Motor and Sensorimotor Systems Flashcards
What were the Held and Hein experiments and what did they show?
Suggested movement through the environment is necessary to develop visual function (provides feedback)
- Kitten experiments where movement was restricted, though vision intact
- Resulted in impaired vision
What are the three basic motor movement types?
Reflex (cough; knee-jerk):
- Require external stimulus
- Few muscle groups which are graded with stimulus
Rhythmic (e.g. walking):
- Several muscle groups
- Relatively stereotyped
Voluntary (e.g. speech; manipulating objects)
- Goal directed
- Highly modifiable
- No external stimulus required
What is thixotropy?
History of a previous movement:
- Can produce different movement from same command or visa versa
What is Moravec’s Paradox?
What artificial systems find east we find difficult and visa versa
- Recall of information vs. movement through environment
How are motor neurons in the spinal cord organised?
Organised in ventral horn (myelinated):
- Brachial and sacral plexus = enlargement of white matter due to arms/legs
- Flexor-extensor rule: dorsal = flex; ventral = extend
- Proximal-distal rule: medial areas = proximal muscles; lateral = distal
What types of muscle fibres exist? How can these fibres be recruited?
Type 1: Slow twitch
- Low tension
- Hight vascular
Type 2A: fast fatigue resistant:
- Higher tension
- Fast twitch
Type 2B: Fast twitch
- Highest force
- Short bursts
Recruited based on type; force required (rate of neuron firing) and number needed
What are two central competing theories of the organisation of the motor system?
Hierarchical
- Goal oriented
- Come from brain (descending)
- Slower
Reflexive
- In reaction to stimuli
- Ascending inputs
How are locomotive patterns coordinated to achieve walking motion? How does speed change muscle recruitment?
Repetitive cycles of swing (flexor muscles) and stance phases (extensor muscles)
- Coordinated between muscles in one limb and between limbs
Increasing speed requires shortening of stance phase (swing phase fixed):
- Reduces time to produce extensor force so higher power muscle units required
- Change of gait allows different pattern
Trade off between balance and complexity (humans need complex balance system but simpler to coordinate 2 legs)
What is the evidence that the spinal cord is a CPG without brain input?
Spinal interneuron circuit (do not need brain to generate movement)
- Dorsal root transected (supraspinal sensory information removed) – Legs of rat can still move in sequence
- Lamprey spinal cord can be isolated (completely from muscle) and still the spinal cord produces patterns of electrical activity
- Primate spinal cord activity shows CPG when all spinal cord inputs transected
- Muscles connected below lesion can still move (no brain input) – not voluntary but there is movement (not paralysed)
- Mike the headless chicken could walk and survived for >1 year
What is Brown’s half-centre theory for movement generation?
One half centre for flexion; one for extension.
- Excitatory interneurons of a half-centre activate both motor neurons and 1a inhibitory neurons for the opposing half-centre
- Activated muscles provide inhibitory feedback (via Renshaw neurons) to excitatory half-centre
- Allows switching between two half centres
[Think about diagrammatic representation]
What are muscle spindle complexes and what information do they provide?
Intrafusal fibres (receptors) act in parallel to extrafusal fibres (provide muscle force)
Muscle spindle fibres = active on muscle stretch:
- Chain fibres give duration of sustained stretch (innervated by static gamma efferent neurons)
- Bag1 fibres give dynamic (velocity) sensitivity (via type 1a adapting afferents)
- Bag2 fibres give static (length) sensitivity – via type II sensory afferents (non-adapting)
- Contractile section allows length determination (and efferent copy to cerebellum) = proprioceptive function
- Efferent γ fibres adjust length of intrafusal fibres to maintain sensitivity during contraction
[Draw diagram representing an intrafusal muscle spindle complex]
How do Golgi tendon organs prevent tendon damage?
Golgi tendon organs transmit information about muscle contraction (via afferent 1b fibres)
- Firing rate increases with tension (via 1b afferent)
- If force too high (danger of tearing tendon), inhibition of muscle contraction caused
Difference between intra and extrafusal length is perceived as stretch (see angel illusion experiment)
Describe how the Knee-Jerk reflex works?
