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OTB 520- Phys Dys > Week 11 to Week 14 > Flashcards

Week 11 to Week 14 Flashcards

1
Q

Supports & Subluxation :

What are reasons for prescription for slings/supports?

A

Weakness, subluxation, hypotonia, pain, neglect, decreased cognition, Pain and subluxation for orthoses

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2
Q

Supports & Subluxation :

Reasons for discontinued use:

A

Improvement in strength

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3
Q

Summarize Article Continued (Foongchomcheay, Ada, & Canning, 2005):

A

Summary:
Supportive devices commonly prescribed by Australian physiotherapists to prevent subluxation

Slings most commonly prescribed

Wheelchair/chair attachments also widely used

Strapping also common

Best for preventing subluxation: Lab tray, arm trough, triangular sling, and Harris sling (sling for standing only/temporary)

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4
Q

Taping for Subluxation:

Taping Overview

A

Beneficial for shoulder impingement, joint sprains, and multi-directional instability

Reposition humeral head with tape to that it is in a neutral position

Taping allows client to feel normal alignment

Can result in immediate pain relief and improved ROM

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5
Q

Taping for Subluxation:

Article: (Peters & Lee, 2003)

A

Case study of shoulder taping on individual with R hemiplegic UE following CVA

Taping significantly reduced pain and relieved tension

Taping method: tri pull method = 3 pieces of tape

1) Mid humerus deltoid tuberosity across the scapula near T3 spinous process
2) Deltoid tuberosity across clavicle to mid clavicle
3) Deltoid tuberosity over acromion process to the neck

Outcome measures:
Results:

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6
Q

CA tri pull method

position

A

1) Medial = 1 inch below deltoid tuberosity - 1 inch above acromial process
2) Posterior = 1 inch below deltoid tuberosity - 1 inch above spine of scapula
3) Anterior = 1 inch below deltoid tuberosity - 1 inch above coracoid process

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7
Q

E-stim & Subluxation

A

May improve muscle strength, joint alignment, spasticity, and sensory deficits

Rationale = allows muscle activity to maintain the glenohumeral joint

No significant evidence of pain reduction with e-stim, did improve pain free PROM

No negative effects found

Functional e-stim found to be effective in reducing shldr subluxation. Most effective early on

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8
Q

Orthotics: Principles

A

Orthotics: Principles
Used to maintain or increase the length of soft tissues by preventing or lengthening shortened tissues and preventing overstretching of the antagonist

Used to correct biomechanical malalignment and protecting joint integrity

Used to position the hand to assist in functional tasks

Used to promote independence in specific areas of occupation

Compensate for weakness by providing an external support

Limited Evidence
Evidence currently does not support one style of orthosis over another
(Gillen, 2016)

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9
Q

Considerations for Prescribing & Designing Orthotics

A

Spasticity
Orthosis may prevent painful contractures and loss of tissue length
Serve to provide a stretch to the distal UE
TX should begin before spasticity becomes severe

Those with severe spasticity should not use Orthosis - Why?

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10
Q

Considerations for Prescribing & Designing Orthotics: Soft Tissue Shortening

A

Evaluate Extrinsics:
Extend the wrist with digits flexed, wrist in ext. and attempt to extend the digits
Next flex the wrist palm upwards

Evaluate Intrinsics:
Normal: MCP are flexed and IP joints are extended
Normal: MCP are extended and IP are flexed
Hold MCP joint in ext and attempt to flex the PIP joint

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11
Q

Extrinsic extensor tightness:

A

full passive composite wrist and digit flexion is not obtainable.

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12
Q

Extrinsic flexor tightness:

A

full passive composite wrist and digit extension is not obtainable.

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13
Q

Intrinsic tightness:

A

PIPs & DIPs can be fully passively flexed when MCP’s are in a position of flexion (puts the interossei on slack)

PIPs & DIPs cannot be fully passively flexed when MCP’s are in a position of extension

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14
Q

Considerations for Prescribing & Designing Orthotics

A

Low Load Prolonged Stress (LLPS)

LLPS in when the tissue is held in a low lengthened position for a total end range time (TERT).

TERT = 1-2 hrs, 3 -4 hours, ideally progresses to 6 - 8 hrs

Stretching manually is not enough and must be followed up with orthotic devices

Orthotic must be readjusted (weekly) to ensure prolonged stretch is occurring

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15
Q

Orthotics: Application Consideration: Normal Posture of the Distal UE

A

Forearm neutral (midway between supination and pronation)

Wrist 10 - 15 degrees of ext

Thumb slight ext and abd, MCP and IP flexxed 15 - 20 degrees

2nd metacarpal aligned w/ radius

Digits: all joints in slight (10-20 degrees) flexion

Palmar arch maintained

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16
Q

Orthotics: Application Consideration: Typical Deviations after Stroke

Wrist Flexion =

A 
Wrist Flexion = 
flattened palmer arches
passive digit extension
shortened collateral ligaments @ MPs 
narrowed thumb web space
decreased grip
decreased wrist deviation ROM
Edema
shortening of wrist & extrinsic digit flexors
lengthening of wrist & extrinsic digit extensors
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17
Q

