Term
| What is the most common dx leading to nursing home placement? Most common cause of disability in adults? |
|
Definition
|
|
Term
| What is an ischemic stoke? |
|
Definition
| death of brain (neurons most sensitive) due to a focal lack of blood supply to brain from occlusion/narrowing of blood vessels. |
|
|
Term
| Describe the 2 types of ischemic strokes. |
|
Definition
Thrombotic- clot formation in a or v, often in already narrowed area or area w/ plaque
embolic- clot travels from heart or larger a to lodge in a smaller one. |
|
|
Term
| What are the 3 types of CVAs? |
|
Definition
1. ischemic stroke
2. Subarachnoid hemorrhage
3. intracerebral hemorrhage |
|
|
Term
| What is a subarachnoid hemorrhage? what is it caused by? |
|
Definition
| bleeding around the brain. Usually from aneurysm, AVM, but can be from extension of intracerebral hemorrhage. May include intraventricular hemorrhage (in brain) (IVH) and ICH. |
|
|
Term
| What is an intracerebral hemorrhage (ICH)? What is it caused by? |
|
Definition
| bleeding within substance of the brain. Usually from HTN, amyloid, but can be from arteriovenous malformation (AVM, aneurysm, and can include SAH and IVH |
|
|
Term
| What can a subarachnoid hemorrhage lead to? What is it commonly caused by? |
|
Definition
| It can lead to hydrocephalus when CSF can't circulate. It is most commonly caused by brain trauma. |
|
|
Term
| What is the most common type of stroke? |
|
Definition
| Ischemic; accounts for 75-80% of strokes. ICH accounts for 10-15% and SAH accounts for 5-10% |
|
|
Term
| What are the mean ages for each type of stroke? What is the mortality rate for each type of stroke? |
|
Definition
Ischemic- 75yr; mortality- 15-20%
ICH- 65yr; mortality: 30-35%
SAH- 50yr; mortality- 35-40% |
|
|
Term
| What accounts for the mortality rate in ischemic stroke? |
|
Definition
| 15-20% of ppl die from embolus, pneumonia, or other things that aren't treated quickly |
|
|
Term
| Which CVA has a better chance of recovery ischemic or ICH? |
|
Definition
| ICH because if they survive, less neurons tend to die than in ischemic stroke. |
|
|
Term
| What do SAH patients present like? |
|
Definition
| They present like Pt's w/ TBI |
|
|
Term
| What are the 5 categories of Ischemic stroke syndromes? |
|
Definition
1. Middle Cerebral a.
2. Anterior cerebral a.
3. Posterior cerebral a.
4. vertebrobasilar system
5. Lacunar syndromes. |
|
|
Term
| What are the sx of middle cerebral a. ischemic stroke? |
|
Definition
| hemiparesis, hemisensory loss, hemianopia, aphasia (left), neglect (more w/ right), visuospatial deficits (right) (problems w/ virticality), apraxia, head and gaze preference. Arm is more affected than leg + face. In the UE- Extensors are weaker than flexors, shoulders and hand are weaker than elbow. In LE- extensors stronger than flexors |
|
|
Term
| What are the sx of ant cerebral a. ischemic stroke? |
|
Definition
| leg > arm hemiparesis, apraxia (problems w/ motor mov't even though strength and sensory components are there), abulia, frontal lobe syndromes (mood, bx, organizational skills, Pt sits and doesn't do much). Note: ant cerebral a. supplies more of leg than arm. |
|
|
Term
| What are the sx of post cerebral a. ischemic stroke? |
|
Definition
| hemianopia, receptive aphasia (left), complex visual disturbances (right), hemisensory loss, verbal (L) or visual (R) memory impairment. |
|
|
Term
| What are the sx of vertebrobasilar system ischemic stroke? |
|
Definition
| dizziness, diplopia, dysphagia, nausea, ataxia (aka dysequilibrium coming from injury to brain stem or cerebellum), hemi or quadriparesis, crossed syndromes (ipsilat face- contralat body), impaired consciousness, "locked-in" syndrome (fully conscious but completely paralyzed), post cerebral a signs. |
|
|
Term
| What are the sx of lacunar syndrome ischemic stroke? |
|
Definition
| penetrating aa to internal capsule, pons, thalamus, resulting in hemiparesis, hemisensory loss, ataxic hemiparesis, dysarthria (clumsy hand), all without cortical signs (i.e. no agraphestsia, 2 pt discrimination, visual field cuts, cognitive, visual-spatial deficits). Note: Pts recover well from lacunar b/c cognition is okay. |
|
|
Term
| Describe general onset and deficit pattern/sx of an iscehmic stroke. |
|
Definition
| Abrupt onset of focal deficit over minutes to hours. Deficit may fluctuate as some ppl have high BP that can break up clot (or rele good circle of willis). |
|
|
Term
|
Definition
| Transient Ischemic Attack is a type of ischemic stroke where deficit resolves in less than 24 hrs, usually less than an hour. It may be true transient ischemia or may actually be a small ministroke. The deficit may come and go over hours, days, weeks, or months. Stroke risk highest w/ TIA clusters (much like unstable angina) |
|
|
Term
| Describe general onset and deficit pattern/sx of a SAH. |
|
Definition
| abrupt onset of severe headache, alteration of consciousness (from confused to lethargic to comatose), stiff neck (blood in subarrachnoid space irritates meninges), seizures, focal deficits if intracerebral component, hx of previous "bad" headaches may signal warning bleeds, rebleeding and vaso spasm major complicating issues, high mortality rate. |
|
|
Term
| Describe general onset and deficit pattern/sx of an ICH. |
|
Definition
| Acute onset of focal deficit usually w/ severe headache, rapid develipment of max deficit often w/ alteration of consciousness esp if large (mass effect), located in pons, assoc w/ SAH/IVH. Sx and signs due to location. Typical locations for HTN-related ICH: basal ganglia, thalamus, pons, cerebellum. amyloid usually causes lobar hemorrhage. Prognosis is most ppl die. In cerebellum, swelling may occlude 4th ventricle leading to hydrocephalus. |
|
|
Term
| When is the IV tPa started and why? |
|
Definition
| usually started at 60 mins after ED arrival (max 3-4.5 hrs post onset of stroke sx) because after too much time, chances of hemorrhage increase. This occurs after everything else including completion of NIH stroke scale CAT scan, ECG..etc |
|
|
Term
| What are the exclusion criteria for tPA post stroke? |
|
Definition
| seizures, clotting medicine |
|
|
Term
| What would happen if the patient was not IV tPA eligible, nut not hemorrhaging, and within 12 hrs from onset or perfusion scan shows viable brain w/ CTA showing retrievable clot? |
|
Definition
| Consider this pt for IA tPA, catheter clot disruption/retrieval. |
|
|
Term
| What should you do if pt is not responsive to IV tPA and clot is in large vessel? |
|
Definition
| pursue catheter clot disruption/retrieval |
|
|
Term
| What are the 14 potential complication after any type of CVA (list the four most important first)? |
|
Definition
| Aspiration pneumonia, DVT-PE, Pressure sores, urinary infection, cardiac complications, GI bleed, dehydration, falls, depression, contractures, deconditioning, constipation, pain, confusion. |
|
|
Term
| What are the 8 modifiable risk factors for CVA? |
