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PHYL2064 > Neuromotor L3 > Flashcards

Neuromotor L3 Flashcards

1
Q

______ (Large/small) alpha motor neurons innervate red fibres (small type I/slow twitch fibre)

A

Small Alpha

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2
Q

_____ (Large/small) Alpha motor neurons innervate type II (fast twitch) fibres

A

Large Alpha

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3
Q

_______ is a sign of chronic denervation (when one fibre dies the other one has to take up the territory that the one next to it that died innervated

A

Muscle fibre type grouping

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4
Q

What is muscle fibre type grouping?

A

a sign of chronic denervation (when one fibre dies the other one has to take up the territory that the one next to it that died innervated

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5
Q

What is a motor unit? What happens when a motor unit is denervated?

A

the one motor neuron to the number of muscle fibres it innervates (if the fibres next to it are denervated, it has to expand its territory to reconnect the innervated muscle fibres.

As a consequence, the motor unit expands and because fibre type is largely dictated by the type of neuron that connects to the muscle eg. slow motor neuron re- connecting to fast muscle fibres, then it would convert the fast muscle fibres to slow (vice versa))

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6
Q

What are the 2 mechanisms that postural adjustment is achieved by?

A
  1. Feed forward (anticipatory)
  2. Feed back (reflex) Requires post birth
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7
Q

What is the activity out of neurons within a deep cerebellar nucleus is governed by?

A

The activity out of neurons within a deep cerebellar nucleus is governed by (note if only had excitatory = no control) Purkinje neurons (will get inhibitory and excitatory inputs)

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8
Q

What is the major inhibitory neurotransmitter within the spinal cord?

A

Glycine

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9
Q

Explain how the knee jerk reflex is an example of reciprocal inhibition

A

Have post-synaptic gating and that neurons can be inhibited if they receive excitation from inhibitory neuron

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10
Q

Explain how motor unit expansion can lead to muscle weakness, poor control of movements and even muscle atrophy

A

In extreme cases where motor units are unable to reconnect to motor fibres

  • Keeps expanding and expanding and then it can’t cope –> no longer able to expand
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11
Q

What are the motor areas of the cerebral cortex?

A
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12
Q

What is the primary motor cortex (PMA)?

A

Controls Simple Features of Movement

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13
Q

What is the pre-central gyrus?

A
  • Somatopic representation of the body (body map)
  • Cell bodies located in lamina V - Betz Cells
  • Controls movts on opposite side of body
  • Excitatory connections to a, g MNs and Ins
  • Descending tract = CORTICOSPINAL tract. (Lateral Cortical spinal Tract, and Ventral Cortical spinal tract)
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14
Q

Disproportionate –> upper motor neuron pools are more in the hands and the face compared to the trunk and lower limbs • Have small muscle that control fine motor movements (eg. no gross movements like trunk ..etc) More weakness in large motor neurons because they are _____ (large/small) In small motor units, if the motor neuron dies then the one next to it can come with reconnection

A

large

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15
Q

What does the lateral cortical spinal track with direction connection to hand motor neuron muscle?

A
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16
Q

What does corticomotorneurons activate complex muscle patterns through divergent connections with spinal motor neurons that innervate different arm muscles?

A
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17
Q

How does Voluntary movement requires integration of all parts of the neuromotor system?

A
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18
Q

What is the pre motor cortex?

A
  • 30% project to spinal cord (corticopsinal tract) & PMA
  • To M1 region; some to spinal Inputs Sensory cortex and Visual feedback
  • Neural activity before PMA (GET SET)
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19
Q

What is the function of the pre motor cortex?

A

setting up the motor programs for learned sequences, - coordination of bilateral MOVTS - active when told to dream movt

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20
Q

What is the lesion of pre motor cortex?

A

impaired ability to execute purposeful MOVTS

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21
Q

What is the function of the pre-motor cortex (lateral regions)?

A

Function thought be involved in the learning of the programmed sequences.

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22
Q

What are the different areas of cortex are activated during simple, complex and imagined Sequences of finger movements?

A
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23
Q

What happens to the cortex when looking, listening, speaking and thinking about words?

A
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24
Q

What are the speech centres and language disorders (aphasias)?

A
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25
Q

What are the 3 types of aphasia (language disorders)?

A
  1. Brocas’s
  2. Wernicke’s
  3. Conduction
26
Q

What is the language disorder called?

A

aphasias

27
Q

What speech is affected in Broca’s (aphasias)?

A
  • Non-fluent
  • Effortful
28
Q

What comprehension is affected in Broca’s (aphasias)?

A

Largely preserved for simple words and sentences

29
Q

What repetition is affected in Broca’s (aphasias)?

A

Impaired

30
Q

What region is affected in Broca’s (aphasias)?

A

Left Posterior frontal cortex

31
Q

What speech is affected in Wernicke’s (aphasias)?

A
  • Fluent
  • Abundant
  • Well articulated
  • Melodic
32
Q

What comprehension is affected in Wernicke’s (aphasias)?

A

Impaired

33
Q

What repetition is affected in Wernicke’s (aphasias)?

A

Impaired

34
Q

What region is affected in Wernicke’s (aphasias)?

A

Left Posterior, superior and middle temporal cortex

35
Q

What speech is affected in Conduction (aphasias)?

A

Fluent with some articulatory defects

36
Q

What speech is affected in Conduction (aphasias)?

