's intended use

Front 161

Hand shaping is highly driven by:

Back 161

sensory and visual input

Front 162

Questions to ask about hand shaping to plan ahead before trying the task:

Back 162

What is the object's size, shape, or weight, and how should i use it?
What type of grip is needed for lifting, throwing, or carrying this object?
Remember to open hand prior to reaching object.

Front 163

Grip assessment-

Back 163

Functional observation gripping objects of different size, weight, outside friction.
Standardized testing (Sollerman's Grips). Toothpaste tube, glass, knife, etc.

Front 164

In grip assessment, ask yourself:

Back 164

Does grip vary according to size, weight, shape of object?
Can they show anticipatory control of grip or adapt accordingly?
Are they using their visual systems to guide grip?
Set up therapy to work on the piece they're missing most.

Front 165

Problems seen in grip phase:

Back 165

Take longer time to contact object before lifting it (sensory issue).
May not be able to adjust force or amplitude. Typical to overcompensate if task is possible.
Lack the variety of grasps needed for function.
Greater visual issues, more impaired grip

Front 166

Interventions for grip phase:

Back 166

Practice: gripping objects of different size, shape, weight, use, outside friction
Grip stationary and moving objects
Power grip first, then precision.
Practice occurs within context of functional and meaningful activity.

Front 167

Assessments for manipulation phase:

Back 167

Stabilization- can patient perform isometric finger forces sufficient to hold object in hand during transport?
Manipulation- Can patient control movement of object through space?
Can patient release an object when and where desired? Is pattern for release abnormal?
Can patient use tools in the manner intended?

Front 168

Standardized assessments for manipulation phase:

Back 168

Purdue Pegboard, Minnesota Rate of Manipulation, Peabody fine motor scales, Bruinicks-Oseretsky Motor Developmen Scales

Front 169

Problems w/ manipulation:

Back 169

in-hand manipulation problems
Slower release or inability to release.

Front 170

Intervention for manipulation:

Back 170

Practice of: In-hand manipulation activities graded in size, shape.
Release on supported (holding object in other hand), then unsupported surfaces, into a container, and stacking.

Front 171

Positive symptoms:

Back 171

Exaggerations or excess of movement: spasticity, spasms, abnormal tone, Babinski

Front 172

Negative symptoms:

Back 172

Deficits or losses of movement: weakness, loss of fine/gross motor coordination, poor muscle endurance

Front 173

Does decreasing positive symptoms increase function?

Back 173

No

Front 174

In reference to PS and NS, what is evidence-based?

Back 174

Prevent loss of mechanical length of muscle (splinting, ROM)
Strengthen, through activity and exercise despite quality of tone..
Address loss of coordination through real occupational performance.

Front 175

When should pain be treated?

Back 175

immediately. may be orthopedic, neurologic, but usually ortho b/c malalignment.

Front 176

Minimize ROM restrictions by:

Back 176

Increasing capsule extensibility (joint mob, modalities, splinting)
Maximize mm resting length (manual therapy, modalities, splinting/casting)
Minimize edema
Minimize tone

Front 177

Minimize pain by:

Back 177

TENS (transcutaneous electrical N stimulation). Sensory impulses into SC to decrease sensory input from pain.
Resolve any ortho issues.
Assess neural tension and treat as needed.

Front 178

Teach patients to be responsible for protection, maintenance, and improvement of the arm by:

Back 178

Make sure arm doesn't fall off wheelchair.
Check temperature of objects before touching them.
Follow splint schedules.
Complete exercise and functional programs.
Make a consistent effort.

Front 179

Train how to handle the arm...

Back 179

During transfers, ADLs, gait, home management and leisure activities.
Shoulder- hand syndrome significantly reduced by not pulling the extremity or causing pain through poor positioning.

Front 180

Causes of edema:

Back 180

Lack of muscle contraction acting as a vascular pump
Entrapment/impingement due to postural change after stroke.
Sympathetic N response to hemiplegia (RSD)
Blood clot/DVT

Front 181

To alleviate edema:

Back 181

Sleep or rest w/ arm in at least 30 degrees of elevation.
Use compression wraps to control edema.
User splints when needed.
Use activity and exercise.
Modalities- heat, cryotherapy, ESTIM to m pump out edema, contrast baths.
Retrograde massage done gently.

Front 182

Intervene w/ tone if:

Back 182

Tone limits PROM, putting client at risk to lose valuable m length needed for strengthening.
It's compromising skin integrity or causing pain
3. It limits functional mobility or activity

Front 183

Modified Ashworth Scale

Back 183

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 range of motion when the part is moved in flexion or extension/abduction or adduction, etc.
1+ = Slight increase in muscle tone, manifested by a catch,followed by minimal resistance throughout the remainder (less than half) of the ROM
2 = More marked increase in muscle tone through most of the ROM, but the affected part is easily moved
3 = Considerable increase in muscle tone, passive movement is difficult
4 = Affected part is rigid in flexion or extension (abduction or adduction, etc.)

Front 184

Is sensory retraining clinically effective?

Back 184

Yes. Gains can be made w/ clients that are even 2 or more years post stroke w/ intensive training 45min/3x/week for 6 weeks.

Front 185

Discriminatory sensory re-education:

Back 185

Incorporate sensory requirements for all tasks (Ex: pick up the corduroy shirt and the cotton pants)

Front 186

Protective sensory re-education:

Back 186

Educate client in how to protect the limb from stimuli that the patient cannot safely detect.

Front 187

How do you maximize fine motor coordination?

Back 187

More sensation. Fine motor coofdination is often sensory based. Provide sensory intervention when coordination is involved. Intervention should be task specific.

Front 188

Key components of fine motor coordination:

Back 188

This includes isolated finger control, thumb opposition, stability of the wrist and thumb, maintaining hand arches, providing sensory feedback, demanding in-hand manipulation

Front 189

Motor learning through:

Back 189

CIMT, NDT, PNF

Front 190

Intervention map to retrain sensation/coordination:

Back 190

No use of arm.
Can provide minimal stabilizing assist w/ involved arm.
Minimal active movement- usually some proximal strength,but no hand function.
Can do lots of active assistance during functional activities w/ involved arm- probably has gross grip, but perhaps w/ no fine motor control
Patient uses both arms and hands- although somewhat hesitantly, has some fine motor control, may need reminders to use both arms and hands.

Front 191

UE function is facilitated by attention to all aspects of motor control:

Back 191

sensory
Visual/visual perception
Cognition
Strength
Coordination
w/in the context of meaningful activity through conscious practice techniques.

Front 192

Shoulder hand syndrome-

Back 192

AKA complex regional pain syndrome or reflex sympathetic dystrophy.
Can have it in any diagnosis
Caused by sympathetic NS overflow.
Causes hypersensitivity to pain and of mechano-receptors. Lack of active/passive ROM and loss of ability to stand WB

Front 193

Stage 1 SHS

Back 193

Diffuse aching in shoulder arm and hand
Swollen tender hand and wrist
Shiny dry skin
Increase in hair and nail growth
Passive ROM to hand and wrist causes sharp and severe pain.

Front 194

Treatment for stage 1 SHS:

Back 194

Treat cause of pain if possible.
Elevate hand and arm to decrease swelling.
maintain ROM as possible.
Check body alignment, biomechanics, hand and arm care
Touching, rubbing, massage
TENS for pain
Slow, gentle increases in WB

Front 195

Stage 2 SHS:

Back 195

Marked decrease in ROM
Pain is severe and diffuse
Hair is scant, nails become brittle and rack
Skin gets more shiny, cold, flaky, and swollen

Front 196

Intervention for stage 2:

Back 196

Joint mob as needed
TENS
CT mobilization
Gradual, but consistent increase in WB

Front 197

Stage 3 SHS:

Back 197

Severe tissue deformity
Joint contractures
Out of realm of PT/OT
Irreversible

Front 198

What happens after stroke (LE)?

Back 198

Weakness
Spasticity
Coordination problems
Sensory problems
Cognitive and perceptual problems
Function

Front 199

After stroke, weakness is a result of...

Back 199

Insufficient recruitment of motor neurons from the cortical and subcortical areas.
Later weakness result of secondary changes in the mm fibers making the muscle unable to produce sufficient force.

Front 200

Why is weakness important?

Back 200

Weakness causes an inability for patients to generate muscle force for concentric, eccentric, and isometric activity during functional activities making compensation or adaptation necessary.

