Week 10 Material

Question 1

What three points of time does plasticity occur?

Answer 1

Beginning of life, “critical period.”
Throughout adulthood, following critical period.
Damage: compensate, re-learn, and maximize function.

Question 2

Recovery of function:
Define function
Define recovery

Answer 2

Function: complex activity directed at performance of task.
Recovery: reacquisition of movement skills lost through injury.
Motor learning underlies recovery of function.

Question 3

Plasticity can occur at many levels such as…

Answer 3

Brain level: glial and vascular support
Network level: cortical remapping
Intercellular level
Intracellular level
Biochemical level
Genetic level

Question 4

Recovery vs compensation.

Answer 4

Recovery: restore function to tissue lost in injury; restoring the ability to perform movement in the same manner as performed before injury; task accomlpished in same way using same structures.
Compensation: neural tissue acquires a function it did not have prior to injury; perform an old movement in a new way; task accomplished using alternate structures.

Question 5

Factors affecting recovery of function:

Answer 5

Age, characteristics of lesion. pre-injury factors (exercise, diet, and environmental enrichment), and post-injury factors (neurotrophic factors, pharmacology, and exercise training).

Question 6

Following injury, we may see the CNS respond by…

Answer 6

Denervation supersensitivity, unmasking of silent synpases, neural regeneration (regenerative synaptogensis), and collateral sprouting (reactive synaptogenesis).

Question 7

With a neural injury, what are the differences we will see with a peripheral vs a central lesion?

Answer 7

Peripheral lesion: cortical maps in nearby areas increase responsiveness of previously weak connections; new connections can form in larger insulted areas.
Central lesions: new regions or redundant pathways take over function; cerebellum activation (working to make things more automatic); and activation of brainstem pathways.

Question 8

Training can induce cortical remapping if used appropriately; so what three strategies can be used to enhance recovery?

Answer 8

Type, intensity, and timing.
You need to work at an intense level to cause an effect, but time is also important because too intense too early on can be a negative thing; we need to build up the intensity over time.

Question 9

Principles of experience-dependent plasticity:

Answer 9

Use it or lose it; use it and improve it; time matters; intensity matters; specificity; salience matters; age matters; transference; interference; and repetition matters.

Question 10

What are the spinal changes that occur in a patient with Ankylosing Spondylitis?

Answer 10

Loss of lumbar lordosis, increased thoracic kyphosis, head protraction, loss of spinal flexibility in all planes, and hip flexion.

Question 11

Posture in a patient with Ankylosing Spondylitis.

Answer 11

Forward shift COM and lowering COG; to maintain balance, they will flex their knees and go into a PPT.

Question 12

Postural control in a patient with Ankylosing Spondylitis.

Answer 12

Steady-state: frontal plane > sagittal plane; 50% increase in displacement with eyes closed compared to healthy individuals.

Question 13

APA and CPAs in patients with Ankylosing Spondylitis.

Answer 13

Some data reveals that changes on static and dynamic clinical tools worsens with disease severity; confirms worse performance with eyes closed; confirms higher incidence of dizziness vs controls; and impacts on dynamic activities such as gait.

Question 14

Information processing in patients with a concussion.

Answer 14

Symptoms post-concussion may include dizziness, noise/light sensitivity, and blurred/double vision.
Impaired sensory integration and delayed speed of information processing.
So, they cannot take information in and cannot make sense of what is coming through.

Question 15

Postural control in patients with a concussion (steady-state, APAs, and CPAs). What measurement tools can be used?

Answer 15

Steady-state: acute increased sway (3-10 days after injury) which is related to sensory integration problems (visual and vestibular problems).
APA and CPA: decreased APA prior to gait initiation, increased latency of reactive balance responses.
Measurement tools: balance error scoring system (BESS), SOT, and instrumentation.

Question 16

Attention, memory, and information processing in patients with a concussion.

Answer 16

Attention: difficulty dividing attention, deficits persist for up to 2 months post-injury.
Memory: working memory has decreased accuracy and verbal fluency.
Motor learning: both recall and task acquisition; attempts at learning can prolong recovery.

Question 17

Alzheimer’s Disease is characterized by slow decline/change in…

Answer 17

Memory, language, visuospatial skills, personality, and cognition.

Question 18

What are the neuropathologic hallmarks of Alzheimer’s?

Answer 18

Amyloid plaques and neurofibrillary tangles.

Question 19

Information processing in individuals with Alzheimer’s Disease.

Answer 19

Slower reaction times, impaired choice reaction time (decreased focused attention), decreased ability to use advanced cues to anticipate and decreased ability to inhibit non-regulatory stimuli.

