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Neuroscience (own deck) > Motor Control and Disease > Flashcards

Motor Control and Disease Flashcards

1
Q

what do simple reflexes involve?

A
  • local circuit control by spinal sensory neurons over spinal motor neurons
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2
Q

what do lower motor neurons do?

A
  • they initiate movements produced by the skeletal musculature
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3
Q

what are central pattern generators?

A
  • they exist in the spinal cord

- they generate complex behaviours without input from the brain i.e. alternate movement of the limbs

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4
Q

what was the Fritsch and Hitzig experiment in 1870s?

A
  • used dogs to demonstrate that electrical stimulation of a part of the cortex elicits contraction of contralateral muscles
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5
Q

what is the primary motor cortex?

A
  • the area in the cortex that is involved in skeletal muscle contraction
  • located in the precentral gyrus (frontal lobe)
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6
Q

what are the neurons that are found in the primary motor cortex?

A
  • the upper motor neurons

- these control motor function

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7
Q

how was the primary motor cortex discovered to be somatotopically mapped?

A

Sherrington and Penfield

  • correlated site of stimulation with location of muscle contraction
  • showed a topographic map similar to that of the somatosensory system
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8
Q

how is the lower body represented in the motor cortex topographic map?

A
  • medially
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9
Q

how is the upper body represented in the motor cortex topographic map?

A
  • laterally
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10
Q

what do the proportions of areas in the motor cortex topographic map represent?

A
  • density of innervation

- behavioural significance of that body part

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11
Q

what is muscle movement innervated by?

A
  • lower motor neurons in the ventral horn of the spinal cord innervate striated muscle
  • innervation is by a specialised synapse called the neuromuscular junction
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12
Q

what 3 kinds of muscles do lower motor neurons innervate?

A
  1. axial muscles: trunk movement
  2. proximal muscles: shoulder, elbow, pelvis, knee movement
  3. distal muscles: hands, feet, digits movement
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13
Q

what kind of neuron inputs into a muscle fibre?

A
  • a single alpha motor neuron
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14
Q

how many muscles does one lower alpha motor neuron innervate?

A
  • each alpha motor neuron innervates the fibres of just one muscle
  • they can innervate more than one fibre of one muscle
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15
Q

what is motor unit?

A
  • the lower motor neuron and all the muscle fibres it innervates
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16
Q

what is a motor neuron pool?

A
  • all the lower motor neurons that innervate a single muscle
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17
Q

how are motor pools organised?

A
  • spatially organised in spinal cord

- grouped in rod-shaped clusters within the spinal cord over several vertebral segments

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18
Q

what experiment showed how motor pools were organised in the spinal cord?

A
  • tracer injected into gastrocnemius and soleus
  • in the spinal cord, a different set of motor neuron cell bodies are labelled for the gastrocnemius compared to the soleus

gastrocnemius occupies a different space compared to the soleus

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19
Q

what areas in the spinal cord do motor pools occupy?

A

the motor pools for each muscle occupy a distinct mediolateral and rostrocaudal position within the ventral horn

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20
Q

what does the mediolateral position of a motor pool reflect?

A
  • whether its motor neurons innervate a proximal or distal muscle
proximal = close to midline
distal = far from midline
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21
Q

what is the name given to the organisation of motor pools?

A

somatotopic organisation:

  • motor pools are organised somatotopically, both medio-laterally and rostro-caudally
  • there is a 3D map of the body’s musculature within the spinal cord
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22
Q

what does the somatotopy in the motor cortex reflect?

A

the location of the upper motor neurons that innervate the lower motor neurons in the spinal cord

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23
Q

where else do lower motor neurons (LMNs) receive inputs from, other than the spinal cord?

A

upper motor neurons (UMNs)

- UMNs project axons to LMNs via the descending tracts of the spinal cord

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24
Q

which descending tract is responsible for the control of voluntary movement?

A

the corticospinal tract (CST)

  • this is a lateral pathway of the spinal cord
  • axons of the CST originate in layer V of the motor cortex
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25
Q

how many layers are in the cortex, including the motor cortex?

A

90% of the cortex has 6 layers:

  • main inputs to the cortex are to the stellate cells in layer IV
  • main outputs are from layers III, V and VI
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26
Q

what cells of the motor cortex project axons in the CST?

A

large pyramidal cells in layer V (Betz cells)

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27
Q

what is the role of motor cortex UMNs?

A
  • fine voluntary control of distal body parts
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28
Q

where do CST outputs to the upper body originate from?

A
  • the lateral motor cortex
29
Q

where do CST outputs to the lower body originate from?

A
  • the medial motor cortex
30
Q

how do axons of the CST project into the spinal cord?

A
  • they cross the midline in the pyramidal decussation in the medulla
  • they then project laterally in the spinal cord
  • they synapse on lateral LMNs that control distal muscles
31
Q

where else are UMNs located, other than in the primary motor cortex?

A
  • in the brain stem
32
Q

where do brainstem UMNs project to?