|
Definition
| 1. HTN, diabetes control, smoking, elevated lipids, heart arrhythmias/disorders, obesity, physical activity, ETOH/drug abuse |
|
|
Term
| What are the 4 nonmodifiable risk factors for CVA? |
|
Definition
| age, gender, heredity, type I diabetes |
|
|
Term
|
Definition
| dysfunction at the organ level (eg neurological deficits- weakness, aphasia, visual loss,...etc) |
|
|
Term
| define activity limitations |
|
Definition
| impact impairments have on a specific task (eg walking, dressing, communicating) |
|
|
Term
| define participation results |
|
Definition
| inability to perform according to expected social roles (eg working, attending school) |
|
|
Term
| define Intrinsic Neuronal Recovery |
|
Definition
| Resolution of neurological deficits (impairments) |
|
|
Term
|
Definition
| use of alternative strategies/equipment to perform an activity (brace/cane, learning how to dress one-handed..etc) |
|
|
Term
| define functional recovery |
|
Definition
| resolution of disability and handicap due to both intrinsic and adaptive recovery |
|
|
Term
| The impairment and disability seen post-stroke and ultimate functional outcome depend on what 3 types of factors (describe each)? |
|
Definition
1. prelesion factors (age, education, IQ additional medical problems, psychological makeup...i.e. go-getter or depressed personality)
2. Lesion factors: size, location of stroke, rate of development
3. post-lesion factors: motication, amt and type of therapy, economics, environment, meds, family and social factors |
|
|
Term
| What are the 3 most common deficits present at or shortly after stroke onset? |
|
Definition
1. hemiparesis
2. Impaired amb
3. visual-perceptual |
|
|
Term
| How fast do stroke survivors recover from hemiparesis ? |
|
Definition
| 50% recover in 6 months, 30% recover in 1 year. |
|
|
Term
| What is the prognosis for UE plegia for stroke survivors 3 months post-stroke? |
|
Definition
| grim. In a study with 56 patients, 8 completely recovered, 14 partial recovery, 34 no recovery. |
|
|
Term
| What is the amt of time before plateu of best UE function is reached in stroke survivors? |
|
Definition
| For mild stroke- 6 wks; for severe stroke 11 weeks. |
|
|
Term
| t/f- For arm recover post-stroke, prognosis is poor if no voluntary mov't at 14 days or no measurable grip strength at 4 weeks. |
|
Definition
|
|
Term
| From the studies, what do we know about ambulation post-stroke at rehab d/c for acute admissions? |
|
Definition
| at rehab d/c, only about 1/3 of survivors were indep in walking in the studies done. |
|
|
Term
| What is the time before best walking function is achieved from stroke onset in 95% of subjects based on? what do the studies show? |
|
Definition
| It is based on severity of initial LE paresis. Those w/ severe paresis or no mov't will take 11 weeks before they reach their best walking function. Those with mild paresis may only take 4 weeks. Bottom line- the weaker you are, the longer u take to plateau. |
|
|
Term
| in studies done, 87% of patients recover from initial neglect by which week? |
|
Definition
|
|
Term
| 25% of those w/ aphasia at onset will remain aphasic at which month? |
|
Definition
|
|
Term
| t/f - 44% of patients and 47% of caregivers felt that language was still impaired in patients declared recovered. |
|
Definition
|
|
Term
| t/f - functional communication may con't to improve for over 1 year, where linguistic recovery plateaus between 3-6 mo. |
|
Definition
|
|
Term
| t/f - dysphagia decreases to 4% in 1 year survivors? why or why not? |
|
Definition
| true because pt's die from aspiration pneumonia |
|
|
Term
| t/f - 25-30% of patients will have persistent cognitive/memory deficits |
|
Definition
|
|
Term
t/f- Depression (which is much more common after L stroke) often persists and has a negative impact on outcomes.
T/f- only 8% receive tx even though tx improves outcome |
|
Definition
|
|
Term
| t/f - incontinence is present in 14% at 6 months |
|
Definition
|
|
Term
| Survival of stroke is based on what? |
|
Definition
| Initial stroke severity...of those w/ very severe strokes, only 38% survived, while 97% with mild strokes survived. |
|
|
Term
| What do the studies say about change in functional status between 6 mo- 1 year for post-stroke pt's? |
|
Definition
| about as many patients got worse as improved...80% stayed the same. |
|
|
Term
| What are 4 potential problems w/ recovery from stroke studies? |
|
Definition
1. "ceiling" effect of ADL scales
2. time span of measurement and measurement interval
3. variations in setting, timing of measurement, instrument used
4. significant recovery measured in groups, individual exceptions. |
|
|
Term
| t/f- those w/ small vessel disease (eg lacunar strokes) fared better, improved more and greater % of home discharge) than other types of strokes. |
|
Definition
|
|
Term
| t/f- R hemisphere strokes improved less and home d/c less than for L hemisphere strokes |
|
Definition
|
|
Term
| t/f- incontinence on admission is associated w/ poorer stroke outcome...i.e. not likely to go home/ |
|
Definition
|
|
Term
| t/f- d/c incontinence is associated strongly w/ placement |
|
Definition
|
|
Term
| t/f- dysphagia on admission associated w/ poorer outcome |
|
Definition
|
|
Term
| t/f- Fim adm score <40 - patients stay in rehab longer and don't get as much better |
|
Definition
|
|
Term
| Which of the following are valid predictors for functional stroke recovery: age, previous stroke, urinary continence, consciousness at onset, disorientation to time and place, severity of paralysis, sitting bal, admission ADL, level of social support |
|
Definition
|
|
Term
| What are the 4 goals of neurotherapeutic interventions? |
|
Definition
1. improve mobility and motor skill acquisition
2. teach pt's to solve motor problems
3. adapt functional strategies to changing task and environmental conditions
4. resolve, reduce, prevent impairments |
|
|
Term
| What are the 4 assumptions underlying neurotherapeutics today? |
|
Definition
1. Mov't emerges as an interaction among many systems (musculoskeletal, neuro, cardiopulm...involves complex actions, segmental linkages, and appropriate spatial/temporal sequence)
2. Mov't is organized around a bx goal and constrained by the environment (rehab environment helps to direct recovery)
3. Mov't deficits involve multi-system impairments (e.g. cognitive)
4. The brain reorganizes after injury and rehab (depends on inputs received and outputs required) |
|
|
Term
| What does motor skill learning and retention involve? |
|
Definition
| purposeful, problem solving thought process. Involves the development of a motor program action plan within the nervous system |
|
|
Term
| During motor skill learning and retention, which parts of the brain are involved in the development of a motor program action plan within the NS? |
|
Definition
