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NHB MVST 1b > Motor and Planning > Flashcards

Motor and Planning Flashcards

1
Q

What do we use muscle contractions for?

A 
Moving limbs
Moving the external world
Moving yourself around
Communication - speech/gesture/writing
To move visual and somatosensory sensors
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2
Q

Define apraxia

A

Movements poorly prepared or planned
Inability to carry out purposeful sequences of action. Perhaps struggle to hold goal in mind while performing individual actions. Have functioning motor equipment

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3
Q

Define noise

A

Random variation in signals, both motor and sensory, which renders them imprecise

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4
Q

Define redundancy

A

There are many possible ways to achieve a goal - the ‘motor equivalence’ problem: which do you pick?

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5
Q

Describe biological delays

A
  • Conduction of AP delays signals
  • Muscle contracts slowly
  • Eye muscles 20ms to full force, limb muscles 30-50ms
  • Must specify when force reaches its peak to produce accurate movement
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6
Q

Define nonlinearity

A

Mixing individual motor commands doesn’t produce predictable results - force depends on length, load and velocity of shortening in a more complex way

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7
Q

Define non-stationarity

A

The behaviour of motor systems can change over time; muscle contraction depends on history e.g. thixotropy (gels becoming fluid when disturbed)

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8
Q

How many synapses does a motorneuron receive?

A

30K

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9
Q

How big is the EPSP of an excitatory synapse?

A

0.1mV

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10
Q

What is the spike threshold for a muscle?

A

> 10mV depolarisation (e.g -55mV)

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11
Q

What are the stages of simple shifts of position?

A

Acceleration (agonist)
Deceleration (antagonist)
Final position holding force (agonist)

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12
Q

What are the sensors of the outside environment?

A 
Auditory
Visual
Somatosensory
Proprioceptors
Vestibular receptors
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13
Q

Define negative feedback

A

System that acts as a regulator to maintain a given parameter at a set point. Deviation from the set point is detected by sensors and a correction generated to nullify the deviation

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14
Q

Define closed-loop feedback

A

A negative feedback system that can shift state when the set point changes

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15
Q

What are the major problems with negative feedback loops?

A

Time delays in the feedback loop (sensory transduction, conduction to and from brain)Leads to instability and oscillation

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16
Q

How do cerebellar lesions affect feedback systems?

A

Damage ability to anticipate motor commands (feedforward), so only leave negative feedback?

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17
Q

Define feedforward/open-loop feedback

A

Sensory information is used to generate a prediction of what is needed in the future

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18
Q

Define internal model system

A 
Simulator in the brain that represents the mechanics of the body and the behaviour of the outside world 
Can learn (with experience) to predict which motor commands would be useful in a given situation
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19
Q

Define inverse model

A

A representation of transformation from motoneuron activity to movement in reverse so that from the desired outcome, motor demands to generate it can be estimated

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20
Q

What are the problems with inverse models?

A

Small errors in the initial stages of the calculation lead to massive errors in the final stages

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21
Q

Define forward model

A

Predicts consequences of motor commands before the slow muscle movement is complete, using information on what the motor commands were via efference copy/internal feedback. This is used to predict the movement that will follow, so the predictions can be set to the desired result and follow up corrections can thus be set up for errors as they are in the process of occurring.

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22
Q

What is the main centres for feedforward control?

A

Cerebellum and motor areas of cerebral cortex

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23
Q

Where in the spinal cord are the alpha-motoneurons?

A

Ventral horn

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24
Q

Define motoneuron pool

A

The 200-500 motoneurons that innervate a given muscle

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25
Q

What is the organisation of motoneurons within the ventral horn?

A

Proximal medial, distal lateral
Flexor posterior, extensor anterior
Somatotopic organisation

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26
Q

What is a motor unit?

A

The muscle fibres that one motoneuron innervates

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27
Q

How many motor units are in a muscle?

A

Several hundred

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28
Q

What are the three categories of motor unit?

A
  1. Slow
  2. Fast fatigue resistant
  3. Fast fatiguable
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29
Q

Describe the anatomy, biochemistry, and physiology of slow fibres?

A

Red
Anatomy: small fibres, few fibres/unit, highly vascular
Biochemistry: oxidative, lots of myoglobin (red)
Physiology: slow twitch, low tension, fatigue resistant, slow axons
Used in endurance training

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30
Q

Describe the anatomy, biochemistry, and physiology of fast, fatigue resistant fibres?

A

Anatomy: intermediate fibres, intermediate fibres/unit, intermediate vascularity
Biochemistry: intermediate oxidative and glycolytic, intermediate levels myoglobin
Physiology: intermediate twitch, intermediate tension, intermediate fatiguability, intermediate speed axons

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31
Q

Describe the anatomy, biochemistry, and physiology of fast, fatiguable fibres?

A

Pale
Anatomy: many fibres/unit, few capillaries
Biochemistry: glycolytic, little myoglobin
Physiology: fast twitch, high tension, fatiguable, fast axons
Used in sprint training

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32
Q

What is the benefit of having motor units with different properties?

A

Slow units can use for continuous generation of small forces (finely graded, low force contractions)
Fast fatigueable units can produce high forces over a short period (strength needed)

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33
Q

How is motor unit utilisation controlled?

A
  1. Rate coding: vary motoneuron firing rate. Fuse into tetanus at quite low freq though
  2. Motoneuron recruitment: recruit more motor units as more force is required
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34
Q

What is the size principle?

A

That motor units are recruited in an orderly sequence from lowest force to highest force units as force increases. Means that force always increments by finest available motor unit, and so is as smooth as possible.

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35
Q

How does the size principle work?

A

Developmental plasticity
Motoneurons with low firing threshold innervate few muscle fibres and induce them to become slow twitch/low force/fatigue resistant. Motoneuons with the highest firing thresholds recruited last innervate many muscle fibres and induce them to become fast twitch.
Reduces work of the motor system.

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36
Q

What are the 3 sources of synaptic input to motoneurons?

