Exam 3 Flashcards
(183 cards)
1
Q
What tracts come out of M1?
A
axons of CST and CBT
2
Q
Motor heirarchy
A
Highest level= mvmnt selection, planning intiation
Middle level= balance, posture, sensorimotor integration
Lowest level= volitional and reflexive mvmnt regulation
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
4
Q
What parts of the CNS do the middle level in the motor hierarchy?
A
cerebellum
vestibular nuclei
reticular formation
5
Q
What parts of the CNS do the lowest level in the motor hierarchy?
A
spinal cord
6
Q
Neural circuit for coordination of voluntary movement
A
UMN from cortex descends to synapse on LMN and interneurons
7
Q
Motor Pathway generalizations
A
Medial= posture and proximal limb movements
lateral= distal limb mvmnts
lateral CST= fine motor hand mvmnts
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
9
Q
Population code
A
activity of everyone together is interpreted as the outcome
10
Q
How is the motor cortex a population code?
A
info that is encoded in the population code has multiple movement parameters
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
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
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
14
Q
Discoveries in 1990s on cortical control of mvmnt
A
Caminiti et al
pop code more accurately reflected movement
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
16
Q
Dorsal premotor area
A
activities performed from memory and planning/holding mvmvnt
17
Q
Medial supplemental motor area
A
bimanual task coordination
important with tool use
18
Q
Parietal area 5
A
receives input from sensory to give update on how things are going
can give course correction
19
Q
What is the Basal Ganglia made of?
A
Collection of nuclei
20
Q
name the principle nuclei of the Basal Ganglia
A
caudate nucleus nucleus accumbens putamen globus pallidus substantia nigra subthalamic nucleus
21
Q
What are the different parts of the substantia nigra?
A
pars compacta
pars reticulata
22
Q
Is the subthalamic nucleus GABA or glutamatergic?
A
Glutamatergic
enhances inhibition to thalamus
23
Q
Define disinhibition
A
removal of inhibition
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
25
What does the Basal Ganglia do?
```
sequencing through movements after initiation
prevent unwanted movement
opponent parallel pathways
learning routines and habits
attention
reward-related learning
```
26
4 Main Loops of Basal Ganglia
skeletomotor
oculomotor
associative cortical
limbic
27
Skeletomotor BG loop controls what?
facial, limb, trunk mm
28
Oculomotor BG loop
saccadic eye movement
29
Associative cortical BG loop
strategic planning of behavior
30
Limbic BG loop
motivation, emotion, learning
31
How are the BG loops arranged in the brain?
parallel along longitudinal axis
32
BG loop sequence
Cortex->striatum->output nuclei->thalamus->cortex
33
Explain the striatum
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)
34
What are the output nuclei
globus pallidus internal
| substantia nigra pars reticulata
35
Which thalamic nuclei are involved in BG loops?
Relay nuclei
| VA/VL/MD
36
Is the BG loop a positive or negative feedback loop? How/why?
Positive (dynamic)
helps derive reptition that derives neuroplasticity
postive feedback to cortices that are doing something relevant to what we want to be doing
37
Is corticotopic mapping present for direct or indirect loops?
Direct
| loops separate from one another in global pattern
38
Direct BG loops
end precisely where they started in cortex
disinhibition of thalamus resulting in increased output to cortex
D1 cells
39
Indirect BG loops
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
40
What does dopamine do with BG loops?
causes release of G protein that can change cell excitability
increases both pathways but the difference between indirect and direct loops is maintained
41
Facilitation (related to dopamine)
more excitabile
| D1 (dopamine) receptors
42
Inhibition (relation to dopamine)
less excitable
| D2 receptor
43
Where is DA made?
substantia nigra pars compacta and VTA
44
What does the cerebellum do?
monitors sensory input and makes changes
45
Name the 3 cerebellar lobes
lateral
intermediate
medial
46
Folia
Ridges of cerebellum
47
Vermal/medial zone of cerebellum function
eye movements, vestibuloocular coordination, axial mm for balance and posture
48
Intermediate zone of cerebellum function
reach and grasp
| neck, trunk, and limb mm
49
What does damage to the intermediate zone of the cerebellum result in?
