Sensorimotor Disorders Flashcards
1
Q
2 different causes of movement
A
- Top-down: you are voluntarily initiating movement (ex. Moving eyes to look for keys)
- Bottom-up: involuntary, automatic movement (ex. Automatically looking at bright, flashing light)
2
Q
Movement pathway
A
- Intention/decision/goal (ex. Make dinner) ->
- Motor plan (ex. Pick up onion, chop with knife) ->
- Motor signal (delivering components of the motor plan to places that will execute them) ->
- Movement ->
- Sensory feedback that influences motor plan and motor signal (ex. Were we chopping the onion well enough?)
3
Q
sensory feedback: what does it include? Case study?
A
- Includes proprioception (knowing where your body is in the world – ie. My legs are crossed)
- Case study: G.O. had damage to somatosensory nerves in arms -> could not get feedback -> numerous problems with movement
4
Q
Hierarchal control of movement
A
- Association cortex ->
- Secondary motor cortex ->
- Primary motor cortex ->
- Brainstem motor nuclei ->
- Spinal motor circuits ->
5
Q
3 main assertions of central sensorimotor program theory
A
- Lower levels of hierarchy possess “sensorimotor programs” that 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 higher levels (becomes automatized, doesn’t need cortex and higher-level structures anymore)
6
Q
Planning out movements - variations
A
- There is more than one way to carry out movement (ex. Signing your name with your toe)
- Primary motor cortex will be different, but secondary motor cortex should be the same
7
Q
practice and sensorimotor programs
A
- Practice can create and/or modify sensorimotor programs
- Most theories talk of two sorts of processes that influence the learning of sensorimotor programs:
- Response chunking
- Shifting control to lower levels
- Basal ganglia heavily involved
8
Q
2 major areas of sensorimotor association cortex and their function
A
- dorsal-lateral prefrontal cortex
- posterior parietal cortex
9
Q
dorsal-lateral prefrontal cortex
A
- Receives projections from posterior parietal cortex
- Projects to secondary motor cortex, primary cortex, and frontal eye field
- Involved in assessments of external stimuli
- May work with posterior parietal cortex in decisions regarding voluntary response imitation
- Fires first in the motor chain
- Decision-making, voluntary movement
- Critically involved in many other functions (ie. Problem-solving, math, working memory, learning)
- Damage here affects a number of sophisticated cognitive functions
10
Q
posterior parietal cortex
A
- Provides information on where body parts are in relation to the external world
- Receives input from visual, auditory, and somatosensory systems
- Output goes to secondary motor cortex
- Stimulation of this area makes the subject feel they are performing an action (even though they aren’t)
11
Q
2 outcomes of damage to posterior parietal association cortex
A
- apraxia
- contralateral neglect
12
Q
apraxia
A
- inability to perform movements on command, imitate gestures – especially non-sensical ones, and use tools
- Occurs when posterior parietal association cortex is lesioned
- Associated with left hemisphere damage
- Symptoms are bilateral
13
Q
contralateral neglect
A
- fail to respond to visual, auditory, or somatosensory stimuli
- Produced by very large right parietal lesions
- Individuals only attend to right side of body or items in environment
- Individuals are capable of unconsciously perceiving objects on the left
14
Q
secondary motor cortex
A
- Eight areas of secondary motor cortex
- Two areas of premotor cortex
- Three supplemental motor areas
- Three cingulate motor areas
- Projects to primary motor cortex, each other, and brainstem
- Produce complex movements (before and during voluntary movements)
- Exact role of these areas is unclear
- Premotor areas encode spatial relations and program movements
15
Q
organization of primary motor cortex
A
- Aka: precentral gyrus, M1
- Somatotopic organization: homunculus (Dr. Penfield played a large role)
- Receives feedback from muscle and joints
- Neurons code for preferred direction
16
Q
what happens when there is damage to primary motor cortex
A
- Damage is not as disruptive as you might think
- Independent movement
- Astereognosis (inability to know what an object is when it’s in your hand)
- Reduced speed/accuracy/force
17
Q
caveats to the movement hierarchy
A
- Cannot account for many notable motor disorders, for ex:
- Cerebellar disorders
- Effect of alcohol
- Parkinson’s disease
- Huntington’s disease
- Stereotypy and impulsivity in psychostimulant addiction
- not all processes that influence movement fit into the hierarchy (ex. 2 pathways of basal ganglia)
18
Q
cerebellum: receives input from
A
- Primary and secondary motor cortex
- Information about descending motor signals from brain stem nuclei
- Feedback from motor responses via the somatosensory and vestibular system
19
Q
cerebellum: functions
A
