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Health.2 > CNS Motor Control & Systems 🧠 > Flashcards

CNS Motor Control & Systems 🧠 Flashcards

1
Q

Motor control: Desc control of spinal circuits and motor cortex

What are the 3 components of the motor system?

A
  • cerebral cortex (and voluntary movement)
  • descending pathways
  • spinal cord
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2
Q

What is the brain part of the motor system?

A

the cerebral cortex

  • motor cortex
  • sensory input
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3
Q

What are the two non-brain components of the motor system?

A

descending pathways

  • lateral= volunatry
  • ventromedial (brainstem control)

spinal cord

  • motor neurons
  • sensory input
  • local reflexes
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4
Q

What neurones within the spinal cord are part of the motor system?

A

alpha motor neurones

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5
Q

Where in the spinal cord are these alpha motor neurones?

A

the ventral horn - they then directly synapse w muscles at neuromuscular junction to initiate movement

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6
Q

What can influence the motor neurone activity in the spinal cord?

A

sensory input

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7
Q

What type of local pathways can be activated in the spinal cord?

A

local reflexes

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8
Q

What are 3 key features of the spinal cord?

A
  • motor neurones
  • sensory input
  • local reflexes
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9
Q

What are the two types of descending motor pathways?

A
  • lateral

- ventromedial

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10
Q

What type of movement is the lateral pathway in charge of?

A

voluntary e.g. decision to stand up

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11
Q

What type of movement is the ventromedial pathway in charge of?
brainstem control

A

involuntary (e.g. maintaining posture)

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12
Q

What are the two key features/functions of the cerebral cortex as part of the motor system?

A
  • voluntary movement

- sensory input

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13
Q

What nuclei are under the cortex and what do they form?

A

subcortical nuclei, form the basal ganglia

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14
Q

What are the 3 key features of the motor system?

A
  • hierarchical organisation
  • feedback loops
  • somatotopic representation
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15
Q

Where does the spinal cord receive input from?

A
  • sensory receptors
  • brainstem
  • primary motor cortex
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16
Q

Where does the the spinal cord output to?

A
  • brainstem
  • sensory receptors
  • cerebellum
  • thalamus
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17
Q

Where does the brainstem receive input from?

A

primary motor cortex

cerebellum

SC

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18
Q

Where does the premotor and supplementary motor cortex receive input from?

A

thalamus

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19
Q

Where does the premotor and supplementary motor cortex output to?

A
  • basal ganglia
  • cerebellum
    blue
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20
Q

Where does the thalamus receive input from?

A
  • basal ganglia
  • cerebellum
  • spinal cord
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21
Q

Where does the thalamus output to?

A

premotor and supplementary motor cortex

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22
Q

Where does the primary cortex output to?

A
  • brainstem

- spinal cord

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23
Q

Where does the basal ganglia receive input from?

A

premotor and supplementary motor cortex

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24
Q

Where does the basal ganglia output to?

A

thalamus

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25
Q

Where is the cerebellum receiving input from?

A
  • precentral and supplementary motor cortex

- spinal cord

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26
Q

Where is the cerebellum outputting to?

A

thalamus

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27
Q

What is meant by ‘somatotopic representation’?

A

sensory info reaches a specific group of neurones in the cortex that expects input from a specific part of the body

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28
Q

What are the 3 types of movement?

A
  • reflex
  • rhythmic motor patterns
  • voluntary
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29
Q

How are reflexes generated?

protective e.g. limb withdrawal

A

by closed loop motor patterns in the SC

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30
Q

What are examples of rhythmic motor patterns? 3

A
  • walking
  • breathing
  • chewing
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31
Q

What are rhythmic motor patterns a combination of?

A
  • voluntary and reflex movements

- e.g. walking is a reflex, but can be sped up or slowed down (voluntary)

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32
Q

What is the nature of voluntary movement?

A

purposeful, goal directed

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33
Q

Where does command originate for voluntary movement?

A

higher centres

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34
Q

Are voluntary movements open or closed loop?