Question 20

Attention in individuals with Alzheimer’s Disease.

Answer 20

Poor selective and divided attention; decreased performance on dual tasks, and we will see no training improvement, associated with risk of falls. The falls are due to the inability to take in environmental cues.

Question 21

Postural control in individuals with Alzheimer’s Disease (steady-state and APAs).

Answer 21

Steady-state: decreased control of sway and decreased performance with eyes closed.
APA: reduced limits of stability and functional reach; postural instability associated with dual-task activity.

Question 22

Memory in individuals with Alzheimer’s Disease.

Answer 22

Early impairments: working memory, episodic memory, and semantic memory. Working and episodic tends to predict those with a mild cognitive impairment who will go on to have Alzheimer’s.
Relative sparring is seen with procedural memory.

Question 23

Motor learning in individuals with Alzheimer’s Disease.

Answer 23

Both implicit and explicit learning strategies can be used but reduced learning. They need repeated practice (implicit) but also observational and guided learning (explicit). We must promote errorless learning because they will not be able to detect their errors.

Question 24

True or False: we want to give individuals with Alzheimer’s Disease verbal feedback.

Answer 24

False, we want visual feedback.

Question 25

Information processing in stroke patients.

Answer 25

Decreased sensory input (homonymous hemianopia, vestibular (brainstem), and/or somatosensory loss associated with loss of function.

Question 26

Attention in stroke patients.

Answer 26

Right hemisphere lesions lead to hemineglect/extinction; decreased ability to sustain, shift, and divide attention.

Question 27

Motor control in stroke patients.

Answer 27

Tone: spasticity
Abnormal synergies: massed patterns of movement, unable to selectively activate individual muscles, and results from increased recruitment of brainstem pathways.

Question 28

Steady-state control in stroke patients.

Answer 28

Impairments in both sitting and standing (sitting: weight is shifted to either side due to collapsing to the other side from lack of muscle activation; standing we will see asymmetrical weight-bearing on the uninvolved side); asymmetrical alignment; and increased and asymmetrical sway.

Question 29

APAs in stroke patients.

Answer 29

APAs: lesions to many areas can impair APAs (motor cortex, basal ganglia, cerebellum); delayed and reduced muscle activity in trunk on affected side; external trunk support can improve performance.

Question 30

CPAs in stroke patients (both in-place and stepping strategies).

Answer 30

In-place: impaired sequencing, timing, and amplitude in paretic limb in response to perturbation; compensate for delays in distal muscles of paretic limb with early proximal activation of non-paretic limb.
Stepping: similar time to foot off paretic vs non-paretic; however, different pattern based on asymmetrical load; delays in non-paretic, but not paretic stepping are associated with falls.

Question 31

Memory in stroke patients.

Answer 31

Dependent upon lesion location.
Possible impairments: decreased STM and LTM

Question 32

Motor learning in stroke patients.

Answer 32

Explicit learning is impaired with medial temporal lobe damage; implicit learning is distributed between brain structures so that not a single lesion completely eliminates it. Ideal practice conditions are dependent upon the type of stroke.
-MCA and basal ganglia strokes: explicit instruction leads to decreased learning.
-Cerebellar stroke: explicit instruction leads to increased learning.

Question 33

Information processing in patients with Parkinson’s Disease.

Answer 33

Difficulty adapting to sudden environmental changes. Difficulty organizing and selecting sensory information.

Question 34

Attention in patients with Parkinson’s Disease.

Answer 34

Difficulty selecting what sensory cues to attend to, so they will benefit from attentional cueing. We will see a decrease in performance under dual-task conditions relative to control subjects.

Question 35

Motor control in patients with Parkinson’s Disease.

Answer 35

Bradykinesia: slow movement time
Hypokinesia: decreased movement amplitude
Akinesia: decreased movement initiation
Rigidity
Tremor
Secondary impairments: decreased ROM (flexors), weakening (extensors).

Question 36

Postural control in patients with Parkinson’s Disease (steady-state, APAs, and CPAs).

Answer 36

Steady-state: increased sway area and velocity, but with medication, we will see a decrease in sway.
APA: smaller anticipatory adjustments, decreased velocity. They do not set their muscles before going to move their extremities.
CPA: in-place responses include abnormal co-contraction of hip and knee musculature; decreased adaptation of postural strategies to environmental and task demands. Stepping strategies include decreased weight shift prior to stepping, slower to initiate step, multiple small steps to recover balance, and increased risk of falls.

Question 37

Memory in patients with Parkinson’s Disease.

