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PSYC2020 > Week 8 > Flashcards

Week 8 Flashcards

1
Q

What is the Spinal Motor Circuits?

A

The descending motor circuits and feedback circuits to the muscles, association cortex, secondary motor cortex, primary motor cortex and brain stem motor nuclei

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2
Q

what are the motor units?

A

• Motor Unit - smallest unit
of control – motor neuron
and skeletal fibres it
innervates
• Neuromuscular Junction –
synapse between neuron
and muscle fibre -
acetylcholine release
activates the motor end
plate (post-synaptic)
causing the muscle fibre
to contract
• Each motor neuron can innervate multiple muscle fibres,
but each fibre innervated by only 1 motor neuron
• Number of fibres innervated reflects fineness of control
– 5 for an eye muscle (22,000 fibres) and 1,800 for a
large leg muscle (1 million fibres) (can range widely
within a single muscle)
• Motor pool –the collection of motor neurons that supply
a single muscle
• Typical muscle controlled by a pool of a few hundred
motor neurons
• 3 properties of motor units - contraction speed,
maximal force, fatiguability

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3
Q

Lower Motor Neurons

A 
• Motor neurons of the
spinal cord and brain
stem that directly
innervate muscle
• Inputs from brain,
muscle spindles, spinal
interneurons
(excitatory or
inhibitory)
• Located in ventral horn
and project out via
ventral root
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4
Q

Spinal Motor Circuits

A 
Motor circuits of spinal cord
show considerable complexity
Reflexes
Recurrent collateral inhibition
Reciprocal innervation
Locomotion
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5
Q

Reflexes

A 
• stretch (e.g. patellar – muscle
spindle afferent synapses
directly onto lower motor
neurons - monosynaptic)
• withdrawal – multisynaptic –
simultaneous excite/inhibit
flexor/extensor
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6
Q

Recurrent collateral inhibition

A 
• motor neuron axon branches
onto inhibitory interneuron
that projects back to itself
• each time it fires, briefly
inhibits itself (for a break) and
shifts responsibility to some
other member of the muscle’s
motor pool
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7
Q

Reciprocal innervation

A 
• constant contraction of
most muscles
• smooth, precise movement
requires adjustments –
antagonistic muscles must
be reciprocally adjusted
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8
Q

Locomotion

A 
• cats with severed spinal
cord walk on a treadmill
• with appropriate
sensory feedback, spinal
walking circuits activate
• basic motor pattern for
stepping in spinal cord
but initiation and fine
control requires range
of brain inputs
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9
Q

Descending Pathways in the brain

A

primary motor cortex to the brain stem motor nuclei

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10
Q

Descending Motor Pathways

A 
• Lower motor neuron has
many inputs
• Major inputs from the
brain
• Can synapse directly
• Most synapse indirectly
via a spinal interneuron
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11
Q

Descending Motor Pathways- tracts

A

From the primary motor cortex, signals descend to the muscles
through 4 pathways - 2 in dorsolateral regions in the spinal cord
and 2 in the ventromedial region in the spinal cord
2 Dorsolateral tracts – one direct and one indirect
• terminate in contralateral half of one spinal cord segment, and sometimes directly on a motor neuron
• limbs - especially independent movement of limbs 2 Ventromedial tracts – one direct and one indirect
• more diffuse, with axons innervating interneurons in several
segments of spinal cord
• body - control of posture and whole-body movements, and they control the limbs movements involved in these activities

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12
Q

Dorsolateral Tracts

A

Dorsolateral to Corticorubrospinal is INDIRECT
Dorsolateral
Corticospinal

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13
Q

Ventromedial Tracts

A 
Ventromedial
Cortico-brainstem-spinal Tract
INDIRECT
Ventromedial
Corticospinal
Tract DIRECT
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14
Q

Dorsolateral Tracts

A

• Corticospinal (direct)
• Descend contralaterally
• Synapse on small interneurons of spinal grey which
synapse on lower motor neurons that innervate distal
muscles – wrist, hands, fingers, toes
• Animals that can move digits independently have
some that synapse directly onto the motor neuron
• Corticorubrospinal (indirect)
• Descend contralaterally
• Ultimately control distal muscles of arms and legs

