Topic 15-Stroke Recovery Flashcards

1
Q

Diaschisis

A

Loss of function in remote areas anatomically connected to region of lesion​ (decrease in blood flow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What does Diaschisis possibly result from?

A

Possibly from disruption of afferent excitatory input from lesioned area to other brain regions.​

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are at least 3 separate but interactive processes associated with recovery​

A

1) 1) Resolution of diaschisis, inflammation etc..​
2) Behavioural compensation​
3) Neuroplasticity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

When does inflammation typically begin after ischemia, and which cells are key players?

A

Inflammation begins hours after ischemia, with microglia and leukocytes playing a key role by removing necrotic tissue and address secondary brain damage.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does the resolution of core damage (umbra) affect the recovery process?

A

As the core damage (umbra) is resolved, the surrounding affected area (penumbra) and diaschisis effects are reduced, facilitating recovery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is a typical sign of an upper motor neuron lesion affecting the facial muscles?

A

Lower facial quadrant weakness with upper face preservation is typical of upper motor neuron lesions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What can cause facial muscle weakness?

A

Facial muscle weakness can result from lesions in the facial nerve or corticobulbar tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does a lesion affect facial movement on the ipsilateral and contralateral sides of the face?

A

The side of the face ipsilateral to the lesion can move normally, while the contralateral side may have hemiparesis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What characterizes a hemiparetic gait?

A

A hemiparetic gait is characterized by flexion at the elbow, wrist, and shoulder due to an imbalance between the flexor and extensor muscles.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Why does an imbalance between flexor and extensor muscles occur in hemiparesis?

A

The imbalance occurs because the descending motor tracts can no longer properly communicate with the rubrospinal tract, which helps regulate the balance between flexor and extensor tone.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is neuroplasticity?

A

Neuroplasticity is the ability of neurons to change their function, chemical profile, or structure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How long must changes in neurons last to be considered neuroplasticity?

A

Changes must be sustained for more than a few seconds to qualify as neuroplasticity and non-periodic changes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the three primary mechanisms of neuroplasticity implicated in stroke recovery?

A

) Redundancy – alternate pathways take over lost function​

2) Unmasking - activation of normally inhibited pathways​

3) Long-term potentiation - increasing efficiency of synaptic connections and formation of new synapses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Can you give an example of redundancy in neuroplasticity?

A

For instance, in a watershed lesion affecting both motor and sensory regions, the brain might reroute signals from the damaged primary motor cortex through the premotor cortex. This allows the premotor cortex to take over and send signals down the pyramidal tract to control muscles, compensating for the lost function.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What differences in brain activation are observed in stroke patients during a motor task compared to control subjects?

A

Stroke patients show more diffuse brain activation in multiple areas, including the primary motor cortex and sensory areas, particularly in the unaffected hemisphere, illustrating redundancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do inhibitory interneurons contribute to maintaining topographic representation in the brain?

A

Inhibitory interneurons prevent excitatory connections from one cortical area from activating adjacent areas, maintaining the separation between different body part representations.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What changes occur in the brain’s inhibitory patterns during stroke recovery?

A

During stroke recovery, changes in inhibitory patterns may occur, allowing previously suppressed areas of the brain to become active and compensate for lost functions.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How do adjacent cortical regions expand in the brain?

A

Adjacent cortical regions expand when preexisting lateral excitatory connections are unmasked by decreased intracortical inhibition.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What effect does a GABA antagonist like bicuculline have on the brain’s cortical areas?

A

Decreases the activity of inhibitory GABA interneurons, leading to disinhibition of cortical areas.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What happens to GABA receptors in response to an ischemic lesion from a stroke?

A

There is a reduction of GABA receptors in response to an ischemic lesion from a stroke, indicating a decrease in inhibitory signaling.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

In stroke patients with left striatal capsular infarction, what neuroplastic changes are indicated by brain scans during a finger tapping task?

A

Brain scans indicate unmasking, shown by posterior displacement (a shift towards the back of the brain) and larger activation areas in sensory and motor regions, and redundancy, evidenced by ipsilateral and supplementary motor area activation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the key features of long-term potentiation in neural function?

A

Characterized by the increased efficiency of synaptic connections, the formation of new synapses, and serves as a means to modify neural circuitry.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What is the critical trigger for the induction of long-term potentiation?

A

The increase in Ca2+ in the postsynaptic cell is the critical trigger for the induction of long-term potentiation.

24
Q

Why are NMDA receptors crucial for long-term potentiation?

A

NMDA receptors are crucial for LTP because blocking them can shut down the process, indicating their active role is needed for LTP to occur.

25
Q

What role does high-frequency stimulation play in long-term potentiation?

A

High-frequency stimulation depolarizes the postsynaptic neuron, which allows calcium to enter, expels magnesium, and activates the NMDA receptor, all of which are essential steps in the process of long-term potentiation

26
Q

What is long term depression? What causes it?

A

The weakening of synaptic connections, induced by low frequency stimulus

27
Q

How does long-term depression (LTD) relate to plasticity?

A

Long-term depression can erase increases in the excitatory postsynaptic potential (EPSP) seen previously with long-term potentiation (LTP), demonstrating plasticity as an increasing and decreasing responsiveness to stimuli.

28
Q

What is one mechanism that can lead to Long-Term Potentiation (LTP)?

A

LTP can result from the rapid insertion of AMPA receptors, which were previously silent but become responsive to glutamate

29
Q

How does the increase of glutamate receptors affect synapses?

