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P2 Head, Neck and Neuro > Eileen - Motor control, PD and functional anatomy of learning > Flashcards

Eileen - Motor control, PD and functional anatomy of learning Flashcards

1
Q

Describe declarative memory

A
  • Factual information
  • Life events
  • Available to the consciousness
  • Easily formed and forgotten
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2
Q

Describe non-declarative memory.

A
  • Procedural memory
  • Motor skills
  • Not available to the consciousness
  • Less easily formed and forgotten
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3
Q

Describe ballistic movements

A

Movement based on pre-programmed instructions

Rapid, but at the expense of accuracy - can’t accommodate unexpected changes

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4
Q

Describe visual feedback movements.

A
  • Motor command continually updated according to sensory feedback (e.g. Visual)
  • Highly accurate - can be modified in progress
  • Slow
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5
Q

Out of ballistic and visual feedback movements, which is used more often in the body?

A

A mixture of both

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6
Q

What does stimulation of the primary motor cortex do?

A

Elicits muscle twitches/movements depending on the amount of stimulation

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7
Q

What is the somatotrophic map?

A

Certain areas of the motor cortex specifically control certain areas of the body

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8
Q

How is the somatotrophic map distorted?

A

Face, hands and digits receive larger representation in the primary motor cortex - due to more through the required for fine control

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9
Q

If there is a stroke or haematoma in or near the primary motor cortex, what (motor) effect will be had on the body?

A

Paralysis and loss of sensation on the side contralateral to the pathology

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10
Q

What sensory information is crucial for co-ordinated movements?

A
  • Proprioception - feedback from peripheral sensory reports on the positions and movements of limbs
  • Vision - eyes, visual system, visual cortex
  • Vestibular - feedback from organ of balance
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11
Q

What are the main non-cortical structures required for movement?

A
  • Basal ganglia
  • Cerebellum
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12
Q

What is the input and output from the basal ganglia?

A
  • Input - prefrontal motor cortex (intended movement)
  • Output - premotor area of the thalamus
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13
Q

What are the functions of the basal ganglia?

A
  • Initiation of movement - puts motor plan into action
  • Planning of complex voluntary movement
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14
Q

What is the input and output for the cerebellum?

A
  • Input - sensory cortex
  • Output - primary motor cortex (via the thalamus)
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15
Q

What are the functions of the cerebellum?

A
  • Co-ordination and smooth execution of movements
  • Motor learning
  • Error detection
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16
Q

What does damage to the cerebellum do?

A

Causes cerebellar ataxia - poor co-ordination

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17
Q

What are the lateral descending motor pathways?

A

Corticospinal and rubrospinal - pyramidal neurons in primary motor cortex project to the spinal cord (corticospinal) and red nucleus (rubrospinal)

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18
Q

What are the functions of the lateral motor pathways?

A

Control of voluntary movements - e.g. Fine control of the hand by distal muscles

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19
Q

What is the function of the vestibulospinal tract?

A

Balance and posture

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20
Q

What is the function of the reticulospinal tract?

A
  • Medial path facilitates voluntary movement and increased muscle tone
  • Lateral path inhibits voluntary movements and decreases muscle tone
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21
Q

What is the function of the tectospinal tract?

A

Co-ordinates movements in the head in relation of visual stimuli

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22
Q

What evidence is there for function of the supplementary motor cortex?

A

Imaging studies show your primary motor cortex, premotor cortex and supplementary motor cortex are involved involved in moving a finger. However, only the SMA is involved in THINKING about moving the finger (but not actually moving it)

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23
Q

What are the symptoms of Parkinson’s disease?

A
  • Resting tremor
  • Bradykinesia
  • Shuffling gait
  • Muscular rigidity
  • Progression to general cognitive decline
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24
Q

What are the two treatments for Parkinson’s?

A
  • Levodopa - and carbidopa to prevent peripheral breakdown
  • Deep brain stimulation
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25
Q

What is Huntington’s disease?

A

Suppression of activity in the basal ganglia

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26
Q

What are the symptoms of Huntington’s disease.

