Week 11 to Week 14 Flashcards
Supports & Subluxation :
What are reasons for prescription for slings/supports?
Weakness, subluxation, hypotonia, pain, neglect, decreased cognition, Pain and subluxation for orthoses
Supports & Subluxation :
Reasons for discontinued use:
Improvement in strength
Summarize Article Continued (Foongchomcheay, Ada, & Canning, 2005):
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)
Taping for Subluxation:
Taping Overview
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
Taping for Subluxation:
Article: (Peters & Lee, 2003)
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:
CA tri pull method
position
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
E-stim & Subluxation
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
Orthotics: Principles
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)
Considerations for Prescribing & Designing Orthotics
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?
Considerations for Prescribing & Designing Orthotics: Soft Tissue Shortening
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
Extrinsic extensor tightness:
full passive composite wrist and digit flexion is not obtainable.
Extrinsic flexor tightness:
full passive composite wrist and digit extension is not obtainable.
Intrinsic tightness:
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
Considerations for Prescribing & Designing Orthotics
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
Orthotics: Application Consideration: Normal Posture of the Distal UE
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
Orthotics: Application Consideration: Typical Deviations after Stroke
Wrist Flexion =
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
Orthotics: Application Consideration: Typical Deviations after Stroke
Wrist & digit flexion
shortened extrinsic flexors lengthened extrinsic extensors decreased normal tenodesis action contractures and deformity skin maceration risk
Orthotics: Application Consideration: Typical Deviations after Stroke
Extreme ulnar deviation
decreased wrist /
shortened tissues ulnar FA
lengthened tissues radial FA
shift of carpal rows
Orthotics: Application Consideration: Typical Deviations after Stroke
Loss of palmar arches
decreased grip
decreased dexterity
TBI
The most common cause of death and disability among young people
TBI: Open
penetrating injury or perforating
Injury depends on shape, mass, direction, and velocity of the object
TBI: Closed
Closed direct or indirect impact without penetration
TBI: Blast injuries =
= can occur in conjunction with open or closed
Pathology: Focal
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)
Pathology: Diffuse vs. Focal:
Focal
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)
Pathology: Diffuse vs. Focal:
Focal
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)
Pathology: Diffuse vs. Focal:
Coup
(the site of direct injury)
Pathology: Diffuse vs. Focal:
Countercoup
(site of indirect injury)
Epidural hematomas (EDHs
associated with skull fractures and disruption of meningeal arteries
Subdural hematomas (SDHs) =
occur between the dura and brain surface due to tearing of bridging veins
Location of trauma dictates symptoms:
Pre-frontal & anterior temporal areas: impaired memory, emotion and motivation
Orbitofrontal area: impulsivity
Frontolateral cortex:impassivity, hemiparesis, impaired attention and mental flexibility
Multifocal & Diffuse Brain injury
Often caused by sudden deceleration of the body and head with variable forces and deeper portions of the brain
Intracerebral hemorrhage (ICH)
nearly always present with missile wounds and common after falls and assault
Subarachnoid hemorrhage (SAH) & Intraventricular hemorrhage (IVH)
occur when the pia or arachnoid is torn.
Diffuse axonal injuries (DAIs)/ Traumatic axonal injury (TAI) =
= prototypic lesions caused by rapid deceleration and rotation of the brain in the skull
Possible symptoms include:
Ataxia Diplopia Dysarthria Impulsivity, irritability Apathy, poor initiative Decreased mental processing speed & efficiency Impaired attention Impaired abstract reasoning, planning, problem solving
Primary injury =
= occurs at the time of trauma
Secondary injury=
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)
State of Consciousness
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.
Coma =
As coma resolves client is either partially aware (minimally conscious) or if no awareness = vegetative
Vegetative State =
- 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
Minimally Conscious State (MCS)
- 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
Post Traumatic Amnesia (PTA)
- 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)
Intracranial Pressure
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.
Second Impact Syndrome (SIS)
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)
Chronic Traumatic Encephalopathy
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
Decerebrate rigidity =
humans results from a midbrain lesion and is manifested by an exaggerated extensor posture of all extremities.