Front 201

What is active during the sit to stand movement??

Back 201

Hip extensors, knee extensors, and PFs are active concentrically.
Stand to sit the same mm are active eccentrically

Front 202

What LE mm are especially susceptible to weakness?

Back 202

PF and DF display weakness due to under recruitment and lack of sufficient strength following stroke and rarely come back.
Quads
Hip flexors, extensors, and abductors

Front 203

PFs produce __% of forward propulsion during gait.

Back 203

85

Front 204

Dorsiflexor weakness leads to what during gait?

Back 204

foot drop

Front 205

Quads are important for...

Back 205

Loading and stance during walking and for standing control and balance.

Front 206

Quad weakness compensation:

Back 206

usually knee hyperextension/forward trunk lean moving the line of gravity forward of knee eliminating need for quad activity.

Front 207

What is wrong with knee hyperextension?

Back 207

can damage structures in knee including ligaments, especially the ACL.

Front 208

Why are the hip flexors important?

Back 208

Allow person to move foot forward for walking, for balance, and for weight shifts.

Front 209

What may occur w/ hip flexor weakness?

Back 209

Knee flexion may be affected, especially if PFs are also weak.
Toe drag can result causing loss of balance.
Hip flexors almost always come back.

Front 210

How may people compensate for hip flexor weakness?

Back 210

Using a posterior pelvic tilt along w/ activation of the abs to move foot forward.
May use hip circumduction (hip hike, forward pelvic rotation, and abduction of hip) to move foot forward.

Front 211

When are hip extensors important?

Back 211

standing and ADLs, ability to balance in standing

Front 212

What compensations may not be used with hip extensor weakness?

Back 212

Can't use backward trunk lean b/c of inadequacy of DF and quads.
Patients using forward trunk lean will have poor stability and accompanying knee hyperextension.

Front 213

Backward trunk lean eliminates need for ___ mm in standing and walking, but imposes greater demand on...

Back 213

hip extensors; greater demand on knee extensors and tibialis anterior which are often weak after stroke.

Front 214

Hip abductors (glut med and TFL) are important for:

Back 214

standing and ADLs

Front 215

When hip abductors are weak, pelvis on __ side drops during one-legged stance.

Back 215

strong

Front 216

How do patients compensate for hip abductor weakness?

Back 216

avoid WB on weak side
Stance on weak leg, patients may use trunk lean toward weak side to compensate.

Front 217

Why do patients w/ weak hip abductors lean towards the weak side?

Back 217

Leaning laterally lessens the load on the hip abducturs or eliminates the need altogether.

Front 218

After stroke, spasticity is a result of:

Back 218

Lack of inhibition of mm tone and activity by the CNS.
Over production of muscle activity or activity that doesn't match the task at hand.

Front 219

In patients w/ stroke spasticity often results when:

Back 219

a quick stretch during transfers, ADLs, or gait.

Front 220

Spasticity can also alter...

Back 220

the mechanical properties of the muscle making it unable to react w/ the speed required of the task.

Front 221

Muscles especially susceptible to spasticity in the LE:

Back 221

PFs and quads

Front 222

When patients shift their weight forward or step forward, the __ mm become stretched producing spasticity.

Back 222

PFs

Front 223

PF spasticity during weight shift forward or step forward causes:

Back 223

the tibia to be pulled posteriorly causing knee hyperextension

Front 224

Spasticity in PFs causes:

Back 224

toe to land first when stepping forward. Also supinate leading to ankle instability.

Front 225

Possible solutions to PF tone:

Back 225

supporting the foot in subtalar neutral through: AFO, foot orthotic, casting or spinting to lengthen muscle

Front 226

Spasticity in quads can lead to...

Back 226

knee hyperextension occuring when quads undergo a lengthening.
This is rare, but spasticity can occur during loading when knee is lengthened to absorb shock.

Front 227

when are coordination problems noted?

Back 227

When one looks at multisegmented movements.

Front 228

One coordination problem seen after stroke is...

Back 228

abnormally high levels of co-activation in agonists and antagonists.

Front 229

Abnormal levels of co-activation may be due to:

Back 229

Need for patients to increase stability.
Altered central pattern generators (motor programs).
Increase in postural support- although altered

Front 230

What are the 2 patterns of abnormal synergies typically apparent after stroke?

Back 230

Total extension and total flexion

Front 231

Flexion synergies (LE)

Back 231

As individuals flex legs after stroke, they experience difficulty isolating flexion at one joint and often use a mass pattern consisting of: PPT, pelvic forward rotation, hip flexion/IR/abd, knee flexion, ankle DF, supination, toe flexion

Front 232

Extension synergies (LE)

Back 232

After stroke have difficulty isolating extension at one joint using pattern consisting of: APT, pelvic backward rotation, hip extension/ER/add, knee extension, ankle PF, STJ supination, and toe flexion

Front 233

Effects of moving in synergy patterns:

Back 233

slow gait speed, affects ADLs, endangers leg joints. Cost from energy expenditure 2-3x increased.

Front 234

As people recover from stroke, do they become better able to isolate joints and muscles?

Back 234

yes

Front 235

Sensory problems in the leg can...

Back 235

disrupt function during gait, standing, and ADLs

Front 236

Most common sensory problems include:

Back 236

somatosensory deficits, visual, and vestibular deficits

Front 237

B/c 3 sensory systems are basis of balance, patients w/ sensory difficulty...

Back 237

will have balance deficits and be at risk for falls.

Front 238

Somatosensation impairments occur due to:

Back 238

Impairment of afferent impulses, usually at the cortical level.
Can occur as result of altered sensory input or absent sensory input.

Front 239

Over time, the sensory component of ___ also becomes altered, affecting...

Back 239

peripheral NN; conduction of nervous impulses

Front 240

Normally, stretch reflexes are modulated in the triceps surae and lead to improved pushoff and stance recognition. These reflexes are inhibited prior to...

Back 240

swing to allow toe clearance.

Front 241

Any disruption of triceps surae stretch reflexes can alter...

Back 241

either the stance and swing phases of gait, or affect the minute balance adjustments we make as we stand in one place.

Front 242

If one sensory system used for balance is affected, the other 2 systems...

Back 242

become hypersensitive thus taking over for the altered system.
In stroke, all 3 systems may become altered or invovled require extensive retraining of balance.

Front 243

Cognitive and perceptual problems related to stroke:

Back 243

Body scheme/image
Spatial relation disorders
Pain
Cognitive impairments
Attention

Front 244

How should patients practice so that they understand how to activate the muscles that perform anterior/posterior pelvic tilt?

Back 244

Practicing while seated allows patients to understand a neutral spine and how to move into and out of it.

Front 245

PEAK

Back 245

Pelvis in neutral
Equal weight on both buttocks
Angles (90)
Knees facing forward

Front 246

After attaining anterior/posterior stability, patients need to understand how to...

Back 246

activate mm that allow them to shift their weight from side to side.

Front 247

How should seated weight shifting be practiced?

Back 247

seated allowing understanding of how to reach laterally and weight shift laterally and to move to involved and uninvolved side. Next move to spinal rotation.

Front 248

When seated and reaching to right, person activates...

Back 248

lateral trunk flexors on L, pelvic elevators on L, and hip abductors on R

Front 249

The hip joint needs a balance between...

Back 249

flexion and extension. Practice in seating allows patients to gain stability and confidence that they won't fall forward or backward.

Front 250

After the initial movement to overcome gravity, leaning forward in sitting uses (in addition to trunk extension discussed previously):

Back 250

hip extensors ECCENTRICALLY. Moving back to upright uses the same muscles concentrically.

Front 251

Practicing leaning forward at the hips in seated position purpose:

Back 251

eliminate fear associated w/ forward falling and allows patients to practice control prior to moving to stand.

Front 252

Proper foot position in seated:

Back 252

STJ neutral and ankle joint neutral. May require under the foot orthosis or AFO

Front 253

An ankle that collapses into DF causes...

Back 253

knee instability (flexion) and leads to a fall or the person purposefully hyperextending knee for stability.S

Front 254

Sit to stand action requires concentric:

Back 254

trunk extension
Hip extension
Knee extension
Ankle PF

Front 255

Stand to sit action requires:

Back 255

same acctions of muscles as sit to stand, but eccentrically

Front 256

Sit to stand action requires what position?

Back 256

Ankle be in DF
Entire foot contacting floor
Knees come forward over feet
Shoulders come forward over feet

Front 257

Does subluxation itself cause pain?

