Final Flashcards
(100 cards)
1
Q
Ischemic stroke
A
80-85%, caused by clot/blockage causing loss of blood supply
2
Q
Hemorrhagic stroke
A
10-15%, caused by rupture/leakage, can be due to trauma
emergent
3
Q
ACA stroke
A
greater motor/sensory loss in CL LE>UE
Frontal lobe involvement causes: memory/behavior impairments
Urinary incontinence
Impairments in imitation, bimanual tasks
Apraxia
Cognitive deficits
4
Q
MCA stroke
A
greater motor/sensory loss in CL UE
CL homonymous hemianopsia
Left sided stroke:
- Aphasia
Right sided stroke: perception
- Unilateral neglect
- Depth perception
- Spatial relations
- Agnosia
- Apraxia: Ideomotor apraxia, Ideational apraxia
5
Q
PCA stroke
A
CL sensory loss
Thalamic sensory syndrome: persistent/unpleasant sensations on hemi side
6
Q
Internal Carotid stroke
A
Massive infarction to ACA/MCA if completely occluded
Often leads to coma and death
Incomplete occlusion will cause mixed MCA/ACA symptoms
7
Q
Vertebrobasilar stroke
A
Catastrophic damage due to damage to major artery
Lethal, comatose, or quadriplegic with poor prognosis
Locked in Syndrome: caused by infarct of pons from basilar artery
Progress from hemiparesis to quadriplegia, dysarthria to anarthria (impaired speech to no speech)
Cranial nerve paralysis V-XII
Pt is AO but unable to move or speak
8
Q
Lacunar stroke
A
small vessel disease deep in cerebral white matter
Pure motor or pure sensory
Motor: lesion to posterior limb of the internal capsule, pons, and pyramids
Sensory: lesion to ventrolateral thalamus or thalamocortical projections
9
Q
Cerebellar stroke
A
lesion in cerebellum which often starts unilateral but can have bilateral effects
Decreased:
coordination in voluntary, gross, fine motor movement
Postural control
Balance
Equilibrium
Eye movement coordination
10
Q
brain stem stroke
A
Decreased:
Alertness
ANS control
Arousal
Sleep regulation
Swallowing ability
balance/movement control
11
Q
Right CVA symptoms
A
L weakness/paralysis
L neglect, perceptual impairments
Poor judgment/impulsive
Decreased attention span
Short term memory loss
Communication problems with facial muscle weakness
Cognitive deficits
12
Q
L CVA symptoms
A
R side weakness/paralysis
Aphasia: Wernicke’s or Broca’s
Personality changes: cautious, compulsive, disorganized
Decreased ability to learn new info, memory, generalize/conceptualize
13
Q
Homonymous Hemianopsia
A
one sided visual field cut to both eyes, most commonly loss of left visual fields
occipital lobe damage
14
Q
hemineglect
A
perceptual issue where patient isn’t aware of one side of space relative to their body
Damage to R hemisphere causing L neglect
15
Q
Interventions for Hemianopsia and hemineglect
A
Awareness; teach use of environment and limb on affected side
Active visual scanning: head turning, axial trunk rotation towards involved side with cuing to get pts attention
16
Q
aphasia
A
communication disorder with language comprehension, formation, or use
17
Q
global aphasia
A
extensive damage causing impaired production and comprehension of language
18
Q
Wernicke’s aphasia
A
“fluent”
Lesion in auditory association complex, L temporal lobe
Smooth speech
Impaired auditory comprehension/unable to follow commands
19
Q
Broca’s aphasia
A
“non fluent”
Lesion in premotor area of L frontal lobe
Slow speech with limited vocabulary and impaired syntax
Good language comprehension
20
Q
spatial perceptual dysfunctions
A
incorrect perceptions of self, illness, space
Neglect of affected side
Agnosia: unable to recognize object
Apraxia: unable to carry out sequence of learned movements on command
21
Q
agnosia
A
unable to recognize object
22
Q
apraxia
A
unable to carry out sequence of learned movements on command
23
Q
spasticity
A
Measure by Modified Ashworth Scale (0-4)
resistance to passive movement
24
Q
Measures to assess arm, hand, finger function
A
Action research arm test
box/block test
Nine hole peg test
Wolf motor function test
25
Brunnstrom's stages of recovery
1. Flaccidity: no active limb movement
2. Minimal voluntary movement with synergy and increased tone
3. Voluntary control of movement synergy, peak spasticity
4. Movement outside of synergy with decreasing tone
5. Increase in complex movement, increase independence from limb synergies
6. Individual joint movement in coordination
7. Normal function
26