tremor
50
Lateral zone of cerebellum function
modulation of fine control of movements and motor learning
| mental agility, smoothness of thought, stability of affect
51
Name the 3 cerebellar layers
granule cell layer
purkinje cell layer
molecular layer
52
What is found in the granule cell layer of the cerebellum
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
53
What is found in the Purkinje cell layer of the cerebellum?
soma
54
What is found in the molecular layer of the cerebellum?
purkinje cell dendrites
55
What are climbing fibers?
to deep cerebellar nuclei
role is under research
wrap around purkinje dendrites
56
what are mossy fibers?
input all along rostral caudal axis
| go through cerebellar peduncles
57
What is the activity type of deep cerebellar nuclei?
spontaneously active
58
How can DCN firing rate be sped up?
through mossy fibers
59
How can DCN firing rate be slowed down?
through purkinje neurons
60
How are cerebellar loops arranged?
along the sagittal plane
61
are cerebellar loops positive or negative feedback loops?
positive
62
Describe the inputs for cerebellar loops
from cortex via contralateral pontine nucleus
from spinocerebellar pathways
cranial nn
Input comes on mossy fibers
63
Describe input divergence for cerebellar loops
input diverges to cerebellar cortex and deep cerebellar nuclei
cortext also connected as input to DCN
64
Purkinje neurons
Gabaergic
provide inhibition
synapse into DCN
spontaneously active
65
Inferior olive
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)
66
What happens when the cerebellum is damaged
results in movements that are erratic in size, force, and direction
67
Development of cerebellum
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
68
Parkinson's disease symptoms
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
69
Parkinson's disease causes
bilateral degredation of dopaminergic neurons in substantia nigra pars compacta with Lewy bodies
70
How would you treat mm spasticity?
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
71
Huntington's disease
progressive and terminal
beings in mid-adulthood with choreoform movements
autosomal dominant
72
Do basal nuclei lesions result in positive or negative symptoms?
positive
result in unwanted behaviors and movements
cortical activity not being inhibited
73
Lesions of UMN: acute phase
posturing then flaccid paralysis
74
What is posturing?
type of paralysis
| decortitate (lesions above MB) or decerebrate (lesions below MB)
75
What is our role in the UMN lesion acute phase?
```
limb protection
PROM
positioning
monitor edema
client/family education
monitor return of reflex and sensation
```
76
Lesions of UMN: chronic phase
```
spasticity
rigidity
hyperreflexia
emergence of voluntary control
loss of fine hand movements
anosognosia
```
77
What is the direction of UMN lesion recovery?
proximal to distal
78
Chorea movements
continuous rapid movements
| fragments of normal voluntary movements
79
athetosis movements
slow and writhing
80
hemiballismus movements
wild and flailing in one arm and leg
81
What type of movements result from an inbalance b/w the direct and indirect basal ganglia pathways?
chorea and athetosis
82
Dystonia
abnormal mm tone in group of mm resulting in asymmetric posture
83
Rett syndrome
```
present typical until 6-18 months
then regression
loss of communication and purposeful hand mvmnts
ataxic gait
disorganized breathing
inconsolable
```
84
Tourette's syndrome
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
How is tourette's syndrome treated
dopamine antagonists
| maybe CBT and mindfulness
86
Chiari malformations
```
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
Limbic lobe makeup
medial temporal lobe
insula
piriform cortex
entorhinal cortex
88
Mossy fibers that synapse into (blank) synapse into (blank)
lateral lobe; dentate nucleus
intermediate lobe; interposed nuclei
medial lobe; fastigual nuclei
89
Input to the hippocampus
from cortex (sensory, prefrontal)
simultaneous from 2 converging pathways (creates opportunity for coincidence detection)
amygdala
hypothalamus
90
Output from hippocampus goes where?