| Primary and secondary sensorimotor cortices; Initiation and retention involves the prefrontal, basal ganglia, and cerebellum. The pt may have problems in these areas as well as CST or wherever else the motor deficit is coming from. |
|
|
Term
| What must be done in order to minimize learned non-use of an involved extremity or trunk? |
|
Definition
| Interventions must require a patient to use these involved body parts- "forced use". Ultimately, you have to minimize opportunities for compensatory strategies and maximize training opportunities focused on task specificity, complexity, intensity, and difficulty. |
|
|
Term
| In order to maximize training, what should we modify (5)? |
|
Definition
1. task duration/speed
2. base of support
3. range/amplitude of mov't
4. establishing mov't boundaries
5. linking mov'ts together |
|
|
Term
| What are 3 progressive challenges for motor skill acquisition? |
|
Definition
1. Postural control
2. Control of transportation, reach, and grasp/release
3. locomotion |
|
|
Term
| How could you modify task duration/speed? |
|
Definition
| Slow sit to stand, walk down steps slowly. |
|
|
Term
| How could you modify base of support to maximize training? |
|
Definition
| progression from larger to smaller BOS. Progress from stable to unstable surface. |
|
|
Term
| How could you modify range/amplitude of mov't to maximize training? |
|
Definition
| progression involves demonstrating control through larger trunk or extremity mov'ts (e.g. puts object on table & have them reach out farther each time) |
|
|
Term
| How could you establish mov't boundaries to maximize training? |
|
Definition
| set task boundaries obligates patients to use preferred movement strategies during skill acquisition. This can be accomplished by manipulating the initial conditions of a task (e.g. have them bring L foot back if you want them to bear weight through it before they stand up in sit to stand.) |
|
|
Term
| How could you use the idea of linking mov'ts together to maximize training? |
|
Definition
| This requires fluid transitions from one mov't to the next and requires pt to expand mov't options and provides practice variability. So you can have them transfer and then go right into walking as opposed to just transferring, stop, and then walk. |
|
|
Term
| How do we know when we have successful motor learning? |
|
Definition
| When the pt can demonstrate retention and transfer to a similar but diff skill set. |
|
|
Term
| What are the 3 phases of motor skill acquisition? |
|
Definition
1. Cognitive phase
2. Associative phase
3. Autonomous phase |
|
|
Term
| Describe the amount of errors, variability in performance, dependence on environment, and feedback during the cognitive phase of motor skill acquisition. |
|
Definition
errors- lots of these
variability in performance- lots
Dependent on environment- highly dependent on cues from environment, PT..etc
Feedback- dependent on visual, verbal, and tactile. |
|
|
Term
| Describe the associative phase of motor skill acquisition (4) |
|
Definition
1. learning shift occurs
2. less reliance on visual and verbal feedback
3. kinesthetic feedback important
4. developing error detection capability (detect their own errors- show insight and will know that they didn't do it right) |
|
|
Term
| Describe the autonomous phase of motor skill acquisition (4) |
|
Definition
1. Automatic (dont need to think about it anymore)
2. Fewer errors
3. Cognitive demands lessen (pay less attn to how they walk and can now hold convo)
4. feedback - requires far less |
|
|
Term
| Why is it important to understand what happens in each of the phases of motor skill acquisition? |
|
Definition
| it tells us how to progress pt, and how we respond to them depending on their phase ...e.g. "how do you think you did?" vs telling them "you need to move slower next time". |
|
|
Term
| List 4 motor learning variables |
|
Definition
1. part vs whole task practice schedule
2. blocked and random order practice
3. variable vs constant practice
4. feedback schedule |
|
|
Term
| Distinguish between part vs whole task practice schedule. |
|
Definition
| there are serial tasks such as rolling and going from supine to sit vs continuous tasks like stair climbing, walking, eating. Things like walking are more complicated to breakdown and then have it transfer over. |
|
|
Term
| Distinguish between blocked and random order practice. which is better? |
|
Definition
In a blocked order- the pt is required to do exact same thing under same conditions...i.e. 3 sets of transfers.
In a random order- tasks are interspersed...i.e. 1 set of transfers, 1 set of something else , 1 set of transfers...etc. Blocked helps develop confidence but random usually shows better ability to retain skills in humans |
|
|
Term
| Distinguish between variable vs constant practice. |
|
Definition
| variable practice may be practicing walking but on different terrains. In constant practice, the environment remains identical. |
|
|
Term
| Distinguish between feedback schedule types. |
|
Definition
| Feedback schedule involves knowledge of results (did they complete their goal) vs knowledge of performance (how did they complete the goal). It takes into account type of feedback- visual, tactile, verbal, how much feedback (as pt's get better, faded schedule is better), and when it feedback is delivered (during vs after) |
|
|
Term
| t/f- As task specific training progresses, so do the exercise variables associated with it. |
|
Definition
|
|
Term
| 4 variables regarding strength intensity/dosing |
|
Definition
1. frequency of sessions
2. duration of training
3. time in activity/repititions
4. physiologic demand |
|
|
Term
| How are body structure/function-focused interventions progressed in relation to motor skill training? what is the goal of body structure/function-focused interventions? |
|
Definition
| body structure/function-focused interventions progressed concurrently w/ motor skill training. The goal is to maximize the resources available to pt (motor, sensory, range of motion, cognition) |
|
|
Term
| What are the 4 goals of impairment-based interventions? |
|
Definition
1. improve ROM (can limit options for safety...reductions of 1 jt movt can have ramifications on other jts and mm down the chain)
2. increase voluntary and purposeful mov't
3. Minimize negative sequela of abnormal muscle tone (emphasis on weight-bearing and increasing upright control & address secondary impairments, i.e. loss of ROM/jt deformity)
4. deconditioning |
|
|
Term
| How do you know how fat to progress a patient? |
|
Definition
| Think of where the patient is right now and about the tasks and functions you are trying to service |
|
|
Term
| What are 3 factors to consider for progression? |
|
Definition
| Safety, task efficiency (how long/cumbersome?), current/future health needs |
|
|
Term
| t/f- motor skill scquisition involves an integration of sensory and motor information that occurs during practice which enables us to develop a sensorimotor solution resulting in accurate, consistent, and skilled mov't |
|
Definition
