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Principles of Med Neuroscience > L.2.1 > Flashcards

L.2.1 Flashcards

1
Q

What is the spinal cord

A
  • a column of nerve tissues that carries nerve impulses from the brain to the rest of the body
  • it consists of grey matter and white matter
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2
Q

What is the function of the ventral horn of spinal cord

A

houses motor neuronal cell bodies

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3
Q

What is the function of the dorsal horn of spinal cord

A

houses neurons receiving sensory input

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4
Q

TRUE OR FALSE: the horns are part of the grey matter in the spinal cord

A

TRUE

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5
Q

What is the function of the ascending tracts in spinal cord

A

carry afferent sensory information/nerve impulses to centres within the brain

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6
Q

What is the function of descending tracts in spinal cord

A

carry efferent motor information from centres within the brain

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7
Q

What is the relationship between tracts and cerebral hemispheres

A
  • tracts to & from cerebral hemispheres are crossed
  • left hemisphere controls right side of the body
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8
Q

What does the dorsal column house

A

ascending tracts

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9
Q

What does the lateral column house

A

ascending & descending tracts

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10
Q

What does the ventral column house

A

descending tracts

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11
Q

What is another name for the corticospinal tract

A

pyramidal tract

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12
Q

What is the corticospinal tract

A

motor pathway which carries motor information from the cerebral cortex to the spinal cord

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13
Q

What are the 2 main types of neurons that are part of the corticospinal pathway

A

upper & lower motor neurons

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14
Q

What are upper motor neurons

A

neurons located in the brain and that transmit nerve impulses from the cerebral cortex to the spinal cord (ventral horn)

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15
Q

What are lower motor neurons

A

neurons located in the spinal cord (ventral horn) and that transmit nerve impulses from the spinal cord to the skeletal muscles

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16
Q

Outline the main anatomical structures in the corticospinal pathway

A
  1. primary motor cortex (pre-central gyrus)
  2. Internal capsule
  3. Cerebral peduncle (midbrain)
  4. Pons
  5. Pyramids of medulla (80% neurons decussate to lateral cortical spinal & 20% neurons stay on same side and join anterior cortical spinal)
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17
Q

Why do upper motor neurons control muscles on the contralateral side of the body

A

upper motor neurons synapse with lower motor neurons in the ventral horn (spinal cord)

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18
Q

What are the main types of lower motor neurons

A
  • alpha motor neurons
  • gamma motor neurons
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19
Q

What muscles do alpha motor neurons innervate and what is their function

A

they innervate extrafusal muscle fibres and generate contractions

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20
Q

What are the features of alpha motor neurons

A

large and fast-conducting neurons

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21
Q

What muscles do gamma motor neurons innervate and what is their function

A

they innervate intrafusal muscle fibres & regulate muscle spindles

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22
Q

What are the features of gamma motor neurons

A

small and slower conducting neurons

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23
Q

What is a motor unit

A

consists of 1 alpha motor neuron and all the muscle fibres it innervates

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24
Q

How do small motor units generate movement/muscle contraction

A
  • innervate few muscle fibres
  • allow precise control
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25
Q

How do large motor units produce movement

A
  • innervate many muscle fibres
  • allow gross movement
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26
Q

What is a motor neuron pool

A

a group of lower motor neurons that innervate 1 muscle

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27
Q

What are features of motor neuron pools

A
  • each muscle has its own motor pool
  • clustered together in rod-shape in spinal cord
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28
Q

What happens if there is damage to a single ventral root or spinal nerve

A

muscle weakness

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29
Q

How is the force of muscle contraction regulated

A
  • firing rate of alpha motor neurons
  • recruitment of additional motor units
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30
Q

How is the firing rate of alpha motor neurons related to muscle contraction generated

A
  • increased firing rate
  • greater muscle contraction
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31
Q

How is the recruitment of additional motor units linked to muscle contraction generated

A
  • more motor units
  • more muscle force
  • more contraction
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32
Q