Back 257

No, but sl clearly puts mm, tendons, and ligament systems at a biomechanical disadvantage and can contribute to ortho and neuro injuries.

Front 258

What does cause shoulder pain?

Back 258

Spasticity of IRs, specifically subscap and pec major.
Significant pain w/ stretching to prevent shortening.
Limited ROM can result in contractures and frozen shoulder.
Multi-factorial requiring individualized assessment and intervention.

Front 259

Is a subluxation reversible and does it affect rehab outcome?

Back 259

No literature to support whether or not s/l inhibit m return or potential (major lit void).
We appear to have more impact acutely, but cannot tie this to better outcomes functionally.

Front 260

Do humeral supports give us a mechanical advantage in rehab?

Back 260

Lack of refuting and supporting evidence:
Proper alignment of static and dynamic structures.
Increase potential for using key kinesiology principles.
Pain prevention.

Front 261

How do we accurately measure inferior s/l?

Back 261

Radiographs are most objective, but costly.
Palpation by finger width had 2nd highest correlation with accuracy.
Assess arm length discrepancy.
Clinical observation.

Front 262

If we choose to use a support, we should evaluate:

Back 262

Application of force and how that impacts the shoulder girdle and s/l.
How teh support moves (or doesn't) w/ the patient as they access environment.
The necessity for reducing the s/l vs the negative impact of the abnormal tone, abnormal posturing of the UE.
Comfort, cosmesis, and control of pain.
Impact on function.
Humeral supports shouldn't be used universally w/ all clients, but considered for each.
Used early as a preventive measure- think ortho.
Horizontal and vertical measurements.

Front 263

Positioning devices as humeral support: laptray, arm rests, foam cushions, pillows. Pros:

Back 263

Low tech/inexpensive
Horizontal measurement
Easy to apply and teach to client
Can be quickly applied in sitting or laying.

Front 264

Using positioning devices as humeral supports: Cons:

Back 264

Don't move w/ your body; fall w/ movement.
Tendency for over/undercorrection in inferior subluxations.
Can put arm in mechanically disadvantaged positions if used incorrectly and as person moves.

Front 265

Slings as humeral support:

Back 265

No slings currently correct trunk imbalances or have significant impact on scapular alignment. Simply work to increase the vertical rise of the humerus toward teh gleinoid so only addresses one reason for s/l.

Front 266

AJOT Chart-

Back 266

Gives us a way to evaluate a sling on an individual.
Looks at desirable and undesirable characteristics: force, impact on tone, access to environment, and cosmesis/acceptability

Front 267

Bobath sling-

Back 267

Allows arm to rest at side of body/use of arm functionally.
Provides support through axilla to minimize vertical displacement.
Straps that support axilla against thorax.
Debate: horizontal displacement, circulation compromise

Front 268

Bobath sling evidence:

Back 268

Does decrease vertical asymmetry, but there was horizontal asymmetry.
Force application is through the axilla, not an upward vertical displacement of humerus. Edema possible.
Do not use for moderate s/l (2-3fingers), only w/ minimal s/l and some muscle tone support.

Front 269

Harris hemi-sling:

Back 269

Intends to provide upward vertical support to minimize inferior s/l.
Displaces weight of arm over both shoulders for improved symmetry.
Places arm in add/IR
Minimizes arm swing and use in functional acitivity.

Front 270

Harris hemi-sling evidence:

Back 270

Good correction of s/l significantly better than bobath, w/ no horizontal displacement.
Significant reduction in vertical asymmetry when placed correctly.

Front 271

Single-strap (conventional) hemi-sling:

Back 271

Intends to provide upward vertical support to minimize internal s/l.
single strap over opposite shoulder.

Front 272

Single strap hemi-sling evidence:

Back 272

Correction in vertical asymmetry, but other supports do better.

Front 273

Roylan humeral cuff sling:

Back 273

Intends to pull humerus vertically w/ force enveloping humerus and pulling superiorly.
Force transmitted to opposite trunk.

Front 274

Roylan evidence:

Back 274

Significant reduction in vertical asymmetry w/ no increase in horizontal asymmetry as compared to bobath and signle strap hemi-sling.

Front 275

Bottom line on using and choosing slings:

Back 275

Use as a preventative measure when the extremity is flaccid.
Weigh advantages of minimizing s/l w/ possible advantages/disadvantages of position, function, circulation, tone changes, pain relief, and gait changes each time you see the patient.

Front 276

What type of e-stim is used as humeral support?

Back 276

neuromuscular stimulation (NMES)

Front 277

In clients w/ neuro disorders, we can use e-stim to:

Back 277

Prevent or retard mm atrophy.
Muscle re-education: Teach patient to activate their own mm; use w/ functional tasks

Front 278

NMES contraindications/precautions:

Back 278

Cardiac pacemakers
Avoid anterior neck and head
Active cancer
Abnormal sensation
Pregnancy

Front 279

For inferior s/l, electrodes should be placed:

Back 279

Over supraspinatus and posterior delt.
Add UT and LT as alternative
Or supra, infra, and UT/LT

Front 280

To decrease s/l, e-stim should be on/off:

Back 280

On no more than 10 sec to avoid fatigue.
Off at least 50 sec moving to 30 sec as muscles strengthen.
ON:OFF ratio 1:5 to avoid fatigue

Front 281

To use e-stim as orthotic aid while decreasing s/l, on/off:

Back 281

Increased from 1:5 ratio to 1:1
Wearing time increased to 6 hours a day
Use 4-6 weeks

Front 282

Reasons for using NMES:

Back 282

See increases in motor recruitment (stronger, faster contractions).
Should see improvements w/in 2 weeks
Should combine voluntary conscious effort w/ stim.
Recovery rate is faster , but in the end similar outcome to those w/o NMES.

Front 283

Shoulder taping as humeral suppport effects:

Back 283

Theory is that effects are proprioceptive in mechanical in nature: Extra sensory feedback
Reminder to maintain proper positioning
Encourages proper positioning and handling techniques
Placebo effect

Front 284

goals of taping:

Back 284

Inhibition of overactive mm synergies.
Facilitation of underactive synergies.
Optimization of joint alignment
Offloading of irritable neural tissue; direct or indirect pain relief.

Front 285

Intervention to prevent and treat s/l:

Back 285

Proper positioning into maximal ER.
Slings are the best method to support a flaccid extremity, but no one sling is better than another.
Aromatherapy and accupressure reduce pain.
Use an actve therapy approach, but avoid over aggressive therapy including use of overhead pulleys.

Front 286

Sensory>___>cognition>___

Back 286

perception; behavior

Front 287

The sense organs...

Back 287

receive info

Front 288

Information is transmitted..

Back 288

to the brain. The brain processes the info into perceptions

Front 289

cognition-

Back 289

How perceptions are used for immediate action or stored for future actions ending in behavioral response.

Front 290

Vision accounts for __% of all sensory receptors, but we must recognize the dynamical relationship between all the senses.

Back 290

70

Front 291

Perception-

Back 291

interpretation of sensory stimuli

Front 292

Visual-receptive components-

Back 292

The anterior visual pathway.

Front 293

Lesions occuring where affect visual reception?

Back 293

Anywhere from the retina, optic N, optic chiasm to the lateral geniculate of the thalamus.

Front 294

Lesions of receptive components affect:

Back 294

Sensory or motor based primary skills.
Ability to receive, detect, orient, and locate.
Acuity, field, oculomotor control, accomodation, fixation, tracking saccades, steropsis, binocular fusion (see one thing w/ 2 eyes), pursuit and scanning.

Front 295

Visual-cognitive components include-

Back 295

Posterior visual pathway.
Lesions may occur anywhere from the thalamus to the primary visual cortex in the occipital lobe, to the parietal, temporal, and frontal lobes.

Front 296

Visual- perception or visual-cognitive components include things such as:

Back 296

Visual attention and memory
Recognition of form, color, and spatial relations (depth perception, figure ground, etc.)

Front 297

Describe the path of sight from the eyes to perceptive areas of the brain.

Back 297

Eyes are sensory receptors.
Transmit info via optic N through visual paths to visual cortex in occipital lobe.
Info then goes through thalamus to associative areas of temporal, parietal, and frontal lobes.

Front 298

What are the foundations of visual perception:

Back 298

Visual acuity, visual field and oculomotor control.