Proper positioning in post stroke pt: supine
keep scapula protracted, slight shoulder abd, arm supported by pillow; knee on pillow or towel to prevent hyperextension
27
Proper positioning in post stroke pt: side lying on affected side
scapula protracted, arm slight abduction/ER, straight elbow/wrist; hip extended and knee flexed
28
Proper positioning in post stroke pt: side lying on unaffected side
towel under rib cage to elongate hemiplegic side, UE - scap protracted, arm forward on pillow, elbow extended and wrist neutral
29
Pusher Syndrome
distorted postural orientation causing pt to use stronger side of body pushing towards the unaffected side, creating a tilt in movement
30
Pusher syndrome: treatment
mirror therapy
tactile cuing
31
stroke specific outcomes
National Institute of Health Stroke Scale: evaluate stroke severity
0-42
Consciousness, motor function, sensory function, speech, vision, neglect
Fugl-Meyer Assessment: performance based, assess motor recovery post stroke
0-226 (higher = better)
UE: 0-66
LE: 0-34
Functional Independence Measure: measure level of disability and assistance level required
18-126 (higher = better)
Stroke Impact Scale: self report, stroke related QoL
0-100 (higher = better)
Action Research Arm Test: UE functioning with ADLs
0-57 (higher = better)
TUG
Wolf Motor Function Test: UE motor skills w functional tasks
6MWT
Berg
10MWT
32
PT approaches to post stroke treatment
1. Task Specific Training: repetition of tasks meaningful to patient
- 5x week, 60 min
- Repetitive reaching, grasping, walking
2. CIMT: restrain unaffected limb to encourage use of affected limb
3. Motor imagery/Mental Practice: mentally visualize movements
4. Mirror Therapy: create illusion of movement
- Every day, 30 min
5. TMS: magnetic fields to stimulate nerve cells in brain
6. Strengthening/Aerobic: improve muscle strength and endurance
7. Treadmill/Gait training: improve gait and aerobic function
33
early mobilization
Greater improvements in walking, spasticity
34
Presentation of Peripheral Neuropathy
Glove and stocking neuropathy
Impaired vibration sense
Decreased ankle DTR
Foot drop
Wide BOS in gait due to loss of proprioception/balance from impaired sensation
35
Symptoms of Peripheral Neuropathy
Slow healing wounds
Burning pain
Touch sensitivity
Lack of sensation
N/T
Trouble sleeping
Trouble walking
36
sensory abnormalities w peripheral neuropathy
absent/diminished
Paresthesia
Hyperesthesia (increased sensation)
Causalgia (burning pain)
Allodynia
37
motor dysfunction in peripheral neuropathy
weakness: loss of motor neuron axons in periphery
balance: decreased somatosensory input
ataxia: abn sequence/timing/duration/magnitude of force, decreased synchronization
38
skeletal dysfunction with peripheral neuropathy
Bunions
toe/arch deformities
Claw foot
Valgus at ankle and knee
39
Diabetic Neuropathy Progression:
Capillary damages due to metabolic and vascular changes
Damage to capillaries results in nerve damage, impairing sensation
Loss of sensation can can integumentary compromise/wounds
Increased risk of infection/gangrene/ulcers due to decreased vascularity and sensation
Can result in amputation
Typical presentation:
- Distal
- BL
- Glove and stocking paresthesia/sensation loss
- LE involved first
40
Diagnosis of Peripheral Neuropathy: testing
Nerve conduction study: decreased NCV
EMG fibrillation potential
41
Assess sensation
qtip/cotton
Semmes-Weinstein monofilament
10g indicates protective sensation
42
Three types of cerebellar disorders;
Vestibulocerebellum
Spinocerebellum
Cerebrocerebellum
43
Spinocerebellar ataxia commonly presents with
Ataxic gait
Limb ataxia
Incoordination
Slow saccades
Optic atrophy
Dysarthria
Balance deficits
Falls
Tremor
Myoclonus
Chorea
Nystagmus
Dementia
Peripheral neuropathy
44
cerebellar atrophy
Balance deficits worsening over time creating issues of gait and rhythmicity
Often don’t have dizziness, vertigo, or hearing loss
45
Cerebellar Evaluation includes
Outcomes include:
Heel to shin
Intention tremor assessment
Dysmetria testing
RAM (expect impaired - dysdiadochokinesia)
Tone (expect hypotonia)
Limits of stability - increased postural sway
SOT
Gait velocity
Visual: nystagmus, VOR, saccades
46
Symptoms of Cerebellar disorder
Balance deficits
Ataxia (Eyes, Trunk, Extremities, Gait: wide BoS inconsistent step length/height/velocity)
