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Unit 19 > From T's Review: Part 2 > Flashcards

From T's Review: Part 2 Flashcards

1
Q

Where is implicit memory formed?

A

Neocortex, striatum, amygdala, cerebellum, reflex pathways

CRANS

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2
Q

Where is explicit memory formed?

A

Medial temporal lobe and unimodal/polymodal association areas

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3
Q

What does imaging of BG and following patients through stages of learning show?

A

Shift in activation from caudate nucleus (executive circuit) to putamen (motor circuit)

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4
Q

Aerobic exercise without rest going into learning creates the highest performance. What is happening physiologically to explain this finding?

A

Mostly BDNF - adrenaline, NE, angiogenesis, dopamine

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5
Q

What does BDNF do?

A

It augments changes at synapses by promoting neuronal growth, differentiation, and maintenance.

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6
Q

What receptor type drives the expression of increases in BDNF?

A

Expressed in glutaminergic pathways, driven by NMDA receptors.

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7
Q

Why is random order practice better for learning (even though it may decrease performance)?

A

You have to reform your plan with every new task = better encoding and different consolidation.

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8
Q

After constant practice your primary consolidation is in which area of the brain?

A

Primary Motor Cortex

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9
Q

After variable practice the site of consolidation is in which area of the brain?

A

Dorsolateral pre-frontal cortex (DLPFC) - so if there is damage to the pre-frontal cortex, this type of learning/practice may not work!

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10
Q

In a study where rats were sacrificed by lesioning the nucleus basalis, their accuracy and plasticity diminished. Which neurons did this affect?

A

Cholinergic neurons

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11
Q

Does this cluster of behavior/sxs indicate a DLPFC or Orbitofrontal cortex lesion? Difficulty initiating behaviors, flat affect, need a little bit less to keep them going thru-out the day.

A

DLPFC

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12
Q

Does this cluster of behavior/sx’s indicate a DLPFS or Orbitofrontal cortex lesion? Often lack of response or concern for things, huge emotional ranges, difficulty w/ impulse control, spiral of despair.

A

Orbitofrontal

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13
Q

Which type of syndrome often leads to behavior changes that are similar to psychiatric diagnoses?

A

Limbic

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14
Q

Do these behaviors/sxs coincide w/ a LEFT hemisphere or RIGHT hemisphere lesion? Pt’s are apathetic, they are risk takers, less aware of errors and have difficulty interpreting emotional tone.

A

RIGHT

right = risk

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15
Q

Do these behaviors/sxs coincide w/ a LEFT hemisphere or RIGHT hemisphere lesion? Pts have intense anxiety reactions w/ failure and are hyper aware of their deficits.

A

LEFT

left = lose

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16
Q

What is anosognosia?

A

lack of awareness of impairments

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17
Q

Which are of the brain, when injured will lead to anosognosia?

A

RIGHT frontal lobe (RIGHT = risk)

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18
Q

What are some of the aspects of the frontal lobes that make them vulnerable to injury?

A

rich connections, last to develop, most NTs project here

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19
Q

What does the word abulic mean, and which prefrontal cortex area is that behavior associated?

A

Not making decisions on their / lack of initiative and is common in DLPFC lesions

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20
Q

What is the difference in presentation bw a patient w/ UMN dysarthria vs. LMN?

A

UMN hypernasal and strained

LMN flaccid, breathy and hypotonic

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21
Q

What is apraxia?

A

Can’t demonstrate a gesture, poor volitional movement

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22
Q

What will a patient w/ non-fluent/expression aphasia present like?

A

Comprehension intact, perseverate on words

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23
Q

What will a patient w/ fluent/receptive aphasia present like and what is another name for this?

A

redux in auditory comprehension, decreased awareness of errors, speech itself not difficult

Wernicke’s

24
Q

Where might a patient’s injury be if they have visual spatial deficits, LEFT neglect, poor insight, maybe dysarthria but all other aspects of language spared?

A

RIGHT hemisphere

25
Q

What are the 3 stages of swallowing?

A
  1. ORAL - bolus control
  2. PHARYNGEAL - transfer to esophagus = reflexive
  3. ESOPHAGEAL - to stomach
26
Q

What 2 critical things compose consciousness?

A

AROUSAL - the LEVEL

AWARENESS - the CONTENT (+ MOTIVATION!)

27
Q

What was learned in a study completed on cats whose reticular formation (nuclei w/in the brain stem) was lesioned?

A

The cats fell asleep, but when the same area was stimmed - they woke. Helped define the ARAS (Ascending Reticular Activating System) which originates in the reticular formation, moves through the thalamus via glutaminergic pathways to the cortex.

28
Q

What is the reticular formation?

A

Not well defined, but believed to be in brain stem and responsible for wakefulness, eye movements, swallowing/vomiting, posture/locomotion, respiration, BP, sensory awareness.