What are muscle proprioceptors

A

they provide sensory feedback about muscle activity to help control movement and balance

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33
Q

What are the 2 types of muscle proprioceptors

A
  • muscle spindles
  • golgi tendon organs
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34
Q

Outline the structure of muscle spindles

A
  • located in skeletal muscles
  • have intrafusal muscle fibres
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35
Q

What is the function of muscle spindles

A

they detect changes in muscle length when the muscle is stretched

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36
Q

How do muscles spindle detect that a muscle has been stretched

A
  • sensory nerve fibres (Group Ia) send signals to brain when muscle is stretched
  • it increases muscle spindles firing rate
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37
Q

What is the function of golgi tendon organs

A

they detect muscle tension

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38
Q

Where are golgi tendon organs located

A
  • tendon
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39
Q

How do golgi tendon organs detect muscle tension

A
  • during muscle contraction, Group Ib fibres send signals to brain
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40
Q

What happens when gamma motor neurons are activated

A
  • they keep muscle spindles tight (taut) even when the muscle changes length
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41
Q

What is the purpose of keeping muscle spindles taut at different muscle lengths

A
  • muscle spindles can keep sending accurate information about muscle stretch
  • no matter how long or short the muscle is
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42
Q

What are reflexes

A
  • involuntary responses to an external stimulus mediated by the spinal cord
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43
Q

What are monosynaptic reflexes

A

simplest reflex and involves only 1 synapse between a sensory neuron and motor neuron

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44
Q

What is an example of a monosynaptic reflex

A

knee-jerk reflex

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45
Q

Outline the knee jer reflex

A
  1. tapping the patellar ligament stretches muscle
  2. Group la fibres from muscle spindles activated
  3. Activates alpha motor neurons in ventral horn
  4. Quadriceps muscle contracts
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46
Q

What are polysynaptic reflexes

A

most reflexes are polysynaptic and have multiple synapses in circuit

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47
Q

Name an example of a poly-synaptic reflex

A

golgi tendon reflex

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48
Q

Outline the golgi tendon reflex

A
  1. Muscle tension increases
  2. Group Ib fibres activated
  3. Inhibitory interneurons activated
  4. Alpha motor neurons inhibited and muscle tension reduced
  5. Stops muscle from contracting for protection
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49
Q

What is reciprocal inhibition

A
  • contraction of muscle with the relaxation of antagonist muscle
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50
Q

What is the flexion/withdrawal reflex

A
  • a spinal reflex to protect the body from damaging stimuli
  • a polysynaptic reflex, caused by nociceptor activation
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51
Q

What is the cause of an upper motor neuron disease

A

disruption of the corticospinal tract

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52
Q

What are the effects of upper motor neuron disease

A
  • spastic paralysis (increased muscle tone)
  • overactive tendon reflexes
  • no significant muscle atrophy
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53
Q

What is an example of an upper motor neuron disease

A

stroke

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54
Q

Explain the reason behind the motor neuron disease effects

A
  • disrupted control over muscle movement causes stiffness and exaggerated reflexes
  • no muscle wasting (atrophy) because some nerve signals can still reach the muscles
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55
Q

What is the cause of lower motor neuron disease

A

degeneration of lower motor neurons

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56
Q

What is an example of a lower motor neuron disease

A

spinal muscular atrophy

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57
Q

What are the effects of lower motor neuron disease

A
  • flaccid paralysis
  • no tendon reflexes
  • muscle atrophy (weakening/shrinking of muscles)
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58
Q

What are the causes of amyotrophic lateral sclerosis

A

both lower and upper motor neurons

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59
Q

What are the effects of amyotrophic lateral sclerosis

A

progressive muscle weakness and atrophy but mind intact

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60
Q

Explain the effects of lower motor neurons diseases

A

Flaccid Paralysis: LMNs degenerate, so muscles no longer receive electrical signals to contract, causing weak and floppy muscles.
No Tendon Reflexes: Reflex arcs are disrupted because LMNs are damaged, preventing the muscle from responding to stimuli.
Muscle Atrophy: Muscles shrink and weaken due to lack of stimulation (trophic support) and disuse when LMNs are lost.