- Hammer stretches the quadricep muscle, activating muscle spindle
- Pathway 1: afferent sensory neurons (1a) synapse with alpha motor neuron in dorsal root ganglion causing contraction of extrafusal fibres in quadriceps
- Pathway 2: sensory (type II) neurons synapse with an inhibitory 1a interneuron to alpha motor neuron, inhibiting hamstring (the antagonistic muscle) contraction
These two pathways prevent further stretch of the muscle which may result in injury.
How are tendon organs and muscle spindles involved in CPG movement?
During programmed motor sequence: tendon organs encourage activity (+ve feedback loop):
- Ankle extensor activity increased during walking
- Overactive tendon organs (+ve feedback) is dangerous (can overextend muscles causing damage) – E.g. grand mal seizure during electroconvulsive therapy
Muscle spindle reflex (keeps tendon organ under control) +ve feedback:
- Inhibit antagonistic muscles once extension reaches threshold.
What evidence is there for modification of stretch reflexes under CPG (rather than brain) influence?
Stim chamber experiment;
- Hoffman reflex evoked by electrical stimulation
- Up or down conditioning trained by giving food reward
Exercise effect in humans:
- Footballers show increased reflex magnitude
- Ballerinas show decreased magnitude (learn to ignore extension reflex)
Treadmill therapy:
- Muscle reflexes can be trained independently of brain (E.g. after lesion)
- Significant increase in motor activity after invoking sensory input (forced walking)
What are the main descending pathways for movement? What are they needed for?
For goal directed movement (not CPG)
Fast pyramidal pathway (mainly ionotropic):
- Corticospinal tracts (both lateral and anterior)
- Conscious
Fast extrapyramidal pathways (mainly ionotropic):
- Reticulospinal: simple motor patterns
- Vestibulospinal: balance
- Tectospinal: eye and head movements
- Rubrospinal: red nucleus connection (blink response?)
Slow pathway (mainly modulation):
- Spinothalamic: pain
- Spinomesencephalic: control and inhibition of pain
- Spinohypothalamic: emotional ties to pain
What are the different corticospinal tracts and what do they control?
Lateral (90% of fibres):
- Contralateral travel from brain level
- Synapse with lower motor neurons in ventral horn
- Innervate limb (distal) muscles
Anterior (10% of fibres):
- Decussate at desired spinal cord level
- Innervate muscles of trunk
What is the function of the reticulospinal tract?
General body orientation/simple patterns:
- Uses CPG and inputs from motor cortex/cerebellum
- Inputs from mesencephalic locomotor region (MLR) in cat: increased stimulation = increasing motor output speed patterns (walking to galloping)
- MLR to reticulospinal formation (RSF) to Spinal cord CPG
What is the evidence for two way communication in descending spinal tracts?
Brainstem spiking caused by fictitious movement:
- CPG activated by NMDA
- NMDA barrier prevents diffusion directly into brainstem
- Therefore activity due to ascending fibres
Efferent copy:
- Necessary for vestibulospinal tract function
- Compare copy with model and correct if necessary (cerebellar activity)
What is the function of the vestibulospinal tract?
Positional information and balance:
- Vestibular system collects positional information
- Vestibulo tract connects to muscles to correct change
- Achieved by efferent copy (feedback) from CNS – comparison of sensory feedback with predicted model from efferent copy (models are subtracted from each other (if the same = no reaction))
What is the function of the tectospinal tract?
Eye and Head movements:
- Coordinates 6 eye muscles in rapid small movements
- Saccade eye movements compensate for adaptation (re-activates areas of retina)
Which modulatory molecules are used by the slow descending pathway?
Predominantly aminergic with some neuropeptides
- Aminergic: 5-HT (Raphe nucleus) slows frequency of output and NA (locus coeruleus)
- Neuropeptides: substance P increases frequency of output, galanin, thyrotropin releasing hormone (TRH), NA, neuropeptide
What is Dale’s principle and how was it disproven?
Dale’s principle: one transmitter type from each neuron
Evidence against:
- Co-localisation of different transmitters from same neuron
- Control of release (amino acids small therefore closer to presynaptic membrane whereas larger may require larger depolarisation and recruitment).
How is cerebral Palsy caused?