Weakness
- Poor posture - decreased postural control
Decreased coordination
- Fine finger movements impaired
- Dyssynergia: unable to perform multi joint movements smoothly
over/undershooting (hyper/hypometria) - dysmetria
saccades/nystagmus impaired
- Impaired VOR
- Nystagmus with gaze shifting
- Ocular dysmetria
- diplopia/blurred vision
Slow gait speed
Dysdiadochokinesia
Intention tremor
Decreased endurance
- Related to hypotonia, limbs feel heavy
Posterior CoM
47
Exercises for cerebellar disorder
gaze stability
trunk stability
controlled mobility
weight legs to increase proprioception and stability
visual cuing
48
common gait deviations post stroke: initial stance
Limited ankle dorsiflexion due to TA weakness
Limited knee flexion/knee hyperextension
49
common gait deviations post stroke: midstance
Lack knee extension
Limited hip extension/ankle DF causing failure to progress body mass over foot
Lateral pelvic shift
50
common gait deviations post stroke: late stance
Lacking knee flexion/ankle PF, impairing push off
51
common gait deviations post stroke: early/mid swing
Limited knee extension/ankle DF impairing weight acceptance
52
Goals of Post Stroke PT
Preventing adaptive changes in lower limb soft tissues
Eliciting voluntary activation in key muscle groups in lower limbs
Increasing muscle strength and coordination
Increasing walking velocity and endurance
Maximizing skill, eg increasing flexibility
Increasing static and dynamic balance
Increasing cardiovascular fitness
Increasing safety awareness
Education on proper use of assistive devices
53
Methods of Post Stroke Rehab
treadmill training
FES: functional electrical stimulation
biofeedback
cortical priming
rTMS
VR training
BWS gait training: lite gait
robot assisted therapy
54
post stroke treadmill training
Goals: improve gait speed, endurance, and distance walked while improving quality/gait mechanics and increase muscle recruitment
Forwards or backwards
HIGT: 70-85% max HR, aerobic capacity
55
FES: functional electrical stimulation
post stroke gait training
Goals: improve muscle coordination, gait biomechanics
Electrical stim improves cycle of muscle activation for antagonistic muscle groups
56
biofeedback post stroke gait training
Include in task oriented stepping to improve quality and quantity for home programs
57
rTMS: high frequency
post stroke gait training
Brain stimulation to LE motor areas to improve gait
58
Body weight supported gait training: lite gait
post stroke gait training
Treadmill or overground
Don’t exceed 30-40% body weight support, want to load LE as much as possible to increase muscle activation
Use to go at higher speeds, goal 2 mph
Pros: less energy expenditure, task specific, decreased pt fear, active problem solving by pt, walk at faster speeds
Cons: harness discomfort, false sense of stability, limitations with treadmill, more work for therapist
59
Robot assisted therapy
post stroke gait training
Walking orthosis/robotic attached to LE and trunk to passively guide through a symmetrical gait pattern
Less degree of muscle activation
60
interventions for low level stroke patients
Low: Increase demand
High sitting w weight shifts
Sit on uneven surface or wedge
STS w/o arm support, high surface
Mini Squats
61
interventions for mid level stroke patients
initiate gait:
Step initiation of involved LE: stance knee control/posture
Swing initiation/limb advancement
stepping/weight shifting
Transfers
62
interventions for high level stroke patients
gait:
fwd/bckwd/sideways/tandem
Various surfaces
Turning
Stepping over obstacles
push/pull
Remove AD
Carry object
63
AD toxic changes in brain
- Beta amyloid proteins: form plaques outside neurons
- Tau proteins: clump together to form tau tangles in neurons
- Vascular system fails to deliver O2 and nutrients due to protein interference
- Chronic inflammation
- Microglia fail to remove debris
- Neurons loss ability to communicate and due, causing hippocampus shrinking
64
AD symptoms
1. withdrawal from social activities
2. Confusion on time/location
3. Difficulty completing familiar tasks
4. Misplacing items
5. Difficulty solving problems
6. Memory loss
7. Unfounded emotions
8. Poor judgment
9. Trouble with images and spaces
10. Difficulty with words
65
increased risk of AD in which populations?