|
|
Term
| What are 4 traditional facilitation approaches? Are these still used? |
|
Definition
1. Brunnstrom
2. Neurodevelopmental treatment (NDT)
3. Muscle Re-education approach (PNF)
4. Sensory/perceptual approaches (Rood)
They are still used but no longer in isolation/exclusively. Now PTs are much more integrative. |
|
|
Term
| Describe the rationale behind NDT |
|
Definition
| abnormal muscle tone and movement patterns predominate after CNS injury. Experiencing normal mov't is important to rehab. This requires an interdisciplinary approach |
|
|
Term
| What were the original key points of NDT according to Bobath (6)? |
|
Definition
1. Use of key points of control and specific handling skills
2. trunk/postural control is essential (emphasis on midline alignment and proximal control important before distal control)
3. approach was originally very therapist-centered
4. emphasis on normalizing tone and inhibiting abnormal mov't (would not even let some1 walk if they showed abnormal mov'ts)
5. developmental sequence
6. Emphasized sequence of recovery - wouldn't develop distal control until proximal first b/c that's how normal motor development works |
|
|
Term
| How is NDT different today? |
|
Definition
| Evidence to support is lacking partly due to inability to define what NDT is. Motor learning literature suggests that reliance on manual guidance on the part of therapist may limit problem-solving in skill training. NDT also requires certification today. |
|
|
Term
| What are some key components of PNF? |
|
Definition
It is based on the concept that functional mov'ts do not occur in strict cardinal planes- there are rotations involved "out of plane mov'ts"
- normalized coordinated activities involve trunk and extremity motions that occur in diagonal directions and are accompanied by rotation (spiral component) |
|
|
Term
| What are the 4 PNF UE patterns? |
|
Definition
1. D1 flexion: flex-add-ER
2. D1 extension: ext-abd-IR
3. D2 flexion: flex-abd-ER
4. D2 extension: ext-add-IR |
|
|
Term
| What are the 4 PNF LE patterns? |
|
Definition
1. D1 flex: flex-add-ER
2. D1 ext: Ext-abd-IR
3. D2 flex: flex-abd-IR
4. D2 ext: ext-add-ER |
|
|
Term
| What are the benefits of working within a PNF diagonal? |
|
Definition
| improving mobility and strengthening within context of function. |
|
|
Term
|
Definition
1. untapped potential exists
2. Responses depend on demands
3. Mov'ts should be specific
4. repition is important
5. tx progression
6. stronger parts help strengthen the weak
7. Pt success (want them to be successful...ie. pnf should not be like a tug of war) |
|
|
Term
| What are 8 basic principles of PNF? |
|
Definition
1. manual contacts
2. visual stimulation
3. verbal stimulation
4. traction
5. approximation
6. appropriate resistance
7. quick stretch
8. normal timing |
|
|
Term
| Who is Brunnstrom? What did she do? What does her method rely heavily on? |
|
Definition
| her keen observation of motor recovery following stroke is still referenced today. She identified specific stages of recovery for both UE and LE. She relied heavily on the use of sensory input as a means of facilitating motor control (overflow- resist an extremity on 1 side that is strong to get a rxn on other side; encouraging primitive postural reflexes- wouldnt do it today; promoting synergistic mov't) |
|
|
Term
| How is Brunnstrom used today? |
|
Definition
| We use her stages of motor recovery as seen in the Fugl-Myer Assessment framework. However, the emphasis on encouraging more primitive mov't patterns is definately out! |
|
|
Term
|
Definition
| Integration of sensory impressions into psychologically meaningful data (interpretation of vision) |
|
|
Term
| What is attention? What are the 5 components of attn according to Sohlberg and Mateer Model? |
|
Definition
capacity for selective perception. 5 components are:
1. Focused- basic responding to stimuli (comes back quickly after coma..the other levels take more time)
2. Sustained: vigilance and working memory
3. Selective: freedom from distractibility (can you pick but 1 voice in a loud room)
4. Alternating: mental flexibility (can shift from one thing to another, like typing and talking)
5. Divided: multi-tasking (most difficult, like driving a car) |
|
|
Term
| What is memory? What are the 7 aspects of memory? |
|
Definition
Memory is the retention of learned info and experiences.
1. Attn and working memory: temporary
2. Encoding: Strategy that makes retrieval likely
3. Storage: Transfer from transient to more permanent storage, involves consolidation.
4. Retrieval: searching/accessing stored info
5. Recall (independent) vs recognition (cued)
6. Remote (pre-injury....memories that are solidified thru repetition like language) vs recent (post-injury....very easily disrupted)
7. Explicit (intentional...unconscious memory) vs Implicit (eg procedural) |
|
|
Term
| What is intellectual functioning? What are the four common factors of intellectual functioning? |
|
Definition
| A generalized mental ability important for success in daily living. Comprised of many skills. Common factors include verbal comprehension (e.g. how 2 things are alike), Perceptual reasoning (e.g. visual/spatial), Working memory, processing speed (how quickly you work w/ hands and eyes..very sensitive w/ impairment) |
|
|
Term
| What is processing/psychomotor speed? |
|
Definition
| includes rxn time and mental efficiency. Among most common impairments in TBI. |
|
|
Term
| What is apraxia? What 3 things must you have to ensure adequacy? |
|
Definition
| disturbance of purposeful bx or learned voluntary acts. e.g. can use a spoon spontaneously but not on command. Must have adequate: motor innervation, sensorimotor coordination, comprehension |
|
|
Term
|
Definition
| Impairment in perceptual integration. Despite adequate recognition w/ some sensory modalities, can't recognize w/ at least one modality. e.g. in visual object agnosia, can recognize by touch but not by sight. |
|
|
Term
| What are executive functions? Where do you commonly see dysfunction in executive function (ie what dx) |
|
Definition
| Capabilities that permit independent purposeful bx (e.g. being organized, coming up with a plan, being insightful). Concerns more how a person approaches a task and whether they will perform than what they are able to do (eg initiation, self-regulation, flexibility, strategy formation/modification, organization, planning, and insight). Common to have dysfunction in TBI. |
|
|
Term
| What is the arcuate fasciculus? |
|
Definition
| It is the major white mater traffic btwn Wernicke's and Broca's |
|
|
Term
| What are 3 characteristics of Behavioral/emotional dyscontrol? |
|
Definition
1. Disinhibition: acts like some 1 who has been drinking too much.
2. Impulsivity: jumping the gun, usually on restraint, eg eat too quickly leading to aspiration.
3. Emotional lability: they are fine and then crying all of a sudden. This is not depression as depression is more consistent |