A
  1. Afferent fibres from muscle spindles
  2. Descending fibres: direct from brainstem or cerebral cortical structures, relatively rare but with an exception
  3. Spinal interneurons: most numerous connection, most cases receive input from sensory pathways and descending pathways
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37
Q

What are the two types of reflex?

A
  1. Targeted at specific small groups of muscles to regulate their force e.g. stretch reflex, associated reciprocal and recurrent inhibition
  2. Complex reflexes that generate functional movements that involve multiple muscles e.g. nociceptive withdrawal reflex
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38
Q

Define a withdrawal reflex

A

Coordinated pattern of muscle contraction to move the stimulated part of the body away from the stimulus

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39
Q

Describe ‘local sign’ of the foot.

A

Different reflexes are evoked from different locations. Stim of plantar (bottom) surface of foot evokes leg flexion, stim of foot dorsum evokes leg (top) extension.

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40
Q

Where do nociceptive afferents terminate?

A

Substantia gelatinosa of the dorsal horn

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41
Q

What are proprioceptors?

A

Sensory fibres from muscles and joints that provide information on the musculoskeletal system. 1/5 of mechanoreceptors.
3 major groups:
1. Muscle spindle afferents = stretch receptors/length
2. Golgi tendon organ afferents = muscle tension receptors/force
3. Joint receptors = signal joint position and movement especially at the extremes

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42
Q

What are exteroceptors?

A

The receptors on the surface of the body, e.g. cutaneous receptors. Especially ruffini endings are involved in movement

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43
Q

What are teloceptors?

A

Receptors that sense the environment at a distance e.g. eyes, ears, nose

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44
Q

Define proprioception

A

The sense of position and movement of the body

Takes information from proprioceptors, exteroceptors, vision and vestibular systems

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45
Q

Describe muscle spindles

A

Proprioceptors: activated by stretch of the central regions of the intrafusal fibres
Spindle-shaped structures embedded in muscles whose afferents signal muscle length and change in muscle length
Comprises an encapsulated bundle of small specialised intrafusal muscle fibres
Striated at the ends of their fibres - contractions change the sensitivity of the sensory nerve endings

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46
Q

How many spindles in a muscle?

A

20-100

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47
Q

What is the difference between extra and intrafusal muscle fibres?

A

Intrafusal aren’t contractile, smaller than extrafusal which are contractile

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48
Q

What are the two types of muscle spindles?

A

Bag fibres: swollen centre and contain many nuclei, contractile ends. 2 forms
Chain fibres: uniform diameter, uniformly contractile along length.

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49
Q

What are the sensory receptors that attach to intrafusal muscle fibres?

A

Primary/1a spindle afferents: very large and fast conducting axons with terminal branches that end in coils/annulospiral endings around the central region of the intrafusal muscle fibre
Secondary/II spindle afferents: end adjacent to the central region of the intrafusal muscle fibre.
Both activated by stretch

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50
Q

What are the motorneurons that attach to intrafusal muscle fibres?

A

Gamma motoneurons
Innervate the ends of the intrafusal fibres
(In some mammalian fibres, beta innervation)
Different gamma neurons innervate bag and chain fibres

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51
Q

What is beta innervation?

A

In amphibian/reptile muscle, where alpha motoneurons innervate the intrafusal (as well as extrafusal) muscle fibres

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52
Q

What is the difference between what bag fibres sense and what chain fibres sense?

A

Chain fibres = uniform mechanical properties along length, so sensory endings esp II afferents, signal static muscle length linearly
Bag fibres = esp 1a afferents, dynamic sensitivity to changes in stretch. Because central region isn’t contractile, but elastic, so rapid stretches rapidly elongate it (rapid strong activation of afferents at stretch onset), which is subsequently relieved as the viscoelastic contractile ends of the fibres elongate - rapid adaptation.

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53
Q

What is the function of gamma innervation?

A

Innervate the ends of the intrafusal fibres
Shorten
Stretch central region of fibres where the receptors are located
Increases both firing and sensitivity of receptors
Lets the muscle signal length changes from different starting muscle lengths (a form of adaptation)

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54
Q

Define adaptation

A

Adjusting the receptor sensitivity to extend the range over which the sense organ operates

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55
Q

How come the brain isn’t confused by both gamma motoneurons or muscle contractions being able to signal the same thing from muscle spindles?

A

Brain receives efference copies of the commands sent to gamma motoneurons

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56
Q

Describe Golgi tendon organs

A

Activated by active tension in the tendon
Passive stretches of relaxed muscle doesn’t increase tension in the tendon, but muscle contractions do.
Signal strongly proportional to the load on the muscle

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57
Q

What is the stretch reflex?

A

Muscles respond to being stretched by contracting, e.g. knee jerk: tap patellar tendon, stretches muscle spindles, reflex contraction of quadriceps, close synergists, and excite interneurons that inhibit antagonist muscles

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58
Q

Which muscles do not have a stretch reflex?

A

Eye, tongue

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59
Q

What is reciprocal inhibition?

A

A spinal reflex. In stretch reflexes, agonist contracts, but also (via interneurone) reflexive relaxation of antagonist

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60
Q

What was Merton’s proposal?

A

That movement was driven by gamma motoneurons altering set points such that the spinal cord itself determines the appropriate force required via negative feedback

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61
Q

What were the problems with Merton’s proposal?

A
  1. For this to work the stretch reflex would need a gain of one (it’s actually less)
  2. Delay which would lead to oscillation
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62
Q

What is clonus?

A

Oscillation following a muscle stretch in pathological situations following damage to descending corticospinal pathway systems such that the stretch reflex is exaggerated

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63
Q

What are the roles of proprioceptors?

A
  1. Spinal reflex action
  2. Kinesthesia (sense of position, movement and effort)
  3. Information for supraspinal motor systems involved in predictive feedforward control
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64
Q

What do proprioceptors contribute to supraspinal control?

A

Information on current state of play at outset of movement to model predictions on
Assessment of the outcome after the movement, critical for learning in the model system to ensure they are accurate

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65
Q

What was the Nashner experiment?