A
  • Choreas
  • Difficulty speaking and swallowing
  • General cognitive decline
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27
Q

How do intrinsic circuits of the spinal cord produce the rhythmic motorneuron activity which drives stepping?

A
  • Alternating activity in flexor and extensor muscles co-ordinated across two limbs
  • Two sets of pattern generating neurons project to flexor and extensor motorneuron pools respectively
  • Reciprocal inhibitory connections between the two sets of pattern generating neurons help to co-ordinate their activity - alternating excitement of flexors and extensors
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28
Q

Motorneuron pools of each muscle form columns in the ventral horn, what are they called?

A

Motornuclei

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29
Q

What is the most important mechanism for grading motor force?

A

Recruitment of motor neurons

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30
Q

Describe the effect of action potential frequency in motor axons on muscle fibre contraction.

A
  • The more action potentials, the stronger the muscle contraction
  • No rest period means each action potential increases contraction form an already elevated level
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31
Q

What does the frontal lobe do?

A
  • Reasoning
  • Behaviour
  • Mood
  • Movement
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32
Q

What is the function of the temporal lobe?

A
  • Hearing
  • Memory (hippocampus)
  • Semantics
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33
Q

What is the function of the parietal lobe?

A

Sensory - pain, pressure, temperature

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34
Q

What is the function of the occipital lobe?

A

Sight

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35
Q

What is the corpus callosum.

A

Connects the cerebral hemispheres and allows communication between them

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36
Q

What is the amygdala and what does it do?

A
  • It is a group of neurons located deep to the medial temporal lobes
  • Processing and memory of emotional reactions
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37
Q

What is the general role of the limbic system?

A

Supports a variety of functions including emotion, behaviour and long-term memory

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38
Q

What is the function of the basal ganglia?

A

Co-ordinates gross, automatic muscle movements and regulates muscle tone

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39
Q

Which brain regions make up the diencephalon?

A
  • Epithalamus
  • Thalamus
  • Hypothalamus
  • Subthalamus
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40
Q

What is the function of the epithalamus?

A
  • Consists of the - pineal gland (melatonin secretion - biological clock and sleepiness)
  • Habenular nuclei (emotional response to olfaction)
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41
Q

What is the function of the thalamus?

A
  • Relays sensory information to the cerebral cortex
  • Includes nuclei involved in voluntary, motor and arousal actions
  • Anterior nucleus functions in emotions, memory, cognition and awareness
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42
Q

Describe the function of the subthalamus

A

Contains

  • subthalamic nuclei
  • portions of basal substantia nigra
  • portions of red nucleus

Helps control body movements

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43
Q

Describe the function of the hypothalamus

A
  • Controls and integrates ANS and pituitary gland activities
  • Regulates emotional and behavioural patterns
  • Controls body temperature
  • Regulates eating and drinking behaviour
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44
Q

What structures make up the midbrain?

A
  • Midbrain
  • Superior colliculus
  • Inferior colliculus
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45
Q

What is the function of the midbrain?

A
  • Relays motor impulses from cerebral cortex to the pons
  • Relays sensory impulses from the spinal cord to thalamus
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46
Q

What is the function of the superior colliculus?

A

Co-ordinates movement of the eyeballs in response to visual and other stimuli

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47
Q

What is the function of the inferior colliculus?

A

Co-ordinates movement of the head and trunk in response to auditory stimuli

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48
Q

What brain parts make up the hindbrain?

A
  • Cerebellum
  • Pons
  • Medulla oblongata
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49
Q

What is the function of the cerebellum?

A
  • Co-ordinates smooth and complex movements
  • Regulates posture and balance
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50
Q

What is the function of the pons?

A
  • Relays impulses from one side of cerebellum to the other, and from medulla to midbrain
  • Contains nuclei of origin for CNV, VI, VII, and VIII
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51
Q

What is the function of the medulla oblongata?

A
  • Relay between brain and spinal cord
  • Reticular formation functions in consciousness and arousal
  • Vital centres regulate heartbeat, breathing and blood vessel diameter
  • Other centres co-ordinate vomiting, swallowing, coughing, sneezing and hiccuping
  • Contains nuclei of origin for CNIX, X, XI and XII
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52
Q

What does the vestibulocochlear nerve do?

