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Year 2 Neuro > session 4 part 2 > Flashcards

session 4 part 2 Flashcards

1
Q

What is lateral inhibition?

A

prevents the overlap of receptive fields so all receptor stimuli can be distinguished
mediated by interneurones within the dorsal horn
facilitates enhanced sensory perception

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2
Q

Describe the gate-control theory of pain inhibition

A

you can modulate a pain response in the dorsal horn by activating an Aβ-fibre
- Aβ-fibre – involved with innocuous mechanical stimulation (e.g. brush)
(- If you hurt yourself, you ‘rub it better’ – this assimilates Aβ-fibres -> inhibits stimulated pain fibres)

The gate control theory of pain asserts that non-painful input closes the nerve “gates” to painful input, which prevents pain sensation from traveling to the central nervous system. Therefore, stimulation by non-noxious input is able to suppress pain.

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3
Q

State the central sensory structures

A
  • SI: Primary somatosensory cortex (in the postcentral gyrus)
  • SII: Secondary somatosensory cortex (in the parietal operculum)
  • Posterior parietal cortex: spatial awareness of the body-
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4
Q

What are the pathways by which sensory inputs reach to the brain? (give the corresponding sensory nerve fibres)

A

2 pathways:

  1. Dorsal column system (transmitting touch and proprioception) - Aβ-fibres
  2. Spinothalamic pathway (pain, temperature and crude touch) - Aδ and C fibres
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5
Q

What type of stimuli does the dorsal column pathway transmit? What types of sensory fibres does this involve?

A

(touch and propiception)
innocuous mechanical stimuli (fine discriminative touch, vibration)

Aβ fibers

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6
Q

Information from the upper and lower limbs are converted through which tracts?

A
  • Information from the lower limbs (below T6) travel ipsilaterally along the gracile tract
  • Information from the upper limbs travel ipsilaterally along the cuneate tract
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7
Q

Give a brief overview of the dorsal column pathway

A
  • 1st order neurones terminate in the medulla
  • 2nd order neurones cross in the caudal medulla
  • 2nd order neurones terminate in the thalamus
  • 3rd order neurones from the VPL terminate in the somatosensory cortex
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8
Q

Where do fibres in the gracile tract have their first synapse?

A

the Gracile Nucleus in the medulla

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9
Q

Where do fibres in the cuneate tract have their first synapse?

A

in the Cuneate Nucleus in the medulla

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10
Q

Where do 2nd order neurones decussate in the dorsal columns?

What tract does this form?

A

in the caudal medulla

forms the contralateral medial lemniscus tract

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11
Q

Where do 2nd order neurones terminate in the dorsal columns?

A

in the VPL nucleus of the thalamus

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12
Q

Where do 3rd order neurones from the VPL terminate in the dorsal columns?

A

terminate in the somatosensory cortex

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13
Q

NOTES for the dorsal columns

A
  • There is a topographic representation of the body in the VPL (lower extremities terminate more lateral)
  • The size of somatotopic areas is proportional to density of sensory receptors in that body region (somatosensory homunculus)
  • Pain and temperature localisation not as precise
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14
Q

What type of stimuli does the spinothalamic (anterolateral) pathway transmit?

A

pain, temperature and crude touch

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15
Q

What are the 2 pathways within the spinothalamic tract and which pathways ascend with which tracts?

A

lateral and anterior spinothalamic tracts

  • Pain and temperature - lateral spinothalamic tract
  • Crude touch - anterior spinothalamic tract
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16
Q

Give a brief overview of the spinothalamic pathway

A
  • 1st order neurones terminate in the dorsal horn
  • 2nd order neurones terminate in the thalamus
  • 3rd peer terminate in the somatosensory cortex
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17
Q

Where do first order neurones terminate in the spinothalamic pathway?

A

in the dorsal horn

Primary afferent axons terminate upon entering the spinal cord

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18
Q

Where do the second order neurones decussate in the spinothalamic pathway?

(in comparison, where does decussation occur in the dorsal column pathway?)

