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206 Cards in this Set
- Front
- Back
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Nagi - enablement of disablement?
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disablement
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ICF model - enablement or disablement
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enablement
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What is the focus of traditional neurologic assessment?
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on system deficits
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What is the difference between tone and spasticity?
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Spasticity is velocity dependent
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8 parts of motor control assessment
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cognition
strength range of motion sensation balance coordination tone synergy |
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What 2 goals do good functional movement have?
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options
& efficiency |
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What is validiity
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ability of tool to measure what it's intended to measure
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what is responsiveness
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the instrument's ability to detect change over time
(like MDC) |
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what is reliability
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ability to repeated measurements to get similar results
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what is sensitivity
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ability to detect fine changes
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what is sensibility?
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the ease and timeliness of administration
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Give examples of health condition/pathology
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GBS
CVA |
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Give examples of body function or impairments
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lacking ROM @ knee
weakness of finger flexors |
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Give examples of acitivty or functional limitations
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can not stand up from chair safely
can not grasp heavy round objects |
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Give examples of participation or disability
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Can not ambulate to bowling alley
Can not hold bowling ball to play |
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+ UE reflex, - LE reflex, with fasciculations suggests
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ALS
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can't walk, blurred vision, can't move UE, typically happens at end of day but gets better with rest
has drooping eyelids, weaker proximally than distally normal reflex/sensation |
Myastenia gravis
NMJ problem |
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middle aged woman with slight termor and discoordination, pain, clonus in ankle,
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possible MS
with UMN problem |
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What area is Broca's
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44
45 |
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What area is Wernicke?
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22
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Neuraxis:
Muscle: |
Myopathy
muscular dystrophy or polymyositis |
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Neuraxis:
NMJ |
loss of synaptic transmission
G, tetanus |
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Neuraxis:
PNS |
Neuropathy/radiculopathy
GBS, ALS, Erb Palsy |
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Neuraxis:
Spinal Cord |
Myelopathy
SCI, MS, VAM |
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Neuraxis:
Brainstem |
Bulbar control
Bulbar Palsy |
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Neuraxis:
Cerebellum |
Motor integration
Degeneration |
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Neuraxis:
Basal Ganglia |
Postural tone / limb control
Parkinson's Huntington's |
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Neuraxis:
Cortex |
Encephalopathy:
CVA, BI, MS |
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Sx of Muscle problem
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proximal muscle weakness
maybe hypotonic |
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Sx of NMF problem
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ptosis, diplopia
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Sx of PNS problem
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myotome problem
dermatome sensation hypotonic or abswent reflex |
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Sx of Spinal Cord problem:
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IL weakness
IL proprioception issue CL pain issue hypo @ level, hyper below |
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Sx of Brainstem problem
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IL facial weakness
CL body weakness @ medulla: ipsi sensation sx @ pons: CL sensation sx hypertonic |
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Sx of Cerebellum problem
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primary coordination problem
secondary weakness hypotonic |
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Sx of Basal ganglia
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Rigidity
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Sx of Cortex problem
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CL weakness/sensation
hypertonic impaired cognition |
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do patients with neuro problem choose mobility strategy favoring force control or momentum?
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force control
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how is vertical forces impaired in sit to stand?
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inability to activate muscles concentrically limit the propulsive vertical forces lifting body
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how is horizontal forces impaired in sit to stand?
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loss of eccentric contro limits ability to control horizontal COM movement
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What rae the speeds for physiological, limited household, unlimited household, most limited community, least limited, and community walker?
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.1
.23 .27 .4 .,58 .8m/s |
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patients with neuro favor "force control" or "momentum"
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force control
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What are the speeds of the walking categories?
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physio .1
limit house .23 unlim house .27 most lim comm .4 least lim comm .58 comm .8 |
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describe measures of modified ashworth scale, 0, 1, 1+, 2, 3, 4
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0 nothing
1 slight increase tone (catch/release or min resistance at end of ROM) 1+ catch in less than 1/2 ROM 2 min/mod resistance thru-out 3 considerable increase, difficult ROM 4 rigid |
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is MAS valid assessment of resistance to passive movement?
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yes
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is MAS valid measure of stretch reflex hyper-excitability
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no
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is Fugl-Meyer valid, reliable, and sensitive?