A

Sensory- hearing and equilibrium

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53
Q

What is the function of the primary motor cortex?

A

Generates nerve impulses that control the execution of movement

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54
Q

What is the function of the posterior parietal cortex?

A
  • Transforms visual information into motor commands
  • Sends this information to premotor and supplementary motor cortex areas
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55
Q

What is the function of the premotor cortex?

A
  • Sensory guide of movement
  • Controls more proximal and trunk muscles
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56
Q

Describe the function of the supplementary motor cortex.

A

Planning and co-ordination of complex movements

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57
Q

What is the input and output for the striatum of the basal ganglia?

A
  • Input - brain regions - motor cortex, premotor cortex
  • Output - globus pallidus internal (inhibitory neurons)
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58
Q

What are the components of the basal ganglia?

A
  • Dorsal striatum - caudate nucleus and Putamen
  • Substantia nigra
  • Globus palidus - internal and external
  • Subthalamic nuclei
  • Thalamus
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59
Q

What is the input and output for the globus palidus internal of the basal ganglia?

A
  • Input - inhibitory neurons of the striatum
  • Output - stops inhibiting the thalamus
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60
Q

What is the input and output for the substantia nigra of the basal ganglia?

A
  • Input - excitatory neurons of the subthalamic nucleus
  • Output - dopaminergic neurons that excite the inhibitory messages the striatum is sending to the globus palidus internal
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61
Q

What is the input and output for the subthalamic nucleus of the basal ganglia?

A
  • Input - excitatory neurons from the motor cortex and inhibitory neurons from the substantia nigra
  • Output - excitatory neurons to the substantia nigra
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62
Q

What is the substrate for dopamine synthesis?

63
Q

In the cytoplasm a of the dopaminergic neuron, what is tyrosine converted to?

A

DOPA via the action of tyrosine hydroxylase

64
Q

How is DOPA converted to dopamine?

A

DOPA-decarboxylase

65
Q

How is dopamine transported into storage vesicles?

A

Active transport carried out by the vesicular transporter mechanism

66
Q

What is dopamine re-uptake 1?

A

When dopamine is released into the synaptic cleft and is then actively transported back into the neuronal terminal (this happens to 50% of dopamine in cleft)

67
Q

What happens to the dopamine in the neuronal terminal that isn’t transporterd into vesicles for storage and release?

A

It’s broken down by the mitochondrial enzyme monoamine oxidase

68
Q

What is re-uptake 2?

A

When some of the dopamine (10%) in the synaptic cleft is actively transported into the effector cell

69
Q

How is dopamine inactivated in the effector cell?

A

Inactivated by the enzyme catchol-o-methytransferase (COMT)

70
Q

What happens the 40% of dopamine still left in the synaptic cleft?

A

Diffuses into the circulation and is broken down by monoamine oxidase and COMT in the liver

71
Q

What are the end products of dopamine metabolism?

A

Organic acids and alcohol - excreted in the urine

72
Q

What are the four main dopaminergic pathways in the brain?

A
  1. Nigrostriatal pathway
  2. Mesolimbic pathway
  3. Mesocortical pathway
  4. Tuberhypophyseal system
73
Q

What is the name of the bundle of monoamine containing fibres that the nigrostriatal, mesolimbic and mesocortical system travel in?

A

Medial forebrain bundle

74
Q

Where are the cell bodies found in the nigrostriatal pathway?

A

In the substantia nigra

75
Q

Where are the cell bodies for the dopaminergic neurons in the mesolimbic pathway?

A

In the midbrain ventral tegmental area (VTA) adjacent to the substantia nigra

76
Q

Where do the neurons in the mesolimbic pathway project to?

A

Parts of the limbic system- especially the nucleus accumbens and amygdaloid nucleus

77
Q

Where are the cell bodies of the neurons in the mesocortical pathway found?

A

In the midbrain ventral tegmental area (VTA)

78
Q

Where do the neurons of the mesocortical pathway project to?

A

Frontal cortex

79
Q

Where do the neurons of the tuberohypopyseal system start and terminate?