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15
Q

Ventromedial Tracts

A

• Corticospinal (direct)
• Descend ipsilaterally, branch diffusely and innervate
interneurons on both sides at several levels
• Cortico-brainstem-spinal (indirect)
• Upper motor feed complex network of brainstem
structures (tectum, vestibular, motor programs in
reticular formation)
• Outputs descend bilaterally (each side carrying info
from both hemispheres)
• Each neuron synapses on interneurons over several
segments – innervate proximal muscles of trunk and
limbs (e.g. should/hip)

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16
Q

Descending Motor Pathways- monkey experiment

A

• Lawrence & Kuypers (1968) transected descending
motor pathways in monkeys
• Dorsolateral (corticospinal)
• After surgery, monkeys could stand, walk and climb
• But could not use limbs for other activities (e.g.
reaching for things; and could not move fingers
independently)
• Ventromedial tracts
• Monkeys had postural abnormalities
• Impaired walking and sitting

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17
Q

Descending Motor Pathways

A

From the primary motor cortex, signals descend to the muscles
through 4 pathways - 2 in dorsolateral regions in the spinal cord
and 2 in the ventromedial region in the spinal cord
2 Dorsolateral tracts – one direct and one indirect
• terminate in contralateral half of one spinal cord segment, and
sometimes directly on a motor neuron
• limbs - especially independent movement of limbs
2 Ventromedial tracts – one direct and one indirect
• more diffuse, with axons innervating interneurons in several
segments of spinal cord
• body - control of posture and whole-body movements, and they
control the limbs movements involved in these activities

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18
Q

Motor Neuron Disease

A

• Group of diseases characterised by degenerative loss of motor
neurons (upper, lower, or both)
• Amyotrophic lateral sclerosis (ALS) most common (many
variations and classifications)
• Progressive muscle weakness and wasting - no cognitive
impairment
• Pattern of weakness, rate and pattern of progression, survival
time all vary
• No cure or treatment - survival 2-5 years from onset
• Cause uncertain – environment, lifestyle, subtle genetic (5 - 10%
of cases have family history)
• Inclusion bodies – cytoplasmic protein aggregates
• Early signs subtle – hard to diagnose (10-18 months) – sometimes
confusion between MND and myasthenia gravis

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19
Q

Motor Cortex- in the brain

A

Secondary motor cortex and primary motor cortex

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20
Q

Primary Motor Cortex (M1)- Part 1

A 
Major outgoing point from
cortex (NOT the only) –
descending motor pathways
• Major point of convergence of
sensorimotor signals - inputs
from PMC, SMA, frontal, basal
ganglia, cerebellum
• Penfield – electrical
stimulation led to activation
of contralateral muscle and
simple movement – motor
homunculus – somatotopic
and cortical magnification
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21
Q

Primary Motor Cortex (M1)- Part 2

A 
2 subdivisions
• Old rostral and new caudal
(primates)
• Caudal are the ones that
synapse directly onto lower
motor neurons for upper
limbs – dexterity –
dorsolateral corticospinal (i.e.
direct) tracts
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22
Q

Primary Motor Cortex (M1)- Part 3

A

• Each neuron in M1 previously thought to encode
direction of movement of a muscle
• Recently – stimulate with long bursts similar to
duration of motor response – elicit complex species
typical natural response sequences (eg feeding
response)
• Natural activity - particular neuron firing related to end
point of movement rather than direction – e.g. 90deg
bend in elbow – different responses depending on
initial configuration – say straight (180) or bent (45)

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23
Q

Primary Motor Cortex (M1)- Part 4

A

• Lesions – hemiplegia
• Very large may disrupt movement of particular
body part independently of others (e.g. finger)
• Reduce movement speed, accuracy, force
• Not eliminate voluntary movement entirely –
descending from secondary motor areas and
subcortical
• Distal extremities much more affected than
proximal limb and truck

24
Q

Secondary Motor Cortex- brain diagram

A 
• Input from
association cortex
(posterior parietal
and dlPFC)
• Output to primary
motor cortex
• Initially – PMC and
SMA; now at least 8
in each hemisphere
• SMA, pre-SMA,
supplementary eye
fields
• Dorsal and ventral
PMC
• 3 small cingulate
motor areas (at least
2 in humans)
25
Q

Secondary Motor Cortex- explaination

A

• Become active just before initiation of voluntary
movement and remain active during movement
• Electrical stimulation results in complex movements,
typically bilateral
• Programming of specific patterns of movement, with
input from the dorsolateral prefrontal cortex
• PMC/SMA functional distinction – externally or
internally guided action
• PMC – strong reciprocal connections with posterior
parietal cortex – sensory guided actions (catch a ball)
• SMA – strong connections with medial frontal cortex –
internally guided goals (playing piano)