|
|
Term
| What are four types of mood and anxiety disorders? |
|
Definition
1. Depression (can look like demensia)
2. pseudodepression
3. euphoria- happy, giddy, silly
4. Anxiety- very pervasive w. brain injury |
|
|
Term
| 5 characteristics of excessive bx and combativeness |
|
Definition
1. Agitation- ppl who wake up from coma, may strike out but not necessarily targeting anyone specificaly
2. Irritability
3. Aggressivity- is more targeting; will have pt who doesn't like some1.
4. Perseveration- this type of person has hard time breaking out of a pattern.
5. Egocentrism |
|
|
Term
| 2 types of dysmotivational bx's |
|
Definition
1. inhibition/poor initiation
2. Dependency |
|
|
Term
|
Definition
1. hypersexuality (too much sexual interest)
2. hyposexuality (too little sexual interest) |
|
|
Term
| List 3 fontal lobe syndromes |
|
Definition
1. Orbitomedial frontal syndrome
2. Dorsal convexity dysexecutive syndrome
3. Medial frontal apathetic syndrome |
|
|
Term
| List 4 anatomical features of orbitomedial syndrome |
|
Definition
1. Limbic connectivity
2. Anterior temporal connectivity
3. lateral orbital is middle cerebral; medial orbital is anterior cerebral
4. rests on orbital bony roof |
|
|
Term
| Behavioral and cognitive correlates of orbitomedial syndrome (4) |
|
Definition
1. inhibitory mechanism
2. elaboration and integration of limbic drives
3. impulsivity
4. socially inappropriate bx |
|
|
Term
| Orbitomedial deficits in orbitomedial frontal syndrome (6) |
|
Definition
1. anosmia (can't smell..olfactory bulb injured)
2. Confabulation (memory mistakes)
3. Go-NO-go defitis (tap no tap)
4. disinhibited personality change
5. hypersensitivity to noxious stimuli (very sensitive to pain/shots)
6. hyperphagia (wants to eat all the time) |
|
|
Term
| Perception of Orbitomedial syndrome deficits (3) |
|
Definition
| may appear manic, may appear antisocial, crimes of passion may result. |
|
|
Term
| Dorsal convexity dysexecutive syndrome anatomical features (secondary associative areas and vascular distribution)? |
|
Definition
secondary associative areas- parietal, occipital, temporal
vascular distribution- middle cerebral (primarily) |
|
|
Term
| behavioral and cognitive correlates of dorsal convexity dysexecutive syndrome (5) |
|
Definition
temporal and sensory integration, planning, goal-directedness, behavioral flexibility, metacognitive organization
(trouble w/ things like planning, making goals, organizing) |
|
|
Term
| dorsal convexity dysexecutive syndrome specific deficits (5) |
|
Definition
1. cognitive flexibility
2. Temporal ordering
3. learning from experience
4. Judgement and insight
5. organization |
|
|
Term
| dorsal convexity dysexecutive syndrome perception of deficits |
|
Definition
| may seem depressed, passive-aggressive. May seem avoidant |
|
|
Term
| Mesial frontal apathetic syndrome anatomical features (3) |
|
Definition
1. cingulum connectivity
2. supplmentary motor area connectivity
3. vascular distribution (ant cerebral a) |
|
|
Term
| Mesial frontal apathetic syndrome behavioral and cognitive correlates (3) |
|
Definition
| dysmotivational syndrome, apathetic, akinetic (won't talk) |
|
|
Term
| Mesial frontal apathetic syndrome specific deficits (6) |
|
Definition
| abulia, inert, loss of motivation, indifference, diminished motor and verbal output, increased response latency |
|
|
Term
| Mesial frontal apathetic syndrome perception of deficits |
|
Definition
| may seem depressed, may seem "willful" |
|
|
Term
| Describe 2 Behavioral management concepts |
|
Definition
1. operant conditioning- control what happens after bx (like time out or reward for bad/good bx)
2. antecedents 0 find triggers (meds, ppl, our bx, too long tx session) |
|
|
Term
| Non-verbal communication strategies to de-escalate a patient (5) |
|
Definition
| soothing voice, open stance, hand position, appropriate distance (out of arms reach if ur with some1 who punches ppl), eye contact |
|
|
Term
| other stimulation strategies to de-escalate a patient |
|
Definition
| reduce stimulation, staff emotional control (keep urself calm, dont look angry or sound critical, breathing, self-instruction), redirection (change of topic, activity, face), empathy, seek information, explanation and teaching (when they aren't too worked up), rapport, avoid questions answered "no", give choices to increase control, give time to cool down, avoid arguing, humor and friendliness, consistency from staff (stay within discipline), family involvement. |
|
|
Term
| Describe 5 Preparedness strategies to de-escalate a patient |
|
Definition
| Be aware of triggers, read reports/consult, consider premorbid characteristics (aggressive pt's are almost always premorbid), attributions, adjust expectatins (if u can eliminate a trigger that's the best) |
|
|
Term
| Pediatric behavioral management risk factors, localization, age, and severity |
|
Definition
risk factors- premorbid dx, prior head injury
localization- frontal/temporal predominantely, axonal shearing
age- before age of 2 "shaken baby syndrome"...worse outcome for brain injuries before 2 yrs old.
severity- span of post-traumatic amnesia (not being awake/alert/oriented) is best predictor of severity |
|
|
Term
| list 4 types of pediatric behavioral syndromes |
|
Definition
Disinhibited/orbitomedial
ADHD
Hypomanic
Posttraumatic stress syndrome (more likely w/ mild injury) |
|
|
Term
| pediatric bx interventions (5) |
|
Definition
1. education to correct attributions
2. Parent training
3. structure and consistency
4. pediatric behavioral management plans
5. Interfacing with schools |
|
|
Term
| General pediatric neuropsychology principles (4) |
|
Definition
1. the earlier the worse for IQ outcome
2. Recently emerged skills most susceptible
3. Behavioral disorders common and risk is long range
4. Sleeper effect: some cognitive sequelae not immediately apparent. |
|
|
Term
| t/f- persistent neurobehavioral and psychosocial impairments are common in TBI and stroke |
|
Definition
|
|
Term
| What brain lesions are associated with depression after TBI (3)? |
|
Definition
| Dorsolateral frontal, temporal, and left basal ganglia lesions |
|
|
Term
| w/ depression in TBI and stroke, there is Decreased glucose metabolism in what regions of the brain? |
|
Definition
| orbital frontal and anterior temporal regions |
|
|
Term
| What have Most class II and class IV studies of cognitive behavioral therapy (CBT) for depression following TBI found? |
|
Definition
| positive effects of treatment on mood. |
|
|
Term
| What does the evidence suggest about the best type of treatment protocol for depression after TBI or stroke? |
|
Definition
| starting with a low dose of SSRI (especially sertaline) or mirtazapine, combining pharmacotherapy with multidisciplinary rehabilitation and psychological treatment is best approach |
|
|
Term
| What are 3 ways of preventing suicide in TBI and stroke Pt's |
|
Definition
1. Proactive assessment of hopelessness and suicidal ideation
2. Treatment of depression and substance abuse
3. Close monitoring by family and physician |
|
|
Term
| Why is Posttraumatic stress disorder (an anxiety disorder) seen more often in mild TBI compared to severe? |
|
Definition
| due to less retrograde and anterograde amnesia in mild TBI |
|
|
Term
| What is anxiety likely to be comorbid with? |
|
Definition
| Anxiety is especially likely to be comorbid with depression, and treatment may address both |
|
|
Term
| Should benzodiazepines be used to treat anxiety in TBI and stroke patients? If not, what is preferable in long term tx? What produces the greatest benefit? |
|
Definition
| Benzodiazepines may have adverse effects on cognitive functioning and outcome and should be used sparingly. SSRIs preferable for long term. Combining cognitive-behavioral psychotherapy and pharmacologic intervention generally produces greatest benefit. |
|
|
Term
| Damage to what area of the brain is associated with behavioral disinhibition, referred to as the orbital frontal disinhibition syndrome. |
|
Definition
| Damage to the orbital prefrontal regions of the brain |
|
|
Term
| Examples of disinhibition in stroke/TBI patients. |
|
Definition
| unfiltered or offensive speech, unwanted sexual talk or advances, impulsivity, or loss of behavioral or emotional control. |
|
|
Term
| What is Intermittent explosive disorder? What is it associated with? |
|
Definition
| IED involves severe episodic outbursts of physical or verbal rage. Has been associated with TBI as well as focal epilepsy |