A

Run from the ventral hypothalamus to the median eminence and pituitary glands

80
Q

What is the function of the tuberohypopyseal system of dopamine action?

A

Controls secretions of the pituitary gland

81
Q

Which dopamine receptors are in the D1 receptor family?

82
Q

Which dopamine receptors are in the D2 receptor family?

A

D2, 3 and 4

83
Q

Which areas are D1 receptors found in?

A
  • Striatum
  • Limbic system
  • Thalamus
  • Hypothalamus
84
Q

Which areas of the brain are D2 receptors found in?

A
  • Striatum
  • Limbic system
  • Thalamus
  • Hypothalamus
  • Pituitary gland
85
Q

What are the function of D2 receptors?

A

Inhibitory autoreceptors

86
Q

What are the effects in the periphery that dopamine receptors (D1) exert?

A
  • Renal vasodilation
  • Increased myocardial contractility
87
Q

What is the function of dopamine in the nigrostriatal system?

A
  • Excites the inhibitory messages being sent to the globus palidus.
  • Fine tunes motor movements
88
Q

What is the function of dopamine in the mesolimbic and mesocortical systems?

A
  • Mediates the pleasure system in the brain (reward pathway)
  • Allows motivational and emotional responses
89
Q

What is the function of dopamine in the tuberohypopyseal system?

A

Acts on lactotrophs in the pituitary gland to inhibit release of prolactin.

90
Q

Where do neurons of the noradrenergic system arise from?

A

Neurons of the locus coeruleus - on one each side of the pons

91
Q

List the places in the brain that the neurons from the locus coeruleus (noradrenergic neurons) innervate?

A
  • All the cerebral cortex
  • Thalamus
  • Hypothalamus
  • Olfactory bulb
  • Cerebellum
  • Midbrain
  • Spinal cord
92
Q

What is the function of the noradrenergic system?

A

Regulates attention, arousal, sleep-wake cycles, leaning, memory, anxiety, pain, mood and brain metabolism

93
Q

Where do the serotonin-containing neurons originate?

A

The nine-raphe nuclei

94
Q

Where do the more caudal (medulla) of the nine raphe nuclei project?

A

The spinal cord - modulate pain-related sensory signals

95
Q

Where do the more rostral (those in the pons and midbrain) of the nine raphe nuclei innervate?

A

Most of the brain, in the same diffuse way as the locus coeruleus neurons

96
Q

When do serotonin neurons fire the most rapidly?

A

Fires the most during wakefulness (when aroused and active) - most quiet during sleep - so involved in the sleep-wake cycles

97
Q

Describe the reticular activating system.

A

Includes the raphe nuclei and the locus coeruleus Included the reticular core of the brainstem in the processes that arouse and awaken the forebrain

98
Q

Define Parkinson’s disease.

A

Progressive degenerative disorder of the basal ganglia that results in variable combinations of tremor, rigidity and bradykinesia

99
Q

What is the pathology that causes Parkinson’s?

A

Dopamine depletion resulting from a degeneration of the dopamine nigrostriatal system

100
Q

What are some other reasons (apart from dopamine depletion) that can cause Parkinsonism.

A
  • Postencephalitic syndrome
  • Side effects of anti-psychotic drugs (block dopamine receptors)
  • Toxic reaction to a chemical agent
  • Outcome of severe CO poisoning
101
Q

What are the pathological processes that destroy the nigrostriatal system.

A
  • Oxidative stress
  • Apoptosis
  • Mitochondrial disorders
  • Auto-oxidation of dopamine may injure the neurons
102
Q

Describe what happens in alpha-synuclein mutations to cause Parkinson’s.

A

Alpha-synuclein are a member of a family of proteins found mostly in the substatia nigra

Mutations cause an autosomal dominant form of the disease - mutation can cause this protein to form Lewy bodies (eosinophilic cytoplasm inclusions found in surviving neurons)

103
Q

Name the two mutations associated with Parkinson’s disease.

A

Alpha-synuclein mutations

Parkin mutations - autosomal recessive early onset form of Parkinson’s

104
Q

Describe the tremors associated with Parkinson’s disease.

