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MOPs II > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What tracts come out of M1?

A

axons of CST and CBT

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2
Q

Motor heirarchy

A

Highest level= mvmnt selection, planning intiation
Middle level= balance, posture, sensorimotor integration
Lowest level= volitional and reflexive mvmnt regulation

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3
Q

What parts of the CNS do the highest level in the motor hierarchy?

A

primary, premotor, and supplementary motor cortices
basal nuclei
thalamus

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4
Q

What parts of the CNS do the middle level in the motor hierarchy?

A

cerebellum
vestibular nuclei
reticular formation

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5
Q

What parts of the CNS do the lowest level in the motor hierarchy?

A

spinal cord

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6
Q

Neural circuit for coordination of voluntary movement

A

UMN from cortex descends to synapse on LMN and interneurons

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7
Q

Motor Pathway generalizations

A

Medial= posture and proximal limb movements
lateral= distal limb mvmnts
lateral CST= fine motor hand mvmnts

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8
Q

Why is the lateral CST control of fine motor hand movements important?

A

Because the other pathways tend to overlap and have similar functions in areas but the lateral CST is the only pathway that does fine motor control of the hand

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9
Q

Population code

A

activity of everyone together is interpreted as the outcome

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10
Q

How is the motor cortex a population code?

A

info that is encoded in the population code has multiple movement parameters

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11
Q

Name the origins of the CST and CBT pathways

A

55% frontal lobe (Brodmann’s 4 (M1), and 6, Betz cells)
10% association cortices
35% sensory cortex

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12
Q

Discoveries in 1960s on cortical control of mvmnt

A

Ed Evarts
recorded from one neuron at a time
saw AP firing 50-150 ms before specific mvmnt

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13
Q

Discoveries in 1980s on cortical control of mvmnt

A 
Georgopolus= recorded from multiple neurons in same area; AP firing correlated with directions and time-course of hand mvmnt; analysis from discharge from pop of neurons could be used to predict what mvmnt occurred
Kalaska= population intensity level varied by needed force
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14
Q

Discoveries in 1990s on cortical control of mvmnt

A

Caminiti et al

pop code more accurately reflected movement

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15
Q

Ventral motor premotor area

A

caudal area active when imagining movement, reaction with visual guidance, and interacting with people in personal space
rostral area active with communicative gestures, hand/face actions

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16
Q

Dorsal premotor area

A

activities performed from memory and planning/holding mvmvnt

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17
Q

Medial supplemental motor area

A

bimanual task coordination

important with tool use

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18
Q

Parietal area 5

A

receives input from sensory to give update on how things are going
can give course correction

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19
Q

What is the Basal Ganglia made of?

A

Collection of nuclei

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20
Q

name the principle nuclei of the Basal Ganglia

A 
caudate nucleus
nucleus accumbens
putamen
globus pallidus
substantia nigra
subthalamic nucleus
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21
Q

What are the different parts of the substantia nigra?

A

pars compacta

pars reticulata

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22
Q

Is the subthalamic nucleus GABA or glutamatergic?

A

Glutamatergic

enhances inhibition to thalamus

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23
Q

Define disinhibition

A

removal of inhibition

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24
Q

How does disinhibition work?

A

input neurons regulate target neurons to produce baseline firing rate
inhibitory synapse on inhibitory input cell decreases output of inhibitory cell
this disinhibits the target and increases firing rate

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25
Q

What does the Basal Ganglia do?

A 
sequencing through movements after initiation
prevent unwanted movement
opponent parallel pathways
learning routines and habits
attention
reward-related learning
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26
Q

4 Main Loops of Basal Ganglia

A

skeletomotor
oculomotor
associative cortical
limbic

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27
Q

Skeletomotor BG loop controls what?

A

facial, limb, trunk mm

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28
Q

Oculomotor BG loop

A

saccadic eye movement

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29
Q

Associative cortical BG loop

A

strategic planning of behavior

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30
Q

Limbic BG loop

A

motivation, emotion, learning

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31
Q

How are the BG loops arranged in the brain?