Front 299

After the foundations for visual perception, the next skills that develop in the hierarchy of visual perception are:

Back 299

Visual attention, scanning, and pattern recognition

Front 300

The final parts of visual perception that develop are:

Back 300

Visual memory and visuocognition develop and allow us to adapt through use of our vision.

Front 301

An acquired assault to the brain can result in visual perceptual deficits due to...

Back 301

Visual field deficits, difficulty attending and scanning the environment.

Front 302

A visual field cut can occur w/ lesions...

Back 302

to either side of the brain in either the temporal field or nasal field and upper and lower quadrants.
Ex: can have a lower nasal visual field cut on the L side as a result of R brain damage.

Front 303

Can people w/ visual field deficits have inattention?

Back 303

Can have some inattention depending on severity, but can quickly learn to compensate.

Front 304

Hemianopia-

Back 304

loss of vision in one half (temporal or nasal) in one eye.

Front 305

Homonymous hemianopia

Back 305

Loss of field (R or L) that's the same in both eyes.

Front 306

Bilateral hemianopia-

Back 306

Loss of the same half of the vision in both eyes.

Front 307

Homonymous hemianopia-

Back 307

los of nasal field in one eye and temporal field in the other resulting in loss of an entire visual field

Front 308

How is loss of visual field different than visual spatial neglect?

Back 308

An individual w/ a field cut will be aware and can compensate after initial training and minimal cues. Person w/ neglect has difficulty compensating no matter how many cues.

Front 309

What lobe lesions often cause visual spatial neglect?

Back 309

often inferior parietal lobe on the R

Front 310

Hemineglect-

Back 310

The impaired or lost ability to react to or process sensory stimuli presented in the hemispace contralateral to a lesion of the human R (or L) cerebral hemisphere.

Front 311

Hemineglect is often accompanied by losses in:

Back 311

Visual field
Body awareness
Hemiparesis
Somatosensation
Spatial awareness

Front 312

Somatagnosia-

Back 312

inability to recognize body parts

Front 313

Anosognia-

Back 313

Denial or lack of awareness of paralysis; particularly hemiparetic arm

Front 314

R/L discrimination issues:

Back 314

difficulty determining L from R or discriminating L versus R side of body.

Front 315

Unilateral body neglect-

Back 315

Failure to orient to stimulus to involved side.

Front 316

Spatial relationships-

Back 316

Relationship of space between objects and space between self and objects.

Front 317

Spatial relationships include:

Back 317

Depth perception
Figure ground
Position in space
Form constancy
Topographical orientation
Spatial attention

Front 318

Figure ground-

Back 318

differentiating foreground from background

Front 319

Position in space-

Back 319

Are objects above or below, inside infront, etc.

Front 320

Form constancy-

Back 320

Objects are recognized as the same despite size, location, or position.

Front 321

Topographical orientation-

Back 321

Knowing ones location in a larger space

Front 322

Spatial attention-

Back 322

Lack of attention to stimulus in the visual environment is unilateral spatial neglect

Front 323

Characteristics of hemineglect:

Back 323

Asymmetry of attention and shift away from L events in favor of R.
Rightward shift of the frame of reference w/ respect to self head turned R.
Distortion of mental representation in space. Describe a room will only describe things on the R side of it.
Contralesional hemianesthesia (impaired position and pain sense).
Deviation of body posture in stance.
Contralesional gaze avoidance. Often don't make eye contact.
Visual-spatial disorders and vidual sensory deficit.

Front 324

___% of people w/ R hemisphere lesions have unilateral neglect syndrome.

Back 324

20-58%

Front 325

Seven days after brain insult, some sign of contralesional hemineglect is seen in __% of patients w/ R hemisphere lesion.

Back 325

50

Front 326

Contralesional neglect is more frequent, severe, and permanent in which hemisphere?

Back 326

R

Front 327

R hemisphere damage may result in:

Back 327

Decreased arousal and attention due to decreased dopamine and there may be more dopamine receptors in the R hemisphere.
Difficulty shifting attention b/c R hemisphere has the dominant mechanisms necessary to shift attention.
Deficits in the internal spatial representation of the contralesional side of space resulting in a rightward error in the bodies spatial orientation.

Front 328

Unilateral neglect syndrome w/ L hemisphere:

Back 328

Detail oriented
Compares and contrasts details in environment
Processes info sequentially
Attends only to R visual field.

Front 329

Unilateral neglect syndrome and R hemisphere:

Back 329

Global orientation
Perceives the environment as a whole
Groups multiple objects into meaningful categories
Attends globally to both L and R visual fields

Front 330

Cognitive deficits are most associated w/ what lobe?

Back 330

frontal

Front 331

Cognitive impairments may be caused by...

Back 331

Frontal lobe lesions or Problems w/ perception from lesions elsewhere.

Front 332

Executive functions:

Back 332

Problem solving/sequencing problem recognition, judgment, and planning, organization initiation, etc. are indicative of the individuals ability to employ new strategies to old tasks and be safe and independent.

Front 333

Test of basic cognitive impairments:

Back 333

Orientation, attention, short term memory, and following verbal commands are often used predictively as precursors for executive functionsa nd for determining d/c environemtn

Front 334

In determining what assessment to use, consider:

Back 334

Can the person participate in the assessment? How much time will it take
Is the assessment relevant for the person?
What additional info do I want to know about th eperson?

Does the assessment cover the areas of cognition and perception that I want?
Is the assessment in line w/ the model guiding my intervention (remidal or adaptive)?
Do I need a sensitive assessment that can measure small changes in performance?
Do I need an assessment that measures change over time for outcomes?
Am I qualified to perform assessment?

Front 335

Benefits of assessments of cognition and perception:

Back 335

More easily recognized by other team members.
Frequenthly more significant research

Front 336

Limitations of assessments of cognition and perception:

Back 336

Relationship to function or occupation may not be apparent

Front 337

Trail making test part b:

Back 337

Starting w/ number 1 draw a continuous line alternating between letters and numbers until you finish w/ number 13. If can't do in less than 3 minutes, it suggests the person shouldn't drive.

Front 338

The Scan Chart Test:

Back 338

Based on Brain Injury Visual assessment batter for adults. Scan chart and ID shapes. Should do this: rectilinear (left to right/top to bottom), clockwise or counterclockwise. Get a plus score for using an organizational strategy.

Front 339

Motor Free Visual Perception test (MVPT)

Back 339

Which shape would look like the initial shape by finishing drawing the shape.

Front 340

Letter cancellation task-

Back 340

used to screen if person has neglect. Tell person to cancel all letter A's and see which ones they miss.

Front 341

Line bisection-

Back 341

put line through center of each line you see. Used to confirm neglect.

Front 342

Intervention for perception and cognition (types):

Back 342

Restorative/remedial
Adaptive/compenssatory
Combined approaches: metacognitive & metaperceptual, environmental approaches, task oriented approach

Front 343

Restorative interventions for perceptual deficits:

Back 343

Computer programs: Hierarchical Cognitive retraining programs, Useful field of view/visual attention
Drill and practice
Table-top activities

Front 344

Hierarchical Cognitive Retraining Programs-

Back 344

Contain multiple cognitive and perceptual aspects frequently including topographical orientation- maze activities

Front 345

Useful field of view/visual attention for perceptual deficit intervention:

Back 345

Central stimulus presented at teh same time that person must discriminate a peripheral stimulus against a cluttered background.

Front 346

Drill and practice interventions for perceptual deficits:

Back 346

Particularly designed for remediation of visual spatial neglect.
Saccades- quckly look from one object to another.
Visual search and scan
Pen and paper exercises- trail making, letter/number cancellation, line bisection, hidden pictures
Do they translate to function?

Front 347

Table-top activities for intervention of perceptual deficits:

Back 347

Constructional praxis- DLM 3 D block designs, parquetry
Body scheme- puzzles (of a person), DLM- L and R hand cards

Front 348

Evidence based intervention for neglect:

Back 348

Contralateral limb activation
CIMT
Mental imagery
Prism glasses
Eyepatching and hemispatial glasses- blocking the good field to cause them to address the bad
Caloric stim- ice water and irrigate the ear canal and do line bisection ebfore and after.
Optokinetic stim- screen in front of person and there are moving dots causing them to pursue toward L field.
Neck vibration
Trunk rotaiton

Front 349

Rapid eye scanning movement in both fields increased...