A

Second order neurons decussate immediately in the spinal cord and form the spinothalamic tract

(Dorsal column tracts decussate in the medulla)

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19
Q

Where do second order neurones terminate in the spinothalamic pathway?

A

terminate in the thalamus

ventral posterior lateral nucleus of the thalamus

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20
Q

What are the key differences between the dorsal column and spinothalamic tracts?

A
  • Dorsal column tracts: transmit light touch, vibration and 2-point discrimination – CROSS IN BRAINSTEM
  • Spinothalamic tracts: transmit pain, temperature and coarse touch – CROSS IN SPINAL CORD
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21
Q

Describe the pathway tat represents the emotional aspect of pain?

A

the spino-reticular system (emotional component of pain).

Pain is transmitted through a pathway from the spinal cord to the parabrachial area (in the brainstem), and then to the limbic system.

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22
Q

How can we test the integrity of ascending somatosensory pathways?

A

QUANTITATIVE SENSORY TESTING

E.g. temperature thresholds, vibration sensitivity, brush sensitivity

23
Q

Describe and explain the consequences of an anterior spinal chord lesion?

A
  • Blocked anterior spinal artery -> causes ischemic damage to the anterior part of the spinal cord
  • Spinothalamic tract damage causes pain and temperature loss below the level of the lesion
  • normal light touch and vibration sensation due to intact dorsal columns
  • If the entire spinal cord was damage, you wouldn’t have ANY SENSATION AT ALL below the level
24
Q

What is ELECTRICAL PERCEPTUAL THRESHOLDS (EPT)?

A
  • Like QST but instead, electrical current is passed through the skin
  • You ask the patient whether or not they can feel it – you can map the whole body through this
  • If you have a spinal cord injury, you begin to lose sensation (so thresholds go up)
  • Depending on where they start to lose sensation, we can determine the vertebral LEVEL of the lesion
25
Q

Define pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage

26
Q

What are the different types of pain?

A
  • Nociceptive – tissue damage, typically acute pain (e.g. skin cut)
  • Muscle – lactic acidosis, ischaemia (e.g. stretching, fibromyalgia)
  • Somatic – well-localized (e.g. inflammation, infection)
  • Visceral – deep, poorly localised (e.g. stomach, colon, IBS)
  • Referred – from an internal organ/structure (e.g. Angina)
  • Neuropathic – dysfunction of the nervous system
27
Q

Chronic pain manifests as _____ and _____

A

hyperalgesia

allodynia

28
Q

Define hyperalgesia

A

increased pain from a stimulus that normally provokes pain

29
Q

Define allodynia

A

pain due to a stimulus that does not normally provoke pain – e.g. brushing the skin

30
Q

What is neuropathic pain?

A

Pain caused by a lesion or disease of the somatosensory nervous system.
Doesn’t have to be from a certain injury, but also from disease.

31
Q

Describe how neuropathic pain presents

A
  • Pain in area of neurological dysfunction (hyperalgesia and allodynia)
  • Typically sharp, burning, ‘electric shocks’
  • Poor response to usual analgesic drugs (e.g. opiates)
32
Q

GIVE SOME EXAMPLES OF NEUROPATHIC PAIN

A
  • Radicular low back pain (sciatica)
  • Diabetic neuropathy
  • Post herpetic neuralgia
  • Post-surgical pain
  • HIV-induced neuropathy
  • Chemotherapy induced neuropathy
  • Complex Regional Pain Syndrome (CRPS)
33
Q

Define sensitisation

A

increased responsiveness of nociceptive neurons to their normal input

34
Q

Define hypoalgesia

A

Diminished pain in response to a normally painful stimulus

35
Q

Define paraesthesia

A

abnormal sensation, whether spontaneous or evoked

36
Q

What is central sensitisation?

A

If you repeat a stimulus a number of times, it becomes more painful
(chronic pain)

37
Q

What is synaptic plasticity?

A

the biological process by which specific patterns of synaptic activity result in changes in synaptic strength and is thought to contribute to learning and memory.

