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Health.2 > CNS Motor Control & Systems šŸ§  > Flashcards

CNS Motor Control & Systems šŸ§  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 ā€˜somatotopic representationā€™?

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 theyā€™re happening

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35
Q

Lower motor neurones

What types of motor neurones are known as the ā€˜final common pathwayā€™ 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 ā€œinterā€?

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 ā€œsee the headless chickens runningā€ 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?
causesā€¦
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 byā€¦

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 pathwaysā€¦
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 areā€¦

A

VOLUNTARY

distal muscle flexors

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53
Q

ventromedial pathways governā€¦

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

ā€¦ 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 ā€œ 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 calledā€¦ 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) controlsā€¦

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 (ā¬† resistance to passive movement)
o ā¬† muscle tone (hypertonia)
o ā¬† 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.

doesnā€™t project outside the brain

89
Q

What are the functions of the cerebellum?

A

Ā· Closely involved with brainstem mechanisms

Ā· Control of muscle tone and body posture

Ā· Sensorimotor coordination

Ā· 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
ā€˜dark basements of brainā€™

integrates sensory + motor info from cortexā€¦ relays back to cortex via thalamus.
loop

selection and initiation of voluntary movement

106
Q

does basal ganglia project outside the brain?

A

no

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

Ā· Responsible for the Integration of sensory and motor information

Ā· Selection and initiation of voluntary movement

109
Q

What is the cortico-basal ganglia-cortical loop?

A

Ā· Integrates motor and sensory information from the cortex

Ā· Relays back to the cortex via thalamus

Ā· Motor loop circuit output to PMA/SMA cortex

Ā· 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 ā€“> Substantia Nigra Regulata OR Globus palidus internal ā€“> Thalamus ā€“> 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 neuronsā€¦ā¬‡ BG output.. movement ā˜ŗ

indirect: act on inhibitory D2 rec on striato- GPe neuronsā€¦ ā¬‡ STN activity ā¬‡ BG outputā€¦ movement ā˜ŗ
- less activity

125
Q

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

A

motor disfunction

  • hypokinetic disorders (Parkinsonā€™s Disease)
  • hyperkinetic disorders (Huntingtonā€™s Disease)
126
Q

What is Parkinsonā€™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 Parkinsonā€™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 Parkinsonā€™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 Parkinsonā€™s Disease?

A

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

driven by ā¬† activity in subthalamic nucleus STN - stimulates Substantia nigra Regulata - inhibits thalamus

130
Q

How can we treat Parkinsonā€™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 Huntingtonā€™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 Huntingtonā€™s Disease?

A

loss of striatal output neurons in indirect pathway

133
Q

What is the rational for treating Huntingtonā€™s Disease?

A

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

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

Ā· Overactive thalamocortical pathway leads to excessive involuntary movemnt

134
Q

How can we treat Huntingtonā€™s Disease?

A

Symptomatic treatments only:

Ā· Tetrabenazine = VMAT inhibitor - decreases Dopamine storage and release

Ā· Chlorpromazine ā€“ Dopamine receptor antagonists (antipsychotic)

Baclofen ā€“ 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 nucleusā€¦

  • 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 Parkinsonā€™s Disease? 3

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

Non of these treatments Ā· 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 ā˜ŗ

p638

142
Q

What is a Disadvantage of L-DOPA as a treatment for Parkinsonā€™s?

A
  • effectiveness ā¬‡ over 2-5 years

ā¬† 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

ā¬‡ in dopaminergic nerve terminals therefore ā¬‡ 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 ā€˜OFFā€™ 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

ā€“ 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 (Parkinsonā€™s disease)
    p640
150
Q

What are the symptoms of Huntingtonā€™s Disease

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

What are the treatments for Huntingtonā€™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 ā€“ Dopamine receptor antagonists (antipsychotic)

o Baclofen ā€“ GABA-B agonist, decreases spinal reflexes

152
Q

What are the treatments for Huntingtonā€™s Disease?

A

no known drugs available, only symptomatic treatment

o Tetrabenazine = VMAT inhibitor - decreases Dopamine storage and release

o Chlorpromazine ā€“ Dopamine receptor antagonists (antipsychotic).. ā¬‡ DA influence on motor circuits, good for symptoms

o Baclofen ā€“ GABA-B agonist, ā¬‡ spinal reflexes

Health.2 (19 decks)

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