Answer 37

Working memory: decreased relative to controls, worsens with disease progression and improves with dopamine.
Long-term: decreased encoding and retrieval

Question 38

Motor learning in patients with Parkinson’s Disease.

Answer 38

Slower rate of learning, worsens with disease progression, difficulty learning sequential tasks, blocked practice improves acquisition and retention, external focus of attention improves performance and motor learning, and cueing can improve performance.

Question 39

What are the possible causes of cerebellar pathology?

Answer 39

MS, stroke, tumor, brain injury, cerebral palsy, neurodegenerative conditions, genetic conditions, and alcohol abuse.

Question 40

Information processing in patients with cerebellar pathology.

Answer 40

Decreased ability to subconsciously compare sensory information to intended motor output. Decreased ability to subconsciously respond to sensory feedback. Slower to respond to unexpected sensory information.

Question 41

Attention in patients with cerebellar pathology.

Answer 41

Must rely more on conscious, attention-demanding pathways for movement adaptation. Performance may deteriorate with other demands on attention (dual-task, fatigue, distraction).

Question 42

Motor control in patients with cerebellar pathology.

Answer 42

Hypotonia, decreased coordination/ataxia, impaired timing and grading of muscle contractions, intention tremor, and improved control of isolated joint vs multijoint movement.

Question 43

Steady-state control in patients with cerebellar pathology.

Answer 43

Steady-state: increased postural sway, direction of sway is linked to lesion location, wide BOS (sway increases as BOS decreases), and vision/somatosensory input decreases sway.

Question 44

APAs in patients with cerebellar pathology.

Answer 44

Able to demonstrate APAs, but we see abnormal timing and mismatched scaling. There is a decreased ability to develop new APAs for novel tasks.

Question 45

CPAs in patients with cerebellar pathology.

Answer 45

In-place responses: decreased ability to grade force of output to match perturbation, hypermetric postural response (larger amplitude and longer duration), and excessive compensatory sway in opposite direction (body oscillations).
Stepping responses: able to demonstrate stepping responses and may require more than one step.

Question 46

Memory in patients with cerebellar pathology.

Answer 46

Decreased verbal working memory, decreased flexibility in previously acquired procedural memories, and decreased consolidation of new procedural memories.

Question 47

Motor learning in patients with cerebellar pathology.

Answer 47

The cerebellum plays an essential role in error correction. If we have damage to the cerebellum, we see a decrease in the extent and rate of adaptation of movement; decreased error-based learning; declarative learning intact; and limited ability to consolidate new skills.

Question 48

Practice and feedback for patients with cerebellar pathology.

Answer 48

Practice: avoid trial and error learning; stepwise movement repetition with verbal prompts to ensure conscious awareness; requires longer duration, increased repetitions, and increased intensity; massed; and less retention.
Feedback: respond well to verbal cues to direct attention; teach patients to consciously attend to movement; providing KP and/or KR assists with error detection; and intermittent better than constant.

Question 49

Information processing in patients with Huntington’s Disease.

Answer 49

Slow response times, difficulty selecting between relevant and irrelevant stimuli, problems with visuospatial awareness, difficulty inhibiting inappropriate responses, and difficulty anticipating due to overestimating abilities.

Question 50

Attention in patients with Huntington’s Disease.

Answer 50

Decreased ability to shift attention; decreased ability to concentrate on more than one task.

Question 51

Motor control in patients with Huntington’s Disease.

Answer 51

Hypotonia; chorea; overtime we will see weakness and decreased ROM.

Question 52

APAs in patients with Huntington’s Disease.

Answer 52

Reduced limits of stability even in pre-manifest HD; limb movements deviate significantly from planned trajectories; and difficult to anticipate.

Question 53

Memory and motor learning in patients with Huntington’s Disease.

Answer 53

Memory: difficulty retrieving memories (applies to both distant and recent memories).
Motor learning: better with part practice, need to increase guidance to put the parts together, and avoid distractions and dual-task.

Question 54

Motor control in patients with MS.

Answer 54

May present with any or all of the following: weakness/paralysis, spasticity, incoordination/ataxia, and loss of ROM.

Question 55

Postural control in patients with MS.

Answer 55

Reduced LOS; slow activation of postural muscles, so they will have slow initiation of APAs and slow CPAs; they will have difficulty under varying/reduced sensory conditions.

Question 56

Information processing in patients with MS.

Answer 56

Sensory deficits are common. Slow conduction may delay response.

Question 57

Attention, memory, and motor learning in patients with MS.

Answer 57

IP: sensory deficits are common and slow conduction may delay response.
The rest: other deficits highly dependent upon lesion locations.