A

parallel along longitudinal axis

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32
Q

BG loop sequence

A

Cortex->striatum->output nuclei->thalamus->cortex

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33
Q

Explain the striatum

A

nucleus accumbens (limbic)
Caudate nucleus (prefrontal/associative)
putamen (somatosensation/motor)
-which nucleus you go through depends on where the loop starts in the cortex
-neurons have either D1 or D2 receptor (medium spiny neurons)

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34
Q

What are the output nuclei

A

globus pallidus internal

substantia nigra pars reticulata

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35
Q

Which thalamic nuclei are involved in BG loops?

A

Relay nuclei

VA/VL/MD

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36
Q

Is the BG loop a positive or negative feedback loop? How/why?

A

Positive (dynamic)
helps derive reptition that derives neuroplasticity
postive feedback to cortices that are doing something relevant to what we want to be doing

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37
Q

Is corticotopic mapping present for direct or indirect loops?

A

Direct

loops separate from one another in global pattern

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38
Q

Direct BG loops

A

end precisely where they started in cortex
disinhibition of thalamus resulting in increased output to cortex
D1 cells

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39
Q

Indirect BG loops

A

goes through globus pallidus external and subthalamic nucleus (extra steps)
increase inhibition to thalamus resulting in decreased output to cortex
D2 cells
GPe inhibits STN and striatum inhibits GPe
slightly wider end projection-not corticotropic

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40
Q

What does dopamine do with BG loops?

A

causes release of G protein that can change cell excitability
increases both pathways but the difference between indirect and direct loops is maintained

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41
Q

Facilitation (related to dopamine)

A

more excitabile

D1 (dopamine) receptors

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42
Q

Inhibition (relation to dopamine)

A

less excitable

D2 receptor

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43
Q

Where is DA made?

A

substantia nigra pars compacta and VTA

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44
Q

What does the cerebellum do?

A

monitors sensory input and makes changes

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45
Q

Name the 3 cerebellar lobes

A

lateral
intermediate
medial

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46
Q

Folia

A

Ridges of cerebellum

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47
Q

Vermal/medial zone of cerebellum function

A

eye movements, vestibuloocular coordination, axial mm for balance and posture

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48
Q

Intermediate zone of cerebellum function

A

reach and grasp

neck, trunk, and limb mm

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49
Q

What does damage to the intermediate zone of the cerebellum result in?

A

tremor

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50
Q

Lateral zone of cerebellum function

A

modulation of fine control of movements and motor learning

mental agility, smoothness of thought, stability of affect

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51
Q

Name the 3 cerebellar layers

A

granule cell layer
purkinje cell layer
molecular layer

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52
Q

What is found in the granule cell layer of the cerebellum

A

axons project through to molecular layer and then perpendicular
internal
round soma of granular cells
white matter int to this later with deep cerebellar nuclei

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53
Q

What is found in the Purkinje cell layer of the cerebellum?

A

soma

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54
Q

What is found in the molecular layer of the cerebellum?

A

purkinje cell dendrites

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55
Q

What are climbing fibers?

A

to deep cerebellar nuclei
role is under research
wrap around purkinje dendrites

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56
Q

what are mossy fibers?

A

input all along rostral caudal axis

go through cerebellar peduncles

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57
Q

What is the activity type of deep cerebellar nuclei?

A

spontaneously active

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58
Q

How can DCN firing rate be sped up?

A

through mossy fibers

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59
Q

How can DCN firing rate be slowed down?

A

through purkinje neurons

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60
Q

How are cerebellar loops arranged?

A

along the sagittal plane

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61
Q

are cerebellar loops positive or negative feedback loops?

