1
Q
what is top-down movement?
A
- we have an internally generated idea of how we want to move, and we generate that
- we are making a decision and controlling movement
2
Q
what is bottom-up movement?
A
- movement that is elicited by external stimuli (reflexes)
- inferior and superior colliculus are responsible for automatic movements elicited by external stimuli
3
Q
what is proprioception?
A
- we know where we are in space even if we can’t see because we can feel the stretch in our muscles
- sensory information allows us to correct our movements
- motor movement and sensory information create a loop that allow us to move in the way that we’d like
4
Q
what is a ballistic response?
A
- movement is so fast and forceful that they can’t be updated on the fly
- exception to the movement flow chart where sensory information allows for changes in motor movement
5
Q
who is patient G.O.?
A
- had damage to somatosensory nerves of his arm
- numerous problems with movement even though damage was sensory
- could no longer correct his movements because sensation was damaged
- sensorimotor feedback loop has been damaged (is now a closed loop)
6
Q
what is the model of hierarchical control of movement?
A
- we have multiple aspects of motor systems stacked on top of each other
- simplest to most complex: spinal cord, brainstem motor nuclei, primary motor cortex, secondary motor cortex, association cortex
- spinal cord - simplest motor control
- brainstem motor nuclei - cranial nerves
- primary motor cortex - last signal before efferent axons move to spinal cord (controlling muscles)
- secondary motor cortex - applying plans to the body
- association cortex - decisions and planning and association (PFC and parietal lobe)
7
Q
what is the central sensorimotor program theory?
A
holds three main assertions:
- the lower levels of the sensorimotor system hierarchy possess “sensorimotor programs”, and those programs represent particular patterns of activity
- a particular movement is produced by activating the appropriate combination of these sensorimotor programs
- once a particular level of the sensorimotor hierarchy is activated, it is capable of operating on the basis of sensory feedback without direct control by the higher levels
8
Q
what movement doesn’t require input from the brain?
A
- reflexes
- stepping responses, limb approach or limb withdrawal to tactile stimuli, stretch reflex
- can’t prepare future or prepare, just reacting to what’s happening right now
9
Q
what is motor equivalence?
A
- we can execute the same movement with different parts of our bodies
- if we learn a motor movement with one limb, the other limb can do it too
- there is an overlapping brain secondary motor cortex
10
Q
what are the two main areas of the sensorimotor association cortex?
A
- dorsal lateral prefrontal cortex - important for executive function
- posterior parietal cortex
11
Q
what process influence the learning of sensorimotor programs?
A
- response chunking - chunking info together helps us keep it in working memory
- shifting control to lower levels - as you become practiced, we don’t need as much activity from the association cortex
- responsibility moves to secondary and primary motor cortex and the association cortex can focus on other aspects of the environment
12
Q
what is the posterior parietal cortex responsible for?
A
- guides and orientates attention
- provides information on where body parts are in relation to the external world
- receives input from visual, auditory, and somatosensory systems (end of dorsal stream)
- output goes to secondary motor cortex
- stimulation of this area makes the subject feel they are performing an action
13
Q
what is the result of dysfunction of the posterior parietal cortex?
A
- apraxia: inability to perform movements on command, imitate gestures, and use tools
- associated with left hemisphere damage but symptoms are bilateral
- contralateral neglect: failure to respond to visual, auditory, or somatosensory stimuli
- produced by very large right parietal lesions
- individuals only attend to right side of the environment/body but are capable of unconsciously perceiving objects on the left
14
Q
what is the dorsolateral prefrontal cortex responsible for?
A
- receives projections from posterior parietal cortex
- projects to secondary motor cortex, primary motor cortex, and frontal eye field
- involved in assessments of external stimuli to make decisions regarding voluntary response initiation (may work with posterior parietal cortex)
- fires first in motor change
- important in decision making, voluntary movement
- also involved in many other functions (problem solving, math, working memory, learning)
- damage here affects a number of sophisticated cognitive functions
15
Q
what is the secondary motor cortex responsible for?
A
- eight areas: two areas of premotor cortex, three supplemental motor areas three cingulate motor areas
- projects to primary motor cortex, each other, and brainstem
- produces complex movements, before and during voluntary movements
- top-down movement
- supplemental motor areas important in planning, is internally guided (top-down)
- premotor movement is externally guided (encode spatial relations and program movements)
16
Q
what are mirror neurons?
A
- found that specific neurons fire when primates were observing, and when performing an action
- neurons in premotor cortex are essential in learning from observation
- are not just concerned with moving, but also with the intention of the movement
- may be related to theory of mind: different people have different internal lives
- may be related to empathy, understanding other’s emotion
17
Q
what is the primary motor cortex? how are the neurons here organized?
A
- is labelled M1, also called the precentral gyrus
- neurons of body parts that are next to each other, are next to each other as well
- somatotopic organization - map of the brain (homunculus)
- receives feedback from muscles and joints
- neurons code for preferred movement/direction, not for a specific muscle
18
Q
what happens when the primary motor cortex is damaged?