A

Intact or largely preserved

37
Q

What speech is affected in Conduction (aphasias)?

A

Impaired

38
Q

What region is affected in Conduction (aphasias)?

A
  • Left superior temporal
  • Supramarginal gyri
39
Q

What are the 5 (interconnection group) nuclei located in the forebrain?

A
  1. Caudate (CN)
  2. Putamen (Pt) 1+ 2 = Striatum (S)
  3. Globus Pallidus (GPe, GPi)
  4. Substantia Nigra (Pars Reticulata [SNr]+ Pars Compactor [SNc])
  5. Sub-Thalamic N. [STN]
40
Q

Inputs from all Cerebral Cortex project back to_____ lobes of Cerebral cortex (Pre-frontal, Pre-motor and Motor cortices). There is no direct connection to _____ MNs . Hence the motor functions of the ______ are therefore mediated in part by motor areas of the ____ cortex.

A

frontal; lower; basal ganglia; frontal

41
Q

What does the gross internal feed back circuit loop of the basal ganglia look like?

A
42
Q

In the basal ganglia, there is Input via the _____ and Output via the ______.

A

Striatum; Ventral Thalamic Nucleus

43
Q

What are the 3 motor control and cognitive functions of the basal ganglia?

A
  1. Old idea: Planning and execution of complex motor strategies (old idea)
  2. Current idea 1: do not generate movements BUT inhibit motor mechanisms that interfere with the desired movement and Dis-inhibit.
  3. Current idea 2: Specification of movement on the bais of the memory of the movement or memory of the outcomes.
44
Q

How have the motor control and cognitive functions of the basal ganglia been revealed?

A

Revealed by clinical observations

  • e.g. Parkinsons’ (Poor control of mvt)
  • Huntingtons’ disease (Over exuberance of movement)
45
Q

What does the basal ganglia loop look like?

A
46
Q

What is Parkinson’s an example of?

A

example of diminished movement.

  • Poverty of movement
47
Q

What are the 5 signs of Parkinson’s neuro denegerative disease?

A
  1. tremors at rest
  2. postural reflex impairment
  3. increase in muscle tone with ratchet - like - characteristics
  4. difficulty in initiating movt & paucity of spontaneous movts
  5. slowness in the execution of movt
48
Q

What is the treatment of Parkinson’s disease?

A

Treatment - L-DOPA

49
Q

What is affected in parkinson’s disease

A
  • Neural pathway affected by Parkinson’s (degeneration of the nigirostriatal pathway) (Diagram)

substantia nigra pars compacta

50
Q

What are the 9 mechanism in Parkinson’s Disease?

A
  1. DA input inhibits cholinergic Ins
  2. Loss Dis-inhibits these Ins
  3. Consequently inhibition of Caudate and Putamen (Striatum) is Reduced
  4. Thus stronger inhibition of GPe
  5. Inhibition of GPe leads to a Reduction in inhibitory out put from GPe
  6. Results in Dis-inhibition of Sub-thalamic N (activation of the indirect circuit).
  7. This causes the Subthalamic N to excite the GPi and SNr more strongly
  8. GPi and SNr inhibits the ventral thalamus more strongly.
  9. Causes a reduction in excitation of the motor cortex (from thalamus) All this leads to a poverty of MOVT.
51
Q

What part of the circuit is affected in Parkinson’s and Huntington’s?

A
52
Q

What is Huntington’s Disease?

A

It is an autosomal dominant disorder and affects 8 in 100 000 people

53
Q

What is the problem in Huntington’s Disease?

A

The Huntingtin gene (Htt) is located on chromosome 4 and it is the mutated version (mHtt) of the gene that is responsible for the disease

Polyglutamine disease: Involves triplet repeat: CAG

54
Q

Only 1-3% of the Huntington’s disease is _____.

A

sporadic

55
Q

What is the adult onset of Huntington’s Disease?

A

Adult onset –90% = 30-40 years old – symptomatic

56
Q

What is the juvenile onset of Huntington’s Disease?

A

10% = symptoms before 20 yrs

57
Q

What is the terminal disease of Huntington’s Disease?

A

death occurring 10-25 years after onset.

58
Q

What is the problem in Huntington’s Disease and what is an example of?

A

Degeneration of intrastriatal and cortical cholinergic neurons and GABA- ergic neurons.

  • An example of excessive movement.
59
Q

What are the 3 progressive signs of Huntington’s Disease?

A
  1. chorea (dance) uncontrolled movts of limbs and facial muscles
  2. dementia (reason goes)
  3. death (progressive)
60
Q

What are the 6 mechanism of Huntington’s disease?

A
  1. Motor impairment due to atrophy of CN and Putamen
  2. Dis-inhibition of the GPe
  3. This leads to stronger inhibition of the STN by the GPe
  4. Thus excitation of GPi and SNr by the STN is reduced
  5. This leads to reduced inhibition of Ventral thalamus by GPe and SNr
  6. Hence the Ventral thalamus excitatory drive to cortex is higher

(ie over excitation of cortex).

All this lead to over-exuberance of movement.

61
Q

What are the 2 treatments for Huntington’s disease?

A
  1. fetal grafting of Striatal tissue (now underway)
  2. inhibition of Caspase I an enzyme proteases associated with cell death & inflammatory cascades

PHYL2064 (29 decks)

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