Orthotics: Application Consideration: Typical Deviations after Stroke

Wrist & digit flexion

A 
shortened extrinsic flexors
lengthened extrinsic extensors
decreased normal tenodesis action
contractures and deformity
skin maceration risk
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18
Q

Orthotics: Application Consideration: Typical Deviations after Stroke

Extreme ulnar deviation

A

decreased wrist /
shortened tissues ulnar FA
lengthened tissues radial FA
shift of carpal rows

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19
Q

Orthotics: Application Consideration: Typical Deviations after Stroke

Loss of palmar arches

A

decreased grip

decreased dexterity

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20
Q

TBI

A

The most common cause of death and disability among young people

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21
Q

TBI: Open

A

penetrating injury or perforating

Injury depends on shape, mass, direction, and velocity of the object

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22
Q

TBI: Closed

A

Closed direct or indirect impact without penetration

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23
Q

TBI: Blast injuries =

A

= can occur in conjunction with open or closed

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24
Q

Pathology: Focal

A

Caused by a direct blow to the head with an external object or fall, penetrating injury from a weapon, collision of the brain with the inner tables of the skull

Common findings from falls = intracerebral and brain surface contusions (inferior and dorsal-lateral frontal lobes, anterior and medial temporal lobes, and less common inferior cerebellum)

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25
Q

Pathology: Diffuse vs. Focal:

Focal

A

Caused by a direct blow to the head with an external object or fall, penetrating injury from a weapon, collision of the brain with the inner tables of the skull

Common findings from falls = intracerebral and brain surface contusions (inferior and dorsal-lateral frontal lobes, anterior and medial temporal lobes, and less common inferior cerebellum)

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26
Q

Pathology: Diffuse vs. Focal:

Focal

A

Caused by a direct blow to the head with an external object or fall, penetrating injury from a weapon, collision of the brain with the inner tables of the skull

Common findings from falls = intracerebral and brain surface contusions (inferior and dorsal-lateral frontal lobes, anterior and medial temporal lobes, and less common inferior cerebellum)

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27
Q

Pathology: Diffuse vs. Focal:

Coup

A

(the site of direct injury)

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28
Q

Pathology: Diffuse vs. Focal:

Countercoup

A

(site of indirect injury)

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29
Q

Epidural hematomas (EDHs

A

associated with skull fractures and disruption of meningeal arteries

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30
Q

Subdural hematomas (SDHs) =

A

occur between the dura and brain surface due to tearing of bridging veins

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31
Q

Location of trauma dictates symptoms:

A

Pre-frontal & anterior temporal areas: impaired memory, emotion and motivation

Orbitofrontal area: impulsivity

Frontolateral cortex:impassivity, hemiparesis, impaired attention and mental flexibility

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32
Q

Multifocal & Diffuse Brain injury

A

Often caused by sudden deceleration of the body and head with variable forces and deeper portions of the brain

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33
Q

Intracerebral hemorrhage (ICH)

A

nearly always present with missile wounds and common after falls and assault

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34
Q

Subarachnoid hemorrhage (SAH) & Intraventricular hemorrhage (IVH)

A

occur when the pia or arachnoid is torn.

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35
Q

Diffuse axonal injuries (DAIs)/ Traumatic axonal injury (TAI) =

A

= prototypic lesions caused by rapid deceleration and rotation of the brain in the skull

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36
Q

Possible symptoms include:

A 
Ataxia
Diplopia
Dysarthria
Impulsivity, irritability
Apathy, poor initiative
Decreased mental processing speed & efficiency
Impaired attention
Impaired abstract reasoning, planning, problem solving
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37
Q

Primary injury =

A

= occurs at the time of trauma

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38
Q

Secondary injury=

A

Occur as a result of the effects of brain swelling in a closed space, loss of perfusion, and decreased delivery of oxygen

The American Association of Neurological Surgeons has developed guidelines for management of severe TBI to minimize secondary injury

Resuscitation of blood pressure and oxygenation, management of elevated intracranial pressure, nutrition after acute trauma and seizure prophylaxis

Secondary effects (Radomski, 2008): hypoxia, hypotension, hypothermia, and hyperthermia (most common)

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39
Q

State of Consciousness

A

TBI typically results in an altered level of consciousness

From Coma to conscious awareness

Progression along this continuum varies depending on age, previous health, severity of injury, and medical/therapeutic/environmental management.