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61
Q

What is dyskinesia

A

involuntary muscle movements (jerks

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62
Q

What is dystonia

A

involuntary muscle contractions (spasm)

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63
Q

What is the spinothalamic tract

A

a sensory pathway in spinal cord that carries information about pain, temperature and crude touch from the body to the thalamus

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64
Q

What are the extrapyramidal tracts

A
  • Descending motor pathways that do not pass through the pyramids
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65
Q

What is the function of extrapyramidal tracts

A

Involuntary motor control, crucial for regulating reflexes and maintaining posture

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66
Q

What are the 3 structures that the extrapyramidal tract descends through

A
  • rubrospinal
  • reticulospinal
  • vestibulospinal
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67
Q

What are the 4 types of movement

A
  • passive
  • stereotypes
  • reflexive
  • self-generated
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68
Q

Definition of passive movements

A

movements happen w/o voluntary muscle contractions

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69
Q

What are the types of passive movements

A
  • hypotonia & hypertonia
  • spasticity
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70
Q

What are reflexive movements

A

involuntary responses to external stimuli mediated by the spinal cord

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71
Q

What are the types of reflexive movements

A
  • hyporeflexia
  • hyperreflexia
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72
Q

What is the cause of hyporeflexia

A

lower motor neuron lesion

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73
Q

What is the effect of hyporeflexia

A

reduced/absent reflexes

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74
Q

What is the cause of hyperreflexia

A

upper motor neuron lesions

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75
Q

What is the effect of hyperreflexia

A

exaggerated reflexes

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76
Q

What is the cause of hypotonia

A

lesion in lower motor neuron or cerebellum

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77
Q

What is the effect of hypotonia

A
  • low muscle tone
  • muscles are weak
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78
Q

What is the cause of spasticity

A

lesion in the corticospinal tract

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79
Q

What is the effect of spasticity

A
  • increase muscle tone
  • resistance to movement
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80
Q

What is a stereotyped movement

A

movements that are automatic, patterned and repetitive

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81
Q

What are examples of stereotyped movements

A
  • chewing
  • walking
  • talking
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82
Q

What are the two types of self-generated movements

A
  • emotional
  • voltional
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83
Q

What are emotional self-generated movements

A

movements driven by emotional state

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84
Q

What is an example of an emotional self-generated movement

A
  • smiling
  • frowning
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85
Q

What are volitional self-generated movements

A

goal-directed movements

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86
Q

What is an example of a volitional self-generated movement

A

reaching for an object

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87
Q

What is the main cause of loss of descending inhibition (reflexive movements)

A

upper motor neuron lesions

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88
Q

How do upper motor neurons lesions result in loss of descending inhibition

A

they disrupt inhibitory signals from brain to the spinal cord

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89
Q

What are the main consequences of loss of descending inhibition?

A
  • increased reflex excitability
  • spasticity
  • Brisk reflexes
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90
Q

Explain why reflexes excitability increases during loss of descending inhibition

A
  • upper motor neurons fail to suppress reflex actions
  • the inhibitory signals have been disrupted
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91
Q

Explain why the spasticity occurs during loss of descending inhibition

A
  • the muscle tension & contraction is not being properly inhibited by the brain, so they become stiff and difficult to move. –> increase muscle tone
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92
Q

How does lower motor neuron damage contrast with upper motor neuron damage in terms of tone and reflexes?

A
  • LMN = reduced tone + loss reflexes
  • UMN = increased tone + brisk reflexes
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93
Q

What are brisk reflexes?

A

they are exaggerated reflexes

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94
Q

What is spasticity

A

an increase in muscle resistance during passive muscle stretching

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95
Q

What is the typical reflex response in spasticity?