Back 349

awareness of the visual deficit and its effect on function

Front 350

Restorative intervention for cognitive deficits:

Back 350

Computer assisted strategies- attention, memory, and executive skills.
Drill and practice- number of repetition, remembering words
Pen and paper- odd, even cross out
Table top task- multivariate sequencing beads

Front 351

Limitation of restorative/remedial intervention for perceptual/cognitive deficits:

Back 351

We assume if the person improves in deficit area generalization of learning or transfer of training to functional tasks will occur.

Front 352

Effectiveness of restoration intervention of cognition:

Back 352

No significant affect on performance of fun ctional tasks
Insufficient evidence

Front 353

Success in remeidal and adaptive approaches contingent on:

Back 353

person's ability to learn

Front 354

Functional Model of Cognitive Rehab-

Back 354

Both restorative and compensatory approaches across teh continuum and settings.
It's possible to use ADLs as an intervention strategy w/in the restorative approach.
Could use context of ADLs to address cognitive or perceptual deficits.

Front 355

Task oriented approach to cognitive/perceptual rehab:

Back 355

Emphasize the relationship of the task to the person w/in an environment.
Focuses on metacognition and metaperception.
Involves patient in problem solving process.

Front 356

Task oriented interventions include:

Back 356

Activity processing- discuss purpose and results of the activity w/ patient
Behavior modification- use of prompts and cues to shape and reinforce to support interdependence
Group treatment- feedback, shared experiences
Multicontextual approach- uses patients' ability to process and self monitor for the transfer of skills
Affolter approach- use tactile and kinesthetic (hand over hand) input to create the connection between movement and its affect on objects.

Front 357

Keep intervention simple:

Back 357

Avoid frustration
Use multiple cues
Decrease environemtnal stimuli
Slow down
Provide basic instructions
Use goal-directed activities in context of normal enviroment.
Frequent practice
Motor learning based in learning theory

Front 358

Environmental/adaptive approach:

Back 358

Structuring the enviornment to improve function and guarentee safety.
Actually setting up environment to prevent failure
Reduce environmental distractions
Use appropriate environment for the activity to enhance performance
Person may not recognize or have the need to know about the intervention.
Family/caregiver must understand the need for the intervention and be involved in implementation
Therapist must have time to develop the intervention and access to family/caregiver for education

Front 359

Adjusting and simplifying the environment to match reduced competency:

Back 359

Appliances w/ auto turn off or plugged in to timers so that the only way the appliance can be turned on is by setting the timer.
Pictures to cover exterior doors to prevent wandering outside.
Outdoor wandering parks
Laying out clothes in correct order to be put on
Use of assistive devices for self-care that don't require new learning and improve safte.

Front 360

How do we measure outcomes?

Back 360

Use of appropriate standardized assessments to measure improvements
At end of services if goals and objectives are met
Specifically ask and document if person/family feel they've improved (COPM)
Evaluate and document if specific intervention strategies have generalized/transferred to other activities.

Front 361

For single-leg stance in frontal plane, where does ground reaction force normally fall?

Back 361

Lateral to STJ
Medial to knee joint
Medial to hip joint

Front 362

For single leg stance in frontal plane, what moments are produced?

Back 362

Pronation at STJ
Varus moment at the knee
Adduction moment at hip (countered by glut med)

Front 363

Adduction moment at the hip in single limb stance...

Back 363

forces the body to respond w/ an eccentric contraction of glut med. Conserves energy by not allowing pelvic drop.

Front 364

Compensations for weak glut med post-stroke:

Back 364

Lateral trunk lean in loading and midstance.
Failure to compensate

Front 365

Lateral trunk lean during loading/midstance:

Back 365

Moves ground reaction force laterally from point of application at foot. B/c vector then passes closer to hip's AP axis, its moment arm is shorter and producess a smaller hip adductor moment.

Front 366

Will lean toward ___ side b/c it brings GRFV closer to hip eliminating need for glut med.

Back 366

weak

Front 367

Failure to compensate for glut med weakness:

Back 367

Seen as a pelvic drop on the strong side b/c the weaker limb can't stabilize w/ glut med/TFL in frontal plane (glut med limp).

Front 368

Failure to compensate makes swing through on the strong leg more difficult b/c...

Back 368

the patient tends to hit his/her toe on the floor.

Front 369

When can the failure to compensate for glut med weakness problem occur during gait?

Back 369

Anywhere from loading through terminal stance when glut med is active

Front 370

Glut med remediation therapeutic interventions:

Back 370

OC: hip abduction in supine progressing to s/l; hip abduction in standing w/ and w/o theraband.
CC: Hip hiking on involved and uninvolved leg,
Slowly lowering and raising strong pelvis while WB on involved leg.
Move on to gait- sidestepping and braiding. Progress doing these activities w/ resistance by theraband or tubing.

Front 371

Glut med immediate compensations- assistive devices:

Back 371

Add a cane on the strong side immediately decreases force demands on glut med moving GRFV laterally.
Move from LBQC (large base quad cane) to SBQC to a single point cane. Most people cannot manage walkers after stroke as one arm is weak, but this is also a possibility.

Front 372

Subtle lack of hip extension (forward trunk lean slight) causes...

Back 372

knee hyperextension

Front 373

During loading, GRF falls:

Back 373

Posterior to ankle
Posterior to knee
Anterior to hip (slightly)

Front 374

During loading, GRF causes what moments:

Back 374

PF moment at ankle
Flexion moment at knee
Flexion moment at hip

Front 375

Loading response forces the body to do what at the hip?

Back 375

Forces body to respond w/ isometric activity in hip extensors

Front 376

In midstance, GRF falls (sagittal):

Back 376

Anterior to ankle
Anterior to knee
Posterior to hip

Front 377

GRF at midstance causes:

Back 377

Dorsiflexor moment at ankle
Extensor moment at knee
Extensor moment at hip

Front 378

Midstance moments force body to...

Back 378

Respond w/ eccentric activity in hip flexors.

Front 379

Compensations post-stroke due to glut max/HS weakness:

Back 379

Backward lean at loading response (rare).
Forward lean at loading response.

Front 380

Backward lean at loading response:

Back 380

Leaning backward inclines GRFV posteriorly passing closer to hip's lateral axis making its moment arm shorter producing a smaller hip flexion moment.

Front 381

What does backward lean do to the knee?

Back 381

Increases demand on quads which are also weak after stroke... more often see forward trunk lean.

Front 382

Forward lean carries through what portions of gait:

Back 382

At loading and through a larger portion of stance phase

Front 383

Is forward lean a stable or unstable position? Why?

Back 383

Unstable position b/c the hip is open and isn't stabilized by any ligaments.

Front 384

When patients assume forward lean during gait, GRFV usually passes:

Back 384

In front of knee joint causing hyperextension of knee during loading.

Front 385

OC therapeutic interventions for glut max remediation:

Back 385

Work on hip extension in s/l progressing to prone if patient is able.
Bridging
Standing w/ and w/o theraband

Front 386

CC therapeutic interventions for glut max remediation:

Back 386

Hip extension on involved and uninvolved leg in standing
Move to gait- forward and backward walking keeping hip stable. Progress to resistance w/ theraband.
Squat until one inch above chair. Lean anterior for gluts.
Wall slides
Up and down a step
Sit to and from stand
Transfer activities

Front 387

Assistive devices for glut max compensation:

Back 387

Cane on strong side to decrease force demands on glut max and allow patient to avoid forward/backward lean by transferring some weight onto cane.

Front 388

Moments in the sagittal plane during loading:

Back 388

PF moment at ankle
Flexion mement at knee,
Flexion moment at hip

Front 389

Flexion moment at knee during loading forces body to...

Back 389

respond w/ eccentric activity in the knee extensors

Front 390

Sagittal plane moments in midstance:

Back 390

DF moment at ankle
Extensor moment at knee
Extensor moment at hip

Front 391

Extensor moment at knee during midstance forces the body to...

Back 391

respond w/ passive force which develops in posterior knee structuers as they elongate during knee extension; knee muscle activity is unnecessary

Front 392

Compensations for quad weakness:

Back 392

Forward trunk lean
Hyperextension of knee w/o forward trunk lean
Avoiding heel strike

Front 393

Use of forward trunk lean in patients w/ quad weakness:

Back 393

Hyperextend knee through loading to midstance to provide stability.
Forward lean moves GRF anterior to knee.
Difficult to differentiate if forward lean is due to quad or glut max weakness, or both.