A
  • Affects distal segments of limbs - hands, feet, head, neck, face, lips and tongue
  • Rhythmic flexion and contraction
  • Usually unilateral
  • Occurs when limb is supported/at rest
  • Disappears in movement or when sleeping
105
Q

Describe the rigidity associated with Parkinson’s disease.

A
  • Resistance to movement of flexors and extensors
  • Most evident during passive joint movements- cogwheel rigidity- requires lots of energy to perform
  • Flexion contraction occur due to rigidity
  • Starts unilateral - becomes bilateral
106
Q

What is bradykinesia?

A
  • Slowness in initiating and performing movements
  • Difficulty with sudden, unexpected stopping of voluntary movements
  • Unconscious movements occur in a series of disconnected steps - not in a smooth manner
107
Q

Describe problems bradykinesia causes.

A
  • Difficulty initiating walking and turning
  • Feet may freeze in place while walking
  • Lean forward when walking to maintain centre of gravity
  • Small, shuffling steps without swinging arms
108
Q

Describe some of the later stage Parkinson symptoms.

A

Loss of postural reflexes

Voluntary/emotional face movements become limited - mask like face

Loss of blinking reflex

Tongue, palate and throat muscles become rigid = drooling

Speech becomes slow and monotonous - no modulation and poorly articulated

Excessive sweating, sebaceous gland secretion and salivation - due to basil ganglia involvement with ANS - also causes lacrimation, dysphagia , orthostatic hypertension, thermal regulation, constipation, impotence and urinary incontinence

109
Q

What are the later stage cognitive problems of Parkinson’s?

A
  • Cognitive dysfunction occurs in 20-30% of people
  • Deficits in executive function disappear first - difficulty planning, starting and carrying out tasks
  • Dementia
  • Slower rate of decline than in Alzheimer’s
110
Q

How does L-DOPA medication help people with Parkinson’s?

A

L-DOPA is a precursor to dopamine

Administering more substrate will increase the amount of dopamine being synthesised in the remaining 20% of healthy dopaminergic neurons

111
Q

What is the disadvantage of L-DOPA?

A

It only manages symptoms - doesn’t fix the destroyed nigrostriatal pathway

Only works while it is present in the body

Only works if there are enough healthy neurons left to convert it into dopamine- doesn’t work in late stage Parksinon’s because the degeneration has progressed too far

112
Q

Which drugs is often co-administered with Levodopa, and why.

A

Carbidopa - a DOPA decarboxylase inhibitor - can’t cross the blood brain barrier- reduces nausea and vomiting often found with L-DOPA administration

113
Q

Why is levodopa given to patients rather than dopamine?

A

Dopamine can’t cross the blood brain barrier, so would remain in the periphery

114
Q

Why are such large amount of levodopa given to patients?

A

Because a lot is converted to dopamine in the periphery before it can enter the brain

115
Q

Describe the mechanism of action of carbidopa.

A

Inhibits dopa decarboxylase, so prevents the peripheral conversion of levodopa to dopamine

Lowers levodopa dose needed by 5-fold

Decreases severity of side effects - vomiting and nausea

116
Q

Define attention

A

A global/domain specific cognitive process, encompassing multiple sensory modalities, operating across sensory domains.

Global = driving

Domain specific = visual awareness

117
Q

What cognitive processes make up attention?

A
  1. Arousal - a general state of wakefulness + responsivity
  2. Vigilance - capacity to maintain attention over prolonged periods of time
  3. Divided attention - ability to respond to more than 1 task at once
  4. Selective attention - ability to ficus on 1 stimulus while suppressing competing stimuli
118
Q

What is the consequence of breakdown of global attention?

A

Delirium/acute confusional state - impaired arousal -> drowsiness - impaired vigilance -> impersistence - impaired divided/selective attention -> distractible

Due to a problem with the ascending reticular activating system

119
Q

What is the consequence of breakdown of domain specific attention?

A
  • visual inattention - sensory inattention - neglect

Could be due to e.g. non-dominant hemisphere stroke -> problem in prefrontal cortex/parietal cortex/limbic cortex

120
Q

What divisions does the prefrontal cortex have? What function are they responsible for?