A

extensor reflexes dominate

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96
Q

Where does the tectospinal tract pathway

A

from the superior colliculus (midbrain) down to the spine

97
Q

What is the function of the tectospinal tract

A
  • associated with visual pathways
  • controls head and neck movements in response to visual stimuli
98
Q

What is the overall pathway of the vestibulospinal tract

A

starts from the vestibular nuclei in the brain stem down to the spinal cord

99
Q

What is the function of the vestibulospinal tract

A
  • ensures postural stability
  • stabilises eyes and head during body movements
100
Q

What are the 2 divisions of the vestibulospinal tract

A
  • lateral vestibulospinal tract
  • medial vestibulospinal tract
101
Q

What is the lateral vestibulospinal tract responsible for

A

activates extensor muscles in arms and legs

102
Q

What is the medial vestibulospinal tract responsible for

A

controls head and neck movements to stabilise eyes during movement

103
Q

What is the function of the reticulospinal tract

A
  • maintains posture and balance
  • coordinates limb movements (ex: walking)
104
Q

What are the 2 divisions of the reticulospinal tract

A
  • medial reticulospinal tract
  • lateral reticulospinal tract
105
Q

What is the medial reticulospinal tract responsible for

A

responsible for extensor motor neurons

106
Q

What is the lateral reticulospinal tract responsible for

A

responsible for flexor motor neurons

107
Q

Which 2 descending pathways are responsible for control of head and neck movements

A
  • tectospinal tract
  • medial vestibulospinal tract
108
Q

Which 2 descending pathways are responsible for activating extensor muscles in arms and legs

A
  • reticulospinal tract
  • lateral vestibulospinal tract
109
Q

What are locomotive movements caused by

A

controlled pattern generators (CPGs) in spinal cord

110
Q

What are the features of locomotive movements

A
  • not consciously controlled
  • rhythmic and repetitive movements
111
Q

How do locomotive movements work

A
  • pacemaker cells start rhythmic activity
  • reciprocal inhibition (one group of muscle is activated, opposing muscle is inhibited)
112
Q

Why is it that during facial palsy damage to the upper motor neuron and emotional movement can occur

A

a genuine smile can elicited by emotion because the emotional pathway bypasses the corticobulbar pathway

113
Q

Which pathway mediates volitional movement

A

mediated by corticospinal tract

114
Q

What is the function of the rubrospinal tract

A

involved in flexion of upper limbs

115
Q

What is posturing in coma

A
  • provides an idea about the location of lesions in brainstem
116
Q

What is posturing

A

abnormal body positions that occur due to severe brain injury

117
Q

Where does the lesion occur in decorticate posturing

A

lesion above the red nucleus

118
Q

What are the effects of decorticate posturing

A
  • rubrospinal tract is disinhibited
  • extensor pathways dominate in lower limbs
  • lower limbs extension & upper limb flexion
119
Q

TRUE OR FALSE: Decerebrate posturing is the MORE severe than decorticate posturing

A

TRUE

120
Q

Where does the lesion occur in decerebrate posturing

A

below the red nucleus

121
Q

What are the effects of decerebrate posturing

A
  • rubrospinal tract is disrupted
  • upper and lower limb extension
  • flexor facilitation in upper limb is lost
122
Q

Which 2 pathways provide extensor dominance

A
  • vestibulospinal tract
  • reticulospinal tract
123
Q

What pathway provides flexor dominance

A

rubrospinal tract

124
Q

What are the features of corticospinal tract damage

A
  • spasticity
  • brisk reflexes
125
Q

What is Parasagittal Meningioma

A
  • tumour which compresses the medial parts of motor corticies
  • causes bilateral leg weakness
126
Q

Where does the middle cerebral artery supply to

A

lateral aspects of the motor cortex

127
Q

What do the lateral aspects of the motor cortex control

A

face and hand

128
Q

What does a proximal lesion to middle cerebral artery

A

causes complete one-sided body paralysis

129
Q

Where does the anterior cerebral artery supply to

A

medial part of frontal lobes

130
Q

What is the main function of the Posterior Parietal Cortex?