A
  • brainstem UMNs project to medial motor pools involved in postural movement
  • axons from the brainstem project ipsilaterally in several tracts e.g. vestibulospinal and reticulospinal tracts
  • they project medially into the spinal cord
  • they synapse on medially located LMNs that control axial muscles
33
Q

what pathway are the brainstem UMN projections involved in?

A

the ventromedial pathway

34
Q

what do the ventromedial pathways control? how do they poject?

A

posture

- they project ipsilaterally and medially

35
Q

what are 3 examples of tracts that project ventromedially?

A
  1. vestibulospinal tract
    - head balance and turning
    - inputs from vestibular system
  2. tectospinal tract
    - orienting response
    - inputs from visual system via superior colliculus
  3. reticulospinal tract
    - control antigravity reflexes
36
Q

where do UMNs and LMNs directly synpase to?

A

UMNs directly synapse onto LMNs, or their interneuron circuitry

LMNs directly synapse onto muscle fibres

37
Q

how is postural control integrated with voluntary movement?

A

Anticipatory feedforward mechanism:

  • when someone lifts a lever, the first muscles to contract are in the leg
  • the anticipatory mechanism pre-adjusts the body posture to compensate for the forces that will be generated when lifting the lever
38
Q

how does the anticipatory feedforward mechanism show how UMNs in the cortex influence spinal cord circuits by two routes?

A

Movement anticipation starts in premotor area (PMA) (area 6)
- anticipation of movement activates an indirect projection to axial muscles via reticular formation

Movement initiation happens in the Primary Motor Cortex (area 4)
- activation of voluntary movement direct to the spinal cord via CST

39
Q

what is Motor Neuron Disease (MND)/ Amyotrophic Lateral Sclerosis (ALS)?

A
  • a degenerative disease of motor neurons
  • muscle atrophy/degeneration and sclerosis (hardening) of the lateral spinal cord
  • degeneration of axons in the CST
40
Q

what are the characteristics of LMN disease?

A
  • muscle paresis (weakness) or paralysis
  • loss of muscle tone due to loss of stretch reflexes
  • muscle atrophy
  • patients can die from lung dysfunction due to atrophy of intercostal muscles
41
Q

what are the characteristics of UMN disease?

A
  • muscle weakness
  • spasticity due to increased muscle tone due to failure of modulation of stretch reflex
  • hyperactive reflexes
  • loss of fine voluntary movement
  • patients can due from loss of input to the bulbar muscles (tongue and pharynx) boa the corticobulbar tract
42
Q

what can cause neurodegerative diseases?

A
  • excitotoxicity: overstimulation by glutamate leading to neuronal cell death
  • glutamate release occuring in hypoxic conditions e.g. after cardiac arrest, stroke or brain trauma
  • 10% cases are inherited: mutation in SOD1, an enzyme involved in removing free radicals that accumulate in metabolically active cells
43
Q

how can neurodegenerative diseases be treated?

A

Riluzole: drug which blocks glutamate release

- this only delays the disease by a couple months

44
Q

what is the overall role of the basal ganglia and cerebellum?

A
  • influence movement by indirectly regulating the function of UMNs
  • they have no direct connections to LMNs
45
Q

what are the key components in the initiation of movement?

A
  1. motor cortex (telencephalon)
  2. basal ganglia (forebrain)
    - caudate and putamen = striatum
    - globus pallidus (external and internal) (GPe and GPi)
    - subthalamic nucleus (STN)
  3. ventral lateral nucleus of the thalamus (diencephalon) (VLo)
  4. Substantia nigra (midbrain)
46
Q

what is the motor loop?

A
  • motor cortex connects to basal ganglia
  • this then feeds back to the premotor area (area 6) via the ventrolateral thalamus (VLo)
  • this controls the initiation of movement

2 pathways:

  • direct
  • indirect
47
Q

what is the direct pathway of the initiation of movement?

A
  1. With no initiating input the Globus Pallidus internal segment (GPi) tonically (continuously) inhibits VLo
  2. input from many cortical regions converges on the striatum (caudate and putamen)
  3. when activated by this input, the striatum inhibits the inhibitory activity of GPi
  4. this releases the VLo so it can activate area 6 and initiate movement
48
Q

how is the direct pathway modulated?

A

The direct pathway is modulated by a complex indirect pathway which involves the substantia nigra (SN) and GP external segment (GPe)

The substantia nigra has a complex role and acts via the striatum (CP) to maintain the balance between inhibition and activation of the VLo.

49
Q

what is the indirect pathway of the initiation of movement?

A
  1. excitatory input from the SN activates the inhibition of GPi through the direct pathway.This activates VLo
  2. in the indirect pathway, the striatum inhibits GPe, which would normally inhibit GPi. GPi is still active and so continues to inhibit VLo
  3. inhibitory input from the SN decreases striatum inhibition of GPe.
  4. this allows GPe to inhibit GPi, meaning VLo is active again to activate area 6 and initiate movement
50
Q

what does degeneration of neurons in parts of the initiation of movement pathways lead to?

A

parkinson’s or huntington’s disease

51
Q

what is Parkinson’s disease?

A
  • second most common neurodegenerative disorder (1:100 people aged over 60)
  • 85-90% sporadic cases
  • 10-15% familial cases caused by mutation

caused by loss of dopamine (DA)

52
Q

what are the symptoms of PD?

