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Semester 3: Mind and Movement > PBL Topic 3 Case 2 > Flashcards

PBL Topic 3 Case 2 Flashcards

1
Q

What do mechanoreceptors detect?

A
  • Mechanical compression or stretching of tissue adjacent to the receptor
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2
Q

What do thermoreceptors detect?

A
  • Changes in temperature, some cold, others warmth
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3
Q

What do nociceptors detect?

A
  • Damage occurring in tissue e.g. physical or chemical damage
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4
Q

What do electromagnetic receptors detect?

A
  • Light on the retina of the eye
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5
Q

What do chemoreceptors detect?

A
  • Taste in the mouth
  • Smell in the nose
  • Oxygen level in the blood
  • Osmolality of blood
  • [CO2]
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6
Q

What is a modality of sensation?

A
  • Any principal type of sensation a person experiecnes
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7
Q

What is the labelled line principle?

A
  • Specific nerve fibres transmit only one modality of sensation
  • Since they terminate at a specific site in the CNS
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8
Q

What is a receptor potential?

A
  • Change in membrane electrical potential whenever the receptor is stimulated
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9
Q

How does a stimulus cause an action potential?

A
  • Stimulus excites a receptor
  • Change in membrane permeability allowing diffusion of ions through the membrane
  • Receptor potential rises above a threshold to generate an action potential
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10
Q

What is meant by receptor adaptation?

A
  • The rate at which a receptor responds to a stimulus until the rate of action potential ceases
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11
Q

What is a tonic receptor? Give an example of a tonic receptor

A
  • Slowly adapting
  • Transmits continuous impulses to the brain as long as the stimulus is present
  • Muscle spindle or Golgi tendon
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12
Q

What is a rate receptor? Give an example of a rate receptor

A
  • Rapidly adapting
  • Transmits signals only when the stimulus changes strength
  • Pacinian corpuscle
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13
Q

How does a type A fibre compare to a type C fibre?

A
  • Type A are larger and myelinated, transmission is faster

- Type C are smaller and unmyelinated, transmission is slower

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14
Q

Give two examples A-alpha fibre

A
  • Annulospiral ending of muscle spindles

- Golgi tendon organs

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15
Q

Give an example of an A-beta fibre

A
  • Cutaneous tactile receptor
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16
Q

Give an example of an A-gamma fibre

A
  • Flower spray ending of muscle spindles
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17
Q

Give an example of an A-delta fibre

A
  • Nociceptor carrying temperature, crude touch and pricking sensation
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18
Q

Give an example of a C fibre

A
  • Pain and crude touch sensation
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19
Q

What is spatial summation?

A
  • Signal strength increases by using progressively greater number of fibres
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20
Q

What is temporal summation?

A
  • Signal strength increases by increasing number of impulses from each fibre
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21
Q

Outline the structure of a free nerve ending

A
  • Nerve loses its Schwann cell sheath as it reaches dermis or epidermis
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22
Q

Identify two modalities that free nerve endings detect

A
  • Temperature

- Pain

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23
Q

Identify a modality that Merkel cells detect? How do Merkel cells adapt?

A
  • Pressure

- Slowly

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24
Q

Identify three encapsulated nerve endings

A
  • Meissner’s corpuscles
  • Ruffini endings
  • Pacinian corpuscles
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25
Q

Where are Meissner’s corpuscles most abundant?

A
  • Finger pads
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26
Q

How do Meissner’s corpuscles adapt?

A
  • Rapidly
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27
Q

What is the role of Meissner’s corpuscles

A
  • Detective work on textured surfaces
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28
Q

Where are Ruffini endings located?

A
  • Hairy and glabrous skin
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29
Q

What do Ruffini endings detect? How do they adapt?

A
  • Drag (shearing stress) over skin

- Slowly adapting

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30
Q

Where are Pacinian corpuscles located?

A
  • Side of fingers and palm
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31
Q

What do Pacinian corpuscles detect?

A
  • Vibration
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32
Q

Where are dorsal root ganglia located?

A
  • Intervertebral foramina

- Where they come together to form spinal nerves

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33
Q

What are satellite cells?

