Cva And Tbi

Front 1

CVA's (cerebrovascular accident) /Strokes:

Definition-?

Back 1

A stroke happens when blood flow to a part of the brain is interrupted because a blood vessel in the brain is blocked or bursts open.

Front 2

CVA's (cerebrovascular accident) /Strokes:

what happens if blood flow stops for more than a few seconds?

Back 2

If blood flow is stopped for longer than a few seconds, the brain cannot get blood and oxygen. Brain cells can die, causing permanent damage

Front 3

CVA's (cerebrovascular accident) /Strokes:

how are motor deficits characterized?

Back 3

Motor deficits are characterized by paralysis (hemiplegia) or weakness (hemiparesis) on the side of the body opposite the side of the lesion

Front 4

CVA's (cerebrovascular accident) /Strokes:

factors affecting severity?

Back 4

The location and extent of the lesion, the nature of the structures involved, and the amount of collateral blood flow determine the severity of the neurologic deficits in an individual patient.

Front 5

CVA's (cerebrovascular accident) /Strokes:

Categories: by Etiology

thrombus- main idea?

Back 5

: A clot may form in an artery that is already very narrow

Front 6

CVA's (cerebrovascular accident) /Strokes:

Categories: by Etiology

embolus- main idea?

Back 6

A clot may break off from somewhere in the body and travel up to the brain to block a smaller artery

Front 7

CVA's (cerebrovascular accident) /Strokes:

Categories: by Etiology

hemorrhage- main idea?

Back 7

abnormal bleeding due to blood vessel rupture. Some people have defects in the blood vessels of the brain that make this more likely. The flow of blood that occurs after the blood vessel ruptures damages brain cells.

Front 8

CVA's (cerebrovascular accident) /Strokes:

management

TIA- main idea

Back 8

temporary interruption to blood flow to the brain. Deficits are temporary and do not last over 24 hours. It is a precursor to both cerebral infarction and MI. Caused by multiple factors including occlusive attacks, emboli, reduced cerebral perfusion due to hypotension, arrhythmia etc

Front 9

CVA's (cerebrovascular accident) /Strokes:

management

minor stroke- main idea?

Back 9

Pt is stable and deficits are minor

Front 10

CVA's (cerebrovascular accident) /Strokes:

management

major stroke- main idea?

Back 10

: Pt is stable but the deficits are severe

Front 11

Cerebral Infarcts

main idea

Back 11

Any pathologic process involving the vessels of the brain can cause a stroke. Cerebral.Infarcts are overwhelmingly the most common cause of a stroke.

Front 12

Cerebral Infarcts

what is an infarct?

Back 12

An infarct is a site of localized necrosis (cell death) precipitated by deprivation of blood (ischemia) and therefore oxygen to that tissue. Usually this is caused by complete occlusion of a cerebral vessel which causes ischemia and leads to cerebral infarct (this is not always true, not all vessel occlusions produce an infarct)

Front 13

Cerebral Infarcts

how many pathological processes?

Back 13

. Two pathological processes account for virtually all cerebral infarcts: thrombus and embolus. Hemorrhage occurs when a blood vessel ruptures, tissue death results from both the ischemia and the mechanical injuries.

Front 14

Cerebral Infarcts

risk factors?

Back 14

primarily same for athlerosclerosis
includes: - HTN
- Diabetes Mellitus
- hyperilipidemia
- smoking
- obesity
- sedentary life style

Front 15

Immediately after the trauma or infarct the patient will go through a varying period of cerebral shock and then recovery will begin. The amount of recovery is dependent on the...?

Back 15

... severity of the stroke and the amount of CNS reorganization

Front 16

Epidemiology

stroke is the X leading cause of death?

Back 16

stroke is the 3rd leading cause of death (behind heart disease and cancer) and the most common cause of adult disability in the US

Front 17

how many new stroke victims a year?

how many with recurrent stroke?

Back 17

around 610,000 new victims each year with an additional 185,000 with recurrent strok

Front 18

what % of people with stroke die in the ACUTE PHASE?

Back 18

30% die in the acute phase

Front 19

of those who survive a stroke, what % will be severely disabled?

Back 19

of the 70 % that survive, 30 - 40 % will be severely disabled

Front 20

what % of strokes happen before 65 years old?

Back 20

20%

Front 21

History and Physical with Stroke:

HISTORY

main idea for collecting it?

Back 21

a complete history is performed on admission to help determine the cause of the stroke: i.e. an abrupt onset with a coma usually is indicative of a cerebral hemorrhage or a brainstem stroke. The history will be obtained from the Pt or family.

Front 22

History and Physical with Stroke:

PHYSICAL

main idea, why collect it?

Back 22

physical: a complete physical will be performed including: VS, a cardiac and a neuro exam and neurovascular tests (palpation of the arteries, auscultation and pressures).

Front 23

History and Physical with Stroke:

DIAGNOSTIC TESTS

main idea, why collect them?

Back 23

diagnostic tests: the Pt may also undergo some or all of the following diagnostic tests: CBC, urinalysis, blood sugars, test for syphillis, erythrocyte sedimentation rate, blood chemistry profile, cholesterol and lipid testing, chest x-ray, ECG, CAT, MRI, PET, and cerebral angiography.

Front 24

Clinical Manifestations

SENSATION

how is loss of sensation associated with vascular lesion?

Back 24

the type and extent of sensory deficits is related to location and extent of the vascular lesion. Sensory deficits include any of the senses. Sensory deficits interfere with the acquisition of new motor skills.

Front 25

Classification of the sensory system:.

exteroreceptors

main idea?

Back 25

sensory receptors responsible for the superficial sensations (skin and subcutaneous tissues)

Front 26

Classification of the sensory system:.

proprioceptors:

main idea?

Back 26

sensory receptors responsible for deep sensations (muscles, tendons, ligaments, joints, fascia, and are responsible for position sense, movement sense (kinesthesia) and vibration.)

Front 27

Classification of the sensory system:.

cortical sensations

main idea?

Back 27

a combination of exteroreceptors and proprioceptor input. Responsible for stereognosis (shape discrimination), 2 point discrimination, barognosis, graphesthesia, tactile localization, recognition of texture, and bilateral simultaneous stimulation.

Front 28

Classification of sensory receptors:

mechanoreceptors

Back 28

respond to mechanical deformation of the receptor or surrounding areas
-golgi tendon organs-reflexes
-massage – Trigger point release

Front 29

Classification of sensory receptors:

thermoreceptors

Back 29

respond to changes in temperature.

Front 30

Classification of sensory receptors:

nocioceptors

Back 30

respond to noxious stimuli and result in the perception of pain

Front 31

Classification of sensory receptors:

chemoreceptors:

Back 31

respond to chemical substances and are responsile for taste, smell, oxygen levels in arterial blood, C02 concentration, and body fluid osmolarity.