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yes
yes yes |
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escribe fugl-meyer 7 stages
1-7 |
1 - flaccid paralysis
2 - spastic paralysis, can cause voluntary synnergies reflexively 3 - can initiate uncoordinated synergies, reduced ROM 4 - simple uncoordinated movements deviating from synergy, voluntary movements in synergy 5 - slow movements without synergy 6 - mostly selective movements, some incoordination w/ reciprocal movements 7 - normal function |
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what is the body's attempt to compensate for weakness?
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subsitution
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window of spontaneous recovery of brain injury
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6mo-1yr
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window of spontaneous recovery for CVA
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3-6mo
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define recovery
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neural recovery '@ cellular level or behavior ompensation
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define recovery of function
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re-acquisition fo movement skills lost through injury
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define learned nonuse
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the behavior shift that occurs with compensation
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define compensation (neural recovery)
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substitutive process in which onthign is recovered but a new and somehwat grossly different behavior is acquired to attenuate the behavioral deficiencies produced by the brain injury
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4 mechanisms for neural recovery:
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1) bilateralization
2) resorption of local edema and necrotic tissue 3) synaptic sprouting and reinforcement of existing circuits 4) formation fo new polysnaptic connections |
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what is diaschisis
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watermelon headshot
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how does brain plasticity affect somatosensory cortex?
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practice expands existing representation
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explain task specificity (neural recovery)
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speicif areas of cortex expand to match task training
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what are the two patterns of cortical reorganization after CVA?
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1) intiial recruitment of bilateral areas, developing to a pattern of activation in CL cortex only
2) persistent recruitment, with intial and sustained recuirtment of ipsilateral activity [seen more often with lesions in primary S/M cortex and internal capsule) |
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3 aspects important to successful rehab of neural plasticitiy
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sensory experience
enriched experience motivating task |
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2 important part of practice in neural rehab
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intensity
specificity |
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examples of recovery of function through skill acquisition, 1 UE, 1 LE
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UE: extremity constraint induced exercise
LE: body weight support treadmill training |
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What are roles of PT regarding swallowing/dysphagia? (3)
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screening
referral oral motor or postural dysfunction |
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what is dysphagia?
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difficulty swallowing
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describe oral preparatory stage
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mouth opening
bolus reception/containment taste mastication soft palate rests on back fo tongue to prevent movement into pharynx |
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describe oral stage
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bolus propelled through oral cavity towards pharynx
(lips, buccal muscles, tongue push bolus back against hard palate to base of tongue) |
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describe the pharyngeal stage
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larynx rises
pharyngeal peristalsis squeezes bolus down pharynx to superior esophagus cricopharyngeal sphincter relaxes and allows food to go into esophagus |
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describe the esophageal stage
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8-12 seconds
bolus go thru esophagus lower esophageal sphincter relaxes, as bolus goes to stomach |
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what components of NS control pre-oral, oral-prep, and oral stages?
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voluntary
cortical CN V, VII (chewing, bolus management) |
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what components of NS control pharyngeal and esophageal stage?
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involuntary
CN IX , X, XI |
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what components of NS control taste?
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CN VII, IX
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describe dysphagia w/ pre-oral stage
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UE str/coordination
judgement, alert, coordination posture |
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how does dysphagia affect oral-preparatory stage
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lip-tongue-cheek control leading to:
drooling food residue in mouth dysarthria (tongue problem) reduced mastication |
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how does dysphagia affect oral stage?
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food held in mouth,
or pooling of food in sulci or reduced tongue movements (ataxia, apraxia, tone alterations, weakness) |
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how does dysphagia affect pharyngeal stage?
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coughing, choking, absents wallow response
increased throat clearing multiple swallows nasal regurgitation |
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how does dysphagia affect esophageal stage?
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reflux:
regurgitation, sour taste heart burn |
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what is aspiration?
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food in ur air pipes
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what are medical complications with dysphagia? (4)
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aspiration
aspiration pneumonia dehydration compromised nutrition |
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role of PT in dysphagia management (3)
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screening
posture strengthening |
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What are ways of screening for dysphagia:
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posture assess
CN exam pharyngeal screen rediologic |
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what are 4 aspects of pharyngeal screen?
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dry swallow
vocal quality volitional cough gag reflex |
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What is body scheme?
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awareness of body parts and their relationsihp to one antoehr and environment
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what is slur speech + LE fasciulations indicate of?