- Compares our intended movements to our actual movements, and then corrects our motor behaviour
- Not involved in ballistic movements (movements that are so fast there is no time for correction -> ie. Swatting a fly)
- Critical for timing and sequence (both motor and cognitive)
20
Q
cerebellum: effects of damage
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 situations
- Difficulties in maintaining steady postures (eg. Standing)
- 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
basal ganglia: parts
A
- Caudate nucleus
- Putamen
- Globus pallidus
- Subthalamic nucleus
- Substantia nigra
22
Q
basal ganglia: functions
A
- Modulates motor output (classical view)
- Critical to habit formation
- Many cognitive roles
- Promotes skill learning
23
Q
striatum
A
- caudate and putamen
- Contains D1 dopamine receptors (excitatory) and D2 dopamine receptors (inhibitory)
24
Q
thalamus is the key regular of…
A
conscious awareness
25
Q
2 pathways of basal ganglia
A
- “GO” pathway
- “STOP” pathway
26
Q
“GO” pathway
A
- direct, excitatory -> encourages behaviour
- In a normal state, GPi is telling motor cortex not to do anything (tonic inhibition)
- In GO pathway, we’re inhibiting that inhibition -> “disinhibition” -> motor cortex can now allow us to move
- Cortex excites striatum -> increases inhibition of GPi (which inhibits its ability to inhibit the motor cortex) -> motor cortex can move
27
Q
“STOP” pathway
A
- indirect, inhibitory -> discourages behaviour
- Cortex excites striatum, stratium inhibits GPe, which means output of GPi will be stronger and motor cortex is inhibited -> no movement
- Encourages inhibition of motor cortex
28
Q
basal ganglia: damage
A
- can affect ability to move
- whether or not movement happens depends on balance of activity between the 2 pathways of the basal ganglia
29
Q
dopamine’s role in 2 basal ganglia pathways
A
- When dopamine released, GO pathway gets stronger, STOP pathway gets weaker
- Substantia nigra releases dopamine onto striatum
- D1 (excitatory) increases transmission of GO pathway
- D2 (inhibitory) decreases transmission of STOP pathway
30
Q
Parkinson’s disease
A
- In PD, most of the dopaminergic neurons of the SNc die
- Therefore, dopamine not released onto striatum -> decreases transmissions in the GO pathway, increased transmission in STOP pathway
- Less GO, more STOP = diminished movement
- Treatment -> L-DOPA (dopamine replacement), deep brain stimulation of subthalamic nucleus
31
Q
Huntington’s disease
A
- Damages neurons in striatum, specifically the neurons that project to the GPe (indirect pathway) -> decreases transmission in indirect/STOP pathway
- Result: no stop -> excessive movement
32
Q
dopamine and reward
A
- Any drugs with addictive properties are increasing dopamine function -> even more GO, less STOP
- Pathways we’ve looked at are similar to those for reward, motivation, learning, habit formation
33
Q
Deep Brain Stimulation (DBS)
A
- Widely-used treatment for Parkinson’s, dystonia, tremor, and other movement disorders
- DBS field is expanding both clinically and technologically
- Clinically, better understanding of outcomes -> better target and patient selection
34
Q
When should DBS be offered as treatment for Parkinsons?
A
Previously offered only in late phases (after 13-14 years with disease), but is now offered earlier in order for greater response to drugs and less risk of surgical complication (one study recommends DBS after 7 years with disease)
35
Q
Pros of DBS to subthalamic nucleus vs. globus pallidus
A
- Motor benefits similar with each target
- Subthalamic nucleus shows greater benefits in reducing severity of symptoms and being cost-effective
- Globus Pallidus shows greater benefits for movement suppression and long-term effects of stability and cognitive outcomes
36
Q
Long-term outcomes of DBS (and ‘long-term DBS syndrome’)
A
- Enduring beneficial effect of surgery on motor fluctuations, tremors, etc. and may improve patient survival
- Does not halt disease progression
- ‘Long-term DBS syndrome’: axial motor problems (ie. freezing of gait, postural instability) experienced by those who use DBS long-term
37
Q
What form of DBS is effective for treating essential tremors?
A
DBS of the ventro-intermedius nucleus (Vim) of the thalamus
38
Q
What forms of DBS are effective for treating dystonia?
A
Globus pallidus pars interna
Motor thalamus and ventralis oralis posterior nucleus (Vop)
39
Q
What other movement disorders has DBS been used to treat?
A
- Huntington’s disease
- Tourette syndrome
- Ataxia in tremor patients
- Other movement disorders
40
Q
Future directions for BDS
A
- Uniting with advances in clinical neurology and neuromodulation from a technical perspective
- Integrating different tools to allow for safer and more accurate placement of electrodes -> optimized benefit
- Other methods will likely be available to correct abnormal neurological circuits and alter disease progression
