Sensorimotor Dysfunction Flashcards
Even “simple” behaviours are mediated by how many parts of the brain?
- MANY
- EX: a tennis player receiving a serve - involves premotor cortex, amygdala, etc.
Sensation, movement planning, and execution are always WHAT? What do they rely on?
- Always intertwined
- Large reliance on feedback
Sensory feedback
Our sensory systems monitor the body’s responses -> feed that information BACK to sensorimotor circuits, so they can take it into account and build on it
Examples of sensory feedback
- Ballistic movements (e.g. swatting)
- Reflexes (e.g. yanking hand away)
Hieararchical organization of the motor system:
- Association cortex
- Secondary motor cortex
- Primary motor cortex
- Brainstem motor nuclei
- Spinal motor circuits
AKA, movement going from a plan -> actual production (sending plan down brain, brainstem, spine, and out towards the body via motor neurons)
* First levels: “chop an onion”
* Middle levels: reach hand toward onion (refining movement)
* Final levels: extending arm and opening hand (specific motor sequence)
Hieararchical organization of the motor system: IN PARALLEL, 2 structures:
- Basal ganglia
- Cerebellum
- Responsible for managing these movements and modifying them as we go (to make sure sequence is good)
During the hierarchical organization of the motor system, how is information being received?
- ALL THE TIME: real time, “online” sensory feedback
What is the role of the lower HOMS levels in this real time, sensory feedback?
- Lower levels of the HOMS have sensorimotor programs
- Once active, these programs can operate without higher control (first learning how to ride a bike - you’re thinking about it a lot, but over time these processes become automatic)
Why should our motor system be flexible?
- Living in a complex, world, reflexes just aren’t enough
- Can see this in the principle of motor equivalence: there;s more than one way to carry out a movement (EX: writing with left hand, right hand, foot - all produce similar letters despite different approaches)
BREAKING DOWN HOMS
In reference to association cortex:
Involves…
* Posterior parietal association cortex
* Dorsolateral prefrontal association cortex
Posterior parietal association cortex
In reference to association cortex:
- Integrates information about the current position of body parts with information about external objects you may act upon
- Receives inputs/raw information from all systems (visual, auditory…) to make a plan of action
- Stimulation can make the patient feel like they’re performing an action
Posterior parietal association cortex DAMAGE
In reference to association cortex:
- Contralateral neglect: dysfunction of attention
- Apraxia: impaired voluntary movement (associated with left hemisphere damage - symptoms are bilateral)
Apraxic errors particularly for:
* Imitation of gestures
* Performance of gestures on command
* Use of tools and objects in unusual contexts
Dorsolateral prefrontal cortex (dlPFC)
In reference to association cortex:
- Involved in evaluation of external stimuli and the initiation of voluntary reactions (decide and react: phone is ringing, do I walk over and pick it up?)
- Gets this initial information from the posterior parietal association cortex
- Some of the first neurons fire here when anticipating a motor movement -> decision to act may begin here
- Also involved in cognition (e.g. problem solving, math…)
What changes with movement practice?
- As a movement is practiced, effort goes away or there’s less activity
- People start response chunking - sequence treated as a unit (opposed to a bunch of different things, when first learning how to do something)
- Shifting control to lower levels
In reference to secondary motor cortex:
- 8 areas of secondary motor cortex (premotor, supplemental, cingulate)
- ALL receive information from the association cortex and send them on to primary motor cortex
- Produce and guide complex movements in space
Mirror neurons
In reference to secondary motor cortex:
- In ventral promotor cortex and other locations
- Have the property of firing both when you carry out an action and when you see that same action being done by the same individual
- Potentially related to the theory of the mind, empathy
- Most ebidence is from monkeys as single-neuron resolution is needed
In reference to primary motor cortex (M1):
+ lesion effects
- Somatotopically organized (PENFIELD = stimulation experiments)
Lesion effects: show less dysfunction than you may think
* disrupted ability to move one body part independently of others
* may produce astereognosia
* may reduce speed, acuracy, and force of movements
Cerebellum
Basal Ganglia + Cerebellum
Receives inputs from:
* primary and motor cortex
* Information about descending motor signals from the brain stem nuclei
* Feedback from motor responses via the somatosensory and vestibular systems
ALLOWS US TO COMPARE intended movements to actual movements
Critical for sequencing and timing of movement
Cerebellar Damage
Basal Ganglia + Cerebellum
Many possible effects:
* Loss of ability to precisely control the direction, force, velocity, and amplitude of movements (ataxia/dysmetria) - affecting gait, eye movements
* Loss of ability to adapt patterns of motor output to changing conditions
* Impairments in learning new motor sequences + others
Basal Ganglia
Basal Ganglia + Cerebellum
- Like cerebellum, modulate motor output
- DON’T contribute to sending information to spinal cord - rather, all activity is receiving information IN the brain and sending information IN the brain
ALSO:
* critical to habit formation
* many cognitive roles
* promotes skill learning
2 pathways in the Basal Ganglia
Basal Ganglia + Cerebellum
- Two pathways in balance involving cortex, basal ganglia, and thalamus
- At rest, BG inhbit the motor/premotor areas = no movement (STOP pathway)
- To activate motor cortex, we must inhibit the inhibition (dishinhibition) via dopamine signalling from the substantia nigra (GO pathway)
Dysfunction within the 2 Basal Ganglia pathways
Basal Ganglia + Cerebellum
Parkinson’s disease:
* Most dopaminergic neurons of the substantia nigra die (thus, less GO)
* Results in diminished movement, particularly movement initiation
* Initial symptoms: stiffness, resting tremor (during inactivity)
* later symptoms: muscular rigidity, slow movement, “mask-like” face, pain, depression
Treatment for Parkinson’s
Dysfunction within the 2 Basal Ganglia pathways
- L-Dopa (dopamine precursor)
- Deep brain stimulation of substantia nigra
Huntington’s Disease
Dysfunction within the 2 Basal Ganglia pathways
- Affect neurons across the brain, particularly striatum
- Decreases tonic inhibition (STOP) leading to excessive movement
- Rare and highly genetically determined
- No strong treatment options