cortex
striatum
hypothalamus
91
Role of hippocampus
memory consolidation
| memory of thought, experience, spatial navigation
92
What is the fornix?
major outflow tract of hippocampus
93
Amygdala
emotional memory
| formation/storage of emotional valence of events
94
What are the limbic structures
```
nucleus accumbens and ventral pallidum (center of reward system; implicated in diseases of addiction)
hippocampus
amygdala
medial temporal lobe
prefrontal cortex
```
95
Medial PFC
context cues
comparing current situation to memories
emotional regulation
96
Dorsolateral PFC
working memory and memory retrieval
97
Orbitofrontal cortex
motivation
| social awareness
98
Anterior cingulate gyrus
inhibition
99
Name the 10 principles of neuroplasticity
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
Hebbian learning
cells that fire together wire together
101
Long term potentiation
needs persistant strong activation
coincident pre and post synaptic activity
postsynaptic CA2+ entry
102
Long term depression
results from persistant weak activation
103
Cognition
thinking and executive function
104
Thinking components (4)
language
calculation
reasoning
concepts
105
Executive function components (4)
self-monitoring
self-awareness
initiating
goal setting/planning
106
Attention enhancement
contrast
movement
meaning
107
Exogenous attention
automatic orientation to stim
| posterior parietal cortex
108
Endogenous attention
voluntary control of attention, choice
prefrontal cortex
can speed exogenous reaction time
109
Selective attention
attention to one thing and exclusion of others
110
sustained attention
can increase through practice
111
Multitasking
not an actual thing
| cannot cognitively attend to more than one thing at a time
112
Task-switching
what we are really doing when we think of multitasking
lose time
requires 3 brain networks (alerting, orienting, executive)
harms productivity
113
Working memory
retain and manipulate information for immediate use
114
inhibition
suppress or delay response to stim or thought
115
Emotion
speeds detection of risk
facilitates interventions and adds value
learned response to stimuli
physiological and motor changes cognitively interpreted as feelings
116
Primary emotions
```
fear
anger
sadness
joy
surprise
disgust
contempt
```
117
Secondary emotions
shame and guilt
| self-conscious emotions
118
Reward
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
Aversive stimuli
```
function opposite of reward
decrease likelihood of behavior
```
120
Motivation
initiates behavior through aim of getting a reward
121
Anticipatory mechanisms
Prepare for need or future reward now
122
Ecological constraints
cost-benefit analysis
123
Hedonic factors
feel good when you receive them
124
How can you tell if someone learned something?
Something changed about a person if they learned
125
Non-associative learning
single-trial learning
| habituation and sensitization
126
Types of learning
operant
associative
non-associative
127
Memory
retain information and reconstruct experiences for present use
128
Process of memory
encoding (multimodal) to consolidation (storage in synapses/synaptic network) to retrieval (recall, recognition, relearning)
129
Types of memory
working memory
procedural (how; cerebellum and basal ganglia)
semantic (what; temporal lobe)
episodic (when; temporal lobe, hippocampus, prefrontal cortex)
130
Dementia
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
Dementia tx first steps
rule out treatable causes that could result in short-term dementia (nutrition, UTI, tumors, hydrocephaly)
132
Alzheimer's Disease
```
memory impairment
word-finding difficulties
visual/spatial confusion
impaired reasoning and judgement
personality changes
hallucinations
delusions
paranoia
```
133
Tx for Alzheimer's
Cognitive/behavior training
Environmental mods
Exercise
Meds
134
What causes Alzheimer's
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
Circadian rhythms
```
primes sleep
adjusts to env
intrinsic cyclical pattern
25 hours
driven by superchiasmatic nucleus
```
136
Drive
behavior to reduce and address intrinsic need
137
Thermoregulation
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
Fever
set point by septal nucleus
| adjusted in response to pyrogens
139
Metabolism states (2)
1. prandial-recently eaten, abundance of nutrients in blood supply (free energy-glucose and lipids)
2. Postabsorptive-stored energy (glycogen and triglycerides)
140
How do we switch metabolism states?