Front 32

Classification of sensory receptors:

photic

Back 32

(electromagnetic receptors): responds to light within the visible spectrum.

Front 33

It is important to remember that pain is not limited to stimulation received by the nocioceptors. High intensities of any stimulation to any type of receptor may be perceived as pain.

Back 33

It is important to remember that pain is not limited to stimulation received by the nocioceptors. High intensities of any stimulation to any type of receptor may be perceived as pain.

Front 34

Transmission of sensory signals

main idea

Back 34

receptors send signals into the spinal cord via the dorsal roots and carries it to the higher centers

Front 35

Transmission of sensory signals

Anterolateral Spinothalamic system

Back 35

responsible for cruder more primitive sensations (pain and touch)

Front 36

Transmission of sensory signals

Dorsal Column Medial Lemniscal system

Back 36

responsible for discriminate sensations such as kinesthesia, vibration etc.

Front 37

How is the sensory system evaluated

what kind of nerves do we test?

Back 37

dermatomes

Front 38

How is the sensory system evaluated

sharp/dull?

temperatures?

Back 38

pin prick

- test tubes

Front 39

How is the sensory system evaluated

light touch?

pressure?

Back 39

-brush, tissue, finger pad, cotton ball

-must be deep enough td indent skin

Front 40

How is the sensory system evaluated

kinesthesia?

Back 40

with pts eyes closed passively move their extremity through small ranges, Pt is to name the direction of the movement

Front 41

How is the sensory system evaluated

-position sense
-vibration

Back 41

-with the pts eyes closed they name the position their limb is placed in.

-tested with a tuning fork

Front 42

How is the sensory system evaluated

-stereognosis

-tactile localization

Back 42

(object recognition) place familiar objects in a bag and see if the Pt can recognize them through touch (keys, pencils, coins etc)

-: recognition of the locality of touch

Front 43

How is the sensory system evaluated

-2 point discrimination

Back 43

start with 2 points of stimulus at the exact same time decreasing the distance until they can only feel one point

Front 44

How is the sensory system evaluated

-bilateral simultaneous stimulation

Back 44

touch proximally and distally to the same extremity or bilateral extremities to see where they perceive the touch

Front 45

How is the sensory system evaluated

-barognosis

Back 45

recognition of weight, can be tested on one hand or bilaterally

Front 46

How is the sensory system evaluated

-graphesthesia

Back 46

recognition of letters, numbers or designs, traced on the palm

Front 47

How is the sensory system evaluated

-recognition of textures

Back 47

: place multiple textures in a bag to determine if the Pt can recognize

Front 48

Sequential recovery stages in hemiplegia

main idea?

Back 48

Motor recovery from a stroke occurs in stereotypical sequential stages. Variability in the clinical picture at each stage is possible and not all patient recovery fully. Patients may plateau at any stage depending upon the severity of their involvement and their capacity for adaptation. Rate of recovery also differs among patients.

Front 49

Brunnstroms' stages of recovery

Stage I

Back 49

Period of flaccidity immediately following the acute episode – slings for UE to decrease shoulder subluxation

Front 50

Brunnstroms' stages of recovery

Stage 2

Back 50

as recovery begins, basic limb synergies may appear as associated reactions or minimal voluntary movement responses may be present. Spasticity begins to develop.

Front 51

Brunnstroms' stages of recovery

Stage 3

Back 51

Patient gains voluntary control of the movement synergies, although the full range of synergies may not always develop. Spasticity has further increased and may become severe.

Front 52

Brunnstroms' stages of recovery

Stage 4

Back 52

: Some movement patterns out of the synergy are developed and begin to be mastered. Spasticity begins to decline.

Front 53

Brunnstroms' stages of recovery

Stage 5

Back 53

If progress continues, more difficult movement patterns are learned as the basic limb synergies lose their dominance over the motor acts.

Front 54

Brunnstroms' stages of recovery

Stage 6

Back 54

Spasticity disappears and individual joint movements become possible and coordination approaches normal. Normal motor function is restored and recovery is complete.

Front 55

Alterations in tone versus Synergy patterns

main idea

Back 55

An important concept in managing a stroke Pt is the ability to recognize tonal changes and synergy movement patterns as separate and distinct clinical findings, and to recognize the relationship between the two. Flaccidity is present immediately and is usually short lived. Spasticity emerges in about 90 percent of cases and tends to occur in predictable muscle groups, commonly antigravity muscles. The effect of spasticity include restricted movement and static posturing of the limbs.

Front 56

Alterations in tone versus Synergy patterns

UE strong in what motions?

Back 56

strong in: -scapular retractors
-shoulder add, depressors and IR
-elbow flexors
-forearm pronators
-wrist and finger flexors

Front 57

Alterations in tone versus Synergy patterns

NECK and TRUNK strong in?

Back 57

strong in: side flexors causing slumping to the hemi side.

Front 58

Alterations in tone versus Synergy patterns

LE strong in what?

Back 58

-pelvic retractors
-hip add and IR
-hip and knee ext
-plantar flexors and supinators
-toe flexors

Front 59

Automatic postural tone

main idea

Back 59

automatic adjustment of muscle tension that occurs normally in preparation before and during a movement task may also be impaired. Thus pts with a stroke may lack the ability to stabilize proximal joints and the trunk.

Front 60

Synergy Patterns

main idea?

Back 60

Mass movement patterns associated with the presence of spasticity. May be elicited reflexively as associated reactions or voluntarily.

Front 61

basic synergy patterns

2 types

Back 61

flexion and extension:

Front 62

basic synergy patterns

UE FLEXION

key points

Back 62

-scapular retraction / elevation or hyperextension
-shoulder abd and E
-elbow flexion *
-forearm supination
-wrist and finger flexion

Front 63

basic synergy patterns

LE FLEXION

key points

Back 63

-hip flexion *, abd and ER
-knee flexion
-ankle dorsiflexion and inversion (supination)
-toe dorsiflexion

Front 64

basic synergy patterns

UE EXTENSION

key points

Back 64

-scapular protraction
-shoulder add * and IR
-elbow extension
-forearm pronation *
-wrist and finger flexion

Front 65

basic synergy patterns

LE EXTENSION

key points

Back 65

hip extension, add * and IR
-knee ext*
-ankle plantarflexion* and inversion (supination)
-toe plantarflexion

Front 66

Stroke and Reflexes:

during the flacid stage?

Back 66

- areflexia

Front 67

Stroke and Reflexes:

with spasticity

what would present?

Back 67

-hyperreflexia
-clonus
-clasp-knife
-+Babinski
-primitive reflexes re-emerge:
- STNR and ATNR

Front 68

Stroke and Reflexes:

with spasticity

what ASSOCIATED REACTIONS may present?

Back 68

-Tonic lab supine = ext, prone = flex)
-Tonic lumbar reflex: rotation of the UE toward the hemi side
results in flexed hemi UE and ext hemi LE, rotation toward the uninvolved side will have the opposite affect
-Positive Support

Front 69

Phenomenon with Stroke:

Souques' phenomenon:

Back 69

elevation of the hemiplegic arm above the horizontal may elicit extension and abd of the fingers.