26
Q

Mirror Neurons

A

• Rizzolatti et al. (90’s) studying monkey premotor cortex
using single cell recordings
• Interested in neurons that respond to complex hand
(and mouth) actions – reaching for a toy or reaching
for food
• Found neurons that fired preferentially when reaching
for one type of object but not for different object
• Then found that some of these neurons responded
identically when reaching for the object and when
observing human performing the same action
• Mirror Neurons – fire when perform a particular goal
directed hand movement or when observing the same

27
Q

Goal Directed Action

A 
• Response to goal directed
actions – no response to same
action if mimed and no object
• Respond to the goal of an action
such as the grasping of a piece of
food even when this action is
performed with different tools
(such as normal or reverse pliers)
requiring opposite sequences of
movements (closing or opening
of the fingers)
• Transform complex visual input
into high level understanding of
observed action
28
Q

Understanding Action

A 
• Don’t need to see the key
action if enough clues to
create a mental representation
• Screen to block and monkey
must imagine what is going on
• But if first show monkey that
no object behind the screen –
no response
29
Q

Purpose of the Action

A 
• Some mirror neurons in
inferior PPC respond to
purpose of action rather than
the action itself
• Fire when food grasped if it
was clear it was to be eaten
• If repeatedly grasp food to put
in bowl – little firing
30
Q

Mirror Neurons

A 
• Social cognition: knowledge of
perception, ideas, intentions
of others
• Action understanding: cooperation,
teaching/learning
• Language
• Emotional understanding -
empathy
31
Q

Mirror Neurons in Humans

A 
• Confirmation in humans not
as strong (single cell
recording) but similar mirror
networks (large scale)
suggested by fMRI and EEG
• Motor imagery – imagine
doing an action – PMC, PPC,
M1 all become active
(imagine observing – weak
motor activation – mainly
visual)
32
Q

Mirror Neurons in Humans- ballet example

A 
• Viewing ballet steps recruits
premotor and parietal mirror
areas more strongly in expert
ballet dancers than in nondancers
or in martial-art
teachers
• Recruitment of motor areas
with mirror properties
strongly correlates with motor
rather than visual expertise
• People can improve their
ability to judge the goal of an
unusual action simply by
practising that action
themselves; this improvement
occurs even when they
practise while blindfolded
33
Q

Association Cortex

A

To move …
• Need to know where things are – objects in the
environment and parts of the body
• Need to make a decision to initiate voluntary movement
• Posterior parietal cortex (PPC) - spatial information
• Dorsolateral prefrontal cortex (dlPC) - decide and initiate

34
Q

Posterior Parietal Cortex

A 
• Input from multiple
sensory systems
(visual, auditory,
somatosensory)
• Localisation of the
body and external
objects in space -
integrates
• Recall PPC in MSI
and dorsal
pathways
• Directs attention
• Outputs to
secondary motor
areas, FEF, and dlPFC
• Subregions
associated with eye,
hand, or arm
movements
• Damage – apraxia
and contralateral
neglect
35
Q

PPC Damage - Apraxia

A

• Disorder of voluntary movement but not a simple motor
deficit
• Difficulty making movements on request, but can make
the same movement under natural conditions when not
thinking about it
• Eg – can hammer a nail but cant demonstrate hammering
when asked
• Bilateral symptoms but damage usually unilateral – left
PPC
• Conscious planning of complex coordinated action

36
Q

PPC Damage – Contralateral Neglect

A

• Disturbance of ability to respond to stimuli on side
opposite lesion
• Usually right lesions and neglect left space
• Patients fail to appreciate that they have a problem
• Egocentric left – left of body – head tilt doesn’t
change (tilt) field of neglect
• Also neglect left side of body

37
Q

PPC Damage – Body Representation

A

• Intrinsic spatial coding: knowing what our own body
parts are doing
• Intrinsic coding is essential when a body part is
obscured from vision at some stage in the movement
planning and execution
• PJ: 50yo F; head injury when 43yo, 30min loss of
consciousness
• Jerking of the right arm at 48years, focal seizures,
presented for assessment
• No visual neglect or extinction, no other visual deficits
• Perceives her right arm and leg to
drift and fade unless she is able to
see them
• In bed, loss of knowledge in limb
position
• In public transport, other
passengers tripping over her leg,
which had drifted into the aisle
• MR: cyst encroaching on the
cortex and subcortical white
matter of left superior parietal
lobe