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40
Q

Coma =

A

As coma resolves client is either partially aware (minimally conscious) or if no awareness = vegetative

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41
Q

Vegetative State =

A
  • Wakefulness without awareness
  • Characteristics: no awareness of self or environment, inability to interact with others, no sustained or voluntary behavioral responses, no language comprehension, sleep wake cycle varies, ability to regulate temp, breathing, and circulation with medical care, incontinence of bowels and bladder, variably preserved cranial nerves and spinal reflexes
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42
Q

Minimally Conscious State (MCS)

A
  • Evidence of awareness of self and/or environment.
  • Must have 1 of the following: ability to follow commands, gesture or verbal yes/no responses, intelligible verbalization, and purposeful movement
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43
Q

Post Traumatic Amnesia (PTA)

A
  • Single best measurable predictor of functional outcomes
  • Length of time from the injury to the moment the individual regains ongoing memory of daily events
  • Longer PTA = poorer outcomes (cognitive and motor abilities, and function)
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44
Q

Intracranial Pressure

A

When the brain is injured, it reacts like other parts of the body that may be injured…it swells.

Unfortunately, the cranial vault where the brain sits inside the skull has a limited volume of about 1,400 milliliters.

When the brain swells, it can damage and kill neurons by squeezing them and stopping oxygen from reaching the cells.

If the (ICP) pressure gets too much, the brain can be forced into the hole at the base of the brain, the foramen magnum, and compress the brainstem.

The brain stem is where the consciousness, breathing, and heart rate are controlled.

Damage here can result in coma or death.

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45
Q

Second Impact Syndrome (SIS)

A

Occurs when an individual suffers a second head injury before the initial injury has fully healed…leads to diffuse cerebral swelling

Can potentially result in death within minutes

Rare enough condition that its frequency of occurrence is debated

Kevin Pearce (snowboarder)

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46
Q

Chronic Traumatic Encephalopathy

A

A neurodegenerative disease associated with repeated head trauma

Results in generalized global atrophy of the brain, ventricular dilation, thinning of the corpus collosum, and neurofibrillary bundles similar to AD

Symptoms include headaches, difficulties with attention and memory, mood disorders, motor dysfunction, and dementia

First identified in 1954 and linked to boxing, it has gained more attention in recent years due to the suicides of NFL football players and a recent movie about Dr. Bennet Omalu

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47
Q

Decerebrate rigidity =

A

humans results from a midbrain lesion and is manifested by an exaggerated extensor posture of all extremities.

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48
Q

Decorticate rigidity =

A

Decorticate posture is an abnormal posturing in which a person is stiff with bent arms, clenched fists, and legs held out straight. … This type of posturing is a sign of severe damage in the brain

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49
Q

Retrograde amnesia =

A

s a loss of memory-access to events that occurred, or information that was learned, before an injury or the onset of a disease.

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50
Q

Anterograde amnesia =

A

Anterograde amnesia is a loss of the ability to create new memories after the event that caused amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remain intact.

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51
Q

Symptoms: Visual & Perceptual:

Visual

A

Blurred vision, convergence insufficiency, reduced blink rate……. Also damage to oculomotor nerve

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52
Q

Symptoms: Visual & Perceptual:

Perceptual

A

Often result of high right hemisphere damage

Visual perception = Right left discrimination, figure ground, position in space

Body schema = anosognosia , unilateral neglect

Speech & Language = aphasia, dyslexia, dysprosody

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53
Q

Symptoms: Psychosocial & Behavioral:

Psychosocial

A 
Self concept
Social roles
Independent living
Dealing with loss
Affective changes
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54
Q

Symptoms: Psychosocial & Behavioral:

Behavioral

A

Common RLA Level IV (agitated/confused) = yelling, swearing, grabbing, biting

55
Q

Assessment:

Glasgow Coma Scale (GCS)

A

Assesses 3 behavioral areas: motor responses, verbal responses, and eye opening

56
Q

Assessment:
Glasgow Coma Scale (GCS):

Motor

A

1) pain, no motor response to pinch,
2) body becomes rigid in extension with pinch,
3) flexes body inappropriately to pain,
4) pulls away with pinch,
5) pulls examiner’s hand away with pinch,
6) follows simply commands

57
Q

Assessment:
Glasgow Coma Scale (GCS):

Verbal:

A

1) no noise to 5) carries on conversation correctly

58
Q

Assessment:
Glasgow Coma Scale (GCS):

Eyes:

A

1) does not open eyes to 4) opens eyes on own/spontaneous

59
Q

Ranchos Los Amigos Levels (RLA)

A

Measurement of levels of awareness and cognitive function

Typical progression is linear although some with very severe injury may skip a level (typically level IV = agitated and confused)

60
Q

The GCS measures the following functions:

Eye Opening (E)

4 = 
3 = 
2 = 
1 = 
NT =
A 
4 = spontaneous
3 = to sound
2 = to pressure
1 = none
NT = not testable
61
Q

The GCS measures the following functions:

Verbal Response (V)