A

open - they can be modulated as they’re happening

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35
Q

Lower motor neurones

What types of motor neurones are known as the ‘final common pathway’ of motor control? Why?

A

alpha neurones - these are the only ones making direct contact with muscle

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36
Q

What are lower motor neurones also known as?

A

alpha motor neurones

a-MNs

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37
Q

Input from what governs spinal motor neurone activity?

A

REFLEXES:

  • sensory input (dorsal roots)
  • spinal interneurones
  • upper motor neurones
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38
Q

Why are spinal interneurones known as “inter”?

A

connections these neurones make are all located within the spinal cord

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39
Q

What of the inputs to spinal motor neurone activity control reflexes?

A
  • sensory input (dorsal roots)

- spinal interneurones

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40
Q

Where are the upper MN located? What does this mean for their function?

A
  • cerebral cortex

- in charge of initiating and controlling voluntary

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41
Q

What does the saying “see the headless chickens running” tell us about spinal cord circuits?

A
  • even if input from descending tracts are severed, the spinal cord can generate coordinated movement
  • hence brain influence is not necessary
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42
Q

What are the circuits generated within the spinal cord sufficient to cause coordinated movement called?

A

central pattern generators

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43
Q

descending inputs from the upper motoneurons?
causes…
superimposed upon what?

A
  • causes sophisticated, adaptable, patterns of movement
  • This is voluntary or otherwise involves input descending from the brain
  • superimposed upon the intrinsic circuitry of the spinal cord
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44
Q

what is an upper motoneuron?

A
  • confined to the CNS
  • initiates voluntary movement
  • maintenance muscle tone for support of the body against gravity
  • regulates posture to provide a stable background upon which to initiate
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45
Q

What is fine motor control?

innervated by…

A
  • ability to make movements using the small muscles (hands / wrists / toes)
  • innervated by lateral motoneurons
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46
Q

What is posture?

A
  • movements made by larger muscles (elbow/knee/trunk)

- innervated by medial motoneurons

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47
Q

what do MEDIAL motorneurons innervate?

A

axial: trunk muscles
proximal: elbow, knee

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48
Q

what do LATERAL motorneurons innervate?

A

distal: hands, feet, digits

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49
Q

What are the 2 lateral descending pathways?

A
  • Direct
    motor cortex -> SC
  • Indirect
    motor cortex -> red nucleus -> SC
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50
Q

How many ventromedial descending pathways are there?

A

2 indirect pathways…
motor cortex > brainstem (Vestibular Nuclei) > SC

or
motor cortex > Reticular Nuclei > spinal cord

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51
Q

How many Lateral descending pathways are there?

A

2: 1 direct, 1 indirect, through red nucleus

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52
Q

lateral pathways are…

A

VOLUNTARY

distal muscle flexors

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53
Q

ventromedial pathways govern…

A

POSTURE

proximal/axial muscles extensors

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54
Q

What are the 2 lateral descending motor pathways?

A
  • Corticospinal (pyrimidal/ direct) Tract

- Rubrospinal Tract (indirect)

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55
Q

What is the corticospinal (pyrimidal) tract? lateral pathway

A

direct line contralateral projection from cortex -> lateral spinal motor neurones

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56
Q

corticospinal (pyrimidal) tract has what kind of contact with aMNs?

A

monosynaptic

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57
Q

corticospinal (pyrimidal) tract- where are majority of axons, and what does it innervate?

A

… from neurons w cell bodies in motor cortex (areas 4-6)

aMNs (a interneurons a bit)
controlling distal muscles and esp flexors

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58
Q

What is the Rubrospinal Tract?

A

contralateral projections from red nucleus running down lateral column of SC

similar role to corticospinal tract, but smaller component of lat pathway

less important in humans

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59
Q

4 ventromedial descending pathways?

pic on p607 too

A

vestibulospinal tract
tectospinal tract
pontine reticulospinal tract
medullary reticulospinal tract

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60
Q

What are the consequences of damage to the lateral ASCENDING spinal sensory pathway?

A
  • can lead to motor deficit

- slower voluntary movements

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61
Q

What is the effect of damage to the lateral ASCENDING spinal sensory pathway on POSTURE?