Decorticate rigidity =
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
Retrograde amnesia =
s a loss of memory-access to events that occurred, or information that was learned, before an injury or the onset of a disease.
Anterograde amnesia =
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.
Symptoms: Visual & Perceptual:
Visual
Blurred vision, convergence insufficiency, reduced blink rate……. Also damage to oculomotor nerve
Symptoms: Visual & Perceptual:
Perceptual
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
Symptoms: Psychosocial & Behavioral:
Psychosocial
Self concept Social roles Independent living Dealing with loss Affective changes
Symptoms: Psychosocial & Behavioral:
Behavioral
Common RLA Level IV (agitated/confused) = yelling, swearing, grabbing, biting
Assessment:
Glasgow Coma Scale (GCS)
Assesses 3 behavioral areas: motor responses, verbal responses, and eye opening
Assessment:
Glasgow Coma Scale (GCS):
Motor
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
Assessment:
Glasgow Coma Scale (GCS):
Verbal:
1) no noise to 5) carries on conversation correctly
Assessment:
Glasgow Coma Scale (GCS):
Eyes:
1) does not open eyes to 4) opens eyes on own/spontaneous
Ranchos Los Amigos Levels (RLA)
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)
The GCS measures the following functions:
Eye Opening (E)
4 = 3 = 2 = 1 = NT =
4 = spontaneous 3 = to sound 2 = to pressure 1 = none NT = not testable
The GCS measures the following functions:
Verbal Response (V)
5 = 4 = 3 = 2 = 1 = NT =
5 = orientated 4 = confused 3 = words, but not coherent 2 = sounds, but no words 1 = none NT = not testable
The GCS measures the following functions:
Motor Response (M)
6 = 5 = 4 = 3 = 2 = 1 = NT =
Motor Response (M)
6 = obeys command 5 = localizing 4 = normal flexion 3 = abnormal flexion 2 = extension 1 = none NT = not testable
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
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
Evaluating TBI: Lower Level
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
Evaluating TBI:Intermediate to Higher Level
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
Interventions: Positioning
Wheelchair Positioning
Effective seating = Pelvis = Trunk = LE = Head =
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
Interventions: Positioning
Bed Positioning
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
Interventions: Splinting & Casting
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
Interventions: Sensory Stimulation
Goal =
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
Interventions: Cognition
Generation effect =
content that is self generated is remembered better than content that is provided/given
Interventions: Cognition= 2 cooking and 2 financial management tasks
- 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.”
Interventions: Cognition= 2 cooking and 2 financial management tasks
- 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.”
Interventions: Behavioral
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
Interventions: Behavioral
Environmental vs Interactive
- Environmental = alter objects or environment to facilitate behavior, inhibit unwanted, maintain safety
- Interactive = used to interact with client, use consistent implementation by all
Interventions: Community Integration
Article (Kim & Colantonio, 2010)
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:
Interventions: Community Integration
Article: Giving Second Chances: The Brain Injury Wellness Program (Klymasz, 2013)
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
Interventions: Family & Caregiver Education
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
D/C Planning
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
What is Parkinson’s Disease?
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
PD Prevalence
PD is the second most common neurodegenerative disorder in the US
Effects approximately 1 million in the US
PD Symptoms: Motor
Bradykinesia Hypokinesia Rigidity Tremor Disturbed postural reflexes
Bradykinesia
slowness of movement and is one of the cardinal manifestations of Parkinson’s disease.
Hypokinesia
partial or complete loss of muscle movement due to a disruption in the basal ganglia.
Rigidity
inability to be to bent or be forced out of shape.
Tremor
involuntary, somewhat rhythmic, muscle contraction and relaxation involving oscillations or twitching movements of one or more body parts.