5 = 
4 = 
3 = 
2 = 
1 = 
NT =
A 
5 = orientated
4 = confused
3 = words, but not coherent
2 = sounds, but no words
1 = none
NT = not testable
62
Q

The GCS measures the following functions:

Motor Response (M)

6 = 
5 = 
4 = 
3 = 
2 = 
1 = 
NT =
A

Motor Response (M)

6 = obeys command
5 = localizing
4 = normal flexion
3 = abnormal flexion
2 = extension
1 = none
NT = not testable
63
Q

The Rancho Los Amigos Scale

Level 1
Level 2
Level 3
Level 4
Level 5
Level 6
Level 7
Level 8
Level 9
Level 10
A

Level 1= No reaction - The brain-injured person is unconscious

Level 2= Generalized reaction - The brain-injured person will react but
inconsistent and without purpose.

Level 3= Level 3: Localized reaction - The brain-injured person is improving.

Level 4= Level 4: Confused/Agitated - The brain-injured person has become very active
but they are not yet able to understand what’s going on

Level 5= Level 5: Confused/Inappropriate - The brain-injured person has become less
agitated.

Level 6= Confused/Appropriate - Things are looking up. The brain-injured
person is motivated but still depends on others to lead the way.

Level 7= Automatic/Appropriate - The brain-injured person seems to act appropriately in the hospital and at home.

Level 8= Purposeful/Appropriate - At last! The brain-injured person remembers how the past fits with the future

Level 9= Purposeful-appropriate, goes through daily routine aware of need fr stand-by-assistance, depression may continue

Level 10= Purposeful-Appropriate/Modified Independent, goes through daily routine but may require more time or compensatory strategies, periodic depression may occur

64
Q

Evaluating TBI: Lower Level

A 
Evaluate: 
Level of arousal - attend, follow commands, communicate, awake
Vision - scan, attend, eye contact 
Sensation - pain, temp, movement
ROM
Motor Control - tone, reflexes
Dysphagia
Emotional and behavioral factors

Interventions: Sensory stim, w/c positioning, bed positioning, splinting/casting, dysphagia, behavioral, family/caregiver edu

65
Q

Evaluating TBI:Intermediate to Higher Level

A

RLA IV to VIII = client is alert, confused, agitated, and inappropriate with responses, may follow 2-3 step commands, easily distracted

Same as Low level with addition of ADLS, work readiness, and reintegration into the community, IADLS

Physical status, dysphagia, cognition, vision

Interventions: Neuromuscular (NDT, PNF), Ataxia, Cognition, Vision, Behavioral, dysphagia & self feeding, Functional mobility

66
Q

Interventions: Positioning

Wheelchair Positioning

Effective seating = 
Pelvis = 
Trunk =
LE = 
Head =
A

Allows interaction with the environment, prevents skin breakdown/ joint contractures, facilitates normal muscle tone, inhibits primitive reflexes, increases sitting tolerance, enhances respiration and swallowing, promotes function

67
Q

Interventions: Positioning

Bed Positioning

A

Crucial early on to prevent sores, facilitate normal tone/ ROM/ mobility

Barriers: spasticity, splints, IVs, tubes, medical precautions

Side lying or semiprone = abnormal tone or posturing

68
Q

Interventions: Splinting & Casting

A

Similar to CVA

When spasticity impacts function
When ROM is limited
When there are soft tissue contractures

Contraindications: uncontrolled hypertension, open wounds, unhealed fx, impaired circulation, acute inflammation

69
Q

Interventions: Sensory Stimulation

Goal =

A

Goal = increase arousal/awareness with sensory stim

Responses measured (Radomski, 2008): respiration, pulse, blood pressure, head movements, eye opening/movements, eye fixation, mimic responses, aimed and non aimed motor responses, and articulations

70
Q

Interventions: Cognition

Generation effect =

A

content that is self generated is remembered better than content that is provided/given

71
Q

Interventions: Cognition= 2 cooking and 2 financial management tasks

A
  • 1 task of each done with provided conditions the other done with generated conditions
  • Provided information: “Scramble two eggs in a bowl. Pour into hot pan on stove. Let cook three minutes. Flip.”
  • Self-generated information: “Scramble two in a bowl. into hot pan on stove. Let cook minutes. Flip.”
72
Q

Interventions: Cognition= 2 cooking and 2 financial management tasks

A
  • 1 task of each done with provided conditions the other done with generated conditions
  • Provided information: “Scramble two eggs in a bowl. Pour into hot pan on stove. Let cook three minutes. Flip.”
  • Self-generated information: “Scramble two in a bowl. into hot pan on stove. Let cook minutes. Flip.”
73
Q

Interventions: Behavioral

A

Post traumatic agitation occurs in 33 - 50% of those with TBI

Clinicians need to determine factors contributing to problem behaviors

Client factors, Social context and environment, & Physical environment

One on one coaching = 24/7
Psychotropic meds = regulate sleep and minimize agitation