A
problems with:
- independent movement (fine motor control) - moving each finger separately
- astereognosia - recognizing something in our hands with no vision
- speed/accuracy/force
suggests that some secondary motor areas must have some control over movement (premotor) and signals might just go from secondary to spinal cord
19
Q
what is the role of the cerebellum in movement?
A
receives from inputs from:
- primary and secondary motor cortex
- information about descending motor signals from the brain stem nuclei
- feedback from motor responses via the somatosensory and vestibular systems
- compares our intended movements to our actual movements, and then corrects our motor behaviour (corollary discharge)
- is critical for both motor and cognitive timing and sequence
- ipsilateral control of the body
20
Q
what happens when there is damage to the cerebellum?
A
- loss of ability to precisely control the direction, force, velocity, and amplitude of movements
- loss of ability to adapt patterns of motor output to changing conditions
- impairments in the learning of new motor sequences
- disturbances in balance, gait, and the control of eye movement
- impairments on measures of attention and executive control, procedural memory, working memory, language and visual-spatial processing
21
Q
what is the basal ganglia?
A
- mainly the striatum and globus pallidus
- also consider the subthalamic nucleus, and substantia nigra pars compacta
- modulates motor output (classical view)
- important to execute effortless skills
- critical to habit formation and skill learning
- many cognitive roles
22
Q
what is tonic inhibition?
A
- our basal ganglia is constantly inhibiting our thalamus which inhibits spontaneous movement
- can activate basal ganglia to cause us to have less or more spontaneous movement
23
Q
what is the direct pathway of the basal ganglia?
A
- input comes from the cortex and feeds into the striatum, making it more active
- cells in striatum project to globus pallidus INTERNAL (GPI) making it less active (inhibits)
- the GPI is not able to fire or release GABA onto the thalamus (doesn’t inhibit)
- thalamus is not being inhibited so it releases glutamate on the frontal cortex which results in more movement
- results in disinhibition - inhibiting the (tonic) inhibitor
24
Q
what is the indirect pathway of the basal ganglia?
A
- input comes from the cortex and feeds into the striatum, making it more active
- cells in striatum project to globus pallidus EXTERNAL (GPE) making it less active (inhibits)
- the GPE is not able to fire or release GABA onto the subthalamic nuclei or GPI (doesn’t inhibit)
- GPI is free the release GABA onto the thalamus and inhibits it
- thalamus doesn’t fire and doesn’t release glutamate on the frontal cortex, which results in no movement
25
what is the role of dopamine on the direct pathway?
- dopamine 1 family receptors (D1R) have a positive modulatory effect (excitatory)
- increases transmission in the direct pathway causing more movement
26
what is the role of dopamine on the indirect pathway?
- dopamine 2 family receptors (D2R) have a negative modulatory effect (inhibitory)
- decreases transmission in the indirect pathway causing more movement
27
what happens to the basal ganglia pathway in parkinson's disease?
- there is a loss of cells in the substantia nigra pars compacta
- no dopamine signal is released onto the striatum
- less activity in the direct pathway and more activity in the indirect pathway
28
what are some treatments for parkinson's disease?
- L-DOPA → gets converted to dopamine and restores functioning in striatum
- but, too much dopamine could result in unwanted motor movements, and problems with gambling
- deep brain stimulation (DBS) of the STN → inhibits the subthalamic nuclei using an electrode
- neurons in the STN don't fire and don't excite the GPI, so the GPI can no longer inhibit the thalamus
29
what happens to the basal ganglia pathway in huntington's disease?
- striatal neurons that project to the GPE in indirect pathway die
- decreases transmission in the indirect pathway so tonic inhibition is eliminated
- is 100% hereditary, opposite of parkinsons, excessive movement, is fatal
30
what is the ventral tegmental area and what is it's role in dopamine transmission?
VTA is also projecting to the basal ganglia and circuits are more strongly related to movement related to motivation
31
how does drug use affect the ventral tegmental area (VTA)?
- all drugs of addiction directly or indirectly increase dopamine transmission from SNc and VTA
- reinforcing basal ganglia learning causes person to seek out more drug use when VTA is involved
- psychostimulant drugs like cocaine or amphetamines increase (at lower doses) goal-directed behaviours, impulsivity, and (at higher doses) repetitive behaviours (called stereotypy or punding)
- if dosage is too high in the pathway, there is an increase in purposeful behaviour and **purposeless** behaviour
- picking at skin and mouth, behaviour in common with primates
32
how is obsessive-compulsive disorder related to the basal ganglia?
- increased size/activity in some basal ganglial structures (caudate & putamen)
- decreased activity in some **basal ganglial structures** (globus pallidus)
- reduced D2R density in the basal ganglia → increased activity in indirect pathway (D2R reduces inhibition)
- marked by intrusive thoughts and behaviours to relieve distress of those thoughts
- they understand that it’s irrational and inefficient but can’t stop
33
how is tourette's syndrome related to the basal gaglia?
- neuroimaging suggests excess DA release in striatum
- overactivate direct pathway → spontaneous movement
- animal models suggest disinhibition in striatum
- block GABA receptors (antagonist) into the striatum → tics emerge
- problem is that there is too little GABA
PSYC 301
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