A

no effect

- no damage to ventromedial tract

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62
Q

Are there any compensatory mechanisms if there is damage to the corticospinal tract?
(selective corticospinal tract legion)

A
  • rubrospinal tract can compensate almost entirely for loss of corticospinal (except fine digit control)
  • Re-routing of cortical output via the rubrospinal tract
63
Q

Where do the ventromedial (extra-pyramidal tract) motor pathways originate?

A
  • brainstem nuclei

- carry motor fibres to the spinal cord

64
Q

What are the ventromedial pathways responsible for?

A

involuntary and automatic control of all musculature, such as muscle tone, balance, posture and locomotion

65
Q

What do extra-pyramidal side effects mean and “ of dopaminergic drugs affect what??

A
  • occur when using anti-psychotics
  • symptoms include an inability to sit still, involuntary muscle contraction, tremors, stiff muscles, and involuntary facial movements.

trunk muscles

66
Q

What are the 2 pairs of ventromedial pathways?

A

reticular nuclei

  • Pontine reticulo-spinal
  • Medullary reticulo-spinal

superior colliculus and vestibular nuclei

  • Vestibulo-spinal
  • Tecto-spinal
67
Q

What is the importance of the 4 ventromedial pathways? 2 pairs

A

controlling balance, body position, visual input

-> modulate spinal reflexes and maintain body balance/posture

68
Q

What is the Pontine reticulo-spinal tract roles? 2

A
  • Enhances anti-gravity reflexes of SC

- Facilitates leg extensors to maintain standing posture

69
Q

What is the Medullary reticulo-spinal tract roles?

A

opposing effect to Pontine reticulo-spinal tract

  • Frees antigravity muscles from reflex control
  • Allows voluntary override
70
Q

What is the Vestibulospinal tract- what info does it relay from inner ear and axial muscles?

A
  • Relays gravitational sensory info from vestibular labyrinth (inner ear) and stretch receptors in axial muscles
  • Maintains head and neck position and also legs
71
Q

What is the tectospinal tract roles? 2

A
  • Relays visual sensory information from retina and visual cortex
  • Orientates head & eyes to visual and auditory stimuli
72
Q

Cerebral cortex and voluntary movement

what do cortical motor areas control?

A

voluntary movement, involves almost all of neocortex

73
Q

other than execution, what 4 things does movement involve?

A
  • sensory input
  • planning
  • deciding appropriate action
  • holding plan in memory
74
Q

What is the primary motor cortex also called… and where located?

A

M1/ Area 4
in the precentral gyrus
near primary sensory cortex

75
Q

where is the pre-motor area (PMA)?

A

next to the primary motor cortex and the supplementary motor area (SMA)

  • SMA and PMA combine to form AREA 6
76
Q

Which 2 areas make up up the motor area of the brain?

A

Area 4: Primary motor cortex
and
Area 6: Pre-motor area and supplementary area

77
Q

which area in motor cortex= lowest stimulus threshold= strong synaptic link?

A

area 4- M1 prim motor

area 6=more complex movement

78
Q

What is a homonculus?

A
  • map along the cerebral cortex of where each part of the body is processed
  • sensations occur all along the body.
  • Larger areas on the homunculus represent the greater supply to these areas of the body
79
Q

Roles of cortical motor areas:

1. primary motor cortex (M1; area 4)

A

control distal musculature (fine motor control)

80
Q

Roles of cortical motor areas:

2. premotor cortex (area 6; lateral) controls…

A

proximal musculature (posture, balance)
movement sequencing
prep for movement, initiation

(planning + movement)

81
Q

Roles of cortical motor areas:

3. supplementary motor area (area 6; fronto/medial)

A

role in planning + initiation

bi-manual co-ordination

82
Q

Which kind of movement is evoked when Area 6 is stimulated?

A
  • complex movement

- some movement can be stored for use once stimulated

83
Q

What are upper motor neurons?

