Sensorimotor Disorders Flashcards

Lecture 12

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
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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
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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
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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
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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)
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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)
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7
Q

what is the central sensorimotor program theory?

A

holds three main assertions:

  1. the lower levels of the sensorimotor system hierarchy possess “sensorimotor programs”, and those programs represent particular patterns of activity
  2. a particular movement is produced by activating the appropriate combination of these sensorimotor programs
  3. 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
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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
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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
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10
Q

what are the two main areas of the sensorimotor association cortex?

A
  1. dorsal lateral prefrontal cortex - important for executive function
  2. posterior parietal cortex
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11
Q

what process influence the learning of sensorimotor programs?

A
  1. response chunking - chunking info together helps us keep it in working memory
  2. 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
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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
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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
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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
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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)
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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
Q

what is the role of dopamine on the direct pathway?

A
  • dopamine 1 family receptors (D1R) have a positive modulatory effect (excitatory)
  • increases transmission in the direct pathway causing more movement
26
Q

what is the role of dopamine on the indirect pathway?

A
  • dopamine 2 family receptors (D2R) have a negative modulatory effect (inhibitory)
  • decreases transmission in the indirect pathway causing more movement
27
Q

what happens to the basal ganglia pathway in parkinson’s disease?

A
  • 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
Q

what are some treatments for parkinson’s disease?

A
  • 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
Q

what happens to the basal ganglia pathway in huntington’s disease?

A
  • 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
Q

what is the ventral tegmental area and what is it’s role in dopamine transmission?

A

VTA is also projecting to the basal ganglia and circuits are more strongly related to movement related to motivation

31
Q

how does drug use affect the ventral tegmental area (VTA)?

A
  • 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
Q

how is obsessive-compulsive disorder related to the basal ganglia?

A
  • 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
Q

how is tourette’s syndrome related to the basal gaglia?

A
  • 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