Front 70

Phenomenon with Stroke:

-Raimiste's phenomenon

Back 70

: (overflow technique) resistance of abd or add in the UE or LE will produce a similar response to the opposite extremity

Front 71

Phenomenon with Stroke:

-Homolateral limb synkinesis:

Back 71

( associated reaction) describes the tendency for flexion of the hemiplegic arm to produce flexion in the hemi leg.

Front 72

Phenomenon with Stroke:

Higher level balance reactions...?

Back 72

...such as righting, equilibrium, and protective extension are frequently impaired or absent.

Front 73

Phenomenon with Stroke:

PARESIS

Back 73

: a common finding in stroke pts where they are unable to generate normal levels of force necessary for initiating and controlling movement or for maintaining posture. Specific changes occur in both the motor neuron and muscle. Not all muscle groups are affected equally

Front 74

Phenomenon with Stroke:

INCOORDINATION

Back 74

can result from cerebellar or basal ganglia involvement (vertebrobasiliar artery), from proprioceptive losses, or from motor weakness. Ataxia is common with cerebellar lesions. Coordination (ch 7) is the ability to execute smooth, accurate, controlled movements. Coordinated movements are characterized by appropriate speed, distance, direction, rhythm, and muscle tension.

Front 75

Examples of diagnosis that typically demonstrate coordination deficits

PARKINSONS

Back 75

- rigidity

Front 76

Examples of diagnosis that typically demonstrate coordination deficits

MS

Back 76

different areas of tightness and weakness

Front 77

Examples of diagnosis that typically demonstrate coordination deficits

Huntington's disease

Back 77

coordination deficits:
>30, 5-15 years post- death; tone, posture, dementia

Front 78

Examples of diagnosis that typically demonstrate coordination deficits

CP

Back 78

increased or decreased tone

Front 79

Examples of diagnosis that typically demonstrate coordination deficits

Sydenham's choria

Back 79

- rheumatic fever- balance, gait, speech, cardiopulmonary

Front 80

Examples of diagnosis that typically demonstrate coordination deficits

cerebellar tumors

Back 80

– increased ataxia

Front 81

Examples of diagnosis that typically demonstrate coordination deficits

cerebellar strokes

Back 81

static ataxia

Front 82

Primary function of the cerebellum is coordination of motor activity,equilibrium and muscle tone. It works as an error-correcting mechanism by comparing the commands from the higher centers and the feedback from the periphery and it adjusts things as needed.

Back 82

Primary function of the cerebellum is coordination of motor activity,equilibrium and muscle tone. It works as an error-correcting mechanism by comparing the commands from the higher centers and the feedback from the periphery and it adjusts things as needed.

Front 83

Clinical Features of a Cerebellar dysfunction

dysmetria

Back 83

disturbance in the ability to judge the distance or range of movement

Front 84

Clinical Features of a Cerebellar dysfunction

dysdiadochokinesia

Back 84

impaired ability to perform rapid alternating movements

Front 85

Clinical Features of a Cerebellar dysfunction

tremor

Back 85

intention or static

Front 86

Clinical Features of a Cerebellar dysfunction

movement decomposition

Back 86

movements not performed as a single smooth activity, they are broken into component parts (ie finger to nose)

Front 87

Clinical Features of a Cerebellar dysfunction

ataxia

Back 87

jerky uncoordinated movements

Front 88

Clinical Features of a Cerebellar dysfunction

dysarthria

Back 88

disorder of the motor component of speech, inability to articulate

Front 89

Clinical Features of a Cerebellar dysfunction

nystagmus

Back 89

uncoordinated eye movement

Front 90

Clinical Features of a Cerebellar dysfunction

rebound phenomenon

Back 90

- inability to keep the limb in position after a resistance is released

Front 91

Clinical Features of a Basal Ganglia dysfunction

main condition?

Back 91

athetosis

Front 92

Changes in coordinated movements with age:

5 main points

Back 92

decreased strength
slowed reaction time
loss of flexibility
faulty posture
impaired balance

Front 93

How coordination is tested

nonequilibrium responses

examples of?

Back 93

finger to nose (self and PT)
finger to finger
alternating nose to finger
finger opposition
alternating pronation and supination
rebound test (elbow flexion)
foot and hand tapping
heel to knee and toe
heel to shin

Front 94

How coordination is tested

equilibrium responses

standing, examples of?

Back 94

feet together
- eyes closed
- tandem
- one foot
- balance displaced

Front 95

How coordination is tested

equilibrium responses

gait, examples of?

Back 95

- balance beam
- heel-toe
- sideways
- backward
- march
- on heels / on toes

Front 96

Motor programming deficits

with a LEFT CVA

ability to initiate movement?

Back 96

difficulty initiating and performing sequences of movement

Front 97

Motor programming deficits

with a LEFT CVA

time to learn task?

Back 97

take longer to learn a task

Front 98

Motor programming deficits

with a LEFT CVA

speed of motion?

Back 98

slower overall movements, with more positioning errors

Front 99

Motor programming deficits

with a LEFT CVA

APRAXIA...

Back 99

-inability to perform purposive movements although there is no sensory or motor impairment

Front 100

Motor programming deficits

with a LEFT CVA

mental state?

Back 100

more realistic about problems
negative, anxious or depressed

Front 101

Motor programming deficits

with a LEFT CVA

defect only in affected side?

Back 101

can present with motor programming problems in both the involved and uninvolved sides
overall more likely to present with motor programming deficits

Front 102

Motor programming deficits

with a RIGHT CVA

MOTOR IMPERSISTENCE

Back 102

-inability to sustain a movement or posture

Front 103

Motor programming deficits

with a RIGHT CVA

ability to pay attention?

Back 103

easily distracted and over stimulated
more perpetual deficits

Front 104

Functional Abilities: are typically impaired or absent and vary considerably from patient to patient. The ability to perform functional tasks is influenced by motor and perceptual impairments, disorientation, communication disorders, sensory loss, and decreased cardiorespiratory endurance.

Back 104

Functional Abilities: are typically impaired or absent and vary considerably from patient to patient. The ability to perform functional tasks is influenced by motor and perceptual impairments, disorientation, communication disorders, sensory loss, and decreased cardiorespiratory endurance.

Front 105

Speech and Language disorders

pts with lesions involving the "X" of the dominant hemisphere (usually the left) demonstrate speech and language impairments.

Back 105

parietoccipital cortex

Front 106

Aphasia

main idea

Back 106

- is the general term used to describe an acquired communication disorder caused by brain damage and characterized by an impairment of language comprehension, formulation and use.