|
|
Term
| When does agitation occur w/ TBI and stroke patients? What will the patient do? How is it managed? Which drugs have been used to treat aggitation? By what mechanism do they work through. |
|
Definition
| Agitation often occurs during the acute coma emergent phase. The patient may lash out impulsively to reduce stimulation or interaction. Management includes reducing level stimulation and frustration. Identifying and managing the antecedents or ‘‘triggers’’ is critical. Amantadine and methylphenidate have been used to successfully treat agitation in frontal lobe dysfunction, especially coma-emerging. Mechanism is through increased arousal, attention, and executive function to help lessen confusion. |
|
|
Term
| When is aggression seen frequently in TBI and stroke patients? What class of drugs used to treat? What should u watch out for with these drugs? |
|
Definition
| Aggression is seen much more frequently in patients who have a premorbid history of aggression or violence. Beta blockers used (propranolol). injuries.Patients treated with propranolol should be monitored for possible depressive side effects as well as hypotension.Other drugs- Antipsychotics, antiepileptics, and stimulants have been used for treatment of aggression or disinhibition following TBI, including IED. Anticonvulsants and mood stabilizers, especially valproic acid, are often used as a first-line treatment for controlling aggression in brain injury. |
|
|
Term
| Why are chronic use of benzodiazepines not recommended in TBI? |
|
Definition
| sedation, cognitive impairment, paradoxical agitation, and tolerance to the medication |
|
|
Term
| What is inhibition and apathy associated with ? What types of lesions do we see inhibition and apathy? |
|
Definition
| Associated with damage to mesial prefrontal region. Frequently seen in conditions resulting in lesions to the ACA distribution such as ACA stroke or aneurysmal hemorrhage. |
|
|
Term
| Abulia can occur with depression, but the apathetic prefrontal syndrome can be differentiated HOW? |
|
Definition
| by the lack of other depressive symptoms |
|
|
Term
| How is apathy and inhibition treated (drugs)? |
|
Definition
| treatments include dopamine agonists (amantadine and bromocriptine) and stimulants. |
|
|
Term
| Which lesions are associted w/ Post-TBI psychosis? |
|
Definition
| Lesions of temporal, parietal, and frontal regions |
|
|
Term
| What are 3 risk factors of psychosis? |
|
Definition
1. Brain injury that is more severe and diffuse
2. Involvement of frontal and temporal areas
3. Onset of injury early in life |
|
|
Term
| How is post-TBI psychosis treated? (pharmaceutically) |
|
Definition
| Highly anticholinergic antipsychotics should be avoided; may compromise rehabilitation and cognitive outcome. Newer atypical agents are better tolerated, although orthostasis may occur and efficacy with TBI is not established. |
|
|
Term
| What are the early warning signs of stroke? What do they all have in common? |
|
Definition
| Visual field changes, face drop, confusion, pain, weakness (1 sided), dizziness, headaches. They all happen acutely (i.e. sudden onset) |
|
|
Term
| which populations are at risk for stroke? |
|
Definition
| Blacks, hispanics, and women |
|
|
Term
| Blacks have higher HTN rates, diabetes, and sickle cell anemia. Why is higher sickle cell anemia rates a risk factor for strokes? |
|
Definition
| because sickle cells can clog up capillaries |
|
|
Term
| t/f - high proportion of HTN found in hispanics (in 72% hispanics who had stroke) |
|
Definition
|
|
Term
| Why do language barriers and lack of transportation limit educational outreach for stroke in hispanic populations? |
|
Definition
| they may be less likely to bring up medical info and relay information about themselves. |
|
|
Term
t/f - stroke incidence rates in women are less than men at younger ages, but not older ages
t/f- stroke is more common in men, but more women die from it
t/f- women tend to be older when they have a stroke |
|
Definition
|
|
Term
| With strokes, women tend to c/o about what at onset? |
|
Definition
| facial pain, nausea, weakness, SOB, hiccups at onset. Pregnant women also more at risk. |
|
|
Term
| What are the 9 risk factors for stroke? |
|
Definition
1. HTN
2. Vascular risk factors/peripheral vascular
3. A-fib (all blood is stagnant in LV which pushes clot to brain...hx of this = 5x more likely to get stroke)
4. diabetes
5. previous hx of heart attack
6. Previous hx of stroke
7. previous TIA
8. Family hx of stroke or vascular disease
9. smoking |
|
|
Term
| t/f - 75% of strokes are ischemic strokes |
|
Definition
|
|
Term
| What is a cerebral thrombosis? |
|
Definition
| area gets narrow over time w/ build up of triglyceride, deposits and clots that decreases blood flow through vessel. The thrombosis itself usually occurs when ppl are lying down cuz BP is lower. |
|
|
Term
| What is the relationship between an a-fib and an embolic stroke? (i.e. how does one lead to the other) |
|
Definition
| With an a-fib, the atria contract poorly, thus blood is stagnant and pools in LV and form clots. The thrombus (clot) breaks off, goes into LV, then through aorta --> common carotid a --> Internal carotid a --> BAM! clogs up blood flow to brain |
|
|
Term
| What does Tissue-plasminogen activator (t-pa) target during an ischemic stroke? |
|
Definition
| tPa targets the ischemic penumbra. it minimizes death of more tissue in the penumbra. Cells are still viable but have decreased metabolic function, decreased EEG, BUT ATP is still being stored, so they have ability to recover thanks to tpa |
|
|
Term
| What are stroke symptoms after an ischemic stroke based on? |
|
Definition
| based on the blood vessel that was occluded. |
|
|
Term
| What are 4 common ischemic syndromes? |
|
Definition
1. middle cerebral a
2. Anterior cerebral a
3. Posterior cerebral a
4. Vertebral-basilar a (cerebellar territory, locked-in syndrome) |
|
|
Term
| What are symptoms associated w/ anterior cerebral artery ischemic stroke? |
|
Definition
| aphasia, apraxia, more loss of motor in leg than arm, abulia, urinary incontinence, hemisensory loss |
|
|
Term
| What are symptoms associated w/ middle cerebral artery ischemic stroke? |
|
Definition
| hemiparesis, arm>face>leg involvement, aphasia (expressive, receptive, or both AKA global), vision, neglect (R sided stroke). |
|
|
Term
| t/f - the middle cerebral a is the largest branch of the internal carotid a and the most common site of emboli. It's deep branches feed the IC and basal ganglia. On the lateral surface, it feeds the parietal, frontal and temporal lobes. |
|
Definition
|
|
Term
| What are symptoms associated w/ posterior cerebral artery ischemic stroke? |
|
Definition
| vision , memory (visual memory), dyslexia (difficulty reading), visual agnosia (cant name what they see), topographical disorientation, contralat homonymous hemianopsia. |
|
|
Term
| t/f - the post cerebral aa branch from basilar a. Supplies midbrain structures and posterior thalamus, temporal lobe, occipital lobe and visual cortex. |
|
Definition
|
|
Term
| t/f- a lesion in the cerebellar territory will produce both cerebellar and brainstem signs and sx |
|
Definition
|
|
Term
| What is Wallenberg's syndrome? What type of ischemic syndrome is it? What type of lesion is it? What are the ipsilat signs? What are the contralat signs? |
|
Definition
| It is a lateral medullary lesion (not a lot of motor fibers, so motor function okay). It is a vertebral-basilar a ischemic stroke. Ipsilat signs include cerebellar ataxia, vertigo/nausea/vomiting, decreased pain/temp sensation in face, horner's syndrome (constricted pupil, ptosis, decreased sweating), hoarseness and dysphagia. Contralat signs include impaired pain and temp over half of body. |
|
|
Term
| What is the cause of Horner's syndrome? What are the sx? |
|
Definition
| Caused from disruption of sympathetic pathways within lateral brainstem (medulla). Sx include pupillary constriction on one side, slight lid ptosis on one side, decreased sweating on one side |
|
|
Term
| t/f- intracerebral hemorrhagic stroke occurs at a lower rate but higher mortality than other strokes. |
|
Definition
|
|
Term
| Name 6 common sites for intracerebral hemorrhage. Include some sx at those sites. |
|
Definition
1. basal ganglia/thalamus - memory problems, initiation issues, pstural control deficits, lots of sensory inputs in thalamus so pt may feel lots of pain.