A
  • Integrates sensory information to create mental images of body and environment
  • Controls exploratory movements like manipulating objects
131
Q

What are the symptoms of Posterior Parietal Cortex damage?

A
  • Neglect syndrome (patient is aware but ignores stimuli)
  • Impaired exploratory movements
132
Q

What are the three motor planning areas?

A
  • prefrontal cortex
  • premotor area
  • supplementary motor area
133
Q

What is the function of the premotor area

A

Coordinates sensory-guided movements and facilitates imitation

134
Q

What is the Bereitschaftspotential?

A
  • Brain activity that precedes voluntary movements by 500-1000 milliseconds
  • Generated by the supplementary motor area
135
Q

What is the role of the supplementary motor area

A

Controls complex motor sequences

136
Q

Compare Ideational and Ideomotor Apraxia

A

Ideational Apraxia:
* Caused by parietal lobe damage
* Cannot plan/execute action sequences

Ideomotor Apraxia:
* Caused by SMA damage
* Cannot use tools properly despite understanding their purpose

137
Q

What is dystonia and its effect

A
  • Sustained involuntary muscle contractions
  • Causes abnormal postures or repetitive movements
138
Q

What is demyelination

A

damage or loss of the myelin sheath

139
Q

Why is demyelination an issue

A

if nerve signals slow down/disrupted it can cause neurological issues

140
Q

Where does multiple sclerosis occur

A

in the CNS

141
Q

What happens in multiple sclerosis

A

the inflammation and destruction of myelin which slows/blocks signals between the brain and the body

142
Q

What are the symptoms of multiple sclerosis

A
  • fatigue
  • muscle weakness
  • coordination issues
143
Q

Define multiple sclerosis

A

autoimmune disease where the body attacks myelin in the CNS

144
Q

What areas are affected by multiple sclerosis

A
  • cerebellum
  • brainstem
  • spinal cord
  • optic nerve
145
Q

How does multiple sclerosis affect the cerebellum

A

it causes balance and coordination problems

146
Q

How does multiple sclerosis affect the brainstem

A

speech and swallowing issues

147
Q

How does multiple sclerosis affect the spinal cord

A

muscle weaknesses, sensory changes and bladder/bowel issues

148
Q

How does multiple sclerosis affect the optic nerve

A

visual problems

149
Q

What are the 2 factors needed for multiple sclerosis diagnosis

A
  • space = plaques must be found in at least 2 different regions of the CNS
  • time = evidence that lesions occurred at different points in time
150
Q

What procedure is used to detect MS

A

lumbar puncture (collects CSF)

151
Q

What elements indicate MS diagnosis

A
  • normal glucose and protein levels
  • an increase in white blood cells
  • oligoclonal bands present
152
Q

What are some treatments for MS

A
  • steroids help reduce inflammation
  • physiotherapy to help improve movement & strength
153
Q

What is the function of the basal ganglia

A
  • helps control muscle movements
  • selects an action plan that is most appropriate and relevant to the goal
154
Q

What are the subcortical structures that are part of the basal ganglia

A
  • corpus striatum
  • globus pallidus
  • substantial nigra
  • thalamus
155
Q

What is the main purpose of the direct pathway in the basal ganglia

A

produce movement

156
Q

What is the main purpose of the indirect pathway

A

stop unwanted movements

157
Q

What is the main purpose of the hyperdirect pathway

A

stops movement quickly before it even starts

158
Q

What are the first 2 steps in the direct pathway of the basal ganglia

A
  1. motor cortex sends excitatory signal (GLU) to corpus striatum
  2. striatum inhibits (GABA) internal globus pallidus & substantia nigra
159
Q

What are the last 2 steps in the direct pathway of the basal ganglia

A
  1. since SN and Gi are inhibted, it stops suppressing the thalamus (can’t send GABA onwards)
  2. thalamus is excited and sends excitatory signals (GLU) to motor cortex
  3. movement produced
160
Q