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ALS - psueobulbar palsy
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what is apraxia?
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motor planning deficit
inability to carry out purposeful movement in presence of intact sensation, movement, and coordination (performane deficits that are not a result of incomprehension) |
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What is constructional apraxia?
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inability to produce designs in 2-3 dimensions by copying/drawing or constructing
eg making bed, setting table |
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what is dressing apraxia?
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inability to dress oneself
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4 possible causes of dressing apraxia?
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constructional apraxia (can't put pieces together)
visual disturbance spatial disorganiation unilateral neglect |
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2 kinds of limb apraxia?
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ideomotor apraxia
ideational apraxia |
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What is ideomotor apraxia?
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movement may occur automatically but not by command
(instinctively respond to wave, climb up stairs...) |
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What is ideational apraxia?
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Purposeful movement is NOT possible neither by command or automatically
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what is transitive testing of apraxia?
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testing movements that require tool (hammer / comb)
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what is INtransitive apraxia testing?
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testing movements without a tool
(wave bye, gestures) |
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What is agnosia?
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Inability to recognize or perceive familiar objects
(but no primary sense impairments) |
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What is anosognosia?
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patient doesn't recognize their hemiplegia
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What are 3 spatial relation disorders?
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topographical - of one place to another
figure ground - fore from background (white shirt on white sheets) position in space (over/under, front/back) |
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What hemisphere is more important for attentional/spatial disorders?
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right
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how do left & right hemisphere relate to left and right stimuli?
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left hem - right stim
right hem - left stim and some right stim |
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where does spatial processing occur?
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parietal association cortex at junction of parietalk, temporal and occipital lobes
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what is unilateral neglecft?
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tendency to ignore stimuli on one side (CL to lesion)
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what is motor neglect?
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tendency to not use the side CL to lesion
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what is motor neglect associated with?
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poor functional outcome
increased hospital duration poor response to rehab |
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how is motor movement of the motor neglected side?
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relatively normal when cued
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what is motor neglect associated with?
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decreased motor performance (eg strength)
decreased motor performance in unaffected limb (suggest generalized effect on function) |
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what is the premotor theory of selective attention and what does it mean for rehab?
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neural circuit that control spatial attention are linked to motor planning so a shift in spatial attention affects motor planning
ie improving visual neglect improves motor neglect |
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how to treat motor neglect?
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train affected limb and perceptual deficit
avoid bilateral or CL movements |
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how to test for motor neglect?
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test performance of bilateral action
(bimanual tapping) motor extinction |
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how to test visuospatial neglect?
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lien bisection
draw a clock cookie thieft picture cancelation task |
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how effective is line bisection test?
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screening only
can be influenced by other syndromes; hemianopia, apraxia... |
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how to interpret line bisection test?
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bisection occurs towards side of lesion is a sign of neglect (6mm)
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how effective is neglect treatment?
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improvement at impairment level
insufficient eviedence at functional level |
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what are 7 ways of neglect treatment?
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1 scanning training (visual cueing)
2 alteration of visual input (glasses) 3 visual imagery 4 limb activation 5 awareness training 6 sustained atten training 7 tactile stimulation |
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What is ataxia?
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incoordination of movement following sensory or cerebellar damage
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what kind of movement does ataxia affect more?
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multijoint
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which side does cerebellar ataxia affect?
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IL
(also true of cerebellar peduncles, pontine nujclei,, dorsal and ventral spinocerebellar pathways) |
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what is result of cerebellar ataxia?
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high amplitude tremor with movement
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how does clothing your eyes differentiate cerebellar and sensory ataxia?
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cerebellar - not much worse
sensory - MUCH worse |
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what is hypermetria?
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ataxia - overshoot of target with rapid single joint movement
agonist magnitude reduce, acceleration time prolonged antagonist delayed |
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what are mechanisms of ataxia?
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hypermetria
exponential difficulty with MJ actions MJ movements in synergy -anticipatory and ineffective postural and leg adjustments to arm movements |
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describe ataxic gait
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uneven step length
irregular width rhythm is absent feet lifted too high cannot walk in straight line w/out lurching arm swing decreased |
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What is the test for ataxia?
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cooperative ataxia rating scale?
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what is dyssynergia?
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movement decomposition
eg finger to nose pointing alternate heel to knee |
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what is dysmetria examination
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look for past shooting
finger to nose pointing, drawing circles or figure 8, heel on shin |
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what is dysdiadochokinesia exmaination?