A

Move a platform backwards with a person on it, pulls feet, measure muscle response in gastrocnemius. The more you do it, the more the early stretch reflex response comes in. Did it again but tilt the platform: caused the same stretch, and get the same strong reflex, which induces a body sway as you expect the previous set of circumstances.

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66
Q

What type of synapse is there between 1a afferents and inhibitory interneurons?

A

Glycinergic

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67
Q

What is recurrent inhibition?

A

Renshaw cells
Motoneuron axons have branches called recurrent collaterals within the spinal cord that innervate a type of inhibitory interneuron called Renshaw cells. Renshaw cells seem to regulate the timing of motoneuron firing, preventing synchrony and so jerkiness or tremor

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68
Q

What does it mean that Golgi tendon reflexes are context dependent?

A

In static positions, activation of tendon organs mainly inhibits the parent muscle
In locomotion, activation of tendon organs mainly leads to excitation, where it supports contraction against a load

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69
Q

What are 3 neonatal reflexes that change with development?

A
  1. Grasp reflex
  2. Babinski’s sign (plantar reflex)
  3. Reflex stepping
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70
Q

Describe the grasp reflex

A

In first 6-12 months then disappears
Babies grasp onto things and generate enough force to support the body
Can reappear after brain damaged

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71
Q

Describe Babinski’s reflex

A

Toes curl up in response to plantar stimulation (in adults they turn down)
Neonatal reflex reappears after brain damage

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72
Q

Describe spasticity

A

Exaggerated stretch reflexes. Muscles are tense and stiff. Stretch elicits strong reflexes and clonus

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73
Q

Describe the clasp knife reflex

A

The limbs snap into flexion or extension during movement (not due to tendon organs)

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74
Q

What are central pattern generators?

A

Biological neural networks that produce rhythmic outputs with the absence of rhythmic inputs. Can function without input from higher brain areas, but are modulated by them. Can also function without sensory inputs, e.g. by cutting dorsal roots of spinal cord.
Made up of spinal interneurons

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75
Q

How much do CPGs generate locomotion in man?

A

Little
Pattern that greater encephalisation is associated with weaker ability to generate locomotion. Mammals less prone to produce movement after removal of the brain

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76
Q

Where do the two descending motor pathways sit in the spinal cord white matter?

A

Dorsolateral

Ventromedial

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77
Q

What do the ventromedial pathways control?

A

Axial and proximal limb muscles
Role in whole body movement (posture/locomotion)
Crossed and uncrossed

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78
Q

What is the ventromedial pathway divided into?

A

Reticulospinal from reticular formation
Vesibulospinal from vestibular nuclei
Tectospinal from superior colliculus (orientation of your head in space)

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79
Q

What are the dorsolateral systems?

A

Control goal directed movements of the limbs esp hands, feet, face, lips

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80
Q

What is the dorsolateral system divided into?

A

Rubrospinal pathway: Red nucleus in midbrain. Probably vestigial in man.
Corticospinal tract: from motor areas of cerebral cortex, largest descending pathway in all mammals, the dominant descending control pathway in man.
Crossed

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81
Q

What and where are the receptors for the vestibular system?

A

Hair cells in labyrinth of semi-circular canals and otolith organs (saccule and utricle)

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82
Q

Describe the utricle and saccule

A

Static information
Hair cells project into jelly-like mass that gravity acts on
Hair cells have different directional sensitivities
Specific sets of hair cells activated when the head in different positions
So inform on effective direction that gravity is acting - when immobile = head position

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83
Q

Describe the semicircular canals

A

Dynamic signal when the head starts or stops to move.
Hair cells embedded in mass that almost closes the canal called the cupula
Cupula neutrally buoyant in the endolymph in the canals so stationary when head is stationary
Head moves –> fluid has inertia so tends to remain stationary but cupula fixed to head so cupula deflected –> activates hair cells.

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84
Q

Why do you feel dizzy when you drink alcohol?

A

Alcohol equilibrates more quickly into the cupula than endolymph cells, so the cupula becomes buoyant and you feel like you’re constantly rotating

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85
Q

Which is more likely to provide signals for feedforward control: otolith or semicircular canals?

A

Semicircular canals

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86
Q

How does the vestibular system being activated affect posture?

A

Activation –> vestibulospinal pathways –> extensor/antigravity muscles

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87
Q

How can the vestibular system get damaged?

A

Labrynthitis, centrally through brainstem stroke or cerebellar damage

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88
Q

How does the body differentiate between body sway, when it needs to move, and head sway, when it doesn’t

A

Efference copy from motor systems that move the head: if the predicted vestibular signals match the actual vestibular signals, the vestibular reflexes are cancelled

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89
Q

What is the point of gaze-fixing mechanisms?

A

Visual system is bad at resolving moving images, so eye needs to be kept fixed relative to the outside world as much as possible.

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90
Q

What are saccades?

A

Very rapid gaze shifting eye movements

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91
Q

What are the two major gaze fixing mechanisms in mammals?

A

Vestibuloocular reflex

Optokinetic reflex

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92
Q

Define the vestibuloocular reflex

A

Moves the eyes equal and opposite to the head

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93
Q

What does the MLF connect?

A

Medial longitudinal fasciculus

Semicircular canal afferents, vestibular nculei, motoneurons of oculomotor nuclei

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94
Q

Which bit of the cerebellum controls vestibuloocular reflexes?

A

Flocculus

Calibrates what oculomotor movement is needed to be done by the cerebellum

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95
Q

How many synapses are thee between the semicircular canals and the eyes moving?

A

4:
1 canal –> nerve
2 nerve to second nerve in vestibular nucleus
3. second nerve to third nerve in oculomotor nucleus
4. third nerve to eye muscle

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96
Q

What is the function of the optokinetic system?

A

Moves the eyes to follow slow movements of the visual field

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97
Q

What drives the optokinetic system?

A

Visual cortex

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98
Q

How does the optokinetic system work?