A
  • ~50% of corticospinal tract axons
  • neuronal cell bodies originate in the 5th cortical layer
  • Somatotopically organised
  • Activate small groups of muscles rather than single ones
  • Individually encode the force OR direction of movement
84
Q

How can upper motor neurons be damaged? 3

A
  • tumours
  • stroke
  • infection
85
Q

What are symptoms of damage to upper motor neurons?

A

Eventual spasticity (⬆ resistance to passive movement)
o ⬆ muscle tone (hypertonia)
o ⬆ reflex responses (hyperreflexia)

86
Q

Which side of the body is affect by damage to upper motor neurons?

A

opposite side to damage

87
Q

Is recovery possible from damaged upper motor neurons?

A

yes. Primary motor cortex shows adaptive alterations

88
Q

Cerebellum

What is the cerebellum?

A

part of the brain associated with voluntary responses.

doesn’t project outside the brain

89
Q

What are the functions of the cerebellum?

A

· Closely involved with brainstem mechanisms

· Control of muscle tone and body posture

· Sensorimotor coordination

· Motor learning

90
Q

What are the 3 anatomical regions of the cerebellum?

A
  • Spino-cerebellum (medial region)
  • Vestibulo-cerebellum (caudal region)
  • Cerebro- (ponto-) cerebellum (lateral hemispheres)
91
Q

Characteristics of the 1. spino-cerebellum?

  • sensory input?
  • output?
  • controls?
A
  • receives sensory input from SC
  • output -> reticular formation + red nucleus
  • from reticular formation/ red nucleus, info sent back to SC via motor cortex
  • this is involved in coordination of motor movements and maintenance of muscular tone.
92
Q

Characteristics of the vestibulo-cerebellum?

  • sensory imput?
  • output?
  • controls?
A
  • receives input from + output to: vestibular nucleus via ventromedial pathway
  • control over posture/ balance and eye movement
93
Q

Characteristics of the cerebro-cerebellum?

A

intracerebral motor loop

cortex -> cerebellum -> back to cortex (M1)

  • Instructs primary motor cortex (M1): movement direction, timing, and force
  • Compares intended movements with actual movements sends compensatory instructions to M1
94
Q

damage to cerebullum 1:

What is ataxia and what functional component of the cerebellum does this affect?

A
  • causes staggering and slurred speech

- affects all functional areas of the cerebellum

95
Q

damage to cerebullum 2:

What is dysmetria and what functional component of the cerebellum does this affect?

A
  • causes inability to control distance/ force of movements

- affects spino-cerebellum and cerebro-cerebellum

96
Q

damage to cerebullum 3:

What is hypotonia and what functional component of the cerebellum does this affect?

A
  • causes reduced muscle tone (over-relaxation of muscle)

- affects spino-cerebellum

97
Q

damage to cerebullum 4:

What is slow saccades/ nystagmus and what functional component of the cerebellum does this affect?

A
  • causes impaired eye movemnt

- affects vestibulo-cerebellum

98
Q

damage to cerebullum 5:

What is Dysarthria and what functional component of the cerebellum does this affect?

A
  • causes slurred speach (weakened speech msucles)

- affects cerebro-cerebellum

99
Q

What are the 2 inputs to the cerebellar cortex (deep cerebellar nuclei)?

A
  • climbing fibers - directly excite Purkinje cells

- mossy fibers - indirectly excite Purkinje cells (via parallel fibres of Granule cells)

100
Q

Where do climbing fibers originate?

A

inferior olivary nucleus in medulla

101
Q

Where do mossy fibers originate?

A

Brainstem nuclei

102
Q

What are the outputs from the cerebellar cortex?

A
  • ONLY purkinje cells
  • project to deep cerebellar nuclei
  • inhibitory output
103
Q

What is the deep cerebellar nuclei (DCN) cells role??

A

compare input from mossy and climbing afferent input

BEFORE: via collaterals from axons to P cell- EXCitatory
AFTER: cerebellar processing via INHIB P cell output

comparison can -> error signal

104
Q 
******************
cerebellar function summary:
- whats it regulate?
- act as...
- role in....
A

regulates: posture indirectky: adjusting output of major desc motor pathways

acts as

  • COMPARATOR: identify + correct discrep in intented movement and actual
  • TIMER: sequencing motor activation-> smooth performance

role in motor memory and learned motor seq when appr.

not required for perception/muscle activation

105
Q

BASAL GANGLIA

what is it? what happpens here?

