Exam 2: Multiple Sclerosis, Orthotics, Guillan Barre Flashcards
1
Q
What is multiple sclerosis?
A
-A chronic progressive inflammatory disease involving damage to the myelin in the brain and spinal cord
-Autoimmune disease
-Can lead to physical dysfunction, depression, participation restrictions
2
Q
What patient populations is MS most common in?
A
-Mean onset 30 years
-70% of onset is between 20-40 years old
-10-20% after 60
-Females > males
-Genetics (first degree relative 20x higher)
3
Q
What can MS be triggered by?
A
Environmental factors such as sunshine, vitamin D deficiency, smoking, and Epstein-Barr virus
4
Q
What is the proposed agent of oligodendrocyte dysfunction?
A
Pro-inflammatory agents released by microglial cells
5
Q
What is the function of astrocytes?
A
Provide synaptic support, neuronal guidance, and maintain the blood brain barriers
6
Q
What is the pathophysiology of MS?
A
-T cells are autoreactive in the periphery of the CNS
-T and B cells cross the weakened BBB
-T cells interact with B cells to create aberrant antibodies that target oligodendrocytes
-T cells and inflammatory microglia
-Antibodies lead to degeneration of myelin
7
Q
What occurs during and after inflammatory demyelination?
A
-Damage to the transmission of nerve impulses occurs during the inflammatory phase
-When inflammation subsides, symptoms improve and oligodendrocytes can remyelinate axons
8
Q
What does repeated inflammation cause? What does this equate to?
A
-Repeated inflammation causes reduced repair and axonal damage
-Axonal damage equates to irreversible disability
9
Q
What is a hallmark sign of MS?
A
-Plaques that are caused by focal loss of myelin
-This leads to fibrous astrocytes and undergoes gliosis
-Associated with loss of axonal function
10
Q
What are the relative percentages of axonal loss in the spinal cord, optic nerve, and brainstem/cerebellum?
A
-Spinal cord: 50%
-Optic nerve: 25%
-Brainstem/cerebellum: 25%
11
Q
What does an MS lesion look like on an MRI?
A
Bright white plaque
12
Q
What is gray matter dysfunction in MS?
A
-The extent and clinical relevance of grey matter pathology in MS is increasingly recognized
-Previous work has shown that GM pathology is more closely associated with some aspects of clinical disability than white matter injury, which has been suggested to arise independently
13
Q
What is the epidemiology of MS?
A
-Over 947,000 affected in the US
-Women vs men 3:1
-Men have a worse prognosis/aggressive disease
-Western European ancestry
-Geographic prevalence: extreme northern and southern latitudes, northern climates in US, Canada, and Scandinavia
-Least common in warm climates such as Asia, Africa, South America
-People who migrate from high to low risk regions before puberty reduce their risk
14
Q
What latitude is MS more common in?
A
Above 45 degrees
15
Q
What are the classifications of MS?
A
-Relapsing-remitting MS (RRMS)
-Secondary progressive MS (SPMS)
-Primary progressive MS (PPMS)
-Progressive relapsing MS (PRMS)
-Benign MS
16
Q
What is relapse remitting MS (RRMS)? What percentage of MS diagnoses are RRMS?
A
-Unpredictable attacks which may or may not leave permanent deficits followed by periods of remission
-85% of cases
17
Q
What is secondary progressive MS (SPMS)? What percentage of MS diagnoses are SPMS?
A
-Initial relapsing-remitting MS that suddenly begins to have decline without periods of remission
-Occurs after RRMS
-75% of RRMS cases are diagnosed with SPMS within 15 years of diagnosis
18
Q
What is primary progressive MS (PPMS)? What percentage of MS diagnoses are PPMS?
A
-Steady increase in disability without attack or periods of remission
-Gradual worsening of symptoms
-Does not respond to medical standard of care/drugs
-Progressive myelopathy
-15% of cases
-Usually in young males
19
Q
What is benign MS?
A
One occurrence with no occurrence
20
Q
What is progressive relapsing MS (PRMS)? What percentage of MS diagnoses are PRMS?
A
-Steady decline since onset with super-imposed attacks
-5% of cases
21
Q
What is the preclinical phase of MS?
A
-May have mild or no symptoms
-Lab tests will be negative
-Can last many years before onset of symptoms
22
Q
What is the relapsing remitting phase of MS? How long does it last?
A
-Onset of symptoms with periods of remission
-Can last 10-15 years
23
Q
When does secondary progressive MS phase come on? How long does it last?
A
-After being in the RRMS phase for about 10-15 years
-Can last 20+ years
24
Q
What is the expanded disability status scale?
A
-A scale that is used by physician’s to grade disability in patients with MS
-Ranges from no disability to confined to bed
-PT’s cannot use this scale
25
What criteria are required for diagnosing MS?
All of the following are required for a diagnosis of MS
-Confirmation of two lesions in at least two separate areas of the brain, spinal cord, or optic nerve
-Find evidence of damage at two different points in time
-Rule out other diagnoses
26
How long can it take after the initial flare/signs and symptoms of MS to have another episode?
Can take years
27
What is a clinical isolated syndrome (CIS)?