A

When eye deviates from it axis within the orbit, saccades reset the eye to the centre: nystagmus.

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99
Q

Define nystagmus

A

Drift and saccade eye sequence resulting in a ‘sawtooth’ motion of the eye
Can occur physiologically due to optokinetic or vestibular stimuli, or pathologically after cerebellar or vestibular damage.

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100
Q

What is the pathway that drives gaze-shifting foveation?

A

Retina –> magnocellular pathway –> superior colliculus –> brainstem reticular formation –> oculomotor nuclei –> saccade
Deep layers of colliculus –> tectospinal tract –> cervical spinal cord –> neck movmeents accompanying eye movements.
Deep layers of colliculus also receive auditory input so can rapidly orientate to sound stimuli too.

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101
Q

Which cortical regions are involved in smooth pursuit?

A

Visual cortex and medial temporal cortex process visual signals, regions of frontal lobe anterior to motor cortex called frontal eye fields also do

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102
Q

What is smooth pursuit?

A

Gaze-shifting mechanism: slower eye movements to follow moving objects. Feedforward

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103
Q

Summarise the main gaze-fixing and gaze-shifting mechanisms:

A

Fixing
VOR
Optokinetic system

Shifting
Foveation
Smooth pursuit

104
Q

What is the function of the primary motor cortex?

A

Execution of voluntary movement via the corticospinal or corticobulbar tracts projecting onto motor neurons

105
Q

What is the effect of unilateral mild stroke in the motor cortex?

A

Contralateral hemiparesis

106
Q

Definition hemiparesis

A

One-sided weakness and partial paralysis

107
Q

What is the effect of unilateral severe stroke?

A

Contralateral hemiplegia

108
Q

Where do: ACA and MCA strokes affect?

A

ACA = lower limbs, MCA = upper limbs and face

109
Q

What is the outflow of the motor cortex called?

A

Internal capsule

110
Q

What is the pathway of the corticospinal tract?

A 
M1
Forebrain internal capsule
Midbrain cerebral peduncle
Ventral brainstem
Inferior olive of medulla --> corticobulbar fibres
Medullary pyramid
Pyramidal decussation
Lateral corticospinal tract in dorsolateral funiculus of spinal cord (90%)
Anterior uncrossed tract (10%)
111
Q

How do you identify corticospinal tract fibres?

A

After a stroke that affects a movement, can find which fibres used to supply it by demyelination

112
Q

What happens to the ventral corticospinal tract fibres?

A

Either cross or provide control for axial muscles

Don’t control distal ipsilateral muscles: after stroke they are not used for recovery of function

113
Q

What is an upper motoneuron lesion?

A

Motor cortex lesions that are complicated by spasticity

114
Q

What is a lower motoneuron lesion?

A

Lesion of spinal cord or peripheral nerve which causes flaccid paralysis

115
Q

What is the function of cortico-motoneuron connections? How do we know?

A

Direct, monosynaptic, bypass spinal interneurons. Allow for precise, independent movement of extremities (fingers)
Lesions –> permanent deficits most prominent in finger movement and manipulation
Comparative neuroanatomy –> projections to motoneurons appear in species that make independent finger movements but not species without
Development –> evidence these direct projections are developed post-natally at 9months, which is when dexterity begins to develop

116
Q

Describe the motor homunculus

A

A simple figure representing the motor cortex organisation

117
Q

Why is the motor homunculus misleading?

A

Misleading in that it suggests the motor cortex contains an orderly representation of individual muscles in a fractionated map, and so that lesions in one location will affect a specific muscle or body part, which isn’t the case

118
Q

What is the representation of the body in M1?

A

 Individual neurons in M1 see sets of synergistic muscles that can be activated together in particular movements
 Different groups of motor cortex neurons thus provide ‘alternative libraries’ of muscle synergies e.g. wrist extensors and finger flexors for a power grip

119
Q

What are the sources of input to the primary motor cortex?

A
  1. Motor association areas via direct cortico-cortical connections
  2. Cerebellum via VL thalamus
  3. Basal ganglia via VL thalamus
  4. Sensory afferents via VL thalamus and sensory cortex (tactile and proprioceptive)
  5. Subcortical areas via VL thalamus
120
Q

What is the function of the sensory afferents reaching M1?

A

Rapid feedback correction of ongoing movement

121
Q

What are the outputs of the motor association areas?

A

Cortico-cortical to M1
Direct to spinal cord
Connections to cerebellum and basal ganglia, through which they can influence plans and preparation or future movement

122
Q

What do the motor association areas do?

A

Plan movement
SMA: Internally generated or self-paced movement, bimanual movement
LPA: Movements that depend on a sensory trigger system

123
Q

Where are the heaviest projections of the cerebellum and basal ganglia?

A

Cerebellum –> LPA

Basal ganglia –> SMA

124
Q

What is the effect of a lateral premotor area lesion?

A

Inability to appropriately incorporate sensory information into motor actions, particularly grasping

125
Q

What are mirror neurons?

A

Neurons that fire in relation to making a movement, but also in relation to seeing another person make the same movement

126
Q

What is the evidence for the function of the SMA?

A
  • PET Scans
    Activity in SMA also occurs during mental rehearsal of imagined movements
    Suggests SMA helps predict the sequence of movements needed to achieve a particular end point and in understanding their consequences
  • SMA more activated when subjects performing a learned sequence of finger movements rather than relying on external cues to signal a novel sequence of finger movements
  • Ablation of SMA in monkeys causes i) deficit in bimanual coordination, ii) failure to orient hands and fingers accurately as they approach food, iii) failure to raise hand in the absence of external cues in order to get peanut reward
  • Alien hand syndrome: patients with SMA pathology may have their actions divorced from conscious control. Hand responds to outside world but the can’t control it.
127
Q

What is the function of the prefrontal cortex?

A

Planning, cognitive and decision making skills

Plans for future strategic goals on which movements are based

128
Q

What is the prefrontal cortex connected to?

A

Basal ganglia and cerebellum

Inputs into supplementary motor areas

129
Q

What are the signs of cerebellar ataxia?