A

positive

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62
Q

Describe the inputs for cerebellar loops

A

from cortex via contralateral pontine nucleus
from spinocerebellar pathways
cranial nn

Input comes on mossy fibers

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63
Q

Describe input divergence for cerebellar loops

A

input diverges to cerebellar cortex and deep cerebellar nuclei
cortext also connected as input to DCN

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64
Q

Purkinje neurons

A

Gabaergic
provide inhibition
synapse into DCN
spontaneously active

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65
Q

Inferior olive

A

additional source of input
gives rise to climbing fibers that synapse onto purkinje neurons
input from collateral descending motor pathways and ascending sensory pathways
speeds purkinje firing rate which increases inhibition of DCN (large burst can turn DCN off)

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66
Q

What happens when the cerebellum is damaged

A

results in movements that are erratic in size, force, and direction

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67
Q

Development of cerebellum

A

one of the last areas of the brain to develop
myelination not complete until about 2 years old
matures from inside out
cortex matures around 1 year old

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68
Q

Parkinson’s disease symptoms

A

bradykinesia, hypokinesia, mm rigidity, resting tremor, characteristic gait, decrease quality of voice, dysphagia, drooling, depression, anhedonia, fatigue, dementia, decreased executive functioning, constipation, orthostatic hypotension, sexual dysfunction

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69
Q

Parkinson’s disease causes

A

bilateral degredation of dopaminergic neurons in substantia nigra pars compacta with Lewy bodies

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70
Q

How would you treat mm spasticity?

A

botox b/c it inhibits Ach at the neuromuscular junction
Baclofen is a tablet, agonist to GABA receptors on motor neurons in SC
best if paired with rehab

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71
Q

Huntington’s disease

A

progressive and terminal
beings in mid-adulthood with choreoform movements
autosomal dominant

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72
Q

Do basal nuclei lesions result in positive or negative symptoms?

A

positive
result in unwanted behaviors and movements
cortical activity not being inhibited

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73
Q

Lesions of UMN: acute phase

A

posturing then flaccid paralysis

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74
Q

What is posturing?

A

type of paralysis

decortitate (lesions above MB) or decerebrate (lesions below MB)

75
Q

What is our role in the UMN lesion acute phase?

A 
limb protection
PROM
positioning
monitor edema
client/family education
monitor return of reflex and sensation
76
Q

Lesions of UMN: chronic phase

A 
spasticity
rigidity
hyperreflexia
emergence of voluntary control
loss of fine hand movements
anosognosia
77
Q

What is the direction of UMN lesion recovery?

A

proximal to distal

78
Q

Chorea movements

A

continuous rapid movements

fragments of normal voluntary movements

79
Q

athetosis movements

A

slow and writhing

80
Q

hemiballismus movements

A

wild and flailing in one arm and leg

81
Q

What type of movements result from an inbalance b/w the direct and indirect basal ganglia pathways?

A

chorea and athetosis

82
Q

Dystonia

A

abnormal mm tone in group of mm resulting in asymmetric posture

83
Q

Rett syndrome

A 
present typical until 6-18 months
then regression 
loss of communication and purposeful hand mvmnts
ataxic gait
disorganized breathing
inconsolable
84
Q

Tourette’s syndrome

A

motor tics and vocal tics that occur in clusters and are exacerbated by stress, anxiety, fatigue and can be voluntarily supressed for a brief period

85
Q

How is tourette’s syndrome treated

A

dopamine antagonists

maybe CBT and mindfulness

86
Q

Chiari malformations

A 
herniation of cerebellum
ranges in severity
symptoms: when increase in cranial pressure results in head and neck pain
vertigo
fine motor incoordination
visual disturbances
difficulty swallowing
choking
gagging
87
Q

Limbic lobe makeup

A

medial temporal lobe
insula
piriform cortex
entorhinal cortex

88
Q

Mossy fibers that synapse into (blank) synapse into (blank)

A

lateral lobe; dentate nucleus
intermediate lobe; interposed nuclei
medial lobe; fastigual nuclei

89
Q

Input to the hippocampus

A

from cortex (sensory, prefrontal)
simultaneous from 2 converging pathways (creates opportunity for coincidence detection)
amygdala
hypothalamus

90
Q

Output from hippocampus goes where?

A

cortex
striatum
hypothalamus

91
Q

Role of hippocampus

A

memory consolidation

memory of thought, experience, spatial navigation

92
Q

What is the fornix?