A
  • Modified Schwann cell in spinal ganglion
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34
Q

What does the medial stream of the dorsal root entry zone consist of? Where do they divide and synapse?

A
  • Medium and large fibres
  • Divide into ascending and descending fibres in the posterior funiculus
  • Which synapse in laminae 2, 4 and 4
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35
Q

What does the lateral stream of the dorsal root entry zone consist of? Where do they divide and synapse?

A
  • Small fibres
  • Divide into ascending and descending fibres in the posterolateral tract of Lissauer
  • Which synapse in the laminae 1 (marginal zone) and the substantia gelatinosa (lamina 2)
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36
Q

Identify the two major somatic sensory pathways

A
  • Dorsal column medial lemniscal system

- Spinothalamic pathway

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37
Q

Where are the first-order neurons of the somatic sensory pathways located?

A
  • Posterior root ganglia
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38
Q

Where are the second-order neurons of the somatic sensory pathways located?

A
  • CNS grey matter on same side as first order neurons
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39
Q

Where are the third-order neurons of the somatic sensory pathways located

A
  • Between thalamus and somatosensory cortex
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40
Q

Outline 3 differences between the DCML and spinothalamic systems

A
  • DCML consists of large fibres which transmit at high velocities
  • DCML has a high degree of spatial orientation of fibres
  • Spinothalamic transmits a broad spectrum of sensory modalities
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41
Q

Identify 4 modalities transmitted in the DCML

A
  • Touch sensation
  • Vibration sensation
  • Proprioception
  • Pressure
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42
Q

Identify 2 modalities transmitted in the anterior spinothalamic tract

A
  • Crude touch

- Firm pressure sensations

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43
Q

Identify 2 modalities transmitted in the lateral spinothalamic tract

A
  • Pain

- Temperature

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44
Q

Identify six sensory receptors that transmit impulses in the DCML

A
  • Meissner’s corpuscles
  • Pacinian corpuscles
  • Ruffini endings
  • Merkel cells
  • Muscle spindles
  • Golgi tendon organs
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45
Q

What are the fasciculus gracilis and nucleus gracilis?

A
  • First order neurons from lower limbs ascend in fasciculus gracilis
  • And terminate in nucleus gracilis in medulla oblongata
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46
Q

What are the fasciculus cuneatus and nucleus cuneatus?

A
  • First order neurons from upper limbs and torso ascend in fasciculus cuneatus
  • And terminate in nucleus cuneatus in medulla oblongata
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47
Q

Where do second order neurons of the DCML project from and to?

A
  • From nucleus gracilis and nucleus cuneatus

- To ventral posterolateral nucleus of thalamus

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48
Q

What terminates in the ventral posteromedial nucleus?

A
  • Fibres from trigeminal lemniscus

- Which subserve same sensory functions for the head that the DCML fibres subserve for the body

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49
Q

Where do third order neurons of the DCML project from and to?

A
  • From VPN

- To somatosensory cortex in postcentral gyrus

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50
Q

Where do second order neurons of the spinothalamic project from and to?

A
  • From lamina 1-2 and 4-5

- To contralateral VPN

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51
Q

Identify the pathway of the spinothalamic system

A
  • Second order neurons enter lamina 1-2, 4-5
  • Decussate immediately
  • Pass in anterior and lateral funiculus
  • Come together at spinal lemniscus
  • Synapse in contralateral VPN
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52
Q

Where does the spinoreticular tract run and terminate?

A
  • Runs alongside spinothalamic pathway

- Reticular activating system

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53
Q

Identify two functions of the spinoreticular tracts

A
  • Report to limbic cortex of anterior cingulate gyrus about the nature of a sensation e.g. pleasurable or painful
  • Arouse cerebral cortex e.g. waking state
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54
Q

Where does the spinotectal tract run and terminate?

A
  • Runs alongside spinothalamic pathway

- Terminates in superior colliculus

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55
Q

Identify a function of the spinotectal tract?

A
  • Mediates reflex postural movements of head in response to visual stimuli
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56
Q

Where does spino-olivary tract terminate and what is its role?