A

Hypotonia (weakness)
Dysmetria (inappropriate displacement e.g. overreaching)
Dysdiadochokinesis (inability to make rapid alternating movement)
Decomposition of movement (lack of coordination of different joint movements)

130
Q

How was cerebellar function found?

A

Lesion studies of WW1 soldiers

131
Q

What is the type of synapse between Purkinje cells and deep nuclei?

A

GABAergic

132
Q

Concisely define the function of the cerebellum

A

Construction of movements from appropriately timed, scaled and patterned contractions of specific groups of muscles
Works out the parameters of movement

133
Q

Describe the organisation of the cerebellum

A

Superficial molecular layer
Purkinje cell layer
Granular layer
White cell layer (deep nuclei and output)

134
Q

What are Purkinje cells?

A

Output of the cerebellar cortex
Dendrites planar
GABA inhibit cerebellar nuclie

135
Q

What is the largest cerebellar nucleus?

A

Dentate

136
Q

Where does the cerebellum project?

A

Superior cerebellar peduncle
VL thalamus –> basal ganglia, primary motor cortex
VA thalamus –> supplementary motor area

137
Q

What are the 5 types of cell in the cerebellum?

A
  1. Purkinje
  2. Mossy
  3. Climbing
  4. Granule (excitatory)
  5. Deep nuclear
138
Q

What is the most numerous cell in the brain?

A

Granule cells

139
Q

What is the function of the climbing fibres?

A

Teach the Purkinje cells which of the parallel fibres carry important information, so cerebellar circuitry could learn which outputs are appropriate to specific inputs
Acts by initiating plasticity

140
Q

Describe synaptic plasticity in the cerebellum

A

LTD

Parallel fibre pathways following conjunctive activation of parallel fibres andclimbing fibres

141
Q

Describe the function of the basal ganglia

A

Decision making = action selection

Selection of movement patterns and triggering of movements

142
Q

Define the basal ganglia

A

Collection of large subcortical forebrain nuclei: largest of these are the putamen and caudate, and globus pallidus

143
Q

What is the striatum?

A

Nuclei with stripes of fibres crossing grey matter: putamen, caudate, globus pallidus

144
Q

What are the 2 midbrain nuclei functionally connected with the basal ganglia nuclei?

A

Substantia nigra

Subthalamic nucleus

145
Q

What are the inputs to the basal ganglia?

A

All lobes of the cerebral corte

146
Q

What is the main output of the basal ganglia?

A

Inhibitory to the thalamus –> excitatory to frontal lobes

147
Q

What are the signs of basal ganglia malfunction?

A

Excess or paucity of movement

  1. Hyperkinesia - often of well coordinated movements at inappropriate times
  2. Dyskinesia - unpredictable movements
  3. Hypokinesia
148
Q

What are the types of hyperkinesia?

A

Chorea (unexpected dancing movement associated with Huntington’s)
Athetosis (writhing movements of hands or face)
Ballismus (flailing ballistic movements)

149
Q

What are the types of hypokinesia?

A
  1. Bradykinesia (slowness associated with Parkinsonism)

2. Rigidity (stiff, fixed position)

150
Q

What does the terminology pyramidal and extrapyramidal mean?

A 
Pyramidal = stroke
Extrapyramidal = basal ganglia disorders. Assumes an alternative descending pathway which is misleading as the main way the basal ganglia affects movements is via motor cortex and pyramidal tract)
151
Q

What is the direct circuit?

A

Corticostriate fibres + caudate or putamen - internal globus pallidus - thalamus so + - - stim disinhibition

152
Q

What is the indirect pathway?

A

Corticostriate fibres + different caudate or putamen neurons - external globus pallidus - subthalamic nucleus + internal globus pallidus - subthalamic nucleus + internal globus pallidus - thalamus so + – + - net - inhibits movement

153
Q

What is the physiology of hypokinesia in Parkinsonism?

A

Loss of dopamine –> imbalances in activity in different pathways as normally dopamine via D1 activates direct pathway, and inhibits via D2 the indirect pathway so loss –> more indirect pathway –> excessive internal globus pallidus activity –> increased inhibition in the thalamus

154
Q

How do you treat Parkinsonism?

A

Radical neurosurgery
Controlled lesions of globus pallidus (pallidotomy)
Deep brain stimulation of subthalamic nucleus
L-DOPA, can lead to too much dopamine and hyperkinesia

155
Q

For the motor circuit

Cortical input and output?

A

Input: motor, sensory association, output, motor and SMA

156
Q

For the oculomotor circuit

Cortical input and output?

A

Prefrontal and visual association

Frontal eye fields

157
Q

For the association cortex

Cortical input and output?

A

About cognition
Parietal and temporal association
Prefrontal

158
Q

For the limbic association cortex

Cortical input and output?

A

About emotion and motivation
Temporal lobe, cortex and amygdala
Output: cingulate, prefrontal

159
Q

What are the dorsal and ventral striata?

A 
Dorsal = related to motor function
Ventral = related to limbic function
160
Q

What stops all peripheral stimuli driving saccades?

A

Superior colliculus tonically inhibited by basal ganglia output (substantia nigra/globus pallidus)
Cerebral cortex can activate appropriate cells in the caudate/putamen to inhibit the output cells, disinhibiting the superior colliculus
BG thus determines whether and when the saccade occurs

161
Q

What is the normal role of dopamine in the basal ganglia?

A

Mediates plasticity of the cerebral corticostriate inputs to the caudate and putamen
If an output from the BG is successful, it reinforces the synapses that were active to generate the successful output, so that when those synapses were activated again, the output is generated again
Underlies habit learning

162
Q

What are the non-motor roles of the basal ganglia?

A

Nucleus accumbens and ventral striatum project to the prefrontal areas of cortex, which are not usually considered to be overtly motor in function. Concerned with high level executive decisions on strategy, so BG seen to select between strategies or potential behaviours
Also reward processes, DA involved in learning what are good decisions (so can be altered in mental illness)

163
Q

What are the characteristic signs of patients with prefrontal lesions?