Front 107

fluent aphasia

main idea

Back 107

speech flows smoothly, with a variety of grammatical constructions and preserved melody of speech, nonsense words, misuse of words and word substitutions. Auditory comprehension is impaired. (receptive language, Wernicke’s)

Front 108

nonfluent aphasia

main idea

Back 108

the flow of speech is slow and hesitant, vocabulary is limited and syntax is impaired. Articulation may be labored. Comprehension is good. (expressive language, Broca’s)

Front 109

global aphasia


main idea

Back 109

severe aphasia characterized by marked impairments of the production and comprehension of language

Front 110

Dysarthria

main idea

Back 110

problems forming words, articulation

Front 111

Damage to Broca's Area
(Broca's aphasia)

key points... can they produce speech, understand language, are words properly formed, rate of speech?

Back 111

Prevents a person from producing speech
Person can understand language
Words are not properly formed  
Speech is slow and slurred.

Front 112

Damage to Wernicke's Area
(Wernicke's aphasia)

can they understand langauge, is their language clear?

Back 112

Loss of the ability to understand language
Person can speak clearly, but the words that are put together make no sense. This way of speaking has been called "word salad" because it appears that the words are all mixed up like the vegetables in a salad.

Front 113

Perceptual deficits

where is the lesion, typically?

Back 113

lesions of the parietal lobe of the nondominant hemisphere usually right). ( anterior or middle cerebral artery).

Front 114

Perceptual deficits

what kind of clinical manifestation?

Back 114

These may include visuospatial distortions (inability to judge distance, size, position, rate of movement, form, or relation to parts as the whole ie: this pt will continuously run their wheelchair into the door frame), topographical disorientation (consistently get lost), disturbances in body image, and unilateral neglect.

Front 115

Cognitive and Behavioral changes

LEFT CVA

ability to process information?
typical mental state?

Back 115

difficulties processing information in a sequential, linear manner


negative, anxious, depressed

Front 116

Cognitive and Behavioral changes

LEFT CVA

assuredness?

Back 116

slower, more cautious, uncertain and insecure
hesitant in tasks and need more frequent feed back
realistic in their appraisal of their existing problems

Front 117

Cognitive and Behavioral changes

RIGHT CVA

ability to see "big picture"?
general mental attitude?

Back 117

difficulty in grasping the whole idea or the overall organization of a pattern or activity
indifferent, quick, impulsive, and euphoric

Front 118

Cognitive and Behavioral changes

RIGHT CVA

confidence in ability?
attentiveness?

Back 118

they overestimate their abilities while minimizing or denying their problems (safety problems)

become distracted and overstimulated easily

Front 119

LABILITY

main idea...

Back 119

they change from laughing to crying quickly and are unable to control their emotions

Front 120

How is attention span and memory impacted with a STROKE?

Back 120

The Pt with stroke typically has a short attention span, and immediate and short term memory is impaired. Long term memory remains intact

Front 121

STROKE pts may also exhibit irritability, confusion, restlessness, and sometimes psychosis, delusions or hallucinations. Dementia may occur with multiple brain infarcts. It is characterized by a general decline in higher brain functions such as faulty judgement, impaired consciousness, poor memory, diminished communication, and behavioral or mood alterations. Seizures occur in a small percentage of stroke patients.

Back 121

STROKE pts may also exhibit irritability, confusion, restlessness, and sometimes psychosis, delusions or hallucinations. Dementia may occur with multiple brain infarcts. It is characterized by a general decline in higher brain functions such as faulty judgement, impaired consciousness, poor memory, diminished communication, and behavioral or mood alterations. Seizures occur in a small percentage of stroke patients.

Front 122

Bladder and Bowel dysfunction with STROKE

main idea

Back 122

Urinary incontinence may require a catheter early on, but generally this resolves quickly. Pts are also frequently impacted requiring stool softeners and diet changes.

Front 123

Orofacial dysfunction with STROKE

dysphagia

main idea

Back 123

- a swallowing dysfunction that is a common complication after stroke. Decreased nutritional intake may require a temporary NG tube. Swallow studies or special diets

Front 124

visual dysfunction with STROKE

homonymous hemianopsia

main idea

Back 124

inability to see half the field of vision in one or both eyes- so either can’t see that side at all, or can’t see it well- Pusher Syndrome

Front 125

psychological problems with STROKE

common reaction include...

Back 125

frustrations in the changes in abilities. Common reactions include: anxiety, depression or denial. Additional their cognitive deficits play a role in their reactions. Depression is extremely common often needing pharmacological management.

Front 126

psychological problems with STROKE

which side (L or R) more commonly associated with secondary psych. issues?

Back 126

L CVA's more common than R CVA's and brainstem strokes.

Front 127

why are Decreasing ROM, Contracture and Deformity often associated with STROKE?

Back 127

may result from the loss of voluntary movement

Front 128

Deep Vein Thrombosis

often seen in stroke patients?

Back 128

DVT's and pulmonary embolism are potential complications for all immobilized patient

Front 129

Common signs of a DVT include...?

Back 129

calf pain or tenderness (+ Homan's sign), swelling and discoloration of the leg.

Front 130

treatments for DVT include...?

Back 130

Treatments include anticoagulants and antiplatelet agents, along with bed rest and elevation of the affected limb

Front 131

with a STROKE where might the patient have pain?

Back 131

Pain the Pt may have pain from muscle imbalances, improper movement patterns, musculoskeletal strain, and poor alignment

Front 132

pain with STROKE

thalamic syndrome

Back 132

from lesions affecting the thalamus resulting in contralateral sensory dysfunction.

Front 133

Shoulder dysfunction with STROKE

what shoulder condition is common (70-84%) with stroke patients?

Back 133

: Shoulder subluxation and pain is extremely common (70-84%) of patients post stroke. Adhesive capsulitis is often an eventual complication. Pain usually starts just during movement but if not addressed can eventually be at rest and extend into the arm and hand

Front 134

Reflex Sympathetic Dystrophy (RSD or shoulder-hand syndrome)

% that present with this, symptoms?

Back 134

also occurs in 12 - 25 % of the cases. The pt experiences swelling and tenderness in the hand and fingers along with shoulder pain. Sympathetic vasomotor changes including warm, red and glossy skin, along with trophic changes. In the latter stages increasing pain, followed by immobilization, stiffness, contractures and muscle atrophy. The skin is now cool, cyanotic and damp. The hand becomes contracted in MP extension and IP flexion. Early diagnosis is essential to prevent the latter deformities.

Front 135

Deconditioning with STROKE

cause?

Back 135

could be premorbid due to their age and cardiovascular status, prolonged bed rest as well as depression will impact their level of motivation as well as exercise tolerance.

Front 136

Recovery from stroke:
a. Mortality rates:

what % at one month
one year
5 years
10 years

Back 136

22 to 37 % at 1 month
25 - 50 % at 1 year
68 - 72 % at 5 years
at 10 years only 35 % are still alive

Front 137

when is the recovery from stroke fastest?