-Only one event of MS symptom with no other signs
-Characterized by acute or subacute onset of a monophasic episode of suggestive MS that has yet to fulfill the current MS criteria
-Usually affects the optic nerve, brainstem, or spinal cord
-Between 30-70% of patients with CIS develop MS
28
What is often the first sign/symptoms of MS, especially in young females?
Intermittent chronic low back pain
29
What is the differential diagnosis for MS?
-Chronic low back pain
-Fibromyalgia
-Cervical spondylosis
-Herniated disc
-Mitochondrial disease
30
What are diagnostic tools for MS?
-MRI to look for plaques
-Lumbar puncture: will have higher levels of proteins during times of inflammation
-Visual evoked potential (VEP): measures the electrical activity of the optic nerve in response to stimulation of visual nerve pathways
31
What are the initial symptoms of MS?
-More common in 20s and females
-Usually transient
-Fatigue
-Visual disturbances (double vision)
-Paresthesias, numbness, weakness, pins and needles accompanied by LBP
-Pain in bilateral LE's sudden and spontaneous (electric shock)
32
What are symptoms and signs during a flare up or relapse?
-Lasts longer than 24 hours (days, weeks, or months)
-Numbness and tingling
-Fatigue
-Visual changes
-Weakness
-Changes in gait
-Brain fog
-Tremors
-Incontinence
-Loss of proprioception
-Ataxia
33
What is the progression of MS?
-Initial diagnosis
-Exacerbation: attacks on myelin
-Period of remission
-Disease management
34
What is the new model for multiple sclerosis?
-Focal disease with isolated areas of inflammation vs "smoldering disease process"
35
What is the "smoldering disease process of MS"?
-There is a continuation of the disease with no quiescent period or periods of evidence of inflammatory activity
-Persons with MS are becoming more involved, yet have no new lesions in the brain or spinal cord are found
36
What is a pseudo exacerbation? What can this be triggered by?
-Less than 24 hours and resolves on its own
-Does not mean that the nervous system is undergoing damage or disease
-Brought on by stress, over exertion, or heat
-Fatigue, brain fog, pain
37
What activities are associated with higher levels of fatigue in individuals with MS? What about with lower levels of fatigue?
-Greater exposure to stress, such as deadlines at work, is associated with higher levels of fatigue
-Positive mood is associated with lower fatigue levels
-Increased fatigue was associated with recent physical activity
38
What is the Uhtoff phenomenon? What percentage of MS patients experience this? What symptoms does this cause?
-Increase in core body temperature that can be triggered by physical exertion or hot water or warm temps
-70% of MS patients experience this
-Temporary increase in MS symptoms that is rapidly reversed when problem is removed
39
What are the motor clinical manifestations of MS?
-Weakness: mono, hemi, or quadriparesis
-Deconditioning
-Dysarthria: speech issues and inability to pronounce words due to motor issues
-Ataxia: 80% experience ataxia at some point in the disease
-Dysmetria or dysdiadochokinesia
-Tremor
-Spasms
40
What are two types of movement based spasms that occur in MS?
-Flexor
-Extensor: crossed/scissoring
-Only occurs with movement
41
What percentage of MS patients experience spasticity? How does this affect the patients?
-84% report spasticity problems
-Highly correlated with reduced QOL and function
-Can lead to contractures, skin breakdown, pain, and sleep disturbances
-Increase in spasticity leads to disease progression
42
What can trigger or increase spasticity in patients with MS?
-Position changes
-Noxious stimuli
-Physiological stress: pain, cold weather, tight clothing, increased body temp
43
What are the different types of neuropathic pain that are associated with MS?
-Acute neuropathic pain: brought on by demyelination of sensory neurons
-Trigeminal neuralgia: stabbing pain in the face or jaw, pain is not constant
-Lhermitte's sign: brief stabbing electrical shock through the spinal cord
-Chronic neuropathic pain: brought on by stress
-Dysesthesias: painful sensations of the UE or LE that burning, lancing, prickling, stabbing, or icy
-Pruritis: a form of dysesthesia, itching, burning, or stabbing
44
What musculoskeletal pain or problems are associated with MS?
-Muscular tightness or loss of ROM
-Spasticity
-Compensatory movement patterns
-Muscular pain from abnormal use
-Muscular fatigue
45
What is optic neuritis? What % of patients experience this during their first event?
-Double vision, blurry, and painful eye movements
-Visual field loss, color desaturation
-Pupillary deficits
-20% experience during their first flare up
46
What are sensory manifestations of MS?
-Optic neuritis
-Dysesthesias
-Anesthesias
-Paresthesias
-Vestibular: dizziness and vertigo (20% of patients)
47
What are 3 postural control problems in MS patients that lead to falls?
-Delayed response to postural perturbations
-Increased body sway to quiet standing
-Inability to move outside the base of support
-Leads to fractures from falls!!!
48
What percent of MS patients experience bowel problems? What types of bowel problems will they encounter?
-35-68%
-Fecal retention
-Incontinence
-Constipation
49
What percent of MS patients experience bladder problems? What types of bladder problems will they encounter?
