Motor and Sensorimotor Systems

Question 1

What were the Held and Hein experiments and what did they show?

Answer 1

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

Question 2

What are the three basic motor movement types?

Answer 2

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

Question 3

What is thixotropy?

Answer 3

History of a previous movement:
- Can produce different movement from same command or visa versa

Question 4

What is Moravec’s Paradox?

Answer 4

What artificial systems find east we find difficult and visa versa
- Recall of information vs. movement through environment

Question 5

How are motor neurons in the spinal cord organised?

Answer 5

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

Question 6

What types of muscle fibres exist? How can these fibres be recruited?

Answer 6

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

Question 7

What are two central competing theories of the organisation of the motor system?

Answer 7

Hierarchical
- Goal oriented
- Come from brain (descending)
- Slower

Reflexive
- In reaction to stimuli
- Ascending inputs

Question 8

How are locomotive patterns coordinated to achieve walking motion? How does speed change muscle recruitment?

Answer 8

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)

Question 9

What is the evidence that the spinal cord is a CPG without brain input?

Answer 9

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

Question 10

What is Brown’s half-centre theory for movement generation?

Answer 10

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]

Question 11

What are muscle spindle complexes and what information do they provide?

Answer 11

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]

Question 12

How do Golgi tendon organs prevent tendon damage?

Answer 12

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)

Question 13

Describe how the Knee-Jerk reflex works?

Answer 13

• 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.

Question 14

How are tendon organs and muscle spindles involved in CPG movement?

Answer 14

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.

Question 15

What evidence is there for modification of stretch reflexes under CPG (rather than brain) influence?

Answer 15

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)

Question 16

What are the main descending pathways for movement? What are they needed for?

Answer 16

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

Question 17

What are the different corticospinal tracts and what do they control?

Answer 17

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

Question 18

What is the function of the reticulospinal tract?

Answer 18

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

Question 19

What is the evidence for two way communication in descending spinal tracts?

Answer 19

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)

Question 20

What is the function of the vestibulospinal tract?

Answer 20

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))

Question 21

What is the function of the tectospinal tract?

Answer 21

Eye and Head movements:
- Coordinates 6 eye muscles in rapid small movements
- Saccade eye movements compensate for adaptation (re-activates areas of retina)

Question 22

Which modulatory molecules are used by the slow descending pathway?

Answer 22

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

Question 23

What is Dale’s principle and how was it disproven?

Answer 23

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).

Question 24

How is cerebral Palsy caused?

Answer 24

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

Question 25

Give 3 examples of pathologies associated with the descending tracts of the spinal cord:

Answer 25

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.

Question 26

What are two techniques to help acute spinal cord lesioning?

Answer 26

• 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.

Question 27

What are the areas contained in the motor cortex?

Answer 27

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)

Question 28

Compare the organisation between the sensory and motor cortical representations of the body.

Answer 28

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

Question 29

What is the evidence for the SMA being involved in movement planning?

Answer 29

• 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

Question 30

What is the function of the lateral motor area and what is the evidence for it?

Answer 30

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

Question 31

What are the feedback mechanisms that feed into the motor cortex?

Answer 31

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

Question 32

What methods have been trialled to recreate movement using artificial hands? What are the problems?

Answer 32

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

Question 33

What is the evidence for cortical plasticity in the motor cortex and how can it be improved?

Answer 33

• 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)

Question 34

Describe the structure of the cerebellum:

Answer 34

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]

Question 35

What is the organisation pattern? How are different patterns of excitation achieved in the cerebellum?

Answer 35

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)]

Question 36

What symptoms result from cerebellum lesions and what to they tell us about its role?

Answer 36

• 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)

Question 37

What are the inputs and outputs for the cerebellum?

Answer 37

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)

Question 38

What is the broad function of the basal ganglia? What are the constitute parts?

Answer 38

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

Question 39

What is the flow of information through the basal ganglia? Which substances cause modulation?

Answer 39

1. Input to caudate and putamen (excitatory = glutaminergic
2. Processing (permit movement?)
3. Output to thalamus
4. Enact in frontal lobes (including motor cortex for movement)

Huge modulation capacity:
- Synaptic plasticity
- Neuropeptides: dynorphin, substance P
- Neurotransmitter: DA, GABA

Question 40

Describe the direct and indirect pathways of the basal ganglia:

Answer 40

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)

Question 41

How does dopamine impact the direct and indirect pathways? How does this cause Parkinson’s disease?

Answer 41

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.

Question 42

What are treatment options for Parkinson’s disease?

Answer 42

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)

Question 43

How is Huntington’s disease caused? What are the symptoms?

Answer 43

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)

Question 44

What are the components of the vestibular system?

Answer 44

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

Question 45

How does the vestibular system account for the position of the rest of the body?

Answer 45

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

Question 46

What are the gaze fixing mechanisms employed to keep an image focussed during movement?

Answer 46

• 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)

Question 47

How are fast VORs achieved?

Answer 47

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

Question 48

How are gaze shifting mechanisms achieved?

Answer 48

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

Question 49

What is the feedforward model for vestibular reflexes and how is cerebellar involvement shown experimentally?

Answer 49

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)

Question 50

What is the Helmholtz model?

Answer 50

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

Question 51

How are VOR reflexes corrected in the cerebellum? What evidence supports the internal feedback model?

Answer 51

1. If VOR not equal and opposite, retinals slip may occur
2. Powerful climbing fibre input stimulated to granule cell in flocculus
3. 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)

Question 52

How do the basal ganglia and superior colliculus generate saccades with purpose?

Answer 52

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

Question 53

Draw Brown’s Half centre arrangement.

Answer 53

See notes.

Question 54

Draw a muscle spindle diagram and label.

Answer 54

See notes (useful diagrams in neuro).