Back 137

fastest within the first few weeks after onset, with most (as high as 90%) of the neurologic recovery occurring by 3 months. Functional gain may continue for up to a year.

Front 138

Medical Management: includes the identification and control of stroke risk factors:

examples of stroke risk factors?

Back 138

regulation of BP
dietary adjustments
smoking cessation
platelet inhibiting therapy (aspirin)
control of associated diseases (heart and DM)
surgery (endarterectomy or angioplasty)
Acute treatment includes returning the Pt to normal body activities.

Front 139

Rehab Management of STROKE

when is rehab most optimal?

Back 139

early onset is optimal
timing of rehab should take into consideration: medical stability, motivation, Pt endurance, stage of recovery and the ability to learn

Front 140

who are the members of the REHAB TEAM with a STROKE patient?

Back 140

physician
nurse
Pt
PT
OT
speech
SW
neurophyscologist
Dietician

Front 141

Assessment of STROKE PATIENT

sense abilities?

Back 141

mental status: cognitive function
communication ability
sensation
perception

Front 142

Assessment of STROKE PATIENT

should you check joint mobility and skin condition?

Back 142

joint mobility include ROM, jt play and soft tissue compliance
skin and edema

Front 143

Assessment of STROKE PATIENT

examples of things to look at with MOTOR CONTROL

Back 143

motor control: muscle tone, reflexes, reactions, strength, voluntary movement patterns, motor planning ability, coordination, and balance

Front 144

Assessment of STROKE PATIENT

examples of things to look at with functional mobility skills?

Back 144

Functional mobility skills: bed mobility, transfers, wheelchair mobility and gait
endurance / cardiorespiratory status

Front 145

Acute stroke rehab

when should rehab begin?

Back 145

as soon as the Pt is stable (typically within 72 hours)

Front 146

Acute stroke rehab

goals

with ROM

Back 146

promote ROM and prevent deformity

Front 147

Acute stroke rehab

goals

use of involved side and trunk control?

Back 147

promote awareness, active movement, and use of the hemiplegic side
-improve trunk control, symmetry and balance

Front 148

Acute stroke rehab

goals

functional mobility? self care?

Back 148

improve functional mobility
-initiate self care activities

Front 149

Acute stroke rehab

goals

positioning?

Back 149

positioning:,-maximize the room to increase awareness of the hemiplegic side (hemi side to the door, family, TV etc) ** be careful to watch for signs of withdrawal in pts with unilateral neglect.

Front 150

how often should a STROKE pt be turned while in bed?

Back 150

-while spending significant time in bed should be on a 2 - 3 hour turning schedule

Front 151

when spending time in bed, a STROKE pt should avoid what kind of positioning?

Back 151

avoid: lateral side flexion of the head and trunk toward the affected side with head rotation toward the unaffected side; depression and retraction of the scapula, IR and Add of the arm, elbow flexion and forearm pronation, wrist and finger flexion; retraction and elevation of the hip, with hip and knee extension and hip add; or hip and knee flexion with hip abduction. Plantar flexion in either.

Front 152

should foot boards be used with a STROKE pt?

Back 152

avoid foot boards, objects in the hand and poor shoulder positions

Front 153

what kind of positioning should be promoted for a patient with STROKE while in bed?

Back 153

promote: lying in the supine position with head and trunk in midline or flexed slightly to the good side, a small pillow or towel under the scapula to promote protraction, the arm can rest on a pillow extended and in abd, with wrist and finger extension see 343-344 for lying on good side, affected side and sitting

Front 154

what is the HEMIPLEGIC ARM at risk for?

Back 154

the hemiplegic arm is at great risk for traction and subluxation injuries.

Front 155

HEMISLING

main idea and use?

Back 155

pads are between the elbow and wrist, these are effective to prevent subluxation but promote contractures in add and IR. They also may impair trunk mobility, balance reactions and a positive body image

Front 156

BOBATH SLING

main idea and use

Back 156

. Bobath slings are an alternative approach which is a humeral cuff maintained by a figure 8 harness. This avoids the internally rotated and flexed arm. A padded arm trough on the wheelchair is option. It is also good for controlling subluxation

Front 157

should slings be used with a STROKE pt with SPASTICITY?

Back 157

As spasticity emerges the use of slings are generally contraindicated; can use weight bearing, FES, approximation

Front 158

ROM after STROKE: usually ROM techniques with special attention to...

UE Focus

Back 158

UE ER and scapular movement (self ROM with overhead pulleys is generally contraindicated)

Front 159

ROM after STROKE: usually ROM techniques with special attention to...

LE Focus

Back 159

LE focus on the deficits; can use icing which can decrease spasticity, contract/ relax and decrease spasticity; increase tone by tapping, vibration and overflow technique

Front 160

functional mobility activities after STROKE

how should they be performed?

Back 160

should be practiced bilaterally, guided and AAROM provide a good base for early learning. The Pt should be given only as much assistance as needed and encouraged to move Indep as much as possible

Front 161

functional mobility with STROKE

examples of positions

Back 161

-bed mobility
-rolling
-bridging
-prone on elbows
-quadruped
-coming to sitting
-sitting
-kneeling
-1/2 kneeling
-modified plantigrade
-standing
-transfers
-gt
-other

Front 162

Post Acute rehab with STROKE

what will pts be continuing with?

Back 162

pts will be continuing with the activities and goals initiated during the acute phase. It is important to remember to monitor cardiorespiratory endurance and avoid overexertion

Front 163

goals with post acute rehab

secondary complications?
sensory and perceptual losses?

Back 163

prevent or minimize secondary complications
compensate for sensory and perceptual loss

Front 164

goals with post acute rehab

movement control and posture?

Back 164

promote selective movement control and normalization of postural tone
improve postural control and balance

Front 165

goals with post acute rehab

functional mobility and ADLs?

Back 165

develop independent functional mobility skills
develop independent ADL's

Front 166

goals with post acute rehab

endurance?
socialization?

Back 166

develop functional cardiorespiratory endurance
encourage socialization and motivation.

Front 167

Motor control training

what kind of movement patterns?

Back 167

stress out of synergy movement patterns

Front 168

Motor control training

what kind of movement tasks should be emphasized?

Back 168

emphasize movement tasks that allow functional success (feeding, dressing, gt)

Front 169

Motor control training

as control develops, what should be tried?

Back 169

as control develops use more difficult postures

Front 170

Motor control training

what kind of resistance to movement?

Back 170

use minimal resistance to movement

Front 171

Motor control training

what kind of contractions will be easier?

Back 171

generally eccentric contractions will be easier than concentric, but all including isometrics should be practiced

Front 172

Motor control training

should spastic or weak muscles be activated first?

Back 172

weak muscles should be activated before spastic in unidirectional patterns followed by slow reversals. (balanced interaction is crucial for development of coordinated movement)

Front 173

Motor control training

what to do if pt is hypotonic?