-52-97%
-Urinary urgency
-Incontinence
-Overactive detrusor/bladder
50
What are the cognitive and psychosocial clinical manifestations of MS?
-Depression
-Verbal fluency and memory problems
-Impaired processing speeds
-Decreased executive functioning
51
What is a quality of life outcome measure for MS?
MS quality of life inventory
52
How are disease modifying drugs helpful for MS?
-Prevents new inflammatory lesions
-Prevents development of secondary progressive MS
-Remyelination can occur
-Slows the progression of MS
-20 different types of DMTs
53
What is the prognosis for those with MS?
-Life expectancy is 6 years less than the general population, 72 with women and 68 with men
-Patients with primary progressive MS demonstrate higher mortality rates
54
What mitochondrial problems are associated with MS?
-Mitochondrial genetic variants are associated with MS
-Deficient mitochondiral metabolism may generate more reactive oxygen species (ROS) that wreak havoc in the cells
-Mitochondiral injury and subsequent energy failure are key factors in the induction of demyelination and neurodegeneration
55
What specific mitochondrial dysfunctions occur in MS?
-Respiratory chain deficiency
-Abnormal mitochondrial transport
-Abnormal gene expression
-Oxidative damage
-Impairment in energy production
56
What types of fibers are not damaged in MS? Why? What does this result in?
-C fibers
-They are unmyelinated
-Results in increased pain in MS patients
57
What do MS patients have more trouble with because of highly myelinated nerve fibers?
-Proprioception
-Proprioceptive fibers are highly myelinated
58
What muscular performance tests are included in the assessment for MS?
-Observe synergies
-Gait assessment for ataxia
-Coordination testing
-Strength assessment
-Speed/accuracy testing
59
What assessments for tone are done with MS?
-Hypertonicity (ROM)
-DTR
-Spasticity
-Observe spasms
60
What cranial nerves are assessed with MS?
-CN II
-CN III
-CN IV
-CN VI
-CN VIII
-CN IX
-CN V
-CN VII
61
What sensory tests are used in an MS examination?
-Proprioception
-Somatosensory
-Visual
-Vibration
62
Will pupillary responses be normal in MS patients?
Will likely appear normal or will be hard to detect changes/delays
63
What pathway does proprioception go through?
-Dorsal column
-Unconscious proprioception goes to the cerebellum via muscle spindles and GTO
-MS involves both pathways
64
What types of fibers are there more of in MS patients? What happens with Henneman's size principle in MS patients?
-Higher proportion of type two fibers (fast twitch)
-Reduced rate of force development due to disruption in Henneman's size principle which leads to inability to recruit motor units
65
What are MS examination areas?
-ROM and muscle tone
-Response time
-Sensory: vestibular, visual, proprioception
-Postural
-Postural reactions and responses
-Bladder questions
-Integumentary
-Short term memory
-Orientation
-Depression screening
-Anxiety screening
-Reduction in processing speed
-Euphoria
-Neuropathic pain assessment
66
What is the primary cause for falls in patients with MS?
Slow conduction speed and impaired central integration
67
What are common postural control problems in people with MS?
-Warm conditions increase the amount of sway in persons with MS
-Delayed responses to perturbations or changes in COM
-Impaired dual task integration
-Increased fear of falling
68
What are different types of gait disorders in MS?
-Spastic gait
-Ataxic gait
-Paretic gait
-Gait pattern can change over time if new lesions occur
69
What are UE outcome measures for MS?
-Boxes and blocks
-Nine hole peg test
70
What are gait outcome measures for MS?
-20 meter walk test
-TUG
71
What are fatigue outcome measures for MS?
Fatigue scale for motor and cognitive function
72
What are physical function outcome measures for MS?
Muscular sclerosis functional composite scale
73
What are important education points for patients with MS?
-Modifiable risk factors: smoking, exercise
-Fatigue
-Vaccinations: anyone with autoimmune diseases should check with their doctor
-Symptom management, especially recognizing remission symptoms
74
What are triggers to avoid for MS patients?
-Lack of sleep
-Stress
-Low vitamin D
-Staying healthy
-Childbirth
-Heat
-Over activity
75
What is a common infection that can cause a relapse?
Urinary tract infection
76
When having a relapse, what should patients do?
-Reduce activity by 1/2 for two weeks
-If relapse is significant, advise patient to seek medical treatment
77
What type of exercise decreases inflammation in every disease process?
Aerobic exercise
78
What DMT are there for MS?
Interferon β
79
What is included in the multi-faceted program for MS treatment?
-Prevention
-Resistance training
-Aerobic training
-Functional & balance training
-Fatigue education
80
What is the best type of intervention for MS patients?
Task based
81
What should a PT do when an MS patient is experiencing fatigue?
-Take vitals (HR, BP)
-Assess fatigue level and symptoms
82
What is MS related fatigue caused by?
-Immune activation
-Activation of glial cells and mitochondrial damage
83
What is chronic persistent fatigue in MS defined as?
> 6 weeks, 50% of the time
84
What is acute fatigue in MS defined as?
Recent onset
85
What is secondary fatigue in MS caused by? How can we as PTs improve this?