A

major outflow tract of hippocampus

93
Q

Amygdala

A

emotional memory

formation/storage of emotional valence of events

94
Q

What are the limbic structures

A 
nucleus accumbens and ventral pallidum (center of reward system; implicated in diseases of addiction)
hippocampus
amygdala
medial temporal lobe
prefrontal cortex
95
Q

Medial PFC

A

context cues
comparing current situation to memories
emotional regulation

96
Q

Dorsolateral PFC

A

working memory and memory retrieval

97
Q

Orbitofrontal cortex

A

motivation

social awareness

98
Q

Anterior cingulate gyrus

A

inhibition

99
Q

Name the 10 principles of neuroplasticity

A
  1. use it or lose it
  2. use it and improve it
  3. specificity
  4. repition matters
  5. intensity matters
  6. time matters
  7. salience matters
  8. age matters
  9. transference
  10. interference
100
Q

Hebbian learning

A

cells that fire together wire together

101
Q

Long term potentiation

A

needs persistant strong activation
coincident pre and post synaptic activity
postsynaptic CA2+ entry

102
Q

Long term depression

A

results from persistant weak activation

103
Q

Cognition

A

thinking and executive function

104
Q

Thinking components (4)

A

language
calculation
reasoning
concepts

105
Q

Executive function components (4)

A

self-monitoring
self-awareness
initiating
goal setting/planning

106
Q

Attention enhancement

A

contrast
movement
meaning

107
Q

Exogenous attention

A

automatic orientation to stim

posterior parietal cortex

108
Q

Endogenous attention

A

voluntary control of attention, choice
prefrontal cortex
can speed exogenous reaction time

109
Q

Selective attention

A

attention to one thing and exclusion of others

110
Q

sustained attention

A

can increase through practice

111
Q

Multitasking

A

not an actual thing

cannot cognitively attend to more than one thing at a time

112
Q

Task-switching

A

what we are really doing when we think of multitasking
lose time
requires 3 brain networks (alerting, orienting, executive)
harms productivity

113
Q

Working memory

A

retain and manipulate information for immediate use

114
Q

inhibition

A

suppress or delay response to stim or thought

115
Q

Emotion

A

speeds detection of risk
facilitates interventions and adds value
learned response to stimuli
physiological and motor changes cognitively interpreted as feelings

116
Q

Primary emotions

A 
fear
anger
sadness
joy
surprise
disgust
contempt
117
Q

Secondary emotions

A

shame and guilt

self-conscious emotions

118
Q

Reward

A

object/stim/event that increase likelihood of behaviors
satisfies biological drive (primary)
result from past experiences (secondary)
can enhance attention and play a role in learning

119
Q

Aversive stimuli

A 
function opposite of reward
decrease likelihood of behavior
120
Q

Motivation

A

initiates behavior through aim of getting a reward

121
Q

Anticipatory mechanisms

A

Prepare for need or future reward now

122
Q

Ecological constraints

A

cost-benefit analysis

123
Q

Hedonic factors

A

feel good when you receive them

124
Q

How can you tell if someone learned something?

A

Something changed about a person if they learned

125
Q

Non-associative learning

A

single-trial learning

habituation and sensitization

126
Q

Types of learning

A

operant
associative
non-associative

127
Q

Memory

A

retain information and reconstruct experiences for present use

128
Q

Process of memory

A

encoding (multimodal) to consolidation (storage in synapses/synaptic network) to retrieval (recall, recognition, relearning)

129
Q

Types of memory

A

working memory
procedural (how; cerebellum and basal ganglia)
semantic (what; temporal lobe)
episodic (when; temporal lobe, hippocampus, prefrontal cortex)

130
Q

Dementia

A

acquired decline in higher functions
not normal aging but occurrence increases with age
higher cognitive achievement the slower rate of decline in normal cognitive aging (dementia supersedes this)

131
Q

Dementia tx first steps

A

rule out treatable causes that could result in short-term dementia (nutrition, UTI, tumors, hydrocephaly)