Back 173

if patient is hypotonic, tone facilitation can be utilized with exteroreceptors, proprioceptors and reflex stimulation. There is a disagreement in theories whether or not to promote synergistic patterns. Can use tapping, quick bounce, stroking, cool pool

Front 174

Tone Reduction

when is spasticity typically seen in recovery?

Back 174

this spasticity is typically seen in the middle phases of recovery

Front 175

Tone Reduction

how should the positioning be?

Back 175

positioning out of reflex dependent postures

Front 176

Tone Reduction

what kind of movement patterns should be emphasized?

Back 176

reflex inhibiting movement patterns (encourages antagonists)
rhythmic rotation out of spastic patterns
stimulate antagonists

Front 177

Tone Reduction

what system do you want to activate?

Back 177

vestibular system

Front 178

Tone Reduction

what effect does prolonged icing have?

Back 178

prolonged icing to slow nerve conduction

Front 179

Sensory Compensation

which side to use?

Back 179

use affected side

Front 180

Sensory Compensation

what effect does repetition of sensory stimuli have?

Back 180

repetition of sensory stim helps with reorganization

Front 181

Sensory Compensation

what kinds of things can increase sensory input?

Back 181

stretch, stroking, superficial and deep pressure, and weight bearing will increase sensory input

Front 182

Sensory Compensation

where should attention be focused?

Back 182

focus attention directly on tasks

Front 183

Postural control and balance

why begin in static postures?

Back 183

begin in static postures to increase symmetrical weight bearing

Front 184

Postural control and balance

progress towards,,,?

Back 184

progress to controlled mobility activities
progress to dynamic surfaces

Front 185

UE control with STROKE

begin with X and work X?

Back 185

begin with scapular activities and work distally

*reinforce OT guidlines*

Front 186

LE control with STROKE

prepare for X?

Back 186

prepares for ambulation

Front 187

LE control with STROKE

incorporate X that are appropriate combinations for X?

Back 187

incorporate activities that are appropriate combinations for gt

Front 188

Gait training with stroke

when should gait training be initiated and why?

Back 188

is usually initiated early for motivation and minimize deconditioning. It should focus on attainment of movement control in selective patterns with appropriate timing

Front 189

Gait training with stroke

what should be done once deficiencies have been noted?

Back 189

Once deficiencies are noted it is important to bring the Pt down to the lower level activities to achieve the selective movement.

Front 190

how can persistent posturing of the upper extremity be controlled?

Back 190

by holding the hemiplegic. arm in extension and abd with the hand open

Front 191

what, if any, orthotic might be indicated with a stroke?

Back 191

the CVA pt will most likely need an AFO if any device, KAFO is rarely prescribed and rarely successful. The ankle position is usually utilized to control knee instability. Prescription will depend on the pts unique problems.

Front 192

Exercise conditioning

what kind of fitness program should be initiated?

Back 192

organized cardiovascular fitness program to increase endurance will be useful for all patients especially those with cardiac compromise. Careful monitoring during exercise is tantamount for success and safety.

Front 193

Patient and family education

how should information be conveyed?

Back 193

1.give accurate and factual information about the pts capabilities and limitations, avoid predicting the future.

Front 194

Patient and family education

how should interventions be structured?

Back 194

2.structure interventions carefully and do not overwhelm the Pt or family with information, be consistent and repeat information.

Front 195

Patient and family education

what kind of forum should be created?

Back 195

3.provide an open forum for communication and discussion

Front 196

Patient and family education

what kind of attitude should you have?

Back 196

4.be supportive, sensitive and maintain a hopeful manner.

Front 197

Patient and family education

role in problem solving with patients and families?

Back 197

5.assist pts and families in confronting alternatives and developing problem-solving abilities.

Front 198

Patient and family education

how should you impact the patients self esteem?

Back 198

6.motivate and provide positive reinforcement in therapy; enhance Pt satisfaction and self esteem.

Front 199

Patient and family education

what additional support in the community might you recommend to the patient?

Back 199

7.refer to support and self help groups.

Front 200

pts who generally do poor in rehab include:

what kinds of mental issues?

Back 200

decreased alertness, inattention, poor memory, and an inability to learn new tasks or follow simple commands

Front 201

pts who generally do poor in rehab include:

ANOSOGNOSIA

definition

Back 201

denial of problem

Front 202

pts who generally do poor in rehab include:

what kinds of medical complications?

Back 202

-significant medical complications (falls, cardiac and DJD)
-serious language disturbances

Front 203

TBI

50% are the result of...?

Back 203

Motor vehicle accidents

Front 204

TBI

which sex is usually more at risk

Back 204

males more than females

Front 205

TBI

typical age of a person with a TBI?

Back 205

15-24

Front 206

a major role of health professionals is education in the prevention of TBI, this includes...?

Back 206

use of passive restraints, helmets, responsible alcohol consumption, proper training in athletics and so on.

Front 207

Classification and Pathophysiology of TBI

how are TBIs assessed?

Back 207

a. mild, moderate or severe based on the Glascow coma scale (492)

Front 208

Classification and Pathophysiology of TBI

what determines if it is OPEN or CLOSED?

Back 208

depending on skull fracture

Front 209

Classification and Pathophysiology of TBI

velocity determinations?

Back 209

high velocity or low velocity

diffuse or focal

Front 210

Factors that Influence outcome of a TBI include...?

Back 210

the preinjury status of the patient, the primary damage, the cumulative effect of secondary brain damage produced by systemic and intracranial mechanisms that occur after the initial injury

Front 211

Premorbid status of TBI include what 3 major categories?

Back 211

prior head injury
older adults
intelligence and cognitive functioning

Front 212

Primary damage with TBI

what does LOCAL BRAIN DAMAGE refer to?

Back 212

damage localized to the site of the impact

Front 213

Primary damage with TBI

what do the terms COUP and COUNTERCOUP INJURY refer to?

Back 213

under the site of impact as well as directly opposite the site of impact

Front 214

Primary damage

POLAR BRAIN DAMAGE refers to...?

Back 214

occurs when the head is subjected to acceleration and deceleration (ie head on collision) causes damage to the poles of the lobes due to the shift and abrupt stop, neurologic damage may not show up until 2 - 3 days later when swelling and shifting occur.

Front 215

Primary damage

DIFFUSE BRAIN INJURY

anatomical picture

Back 215

diffuse axonal injury, refers to widely scattered shearing of subcortical axons within their myelin sheath, it can be isolated or also have localized or polar damage with it, it can also extend down into the midbrain and brainstem

Front 216

Primary damage

DIFFUSE BRAIN INJURY

functional picture

Back 216

With this type of injury, the Pt is deeply comatose from the time of injury, has abnormal and autonomic dysfunction (control of involuntary bodily functions).