Front 394

Hyperextension w/o forward trunk lean:

Back 394

Allows for stability of weak knee from loading to midstance.
Can be hard on knee joint providing stress to ACL esp if knee "jerks" back into hyperextension.

Front 395

4 most common causes for knee hyperextension:

Back 395

Poor proprioception
Glut max weakness
Quad weakness
PF tone or contracture

Front 396

Avoiding heel strike:

Back 396

Contacting ground initially on a flat foot, moves GRFV anteriorly.
Anteriorly placed vector is closer to knee joint through loading and produces a smaller knee flexor moment.
Then produces a knee extensor moment- compensate for knee extensor weakness.

Front 397

Quad remediation- OC strengthening:

Back 397

Knee extension in s/l progres to supine or sitting.
Work on bridging activities combining hip extension w/ knee extension.
Work on knee extension in sitting= increase resistance

Front 398

Quad remediation- CC strengthening:

Back 398

Knee extension on involved and uninvolved in standing through shallow moving to deeper knee bends.
Move on to gait
Wall slides
Sit to and from stand
Transfer activities
Staires, curbs, and stepping up.

Front 399

Quad compensation- assistive devices:

Back 399

Cane on strong side will decrease force demands on quads and provide stability
Solid AFO in 5 degrees of DF changes GRFV to allow knee to have flexion moment instead of extension. If quads aren't strong enough to accept the load may become unstable.
If patient has problem stabilizing the knee in extension provide solid AFO in 5 degrees PF to allow knee to have a greater extension moment. May cause problems w/ a jerking hyperextension causing ACL stress.

Front 400

PF moment at ankle during loading forces the body...

Back 400

to respond w/ eccentric activity of ankle DF.

Front 401

DF moment during midstance forces body to...

Back 401

respond w/ eccentric activity in PFs

Front 402

GRF in terminal stance falls (sagittal):

Back 402

anterior to ankle
anterior to knee
posterior to hip

Front 403

GRF in terminal stance causes what moments:

Back 403

DF at ankle
Extensor at knee and hip

Front 404

DF moment in terminal stance forces body to...

Back 404

respond w/ activity in ankle PF. PF which have acted eccentrically through midstance, now act isometrically. Continued advancement of pelvis and lower extremity now move tibia anteriorly which causes heel to rise at 35-40 percent of gait cycle.

Front 405

Preswing in sagittal plane GRF falls:

Back 405

Anterior to ankle
Posterior to knee and hip

Front 406

Moment in sagittal plane in preswing:

Back 406

DF moment at ankle
Flexor moment at knee
Extensor moment at hip

Front 407

DF moment in preswing forces body to...

Back 407

respond w/ activity in ankle PF. PF activity becomes concentric as they develop the important "push off" force for propulsion

Front 408

Compensations for weak PFs:

Back 408

Lack of push-off
Overuse of hip flexors if available (pull-off)
Short step length w/ swing on stronger leg and subsequent landing on stronger leg.
Inadequate knee flexion in swing due to lack of push off.

Front 409

Therapists who see a short step length should interpret it as...

Back 409

decrease in stance time and stability on opposite limb.

Front 410

When R step length is short, likely has weakness in muscles controlling ____ limb.

Back 410

L

Front 411

Gastroc/soleus remediation OC strengthening:

Back 411

Not very useful, but consists of pointing toes or making foot circles

Front 412

Gastroc soleus remediation cc strengthening:

Back 412

Heel-off exercises on a level progressing to raised surface.
Move to gait w/o then w/ resistance
Walking forward and backward, up and down inclines.
E-stim to work on timing and force of contraction

Front 413

Gastroc/soleus compenstion- assistive device:

Back 413

Add cane on strong side to assist in improving swing on involved side.
Emphasize pull-off and strengthen hip flexors
If there's collapse of tibia (knee flexion/DF) from midstance through terminal stance and push off, provide solid AFO to assist in substituting for triceps surae function to allow heel rise

Front 414

GRFV at ankle in loading forces body to respond w/

Back 414

eccentric activity in ankle DF.

Front 415

What is the activity at the ankle during swing phase?

Back 415

Ankle dorsiflexors act concentrically to clear toe.

Front 416

Compensations for tibialis anterior weakness:

Back 416

Foot slap
Foot flat at initial contact

Front 417

Foot slap:

Back 417

During loading, GRF produces PF moment at ankle
When DF are inadequate, foot slaps audibly on walking surface

Front 418

Foot flat at initial contact:

Back 418

B/c anterior tib weakness, people may contact ground late and initially land on flat foot. Moves GRFV anteriorly potentially causing knee hyperextension

Front 419

Anterior tib strengthening:

Back 419

Toe raises w/ eversion
ankle circles
PNF patterns

Front 420

Anterior tib compensations we provide:

Back 420

E-stim
Hinged AFOs to allow foot to freely DF past neutral, but w/ a stop to prevent fot drop past 90 (or neutral) PF/DF
Canes may assist in stabilizing during swing phase on weaker foot.

Front 421

All gait is made easier through the use of....

Back 421

supported body weight systems.

Front 422

In the EXCITE article, which CIMT group showed more improvement in time on the Wolfe Test?

Back 422

The CIMT lower functioning group showed greater change, though scored worse than the higher functioning group.

Front 423

What do people learn quickly after stroke?

Back 423

Quickly learn how to do things w/ only one arm and leg (learned non-use).
Quickly learn to compensate for weakness.
Quickly learn to quit trying to use their involved extremities.

Front 424

when does learned non-use occur?

Back 424

During the initial period after brain injury.
The brain is in a period of recovery in which the client loses most voluntary or involuntary motor function.

Front 425

What happens in learned non-use?

Back 425

Patient learns to compensate w/ the stronger limbs and do functional activities w/ them.
When motor function begins to return, the person has learned not to use the involved limb through failed attempts.

Front 426

During the period in which the patient learns non-use, potential motor recovery is limited by...

Back 426

learned over reliance on the unaffected limb.

Front 427

What is CIMT?

Back 427

Constraining the use of the uninvolved (strong) UE for a period of approx 2 weeks.
Giving the involved arm increasing amounts of practice at a variety of functional motor tasks.
Behavioral training involves shaping or guiding use of the arm.
Also called forced-use

Front 428

Shaping-

Back 428

Psychology term used to describe "shaping" behavior by rewarding the patient or client w/ enthusiastic approval for improvement. Rewarded for using involved arm, but not punished for failure.

Front 429

Taub's research on monkeys:

Back 429

Severed sensory NN of limbs of monkeys. Restrained normal limb for two weeks. They learned to use their involved limb again.

Front 430

EXCITE trial used individuals how far post-stroke?

Back 430

3-9 months.

Front 431

Requirements of UE function in EXCITE trial in order to use CIMT:

Back 431

Ability to extend their MCP and IP joints of all digits at least 10 degrees and extend wrist at least 20 b/c they have some sort of functional hand use.
Second level- Less functioning; At least 10 degrees of active wrist extension, 10 degrees of thumb abduction/extension, and at least 10 degrees of extension in at least 2 additional digits. Ability to repeat 3 times in one minute.

Front 432

Were patients w/ balance difficulty included in EXCITE? Why//why not?

Back 432

No balance problems that might compromise their safety. If constrain uninvolved UE of someone with balance problems it prevents them for catching themself if they begin to fall and futher disturbs balance. Put in WC for CIMT if they have balance problems.

Front 433

Why was it important to the EXCITE trial that participants scored at least 24 on Mini-mental status?

Back 433

Need to be able to understand the purpose of the restraint.

Front 434

What did CIMT consist of in the EXCITE study?

Back 434

Individuals wore restraints and did six hours/day of shaping activities for an intensive 2 week period. Resume previous activities after trial.

Front 435

Results of EXCITE trial:

Back 435

Improvements in function as measured by Wolf Motor Function Test (WMFT) and MAL Quality of Movement Assessment.
Decrease in disability in SIS.
Retention at 12 months post intervention./

Front 436

CIMT supported by evidence:

Back 436

Neuroplasticity and cortical reorganization are supported by MRI/PET scans.
Ipsilateral association areas and contralateral motor cortex areas (hemispheric shift) compensate for loss of function.

Front 437

Potential side effects of CIMT:

Back 437

Uninvolved arm stiffness, cramping, and numbness. May have overuse problems in shoulder.
Involved arm- fatigue, painful overuse syndromes.
Frustration due to focusing on weak and clumsy limb.
Compromised safety
Increased stroke lesion volume may occur if treatment is introduced immediately after stroke (maybe).