A

Lack of initiative, poor planning ability and inability to cope in novel situations, poor social skills

164
Q

Define apraxia. What are the major types?

A

Motor disorder where there is a difficulty performing purposeful or voluntary movements
4 major types: limb, oral, agraphic, constricutional

165
Q

Define limb apraxia. What causes it?

A

Problems with arm, hand and finger movements, but general intent or planning of act intact
Bilateral damage to parietal or premotor cortex
Execution and recognition deficits parietal, execution but not recognition premotor (removal and loss of ability to store action plans)

166
Q

Define oral apraxia. What causes it?

A

Problems with programming movements of the tongue, lips and throat to produce sequences of speech

167
Q

Define agraphic apraxia. What causes it

A

A particular type of writing deficit

168
Q

Define constructional apraxia. What causes it?.

A

Inability to copy mental or visual pictures

Right parietal damage

169
Q

Define ideomotor apraxia

A

Represent the inability to perform purposeful movements either to command or on imitation

170
Q

Discuss the Kimura box test

A

illustrates impairments in learning new sequences of actions. Have to push top button with index finger, pull the handle and then press down on the bar with your thumb. Can’t

171
Q

Which areas of the brain when damaged are associated with apraxia?

A

Posterior parietal cortex and frontal premotor areas and the connections between them
Post parietal –> hand and limb apraxias
Ant premotor –> oral
These two are the ideomotor apraxias

172
Q

What does the posterior parietal cortex do?

A

Rostral = integration of somatosensory and proprioceptive information relating the relative position of body segments to their movement
Posterior = integration of visual information about events located in the external environment
Mediates reaching into extra-personal space, mediates between spatial perception and the direction of action

173
Q

What is the evidence that the posterior parietal cortex mediates reaching into extra-personal space?

A
  1. Posterior parietal lesions in monkeys impair sequential reaching movements e.g. removing polo mints from a bent wire
  2. Recordings of the posterior parietal cortex from single units in monkeys demonstrate the existence of neurons within area 7 that
    i. Fire when the monkey detects a visual target, increase firing as an arm is projected towards the target and decrease firing when the target is reached (arm projection neurons)
    ii. Fire when the target is manipulated (manipulation neurons)
174
Q

What are the connections from the posterior parietal cortex?

A

Reciprocally connected to the lateral and medial premotor areas of the frontal lobes

175
Q

What is the evidence for the function of the lateral premotor area?

A
  1. Ablations of PM in monkeys causes i) deficit in performing hand actions based on, or directed by, external cues
  2. PET studies reveal greater activity in PM when subjects relying on external cues to determine a sequence of finger movements compared to when they are performing a sequence of finger movements from memory
176
Q

Explain ‘release of reflexes’

A

Premotor areas (LPA, SMA) inhibit inappropriate actions, especially inappropriate reflexes. Many reflexes present at birth that become inhibited during development re-appear following damage to premotor areas e.g. suckling, rooting, grasping. Think mechanisms reside in the parietal lobe, normally inhibited by the frontal lobes

177
Q

What is the function of the inferotemporal area of the posterior cortex?

A

Feature attention

178
Q

What is the function of the rhinal cortex of the temporal lobe?

A

Recognition memory - declarative

179
Q

What is the function of the hippocampus?

A

Scene/episodic memory - declarative

180
Q

What is the function of Wernicke’s area?

A

Speech comprehension

181
Q

What is the function of Broca’s area?

A

Speech production

182
Q

What is the prefrontal cortex connected to?

A
  1. Specialised processing modules in posterior cortex (parietal spatial attention and inferotemporal feature attention)
  2. Declarative memory in temporal lobes (rhinal cortex recognition memory and hippocampus scene/episodic memory)
  3. Limbic structures involved in emotional processing amygdala and hypothalamus
  4. Basal ganglia – higher order control of action
  5. Language processing in post + ant cortex: Wernicke’s and Broca’s
183
Q

Describe the Winsconsin Card Sort Test

A

Deficit in inhibitory control seen following damage to the lateral prefrontal cortex. Failure to inhibit previously relevant rules governing behaviour. If patients learn to sort a pack of cards according to colour, they are then unable to switch to sorting according to a different dimension, i.e. shape. Instead persevere with the previously correct dimension.

184
Q

Describe behavioural inflexibility

A

monkeys with prefrontal damage, after learning that one object, out of a pair, is associated with reward, cannot switch their responding to the other object when that object becomes rewarded instead

185
Q

Describe the evidence about spatial and feature detection in the prefrontal cortex.

A

subjects required to attend to one of three different perceptual features: colour, form or movement (selective attention conditions) or all three (divided attention). Dorsolateral Prefrontal cortex activated spatial, ventrolateral activated most when attending to visual features.

186
Q

Which brain areas are used in processing spatial info?

A

Posterior parietal cortex, dorsolateral prefrontal cortex

187
Q

Which brain areas are used in processing visual info?

A

Inferotemporal cortex, ventrolateral prefrontal cortex

188
Q

How does the ventrolateral prefrontal cortex influence the processing of visual information?

A

Top down control of selective attention
Enhances processing of relevant information by enhancing activity in the sensory cortex involved in processing that information

189
Q

How does the dorsolateral prefrontal cortex influence the processing of spatial information?

A

Enhances activity for divided attention linked to spatial attentional mechanisms
Thought dorsolateral region involved in learning and planning of higher-order strategies to achieve the goal

190
Q

What is the evidence for the prefrontal cortex’s control of short term memory?

A
  1. Delayed response tasks: Lesions of regions of prefrontal cortex impair delayed response tasks that require monkeys to remember spatial, object or proprioceptive information over a brief delay. Sample stage where monkey a) shown peanut hidden in one of two locations (spatial), b) shown one of two objects (object), c) or required to press a lever one or five times (proprioceptive). After a few s, choice stage, where monkeys choose the location/object/do the same response. Lesions of pfc do not affect this choice if there is no delay. Implicates the pfc in short term memory
    2, Some neurons in lateral regions of pfc in monkeys have been shown to fire during the delay period of the spatial and object versions of the delayed response task
191
Q

Which region of the prefrontal cortex is involved in emotion?