Defects in descending system associated with changes to regulation of spinal reflexes:
- In normal infants spinal stretch reflexes occur in both flexor and extensor muscles. Adults only show stretch reflex in stretched muscle.
- Cerebral palsy adults show infant pattern – CPG never learns/matures appropriate response to forced extension
Give 3 examples of pathologies associated with the descending tracts of the spinal cord:
Cerebral palsy
- Defects in descending system associated with changes to regulation of spinal reflexes. - Shows importance of descending inputs to mature spinal function
Early lesion of corticospinal tract:
- Nociceptive inputs and corresponding movements are not coupled appropriately (increased chance of moving towards input)
Spinal cord Injury – CPG not lost but modulation and activation is.
What are two techniques to help acute spinal cord lesioning?
- Drugs to mimic activation (glutamate) and modulation (e.g. 5-HT) have had success in trials of acutely lesioned cats. E.g. clonidine (NA agonist)
- Create environment for neuronal growth – implant olfactory ensheathment cells (OECs) to provide route for neuronal growth.
What are the areas contained in the motor cortex?
Premotor cortex = planning movement
- No direct inputs to motor neurons but projections to brainstem/reticular formation
- Lateral premotor area: prepares motor system for movement
- Supplementary motor area (SMA): complex sequence planning (E.g. finger movement)
Motor cortex (homunculus representation) = execution of movement
Links to motor association areas (basal ganglia, cerebellum, prefrontal cortex)
Compare the organisation between the sensory and motor cortical representations of the body.
Similarities:
- Both on contralateral sides
- Both show homunculus with disproportionate area for functional activity (not actual size)
Differences:
- Motor cortex organised by functional programmes not anatomical representation (Fractured somatotopy vs. somatotopy)
- All sensory areas represented in brain; motor cortex mainly for distal muscles (proximal mainly spinal control)
- Not a line labelled code since single cortical neurons project to multiple spinal cord paths
What is the evidence for the SMA being involved in movement planning?
- Readiness potential: neurons fire ≈800ms before voluntary movements (Libet experiments)
- Preparation time increases with complexity
- Mirror neurons fire when observing someone else perform a task
- No direct links to motor neurons (cannot cause a muscle contraction directly) but fires during movement
What is the function of the lateral motor area and what is the evidence for it?
Prepares motor system for movement:(integrates sensory information):
- Inputs from posterior parietal cortex and projections to brainstem and reticulospinal system
- Lesions affect ability to develop movement strategies (subtle) – e.g. right superficial movement but inability to shape the hand correctly for obstacle avoidance
What are the feedback mechanisms that feed into the motor cortex?
Transcortical/Long loop stretch reflexes (60ms):
- Longer than muscle stretch reflex (35ms) but shorter than voluntary (120ms)
- Muscle spindle to thalamus to sensory/motor area to muscle (corticospinal tract)
- Mainly for distal muscles (modulated by cerebellum)
Higher order:
- Somatosensory, visual, vestibulocochlear input
What methods have been trialled to recreate movement using artificial hands? What are the problems?
Implantation of electrode array in motor cortex:
- Record ‘imagined’ movement; decode and then re-play to induce desired movement
- Problems: short lived effect (6-9 months) and lots of personal variation
Brain-machine-brain interfaces:
- Record activity from motor cortex to control a cursor (movement) and use stimulation of somatosensory cortex to provide feedback.
- Feedforward with feedback = much more successful
What is the evidence for cortical plasticity in the motor cortex and how can it be improved?
- Motor maps initially absent but develop with usage
- Small lesions can be overcome by reorganisation (larger regions cause representation loss)
- Reorganisation encourages by forcing activity of phantom limb
Problems:
- Phantom limb syndrome
- Training hand-arm transplant patients (initial activity is diffuse/inaccurate)
Describe the structure of the cerebellum:
Outer cortex: 3 layers with different cell types (repeating ‘folia modules’ = repeated computation in parallel):
- Molecular layer: parallel fibres of GC; basket cells (inhibitory); stellate cells (inhibitory)
- Purkinje layer: Purkinje cell bodies = inhibitory
- Granular layer: Granular cell bodies = excitatory; golgi cells (inhibitory)
Inner cortex (white matter and brain stem):
- Mossy fibres
- Climbing fibres (from interior olive)
Connections:
- Basket and Stellate cells synapse only Purkinje
- Golgi on mossy fibre
- Climbing fibre on purkinje (complex spike)
- Purkinje, climbing and mossy all feed into cerebellar nuclei
[draw diagram of connections]
What is the organisation pattern? How are different patterns of excitation achieved in the cerebellum?