29
Q

What are the pathways w/in the ARAS (Ascending Arousal System) have and what significance does this have?

A

2 pathways (allow for redundancy):

1) THALAMIC (from RF to thalamus and then to rest of cortex
2) EXTRATHALAMIC (bypass to hypothalamus -> basal forebrain and then cortex)

30
Q

What nuclei are inside the thalamic pathway and what do they both secrete?

A

Peduncular Pontine Nucleus (PPT)
Lateral Dorsal Tegmentum (LDT)

Ach

31
Q

What does the thalamus do?

A

It’s a relay station, but this also means that it filters / modulates info.

32
Q

The thalamus has its strongest/output interaction with _____.

A

the striatum

33
Q

What is the range of wakefulness?

A

stage 3 non REM to high vigilance

34
Q

What is the difference bw a COMA and a VS?

A

global dysfx of cortico-thalamic loop, eyes stay closed, immobile, no reflexes for both EXCEPT for VS there is some eye opening and functioning of the upper brainstem.

35
Q

What is akinetic mutism? And what abilities will these individuals have that differentiates them from those in COMA or VS?

A

disorder of motivation (prefrontal cortex disorder), severe form = eye tracking only otherwise decreased initiation of goal-directed behavior and retained response to commands

36
Q

Is locked-in state a disorder of consciousness?

A

NOPE. These poor people have lost their CST in ventral pons OR have a white matter injury.

37
Q

What’s the difference bw decorticate and decerebrate posturing? Which one is better prognostically?

A

4 e’s in decerebrate so 4 limbs in extension vs. 2 - decorticate is better (bilateral damage for both, but decerebrate indicates damage is moving down)

38
Q

What is one potential pharmacological intervention strategy that can be used in disorders of consciousness?

A

Amantadine HCL (standard of care)

39
Q

What is the mechanism of action of Amantadine HCl?

A

The striatum inhibits the globus pallidus which normally inhibits the thalamus (so that the thalamus IS working). But in the case of disorders of consciousness - the striatum stops inhibiting the inhibitor and we have a problem! Amantadine affects the striatum so this doesn’t happen.

40
Q

When are Alpha waves more prominent?

A

eyes closed/relaxation

41
Q

When are Beta waves more prominent?

A

mentation, but not a high-level task

42
Q

When are Gamma waves more prominent?

A

high level cognitive task

43
Q

What’s the difference bw theta and delta waves?

A 
Theta = Sleepy
Delta = DEEP (D-> D)
44
Q

What kind of waves do we expect to see throughout a sleep cycle?

A
  1. Theta waves as you get sleepy.
  2. Stage 4 sleep / DEEP Delta Waves!
  3. Back up to REM = Beta
  4. Stage 2 (possible spindles and k-complexes to note sounds) = Delta
  5. Back to REM = Beta
  6. Stage 3 (possible spindles and k-complexes to note sounds) = Delta
45
Q

What is the suprachiasmic nucleus of hypothalamus responsible for?

A

Circadia Rhythm

Stims pineal gland which secretes serotonin

46
Q

What is the difference between primary and secondary brain tumors?

A

Primary originates in brain (or surrounding tissues). Secondary metastasizes to other parts of the body.

47
Q

How are brain tumors staged?

A

From benign to most malignant, Stage I-IV

Stage I - benign, slow growing
Stage II - relatively slow growing, spreads to normal tissue and comes back
Stage III - malignant, actively reproducing abnormal cells
Stage IV - most malignant, vascular w/ necrosis

48
Q

What distinguishes having seizures regularly from epilepsy?

A

Epileptic seizures are unprovoked.

49
Q

What are 3 key features of seizures?

A
  1. Where in the brain it happens
  2. Level of awareness during
  3. Movements or not
50
Q

What kind of seizure has an impaired awareness OR awareness, could be motor OR non-motor?

A

Focal Onset

51
Q

What kind of seizure has an impaired awareness and motor?

A

Generalized Onset

52
Q

What are the stages of a seizure?

A

Prodromal - sx start before (can be behavioral, urinary, GI) - days ahead of time

Aural - usually w/ focal, not all (altered senses, deja vu, dread)

Ictus - seizing (GREATER THAN 5 MIN NEEDS MED ATTN)

Post-ictus: recovery period

53
Q

A patient you are testing for POTs has a HR change of 20 bpm accompanied by >40 changes in BP. What effect might this have on diagnosis?

A

If both HR and BP = hypovolemic.

If only HR = neurogenic.

54
Q

If you worked in a SNF, what percentage of your patients could receive concurrent group therapy?

A

25%

55
Q

If you worked in an IRF, what percentage of the cases in your facility must have one or more of HOW many conditions?

A

60%, 13 conditions ( they’ve added a group for “3 arthritis conditions that failed OP”)

56
Q

What is a normal score for cervical joint position testing?

A

<4.5 deg off for each direction

Unit 19 (2 decks)

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