What are the 3 first steps in the indirect pathway in the basal ganglia

A
  1. motor cortex sends excitatory signals (GLU) to corpus striatum
  2. corpus striatum inhibits (GABA) the external globus pallidus
  3. GABA signals are passed onwards, disinhibiting subthalamic nucleus
161
Q

What are the last 2 steps in the indirect pathway of basal ganglia

A
  1. subthalamic nucleus sends excitatory signals (GLU) to internal Gi & substantia nigra
  2. they are activated and can inhibit the thalamus
  3. the thalamus can’t excite the motor cortex so no movement is produced
162
Q

Outline the hyperdirect pathway in the basal ganglia

A
  1. motor cortex sends excitatory signals to subthalamic nucleus
  2. it activates the internal globus pallidus –> inhibiting thalamus
  3. thalamus can’t send signals to motor cortex and movement is stopped
163
Q

Which 2 beurotransmitters does the balance of the direct & indirect pathway depend on

A
  • acetylcholine
  • dopamine
164
Q

What are medium spiny neurons

A
  • neurons are responsible for deciding whether movement will happen
  • influenced by dopamine
165
Q

How does dopamine affect the direct pathway

A
  • dopamine binds to D1 receptors
  • excites medium spiny neurons
  • direct pathway is more active and movement is produced
166
Q

What effect does dopamine have on D1 receptors

A
  • excitatory effect
  • encourages movement
167
Q

What effect does dopamine have on D2 receptors

A
  • inhibitory effect
  • facilitates movement
168
Q

How does dopamine affect the indirect pathway

A
  • dopamine binds to D2 receptors
  • inhibits medium spiny neurons
  • dampens the inhibitory effect of the indirect pathway
  • facilitates movement
169
Q

What is the effect of acetylcholine in the direct pathway

A
  • Ach decreases the activity direct pathway
  • making movement less likely
170
Q

What is the effect of acetylcholine in the indirect pathway

A
  • Ach increases the activity of indirect pathway
  • making it harder to move
171
Q

What are the overall effects of dopamine and acetylcholine on the basal ganglia

A
  • dopamine = promotes movement
  • acetylcholine = inhibits movement
172
Q

What is hypokinetic movement?

A

Moving too little

173
Q

What are examples of hypokinetic movement

A
  • akinesia (no movement)
  • bradykinesia (slowed movement)
174
Q

What is hyperkinetic movement?

A

Moving too much, such as tics

175
Q

Define ataxia

A

disturbance of coordination, resulting in clumsy or uncoordinated movements.

176
Q

Define apraxia

A

A disturbance of planning movements, leading to difficulty planning and performing movements.

177
Q

What is parkinsonism?

A

A group of movement problems characterized by slow or reduced movement, including rigidity, tremor, and bradykinesia.

178
Q

What are the clinical features of parkinsonism?

A
  • rigidity
  • tremor
  • bradykinesia
179
Q

What is genetic parkinsonism?

A

Parkinsonism caused by specific gene mutations, often with a family history of the condition

180
Q

What is atypical parkinsonism?

A

Parkinsonism with initial symptoms that differ from typical Parkinson’s disease, such as Lewy body dementia or supranuclear palsy.

181
Q

What is secondary parkinsonism?

A

Parkinsonism caused by external factors like brain injury, stroke, or medication.

182
Q

What is genetic parkinsonism?

A

It is caused by specific gene mutations, often with a family history of the disease.

183
Q

What is akinesia?

A

Decreased overall movement, such as reduced blinking, lack of facial expression, and sitting very still

184
Q

What is bradykinesia?

A

Slowness of movement, worsening as the condition progresses.

185
Q

What is apraxia in Parkinson’s disease?

A

Difficulty initiating voluntary movements.

186
Q

What is rigidity in Parkinson’s disease?

A

Stiffness throughout movement.

187
Q

What are three important negatives in Parkinson’s disease?

A
  • Normal reflexes
  • no ataxia (coordination is unaffected)
  • normal eye movements
188
Q

What is idiopathic Parkinson’s disease (IPD)?