Organised in IPSIlateral fractured somatotopic map
Direct pathway: input to deep nucleus to output:
- E.g. efferent copy
Indirect pathway: input through cortex (parallel processing) to output:
- Feedforward disinhibition of GCs (since stellate and basket cells excited (inhibit Purkinje so Granule cells less inhibited): leads to temporal window of excitation
- Feedback inhibition from Golgi cells which receive parallel input and inhibit granule cells: allows complex patterns of activation
Having tonic level of activity allows information through both mechanisms (particularly disinhibition)
[Think about circuit diagram (see notes)]
What symptoms result from cerebellum lesions and what to they tell us about its role?
- Ataxia = disruption of smooth movements (no sensory loss but bad integration)
- No paralysis (like lesion in motor area) but disruption of planning and execution
- Dysmetria = inappropriate displacement (E.g. overreaching) –> shows cerebellar role in movement modification
- Hypotonia = weakness
- Dysdiadochokinesia = inability to make rapid movements and decomposition of movements (reach by arm then wrist then hand movement not all together)
- Limb perturbation results in continued oscillation (rather than recovery to stability)
What are the inputs and outputs for the cerebellum?
Inputs:
- Feedforward inputs (for planned movements) from motor cortex
- Feedback: sensory information from dorsal spinocerebellar tract; muscle efferent copy from ventral
- Sensory feedback on the actual movement (visual; somatosensory)
- Vestibulocerebellum coordinates head and eye movements (input from vestibular nuclei in brainstem)
Output (modulation):
- Reticulo; rubro and vestibulospinal pathways
- Parallel processing (between cortex and nuclei as well as individual)
What is the broad function of the basal ganglia? What are the constitute parts?
Influences cognitive aspects of motor control (no direct spinal connections) – highly flexible system with physiological and limbic inputs.
Organised in striomes (chemical systems)
- Striatum including putamen (motor control) and caudate nucleus (eye/cognitive function)
- Globus Pallidus: external = input and connection to subthalamic nucleus; internal = output
- Subthalamic nucleus
- Substantia nigra: DA production
What is the flow of information through the basal ganglia? Which substances cause modulation?
- Input to caudate and putamen (excitatory = glutaminergic
- Processing (permit movement?)
- Output to thalamus
- Enact in frontal lobes (including motor cortex for movement)
Huge modulation capacity:
- Synaptic plasticity
- Neuropeptides: dynorphin, substance P
- Neurotransmitter: DA, GABA
Describe the direct and indirect pathways of the basal ganglia:
Direct pathway:
Caudate ➡ IGP and SN ➡ thalamus ➡ motor cortex ➡ movement
- Upregulation causes disinhibition of thalamus = more movement
Indirect pathway:
Caudate ➡ EGP ➡ subthalamic nucleus ➡ IGP ➡ thalamus ➡ cortex
- Upregulation causes disinhibition of subthalamic nucleus = less movement
Only output from thalamus and subthalamic nucleus are excitatory (all others inhibitory)
How does dopamine impact the direct and indirect pathways? How does this cause Parkinson’s disease?
D1R = upregulates direct pathway (increases cAMP in caudate = increase inhibition)
D2R = inhibits indirect pathway (reduces cAMP in caudate = less EGP inhibition)
Loss of dopaminergic cells from SN causes reduction of both pathways reducing initiation of movement.
What are treatment options for Parkinson’s disease?
Chemical:
- L-Dopa (dopamine itself cannot cross BBB)
- Dopamine receptor agonists;
- Foetal SN tissue transplants;
Electrical:
- Deep brain stimulation in IGP: subthalamic nucleus responds most (variable response due to exact neurons stimulated)
How is Huntington’s disease caused? What are the symptoms?