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test with rapid alternating movements
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when is Fugl-Meyer usefor for ataxia?
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used for screening to determine if CVA is typical MCA infarct or of other origin
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what is cognition?
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ability to process sort retrieve and manipulate information
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what is perception?
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integration of sensory impiressions into psychologically meaningful information
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what is attention?
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ability to focus on a specific stimulus without being distracted
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what is focused attention?
sustained attention? selective attention? alternating attention? divided attention? |
focused - respond repeatedly
sustained - over time selective - ignore distraction alternate - shift between tasks divided - multi-task |
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what is concentration?
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ability to process information you're attending to
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what are 3 different source of problem with orientation?
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impaired wakefulness
imparied attention aphasia |
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what are the 4x orientation?
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people
place time situation |
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what is Folstein Mini-Mental State Examination? (MMSE)
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originally detect dementia
now widely used - lesions, amnesia, cognitive defects |
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What is remote memeory?
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ability to preserve information and recall it later
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what is semantic memory?
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memory of general knowledge
(eg state capitals, Poo's friends) |
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what is episodic memory?
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remembering events of your life
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what is declarative learning?
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explicit learning
can be consciously recalled cognitive learning |
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what is procedural learning?
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implicit learning
learned tasks that can be performed without attention/thought develops slowly after repetition motor learning |
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what is anterograde amnesia?
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deficit to form new memories
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what is retrograde amnesia?
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loss of memory prior to brain injury
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what is problem solving?
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ability to manipulate and apply knowledge to new or unfamiliar situatiosn
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what is 3 stage of problem solving?
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preparation (understand problem)
production (generating solutions) judgement (evaluate solutions) |
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What is alertness?
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basic arousal process allowing patient to respond to the environment
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What is insight?
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awareness of cognitive impairments
insight into how they affect your ability to perform |
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what is safety judgement?
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patient's ability to judge situations, perform in safe manner, and relationship between impariements and ability to perform tasks
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what are some strategies for cognitive problems?
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identify impairment
speak slowly/clearly use simple sentences repeat / reword info demonstrate provide handouts |
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What are effective techniques for cognition problems?
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calendars
watches (with timers) memory books breaks eliminating distractions one person at a time |
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what # are broca's areas?
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44, 45
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what # are wernicke's areas?
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22
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what part of brain is responsible for repeating spoken word?
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arcuate fasciculus connecting wernicke to broca.
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what happens when u have dysarthria?
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slurry speech
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what is aphasia?
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defect in language processing caused by dominant cerebral hemisphere dysfunction
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what are 4 aspects of Broca's aphasia?
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expressive
motor anterior non-fluent |
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what are 4 aspects of Wernicke's aphasia?
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receptive
sensory posterior fluent |
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what kind of words do Broca's pt usually do better with?
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content words (nouns) monre than function words (prepositions/articles)
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what is most common cause of broca's aphasia?
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infarct in left MCA, superior division
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what do Broca's patietn do better with?
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overlearned, semi-auto tasks...
bday song, counting, days of weeks and improves with cueing |
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"no ifs ands and buts" helps rule in what?
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broca's
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what is associated with naming difficulties?
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broca's
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how is comprehension is broca's?
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relatively intact
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which aphasic patietn is frustrated?
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broca's
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how is writing/reading in broca's?
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have slow, effortful, aggramatical quality like the spoken
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what are some characteristics of wernicke? (3)
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do not respond appropriately to questions
do not follow commands (most) speech has normal prosody/grammar/fluency, but with broken lexicon |
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what are some mistakes made by wernicke pt (3)
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paraphasic error (word substitution)
neologism (non words) naming is impaired |
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what is common cause of wernicke?
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infarct of left MCA inferior division
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how is reading/writing in wernicke pt?
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show similar deficits as those seen in speech
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what are some associated features of broca?
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dysarthria
hemiparesis frustration apraxia (frontal lobe) |
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what are some associated features of wernicke?
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MILD dysarthria/ hemiplegia
apraxia (hard to prove) anosognosia angry (it all makes sense to them) contralateral field cut, upper quadrant esp. |
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what is transcortical aphasia?
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repetition is spared
(otherwise like broca's, wernicke, and global) |
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is repetition intact in wernicke? or broca?