Front 217

Secondary injury

HyYPOXIC-ISCHEMIC INJURY

anatomical picture

Back 217

vascular compromise due to shifting brain structures

Front 218

Secondary injury

HYPOXIC-ISCHEMIC INJURY

anatomical picture

Back 218

vascular compromise due to shifting brain structures

Front 219

Secondary injury

HYPOXIC-ISCHEMIC INJURY

injury picture

Back 219

. A more diffuse form of this would caused by arterial hypoxemia due to such things as airway obstruction and chest trauma.

Front 220

Secondary injury

INTRACRANIAL HEMATOMAS

what are they associated with?

Back 220

often associated with the "talk and die" pts. This late appearing complication results from compression of the brain by the expanding hematoma.

Front 221

Secondary injury

INTRACRANIAL HEMATOMAS

how are they usually classified?

Back 221

They are usually classified by their site (epidural, subdural or intracerebral) and by the time in which they develop after the injury: acute, subacute and chronic.

Front 222

Secondary injury

INTRACRANIAL PRESSURE

what is this associated with?

Back 222

even mildly increased ICP is associated with increased morbidity.

Front 223

Secondary injury

INTRACRANIAL PRESSURE

if severely increased?

Back 223

Severely increased ICP may result in herniation of the brain (uncal, central (transtentorial), and tonsillar (foramen magnum).

Front 224

Other causes to secondary brain damage include...?

Back 224

intracranial infection
-cerebral artery vasospasm
-obstructive hydrocephalus
-post traumatic epilepsy
-neurochemical changes

Front 225

Common clinical rating scales with TBI are used to...?

Back 225

used to standardize the description of patients who have sustained head injuries.

Front 226

The Glascow Coma Scale (GCS) is used to...?

Back 226

used to document level of consciousness and define severity of the injury (24-1) shown to be statistically reliable

Front 227

The GLASCOW COMA SCALE (GCS) has 4 stages, what are they?

Back 227

8 or less = severe
9 - 12 = moderate
13 -15=mild
l5=normal

Front 228

Ranchos Los Amigos level of cognitive functioning (LOCF) is...?

Back 228

descriptive scale that outlines a predictable sequence of cognitive and behavioral recovery seen in pts with TBI

Front 229

Ranchos Los Amigos level of cognitive functioning (LOCF)

is it certain and specific?

Back 229

No data on reliability and does not address specific cognitive deficits

Front 230

Ranchos Los Amigos level of cognitive functioning (LOCF)

general use with TBI

Back 230

It is useful for reporting general cognitive and or behavioral status. (24-3)

Front 231

Rappaport's Disability rating scale (DRS):

general use in TBIs?

Back 231

covers a wide range of A functional areas and is used to classify level of disability from none - to death. Statistical reliability is high. (24-4)

Front 232

Glascow Outcome Scale (GOS)

how different from the original and what is its use?

Back 232

original scale expanded to 8 categories, used for research to quantify outcomes. Statistically high reliability

Front 233

Diagnostics with TBI

electroencephalograms (EEC)

what do they measure?

Back 233

measures CNS activity. One form of EEC is evoked potential where the EEC signals are averaged in response to stimuli and used to evaluate sensory function.

Front 234

Diagnostics with TBI

computed tomography (CT):

what are they usefull for?

Back 234

useful for identifying hematomas, atrophy and ventricular enlargement. Not as sensitive as MRI.

Front 235

Diagnostics with TBI

magnetic resonance imaging (MRI):

sensitivity?

Back 235

more sensitive than CT's especially to nonhemorrhagic lesions

Front 236

Diagnostics with TBI

cerebral blood flow mapping

what does it use and what is its use?

Back 236

use PET scans (positron emissions tomography) to measure cerebral metabolism (only 60 worldwide) so limited clinical value. Their is a more common SPECT scan but it is not as sensitive.

Front 237

Deficits related to head injury

how does a decreased level of consciousness relate to accelration-deceleration injures?

Back 237

occurs consistently in acceleration-deceleration injuries as well as some focal injuries.

Front 238

Deficits related to head injury

what characterizes the coma: GCS <8 stage of a TBI?

Back 238

"not obeying commands, not uttering words and not opening the eyes", usually lasts only a few weeks at most

Front 239

Deficits related to head injury

persistent vegetative state (PVS) is characterized by what?

Back 239

postcomatose unawareness, may have a wide range of responses including eye opening and sleep - wake cycles , these may occur at subcortical levels. pts in PVS do not speak or produce any type of behavior that is purposeful or psychologically meaningful.

Front 240

Deficits related to head injury

post traumatic amnesia is characterized by what?

Back 240

: appear to be conscious, this describes the time between injury and the time when the Pt is able to remember ongoing events.

Front 241

Deficits related to head injury

cognitive deficits generally affect what abilities?

Back 241

most pts will have residual cognitive deficits. disorders of learning, memory and complex information processing

Front 242

Deficits related to head injury

cognitive deficits will generally manifest as?

Back 242

problems with selective attention to problems understanding a task, to problems planning a strategy for a solution.

Front 243

Deficits related to head injury

can communication be affected?

Back 243

deficits in communication: expressive as well as receptive

Front 244

Deficits related to head injury

behavioral defecits

in what way are they the most disabling TBI defecits?

Back 244

these are the most socially disabling of all the TBI deficits. Long term changes in behavior such as sexual disinbibition, apathy, aggression, low frustration tolerance and depression often lead to a life of loneliness and seclusion.

Front 245

Deficits related to head injury

sensorimotor defecits

general deconditioning due to?

Back 245

due to significant medical complications, effects of coma and other changes

Front 246

Deficits related to head injury

sensorimotor defecits

what kinds of paresis?

Back 246

hemiparesis
bilateral hemiparesis

Front 247

Deficits related to head injury

sensorimotor defecits

how can they present?

Back 247

balance deficits
ataxia and incoordination (cerebellar or basal ganglia damage)

Front 248

Deficits related to head injury

sensorimotor deficits

what injuries are associated with this?

Back 248

fractures, peripheral nerve injuries and SCI

Front 249

Acute management of TBI

where is the focus, medically?

Back 249

: focuses on determination of the severity of the injury, preservation of life, and prevention of further damage. ICP may be monitored with a camino bolt (should remain below 20 mmHG

Front 250

Acute management of TBI

where is the focus for PT

Back 250

pulmonary hygiene, prevention of contractures (ROM, splinting; casting, passive weight bearing on the tilt table), and prevention of pressure sores. Functional mobility may begin when the Pt stabilizes. Always check with the nurse before initiating treatment in the NICU.

Front 251

Rehabilitative management with TBI

what is the #1 goal?

Back 251

prominent goal is to return the Pt to society at the highest possible level of functioning.

Front 252

Rehabilitative management with TBI

for low level patients (LOCF I-III), what does the treatment picture look like?

Back 252

these pts have little if any interaction with the environment. Goals of tx to prevent contractures, decubitus ulcers, and increase the level of interaction with the environment.

Front 253

Rehabilitative management with TBI

for low level patients (LOCF I-III) how should sensory stimulation be done?