Plasticity is the ability of the brain to change and adapt to new information. Synaptic plasticity is change that occurs at synapses.

38
Q

Which receptors are involved with inducing plasticities in the CNS?

A

NMDA receptors

39
Q

Describe how the mechanism of action by which synaptic plasticity can lead to central sensitisation

A
  • Initiated by NMDA receptor activation
  • They allow a big post-synaptic depolarisation -> Ca enters the neurone
  • (Ca2+ mediated synaptic plasticity in dorsal horn neurones - Ca involved in activating signalling pathways) Therefore there is increased synaptic strength (efficacy) -> increased sensitivity
  • The inhibitory interneurons in the dorsal horn become less influential
  • Persistent activation of NMDA receptor can result in the development of chronic pain (e.g. arthritis)
40
Q

What is the normal actions of inhibitory neurones (that stops central sensitisation)?

A

normally prevent touch (abeta fibres) causing pain

41
Q

What will loss of inibitory neurones in the dorsal horn cause?

A

allodynia

42
Q

How does central sensitisation (chronic pain) usually present?

A

allodynia and hyperalgesia

43
Q

How is chronic pain reduced?

A

monoamines in the brainstem are released that work to inhibit spinal chord excitability

44
Q

Name the main monoamine neurotransmitters and where in the brainstem they are released from

A
  • serotonin (from serotinergic nuclei) - medulla

- neuroadrenergic neurones - pons

45
Q

Describe how nociception is controlled using the PAG-RVM axis

A
  • RVM contains serotonergic neurones, which project to the dorsal horn, releasing serotonin
  • (this will either inhibit of facilitate pain):
  • —-> 5-HT1a receptors - inhibitory
  • —-> 5-HT3 receptors - facilitatory
46
Q

Describe how nociception is controlled in the locus cereleus

A

(in the pons)

  • main nuclei is located in the dorsal horn
  • predominantly inhibitory (can be thought of as a pain-braking-mechanism) - dampens down the resins to pre-synaptic alpha-2 receptors on primary afferents and projection neurones
47
Q

Describe how opioids increase descending inhibition in an endogenous analgesic system

A
  • The PAG and RVM contain high concentrations of µ opioid receptors
  • Endogenous opioids (enkephalin, dynorphin) enhance descending inhibition from the PAG-RVM axis
  • —-> in the dorsal horn by inhibiting glutamate release
    (i. e. INHIBITNG activation of spinothalamic neurons -> less excitation)
48
Q

Give another form of endogenous analgesia

A

Placebo-induced analgesia

  • PAG and RVM show activity following a placebo analgesia
  • The spinal cord is either inhibited or facilitated in placebo analgesia
49
Q

What descending controls are targeted for pain relief?

A

• Opioids – work in the PAG and RVM
• Antidepressants treat neuropathic pain (opioids are ineffective) – TCA, SNRI, SSRI
NOTE that SSRIs are not effective in neuropathic pain patients – low analgesic efficacy. TCAs and SNRIs have better efficacy
• Amitriptyline (TCA) is widely prescribed for neuropathic pain due to its noradrenergic component

50
Q

Give an example of an SSRI

A

fluoxetine, citalopram

NOTE that they are not effective in for treatment of neuropathic pain

51
Q

Give an example of a TCA

What is good about TCA in the target of descending control systems?

A

Amitriptyline

it is widely prescribed for neuropathic pain due to its noradrenergic component

52
Q

How to antidepressant drugs (e.g. SNRIs) enhance descending noradrenergic inhibition?

A

damage to a primary afferent neurone -> increase in excitability -> central sensitisation in the spinal chord

Antidepressant drug —> NA increases in the synaptic cleft —> binds to α2 receptors (inhibitory) —> inhibits activity within the neurones —> sensory input to brain is reduced —> reduced pain.

53
Q

What is an SNRI? Give an example

A

serotonin and norepinephrine reuptake inhibitors

e.g. duloxetine

Year 2 Neuro (16 decks)

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