A

group of associated subcortical nuclei
‘dark basements of brain’

integrates sensory + motor info from cortex… relays back to cortex via thalamus.
loop

selection and initiation of voluntary movement

106
Q

does basal ganglia project outside the brain?

107
Q

what happens if basal ganglia gets damaged?

A

movement disorderes

108
Q

What are the functions of the basal ganglia? 2 distinct

A

· Responsible for the Integration of sensory and motor information

· Selection and initiation of voluntary movement

109
Q

What is the cortico-basal ganglia-cortical loop?

A

· Integrates motor and sensory information from the cortex

· Relays back to the cortex via thalamus

· Motor loop circuit output to PMA/SMA cortex

· Involved in selection and initiation of voluntary movement

110
Q

What is the motor loop at rest?

A
  • Cortex sends info to the basal ganglia (excita)
  • Basal ganglia sends outflows to the thalamus (inhibitory)
  • Thalamus is unable to send info to the cortex to cause movement
111
Q

whys inhibi BG outflow paused?

A

to allow thalamus to be free to stimulate cortex= initiate movement

112
Q

What is the motor loop when we want to move?

A
  • prefrontal cortex thinks about this and sends EXCITATORY info to the basal ganglia
  • Excitatory outflow to the basal ganglia REMOVES the inhibitory outflow to the thalamus
  • Thalamus Dis-inhibition allows for excitatory outflow to be passed to the cortex (causing movement)
113
Q

What are the structures of the Basal Ganglia?

A

STRIATUM (STR)

  • Caudate nucleus
  • Putamen
  • Nucleus accumbens
  • Subthalamic nucleus (STN)
  • Globus pallidus (2 segments - internal/external)
  • Substantia nigra (2 segments - regulata/ pars compacta)
114
Q

What is the collective term for the Caudate nucleus, Nucleus accumbens and Putamen?
and is it input/outflow?

A

Striatum STR

input from cortex

115
Q

What is the INTERNAL segment of the Globus pallidus responsible for?

A
  • sending Inhibitory Outflow to the Thalamus

- uses GABA as a neurotransmitter

116
Q

What is the RETICULATA segment of the Substantia Nigra responsible for?

A
  • sending Inhibitory Outflow to the Thalamus

- uses GABA as a neurotransmitter

117
Q

At rest what is the effect of the basal ganglia output on the excitatory drive to the cortex?

A
  • output inhibits the excitatory drive of the thalamus to the cortex

circuit pic p628

118
Q

What are the pathways of the basal ganglia? and role of each?

A
  • direct: promote movement

- indirect: suppress movement

119
Q

What is the (Dopamine +) direct pathway of the basal ganglia?

A

Striatum –> Substantia Nigra Regulata OR Globus palidus internal –> Thalamus –> cortex

120
Q

How is movement generated via the DIRECT pathway?

A

cortex STIMULATES inhbitory effects of striatum on the Substantia Nigra Regulata (SNr)

  • Inhibitory effects of SNr on the thalamus are stopped (stimulates thalamus)
  • Thalamus sends EXCITATORY information to Cortex
121
Q

What is the effect of dopamine in the Direct pathway of the basal ganglia?

A
  • acts on D1 receptors on the Striatum
  • increases the inhibitory effects of striatum on the substantia nigra reticulata

DEC BG output
facilitates movement

122
Q

How is movement suppressed via the INDIRECT pathway?

A
  • cortex sends excitatory signals to striatum which inhibits Globus palidus external (GPe)
  • Inhibitory signals from GPe to Subthalamic nucleus (STN) are stopped
  • Dis-Inhibition of STN, increases excitatory signals from STN to Substantia Nigra regulata/ SNr

(inhibitory)

  • Increased stimulation of SNR increases inhibitory signals to thalamus
  • inhibition of the thalamus inhibits excitatory signals to cortex (stops movement)
123
Q

What is the effect of dopamine in the Indirect pathway of the basal ganglia?