132
Q

Alzheimer’s Disease

A 
memory impairment
word-finding difficulties
visual/spatial confusion
impaired reasoning and judgement
personality changes
hallucinations
delusions
paranoia
133
Q

Tx for Alzheimer’s

A

Cognitive/behavior training
Environmental mods
Exercise
Meds

134
Q

What causes Alzheimer’s

A

amyloid plaques, neurofibrillary tangles, Apo-e4 which are associated with death of cells in that region
pathology predates symptoms
begins in hippocampus and spreads
cholinergic neurons affected most

135
Q

Circadian rhythms

A 
primes sleep
adjusts to env
intrinsic cyclical pattern
25 hours
driven by superchiasmatic nucleus
136
Q

Drive

A

behavior to reduce and address intrinsic need

137
Q

Thermoregulation

A

detection in HT from STT and temp sensitive neurons in HT
Ant HT-when temp increases, sweat
Post HT-when temp decreases, shiver
endocrine funct for longer term regulation
behavior correction for regulation

138
Q

Fever

A

set point by septal nucleus

adjusted in response to pyrogens

139
Q

Metabolism states (2)

A
  1. prandial-recently eaten, abundance of nutrients in blood supply (free energy-glucose and lipids)
  2. Postabsorptive-stored energy (glycogen and triglycerides)
140
Q

How do we switch metabolism states?

A

brain

responds to presence of insulin secreted that triggers to transform nutrients into stored energy

141
Q

Satiety

A

signal that we have consumed what we need to

smell/texture/taste, stomach distentation (CN X, area postrema), caloric intake signaled by liver

142
Q

What satiety signal are infants missing?

A

caloric intake

143
Q

Hunger signals

A

limbic and prefrontal cortex
ventral HT
PNS (stomach growling)
GI secretion of ghrelin

144
Q

Thirst functions

A

need enough water to maintain correct concentrations, volume, and to get rid of waste

145
Q

Osmoreceptors

A

extend beyond blood brain barrier

sample concentration of blood

146
Q

HT role in thirst

A

HT smaples concentration of blood

if too concentrated secretes antidiuretic hormone

147
Q

Sleep stages

A 
Non REM (stage 1 light sleep to stage 4 deep sleep)
REM (dreaming, rapid eye movement)
148
Q

Which sleep stages are low amplitude high frequency

A

Stage 1, REM, wakefulness

149
Q

Which sleep stages are high amplitude, low frequency

A

Stage 4

delta waves

150
Q

What is the function of sleep

A

energy conservation
restoration
repair
memory consolidation

151
Q

Narcolepsy

A

daytime sleepiness with sudden and unwanted episodes of REM sleep

152
Q

Sleep apnea

A

obstruction of upper airway leads to frequent brief arousals from sleep

153
Q

Insomnia

A

difficulty falling asleep

154
Q

Insufficient sleep syndrome

A

voluntary restriction of daily sleep time requiring a week or more of restorative sleep

155
Q

What layer does the nervous system develop from? ectoderm, mesoderm, or endoderm

A

Ectoderm

156
Q

List process from neural plate to neural tube

A

neural plate stimulated by notochord to become neural crest (sonic hedgehog protein and chem)
then neural crest to neural tube

157
Q

Notochord

A

part of mesoderm

becomes body of vertebrae

158
Q

Components of neural development

A

neurogenesis (neurulation and directionality)
segmentation
neural migration and differentiation
axonal pathfinding

159
Q

Segmentation (3 + 5)

A

3 vessical differentiation:
prosencephalon=forebrain
mesencephalon=midbrain
rhombencephalon=hindbrain

5 vessicle differentiation:
prosencephalon to telencephalon (cortex) and diencephalon (thalamus and HT)
Mesencephalon
Rhombencephalon to metencephalon (pons) and myelencephalon (medulla)

160
Q

describe crest cell migration

A

neural crest cells squeezed out of neural tube
project distally then follow projection to body part
ride along with that body part as it grows

161
Q

How does the brain develop inside out?