A
  • Inferior olivary nucleus in medulla

- Motor learning through its action on contralateral cerebellar cortex

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57
Q

Identify the three nuclei of the trigeminal sensory nuclei and their roles?

A
  • Mesencephalic: proprioception
  • Chief: Touch and pressure
  • Spinal: Pain
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58
Q

Identify three other cranial nerves that convey sensory information to the trigeminal sensory nucleus

A
  • Facial
  • Glossopharyngeal
  • Vagus
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59
Q

Where does the trigeminothalamic tract run from and to?

A
  • Spinal trigeminal lemniscus
  • Terminates in ventral posteromedial nucleus of the thalamus
  • Third order afferents to somatosensory cortex
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60
Q

Describe the layout of the homunculus of the somatosensory cortex

A
  • Tongue and larynx closest to horizontal fissure
  • Large representation of lips and thumb
  • Lower limb and foot closest to longitudinal fissure
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61
Q

Which of Broadmann’s areas does the somatosensory cortex reside in?

A
  • 3, 1 and 2
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62
Q

Area 3a of the somatosensory cortex receives information from which receptors?

A
  • Muscle spindles
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63
Q

Area 3b of the somatosensory cortex receives information from which receptors?

A
  • Cutaneous receptors
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64
Q

Identify three afferents to the somatosensory cortex

A
  • Thalamic afferents
  • Commissural fibres from opposite somatosensory cortex
  • Association fibres form motor cortex
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65
Q

What is stereoanesthesia and what is a common cause?

A
  • Reduction of sensory acuity on opposite side of body
  • Including raised sensory threshold, poor two-point discrimination, and impaired vibration sense and position sense
  • Middle meningeal artery is compromised
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66
Q

Identify three efferents to the somatosensory cortex

A
  • Association fibres to ipsilateral motor cortex
  • Commissural fibres to contralateral somatosensory cortex
  • Projection fibres to pyramidal tract to terminate on inhibitory internuncial neurons
67
Q

Where are somatosensory association areas located and what is their role?

A
  • Broadmann’s areas 5 and 7

- Deciphering deeper meanings of inputs to somatosensory cortex

68
Q

What is pain?

A
  • Unpleasant emotional experience associated with tissue damage
69
Q

What is allodynia?

A
  • Pain produced by an innocuous stimuli

- For example stroking sunburned skin or moving an inflamed joint

70
Q

What are central pain-projecting neurons?

A
  • Posterior horn neurons projecting pain-encoded information to the contralateral brainstem and thalamic nuclei
  • Includes spinothalamic, spinoreticular and spinoamygdaloid pathways
71
Q

What is wind-up phenomenon?

A
  • Sustained state of excitation of central pain pathways induced by glutamate activation of NMDA receptors
72
Q

What is fast pain?

A
  • Stabbing pain perceived by activation of A-delta nociceptors
73
Q

What is hyperalgesia?

A
  • Hypersensitivity to stimulation of injured tissue and of surrounding tissue
74
Q

What is neurogenic inflammation?

A
  • Inflammation caused by liberation of substance P

- Following depolarisation of antidromic fine peripheral nerve fibres

75
Q

What is neuropathic pain?

A
  • Chronic stabbing or burning pain associated to peripheral nerve
76
Q

What are nociceptors?

A
  • Receptors whose activation generates a sense of pain
77
Q

What are polymodal receptors?

A
  • Peripheral nociceptors responsive to noxious stimulation
78
Q

What is sensitisation?

A
  • Lowering of threshold of peripheral nociceptors by histamine
  • Following peripheral release of peptides via the axon reflex
79
Q

What is slow pain?

A
  • Aching pain perceived following activation of C-fibre nociceptors
80
Q

Identify three molecules that lower the activation threshold of nociceptors following tissue injury

A
  • Bradykinin
  • Prostaglandin
  • Leukotrienes
81
Q

What does substance P bind to? How does this result in production of arachidonic acid?

A
  • Substance P binds to mast cells
  • Mast cells secrete histamine
  • Which binds to histamine receptors on nerve terminals
  • Causing production of arachidonic acid
82
Q

What happens to the arachidonic acid during tissue damage?