Environmental modifications = alarm system, helmet, quiet room

74
Q

Interventions: Behavioral

Environmental vs Interactive

A
  • Environmental = alter objects or environment to facilitate behavior, inhibit unwanted, maintain safety
  • Interactive = used to interact with client, use consistent implementation by all
75
Q

Interventions: Community Integration

Article (Kim & Colantonio, 2010)

A

Systematic review of 10 articles to determine best practice for OT in community integration

Assessment:
Reintegration to Normal Living Index

Community Integration Questionnaire (most widely used)

Findings:

76
Q

Interventions: Community Integration

Article: Giving Second Chances: The Brain Injury Wellness Program (Klymasz, 2013)

A

Patient’s and caregivers report frustration with being discharged from therapy before they feel ready

Brain Injury Wellness Program:

6, 1-hour sessions that focus on community integration, wellness, function, and QOL

Results: increased community participation, success in implementation of compensatory strategies, gained confidence

77
Q

Interventions: Family & Caregiver Education

A

May have unrealistic expectations or interpret information differently than medical staff (unresponsiveness may be laziness, deafness…. When it is cognitive status)

Provide family with concise information

Involved throughout the rehab process
Educated on ROM, positioning, transfers…….

Substance Use
Drug rehab services

78
Q

D/C Planning

A

Home safety
Complete home eval to determine needed home modifications

Equipment Eval and Ordering
May refer to driver training/eval

May refer to work/vocational training

79
Q

What is Parkinson’s Disease?

A

ICD 10: G20
Chronic progressive condition
Loss of dopamine-producing cells in the basal ganglia
Cause is unknown. Recent studies point to environmental and genetic factors

80
Q

PD Prevalence

A

PD is the second most common neurodegenerative disorder in the US
Effects approximately 1 million in the US

81
Q

PD Symptoms: Motor

A 
Bradykinesia
Hypokinesia
Rigidity
Tremor
Disturbed postural reflexes
82
Q

Bradykinesia

A

slowness of movement and is one of the cardinal manifestations of Parkinson’s disease.

83
Q

Hypokinesia

A

partial or complete loss of muscle movement due to a disruption in the basal ganglia.

84
Q

Rigidity

A

inability to be to bent or be forced out of shape.

85
Q

Tremor

A

involuntary, somewhat rhythmic, muscle contraction and relaxation involving oscillations or twitching movements of one or more body parts.

86
Q

PD Symptoms: Non-Motor

A 
Mental Functions
Sleep Disorders
Voice and Speech
Depression
Psychosis
Anxiety
Fatigue
Smell disorders
Constipation
87
Q

PD Symptoms: Progression

A

Motor symptoms often precede non-motor symptoms
Motor symptoms often begin unilaterally
Less than 5% end up w/c or bedridden
Life expectancy is almost average with medical advances
Slower progression:
Faster progression:

88
Q

PD OT Interventions: Physical Exercise

A

Progressive resistive, joint mobilization, postural stability/balance training, gait training, aerobic activities
More likely to improve performance skills and not task performance itself
Encourage clients to engage in regular physical activity

89
Q

PD OT Interventions: Physical Exercise

A

Progressive resistive, joint mobilization, postural stability/balance training, gait training, aerobic activities

More likely to improve performance skills and not task performance itself

Encourage clients to engage in regular physical activity

90
Q

PD OT Interventions: Physical Exercise

A

Progressive resistive, joint mobilization, postural stability/balance training, gait training, aerobic activities

More likely to improve performance skills and not task performance itself

Encourage clients to engage in regular physical activity

91
Q

PD OT Interventions: Environmental Cues

A

Auditory rhythmic cues stronger than visual and tactile cues for regulating walking

Moderate evidence to support client-preferred external cues during performance of ADLs had positive effects on motor control

Provide Targeted external cues

92
Q

PD: OT Interventions: Self Management

Cog behavioral:

A

education, goal setting, practice, and feedback to incorporate into daily life
Plan for and manage the progression of the disease

93
Q

PD: General Interventions

A 
Optimizing daily schedule
Dealing with stress and time pressure
Practicing arm/hand motor skills
Attention to Task
Cognitive movement strategies
Minimize dual task
Use Cues
Rhythmic and single
Auditory, Visual, Tactile/Proprioceptive
Environmental modifications
Caregiver support and education
94
Q

PD Early & middle/Late stages

Stages 1 to 5

A

Stage 1: minimal symptoms; usually tremors; symptoms don’t affect daily routine

Stage 2: Diseases starts to affect whole body; routine activities may take longer to complete

Stage 3: loss of balance and coordinaton; routine activities may become difficult

Stage 4: nearly impossible to live on your own; routine activities should not be performed alone

Stage 5; final & most severe stage; confined to bed; dementia; confusion; and hallucinations begin

95
Q

General Taping Information

KT is good for..?