brain
| responds to presence of insulin secreted that triggers to transform nutrients into stored energy
141
Satiety
signal that we have consumed what we need to
| smell/texture/taste, stomach distentation (CN X, area postrema), caloric intake signaled by liver
142
What satiety signal are infants missing?
caloric intake
143
Hunger signals
limbic and prefrontal cortex
ventral HT
PNS (stomach growling)
GI secretion of ghrelin
144
Thirst functions
need enough water to maintain correct concentrations, volume, and to get rid of waste
145
Osmoreceptors
extend beyond blood brain barrier
| sample concentration of blood
146
HT role in thirst
HT smaples concentration of blood
| if too concentrated secretes antidiuretic hormone
147
Sleep stages
```
Non REM (stage 1 light sleep to stage 4 deep sleep)
REM (dreaming, rapid eye movement)
```
148
Which sleep stages are low amplitude high frequency
Stage 1, REM, wakefulness
149
Which sleep stages are high amplitude, low frequency
Stage 4
| delta waves
150
What is the function of sleep
energy conservation
restoration
repair
memory consolidation
151
Narcolepsy
daytime sleepiness with sudden and unwanted episodes of REM sleep
152
Sleep apnea
obstruction of upper airway leads to frequent brief arousals from sleep
153
Insomnia
difficulty falling asleep
154
Insufficient sleep syndrome
voluntary restriction of daily sleep time requiring a week or more of restorative sleep
155
What layer does the nervous system develop from? ectoderm, mesoderm, or endoderm
Ectoderm
156
List process from neural plate to neural tube
neural plate stimulated by notochord to become neural crest (sonic hedgehog protein and chem)
then neural crest to neural tube
157
Notochord
part of mesoderm
| becomes body of vertebrae
158
Components of neural development
neurogenesis (neurulation and directionality)
segmentation
neural migration and differentiation
axonal pathfinding
159
Segmentation (3 + 5)
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
describe crest cell migration
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
How does the brain develop inside out?
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
Critical period vs sensitive period
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
Explain axonal pathfinding
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
Types of cues for axonal pathfinding
contact attraction and chemoattraction (filopodia contact and move in that direction
contact repulsion and chemorepulsion (filopodia repulsed and move in opposite direction)
165
Spina Bifida
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
Chiari Malformation
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
Holoprosencephaly
sonic hedgehog gene
Alobar-not survivable
semilobar- lifespan of 5 years; seizures, blindness, little voluntary movement
lobar- IDD pathologies
168
Agenesis of Corpus callosum
subtle to mild to severe
corpus callosum not formed
can go undetected
169
Enriched vs sparse environment
enriched is better for development
| sparse env can lead to brain underdevelopment
170
What is the most common cause of TBI?
motor vehicle accidents
171
TBI
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
Primary TBI damage
damage at tissue level or cellular level
173
Secondary TBI damage
brain/body responding to primary damage
neurochemical changes leading to futher apoptosis
atrical hypotension, ischemia, edema, hypoxia, increased ICP, hydrocephaly
174
Concussion
```
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
TBI classifications based on
Skull injury (open, closed, linear, depressed, comminuted, compound)
injury mechanism (blast, impact, missile)
primary vs secondary damage
severity (severe, moderate, mild)
176
Impact injury types
acceleration or decceleration
| coup or countercoup
177
Missile injury types
penetrating (doesn't exit)
| perforating (enters and then exits)
178
Clinical measurement of TBI
```
LOC
AMS
GCS
PTA
Neuroimaging
```
179
Consciousness for TBI
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
Mental State TBI
level of arousal (responsive, clouding, lethargic, obtunded, stuporous)
content (appropriateness of responses)
181
GCS
8 or less is severe
9 to 12 is moderate
13 or more is mild
182
Medical management of TBI
```
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
Factors that influence TBI outcomes
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)