A
  • Cyclooxidase converts arachidonic acid into prostaglandin
  • Which results in sustained activation of large numbers of C-fibres and sensitisation of nociceptors
  • Manifested by allodynia and hyperalgesia
83
Q

What is the lateral pain pathway?

A
  • Projecting of pain via the lateral spinothalamic tract to the contralateral ventral posterolateral nucleus to the primary motor cortex
  • This pathway activates spinotectal tract which causes eye to look towards source of pain
84
Q

What is the medial pain pathway?

A
  • Projecting of pain via the spinoreticular tracts to anterior cingulate cortex via intralaminar nucleus of thalamus
  • This area is concerned with the affective component of pain
85
Q

Identify three causes of central pain states

A
  • Repetitive activation of NMDA glutamate receptors
  • Gene transcription involving addition of glutamate receptors
  • Non-serotonergic neurons near the magnus raphe nucleus facilitate central pain states
86
Q

Identify the pathology of neuropathic pain

A
  • Peripheral nerve is severed
  • Proximal and distal end become separated by developing scar tissue
  • Intermediate regenerating axon from a thread like ball known as a neuroma
87
Q

Identify one cause of neuropathic pain

A
  • Postherpetic neuralgia (shingles)
88
Q

Outline the axon reflex

A
  • Skin is stroked by a sharp object
  • Red flare owing to arteriolar dilatation
  • White wheal owing to exudation of plasma
  • Due to release of Substance P which binds to surface of mast cells which release histamine
89
Q

What is segmental antinociception?

A
  • Large type A mechanoreceptive afferents from hair follicles synapse upon anterior spinothalamic relay cells
  • They (mainly GABA) gelatinosa cells which synapse in turn upon lateral spinothalamic relay cells.
  • Some of the internuncials also exert presynaptic inhibition upon C-fibre terminals.
  • Gating of the spinothalamic response to C-fibre activity can be induced by stimulating the mechanoreceptive afferents, thereby recruiting inhibitory gelatinosa cells.
90
Q

What is supraspinal antinociception?

A
  • Raphespinal tract descends from magnus raphe nucleus
  • Which descends in Lissauer’s tract to terminate in substantia gelatinosa
  • Liberation of serotonin excites inhibitory internuncials causing synaptic inhibition.
91
Q

Stimulation of which brain region results in stimulation of the magnus raphe nucleus?

A
  • Periaqueductal grey of the midbrain
92
Q

What is the role of beta-endorphin in analgesia?

A
  • Released from hypothalamic neurons which project to PAG during stress
  • These neurons inhibitory internuncials on the PAG
  • Resulting in increased stimulation of the MRN and hence antinociception
93
Q

What is cervical spondylosis?

A
  • Osteoarthritis in the cervical spine

- Characterised by degeneration of the intervertebral disc and osteophyte formation

94
Q

What is cervical spondylotic radiculopathy?

A
  • Compression of a nerve root when a disc prolapses laterally
95
Q

Outline the clinical features of cervical spondylotic radiculopathy.

A
  • Pain in the neck and affected segment
  • Neck held rigidly and movements may exacerbate pain
  • Paraesthesia and sensory loss in the affected segment
  • Weakness, wasting, reflex impairment
96
Q

Outline the muscle weakness, sensory loss and reflex loss associated with a C5 root compression

A
  • Biceps, deltoid
  • Upper lateral arm
  • Biceps reflex
97
Q

Outline the muscle weakness, sensory loss and reflex loss associated with a C6 root compression

A
  • Brachioradialis
  • Lower lateral arm, thumb, index finger
  • Supinator
98
Q

Outline the muscle weakness, sensory loss and reflex loss associated with a C7 root compression

A
  • Triceps, fingers and wrist extensors
  • Middle finger
  • Triceps
99
Q

Outline the treatment options for cervical spondylotic radiculopathy.

A
  • Analgesics and physiotherapy

- Disc excision (MRI required)

100
Q

What is cervical spondylotic myelopathy?

A
  • Pressure on the spinal cord in the cervical region due to herniation of a disc
101
Q

Outline the clinical features of cervical spondylotic myelopathy.