2. Temporal lobe- hearing issues, aphasia
3. Frontal lobe
4. Parieto-occipital lobe- R sided perceptual deficits
5. cerebellar
6. Pontine (brain stem function in general) |
|
|
Term
| Characterize the sx of subarachnoid hemorrhage. |
|
Definition
| will not necessarily have localized sx. More likely to have global sx- blood leaking all around brain. |
|
|
Term
| What is a berry aneurysm? where does it occur? |
|
Definition
| an abnormal bulge in an arterial wall; 90% of subarachnoid hemorrhages. |
|
|
Term
| What is an arteriovenous malformation (AVM)? What affects does it produce? what type of hemorrhage is it associated with? |
|
Definition
| Direct communication btwn artery and vein w/o intervening capillary bed. Increases pressure in venous side that vv arent't normally meant to handle. Thus, vv get weaker over time & u get burst at this junction. Associated with SAH. |
|
|
Term
| Describe the general difference in sx between R and L sided stroke. |
|
Definition
Left CVA --> R hemiplegia (language impairments, processing delays, apraxia, easily frustrated, intellectual impairment), person tends to be more insightful & more aware of what they cant do, frustrated more easily.
R CVA --> L hemiplegia (spatial/perceptual deficits, poor judgement, impulsivity, L visual field deficit, emotional lability, difficulty w/ abstract reasoning, safety is a huge issue here). |
|
|
Term
| list 5 influences of neurological impairment post-stroke |
|
Definition
1. Size of lesion
2. lesion location
3. Amount of collateral blood flow
4. interruption of carotid vascular system
5. interruption of basilar system |
|
|
Term
| What is the National Institute of Health Stroke Scale (NIHSS)? How is the score interpreted? When is it used? |
|
Definition
| It is a 15 item impairment scale w/ ordinal scoring. Total on scale = 42 points. >= 25 means very severe neurological impairment. <5 means mild impairment. Performed as a baseline measure in conjunction w/ tPA or other therapies. As repeat assessment done in 24 hours and also performed at d/c from acute hospital. |
|
|
Term
| Name some items that are addressed in the National Institutes of Health Stroke Scale (NIHSS). |
|
Definition
| levels of consciousness (responsiveness, orientation, commands), best gaze, visual field, facial palsy, motor (R & L arm/leg), limb ataxia, sensory function, best language, dysarthria, extinction and inattn (for neglect) |
|
|
Term
| On the NIHSS, What score indicates that some indicates that the individual with a stroke will have to get long term care in a nursing facility |
|
Definition
| >=14 (severe). 6-13 is adequate and pt will receive acute inpt rehab. <=5 is mild...most of these scores d/c home |
|
|
Term
| Does the NIHSS have a floor or ceiling effect? |
|
Definition
| floor effect for severe stroke |
|
|
Term
| Describe the 3 goals of acute stroke medical management |
|
Definition
1. increase cerebral perfusion (ciculation, oxygenation)
2. maintain adequate blood pressure (ischemic and hemorrhagic stroke)
3. Manage cardiac factors that may have contributed to stroke (A-fib) |
|
|
Term
| Describe 3 goals of acute stroke medical management. |
|
Definition
1. fluid/electrolyte/glucose in balance
2. control for seizures
3. control for increased intracranial pressure (especially w/ hemorrhagic stroke) |
|
|
Term
| How do you prevent DVTs in ischemic stroke? |
|
Definition
| early mobilization, anticoagulation therapy (heparin), intermittent pneumatic compression devices/compression stockings |
|
|
Term
| How do you prevent DVTs in hemorrhagic stroke? |
|
Definition
| anticoagulation avoided, mechanical filter may be used |
|
|
Term
| How do you prevent pressure ulcers in stroke patients? |
|
Definition
| altho not a lot of patients w/ skin breakdown post stroke, look at risk factors such as dependence in mobility , diabetes/peripheral vascular disease, urinary incontinence, low body mass index |
|
|
Term
| t/f- persistent bladder incontinence generally associated w/ poorer outcomes in stroke patients |
|
Definition
|
|
Term
| What is the danger w/ dysphagia post-stroke? |
|
Definition
| aspiration pneumonia, interferes w/ adequate nutrition, silent aspiration. |
|
|
Term
| What meds can be used to prevent stroke recurrence? |
|
Definition
cerebral ischemia- aspirin (antiplatelet medication...the gold standard) and Plavix (antiplatelet med)
Coumadin: anticoagulant med also frequently used in pt's w/ a-fib |
|
|
Term
| When do neurologic and functional recovery occur at the quickest rate post CVA? does recovery continue beyond that time? |
|
Definition
| first 1-3 months; recovery continues at 3 mo-12 mo but at slower rate. After 1 yr, recovery can be made but its slower. |
|
|
Term
| After a stroke, how much time before the patient reaches their best walking function? |
|
Definition
Depends on severity of initial LE paresis
Mild: 4 weeks
Mod: 6 weeks
Severe paresis/no mov't: 11 weeks |
|
|
Term
| What is the Barthel Index (BI)? What does it measure? What does the highest score mean? what is the assisted score? |
|
Definition
| It is an outcome measure that assesses the best walking function. Highest score indicates that pt ambulates indep for >50 yards (pretty small distance, not very functional); may walk w/ device. The assisted score indicates that the pt walks >50 yds w/ physical/verbal assistance. |
|
|
Term
| t/f - poor stoke prognosis if no voluntary mov't at 14 days or no measurable grip strength at 4 weeks |
|
Definition
|
|
Term
| Time to best UE function post stroke |
|
Definition
mild initial paresis: 6 weeks
Severe: 11 weeks |
|
|
Term
| t/f - for both acute and chronic stroke, pt's will show significant spontaneous improvement BUT the rehab specialist can facilitate the extent and time course of recovery w/ specific interventions. |
|
Definition
|
|
Term
| name a positive sx of UMN syndrome |
|
Definition
|
|
Term
| name a negative sx of UMN syndrome |
|
Definition
| weakness, loss of isolated mov'ts, decreased endurance |
|
|
Term
| What are the Brunnstrom Sequential Recovery stages for volitional motor control? |
|
Definition
| they are based on qualitative observations of individuals post-stroke. Influenced by neurophysiologists who believed that recovery followed an orderly progression of phenomena. Normal motor development was the basis. |
|
|
Term
| what are the benfits of WBing w/ stroke patients? |
|
Definition
| WBing increases proprioception/awareness, support of trunk control, prevents Osteoporosis, helps w/ rxns and uses stabilizers. |
|
|
Term
| According to Brunnstrom sequential recovery stages, what is stage 1? What are the goals of limb management during this phase? |
|
Definition
| Initial Stage of recovery where no volitional mov't in extremities. Hypertonicity present. Maintain ROM, gravity will deform/impact pt...in UE, shoulder may sublux. Use equipment to help w/ positioning so u can stabilize and maintain alignment, as well as encourage weight bearing. |
|
|
Term
| According to Brunnstrom sequential recovery stages, what is stage 2? What is emphasized w/ PT? |
|
Definition
| Little or no volitional mov't; it is associated w/ rxns/reflexive movt. Spasticity may begin to develop. Alignment (keep using equipment if necessary) is emphasized. Gravity and spasticity may be deforming forces now. May see overflow now. |
|
|
Term
| According to Brunnstrom sequential recovery stages, what is stage 3? What is emphasized w/ PT? Which mov't combos define limb synergies? Why does this matter in terms of exercise prescription? |
|
Definition
| Stage 3 is Volitional movement in synergy. Full range of synergies may not develop. spasticity may continue to develop. May see UE flexion synergy (flex, abd, flex, ER) or ext synergy, may see pronation occuring distally. May see LE synergy (hip ext, add, PF, inversion). Don't give them exercise program that encourages going through synergies. Instead, try to break up tasks to encourage isolated movements. |
|
|
Term
| According to Brunnstrom sequential recovery stages, what is stage 4? What is emphasized w/ PT? |
|
Definition
| stage 4= Movements deviate from synergy. Strengthening is important here. Look at concentric/eccentric control w/ task training. Look at how speed interplays w/ isolated motion |