A

Orbital regions of prefrontal cortex

192
Q

Describe monkeys with orbitofrontal damage

A

female monkeys normally submissive and solicitative of the advances of a male, when damaged, replaced either by indifference or aggression. Show indifference towards own offspring.

193
Q

What is the function of the prefrontal cortex?

A

Executive function - management and regulation of cognitive processes
Seems like the prefrontal cortex inhibits complex behaviours, is involved in attention, is involved in short term memory, and enables emotions to contribute to complex decision making

194
Q

What are the different ways that you can divide the prefrontal cortex?

A
  1. Type of information that they process

2. Type of cognitive operations that they perform

195
Q

What is needed to select a goal?

A
  1. Hold information in mind
  2. Filter out irrelevant info (determined by what we have learnt in the past)
  3. Choose an appropriate goal
  4. Select appropriate responses to fulfil the goal
  5. Inhibit inappropriate responses
196
Q

Are the pyramids dorsal or ventral?

A

Ventral

197
Q

Which neurons form the corticospinal tract?

A

Layer V pyramidal neurons of motor cortex

198
Q

What histologically distinguishes the primary motor cortex from other areas?

A
  1. Layer V contains a population of giant pyramidal neurons only round in M1.
  2. Motor cortex is thickest area of cortex, but contains few small rounded cells (so sometimes called agranular cortex)
199
Q

Where does the internal capsule run through?

A

Between basal ganglia nuclei and thalamus

200
Q

What is the boundary between medulla and spinal cord?

A

The motor decussation

201
Q

What is just deep to the peduncles in the upper midbrain?

A

The substantia nigra and the red nuclei

202
Q

Describe the vestibulospinal tracts

A

Descend in the ventral columns
Arise in vestibular nuclei in the dorsal medulla
Exerts actions mainly on extensor limb muscles and proximal muscles
Involved in maintaining posture and equilibrium

203
Q

Describe the reticulospinal fibres

A

Originate from reticular formation of pons and medulla
Several groups of neurons give rise to descending fibres, which are fast conducting and project through the length of the spinal cord
Important for posture and coordinated body movement

204
Q

Describe the rubrospinal tract

A

From Red nucleus of midbrain
Large nucleus in man but few fibres that descend to spinal cord
Gets input from cerebellar nuclei and motor areas of the cerebral cortex and output mainly to inferior olivary nucleus (–> climbing fibres)
Thought to function in motor skills learning

205
Q

What are the folds of the cerebellar cortex called?

A

Folia

206
Q

What is the fat middle part of the cerebellum called?

A

Vermis

207
Q

What is the flocculus?

A

Small, semi-detatched part of cerebellum
Concerned with vestibular function
In cerebello-pontine angle

208
Q

What are the tonsils?

A

Bilateral small parts of cerebellar cortex that overhang the dorsolateral aspect of the medulla

209
Q

What is the clinical importance of the tonsil?

A

In patients with raised intracranial pressure, risk of tonsils collapsing into the foramen magnum if CSF is withdrawn by lumbar puncture. Results in pressure on the brainstem and sudden death due to pressure on vital centres for respiratory and autonomic control: coning.

210
Q

What are the deep cerebellar nuclei?

A

Dentate nucleus
Nucleus interpositus
Fastigial nucleus

211
Q

How does the cerebellum output information?

A

All via deep nuclei

Except flocculus directly to vestibular nuclei in the medulla

212
Q

Where do each of the cerebellar peduncles come from?

A 
Superior = deep nuclear output --> thalamus
Middle = pons
Inferior = medulla
213
Q

Where and what can you see regarding the superior cerebellar peduncle?

A

Midbrain dorsally
Can see decussation in low midbrain
Then sends some fibres to the red nucleus
Bridge between the two is the roof of the rostral part of IV ventricle

214
Q

Where do the ventrolateral and ventroanterior thalamic nuclei project to?

A

VL –> primary motor cortex

VA –> premotor and supplementary motor

215
Q

What is the projection through the middle cerebellar peduncle? What does it carry?

A

Pons to contralateral cerebellum as mossy fibres

Infromation from sensory and sensory association areas

216
Q

What is the projection through the inferior cerebellar peduncle? What do the fibres carry?

A

Ascending spinocerebellar mossy fibres (juncrossed)
Somatosensory information (e.g. from Clarke’s nucleus, proprioceptors)
Also fibres form inferior olive climbing fibres - mediate learning

217
Q

Is the representation in the cerebellum ipsi or contralateral?

A

Ipsilateral

218
Q

Do parallel fibres and Purkinje cell fibres run along with the folia or perpendicular to them?

A 
Parallel = parallel
Purkinje = perpendicular
219
Q

How do you stain Purkinje cells?

A

Silver impregnation (the Golgi method) - selects only some neurons and glia

220
Q

What can cause upper motoneuron signs? What are they?

A

Strokes, cerebral palsy, multiple sclerosis
Immediate flaccid paralysis, gradually becomes spastic with hyperreflexia, clonus and + Babinski sign, voluntary movement impaired, reflex contraction remains

221
Q

What can cause lower motoneuron signs? What are they?

A

Lesions in spinal cord or peripherally, e.g. poliomyelitis. Muscular weakness, flaccid paralysis, muscle wasting, areflexia

222
Q

When can ventromedial corticospinal pathways reorganise to allow recovery of function after a stroke?

A

Prenatally or in early neonatal life

223
Q

What are AVMs?

A

Arteriovenous malformations
congenital vascular anomalies consisting of direct fistulas artery –> vein iwhtout an intervening capillary bed
Propensity to bleed/haemorrhage
Treat with surgical resection, focused radiotherapy or endovascular embolisation

224
Q

What are cavernomas?