Front 438

Task specific gait training-

Back 438

Can enable patients w/ stroke to practice walking repetitively rather than in conventional treatment where tone inhibiting manoevres and gait preparatory tasks during sitting and standing dominate.
Practice early w/ best biomechanical gait possible- use assistive devices.

Front 439

What is task specific gait training?

Back 439

Practice walking
Done effectively in group settings.
Significant results in circuit training.
In most trials patients walked distances as long as they could tolerate from specific ADL task to task, performing the task, then walking to the next.

Front 440

Results of task specific gait training:

Back 440

Increased walking distance (no significant speed increase).
Improvement in timed get up and go test.

Front 441

How do we get patients to the level that they can ambulate over long distances safely?

Back 441

Robotic assisted gait training
Supported body weight treadmill training

Front 442

What is partial bodyweight treadmill training?

Back 442

Form of training using body weight support (BWS) system to offset a percentage of body mass and provide external balance support, permitting treadmill walking of people in early stages of neuro recovery.

Front 443

Why is partial bodyweight treadmill training effective?

Back 443

PBW gait training allows earlier mobilization following neuro insults.

Front 444

How do we support person's weight in PBW treadmill training?

Back 444

Harnesses connected to: treadmills, gait trainers, walkers, lift systems in homes via tracking devices.

Front 445

Why use partial body weight?

Back 445

Reduces amount of weight patient must bear during gait training.
Decreases demands on the mm, promotes coordination of LEs, and improves posture and balance to minimize risk to patient.
Biomechanically erect gait cycle w/o requiring full support.
Encourages entire gait cycle at early stages of strength and stability enabling correct weight transfer, loading of affected limb, and selective activity of antigravity mm.
By reducing support during intervention, loading of weak extremities and trunk are accomplished gradually.

Front 446

How much body weight should be supported in treadmill training?

Back 446

10-20% of body weight support provided optimal sensory feedback and symmetry of loading to patient. Individualize.

Front 447

Frequency of treadmill training:

Back 447

As many reps as possible each day, coupled whenever possible w/ functional contexts.
Direct supervision at all times to assure good body and gait mechanics.

Front 448

What kind of patients can use PBW treadmill trailing for neuro-rehab?

Back 448

SCI
TBI
Stroke- addresses posture, balance and coordination
CP

Front 449

Contraindications for treadmill training:

Back 449

Lightheadedness
Confusion
Dyspnea
Angina
Excessive BP changes
Bradycardia

Front 450

Advantages of PBW training:

Back 450

Using support increases patient confidence causing patients to use a more symmetrical gait pattern and tend to walk longer distances and for longer time frames.
Safer for patient and therapist.
Therapist can carefully eval gait pattern.

Front 451

Disadvantages of PBW training:

Back 451

Not task oriented
Harness is uncomfortable.

Front 452

What is the research behind use of PBW training?

Back 452

Generation of cyclic locomotor patterns can be attributed in some animals to rhythmic neural activity produced by CPG networks in brain stem or SC.
Below lesion SC centers can learn to use lower limb afferents to generate locomotor pattern and treadmill and body support training is effective in activating spinal circuits.

Front 453

Evidence to support treadmill training:

Back 453

Performed better on speed, distance, and function than conventional therapy.
Better stride length, more even step lengths, decreased spasticity, and better CV training.
Significant benefits when combined w/ more traditional sessions (functional activities). Improved speed and function.

Front 454

Lokomat-

Back 454

Robot-assisted walking therapy is a form of PT that uses a robotic device to help a person whose ability to walk has been impaired due to stroke, SCI, TBI, neuro or ortho condition, learn to walk again.

Front 455

How does lokomat work?

Back 455

Person suspended in a harness over a treadmill and the frame of the robot, attached by straps to outside of legs, moves the legs in a natural walking pattern. A computer controls the pace of walking and measures the body's response to the movement.

Front 456

What effect does robot- assisted walking have on body?

Back 456

Repetitive walking pattern in biomechanically correct manner helps the brain and SC work together to re-route signals that were interrupted by injury or illness.
May help strengthen mm and improve circulation.
May help strengthen bones at risk for osteoporosis due to lack of use.

Front 457

What does the robotic device do?

Back 457

does most of the heavy work, pattern and pace are consistent throughout session, and exercise can be sustained over longer periods of time. You control resistance

Front 458

Who is mobile earlier: patient in traditional PT or in robotic gait training.

Back 458

robotic gait training

Front 459

Functional e-stim combined w/ biofeedback produced...

Back 459

greater improvements in functional gait speed, cadence, and stride length. These effects didn't last once e-stim was discondinued.

Front 460

E-stim to spastic mm causes...

Back 460

significant reduction in muscle tone and increase in ROM, especially when combined w/ casting/splinting.

Front 461

How does the Bioness L-300 work?

Back 461

Delivering electrical impulses to common peroneal N which controls mm that cause foot to DF in swing phase of gate and prevent foot drop.

Front 462

Where is the bioness connected to the person?

Back 462

Patient wears a lower leg electronic orthosis housing integrated stim unit and electrodes.
Gait sensor worn in shoe detects heel off and heel on positions and signals stimulator to initiate or pause.
Doesn't stabilize ankle making them at risk for sprain.

Front 463

Evidence for strengthening interventions:

Back 463

Produced CV effect as well as strength difference w/ no increase in spasticity, but no significant difference in function.
Make sure use the shoulder rules!

Front 464

CV training evidence:

Back 464

Using treadmills and stationary bikes improved gait speed, distance, and sensation.
Must be medically stable.

Front 465

Paradigm shifts in stroke rehab:

Back 465

Muscle reeducation
Neurotherapeutic/neurorestorative approaches
Functional Task-oriented restorative approach.

Front 466

Muscle reeducation used in-

Back 466

polio

Front 467

Neurotherapeutic/neurorestorative approaches to stroke rehab:

Back 467

PNF
NDT
Brunnstrom

Front 468

Functional task-oriented restorative approach:

Back 468

CIMT
BWSTT
Robot-aided UE movement
Adjunct interventions- mental practice, biofeedback, e-stim

Front 469

Consensus recommendations for UE intervention: When will it be successful?

Back 469

Remedial intervention for recovery of the UE won't be successful unless the patient has experienced some recovery.
At least stage 4 of Stages of Motor Recovery of Chedoke McMaster Stroke Impairment Inventory.

Front 470

If the patient isn't at stage 4 of the Stages of Motor Recovery of Chedoke McMaster Stroke Impairment Inventory, what intervention should be used?

Back 470

Use compensatory approach.
Any additional intervention won't result in any significant change.

Front 471

Stages of Motor Recovery of Chedoke McMaster Stroke Impairment Inventory vs. Modified Ashworth:

Back 471

Used as a predictive scale for potential of making a difference compared to Ashworth which is evaluative.

Front 472

What does the compensatory approach include?

Back 472

Maintain a comfortable, pain free, mobile arm and hand.
Proper positioning while at rest
Careful handling during functional activities.
Instruction to provide appropriate self-ROM exercises.
Use humeral supports for first 2 stages during transfers and mobility.
Teach compensatory strategies (one handedness; change in hand dominance)

Front 473

Function based restorative approach-

Back 473

Task oriented approach results in motor learning and creates cortical reorganization.

Front 474

Intervention techniques for function-based restorative approach:

Back 474

Visual demonstration
Verbal instructions
Manual guidance doing meaningful and valued activities and tasks (ideally self-initiated movement)
Appropriate feedback w/ active problem solving.
Consistent and repetitive practice

Front 475

Impairment-based restorative intervention:

Back 475

Result in improvements in impairments, but not function.
Neurorestorative intervention.

Front 476

Neurorestorative intervention-

Back 476

NDT, Brunstrom, PNF
Address positive signs and are no more effective than any other impairment based intervention.

Front 477

NDT-

Back 477

Neuromuscular development theory/therapy?- Need to work on abnormal before you get normal. All about normal movement and tone. Work to normalize tone.

Front 478

Bilateral arm training-

Back 478

Type of evidence-based restorative intervention (EBRI)
Practice the same tasks w/ both hands simultaneously often to rhythm.
Theory- activates the damaged hemisphere via the corpus callosum
Improvements in impairment based tests.