A
  • Spasticity of legs comes first

- Sensory loss in upper limbs, tingling, numbness, proprioception loss in hands, with progressive numbness

102
Q

Outline the treatment options for cervical spondylotic myelopathy.

A
  • Anterior discectomy

- Which may arrest progression but may not result in neurological improvement

103
Q

What is lumbar spondylosis?

A
  • Degenerative disc disease and osteoarthritic changes in the lumbar spine
  • Sciatica
104
Q

Outline the pathology of lumbar disc herniation

A
  • Precipitated by trauma
  • Nucleus pulposus may budge or rupture through annulus fibrosus
  • Giving rise to pressure on nerve endings in spinal ligaments
105
Q

Outline the clinical features of lumbar disc herniation

A
  • Lasegues sign: limitation of flexion of the hip on the affected side if the straight leg is raised
  • Acute onset lower back pain and sciatica
  • Reflex loss
  • Sensory loss in affected dermatome
106
Q

Outline the muscle weakness, sensory loss and reflex loss associated with a L4 root compression

A
  • Inversion of foot
  • Inner calf
  • Knee
107
Q

Outline the muscle weakness, sensory loss associated with a L5 root compression

A
  • Dorsiflexion of great toe

- Outer calf and dorsum of foot

108
Q

Outline the muscle weakness, sensory loss and reflex loss associated with a S1 root compression

A
  • Plantar flexion
  • Sole and lateral foot
  • Ankle
109
Q

Identify 4 things that X-rays of the skull and spine show

A
  • Fracture
  • Vault and skull disease
  • Enlargement or destruction of pituitary fossa
  • Intracranial calcification
110
Q

What is an opioid?

A
  • A substance that produces morphine like effects

- That is blocked by naloxone, a complete antagonist

111
Q

Identify the opioid receptor responsible for most of the analgesic effects.

A
  • u receptor
112
Q

Describe how opioids decrease neuronal excitability

A
  • Opening inward-rectifying potassium channels, causing hyperpolarisation
  • Inhibiting the opening of N-type calcium channels, resulting in reduced neurotransmitter release
113
Q

How are opioids inactivated?

A
  • Hepatic metabolism

- In conjunction with glucuronide

114
Q

Outline five adverse effects of opioids

A
  • Tolerance
  • Dependence
  • Euphoria
  • Sedation
  • Respiratory depression
115
Q

Outline the roles of COX-1 and COX-2

A
  • COX-1 is involved in tissue homeostasis and prostaglandin production
  • COX-2 is involved in production of prostanoid mediators of inflammation
116
Q

Describe the mechanism behind the anti-inflammatory effect of NSAIDs

A
  • Decrease in prostaglandin E2 and prostacyclin

- Which reduces vasodilation and oedema

117
Q

Describe the mechanism behind the anti-analgesic effects of NSAIDs

A
  • Decrease prostaglandins generation

- So less sensitisation of nociceptive nerve endings to inflammatory mediators such as bradykinin and 5-HT

118
Q

Describe the mechanism behind the anti-pyretic effect of NSAIDs

A
  • Inhibit IL-1 beta release
119
Q

Identify two examples of NSAIDs

A
  • Ibuprofen

- Naproxen

120
Q

What is the dosage of ibuprofen?

A
  • 300-400 mg

- 3 - 4 times a day

121
Q

Outline two unwanted effects of NSAIDs

A
  • GI disturbances (gastric ulceration / bleeding)

- Skin reactions

122
Q

Explain the rationale behind co-administration of NSAIDs and opioids

A
  • Same degree of analgesia

- But reduced addiction

123
Q

Explain the actions of paracetamol

A
  • Antipyretic
  • Analgesic
  • But less anti-inflammatory effects
124
Q

Identify two drugs that can prevent liver damage and how they work

A
  • I. V Acetylcysteine
  • Oral methionine
  • Increase glutathione
125
Q

What is the dosage of paracetamol?

A
  • 0.5-1g

- Every 4-6 hours

126
Q

What is neuropathic pain and when does it occur?