A

Thin dilated vascular channels that don’t have a feeding artery and so don’t appear on angiograms
In brain or spinal cord
Some familial
Risk of bleeding lower than AVM but if multiple haemorrhages, then surgical resection

225
Q

Which corticobulbar fibres provide bilateral innervation to motor nuclei?

A

V upper VII XII

226
Q

Where do you find the cingulated motor areas?

A

buried medially

227
Q

What is Clarke’s nucleus?

A

Part of the spinocerebellar tract (up through inferior cerebellar peduncle)
T1-L3/4
Proprioception related
Spinal interneurons in lamina VII

228
Q

How do you find the caudate nucleus?

A

Remove the septum pellucidum on a saggital section, can just about see the caudate inside the lateral ventricle
Follows the course of the lateral ventricles (ant horn, body, inf horn)
Tail of caudate into the temporal lobe

229
Q

Which part of the brain is the basal ganglia in?

A

Forebrain

230
Q

What composes the neostriatum?

A

Caudate and putamen, separated in development by the internal capsule

231
Q

Where is the putamen?

A

Lateral to the internal capsule, medial to the insula

232
Q

What are the two major divisions of the substantia nigra?

A

Pars compacta = dopaminergic, innervates the neostriatum

Pars reticulate = non-dopaminergic control of eye movements

233
Q

What is the shape of the caudate?

A

Large head anteriorly

234
Q

Where is the globus pallidus?

A

More posteriorly, medial to the putamen, inferior to the caudate and internal capsule

235
Q

Where is the thalamus?

A

More posteriorly, either side of the third ventricle so medial to the internal capsule

236
Q

What is the counterpart of the corpus callosum more anteriorly? What else can be seen at this level?

A

Anterior commissure
Hypothalamus
Caudate, putamen, globus pallidus

237
Q

How do the basal ganglia structures appear anteriorly to posteriorly?

A

Caudate (getting smaller), putamen (getting bigger then smaller), then globus pallidus, then thalamus. Most posteriorly thalamus large but putamen and globus pallidus is not present. Internal capsule now ventral and tightly bundled and form cerebral peduncles

238
Q

Where does the caudate input predominantly originate from?

A

Prefrontal cortex

239
Q

Where does the putamen input predominantly originate from?

A

Sensorimotor cortex

240
Q

Where do fibres from the internal globus pallidus terminate?

A

VL VA thalamus, medial nucleus of the thalamus

241
Q

What does the substantia nigra pars compacta look like in fresh and fixed tissue?

A

Dark pigmented area in midbrain next to the cerebral peduncles
In a cross section through the brain where myelin has been stained it appears as a lighter area

242
Q

Where is the subthalamic nucleus?

A

At the junction of the midbrain and diencephalon

Probably unable to find

243
Q

Where does the medial dorsal nucleus of the thalamus project to?

A

Prefrontal cortex, involved in complex executive functions

244
Q

What does the internal capsule carry?

A

Corticospinal tract
Other cortical output fibres
Thalamocortical input fibres

245
Q

What is the clinical significance of the genu?

A

Where MCA haemorrhage or thrombosis commonly affects the internal capsule

246
Q

What is the clinical significance of the genu?

A

Where MCA haemorrhage or thrombosis commonly affects the internal capsule
At the genu there are corticospinal fibres to the the head, neck and part of the upper limb

247
Q

Give two examples of thalamocortical fibres

A

LGN –> runs around lateral ventricle –> post –> visual cortex as optic radiation
MGN –> auditory radiation

248
Q

What is the blood supply of the striatum and internal capsule?

A

Small arteries originating from the middle and anterior cerebral arteries
End-arteries
Termed striate arteries from the MCA

249
Q

What is the cause of Hungtington’s chorea?

A

Partly due to death of cells in the neostriatum

250
Q

What do lesions of the subthalamic nucleus lead to?

A

Hemiballismus, violent disorder in which flailing limb movements are produced

251
Q

What is Wilson’s disease?

A

Copper deposits in the basal ganglia, kidney, liver, and Kayser-Fleischer rings.

252
Q

Which deep nuclei are targeted in deep brain stimulation?

A

Subthalamic nucleus, globus pallidus internal, ventral anterior thalamus, pedunculopontine nucleus

253
Q

What is ETV?

A

Endoscopic third ventriculostomy
Surgical procedure involving placing an endoscope through the frontal lobe into the lateral ventricle, then through the foramen of Munro into the third ventricle. There make a hole (ventriculostomy) in the floor of the third ventricle to allow CSF to drain from the ventricle into the subarachnoid space, then onwards to be absorbed. Diverts CSF from any blockage downstream of the third ventricle, e.g. from a tumour obstructing the aqueduct, so preventing hydrocephalus

254
Q

What is stereotaxy?

A

coordinate based system used to localise brain regions

255
Q

Discuss prefrontal damage, and tests for it

A

Executive function. Inability to inhibit behaviours. Emotional lability.
1. Winsconsin Card Sort Test - perseveration, despite not ‘wanting’ to
2. Sentence suppression task - give someone a sentence with the last word missing out. Ask to complete with a logical word, and can. If you ask to finish with an illogical word, really struggle.
3. Stroop - colour words written in different colours. Told to say what the colour it is printed in is.
Attention - anterior cingulate so dorsomedial and lateral
4. Respond to words with an x - start pressing with non targets after a while.
Working memory - tends to be dorsolateral
5. Delayed matching to sample - Monkeys with two choices, one with food, pause, has to hold on line. Prefrontal firing during delay period sustained.
Emotion - medial and orbital prefrontal
6. Iowa gambling task - risky or non risky gambles. Can manipulate so certain behaviours are optimal. People should be able to resist the big gambles. Medial prefrontal damage struggle with this
Planning - prob lateral (combination of attention, behavioural inhibition etc)
7. Tower of London Task - pegs of different lengths, have to reach a target by moving multiple pegs. Subgoals may be out of keeping with ultimate goals.

256
Q

Which areas are involved in attention?

A

Prefrontal and right parietal generally

NHB MVST 1b (11 decks)

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