A
  • hypokinesis - insufficiency of movement
  • bradykinesis - slow movements
  • akinesis - no movements
  • increased muscle tone - rigidity
  • resting tremor at 4-5Hz
  • shuffling gait and flexed posture
  • impaired balance
  • mood disorders
  • loss of sense of smell
53
Q

how is PD caused?

A
  • dopamine loss/reduction due to loss of dopaminergic neurons in the SN
  • degeneration of these neurons is marked by the presence of Lewy bodies (intracellular protein aggregates)
  • DA falls over time as the neurons that make it are dying
54
Q

how much of the brain’s dopamine is found in the basal ganglia?

A
  • 80%

- specifically in the SN

55
Q

what is the L-DOPA therapy for PD?

A
  • L-DOPA is a dopamine precursor
  • can briefly reverse the symptoms of PD
  • oral L-DOPA can halt the disease
  • works by boosting capacity of surviving DA-ergic neurons in the SN to make DA
56
Q

what are the limitations of L-DOPA therapy for PD?

A
  • it does not stop the degeneration of SN DA-ergic neurons
  • eventually, there are insufficient SN neurons left to make DA
  • side effects: increase in motor response fluctuations and drug related dyskinesias
57
Q

what does reduced dopaminergic input from the SN to the striatum cause?

A
  1. decreased activity of the direct pathway
  2. increased activity of the indirect pathway
  • this means less inhibition of GPi, so its inhibitory action of VLo is increased
  • this leads to decreased VLo activity so less motor cortex activation
  • leads to hypokinesis (reduced movement)

L-DOPA can reverse this effect as long as some DA-ergic neurons survive

58
Q

aside from L-DOPA, what other ways can reverse the effects of PD?

A
  1. surgical removal of the GPi

2. deep brain stimulation to inhibit GPi hyperactivity

59
Q

what is Huntington’s disease?

A
  • a rare, hereditary disease
  • progressive and fatal
  • 3-7/100000 with European ancestry

caused by an autosomal dominant genetic disease resulting in neuronal degeneration:

  • firstly affects indirect pathway components of the striatum
  • then affects direct pathway components and the GPe
60
Q

what are the symptoms of HD?

A

early:

  • hyperkinesia or dyskinesia
  • chorea: involuntary twitching movements

late:

  • akinesia and dystonia (spasms)
  • dementia
  • psychosis (personality disorder)
61
Q

how is the basal ganglia affected in HD?

A

early: degeneration in the striatum reduces the indirect pathway inputs to the GPe
- this increases inhibition of GPi, meaning VLo is active and there is an inappropriate initiation of movement
- hyperkinesis, chorea

late: the striatal direct pathway and GPe neurons degenerate
- this releases GPi to over-inhibit the VLo
- akinesis

62
Q

what is the difference between PD and HD?

A
  • PD is due to degeneration of the SN and leads to hypokinesis
  • HD is due to the degeneration of the striatum and leads initially to hyperkinesis, and then to akinesis
63
Q

how are genetics involved in PD?

A
  • most cases of PD are sporadic, and only 10-15% cases are inherited
  • mutations in multiple genes predispose you to PD
  • some mutations are rare but with high penetrance (SNCA)
  • some mutations are common but with low penetrance (GBA1)
  • PD genes encode proteins involved in protein degradation pathways (e.g. SNCA, hence Lewy bodies), or mitochondrial function (PINK1, DJ-1)
64
Q

how are genetics involved in HD?

A
  • HD is rarely sporadic (0.005%) and mainly inherited
  • only mutations in HTT (encoding the huntingtin protein) causes HD
  • a specific mutation in HTT means a patient is certain to get HD at some point
  • function of HTT is possibly involved in intracellular transport
  • mutant HTT contains extensions of poly-glutamine which contributes to aggregation of proteins in inclusion bodies of affected neurons
65
Q

what is the cerebellum?

A
  • modulates UMNs - no direct connection to the spinal cord

- required for the learned execution of planned, voluntary, multi-joint movements

66
Q

how is the cerebellum important in throwing a ball?

A
  • cerebellum instructs motor cortex with respect to direct, timing and force of movement
  • based on predictions of outcomes
  • movements are too fast to feed back sensory info to be of immediate use
  • predictions are based on past experiences of movements
  • cerebellum compares what is intended with what actually happens
  • key in motor learning
67
Q

how does the cerebellum form a loop with the motor cortex?

A
  • it receives massive input from many areas of the cortex, corticopontocerebellar projection and sensory info from spinal cord and vestibular system
  • it then projects back to the motor cortex via the thalamus (doesn’t output to spinal cord)
68
Q

what is the function of the the cerebellum-motor cortex loop?

A
  • detect and correct differences between the intended movement and the actual movement
  • ‘motor error’
  • it records the motor error detected and builds it into its prediction for the next time the same movement is made
69
Q

what does lesions in the cerebellum cause?

A

cerebellar ataxia: poorly integrated movement

- dyssynergia: ability to perform a simple task like touching your nose is lost

Neuroscience (own deck) (14 decks)

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