women
hispanic/african american
65+
66
types of dementia
Alzheimers
Vascular dementia
Lewy body
Frontotemporal
67
AD disease progression
Mild cognitive impairment
Mild -> moderate -> severe alzheimer's
68
Alzheimer's disease progression: mild cog impairment
Lasts ~7 years
Medial temporal lobe
Short term memory loss
69
AD disease progression: mild AD
Lasts ~ 2 years
Spread to lateral temporal and parietal lobes
Reading problems, poor object recognition, poor direction sense
70
AD disease progression: moderate AD
Lasts ~2 years
Spreads to frontal lobe
Poor judgement, impulsivity, short attention
71
AD disease progression: severe AD
Lasts ~3 years
Spreads to occipital lobe
Visual problems
72
AD vs PD
PD has a quick progression with symptoms that come and go, meds can cause hallucinations
Alzheimer’s has a slow progression with symptoms that don’t go away and hallucinations in late stages
73
Early signs of Alzheimer's
1. Memory changes disrupting daily life
2. Trouble making decisions, planning/solving problems
3. Trouble completing familiar tasks
4. Confusion on time/place
5. Trouble understanding images/spatial relationships
6. Not finding right words when speaking
7. Misplacing items/can’t retrace steps
8. Poor judgment on safety
9. Withdrawal from work/social
10. Changes in mood/personality
74
Neuro Eval of AD includes:
Cognition assessment: MOCA, MMSE
Mood: depression screen
Motor: voluntary movement, coordination testing
balance/gait: cognitive decline impacts attention/motor symptoms
Functional outcome measures
Caregiver education/training
75
Effects of exercise on AD
- Slow rate of progression of AD (meds also help but come with side effects)
- Increase mitochondria function
- Decreased neuroinflammation/oxidative stress/decreased TNF-alpha and IL-6
- Protect neurogenesis/hippocampal proliferation/neuronal growth
- Reduce amyloid beta cells
- Increase cognitive ability and synaptic plasticity/neuroplasticity
- Ideal intensity: 30-50% VO2Max
- Use exercise to maintain current level with strength training to reduce falls, flexibility, aerobic for cognitive benefits
Balance for confidence and safety in movement
Gait training: recommend AD
Functional training: maintain ability to complete ADLs
76
Multiple Sclerosis
chronic autoimmune disease causing inflammation, demyelination, gliosis of CNS (cortical, subcortical, cerebellum, spinal cord)
77
MS etiology
white blood cells attack neurons, affecting myelin around nerve fibers produced by oligodendrocytes
Causes sclerosis/scarring, which impacts nerve signals and causes symptoms
78
MS diagnosis
MRI findings of two separate CNS lesions
CSF analysis: elevated immunoglobulins, oligoclonal IgC bands, slight protein elevation
NCV: decreased
79
MS common symptoms
clumsiness/muscle weakness/motor impairments
Intention tremor
Fatigue: most common symptom
Cognitive impairments
bowel/bladder dysfunction
Emotional disturbance/psychosocial problems
Optic neuritis/visual impairments
Paresthesia/numbness/proprioception or vibration loss
Lhermitte sign: cervical flexion produces electric shock
Uhtoff’s phenomenon: neuro symptoms increase in response to heat
- Fatigue, weakness, and spasticity lead to heat sensitivity
spasticity/UMN impairments/paresis
- Increased DTR
- + babinski
Spasms
Pain: neuropathic pain, trigeminal neuralgia (severe pain on face from trigeminal nerve), paroxysmal limb pain, headache
80
types of MS
relapsing remitting
secondary progressive
primary progressive
progressive relapsing
81
relapsing remitting MS
most common