Front 479

Mental practice-

Back 479

Type of EBRI
AKA visualization, visual imagery, mental practice, and mental rehearsal.
The symbolic rehearsal of a physical activity in the absence of any gross muscular movement.
Person is instructed to visualize or remember a task and then imagine it occur.

Front 480

Neural basis for mental practice:

Back 480

As person imagines movement or task, EMG can detect slight muscle impulses that are similar to those emitted by actual movement.
As a person imagines a function/task, fMRI can detect the same brain activity that's elicited by the actual movement.

Front 481

Results found from use of mental practice:

Back 481

Increasing performance of elite athletes.
Reducing falls and social skills training.
Line tracing accuracy w/ hemiparetic limb.
Gross and fine motor skills.
Gait rehab

Front 482

Limitations of mental practice:

Back 482

Dependent on person's ability to consistently practice in order to develop a skill.
Unknown whether person must have experience to effectively use it.
Dependent on person's ability to accurately imagine. Accuracy of mind's eye may be affected by neuro damage.

Front 483

Assets of mental practice:

Back 483

Cost effective
Conserves energy
Allows imaginers to gain insights into movement allowing the person to develop strategies and correct errors.
Most effective in combo w/ physical practice.

Front 484

Robot-aided motor training-

Back 484

mechanical devise designed to train arm movements through intensive practice of repetitive and sterotyped movements at the shoulder and elbow joints using an assistive force or resistive force.
Enhance labor intensive one-to-one intervention in a quantifiable and evaluative way.

Front 485

Assets of robotics:

Back 485

Robot can aide w/ PROM
Robot can help maintain range and flexibility, temporarily reduce hypertonia or resistance to passive movement.
Robot can also assist when patient has active, but non-functional movements.
Robot can be used w/ higher level patients who wish to increase strength by providing resistance during movement.

Front 486

When may use of active-assisted movement w/ robotics be beneficial?

Back 486

In more severely impaired patients esp. during acute and subacute phases when patients experience spontaneous recovery.

Front 487

Robotic devices rely on...

Back 487

the repetition of specific movements to improve functional outcomes.

Front 488

Robotic devices focus on retraining...

Back 488

UE, specificaly shoulder, elbow, and wrist movements. Best when movement is self-initiated.

Front 489

Myomo stand for...

Back 489

my own movement

Front 490

Limitations of robotics:

Back 490

Improves motor outcomes of shoulder and elbow, but doesn't improve functional and motor outcomes of the wrist and hand.
Restrains other movement (trunk-arm and wrist-hand complexes).
No long-term improvements except at impairment level.

Front 491

Other EBRIs include:

Back 491

Music, rhythmic, metronome training
Variations of biofeedback
E-stim- bioness
Virtual reality- Wii
Surgical brain implants

Front 492

How long should you try restorative interventions and what should be used after this period?

Back 492

2 weeks; d/c w/ compensatory strategies if no functional gains.

Front 493

Speech and language disorders occur in as many as __% of people w/ strokes.

Back 493

40

Front 494

What is common when a stroke survivor has a persistent communication impairment?

Back 494

Reactive depression, withdrawal, disruption of family roles, and loss of income.

Front 495

Broca's aphasia AKA

Back 495

expressive aphasia

Front 496

Where is the lesion in Broca's aphasia?

Back 496

L prefrontal motor cortex/frontal lobe

Front 497

Characteristics of Broca's aphasia:

Back 497

Speech takes effort and is slow, and pauses between words may outnumber words themselves.
May be perseverate.
May be able to correctly use automatic speech or habitual responses (thank you, lines from familiar songs, sayings, or prayers)

Front 498

In Broca's aphasia, is the patient aware of errors?

Back 498

Usually aware of communication errors and may be frustrated, angry, or depressed.

Front 499

Wernicke's aphasia AKA

Back 499

receptive (sensory)

Front 500

Where's the lesion in Wernicke's aphasia?

Back 500

Lesion of L temporal lobe resulting in no auditory feedback when speaking and inability to comprehend spoken language.

Front 501

Characteristics of Wernicke's aphasia:

Back 501

Effortless and produced at normal or even faster than normal rates.
Often shift the order of intended sounds or words.
Doesn't select words that accurately represent their intended meaning.
May use jargon or fluent, but unintelligible speech.
May use neologisms or new words

Front 502

In Wernicke's aphasia, is the patient aware of errors?

Back 502

Usually unaware of language errors

Front 503

Where is the lesion in conduction aphasia?

Back 503

Results when arcuate fasciculus, the connective path between Broca's and Wernicke's is involved.

Front 504

Characteristics of conduction aphasia:

Back 504

Relatively preserved speech production and auditory comprehension.
Difficulty repeating sentences, and their ability to select correct words is impaired.
Marked inability to find the correct word in spontaneous speech and writing or when asked to name objects.
Often use circumlocution, a form of talking around things to communicate or empty speech.

Front 505

Where is the lesion in global aphasia?

Back 505

Results from extensive involvement of the frontal and temporal areas of the brain.

Front 506

Characteristics of global aphasia:

Back 506

nearly complete loss of ability to comprehend language and formulate speech.
Some automatic speech expressions, including expletives, may be intact.
Other automatic speech routines such as ability to name or count days of the week or hum or sing previously learned songs may also be intact.

Front 507

Interventions for communication disorders:

Back 507

Treat patient as an adult.
Provide a quiet, controlled environment w/ minimal distractions.
Avoid talking loudly or more slowly.
Use eye contact and stand in front of field of vision.
Don't assume patient can't understand b/c they can't give verbal feedback.
Simplify communication
Be honest if you don't understand what the patient's trying to communcate.
Point out progress, give realistic feedback.
Adequate time for patient to respond.
Opportunities for natural conversation.

Front 508

Dysarthria-

Back 508

An alteration in speech sounds that results from impaired mm control of speech mechanism. Speech is garbled and difficult to understand.

Front 509

Apraxia of speech-

Back 509

The inability to program the sequence of movements for speech despite the absence of motor deficits.
Know what they want to say, but lack ability to transform thoughts into verbal content and often become frustrated.

Front 510

Mrs. C speaks slowly and has anomia. She becomes frustrated as she tries to express herself. This is indicative of ___, caused by cortical damage to the ___ lobe.

Back 510

Broca's/expressive aphasia; frontal lobe

Front 511

Do people who have aphasia have cognitive deficits?

Back 511

no

Front 512

Dysphagia-

Back 512

Difficulty swallowing due to- weakness, tone, motor incoordination of oral structures, pharynx, and larynx.

Front 513

Approx. __% of people w/ strokes have dysphagia.

Back 513

47

Front 514

What does dysphagia result in?

Back 514

Compromised nutrition and hydration, potentially life threatening aspiration (30% of those w/ dysphagia)

Front 515

Are changes in urinary elimination common w/ stroke?

Back 515

yes, esp. in acute phase

Front 516

Urge incontinence-

Back 516

Type of incontinence most likely to occur after stroke b/c of an uninhibited neurogenic bladder.
Detrusor m of bladder is hyperactive. Involuntary voiding occur due to contractions.

Front 517

Sexual issues following stroke include:

Back 517

Sexual function and changes in body image.
Decreases in libido, impotence, or ability to achieve orgasm are common and can result in depression.
Psychological factors including changes in dependency in self-care activities, and changes in sexual roles may also be important.
May feel unattractive or inadequate.
Positioning may be difficult and spasms may increase.

Front 518

Is sexual activity contraindicated post-stroke?

Back 518

no, need to recognize need to adjust for affects of fatigability, changes in body image, and decreased self-esteem.

Front 519

PLISSIT model:

Back 519

Permission, limited info, specific suggestions, and intensive therapy.
Appropriate for PT/OT to address the first two levels.

Front 520

Social consequences of stroke:

Back 520

Social isolation (more severe in women)
Decreased community involvement
Economic strain
Disruption of family function, poor motivation, dependency, loss of control.

Front 521

__ hemisphere lesions are characterized by anxiety and depression. __ hemisphere lesions are characterized by denial, indifference, emotional lability, and euphoria.

Back 521

L; R

Front 522

Is depression common in stroke survivors?

Back 522

Yes

Front 523

dysthymia-

Back 523

type of depressive disorder

Front 524

Untreated depression post-stroke leads to:

Back 524

loss of functional gains, failure to continue improvement, failure to resume social activities

Front 525

Contacts w/ family __ post-stroke, interactions w/ friends __.

Back 525

maintained; decrease