-Medications, stress, weather, depression
-LE weakness: strengthening
-Fatigue related to respiratory system: aerobic exercise
-Environmental issues: make modifications
86
What are educational strategies to manage fatigue in MS?
-Stop smoking!!!
-Encourage a 10-30 minute mid day nap
-Breathing activities
-Adjust activity levels
-Well balanced low fat diet (???)
-Drink cool liquids, as it reduces myelin loss
87
What is a possible intervention to reduce core body temperature in MS?
Cooling vests
88
What is the evidence surrounding exercise, cognitive function, and size of lesions in MS?
-Exercise early in the process spares the cognitive status of the patient
-Physically fit MS patients had fewer and smaller lesions than those who weren't as fit
89
What enhances the ability of oligodendrocytes to generate additional myelin and to maintain preexisting sheaths?
-Exercise!!!
-Aerobic exercise was associated with less damaged brain tissue in both the white and gray matter
90
What are the exercise guidelines from the MS society?
150 minutes per week or more of exercise
91
What is the AM Journal of Physical Medicine Rehab guidelines for exercise in MS?
-2-3 days/week of aerobic exercise, 10-30 minutes at moderate intensity
-2-3 days/week of resistance training, 1-3 sets of 8-15 reps max
92
How did aerobic exercise effect the hippocampus?
-Intervention was 30 minute sessions 3x/week for 3 months
-Aerobic exercise resulted in 16.5% increase in hippocampal volume and 53.7% increase in memory, and increased hippocampal resting-state functional connectivity
93
What position should someone lay in to manage flexor spasticity? How long should they lay like this for?
-Feet hang over the edge
-Arms overhead
-20 minutes is optimal!!
94
What position should someone lay in to manage extensor spasticity? How long should they lay like this for?
-Side lying with hips and knees bent
-Place a pillow between the legs and at the chest level
-20 minutes is optimal!!!
95
What other interventions can help to manage spasticity in MS?
-Daily ROM stretching program through full ROM with holds at end range for one minute
-Medications
-Fatigue management
96
How is dual tasking effected in MS?
-White and gray matter lesions effect areas of the CNS that are involved in dual task training
-These have also been negatively associated with postural control and motor learning performance
97
What type of resistance training has been shown to be the most helpful in MS?
Eccentric exercise
98
How does sensory input effect balance in MS patients?
-Slow conduction of proprioception
-Impaired central integration
-Leads to balance problems, reduced confidence and fear, especially during unpredictable environments
99
What % of MS patients have postural sway during quiet stance? What did they require to maintain balance?
-75%
-Required vision for balance due to proprioceptive and vestibular deficits
100
What wearable device can have immediate results for static and dynamic balance in MS patients?
-Sensory weighted vest
-Provides weighted information for balance
-Improves postural control in gait
101
Why does a weighted vest assist with postural control with MS?
-Axial loading
-It increases the sensory and proprioceptive stimuli
102
What is the evidence for interventions for gait activities in MS?
-Strengthening does not improve gait
-VR was not any different from conventional therapy
-Task based practice targets specificity and salience for gait training: 40 minutes or more, and must be challenging
-Very few studies show positive results in gait activities
103
How is speed interval training effective for patients with MS?
-20 second intensive walking periods
-1-6 minutes of slow walking or relaxation
-Milder degrees of disability were seen in treatment group
-Allows for rest
-Allows persons with MS to continue to take short steps but work on increasing limb speed
104
What type of steps should patients with MS be taking? Why?
-Shorter steps but not as fast
-For safety!!!
105
When should assistive devices be provided for MS patients?
-Provide at first sign of postural deficiencies to reduce energy expenditure and increase safety
-Start with single point cane or trekking poles (best)
106
What is a commonly used cardiorespiratory training program for MS with EDSS levels less than 7?
-Moderate intensity: 40-60% of HR max or 11-13 on RPE scale
-10-30 minutes
-2-3x/week
-Gradually increase to maintain target HR and RPE
107
What problems can spasticity in MS cause?
-Biomechanical and connective tissue problems: becomes more rigid and more connective tissue
-Hyperactive stretch reflex
-Muscle weakness
108
What type of spasticity is seen in MS?
-Dynamic spasticity
-Spasm
-Co-contraction
-Clonus
-Flexor withdrawal
109
What is used to treat generalized spasticity?
Oral medications
110
What is used to treat focal spasticity?
Botulinum toxin
111
What is used to treat regional spasticity?
Intrathecal baclofen
112
What questions should be used to determine if spasticity should be treated in MS?
-Does the spasticity affect function?
-Does spasticity result in pain or discomfort?
-Is there a risk of or presence of complications?
-If yes, then treat!
-If no, then no treatment is required
113
What can increase spasticity in MS?
-Pressure ulcers
-Bowel and bladder dysfunction
-Infections
-Pain
114
What are the first and second line medications for treating spasticity in MS?
-Oral baclofen is first line
-Gabapentin is second line
115
How can whole body vibration be helpful in treating spasticity in MS?
-Provides sensory information
-Resets the spinal reflex by responding to the length and velocity that whole body vibration provides
115
What are the parameters for using TENS to treat spasticity in MS? What mechanism does TENS use to treat spasticity?