Symptoms: heritable, fatal disease with impairment in movements (chorea), speech and cognitive
- Both due to cell death itself and inflammation/distress following
- No treatment (late onset)
Cause: death of (up to 90%) cholinergic and GABAergic cells in caudate:
- Reduces indirect pathway activity: overexcitation of thalamus (excessive movement)
What are the components of the vestibular system?
Semicircular canals: detection of head movement
- 3 perpendicular canals (for each dimension)
- Hairs in both directions (head movement compared to endolymph (with inertia))
Utricle (horizontal) and saccule (vertical) orientation of the head:
- Combinatorial code determine head orientation
- Translational movement
- Hairs arranged in radii along (striola) to give directional selectivity = kinocilium
- Otoliths in cupula (gel-like substance) stimulate hair cells
How does the vestibular system account for the position of the rest of the body?
Neck:
- Feedforward control equal and opposite movement to the vestibular reflex
- Adjusted relative to reflex size and learned (achieved by cerebellum)
Body:
- Efferent copy from proprioceptors indicate body movement
- Vestibulospinal pathway activates antigravity (extensor)muscles to compensate
What are the gaze fixing mechanisms employed to keep an image focussed during movement?
- Vestibulocollic reflex: move head equal and opposite to body (pronounced in birds but not possible in humans with heavy head)
- Vestibuloocular reflex: move eyes equal and opposite to head/body (using set of 3 muscles on each eye; eyes move consensually)
- Optokinetic system: move eyes to follow slow movements of visual field (when too slow to activate VOR)
- Nystagmus: prevents reaching limit of ocular movement by ‘resetting’ gaze to central area (gives saw-tooth eye movement)
How are fast VORs achieved?
Feedforward mechanism: predicts eye movements:
- Afferents from semicircular canals ➡ vestibular nuclei and flocculus ➡ oculomotor nuclei neurons ➡ extraocular muscles
- Very fast pathway (large neurons; one interneuron and fastest twitch muscles)
Relies on calibration: eyes must move in equal and opposite direction and velocity to head
- Learned calibration from input to flocculus in cerebellum (flocculus) which feeds back to vestibular nucleus
How are gaze shifting mechanisms achieved?
Saccades – foveate stimuli:
- Organised by superior colliculus (contains retinotopic map of visual world)
- Retina ➡ SC ➡ brainstem ➡ eye muscles
- Deeper SC layers project to brainstem (control oculomotor nuclei) to focus on new target area (e.g. move central vision to target in peripheral vision)
- Inputs from basal ganglia to process conflicting desires
What is the feedforward model for vestibular reflexes and how is cerebellar involvement shown experimentally?
Estimate future state based on current information then compare intention to actual outcome to modify future events (E.g. Helmholtz model)
- Cerebellar reliance
- Visuomotor adaptation – use mediolaterally inverting glasses to flip world then learning occurs to become accurate again over time
- Control of spinal reflexes – standing on a shifting platform, second movement will be much better compensated for (Nasher experiments)
What is the Helmholtz model?
Cerebellum compares exafference signal (from outside world) to re-afference signals (from own movement) for visuomotor system.
- Not proprioceptor afferent as cutting them has no affect on visuomotor perception
How are VOR reflexes corrected in the cerebellum? What evidence supports the internal feedback model?
- If VOR not equal and opposite, retinals slip may occur
- Powerful climbing fibre input stimulated to granule cell in flocculus
- Modulates Purkinje cell activity (via parallel fibres)
Experiments comparing passive head movement to voluntary movement:
- Similar movement but only activity in cerebellum when movement enforced (not expected from efferent copy)
How do the basal ganglia and superior colliculus generate saccades with purpose?
Superior colliculus gives ‘robotic’ mechanism to generate saccade towards a visual stimulus.
Basal ganglia compares conflicting stimuli and triages.
- Superior colliculus under continuous inhibition from GP
- Inhibition released if inputs activate appropriate cells in caudate/putamen (to inhibit output cells) ➡ allowing disinhibition of superior colliculus
Draw Brown’s Half centre arrangement.
See notes.
Draw a muscle spindle diagram and label.
See notes (useful diagrams in neuro).