A

A neurodegenerative condition affecting dopaminergic cells of the substantia nigra

189
Q

What happens when dopamine-producing cells in the substantia nigra die?

A

Lewy bodies build up, worsening neuronal function.

190
Q

What happens to movement pathways when dopamine levels are low?

A
  • Direct pathway activation decreases, reducing movement promotion.
  • Indirect pathway inhibition decreases, overly suppressing movement.
191
Q

What is the overall result of dopamine deficiency in Parkinson’s on movement ?

A

Movements slow down, causing stiffness and tremors

192
Q

What are the goals of Parkinson’s disease treatment?

A
  • Manage symptoms through lifestyle changes, medications, and brain stimulation
  • slow down progression
193
Q

What enzymes reduce dopamine availability in Parkinson’s disease?

A

Dopamine is broken down by COMT and MAOB enzymes

194
Q

How is L-DOPA used in Parkinson’s treatment?

A

It is combined with a Dopa decarboxylase inhibitor to prevent dopamine conversion in the bloodstream before reaching the brain

195
Q

What are the benefits of Levodopa treatment for Parkinson’s disease?

A

Improves motor symptoms

196
Q

What are the side effects of Levodopa treatment?

A
  • Low blood pressure.
  • Dyskinesias (uncontrolled movement).
  • Dopamine dysregulation syndrome (addiction-like behavior).
  • Excessive daytime sleepiness (e.g., falling asleep during activities).
197
Q

How can continuous dopamine intake affect the brain?

A

dopamine dysregulation syndrome (addiction-like behavior)

198
Q

What do dopamine agonists do in Parkinson’s treatment?

A

Mimic dopamine and stimulate dopamine receptors.

199
Q

What are dopamine agonist benefits in treatment

A
  • Work even if dopamine-producing neurons are damaged.
  • Don’t need enzymatic conversion, making them stable and long-acting.
200
Q

What are the two types of dopamine agonists?

A
  • Ergot-based Agonists: Rarely used due to serious side effects
  • Non-Ergot Agonists: Commonly used
201
Q

What are the side effects of dopamine agonists?

A

Can cause impulse control issues, such as gambling

202
Q

How do monoamine oxidase inhibitors (MAOIs) work in Parkinson’s treatment?

A

Prevent the breakdown of dopamine in the brain, increasing its levels.

203
Q

What are the two types of monoamine oxidase inhibitors?

A
  • MAO-A: Affects serotonin, adrenaline, and dopamine
  • MAO-B: Targets dopamine and is used for Parkinson’s disease
204
Q

What is a key benefit of MAO-B inhibitors in Parkinson’s treatment?

A

Slight improvement in motor symptoms.

205
Q

How do anticholinergics help in Parkinson’s treatment?

A
  • Reduce tremors by balancing the effects of acetylcholine.
  • Excess acetylcholine occurs due to low dopamine levels.
206
Q

What does Amantadine do in Parkinson’s treatment?

A

Functions as a glutamate agonist, increases dopamine activity, and reduces involuntary movements.

207
Q

How do COMT inhibitors work in Parkinson’s treatment?

A
  • Block COMT enzymes that break down dopamine in the brain.
  • Reduce L-dopa metabolism, enhancing its effectiveness.
208
Q

What are the benefits of COMT inhibitors?

A
  • increase the duration of L-dopa’s effects.
209
Q

What are the side effects of COMT inhibitors?

A
  • May increase involuntary movements (dyskinesia)
  • diarrhoea
210
Q

What are the infusion therapies for Parkinson’s?

A
  • Apomorphine: Provides rapid relief from OFF periods.
  • Levodopa-Carbidopa Intestinal Gel: Maintains steady L-dopa levels.
  • Foslevodopa: New formulation for improved levodopa delivery
211
Q

Where is L-dopa absorbed

A

Duodenum

212
Q

what factors can impact L-Dopa absorption in Parkinson’s disease?