A
  • Dopamine acts on inhibitory D2 receptors on the striatum - inhibiting the striatum
  • Inhibiting the striatum stops the inhibitory effect on the Globus palidus external (GPe)
  • Dis-inhibition of the GPE increases the inhibition of the excitatory Subthalamic nucleus (STN)
  • Inhibition of the STN decreases the inhibitory effect on the Substantia Nigra regulata/ SNr on the thalamus
  • Dis-inhibition of the thalamus allows for excitatory effects on the cortex (stimulating movement)

pic p 629

124
Q

what is dopamines role in both direct and indirect pathways? BG

same end result

A

direct: act on excitatory D1 rec on striato- Gpi/SNr neurons…⬇ BG output.. movement ☺

indirect: act on inhibitory D2 rec on striato- GPe neurons… ⬇ STN activity ⬇ BG output… movement ☺
- less activity

125
Q

What is the consequence of imbalance between the indirect and direct pathways?

A

motor disfunction

  • hypokinetic disorders (Parkinson’s Disease)
  • hyperkinetic disorders (Huntington’s Disease)
126
Q

What is Parkinson’s disease?

A

Movement disorder caused by the death of cells that generate dopamine in the basal ganglia and substantial nigra pars compacta.

127
Q

What are 4 symptoms of Parkinson’s Disease?

A

1) Resting tremor (shaking)
2) Bradykinesia: Slowed movement
3) Rigidity of movements of the face
4) Akinesia (the absence or reduction of movement)

128
Q

What is the primary pathology of Parkinson’s Disease?

A
  • Progressive degenerative loss (> 80%) of nigro-striatal dopaminergic pathway
  • -> excessive inhibition of thalamo-cortical pathway
129
Q

What is the rational for treating Parkinson’s Disease?

A

Dopamine loss in basal ganglia-> excessive inhibition of thalamo-cortical pathway

driven by ⬆ activity in subthalamic nucleus STN - stimulates Substantia nigra Regulata - inhibits thalamus

130
Q

How can we treat Parkinson’s disease?

A

need to boost dopamine in brain

Dopamine boosting agents

  • L-DOPA
  • Drugs that slow Dopamine Metabolism (MAO-B inhibitors)
  • Deep brain stimulation
131
Q

What is Huntington’s disease?

A

A degenerative disease of the nervous system.

uncontrollable, rel rapid motor patterns disrupts normal motor activity

autosomal dominant disorder

132
Q

What is the primary pathology of Huntington’s Disease?

A

loss of striatal output neurons in indirect pathway

133
Q

What is the rational for treating Huntington’s Disease?

A

· Loss of striatal cells in indirect pathway leads to the suppression of STN

· This leads to the dominance of the direct pathway, leading to decreased Basal Ganglia output and an overactive thalamocortical pathway

· Overactive thalamocortical pathway leads to excessive involuntary movemnt

134
Q

How can we treat Huntington’s Disease?

A

Symptomatic treatments only:

· Tetrabenazine = VMAT inhibitor - decreases Dopamine storage and release

· Chlorpromazine – Dopamine receptor antagonists (antipsychotic)

Baclofen – GABA-B agonist, decreases spinal reflexes

134
Q

What are other Hyperkinetic disorders of the Basal Ganglia origin? 2

A
  • Hemiballismus

- Tardive Dyskinesia

135
Q

cause and effect of..
- Hemiballismus

  • Tardive Dyskinesia
A
  • Hemiballismus
    damage to subthalmic nucleus (from stroke)
    violent flailing movement of limbs
  • Tardive Dyskinesia
    long term exp to antipsychotics (DRAnt.. inc sensitivity?)
    uncontrolled movement esp facial, trunk muscles
136
Q

dopamine therapy in PD can also ->?

A

acute dyskinesia

uncontrolled movement esp face + trunk muscles

137
Q

what does deep brain stimulation for PD target?