-100 Hz
-0.3 ms pulse
-20 minutes per day
-4 weeks
-Gating mechanism by stopping the ongoing stimulus
116
What are other methods of combating spasticity? How does this work?
-Touch and pressure
-Compressive blanket
-Influences the AHC
117
What is the primary mechanism for slow, low load prolonged stretches?
As you hold the muscle in a stretched position, the muscle spindle habituates by becoming accustomed to the new length, which reduces signaling
118
What does Brain Derived Neurotrophic Factor (BDNF) help with? How was BDNF effected by exercise in MS?
-Supports neurogenesis
-Improved synaptic connections
-Promotes brain vascularization
-Serum BDNF levels are higher in exercise groups compared to control
119
What is compensation and recovery/restoration in neurorehab?
-Compensation is optimizing new skills while learning new methods of performing tasks to minimize loss of motor function (use of an AFO)
-Recovery/restoration is the process of restoration of the loss of a motor skill or function
120
What are the 5 main principles of effective exercise in neurorehab?
-Specificity
-Repetition
-Intensity
-Time
-Salience
121
What types of neuroplasticity are there?
-Experience expectant
-Experience dependent
122
What is experience expectant neuroplasticity?
-Neuroplasticity that is dependent upon genetics: developmental process
-Brain is producing connection by innate processes and normal development
-Example: vision
123
What types of stimuli provide experience dependent neuroplasticity?
-Diet
-Exercise
-Environment
-Stress
-Natural aging
-Neurotrophic factors
-Brain reserves (lifetime of experiences)
124
What is linked to better recovery in acute patients with brain injury/CVA?
-Normalization of motor activity patterns
-Task oriented practice promotes localized brain changes that may be more beneficial at the acute stage after stroke
125
What type of rehab should be provided early after CVA?
-Early rehab program regardless of intensity
-15-20 minute bouts
-Shorter bouts, more times/day
126
What is long term potentiation (LTP)?
-Involves persistent strengthening of synaptic connections occurring from high-frequency pre-synaptic acitvity
127
What is the key to permanent change?
Long term potentiation
128
What changes occur at the cellular level during long term potentiation?
-Presynaptic neurotransmitter levels increase
-Number of postsynaptic receptors increase
129
What is the role of aerobic and resistance exercise in neurogenesis?
-Increased cerebral blood flow
-Enhanced memory
-Leads to increased neurogenesis
130
What are neuroplastic mechanisms that are known contributors to neural remodeling?
-Modified gene expression
-Dendritic remodeling
-Myelin plasticity
-Cytogenesis
-Synaptic strengthening
-Increased circulating neurotrophins
131
What is the role of motor learning in neuroplasticity?
-Learning new motor skills enhances neuroplasticity
-Increases dendritic spine density
-Increased survival for new spine in motor cortex
-Forms specific connections to the striatum and basal ganglia which is responsible for selection of motor programs
132
What are some examples of new motor skills for individuals with brain injury?
-Ping pong: reaction time, eye hand coordination, postural control, visual tracking (can be seated or standing)
-Swiss ball bowling or rolling
-Sticks drill
133
What do task based activities help with in CVA?
-Reduce the chance of non-use
-It is essentially learning a new skill due to their hemiparesis
134
What is the time and dosage for neuroplasticity after stroke?
-Wait 24 hours after stroke so they are medically stable
-Smaller doses, more frequent
-Exercise in larger amounts 2-3 months after stroke
-Greater than 3 hours of rehab shows better outcomes than less than 3 hours
135
What is the difference between spinal cord and brain neuroplasticity?
-Strength training increases spinal motor neuron excitability and increase in synapses
-Co-contraction activities lead to changes in spinal cord with reduction in muscle spindle transmission
-Skilled motor training leads to brain plasticity
136
What is multimodal stimulation/exercise? What does research say about multimodal exercise?
-More than one sensory or motor activity that targets brain activity
-Working memory and attention can be directly related to successful multi-sensory processing
-Many cognitive abilities and processes are dependent on successful multi-sensory processing
137
What is multisensory integration associated with? What area of the brain is this process associated with?
-Enhances speed, detection, localization, and reaction to biologically significant events
-Single neurons in the superior colliculus (SC), which synthesize concordant combinations of visual, auditory, and/or somatosensory signals to enhance the vigor of their responses
138
What populations should multimodal training be used in?
-Parkinson's disease
-Stroke
139
What does multimodal stimulation improve with Parkinson's?
Turning and festination
140
What intervention improves gait outcomes in CVA patients? What are the parameters for this?
-High intensity gait training
-70-85% of HR max
141
What area of the brain is improved with goal oriented motor activity?
Premotor cortex
142
What area of the brain is improved by aerobic exericse?
Frontal lobe and executive function
143
What area of the brain is improved with skilled performance?
Cerebellum (only while performing)
144
What area of the brain is improved from learning new motor skills?
-Parahippocampal gyrus
-Dendritic growth
-Brain reorganization
145
Is high intensity variable gait training or forward gait training better for recovery in CVA?