A
  1. Dorsolateral - Attention
  2. Ventrolateral - Behaviour & Judgement
  3. Orbitofrontal - Emotional reponses
121
Q

What structures make up the parietal cortex? What is its function?

A

Functions to recieve + process sensory info from body & skin (somatosensory info) -> transmits info to other parts of brain -> co-ordinates info from other parts of brain.

Alsom involved in visual attention + spatial reasoning

122
Q

What are the components of the limbic system? What is its function?

A
  • cingulate gyrus
  • hippocampus
  • fornix
  • amygdala
  • orbital + prefrontal cortex
  • mamillary bodies

Function:

  • memory, learning
  • emotion: aggressive + sexual behaviour
  • homeostasis mainentance by hypothalamus
123
Q

What makes up the ascending reticular activating system? Function?

A
  • brainstem nuclei
  • thalamic nuclei
  • cortex

Functions to:

  • recieve fibres from sensory pathways via long ascending spinal tracts
  • alertness, maintenance, wakefulness, attention
124
Q

What happens in disorders of ascending reticular activating system function?

A
  • impaired arousal/delirium
  • metabolic disturbances
  • neurodegernative diseases
125
Q

How do you test attention?

A
  1. orientation in time + place?
  2. serial 7s (count down from 100 in 7s)
  3. digit span + digits backwards (repeat back or write down a series of no’s)
  4. months of the year/days of the week in reverse
  5. stroop test (say the name of the colour written not filled in)
  6. star cancellation test
  7. trail making test
126
Q

How is memory classified?

A

Into long term & immediate/working memory

127
Q

What are the features of working memory?

A
  • immediate recall of smal amounts of verbal/spatial info
  • functions independently of long-term memory

Central executive function in the dorsolateral prefrontal cortex splits into:

  • visual sketchpad (parieto-occipital lobe) -> spatial info
  • phonological store -> words, numbers, melodies
128
Q

What are the divisions of long-term memory?

129
Q

Describe episodic memory

A
  • a form of explicit/declarative memory: availabel for conscious access + reflection
  • personally experiences, temporally specific events

Involves:

  • extended limbic system (medial temporal lobe, hippocampus, entorhinal cortex, diencephalon, mamillary bodies, thalamic nuclei)
  • dorsolateral prefrontal cortex (for temporary organisation of episodic memory + interaction with structures within the extended limbic system)
  • impairment by e.g. Korsakoff’s, amnesia, subarachnoid haemorrhage, can lead to acute (delirium) or chronic (dementia) results
130
Q

How do you test episodic memory?

A
  1. Recall complex verbal info
  2. Word-list learning
  3. Recognition of newly encountered words + faces
  4. Recall of geometric figures
131
Q

Describe semantic memory

A
  • another form of explicit/declarative memory: availabel for conscious access + reflection
  • factual info/general knowledge & vocab
  • independant of context, time, personal relevance (as opposed to episodic)
  • storage, maintenance + retrieval are NOT based on limbic system
  • info initially process via episodic memory systems, then repeated rehearsal -> semantic storage

Involves:

  • left hemisphere anterior temporal lobe
  • anterior temporal cortex + angula gyrus integrate incoming info

Clinical damage could be: herpes simplex, right temporal lobe atrophy, alzheimer’s dementia

132
Q

How do you test semantic memory?

A
  1. Test general knowledge + vocab
  2. Fluency (e.g. name as many animals as possible in 60secs)
  3. Object naming to confrontation
  4. Test of verbal knowledge (e.g. what colour is a banana)
  5. Person-based tasks (e.g. name photos of famous people)
133
Q

Describe implicit/procedural memory

A
  • no conscious access to implicit memory stores
  • we progressively acquire motor skills to perform tasks, but we cannot explain them (e.g. riding a bike, playing an instrument)
  • Korsakoff’s -> amnesia
  • Involves basal ganglia, cerebellum
134
Q

What are ballistic movements?

A

Movement based on a set of pre-programmed instructions - rapid delivery but at expense of accuracy

135
Q

What are pursuit/visual feedback movements?

A
  • motor command continually updated according to sensory feedback -> high accuracy as movement can be modified while in progress BUT slow
136
Q

What are the areas of the brain involved in planning + instructing voluntary movement?