A

subthalmic nucleus…

  • neurosurgical procedure involving the placement of a medical device called a neurostimulator.
138
Q

L: Drugs used in movement disorders

What drugs can be used to treat Parkinson’s Disease? 3

A
  • Dopamine replacement agents (L-DOPA)
  • Dopamine agonists
  • Dopamine breakdown inhibitors (MAO-B inhibitors)

Non of these treatments · address the underlying degeneration of dopamine

139
Q

How can L-DOPA cause an increase in (Nor)adrenaline production

A

L-DOPA is metabolised -> Dopamine via DOPA-carboxylase in the dopaminergic neuron

Dopamine metabolised -> NAd via Dopamine-Beta-hydroxylase enzyme

NAd then broken down into adrenaline

140
Q

What is the function of carbidopa/ benserazide?

A
  • coadministered for inhibition of DOPA-decraboxylase
  • stops conversion to dopamine in the periphery
  • Lack of dopamine slows the production of Noradrenaline from that dopamine
141
Q

how does an enzyme inhibitor (carbidopa/ benserazide) restore normal movements?

A

inhibits LDOPA-> dopamine (DOPA decarboxylase

allow brain to pick up LDOPA + make more dopamine ☺

p638

142
Q

What is a Disadvantage of L-DOPA as a treatment for Parkinson’s?

A
  • effectiveness ⬇ over 2-5 years

⬆ dose frequency can cause:

  • ON-OFF effect (sudden transitions between symptom relief and hypokinesia)
  • dyskinesias (involuntary writhing movements)
143
Q

Why does the effectiveness of L-DOPA decrease over time?

A

⬇ in dopaminergic nerve terminals therefore ⬇ capacity to convert L-DOPA to Dopamine

144
Q

When using Dopamine Agonists, which receptors should we target ideally? 2 examples

A
  • D2 recepetors

- examples are Pramipexole / Ropinirole

145
Q

What is apomorphine and when is it used?

A
  • a dopamine agonist

- reserved for advanced stage PD and ‘OFF’ L-DOPA episode treatment

146
Q

What are some drawbacks of Dopamine agonists?

A
  • Nausea/emetic effects (especially apomorphine) - Psychotomimetic effects (schizophrenic symptoms)
147
Q

What are the other alternatives to Dopamine Agonists/ L-DOPA?

  • MAO-B inhibitor
  • dopamine releaser
  • Muscarinic ACh Receptor antagonists
A
  • Selegiline = MAO-B inhibitor selectively elevates [DA]
  • Amantadine = dopamine releaser
  • Benzhexol = Muscarinic ACh Receptor antagonists (offsets local circuit consequences of DA deficiency on cholinergic striatal interneuron)
148
Q

Can alternatives be used with L-DOPA?

A

yes or alone

149
Q

How does deep brain stimulation work?

A
  • sends electrical impulses, through implanted electrodes, to specific targets in the brain (the Subthalamic nucleus).
  • This makes the STN overactive and shuts it down

– Increased stimulation of the STN increases the inhibitory outflow from the Substantia nigra Regulata on the thalamus

  • This is used for treatment of movement disorders (Parkinson’s disease)
    p640
150
Q

What are the symptoms of Huntington’s Disease

A
  • Tremors
  • clumsiness
  • memory loss
  • mood changes
  • poor concentration
151
Q

What are the treatments for Huntington’s Disease?

A
  • There are no known drugs available for treating this disease
  • there is only symptomatic treatment

o Tetrabenazine = VMAT inhibitor - decreases Dopamine storage and release

o Chlorpromazine – Dopamine receptor antagonists (antipsychotic)

o Baclofen – GABA-B agonist, decreases spinal reflexes

152
Q

What are the treatments for Huntington’s Disease?

A

no known drugs available, only symptomatic treatment

o Tetrabenazine = VMAT inhibitor - decreases Dopamine storage and release

o Chlorpromazine – Dopamine receptor antagonists (antipsychotic).. ⬇ DA influence on motor circuits, good for symptoms

o Baclofen – GABA-B agonist, ⬇ spinal reflexes

Health.2 (19 decks)

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