-Studies have shown that the paretic leg got stronger with variable high intensity gait training compared to just forward gait training
-Unimpaired leg got stronger with just forward gait training
-Increase in paretic leg strength, balance, over obstacles with variable
146
How can TENS or FES be used to treat spasticity in CVA? What amount of time is best? What electrode placement was the best?
-Has been shown to improve spasticity post-stroke
-60 minutes was more effective than 30 minutes
-Over the nerve
147
When should TENS be used during pain treatment?
Should be used at every stage of the stepped care model for pain
148
How does TENS modulate pain?
-Gate control theory
-Releases inhibitory neurotransmitters on the pain fibers at the dorsal horn of the spinal cord
149
What type of neuroplasticity can happen with neuropathic pain?
Negative neuroplasticity where dendrite density is increasing and so are receptors, which hyperexcitability of pain fibers
150
What is the evidence in neuroplasticity with Parkinson's disease?
Exercises that incorporate goal-based training and aerobic activity have the potential to improve both cognitive and automatic components of motor control
151
What is the evidence in neuroplasticity with Multiple Sclerosis?
-Task based training increases volume of white and gray matter
-Two months of training for white matter changes
-High intensity exercise with visual feedback
-Resistance training
152
What is motor priming? What does this show with cardiovascular activities?
-Preparing the nervous system to perform
-Shows that cardiovascular activity induces plasticity within neural circuits that are directly relevant for the acquisition or performance of another behavior
-Ex: stair climber then practice walking
153
What is the evidence for dosage in neuro rehab?
-Typically inpatients only receive 22-60 minutes of training a day
-At least 16 hours (71 more minutes/day for 3 months) extra training within the first 6 months is required for functional gains
-High dose rehab protocols
-Should focus both on specific brain areas as well as networks of the brain
154
How many hours a week should neuro patients get?
More than 5 hours
155
What is structured practice?
Training schedule with frequent and longer breaks
156
What is variable practice?
Several tasks that require different movements
157
What is explicit feedback?
Knowledge about results
158
What is implicit feedback?
Knowledge about performance that is obtained from tracking, analyzing, and visualizing kinematic movement
159
What gait outcomes occur from static and dynamic balance activities in stroke patients?
These interventions do not contribute to improvements in locomotor function
160
What are the 4 factors in decision making for orthotics?
-The advantages or positive outcomes expected
-Any disadvantages or concessions
-The indications that the orthosis may be useful
-The circumstances or characterisitics of the individual
161
What are the characteristics of an ideal orthosis?
-Meets the individual's mobility needs and goals
-Maximizes stance phase stability
-Minimizes abnormal alignment
-Minimally compromises swing clearance
-Maintains or reduces joint contractures
-Effectively prepositions the limb for initial contract
-Is energy efficient
162
What assessments should be done when determining if a patient should get an orthotic?
-ROM
-Synergistic versus muscular weakness
-Sensation
-Gait deviation assessment
-Injury or instability prevention?
-Muscular adaptation
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What must be done for skin protection when someone has an orthotic?
-Wear athletic socks that covers the entire area of the orthotic
-Check brace and all boney prominences 20 minutes after the first wear
-If any redness on the skin, request that the person do not wear and go to the orthotist
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When will changes in gait from an orthotic appear?
Immediately
165
What team members are involved in prescribing orthoses?
-Orthotist
-MD
-PT
-Patient and family members
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What diagnoses are typically prescribed AFOs?
-Weakness
-Stroke
-Cerebral palsy
-Head injury
-Peripheral neuropathy
-Alignment
-Spinal cord injury
-Progressive disease
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What principles does every orthosis use to accomplish the goals of its design?
Force principles
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When is an orthosis most comfortable?
-Pressure= force/area
-Control direction of primary force and direction of counterforces
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What are characteristics of leather and metal AFOs?
Heavy and less malleable
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What are characteristics of thermoplastic AFOs?
-More commonly used
-Thicker and stronger
-Adjustable
-Lighter than metal
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What are newer basis for orthotics?
-Carbon fiber
-Light weight and durable
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What is a KAFO? What diagnoses is it most commonly used for?
-Knee ankle foot orthosis
-Spinal cord injury
-Muscular dystrophy
-Spina bifida
-Polio
-Used for limited community or household ambulation
-Muscular weakness
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What are considerations for decision making for orthoses?
-Body structure
-Function
-Participation
-Stable disease, improving, or degenerative (MS, ALS)
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What are the functional priorities with orthotics?
-Gait
-Sit to stand
-Floor to stand
-Balance
-Incline and stairs
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What are other essential attributes for orthotics?
-Can be worn for long periods of time, 6-8 hours/day
-Can be easily donned and doffed
-Cosmesis (cosmetically appealing)
-Considerations for job and recreation
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What are critical phases of gait for orthotics?
-Mid stance
-Mid swing
-Terminal swing
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What are the distinct types of AFOs?
-Solid AFO
-Dynamic AFO
-Hinged AFO
-Ground force AFO
-Leaf spring AFO/posterior leaf spring AFO (PLS AFO)
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What are custom molded orthoses?
Provide the optimal control of the limb and, because of their intimate fit, are especially important for patients with impaired sensation, significant hypertonicity, or risk of progressive deformity associated with their condition
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What are the off the shelf AFOs?