A
  • Gastric motility issues.
  • Constipation.
  • High-protein meals (compete with L-dopa for absorption)
213
Q

How does Duodopa infusion help in advanced PD

A

Delivers L-dopa directly to the duodenum, stabilizing levels and reducing motor fluctuations.

214
Q

what are Duodopa limitations?

A

Costly

215
Q

What is Apomorphine, and how is it delivered in PD treatment?

A
  • Dopamine agonist mimicking dopamine’s effects.
  • injection under the skin
216
Q

How does Deep Brain Stimulation work in treating Parkinson’s disease?

A

Disrupts abnormal activity in the basal ganglia causing motor symptoms

217
Q

What are the limitations of DBS in Parkinson’s treatment?

A

Does not improve non-motor symptoms, such as dementia

218
Q

What is Hemiballismus

A

Hyperkinetic movement disorder with violent limb movements, typically on one side of the body

219
Q

what causes Hemiballismus

A

Cerebrovascular event, such as a stroke.

220
Q

What are the types of tic disorders?

A
  • Simple Tics: Blinking, coughing.
  • Complex Tics: Jumping, twirling
221
Q

What are key features of tic disorders?

A
  • Preceded by urgency, relieved by performing the tic.
  • Reduced by distraction and concentration
  • Worsen with anxiety or fatigue
222
Q

What are the main causes of chorea?

A

Huntington’s disease.
- drugs

223
Q

What are the characteristics of chorea?

A
  • Jerky, brief, irregular contractions.
  • Not repetitive or rhythmic but flow between muscles.
  • Appears as fidgetiness or restlessness.
224
Q

What are the cognitive symptoms of Huntington’s Disease?

A

Inability to make decisions.
Difficulty multitasking.
Slowness of thought.

225
Q

What are the behavioral symptoms of Huntington’s Disease?

A
  • depression
  • anxiety
226
Q

What is myoclonus

A

Brief, involuntary muscle contractions.

227
Q

What is dystonia?

A

An abnormal twisting posture

228
Q

How is dystonia influenced by dopamine?

A

blocking dopamine receptors can cause dystonic symptoms.

229
Q

What is long-term depression (LTD) in the context of Purkinje cells?

A

LTD is the weakening of synaptic connections between parallel fibers and Purkinje cells, making specific synapses less effective over time

230
Q

What are the two key input pathways to Purkinje cells?

A
  • Parallel Fibers:
  • Climbing Fibers
231
Q

What is required for LTD to occur in Purkinje cells?

A

The Purkinje cell must be simultaneously stimulated by climbing fibers and parallel fibers.

232
Q

What happens intracellularly during simultaneous activation of climbing and parallel fibers?

A

A large influx of calcium occurs in the Purkinje cell.

233
Q

How does the calcium surge affect synaptic transmission in LTD?

A
  1. Calcium activates protein kinases.
  2. These kinases phosphorylate proteins involved in receptor trafficking.
  3. AMPA receptors are removed (internalized) from the postsynaptic membrane of the Purkinje cell.
234
Q

What is the consequence of AMPA receptor internalization during LTD?

A

Synaptic transmission is weakened, reducing the effectiveness of the synapse

235
Q

How does the weakening of the synapse between the parallel fiber and the Purkinje cell help with motor control?

A

The weakening prevents excessive or incorrect motor commands, aiding the cerebellum in refining movements

236
Q

Why is long-term depression (LTD) important for motor control?

A
  • Error Detection and Correction
  • Refinement of Movements:
  • Adaptive Motor Skills:
237
Q

What happens during error detection and correction

A

LTD weakens ineffective synapses when movements are incorrect, enabling better future motor adjustments

238
Q

What happens during refinement of movements

A

Over time, LTD helps optimize motor responses by reducing unnecessary or incorrect pathways

239
Q

What happens during adaptive motor skills

A

LTD allows long-term changes in motor behavior, which is essential for learning new skills and adapting to new environments

Principles of Med Neuroscience (12 decks)

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