137
Q

Why does the face & hands have the largest representation in the motor homuculus?

A

Because they’re used in fine control

138
Q

Describe the motor pathway

139
Q

Describe the sensory pathway

140
Q

Describe proprioception

A

Feedback from peripheral sensory receptors on the positions & movement of limbs - somatic sensory cortex

141
Q

What is the input & output of the cerebellum?

A

Input - Sensory cortex

Output - Primary motor cortex (via thalamus)

142
Q

What is the function of the ventromedial descending motor pathway?

A

control of proximal + axial (trunk) muscles -> maintain posture

  • descending systems synpase on motor neurones/ interneurones in the spinal cord
143
Q

Describe the knee jerk reflex

A

Tapping the tendon stretches the muscle to which it is attached -> a monosynaptic reflec which produces contraction of the stretched muscle:

  • muscle spindle is stretched -> nerve activity increases -> a motor neuron activity increases -> muscle fibres contract -> resist stretching
144
Q

Define motoneuclei

A

Collections of motor-neurones in the VENTRAL HORN.

Collections formed from columns of all the different motor-neurons of each muscle

(a-motor neurons0

145
Q

Describe 2 methods of non-invasive brain stimulation - used for diagnosis + therapy

A
  1. Transcranial electrical stimulation
  2. Transcranial magnetic stimulation
146
Q

Define muscle recruitment

A

When the nervous system adjusts the number of motor axons firing, which controls the number of twitching muscle fibres

147
Q

Define muscle summation

A

When the nervous system varies the frequency of action potentials via the motor axons to be between 200-75 ms -> Ca2+ in the muscle is still above baseline levels from a previous action potential = the muscle fibre is not completely relaxed so the next contraction is stronger than normal

148
Q

Define muscle tetanus

A

When muscle fibres are stimulated at very high frequencies, the muscle has not time to relax between successive stimuli -> a smooth contraction many time stronger than a single twitch

149
Q

Define ‘motor point’

A

Points on the muscle which are more sensitive to electrical stimulation than the rest of the muscle.

  • usually lie over where the nerve ENTERS the muscle (muscle belly) -> muscle contraction produced by stimulation of innervating nerve
150
Q

Why does electrical stimulation of an area sometimes cause pain?

A

At these places, a cutaneous sensory nerve is being stimulated. If the left wrist is being stimulated this is being sent to the right somatosensory cortex etc

151
Q

Curare is a nicotinic acetylcholine receptor antagonist. What effect do you think do you think this drug would have on electrical stimulation of an arm muscle?

What clinical use can Curare provide?

A

As it would block the ACh receptor, the nerve would not be able to pass the signal on to the muscle so the muscle would not respond to the stimulus.

Clincally:

It could be used as a neuromuscular blocker – sometimes called a “muscle relaxant”, e.g. in the treatment of tetanus, as part of general anaesthesia or in intensive care – to allow assisted ventilation. as a paralysing poison. There are other classes of drugs also sometimes called muscle relaxants, these are anti-spasmodics, used for treatment of spacticity, for example in multiple sclerosis. These latter have different mechanisms of action.

152
Q

Describe how radial nerve compression can cause damage

A

Compression of the nerve occurs in the spiral groove of the humerus - Normally compression of the nerve causes tingling and pain to alert the sleeper, however after alcohol the warning symptoms may not be noticed. The compression continues for a longer period, resulting in damage to the nerve.

Motor fibres would be affected BEFORE pain fibres

153
Q

Describe the mechanism of damage to a body part due to compression of a nerve

A

There’s both mechanical compression + ischaemia.

  • External compression restricts blood supply of nerves in the vasa nervorum. The ischaemia affects transmission of action potentials.
  • If compression continues, demyelination occurs which can cause a conduction block.
  • Finally continued ischaemia causes axonal damage.
  • Compression initially affects the large motor fibres -> pain fibres
  • Effects irreversible if ischaemia occurs for >8hrs
154
Q

What symptom can compression of the common peroneal nerve result in?

A

Foot drop - weakness in dorsiflexing foot

P2 Head, Neck and Neuro (11 decks)

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