PD Symptoms: Non-Motor
Mental Functions Sleep Disorders Voice and Speech Depression Psychosis Anxiety Fatigue Smell disorders Constipation
PD Symptoms: Progression
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:
PD OT Interventions: Physical Exercise
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
PD OT Interventions: Physical Exercise
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
PD OT Interventions: Physical Exercise
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
PD OT Interventions: Environmental Cues
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
PD: OT Interventions: Self Management
Cog behavioral:
education, goal setting, practice, and feedback to incorporate into daily life
Plan for and manage the progression of the disease
PD: General Interventions
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
PD Early & middle/Late stages
Stages 1 to 5
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
General Taping Information
KT is good for..?
: pain, swelling, inflammation, postural malalignment, muscle imbalance, trigger points
What are the benefits of K-tape?
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
Cuts of K-Tape
Y-tape
I-tape
X-tape
Donut
Web/Fan
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
Application of KT
Insertion to Origin is used to…..?
Origin to Insertion is used to….?
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%)
CA Tri Pull Method
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
Kinesio Taping in Stroke
Origin to insertion or insertion to origin?
What are the 5 steps to placing tape onto your ct?
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
Definition:ALS
A group of progressive, degenerative neuromuscular diseases:
ALS: Progressive bulbar palsy
Destruction in corticobulbar tracts and brain stem
Symptoms: speech, swallowing, breathing may be affected
ALS: Progressive spinal muscular atrophy (Lower Motor Neuron)
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
ALS: Primary lateral sclerosis (Upper Motor Neuron)
Destruction of cortical motor neurons
Symptoms: results in: general weakness. Spasticity, and hyperreflexia
Clinical Picture:ALS- Early
- Focal weakness in arms, legs, or bulbar muscles
- Trip or drop things
- Slurred speech
- Abnormal fatigue
- Uncontrollable laughing/crying
Clinical Picture: ALS- Progresses
Progresses
Marked muscle atrophy
Weight loss
Spasticity
Muscle cramping
Fasciculation
Difficulty walking, dressing, fine motor, swallowing, breathing
OT’s Role: ALS
What are the 6 stages?
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?
Huntington’s Disease
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
Huntington’s Disease: Presymptomatic Stage
Decreased speed of finger tapping
Unified Huntington’s Disease Rating Scale
Huntington’s Disease: Early Stage
Alterations in behavior, changes in cognitive functioning, choreiform movements of the hands
Huntington’s Disease: hands
Middle Stage
Memory and decision making skills
Help them maintain meaningful habits and routines
Better with familiar and routine tasks
Gait and balance disturbances
Huntington’s Disease: Late Stage
Verbal comprehension Dysarthria Depression worsens Bradykinesia and akinesia Increasing difficulty with handwriting Slowed saccadic and ocular eye movements Dysphagia and choking hazard
Huntington’s Disease: Clinical Picture: Medical treatment for HD
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
OT’s Role: HD (early/middle/end?)
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?
Definition MS
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
Clinical Picture: MS (early symptoms and advance stages?)
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
Clinical Picture: MS
1) Relapsing and Remitting
2) Secondary Progressive
3) Primary Progressive
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
Clinical Picture:MS Life expectancy
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
OT’s Role: MS Evaluation:
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
OT’s Role: Treatment:
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
Guillain-Barre Definition
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
Guillain-Barre Clinical Picture
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
Guillain-Barre
1) Initial/Acute Phase:
2) Plateau Phase:
3) Recovery Phase:
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
Postpolio Syndrome Definition (PPS)
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
6 criteria to diagnose Postpolio Syndrome (PPS):
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
PPS: Clinical Picture
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
PPS: Role of OT
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
Define
- Feeding
- Eating
- Dysphagia
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: ???
Preparatory Phase & Stage 1 of Swallowing
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
Stage 2 & 3 of Swallowing
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
Final Stage of Swallowing
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
Dysphagia & Aspiration
Symptoms of Dysphagia:
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
Interventions & Goals
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
Diet selection for Dysphagia
Food: 4 Levels of Dysphagia
Dysphagia Level 1:
Dysphagia Level 2:
Dysphagia Level 3:
Dysphagia Level 4:
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