38
Q

Dorsolateral Prefrontal Cortex

A 
• Input from PPC
• Outputs to M1,
secondary motor,
FEF
• Evaluate external
stimuli and
decide to act –
goals based
• Decisions to
initiate voluntary
movement
39
Q

Basal Ganglia

A

• Complex heterogenous collection of interconnected nuclei
• Modulatory function – loops receiving cortical
input then back to cortex via thalamus (other nonmotor functions)
• Caudate and putamen (striatum), globus pallidus, subthalamic nucleus, substantia nigra
• Inputs from all over cortex (sensory, motor,
association) to striatum; output from GP and SN to motor and frontal cortex via thalamus
• Critical role in selection and initiation of action
• Complex, heterogenous
interconnected nuclei
• Connections excitatory or inhibitory
• Initiate selected movement

40
Q

Basal Ganglia- brain diagram

A 
Direct – enhances thalamic
output
Indirect – inhibits thalamic
output
But – indirect slightly
delayed so brief
enhancement then balance
SN input – turns up DIRECT
and turns down INDIRECT
To Enhances overall process
41
Q

Basal Ganglia

A

• This circuit model is speculative – details are way
more complicated
• Other inputs, outputs, connections, and
complexities not mentioned here
• Output (discharge rates) likely not the only
important factor
• Neuronal firing patterns likely important
• Synchrony of higher level activity likely important
• Complex coordinated activity of multiple
interconnected nuclei – fine balance
• Basics of function from disorders

42
Q

Basal Ganglia - Disorders

A

Disorders of motor control:
• Parkinson’s Disease – loss of modulatory dopaminergic
neurons in the substantia nigra
• Huntington’s Disease – loss of inhibitory GABAergic
neurons in the striatum
Note – these disorders have broader effects than just
motor and involve neurodegeneration in multiple regions

43
Q

Parkinson’s Disease- part 1

A

• Loss of dopaminergic neurons in the substantia nigra
• Increase indirect and decrease direct – decrease
thalamic output
• Latest – changes in neuronal firing patterns and
synchrony rather than reduced discharge rate
• Primarily affect indirect pathway
• Ultimately - decreased cortical activity
• Cardinal features – akinesia (slowed initiation),
bradykinesia (slowed movement), muscle rigidity,
tremor

44
Q

Parkinson’s Disease- part 2

A

• Reduction in spontaneous movement (hypokinesia)
• Slow initiation of movement (akinesia);
• Progressive slowing or freezing during a movement and
reduced range and scale of movement
• Micrographia
• Slow gait, often with freezing and small steps
• Poor arm swing
• Postural instability = many falls
• Dull, weak voice without inflections (hypophonia) and
slow speech
• Mask-like, unemotional expression

45
Q

Parkinson’s Disease Treatment

A 
• Dopamine agonist: L-Dopa (precursor)
• Increase dopamine generally
• Efficacy drops with usage
• Numerous side effects
• Chronic high frequency deep brain stimulation (DBS)
• Implanted device to stimulate STN (usually)
• High frequency disrupts activity
• Not sure how/why it works
• Reduce inhibition of thalamus?
• Replace irregular BG output to cortex with a regular, better
tolerated pattern?
• Disrupt abnormal frequencies?
46
Q

Huntington’s Disease

A

• Genetic neurodegenerative disease – manifests in
adulthood (35-55); life expectancy 10-25 years post
onset
• Autosomal dominant with complete lifetime
penetrance, chromosome 4 – excessive build up of
Huntingtin protein
• Destruction of GABAergic neurons in striatum (caudate
and putamen) – primarily affecting indirect pathway
• Progressive striatal atrophy: medial caudate first (small
spiny neurones), then putamen, then tail of caudate
• Reduced (indirect) basal ganglia output

47
Q

Parkinson’s Disease

A 
Direct – enhances thalamic
output
Indirect – inhibits thalamic
output
Enhancement of direct
versus indirect reduced
Decreased thalamic output
48
Q

Huntington’s Disease- diagram

A 
Direct – enhances thalamic
output
Indirect – inhibits thalamic
output
Thalamic inhibition reduced
– increased thalamic
excitation of motor cortex
49
Q