A
  • Dysfunction of pain perception apparatus
  • Caused by trigeminal neuralgia / diabetic neuropathy
  • Opioid resistant
127
Q

Explain how TCAs can be used to treat neuropathic pain

A
  • Inhibit noradrenaline re-uptake
128
Q

Explain how gabapentin can be used to treat neuropathic pain

A
  • Bind to alpha 2 delta 1 and alpha 2 delta 2 subunits of potassium channels
  • And inhibit neurotransmitter release
129
Q

What is the dosage of gabapentin?

A
  • 300 mg once daily on day 1
  • 300 mg twice daily on day 2
  • 300 mg three times daily on day 3
130
Q

Explain how lidocaine can be used to treat neuropathic pain

A
  • Blocks spontaneous discharges from damaged sensory nerve terminals
131
Q

How is lidocaine administered?

A
  • Topically as a patch

- Or intravenously

132
Q

Outline the WHO Analgesic Pain Ladder

A
  • Step 1: Paracetamol
  • Step 2: If pain persists or increases (moderate pain), weak opioid such as codeine
  • Step 3: Severe pain, give a strong opioid such as morphine
133
Q

What is drug dependence?

A
  • Condition in which drug taking becomes compulsive, often with serious adverse consequences
134
Q

Explain why psychoactive drugs produce a rewarding experience e.g. elevation in mood or feeling of euphoria

A
  • Activate mesolimbic dopaminergic pathway running from the VTA to the nucleus accumbens
  • They enhance firing of VTA dopaminergic neurons
  • By reducing the level of GABAergic inhibition within the VTA
135
Q

Explain how drugs alter memory formation to enhance the recollection of previous drug experiences

A
  • Changes in synaptic plasticity by enhancing long-term potentiation
  • By increasing expression of AMPA receptors
136
Q

What is withdrawal syndrome?

A
  • Cessation of drug administration / administration of an antagonist producing adverse effects characteristic of the drug taken
137
Q

Outline the mechanisms responsible for the withdrawal syndrome

A
  • Increase in cAMP production as a result of super activation of adenylyl cyclase
  • Activation of protein kinases
  • Resulting in excitation of nerve terminals by phosphorylation neurotransmitter transporters
  • Thus increasing conductance and increasing neurotransmitter release
138
Q

What is tolerance?

A
  • Decrease in pharmacological effects on repeated administration of a drug
139
Q

Outline the mechanisms responsible for tolerance

A
  • u receptor is phosphorylated by various intracellular kinases
  • That desensitise the receptor or cause the receptor to be blocked by other binding proteins
140
Q

Outline the process of plain radiography

A
  • X rays are collimated (directed) to appropriate area
  • The X-rays are attenuated by the tissue
  • Air attenuates X-rays a little
  • Fat attenuates X-rays more than air but less than water
  • Bone attenuates X-rays the most
  • Differences in attenuation result in differences in level of exposure on the film
141
Q

Why does bone appear white on plain radiography?

A
  • Most attenuation of X-rays

- Meaning it is exposed to least amount of X-rays

142
Q

Why does air appear black on plain radiography?

A
  • Least attenuation of X-rays

- Meaning it is exposed to most amount of X-rays

143
Q

Identify a substance used to fill structures to increase attenuation of X-rays

A
  • Barium sulfate
144
Q

Identify a contrast agent injected directly into veins or arteries during plain radiography

A
  • Iodine based molecules
145
Q

What does Computed Tomography involve?

A
  • X-ray tube passes around the body
  • Creating a series of images
  • Which are transformed using a computer to produce final image
146
Q

Identify 5 limitations of CT

A
  • Lesions under 1 cm in diameter may be missed,
  • Lesions with attenuation close to bone may be missed if near the skull,
  • Lesions with attenuation similar to brain are poorly displayed e.g. MS plaques, isodense subdural haematoma.
  • CT is not good at detecting posterior fossa lesions because of surrounding bone,
  • Patient co-operation: an anaesthetic is very occasionally needed.
147
Q

Outline the process of magnetic resonance imaging

A
  • Protons in water molecules of patient act as magnet
  • Patient is placed in strong magnetic field which aligns the protons
  • Radio waves are passed through the body and cause the magnets to deflect
  • As they return to their aligned position they emit small radio pulses
  • The strength and frequency of pulses produces a signal which is analysed by a powerful computer
148
Q

What are T1 and T2 images and how are they produced?