Back 253

Sensory stimulation.should be done in short tx sessions (15 - 30 min). Be careful to only administer one stimulus at a time and not to overload.

Front 254

Rehabilitative management with TBI

for low level patients (LOCF I-III) how should they be monitored?

Back 254

should be closely monitored for response and the following should be noted: latency(time delay between stim and response), consistency (how many times out of a given number of stimulus does the Pt respond the same), intensity (is the response proportional to the stimulus), and duration (how long the response lasts).

Front 255

Rehabilitative management with TBI

with types of stimulation, how does the order of loss impact the return?

Back 255

Last to shut down is the first to start up

Front 256

Rehabilitative management with TBI

general ideas for AUDITORY STIMULATION?

Back 256

use normal tones, discuss meaningful topics to the Pt, intermittent use of the radio or television is ok, but discourage background noise during tx.

Front 257

Rehabilitative management with TBI

general ideas for VISUAL STIMULATION?

Back 257

use familiar objects and pictures, watch for attentiveness and tracking.

Front 258

Rehabilitative management with TBI

general ideas for OLFACTORY STIMULATION?

Back 258

place scents under pts nose for 10 -15 seconds (may not responds if trached) try and use favorite or familiar smells

Front 259

Rehabilitative management with TBI

general ideas for GUSTATORY STIMULATION?

Back 259

: watch out for swallowing precautions, use cotton swabs dipped in flavored solutions

Front 260

Rehabilitative management with TBI

general ideas for TACTILE STIMULATION?

Back 260

provided during functional activities such as turning and bathing, allow Pt to feel the motion of these activities

Front 261

Rehabilitative management with TBI

general ideas for VESTIBULAR STIMULATION?

Back 261

can be provided with neck ROM, rolling, rocking or WC rides.

Front 262

Rehabilitative management with TBI

what range typifies a MID LEVEL for cognitive function?

Back 262

mid level: (LOCF IV - VI)

Front 263

Rehabilitative management with TBI

what characterizes a MID LEVEL patient who is at LEVEL IV?

Back 263

level IV: these pts are in a confused and agitated state and require a tremendous amount of structure. Goals include maintenance or improvement of ROM, prevention of further deconditioning, improved response to simple commands, and prevention of agitated outbursts

Front 264

Rehabilitative management with TBI

when working with a MID LEVEL patient how should the treatment proceed?

Back 264

It is important to work at the pts physical level and strengthen instead of push to more challenging skills. Sometimes it is easier to use fun activities to get treatment goals

Front 265

Rehabilitative management with TBI

when working with a MID LEVEL patient is routine important?

Back 265

remember the pt is confused: see the Pt at the same time, same place and same person everyday. establish a routine, provide orientation do no test at this stage

Front 266

Rehabilitative management with TBI

when working with a MID LEVEL patient is it important to teach new skills?

Back 266

expect no carryover: teaching new skills is unrealistic. Use charts and graphs to help recall.

Front 267

Rehabilitative management with TBI

when working with a MID LEVEL patient what importance does your behavior have on them?

Back 267

model calm behavior: be calm and so will the Pt

Front 268

when working with MID LEVEL TBI patients, how should you accommodate low attention spans and how can you provide a sense of control to the patient?

Back 268

be prepared with numerous activities: low attention span requires numerous activities
-offer options: this gives the Pt a sense of control, be careful with the phrasing of your questions

Front 269

when working with MID LEVEL TBI patients, is it beneficial to try and get the patient to understand other points of view?

Back 269

expect egocentricity: do not attempt to make the Pt understand other points of view

Front 270

Rehabilitative management for TBI

for patients at LEVEL V and VI, what are the common characteristics?

Back 270

at this level pts are confused but no longer agitated, they are able to follow simple commands fairly accurately and consistently, if overstressed their abilities will deteriorate

Front 271

Rehabilitative management for TBI

for patients at LEVEL V and VI, what should the goals focus on?

Back 271

While carryover is now present, new learning is limited. Goals should include increasing the patients participation in the program, increasing or maintaining ROM, increasing physical conditioning, and treating any focal motor defects

Front 272

Rehabilitative management for TBI

for patients at LEVEL V and VI, should the treatment schedule be fixed or fluid?

Back 272

maintain structure: keep their schedule

Front 273

Rehabilitative management for TBI

for patients at LEVEL V and VI, how should instructions be given?

Back 273

keep instructions to a minimum: speck slowly and allow for processing delays. Use familiar activities.

Front 274

Rehabilitative management for TBI

for patients at LEVEL V and VI, what is the benefit of using physical props?

Back 274

use physical props to improve compliance: use timers, charts, graphs. Videotaping may be useful for realism.

Front 275

Rehabilitative management for TBI

for HIGH LEVEL (LOCF VII & VIII), is the structure utilized early on still a priority?

Back 275

): it is at this level (late VII, early VIII) that pts are usually discharged home. It is important to wean them from the structure utilized early on

Front 276

Rehabilitative management for TBI

for HIGH LEVEL (LOCF VII & VIII), what role should decision making in the patient play?

Back 276

Pts should be involved in decision making, and reintegrated into their homes and communities. The focus is maintaining performance while decreasing structure and supervision.

Front 277

Rehabilitative management for TBI

for HIGH LEVEL (LOCF VII & VIII), what is a common residual problem?

Back 277

One residual problem in most brain injuries is some degree of sensorimotor integration dysfunction. Subtle problems with activities that require speed, flexibility, interlimb coordination, rhythm and timing.

Front 278

Rehabilitative management for TBI

for HIGH LEVEL (LOCF VII & VIII), what is ROBOT SYNDROME?

Back 278

robot like motion, excessive eating, and sedentary avocational activities. Pts at this level should be involved in pleasurable scheduled physical activity. pts who recover to level VIII will need vocational and driving services.

Front 279

Rehabilitative management for TBI

issues that cross all levels include the folowing facets in regards to ROM

Back 279

: often a combination of treatments is necessary: oral spasticity medications, nerve or motor point blocks, serial casting and positioning systems. If all conservative measures fail the Pt may undergo manipulation under anesthesia or surgical releases. most disabling of all is equines deformities. Use prophylactic casting, serial casting prior to surgery. short leg casts are also useful functionally for tone inhibition.

Front 280

Rehabilitative management for TBI

issues that cross all levels include the folowing facets in regards to MOBILITY

Back 280

use same techniques as discussed in CVA's but must keep the cognitive difficulties in mind. Improved mobility can result in improved cognitive function.

Front 281

Rehabilitative management for TBI

what should not be done if cognitive impairments cause safety issues?

Back 281

be careful not to document independence in activities if cognitive impairments cause safety issues.

Front 282

Rehabilitative management for TBI

in regards to goal setting and predictions, is there certainty in the projections?

Back 282

very Pt specific with outcome predictions very difficult due to the individuality of the injuries.