A

: pain, swelling, inflammation, postural malalignment, muscle imbalance, trigger points

96
Q

What are the benefits of K-tape?

A

May encourage realignment of joint structures

Offers proprioceptive feedback

Beneficial for shoulder impingement, joint sprains, and multi- directional instability

Reposition humeral head with tape to that it is in a neutral position

Taping allows client to feel normal alignment

Can result in immediate pain relief and improved ROM

May help with inflammation by encouraging lymphatic drainage

97
Q

Cuts of K-Tape
Y-tape

I-tape

X-tape

Donut

Web/Fan

A

Y-tape
Used to surround a muscle
To facilitate or inhibit muscle stimuli, should be 2 inches longer than muscle

I-tape - most commonly used
Used for more acute injuries
Edema and pain management, correct alignment

X-tape
Used when origin and insertion change depending on movement

Donut
Specifically for edema
Overlapping strips and the center is cut our over areas of focus

Web/Fan
Primarily used for edema

98
Q

Application of KT

Insertion to Origin is used to…..?

Origin to Insertion is used to….?

A

Insertion to Origin
Used to inhibit overused or stretched muscles
Light stretch required (15 – 25%)

Origin to Insertion
Used to facilitate weak or under performing muscles
Light to moderate stretch required (50-75%)

99
Q

CA Tri Pull Method

A 
1) Identify the 3 landmarks on your client
Deltoid Tuberosity
Coracoid process
Acromial Process
Spine of scapula

2) Measure out and cut the 3 pieces of tape
3) Clean and prepare the skin

4) Apply Tape
1) Medial = 1 inch below deltoid tuberosity - 1 inch above acromion process (ends at neck)

2) Posterior = 1 inch below deltoid tuberosity - 1 inch above spine of scapula
3) Anterior = 1 inch below deltoid tuberosity - 1 inch above coracoid process

100
Q

Kinesio Taping in Stroke

Origin to insertion or insertion to origin?

What are the 5 steps to placing tape onto your ct?

A

Origin to insertion method as the deltoid is noted to be weakened or paralyzed

1) Pt positioned with head, trunk, and scapula in best alignment
2) Abduct shoulder to 90 degrees
3) Cut Y tape and place anchor on the acromion process with no stretch
4) Move shldr to Extension and apply first tail to anterior deltoid as it is stretched (end at insertion) with no stretch in tape
5) Move shoulder in horizontal abduction and apply second tail over posterior deltoid ending at insertion

101
Q

Definition:ALS

A

A group of progressive, degenerative neuromuscular diseases:

102
Q

ALS: Progressive bulbar palsy

A

Destruction in corticobulbar tracts and brain stem

Symptoms: speech, swallowing, breathing may be affected

103
Q

ALS: Progressive spinal muscular atrophy (Lower Motor Neuron)

A

Destruction in LMN in the spinal cord (sometimes brainstem)

Symptoms:weakness or muscle atrophy of extremities, cervical extensor weakness, fasciculation, muscle cramps, and loss of reflexes

104
Q

ALS: Primary lateral sclerosis (Upper Motor Neuron)

A

Destruction of cortical motor neurons

Symptoms: results in: general weakness. Spasticity, and hyperreflexia

105
Q

Clinical Picture:ALS- Early

A
  • Focal weakness in arms, legs, or bulbar muscles
  • Trip or drop things
  • Slurred speech
  • Abnormal fatigue
  • Uncontrollable laughing/crying
106
Q

Clinical Picture: ALS- Progresses

A

Progresses

Marked muscle atrophy

Weight loss

Spasticity

Muscle cramping

Fasciculation

Difficulty walking, dressing, fine motor, swallowing, breathing

107
Q

OT’s Role: ALS

What are the 6 stages?

A

1) Ambulatory, no ADL problems, mild weakness
How would you treat?

2) Ambulatory, moderate weakness in certain muscles
How would you treat?

3) Ambulatory, severe weakness in certain muscles
How would you treat?

4) Wheelchair confined, almost independent, severe weakness in legs
How would you treat?

5) Wheelchair confined, dependent, pronounces weakness in legs, severe in arms
How would you treat?

6) Bedridden, Dep ADLs, Max A - Dep in all tasks
How would you treat?

108
Q

Huntington’s Disease

A

Fatal degenerative neurologic disorder

Genetic, transmitted in an autosomal dominant pattern

Damage to the corpus striatum which is responsible for motor control

Damage to the caudate nucleus is linked to cognitive and emotional function

109
Q

Huntington’s Disease: Presymptomatic Stage

A

Decreased speed of finger tapping

Unified Huntington’s Disease Rating Scale

110
Q

Huntington’s Disease: Early Stage

A

Alterations in behavior, changes in cognitive functioning, choreiform movements of the hands

111
Q

Huntington’s Disease: hands

Middle Stage

A

Memory and decision making skills
Help them maintain meaningful habits and routines
Better with familiar and routine tasks
Gait and balance disturbances

112
Q

Huntington’s Disease: Late Stage

A 
Verbal comprehension
Dysarthria
Depression worsens
Bradykinesia and akinesia
Increasing difficulty with handwriting
Slowed saccadic and ocular eye movements
Dysphagia and choking hazard
113
Q

Huntington’s Disease: Clinical Picture: Medical treatment for HD

A

Medical Treatment
Can address the symptoms but not stop the progression of the disease
Antidepressants

Goal: manage symptoms, reduce burden of symptoms, maximize function, and provide pt and family education

114
Q

OT’s Role: HD (early/middle/end?)

