Motor systems

Question 1

Damage to motor neurons

Answer 1

Flaccid paralysis

Question 2

Damage to primary motor cortex

Answer 2

Spastic paralysis with exaggerated spinal reflexes

Question 3

Damage to brainstem pathways

Answer 3

Postural defects and problems with walking

Question 4

Damage to higher cortical areas

Answer 4

Apraxia: movements aren’t ordered or appropriate to the situation

Question 5

Damage to the cerebellum

Answer 5

Ataxia: poorly coordinated movements that may be the wrong size or shape

Question 6

Damage to the basal ganglia

Answer 6

Hyper/hypokinesia since BG involved in action selection

Question 7

Problems with negative feedback

Answer 7

Biological delays, so signal continues while correction starts
-> Over correction and oscillation around a set point

Question 8

Slow fibre properties

Answer 8

Anatomical: few fibres/unit, small
Biochem: oxidative, high myoglobin
Physiological: slow twitch, low tension, fatigue resistant, slow axons

Question 9

Fast fibre properties

Answer 9

Anatomical: large, lots of fibres/motor unit
Biochem: glycolytic, little myoglobin
Physiological: fast twitch, high tension, fast axons, fatiguable

Question 10

Size principal of motoneuron recruitment

Answer 10

Low force units, the slow fibres, are active at low rates of stimulation
As force increases, get recruitment of higher force units
This means the increase in force is via the smallest increments possible to give smooth contraction

Question 11

How does size principal of motoneuron recruitment come about

Answer 11

Lowest threshold motoneurons innervate few fibres and induce them to become slow, low force, fatigue resistant
Higher threshold motoneurons innervate more fibres, inducing them to become fast, fatiguable fibres

Question 12

Muscle spindle afferents

Answer 12

Signal passive stretch

Question 13

Tendon organ afferents

Answer 13

Signal tension, including active tension from muscle contraction
(as well as due to bones being pulled apart with passive stretch)

Question 14

Bag fibres

Answer 14

Central region full of nuclei with no striations

Signal changes in length very well, mainly via primary spindle afferents

Question 15

Chain fibres

Answer 15

Nuclei and striations throughout so stretch acts equally along fibre
Signal static length via secondary spindle afferents mainly

Question 16

Gamma motoneurons

Answer 16

Innervate the ends of intrafusal fibres to make them contract to alter sensitivity of the spindles; so they have similar sensitivity despite changes in starting length of the spindle

Question 17

Problems with stretch reflex proposal

Answer 17

Gain is measured to be less than 1 so can’t be a fully compensatory contraction for unexpected loads

Delays due to negative feedback would lead to muscle oscillation

Question 18

Spasticity

Answer 18

Due to damage to descending pathways

• Exaggerated high gain stretch reflex
• Brisk response to tendon tapping and oscillating contraction; myoclonus

Question 19

When are gamma motoneurons very active

Answer 19

During slow high gain reflexes such as walking on a beam

Question 20

Reciprocal inhibition

reflex inhibition accompanying stretch reflex

Answer 20

Primary spindle afferents innervating inhibitory motoneurons off antagonistic muscles to prevent them working against the other contraction

Question 21

Recurrent inhibition

reflex inhibition accompanying stretch reflex

Answer 21

Via Renshaw cells
Primary spindle afferents activate inhibitory interneurons of the same motoneuron pool (renshaw cells); type of negative feedback to prevent jerkiness and tremor

Question 22

Tendon organ context dependent reflexes

Answer 22

Tendon afferents can activate alternate pathways depending on context e.g when walking compared to at rest

Question 23

Infant specific reflexes

Answer 23

Babinski’s sign/plantar reflex
Grasp reflex
Reflex stepping

Question 24

Central pattern generators

Answer 24

Intrinsic circuit within spinal cord to simplify a patterned movement e.g walking; just need brain input to start and stop

Most vertebrates have spinally generated locomotion but humans have lost this (except reflex stepping)

All have CPG in brainstem for breathing

Question 25

Reticulospinal pathway

Answer 25

Ventromedial From reticular formation Drives spinal motor control, activating CPGs and whole body stereotypical actions

Question 26

Vestibulospinal pathway

Answer 26

Ventromedial From vestibular nuclei For balance and anti-gravity extensor action

Question 27

Tectospinal pathway

Answer 27

Ventromedial From rostral/superior colliculi For sensory orientation of the body; head, eye, trunk movements

Question 28

Rubrospinal pathway

Answer 28

Dorsolateral Crossed From red nucleus in midbrain Involved in limb movement

Question 29

Corticospinal pathway/pyramidal

Answer 29

Dorsolateral From cortex via brainstem to spinal cord Goal directed movement esp upper limbs used for manipulation

Question 30

Vestibular reflex: postural instability

Answer 30

Head movement generates vestibular signal which acts via feedforward pathway to generate extensor contraction to hold body up -> Predictive feedforward command learnt using cerebellum

Question 31

Vestibular reflex: neck reflexes

Answer 31

Neck proprioceptors used to work out if we are falling or if neck just being bent They generate equal and opposite signals to vestibular reflex so there is no loss of equilibrium Cerebellum learns this; uses efferent copy to predict expected head movements (when bending neck) to work out what vestibular signals will be

Question 32

Vestibulocolic reflex

Answer 32

In small animals and babies | Compensatory neck contraction when body moves to keep head stable and fix gaze

Question 33

Vestibuloocular reflex

Answer 33

Equal and opposite movement of the eyes to the head movement to keep eyes fixed relative to image