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no
no |
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what are common causes of transcortical aphasia?
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watershed
basal ganglia thalamus |
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what is dysarthria?
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disturbance of msucular control in speech mechanism
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what are signs of dysarthria
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weaknes, slowness, incoordination
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what causes dysarthria?
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damage to central or peripheral processes
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what is flaccid dysarthria?
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breathy voice
hypernasality |
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what is spastic dysarthria?
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strained/strangled voice
hypernasality slow rate |
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what is ataxia dysarthria?
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excess and equal stress
irregular articular breakdown |
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what is hypokinetic dysarthria?
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monopitch,
monoloud, short rushes |
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what is hyperkinetic dysarthria
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prolonged intervals
monotone harsh voice loud |
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what is apraxia of speech?
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disconnect from brain to mouth,
result of damage to brain |
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what are characteristics of apraxia speech (3)
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subsitution errors more frequent than other types
more consonant errors slow speech, with pauses |
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what are ways to assess apraxic speech?
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diadochokinetic tasks (da ka da ka)
multisyllabic words words with increasing length (please pleasing pleasingly) words with same initial and final phoneme (coke dad) |
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what are other ways of assessing speech (horrible question i know) 4
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repeating sentence
describing a picture counting non-verbal tasks (tongue/lip movement) |
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what to do in therapy with expressive aphasia? (3)
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counting
require short answer responses priming |
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what to do in therapy with receptive aphasia? (2)
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demonstration
initiate task for patient |
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what can be done in therapy w/ dysarthria? (4)
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remind to speak slowly
postural breath support repeat what you are hearing for clarification don't pretend to understand if u don't! |
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where is site of injury for tetraplegia?
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cervical spine
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where is the site of injury for paraplegia?
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below cervical
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how to define ASIA neural level?
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most caudal segment with normal sensory AND motor on both sides
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how to define ASIA sensory or motor level?
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most caudal segment with normal function on both sides
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how to define ASIA incomplete injury?
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if partial preservation of sensory or motor is found below neural level
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how to define ASIA complete injury?
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absence of sensory or motor function in the lowest sacral segment
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how to define zone of partial preservation?
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only with completes.
refer to dermatome/myotome caudal to neural level that remain partially innervated |
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ASIA motor examination C5-S1?
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C5 elbow FX
C6 wrist EX C7 Elbow EX C8 finger FX T1 Finger AB === L2 hip FX L3 knee EX L4 DF L5 Long toe EX S1 PF |
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what are ROM precautions with ASIA MMT?
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cervical injuries: ROM > 90
lumbar injuries, FX > 90 |
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Define ASIA scales A B C D E
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A = complete (no sensory/motor in S45)
B = Incomplete, preserved sensation below neural level C = incomplete, preserved motor below neural level, more than half the key muscles below neural have <3/5 D = incomplete, > 1/2 below neural have 3/5 E = normal |
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What is central cord syndrome?
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lesion (usually cervical) that produce sacral sparing
weakness more in UE than LE |
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what is anterior cord syndrome?
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produces variable loss of motor
variable loss of pain & temperature preserve proprioception |
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what is brown sequard syndrome?
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produces greater IL proprioceptive loss
greater IL motor loss CL pain/temp loss |
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what is conus medullaris syndrome?
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injury of sacral cord and lumbar roots within canal:
areflexive bladder,bowel, lower limbs sacral segments may have preserved reflexes |
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what is cauda equina syndrome?
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injury to lumbosacral nerve roots within neural canal
results in areflexive bladder, bowel, and lower limbs |
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how to deal with sCI osteoporosis?
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nothing appears to be effective in lower limbs
(standing frame?) |
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what is heterotopic ossificatio?
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ectopic bone formation in muscles/ CT
(in SCI patients can happen) |
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how to treat heterotopic ossification?
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gentle ROM, functional training
MD perscribe NSAID, resection of MATURE bone |
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what is autonomic dysreflexia?
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in patients with sCI above T6,
disconnet between brain and sympathetic neurons of the spine noxious stimuli below lesion trigger excessive sympathetic response |
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what are symptoms of autonomic dysreflexia?
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sudden increase in BP
brady cardia pounding headache flushing /profusing sweating above lesion |
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how to treat autonomic dysreflexia?
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STAND UP
remove stimuli loosen clothing check catheter bag |