A
  • Sequence of radio waves is altered to produce either T1 or T2 images
  • T1 images show dark fluid
  • T2 images show bright fluid
149
Q

What i.v contrast is used during MRI when assessing cerebral circulation?

A
  • Gadolinium
150
Q

Identify five advantages of MRI

A
  • Distinguishes between white and grey matter in the spinal cord,
  • MRI has resolution superior to CT (around 0.5 cm),
  • No radiation is involved
  • Capable of pituitary imaging
  • Tumours, infarction, haemorrhage, MS plaques, posterior fossa, foramen magnum and cord are demonstrated well by MRI.
151
Q

Identify four disadvantages of MRI

A
  • Time
  • Cost
  • Patients need to keep still within a narrow tube and thus claustrophobia is an issue
  • Patients with pacemakers or metallic fragments in the brain cannot be imaged
  • MR imaging frequently shows diffuse meningeal enhancement with gadolinium for some days after lumbar puncture.
152
Q

Outline the process of PET scanning

A
  • Positrons are positively charged ‘anti-electrons’.
  • Which are emitted from the decay of proton-rich radionuclides.
  • The most commonly used radionuclide is fluorodeoxyglucose (FDG)
  • Tissues actively metabolising glucose take up FDG, the resulting localised high concentration of this molecule compared to background emission is detected as a “hot spot.”
153
Q

Define Gate Control Theory

A
  • A gate exists that, when opened sends information to an action system which results in perception of pain
  • Pain is not only understood in terms of stimulus response pathways
  • But is also affected by emotional and behavioural factors
154
Q

According to Gate Control Theory, identify physical factors that open and close the gate.

A
  • Open: Injury or activation of large nociceptive fibres

- Closure: Medication, stimulation of small fibres

155
Q

According to Gate Control Theory, identify emotional factors that open and close the gate.

A
  • Open: Anxiety, worry, tension, depression

- Closure: Happiness, optimism, relaxation

156
Q

According to Gate Control Theory, identify behavioural factors that open and close the gate.

A
  • Open: Focussing on pain

- Closure: Concentration, distraction or involvement of other activities

157
Q

Explain how learning plays a role in the processing of pain

A
  • Classical conditioning: associating an environmental stimulus with pain
  • Operant conditioning: positive reinforcement includes sympathy, time off work
158
Q

What are fear avoidance beliefs?

A
  • Pain related fear results in hyper-vigilance towards the pain
  • Which would contribute to the progression from acute to chronic pain
159
Q

Identify the three components of catastrophising

A
  • Rumination: a focus on threatening information e.g. a symptom
  • Magnification: overestimating the extent of the threat e.g. the severity of the symptom
  • Helplessness: underestimating personal and broader resources that might help mitigate the danger e.g. visiting doctor / treatments
160
Q

How does treatment of chronic pain differ to that of acute pain?

A
  • Acute pain = pharmacological interventions
  • Chronic pain = multidisciplinary approach to pain with focus on:
  • Improving functioning
  • Decreasing reliance on medical services
  • Increasing social support
161
Q

Outline three methods of pain relief that reflect an interaction between psychology and physiological factors

A
  • Respondent methods: Reducing muscular tension and anxiety to reduce pain
  • Cognitive methods: modifying thoughts about pain that may exacerbate pain
  • Behavioural methods - Which draw upon operant conditioning and reinforcement
162
Q

Outline Black Report

A
  • Cultural explanation: health influenced by culture
  • Materialist explanation: health influenced by economic factors
  • Social selection hypothesis: health influences social class not the other way around
  • Artefact explanation: No significant relationship between health and class
163
Q

What is drift hypothesis?

A
  • Mental illness causes a downward shift in social class
164
Q

What is social causation theory?

A
  • Low social status causes stress that leads to mental illness

Semester 3: Mind and Movement (21 decks)

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