A

Early stages
Address memory and concentration: How?
Assist with strategies for employment: How?
Address anxiety, depression, and irritability: How?
Address the effects of Chorea
Modifications for fine motor control: How?

Middle Stages
Provide visual cues to prompt actions
Watch for signs of Suicide: How?
Address fatigue: How?
Address increase chorea: How?
Address dysphagia: How?

Final Stages
Address chorea replaced with rigidity: How?

115
Q

Definition MS

A

Progressive, inflammatory neurologic disease

Damage to the myelin sheath in the CNS

Onset between the ages of 20 - 45

Etiology: unknown, suspected combination of environmental and genetic factors

116
Q

Clinical Picture: MS (early symptoms and advance stages?)

A

Early symptoms:
Paresthesia, diplopia, visual loss in one eye, fatigue, emotional lability, sensory loss in extremities
Trigeminal neuralgia, symptoms exacerbated with increased body temperatures

Advance stages:
Varying degrees of paralysis, dysarthria, dysphagia, severe visual impairment, ataxia, spasticity, nystagmus, neurogenic bladder, impaired cognition

117
Q

Clinical Picture: MS

1) Relapsing and Remitting
2) Secondary Progressive
3) Primary Progressive

A

Patterns of symptoms:
1) Relapsing and Remitting
85% of cases
Slow, step like progression as deficits accumulate

2) Secondary Progressive
Begins with relapsing and remitting that progresses into primary progressive
50% of those with relapsing/remitting progress to secondary progressive

3) Primary Progressive
10% of MS population
Downward slope with little recovery after an exacerbation
Become non ambulatory, incontinent, dysphagia, dysarthria, severely compromised LE function, varying UE function

118
Q

Clinical Picture:MS Life expectancy

A

Life expectancy
Favorable Prognosis: (chart page 937)
Minimal disability after 5 years of onset
complete/rapid remission of initial symptoms
Age of onset less than 40 y/o
Only 1 symptom the first year
Onset with sensory symptoms or mild optic neuritis

Poor Prognosis:
Progressive course
Age of onset greater than 40
Cerebellar involvement
Polysymptomatic
Male sex
119
Q

OT’s Role: MS Evaluation:

A

Assess motor and praxis, sensory perceptual, emotional regulation, cognitive, communication skills

As fatigue is often an issue assessments results may vary depending on time of day
Self report often inaccurate
Assess sleep and sleep patterns

Assess visual tracking, scanning, and acuity
Assess cognition

120
Q

OT’s Role: Treatment:

A

Treatment:
MS Society resources for clinicians:

Articles: Systematic Reviews Part I and Part II (Yu & Mathiowetz, 2014a&b)
Part 1 = activity and participation
-Goal directed interventions, health promotion programs, and fatigue management programs
-Direct training in functional performance
-Group fatigue management delivered face to face or long distance

Part 2 = Impairment
Cognition
Emotional Regulation
Exercise
Motor Training
121
Q

Guillain-Barre Definition

A

A rare autoimmune disease with no known cure, no established treatment, requiring a long period of recovery, no clear cause

Acute, Inflammatory disorder in which the body’s immune system attacks the peripheral nervous system

Damage to the myelin sheath prevents nerve conduction that leads to muscle weakness, pain, and/or paralysis of the entire body

122
Q

Guillain-Barre Clinical Picture

A

Rapidly progressive weakness of bilateral extremities distal to proximal

Brain does not receive signals from the body

Body does not receive signals from the brain to move

Often first symptom is tingling, crawling skin, painful sensations that begin in the hands and feet

If demyelination continues may impact breathing, speaking, swallowing, blood pressure, and/or heart rate

123
Q

Guillain-Barre

1) Initial/Acute Phase:
2) Plateau Phase:
3) Recovery Phase:

A

Initial Phase:
Passive ROM, positioning, splinting to prevent contractures/deformity
Passive activities like watching tv
Address anxiety, fear, and panic

Recovery Phase:
Precautions: prevent muscle belly tenderness, fatigue, and further damage to nerves
Address proximal joints first as they recovery then move to distal
Introduce activities as they are able to tolerate them, just right challenge, opportunities for success
AE, compensatory strategies, energy conservation, joint protection
Lifestyle redesign