A

increase of glutamate receptors can convert silent synapses into active synapses, enhancing signal transmission between neurons.

30
Q

What is the role of AMPA receptors in LTP?

A

Facilitate the rapid and increased transmission of signals between neurons by becoming more responsive to glutamate, thus strengthening the synaptic connection.

31
Q

What happens to the postsynaptic membrane during Long-Term Potentiation (LTP)?

A

In LTP, high-frequency stimulation leads to calcium upregulation and the insertion of AMPA receptors, causing the entire postsynaptic membrane to remodel and form new dendritic spines, which increases its responsiveness to input.

32
Q

What is one effect of Long-Term Potentiation (LTP) on synaptic contacts?

A

LTP may increase size and number of synaptic contacts ​

33
Q

How did the study about Constraint-induced rehab training show unmasking and redunancy?

A

The study showed unmasking as brain areas not usually used for movement were more active after therapy. It showed redundancy as the brain used different paths to control movement, helping in stroke recovery.

34
Q

What is Forced Use / Constraint-Induced Training​? How is this beneficial’?

A

Patients practice using affected limb while other limb is restrained. ​Can increase patient’s ability to use affected limb.​

35
Q

Why is post-lesion training important for optimizing plastic change?

A

Post-lesion training is important because an absence of training can lead to a further reduction in the representation of the affected limb.

36
Q

What was the effect of rehabilitation on the hand representation areas in M1 after a lesion was induced?

A

After rehabilitation, spared hand representation increased in size

37
Q

What happens to the hand representation area in M1 when a lesion is induced without post-stroke rehabilitation?

A

When a lesion is induced in the part of the hand representation area in M1 and there is no post-stroke rehabilitation, the representation of digits in the non-lesioned regions diminishes.

38
Q

What are some alternative approaches in stroke rehabitlation?

A

1) Observation therapy
2) “Mirror-box” therapy

39
Q

Observation Therapy- Alternative Stroke Rehabitliation

A

Involves a patient observing someone else moving with the intent to imitate those movements. It may involve the “mirror neuron” system.

40
Q

Mirror Box Therapy

A

A technique where the movements of a patient’s unaffected arm appear to be made by the patient’s impaired limb. This can help improve motor function and perception in rehabilitation.

41
Q

What does acute stroke treatment focus on?

A

Focuses on restoring blood flow to the affected area of the brain (reperfusion) and to protect the brain cells from further damage (neuroprotection).

42
Q

What is the time window for acute stroke treatment?

A

Acute stroke treatment must be administered within a limited time window of hours.

43
Q

What are the main targets of acute stroke treatment?

A

Acute stroke treatment primarily targets the ischemic core (already damaged brain tissue) and the penumbra (at-risk tissue) to minimize brain injury and improve outcomes.

44
Q

What is the target of stroke recovery and rehabilitation?

A

The target of stroke recovery and rehabilitation is the unaffected areas of the brain.

45
Q

What plays a significant role in stroke recovery and rehabilitation?

A

Innovative rehabilitation techniques and the development of “stroke recovery drugs” are crucial components of stroke recovery and rehabilitation.

46
Q

What are the associated risks and limitations of acute stroke treatment?

A

Acute stroke treatment has a narrow time window for effectiveness, and carries the risk of bleeding in the brain (hemorrhagic transformation) if administered inappropriately

47
Q

What is spasticity?

A

Muscle stiffness and tightness in the affected limbs due to damage to the upper motor neurons.

48
Q

How does spasticity differ when it is focal versus generalized?

A

Focal spasticity affects a small area such as one hand or foot, while generalized spasticity affects larger areas, potentially the whole body.

49
Q

What is a common treatment for focal spasticity and how does it work?

A

Focal spasticity can be treated with botulinum toxin (Botox), which works by preventing neurotransmitter release at the neuromuscular junction, temporarily paralyzing the muscle.

50
Q

What is used to treat generalized spasticity?

A

1) Baclofen (GABAb agonist)​

2) Phenobarbitol (GABAa agonist)​

3) Tizanidine (adrenergic agonist)​

4) Physiotherapy! ​gonists Agonists activates or stimulates a specific receptor in the body.

51
Q

Clonus

A

Characterized by involuntary, rhythmic, and repetitive muscle contractions or spasms that typically occur in response to a sudden stretch of a muscle.

52
Q

What two medications can be used to enhance stroke recovery?

A

1)Amphetamines can be used for stroke recovery by potentially enhancing motor function through increased levels of central norepinephrine
2) Fluoxetine -SSRI used as an antidepressant, increasing serotonin levels helped in stroke recovery

53
Q

Stem Cell Therapy

A

Stem cell therapy involves using cells that can continuously divide and have the potential to become various cell types. This therapy has the potential to replace damaged tissues

54
Q

Where are neural stem cells located in the adult human brain?

A

Neural stem cells are located in the lateral ventricular walls of the adult human brain.

55
Q

What is the main challenge with neural stem cells in the brain?

A

The main challenge is that these stem cells do not naturally migrate or function in the brain, and researchers need to figure out how to activate them for brain healing.

56
Q

What is the time window for stroke recovery and rehabilitation?

A

Stroke recovery and rehabilitation can occur over an extended time window, including days, weeks, months, and even years.

57
Q

What is the target of stroke recovery and rehabilitation?

A

The target of stroke recovery and rehabilitation is the unaffected areas of the brain.