Huntington’s Disease

A

• First signs usually affective: depression, anxiety, irritability,
impulsivity, aggression
• Followed by: restlessness, clumsiness, poor coordination,
forgetfulness and personality changes
• Characteristic - athetosis (writhing movement) and chorea
(jerky movement)
• Poor motor dexterity, unsteadiness, reduced speed
• Altered speech and writing, saccadic changes
• They involve multiple joints and thus resemble voluntary
action
• They are briefly suppressible, and decrease during sleep
• They increase with stress and with voluntary movements
like walking

50
Q

Cerebellum

A

• Modulatory – fine-tuning and learning (other non-motor functions)
• Inputs from cortex (M1 and secondary motor), descending
motor signals from brain stem nuclei, somatosensory and vestibular feedback
• Compare signals with
feedback to correct ongoing movement that deviates from intended
• Project to brainstem nuclei and cortex (M1 and secondary) via
thalamus
• Role in motor learning especially when sequence timing critical
• Diffuse damage – lose precise control of direction, force, velocity
and amplitude of movement; lose ability to adapt movement to
changing conditions, disturbances in balance, gait, speech, eye
movement
• Cells in cerebellum that project to spinal cord especially sensitive to effects of alcohol – unsteady gait, disturbance of balance

51
Q

Cerebellar Dysfunction - Ataxia

A

• Loss of sensory co-ordination of distal limbs disrupting fine
coordination – finger to nose test
• Lack of muscle control or coordination of voluntary movements,
such as walking or picking up objects.
• Speech impacts
• Alcohol abuse, certain medications, stroke, tumour, cerebral palsy,
brain degeneration and multiple sclerosis

52
Q

Motor Acts, Volition, and Free Will- part 1

A

• Described voluntary behaviour as wilful –
intentionally initiated following a decision to act
(including rejection of the alternative of doing
nothing)
• Subjective experience – ownership of action,
agency, conscious control – ‘I’ did something on
purpose
• But ….

53
Q

Motor Acts, Volition, and Free Will- part 2

A

• Often act unconsciously or with minimal conscious
control
• Split brain patients – dissociation of action and awareness
• Confabulation – plausible (but incorrect) reasoning about
decisions to act with feeling of agency
• People are subject to other illusions of ownership
• People are subject to other illusions of control

54
Q

Motor Acts, Volition, and Free Will- part3

A

• A bilateral slowly increasing negativity (EEG of SMA) (termed
the ‘readiness potential’) was shown to precede voluntary
action by Kornhuber and Deeke (1965)
• Libet – have subjects perform a simple motor at random act
while looking at a fast moving ‘clock’ – note the position of the
clock when first aware of the intention to act
• Onset of the readiness potential hundreds of ms before
awareness of intention to act
• “the brain evidently ‘decides’ to initiate or, at the least,
prepare to initiate the act at a time before there is any
reportable subjective awareness that such a decision has
taken place”

55
Q

Motor Acts, Volition, and Free Will- part 4

A

• Soon et al (2008) – similar approach but using fMRI
• Look at a letter stream – freely press one of two buttons –
recall letter when motor decision was consciously made
• Intentions mostly formed 1000ms before press
• 2 brain regions encoded left vs right decision early –
frontopolar cortex and parietal
• Over 10 seconds before the decision to act (7 seconds on fMRI
signal)
• Timing of decision predicted in preSMA and SMA
• 5 seconds before the decision to act
• Dissociation between outcome of motor decision and timing

56
Q

Key Learnings- part 1

A

• Hierarchical, functional segregation, parallel, feedback
• Simple spinal circuits control some movement
• 4 descending pathways dorsolateral for fine control of
limbs, ventromedial for axial muscles/ whole body
movement (direct and indirect for each)
• MND – neurodegeneration of upper and/or lower
motor neurons
• Motor cortex – primary (M1) and several secondary
• Stimulate M1 – complex unilateral movement – motor
homunculus

57
Q

Key Learnings- part 2

A

• Stimulate secondary – complex bilateral movements
• Secondary – functional distinction – internally or
externally guided action
• Mirror neurons – goal directed actions
• Association cortex – functional distinction - spatial
information and decide/initiate
• Basal ganglia – selection and initiation of action – PD
and HD
• Cerebellum – fine tuning and learning – cerebellar
ataxia
• ‘Voluntary’ action

PSYC2020 (14 decks)

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