Question 34

Optokinetic system

Answer 34

Drift and saccade sequence (nystagmus) to fix image on retina (gaze fixing) when following slow movement Fast movement of eye because harder to get detail when moving it

Question 35

Gaze shifting

Answer 35

Moving eyes to seek out different images i.e to foveate on visual stimuli detected on retina - Involves the superior colliculus (and its projections)

Question 36

Smooth pursuit

Answer 36

Feedforward mechanisms to move eyes with the (predicted) movement of an image to track it Involving cortex and cerebellum

Question 37

Additional tract found in apes and humans

Answer 37

Cortico-motoneuronal pathway to bypass interneurons and project straight to spinal motoneurons For finger movement -> Development of these pathways starts at 9 months, same age dexterity starts to develop

Question 38

Problems with motor cortex homunculus

Answer 38

There is overlap between areas of cortex from which different body part movements can be evoked Corticospinal axons terminate in multiple motor nuclei from different motoneuron pools; can activate synergistic muscles used in specific movements

Question 39

Lateral premotor cortex

Answer 39

Integrates visual and proprioceptive information into the movement pathway - Lesions here cause inappropriate movement of the contralateral hand in space Mirror neurons

Question 40

Supplementary motor area

Answer 40

For planning movements and mental rehearsal | - Get activity here both when doing a movement pattern and thinking about doing it

Question 41

Cingulate motor areas

Answer 41

For emotionally driven gestures like the limbic laugh

Question 42

Mirror neurons

Answer 42

Active both when performing a movement and when watching someone else do it Suggested to be involved in learning by imitation and empathy First discovered (and mainly found in) the premotor cortex

Question 43

Long latency reflexes

Answer 43

Cutaneous: tactile mechanoreceptors can detect slips between object and fingertips and signal to motor cortex (via DCN and ventrolat thalamus) to activate muscles to reinforce grip (requires slowing down of the original action) Stretch: as well as past stretch reflex, get projection via DCN and ventrolat thalamus to the motor cortex to cause smaller long latency reflex to reinforce the movement

Question 44

Dysmetria

Answer 44

Inappropriate displacement of movement i.e under or over reaching (cerebellar damage)

Question 45

Dysdiadochokinesia

Answer 45

Inability to make rapid, alternating movements | cerebellar damage

Question 46

Signal carried by mossy fibre

Answer 46

From cortex and proprioceptors Error signal (using sensory info and efferent copy) Carries context; the conditional stimulus e.g sound in eyeblink conditioning

Question 47

Climbing fibre input

Answer 47

From the inferior olivary nucleus Carries instructive signal; i.e unconditional stimulus like periocular eye puff Helps establish what movement is the right one to strengthen for that context?

Question 48

Motor learning in cerebellum

Answer 48

Learned pattern of activity in mossy fibres will automatically generative the appropriate movement (by not inhibiting certain outputs) Automating outputs to free it from conscious control

Question 49

Movement calibration in the vestibule-ocular reflex

Answer 49

Canals signal to the cerebellum (flocculus) and the vestibular nuclei Vestibular nuclei activity is balance of excitation from canals and inhibition from cerebellum

Question 50

Adjusting vestibular-ocular reflex

Answer 50

Climbing fibres activated by retinal slip; carry error signal Leads to adjustment of the feedforward model

Question 51

Chorea

Answer 51

Involuntary, unpredictable movements (BG damage)

Question 52

Ballismus

Answer 52

Unpredictable flailing movements (BG damage)

Question 53

Bradykinesia

Answer 53

Slowness of movement (BG damage)

Question 54

Hyperkinesia

Answer 54

Too much movement and at inappropriate times but still well coordinated

Question 55

Direct pathway in basal ganglia

Answer 55

Dopamine from substantial nigra acts on D1 receptors in striatum This activates the direct pathway to inhibit GPint This relieves the inhibition on the thalamus so motor plans can get through

Question 56

Indirect pathway in basal ganglia

Answer 56

Lack of dopamine from substantial nigra means it doesn't inhibit indirect pathway via D2 receptors So get inhibition of GPext This relieves inhibition on sub thalamus so it is free to excite GPint GPint can then inhibit the thalamus to stop motor plans getting through

Question 57

Hyperdirect pathway in basal ganglia

Answer 57

Motor cortex can direction excite sub thalamic nucleus to excite GPint, causing inhibition on thalamus for rapid braking of movement

Question 58

Treating Parkinson's

Answer 58

Provide L-DOPA to replacement dopamine Pallidotomy; controlled GPint lesions Deep brain stimulation of sub thalamic nucleus to reduce excitation on GPint

Question 59

Dorsal striatum output function

Answer 59

Related to motor function

Question 60

Ventral striatum output function

Answer 60

To limbic function which motivates decisions about future movement - Projects to prefrontal cortex and cingulate prefrontal cortex

Question 61

Role of BG in controlling visual saccades to foveate on stimuli

Answer 61

GP acts to tonically inhibit the superior/rostral colliculus that drives visual saccades So must disinhibit this with striatum activity (need cortical input for this)

Question 62

Spiny neurons in the striatum

Answer 62

Get corticostriate input (excitatory); this is instructive signal for learning Input from dopaminergic neurons of substance nigra to act as reinforcer -> If an output from BG was successful, there will be a release of dopamine which reinforces the synapses used via LTP Habit learning

Question 63

Fact that motor system ca achieve a goal in multiple ways

Answer 63

Motor equivalence problem