short relapses
No symptoms between for many pts
Relapse: acute worsening of neuro function
Remission: period without disease progression, partial or complete recovery
82
secondary progressive MS
slow steady progression with relapses that pt doesn’t fully recover from
83
primary progressive MS
steady worsening without relapse/remission
84
progressive relapsing MS
steady worsening with relapses that may or may not remit
85
MS gait impairments
Weakness: foot drop, vaulting, hip hike, trunk lean, circumduction
Spasticity: muscle tightness/length
Balance: swaying, ataxic gait
Sensory: numbness in feet causing sensory ataxia
Fatigue: increases gait problems
86
MS visual impairments
Optic neuritis: pupil decreased response to light (marcus gunn), inflammation of the optic nerve causing blurred vision
Nystagmus: cerebellum or central vestibular involvement
Diplopia: ocular muscle discoordination, common, impairs balance and movement
87
goals of PT for MS
| intensity?
Optimize mobility
Heat sensitivity limits exercise for pts
Maximize physical function
Minimize functional loss
Intensity: submaximal: 50-70%
88
Myasthenia Gravis
neuromuscular junction disorder from autoimmune response causing ACh receptor damage and creating NM transmission deficit
causes muscle weakness
89
s/s of myasthenia gravis
Weakness, worsening during activity, improves with rest
Variable periods of weakness: ptosis, diplopia, critical respiratory weakness
Involvement: of speech, facial, mastication, swallowing, breathing, neck and limb muscles/movements
90
PD
hronic, progressive neurodegenerative dx from dopamine depletion in substantia nigra/loss of dopaminergic cells
91
PD Cardinal Signs
Tremors
Rigidity
akinesia/bradykinesia
Postural instability
92
other early PD signs
loss of smell, constipation, sleep disorder
93
huntington's disease
genetic neurodegenerative disease of basal ganglia and cerebral cortex
Autosomal dominant: CAG expansion on chromosome 4
94
Huntington's disease s/s
Muscle incoordination: involuntary jerking/writhing movements/chorea
Cognitive decline/psychiatric problems
rigidity/muscle contracture/dystonia
slow/abn eye movements
Impaired gait, posture, and balance
Difficulty with speech production and swallowing
95
Guillain Barre Syndrome
autoimmune LMN disorder where antibodies attack pt’s peripheral nerve cells, triggered by respiratory infection, GI infection, surgery, vaccines, or childbirth
96
Guillain Barre presentation
rapid onset weakness distal to proximal, bilateral
Develops over 2-3 weeks, max 4
Wide variation, most recover in 3-6 months
97
Guillain Barre symptoms
Decreased peripheral n strength causing: Weakness, atrophy, diminished DTRs, paralysis, respiratory involvement, facial/oral weakness, vision/speech/swallowing problems
Ataxia
Problems with respiration, talking, swallowing, bowel/bladder
Glove and stocking sensory symptoms: burn/tingle/pins and needles/numbness
Pain in large muscles: stiff/cramping/deep ache
98
Diagnosis of guillain barre
Clinical exam of BL, ascending symptoms
blood/urine tests
Lumbar puncture: CSF with high protein
MRI/CT/nerve biopsy
Stool test: viral/bacterial cause
NCV test/EMG
99
ALS
UMN and LMN, idiopathic genetic condition
diagnosed 50s
100
ALS symptoms
LMN: weakness, hyporeflexia, hypotonic, atrophy, muscle cramps, fasciculations
UMN: spasticity, pathological reflexes, hyperreflexive, weakness
Bulbar: weakness, dysphagia, dysarthria
Respiratory: weakness, dyspnea, esp w exertion
Frontotemporal dementia
Cognitive impairments
Behavioral changes