-Standard AFO
-Leaf spring AFO
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What is a leaf spring AFO?
-Dynamic thermoplastic AFO
-Supports the weight of the foot during swing phase as a means of enhancing swing clearance
-Assists with controlled lowering of the foot during loading response in stance as part of the first heel rocker
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What are dorsiflexion assist AFOs?
-Designed to preposition the foot for heel strike at initial contact
-Not ideal for CNS issues as it does not control rear foot
-Contributes to push off in the transition from stance to swing phase
182
What is a solid AFO?
-Larger trim lines allow for more control of the tibia
-Support the calcaneus
-Wider control of footplate to prevent excessive eversion or inversion
-Resists plantar flexion during swing phase
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What are disadvantages of a solid AFO?
-Interferes with all three ankle rockers in stance phase
-Prevents controlled lowering of the foot
-Prevents forward progression of the tibia during the second ankle rocker
184
What is a hinged AFO?
-Allows for sagittal plane motion at the ankle by incorporating a mechanical ankle joint between the foot and calf sections of the orthosis
-Provides mobility in many functional activities
-Reduce risk of falls
-Less negative impact on dynamic postural control
-Allows for tibial advancement during stance phase
185
What are different aspects that can be added to hinged AFOs?
-Plantar flexion stops that prevents excessive plantar flexion and equinus
-Permits dorsiflexion
-Can have increased trim lines with patients who have limited muscular control
-Elastic dorsiflexion check strap
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What is an anterior floor reaction orthosis?
-Ground reaction orthosis
-Evolved from basic SAFO design to better address impaired motor control of the knee and weakness of the quadriceps
-Restricts the ability of the tibia to roll forward over the foot, creating an extensor moment to stabilize the knee during stance
-Used for poor ankle support in stance, minimal dorsiflexion in swing, and knee collapse during stance
-Prevents knee flexion in stance
187
What is a dynamic AFO?
-Used for tone reduction
-Mostly in children
-Stabilizes rear foot and calcaneus
-Surrounds the whole ankle, foot, and calf
-Controls ankle through stance
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What is the pathophysiology of Guillan Barre Syndrome?
-Immune mediated polyneuropathy
-Results from a preceding infection that reacts with the autonomic nervous system that causes inflammation in the peripheral nerve
-Directed toward nerve root
-Leading to a motor & sensory neuropathy
-Most common severe paralytic neuropathy
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What are the three other types of Guillan Barre?
-Acute motor axonal neuropathy (AMAN)
-Acute motor-sensory axonal neuropathy (AMSAM)
-Miller-Fischer syndrome
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What is acute motor axonal neuropathy (AMAN)?
-Attacks nerve fibers rather than myelin sheath
-UE and LE involvement
191
What is acute motor-sensory axonal neuropathy?
Combination of myelin and axons damage
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What is Miller-Fischer syndrome?
-Rare variant
-Weakness or paralysis of the eye muscles
193
What is the incidence of Guillan Barre?
-1-2/100,000 per year in the US
-Incidence increase by ~20% with every decade of life beyond 10 years of age
-Greater in males than females
-Children 0-18 years
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What is the pathology of Guillan Barre?
-Autoimmune disease
-Acute demyelinating process
-Cell mediated peripheral nerve disruption
-Immune cell mediated
-Secondary hypersensitivity reaction
-Elevated cytokines in CSF
-2/3 associated with bacterial or viral infection 2 weeks before
-Moves through the GI or respiratory system mucosa or epithelium
-Ingestion of Campylobacter
-Infiltration of macrophages & T lymphocytes into the spinal roots and PN
-Macrophages attack and strip myelin
-In severe cases, axons are destroyed
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What are common pathogens that cause Guillan Barre Syndrome?
-Respiratory or diarrhea prior to illness (2-3 weeks)
-Campylobacter jejuni infection is the most commonly identified
-Cytomegalovirus, Esptein-Barr virus (herpes), and human immunodeficiency virus (HIV)
-A small potion of patients develop GBS after another triggering event such as immunization, surgery, trauma, and bone marrow transplantation
196
What is Chronic Inflammatory Demyelinating Polyneuropathy (CIDP)?
-Similar clinical presentation to GBS
-Slow progression up to 8 weeks
-Persists for years (chronic)
-Does not involve the respiratory system
-Relapses are much more frequent
-Longer recovery time
-Corticosteroids are effective
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What is the clinical presentaiton of GBS?
-Acute or develops slowly over 3-4 weeks
-Symmetrical ascending weakness from distal LEs to UE and respiratory system
-Varies from mild distal to total paralysis and intubation
-Accompanied by severe fatigue
-20-38% are intubated from intercostal and diaphragmatic weakness
-Ascending loss and hypotonia
-Sensory loss (proprioception, vibration, paresthesias, stocking and glove pattern)
-Pain: muscular aching, severe burning or hypersensitivity
-Significant fatigue
198
What are autonomic symptoms of GBS? What percentage of patients does it occur in?
-Tachycardia
-Low cardiac output
-Hypotension
-Cardiac arrhythmias
-Hypertension: BP dysregulation
-peripheral pooling of blood
-Urinary retention
199
What helps sensory regrowth in GBS?