|
|
Term
| According to Brunnstrom sequential recovery stages, what is stage 5 and 6? What is emphasized w/ PT? |
|
Definition
| These are the "isolated movements develop" stage- where movements become indep of synergies. All mov't combos are possible, spasticity declines. In this stage, you want to see how they're coming along w/ isolated mov'ts, so do MMTs. Look at endurance and fine motor mov't, transitioning btwn mov'ts, stability, reciprocation (being able to access isolated mov'ts quickly), and power (fxv...necessary for patients who want to run) |
|
|
Term
| t/f- variability in post stroke recovery is the rule rather than the exception. |
|
Definition
|
|
Term
| What 2 outcome measures are done for Quantitative motor assessment in stroke? |
|
Definition
| Fugl-meyer assessment, STREAM |
|
|
Term
| What is the fugl-meyer assessment? What is it based on? What about its reliability? Any MDC/MDIC values? Is it long or short? Do you want a high score or low score? |
|
Definition
| widely used clinical and research tool to measure post-stroke motor impairment. It is based on Brunnstrom's stages of recovery. It has excellent intra/interrater reliability. MDC values published but NO MDIC. It is a lengthy tool. Higher score is better. |
|
|
Term
| What is the STREAM assessment? What is it based on? What about its reliability? Any MDC/MDIC values? Is it long or short? Do you want a high score or low score? |
|
Definition
| It is the stroke Rehabilitation Assessment of Movement. It measures voluntary mov't and basic mobility. It has adequate to excellent interrater reliability. Predictive of d/c destination. It is responsive to changes in motor function. It has both MDC and MCID values.It only takes 15 mins to complete. |
|
|
Term
| In terms of post-stroke weakness, what are some characteristics of paresis? |
|
Definition
| Impairment in most ppl w/ stroke. Fiber type transformation is different amongst diff studies/individuals/findings. Overall reduction in ability to initiate movt. Reduced speed in producing muscle force. Rapid onset of m fatigue. Excessive sense of effort. Increased intramuscular fat. Reductions in muscle mass may be seen over time (not right away...it's a UMN, so you'll see atrophy w/ disuse) |
|
|
Term
| Does co-contraction aka spasticity of antagonist muscles impair force magnitude, rate of force production, or intersegmental coordination? |
|
Definition
| No evidence to support this claim. Agonist activation is the real problem. This should direct ur tx away from spasticity and tone and now back on the agonist. |
|
|
Term
| With post-stoke weakness, where do u see greater weakness? Where is the weakness most pronounced, ispilat or contra lat to lesion? |
|
Definition
| Distally...so PFs and DFs are most affected.Weakness is most pronounced contralat limbs but ipsilat weakness noted. |
|
|
Term
| t/f- patients post-stroke can not always transition to single limb support on nonparetic side w/ success. they fail 50% of time or undershoot. This is because there is a problem generating a propulsatory impulse and shifting COM over BOS. |
|
Definition
|
|
Term
| List 3 motor control deficit types post-stroke |
|
Definition
1. muscle tone alterations
2. Coordination deficits
3. motor planning dificits |
|
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Term
| What tool is used to assess trunk control post stoke? What exactly does it assess? Is it applicable to all patients? What is the best score possible? When is it most useful? What does it have a high correlation with? |
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Definition
| Postural Assessment Scale for Stroke (PASS). It assesses the ability to maintain a posture in sitting/standing or change a specific reclined, sitting, or standing posture. It is applicable for all patients, even those w/ very poor postural performance. Best score is 36. Most useful in acute stroke. High correlation w/ FIM scores. |
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Term
| What are the 3 types of postural control strategies? Describe each in terms of safety and efficiency |
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Definition
1. Preparations- very safe but not efficient
2. Accompaniments
3. reactions- More efficient but not safe. |
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Term
| What are postural preparations? |
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Definition
| it is a postural control strategy that is initiated before the intended mov't (e.g. some 1 reaches out for hand rail before they go down steps). It is safe and favors stable postures, but not efficient. |
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Term
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Definition
| it is a postural control strategy that relies on sensory feedback. Arrives 100msec after mov't initiation. It is efficient but not safe because it is highly dependent on timing, magnitude, and accuracy of sensory input...think ankle strategy |
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Term
| What are postural accompaniments? |
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Definition
| it is a postural control strategy that focuses on anticipatory postural adustments (APAs). These occur with or just before mov't initiation. e.g. if u want to raise arm in air, erector spinae becomes active to stabilize spine JUST BEFORE u raise arm. It has an equal trade off between safety and efficiency. |
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Term
| What are anticipatory postural adjustments? |
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Definition
| Sophisticated CNS control that predicts the potential effect a disturbance might have on a mov't variable. It allows u to anticipate the force needed to counteract that disturbance. It involves the circuitry in supplmentary motor cortex, basal ganglia, and cerebellum. It involves a feedforward process and predictive postural control (helps u to predict displacement and preturbation u are going through) |
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Term
| How is your CNS able to make anticipatory postural adjustments? Does it occur in standing or sitting? What type of mov't sets it off? What is the purpose of APA? |
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Definition
| It adjusts movement based on past experience, knowledge of one's body and the physical world. It generally occurs in standing (ur pretty safe in sitting). It occurs in response to internal preturbation i.e. mov't that is voluntarily initiated. Its purpose is to constrain COM displacement and assist in repositioning COM over new BOS. |
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Term
| What is the status of APAs post stroke? |
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Definition
| You will see delayed activation of APA muscle activity on the involved side. May see earlier activation on nonparetic side. Impairments in APAs increase risk of falling post-stroke. APA patterns can change over time |
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Term
| Describe 5 factors that influence APAs |
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Definition
1. Mass of moving limb- will influence magnitude of APA
2. Symmetry of mov't- response usually diminished w/ symmetric mov't due to COM displacement decrease
3. Effects of external support- may decrease b/c you're supporting yourself w/ other arm.
4. Speed of focal mov't- moving quickly increases APA
5. Behavioral conditions of the task: self-paced vs reaction time...Rxn time increases APA |
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Term
| What are some predictive factors of falls post-stroke? Which ones are the best predictor of falls? |
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Definition
1. <30 on berg balance
2. Apraxia
3. cognitive deficits
4. lower function independence measure scores (FIM)
5. Self-report balance problems while dressing
NO consistent agreement exists between which risk factor is greatest or degree to which impaired balance and gait can predict falls post-stroke. The problem is multifactorial. |
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