124
Q

Postpolio Syndrome Definition (PPS)

A

Peak of Polio in the US was 1952

After 30 - 40 years 25% - 40% of these adults deal with new muscle pain, weakness, and/or paralysis = postpolio syndrome PPS

125
Q

6 criteria to diagnose Postpolio Syndrome (PPS):

A

1) Pervious paralysis due to polio
2) Period of partial or complete recovery
3) Gradual or sudden onset of progressive muscle weakness or fatigue
4) New difficulties with breathing and swallowing
5) A year or more of the above symptoms
6) Other causes have been ruled out

126
Q

PPS: Clinical Picture

A

Slow progression with periods of stability (plateaus)

Fatigue is found to be the most debilitating symptom

Risk of muscle atrophy, scoliosis, osteoporosis, fractures, contractures, and depression

Difficulty with ADLs, IADLs, ambulation, stairs, home mang, transfers, driving, eating and swallowing, bladder and bowel control

While symptoms greatly impact quality of life there are rarely life threatening

127
Q

PPS: Role of OT

A

Work simplification, pacing and energy conservation, adaptive equipment, passive and active ROM, muscle re-education, proper posture and body mechanics, joint protection

Connect with support groups for feelings of denial, anger, hopelessness, feel a burden

Introduce changes gradually with just right challenge to provide confidence and success

Caution with exercise:

In general body weight reduction, work with dietician

128
Q

Define

  • Feeding
  • Eating
  • Dysphagia
A

Feeding: “the process of setting up, arranging, and bringing food (fluids) from the plate or cup to the mouth, sometimes called self feeding” OTPF

Eating: “The ability to keep and manipulate food/fluid in the mouth and swallow it; eating and swallowing are often used interchangeably” OTPF

Dysphagia: inability to swallow or difficulty with swallowing
Clients who may have difficulty feeding or eating: ???

129
Q

Preparatory Phase & Stage 1 of Swallowing

A

Preparatory Phase
Before the 4 stages of eating
Begins when client enters the dining area
Considers variety of foods, presentation of food, seating during meals, meal time atmosphere, mealtime habits
Sensory quality of the food and items, appetite & hunger

1) Oral Preparatory Phase
Action:
Visual and olfactory information stimulates saliva production
Jaw opens and lips close around food with musculature creating a seal to prevent spillage
Chewing:
Time to form bolus is shorter for softer foods

130
Q

Stage 2 & 3 of Swallowing

A

Stage 2 & 3 of Swallowing
2) Oral Phase
Begins when tongue initiates movement of bolus towards the pharynx
Tongue elevates, pushing bolus against the hard palate and guides the bolus back
Thicker foods require more pressure of tongue on the palate
This is a voluntary phase, person must be alert and involved

3) Pharyngeal Phase
Closure of the larynx, the laryngeal entrance, and epiglottis to prevent material from entering airway
Bolus moves through the pharynx towards the esophagus, passes through pharynx divided in half at the valleculae and down each side of the pyriform sinuses
Upper esophageal sphincter relaxes and opens allowing material to enter the esophagus

131
Q

Final Stage of Swallowing

A

4) Esophageal Phase
Begins when bolus enters the esophagus through the cricopharyngeal juncture or upper esophageal sphincter (UES)
Esophagus is a straight tube 10 inches long that connects the pharynx to the stomach
UES separates pharynx from esophagus and LES separates esophagus from the stomach
Muscles of esophagus contract and push bolus down = peristaltic wave contractions
Epiglottitis returns to a relaxed state to allow airway to open, return to breathing

132
Q

Dysphagia & Aspiration

Symptoms of Dysphagia:

A 
Difficulty shaping food into bolus
Loss of food from mouth or nose
Coughing, throat clearing 
Wet or gurgling voice after
Changes in mealtime behavior
Food residue in mouth
Delayed or absent swallow
Weak cough
Reflux of food 
Aspiration
133
Q

Interventions & Goals

A 
Trunk and head positioning
-Improve swallow
-Reduce risk of aspiration
Rehabilitative:
Exercises

Compensatory:
Oral hygiene
Modify food texture

1) facilitate appropriate positioning during eating
2) Improve motor control at each stage of swallowing
3) Maintenance of adequate hydration and nutrition
4) Prevention of aspiration
5) Reestablishment of oral eating to the safest/optimum level on least restrictive diet

134
Q

Diet selection for Dysphagia
Food: 4 Levels of Dysphagia

Dysphagia Level 1:

Dysphagia Level 2:

Dysphagia Level 3:

Dysphagia Level 4:

A

Dysphagia Level 1: Dysphagia Puree

Dysphagia Level 2: Mechanical Soft

Dysphagia Level 3: Dysphagia Advanced

Dysphagia Level 4: Normal
Liquids
Thin
Nectar like
Honey like
Spoon thick

OTB 520- Phys Dys (12 decks)

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