Weight bearing and exercise
200
What is the clinical progression of GBS?
-Progression of disease process over 2-4 weeks
-90% reach nadir (when disease stops) by 4 weeks
-Progressive weakness distally and ascending
-May involve respiratory musculature and diaphragm
-If placed in ICU on ventilation is a poor prognosis
201
What does the medical diagnosis of GBS include?
-Based upon clinical presentation: progressive weakness, absent or depreesed DTRs, absence of fever, symmetrical, CN nerve involvement
-CSF lumbar puncture: decreased leukocytes, elevated CSF protein
-Nerve conduction velocity (gold standard)
202
Where is the lumbar puncture performed?
-Side lying fetal position
-L3 or lower where cauda equina is
203
What are the 3 phases of GBS?
-Initial phase with definitive symptoms: 1-3 weeks
-Plateau phase: several days to two weeks
-Recovery phase: 4-6 months up to 2 years
204
What is the first medical treatment option of GBS?
-Plasmapharesis: plasma exchange which includes removing plasma from blood and centrifuging it to remove immune complexes and antibodies, re-inject plasma into patient with albumin (to combat protein loss)
-Variable outcomes
-Initiated within two weeks
205
What are other medical treatments for GBS?
-IV administration of immunoglobulins (IVIg) which inhibits autoantibodies and reduces or blocks secondary immune attack
-Just as effective as plasmapheresis
-Must be implemented immediately
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What is immunoglobulin?
A protein that helps fight diseases
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What is the medical prognosis of GBS?
-50% reach nadir by one week
-70% by two weeks
-80% by 3 weeks
-3-5% expire due to respiratory or organ failure
-Recovery emerging in two to four weeks
-Fatigue or endurance long term consequence
208
What are negative prognostic indicators of GBS?
-Older age > 40
-rapid rate of progression from onset (< 7 days)
-Length of time until nadir
-Severe muscle weakness
-CN involvement with loss of eye movement and swallowing
-need for ventilatory support
-Average distal motor response amplitude reduction to < 20% of normal (80% reduction)
-Preceding diarrheal illness or cytomegalovirus
209
What are long term outcomes of GBS?
-Independent ambulation at 6 monhts: > 80%
-Full strength recovery at 1 year: 60%
-5-10% have prolonged course with several months of ventilator dependency
-Death: 5% of those with GBS, 20% who become ventilator dependent
-Relapse: up to 10%
-Develop CIDP: 2%
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What is included in the physical therapy exam of GBS in inpatient setting?
-Medical hx
-Co-morbidities
-Medications
-Social hx
-Environment
-Launguage and learning style
-Cognitive screen
-Integumentary assessment
-Neuromsucular: full assessment
-Muscular: full assessment
-Cardiopulmonary: full assessment
-Cardiovascular assessment
-CN: full assessment
-Pain
-Sensation: prop, touch
-Bed mobility
-Sitting tolerance
-Transfers and standing
-Gait
211
What are special considerations for GBS?
-Skin integrity
-DVT
-Autonomic dysfunction: hypotensive events
-Aspiration
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What should be done if aspiration is a concern for GBS?
Always elevate the head of the bed and never leave the patient flat
213
What should be done if a patient with GBS says "I'm tired" or "I'm feeling weak"? Why?
Get a chair immediately because they will collapse and not know they are going to fall
214
What is ICU care management of GBS?
-Ventilator
-Nursing and family training
-ROM and positioning
-Supported upright sitting with close cardiac and respiratory monitoring (10-20 minutes initially, while checking BP and HR every 3 minutes)
-Prevent contractures and skin breakdown
215
What are overall goals for ICU and acute care with GBS?
-Prevent contractures with ROM and resting splints, positioning, and AFOs
-Promote mobility (OOB): as soon as nadir is achieved
-Management of orthostatic hypotension with abdominal binder, stockings or leg wraps, and W/C with tilt and elevated LE
-Upright sitting in chair 2-3 hours per day
-Transfers and bed mobility
-Promote graded activity
-Initiate weight bearing activities
-Avoid prolonged positioning
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What positions should be avoided for GBS in acute care? How often should position be changed?
-Avoid porlonged hip and knee flexion to prevent contractures
-Change position every 2 hours
-Float heels to prevent pressure sores
217
What should be avoided in the acute phase with GBS?
-Avoid over fatigue or over-exertion in acute phase
-Up to 86% have fatigue
-Can exercise up to level of movement without pain and/or fatigue
-Halt at first signs of fatigue
-Upright tolerance is exercise!
218
What are the exercise guidelines for GBS?
-Passive to active- assisted when below 3/5
-Low reps and low resistance
-Powder board or hydrotherapy
-Painful muscles greater than 12 hours- reduce activity
219
Why are GBS patients at high fall risk? What equipment can help reduce fall risk?
-Lack of equilibrium and protective responses due to demyelination
-Orthotics (AFO or ground reaction AFO)
-Parallel bars
-Walker
220
How do individuals with GBS fall?
-Straight down!!!
-Collapse secondary to muscular fatigue
221
What type of tremors will MS patients have?
Active