A

subventricular zone produces neural stem cells
stem cells migrate by climbing radial glial cells attached to Cajal retzious cells
climb until they are just passed the previously born neurons that migrated before
once they arrive in appropriate layer they are signaled on what cell type to become

162
Q

Critical period vs sensitive period

A

critical period more in animals, stronger defined window when experience has to occur for something to develop (if it doesn’t happen in that window it will not ever happen)
humans have sensitive periods with more soft windows and not necessarily exclusion of development if it doesn’t happen in that window

163
Q

Explain axonal pathfinding

A

axon is extension of soma
sends out filopodia from growth cone
short and long range cues paired with post synaptic release attraction (Agrin) that forms synapse

164
Q

Types of cues for axonal pathfinding

A

contact attraction and chemoattraction (filopodia contact and move in that direction

contact repulsion and chemorepulsion (filopodia repulsed and move in opposite direction)

165
Q

Spina Bifida

A

neural tube doesn’t fully close
can be surgically tx
severity levels:
meningiocele (least; protruding meninges)
meningiomyocele (protruding meninges with neural tissue, bubble)
myeloschisis (most severe; malformed SC opened to surface)

166
Q

Chiari Malformation

A

neural tube deficit
enlarged foramen magnum b/c skull didn’t close fully
sensorimotor deficits of tongue, face, eye mvmnt, and vital signs
blocks CSF flow
surgical tx but painful

167
Q

Holoprosencephaly

A

sonic hedgehog gene
Alobar-not survivable
semilobar- lifespan of 5 years; seizures, blindness, little voluntary movement
lobar- IDD pathologies

168
Q

Agenesis of Corpus callosum

A

subtle to mild to severe
corpus callosum not formed
can go undetected

169
Q

Enriched vs sparse environment

A

enriched is better for development

sparse env can lead to brain underdevelopment

170
Q

What is the most common cause of TBI?

A

motor vehicle accidents

171
Q

TBI

A

caused by external force
may result in diminshed/altered mental state, cognition, or physical function
symptoms: impaired behavior and motor function
can be temporary or permanent

172
Q

Primary TBI damage

A

damage at tissue level or cellular level

173
Q

Secondary TBI damage

A

brain/body responding to primary damage
neurochemical changes leading to futher apoptosis
atrical hypotension, ischemia, edema, hypoxia, increased ICP, hydrocephaly

174
Q

Concussion

A 
mild TBI
one increases the risk of another
LOC 0-30 min
AMS up to 24 hrs
neurocog changes, balance deficits, blurred vision, light/auditory sensitivity, sleep distrubances, ringing in ear
175
Q

TBI classifications based on

A

Skull injury (open, closed, linear, depressed, comminuted, compound)
injury mechanism (blast, impact, missile)
primary vs secondary damage
severity (severe, moderate, mild)

176
Q

Impact injury types

A

acceleration or decceleration

coup or countercoup

177
Q

Missile injury types

A

penetrating (doesn’t exit)

perforating (enters and then exits)

178
Q

Clinical measurement of TBI

A 
LOC
AMS
GCS
PTA
Neuroimaging
179
Q

Consciousness for TBI

A

needs reticular formation
oriented and aware
syncope or bLOC= partial or complete interruption in awareness
coma= LOC no responsiveness, no sleep/wake cycles
vegetative state= no response, may have sleep/wake cycles, reflexive mvmnts

180
Q

Mental State TBI

A

level of arousal (responsive, clouding, lethargic, obtunded, stuporous)
content (appropriateness of responses)

181
Q

GCS

A

8 or less is severe
9 to 12 is moderate
13 or more is mild

182
Q

Medical management of TBI

A 
maintain ventilation and temp
reduce edema and ICP
medications
avoid anticholinergics and catecholamine blockers
growth factors
nutrition (protein rich diet)
gangliosides
stem cell transplant (?)
183
Q

Factors that influence TBI outcomes

A

features of lesion (smaller is better, primary cortex=more deficits)
time course of onset (slow progression=less deficits)
gender (women have more sparing b/c progesterone)
age (perinatal and older adults=greater impairment)

MOPs II (4 decks)

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