Neuro 7: Sensory pathways Flashcards

1
Q

What is a sensory modality

A

Type of stimulus (hot cold etc)

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2
Q

How does information about such modalities get to brain

A

Modalities have specialised receptors which transmit inforatmion through specific anatomical pathways

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3
Q

Outline the receptors detecting following modalities:

  1. Touch Pressure Vibration and Proprioception (joint position, muscle length, muscle tension)
  2. Temperature
  3. Nociception
A
  1. Mechanoreceptor
  2. Thermoreceptor
  3. Nociceptor
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4
Q

Classify sensory fibres

A

Aalpha group I- skeletal muscle proprioceptors (very rapid, large diameter and lots of myelination

Abeta-group II. Very large and myelinated so fast. Innocous mechanical stimulation. Mechanoceptors of skin

Adelta- group III. Not as large but still myelinated so kind of fast. Noxious mechanical and thermal stimulation. Involved in pain and temperature transduction

C fibres- group IV- very slow, no myelination and thin. Noxious mechanical, thermal and chemical stimulation (slower achey pain and temperature and itch)`

ALL MYELINATED EXCEPT C FIBRES

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5
Q

T/f peripheral nerves contain one type of sensory fiber

A

FALSE: different fiber types containing information about different modalities present in peripheral nerve

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6
Q

Differentiate the nerve endings for the receptors of different modalities

A

Thermoceptors and nociceptors have branched nerve endings

Mechanoceptors have encapsulated nerve ending morphology

I.e. the nerve ending type differs depending on the modality being served by that receptor

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7
Q

Define sensory receptor

A

Sensory receptors are transducers that convert energy from the environment into neuronal action potentials

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8
Q

Define absolute threshold

A

The absolute threshold is the level of stimulus (stimulus strength) that produces a positive response of detection 50% of the time

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9
Q

Put in correct sequence
Neurotransmitter release
Generator potential
action potential

A

Generator potential
action potential
Neurotransmitter release

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10
Q

What is the consequence of a longer and stronger stimulus

A

Larger Generator potential,
larger action potential (and threshold potential reached for longer), increased Neurotransmitter release and greater intensity of feel

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11
Q

What type of channels do thermoreceptors have

On which fibres are thermoceptors present

A

Present on Alpha-delta and c fibres

TRP (transient receptor potential) channels.

TRPV1-4 are activated by heat

TRPM8 and TRPA1 activated by cold!

Look at the different heats and different receptors

(TRPV2 activated at higest temperature).

The nerve endings might have a combination of different types of receptor

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12
Q

4 different types of mechanoreceptors and what they fire based on

A

Meissners corpuscle- Fine discriminative touch

Merkel cells- Light touch and superficial pressure

Pacinian corpuscle-
Detects deep pressure, vibration and tickling (P for deeP pressure)… think cheeky pacini (likes deep pressure, vibration and tickling)

Ruffini endings- Continuous pressure or touch and stretch
(think of ruffles which go on forever, so continuous)

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13
Q

Differentiate tonic and phasic receptors

A

TONIC- slow adapting. Fire continuously until stimulus is removed, then stop firing. Keeps the brain constantly informed of the status of the body

PHASIC- fast adapting. Detect a change in stimulus strength. Transmit an impulse at the start and the end of the stimulus.
Also called ‘’movement receptors’’ or ‘’rate receptors’’

phasic is phast adapting!

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14
Q

Given an exampe of a tonic and phasic receptor

A

TONIC:
Merkel cells
Slowly adapt allowing for light touch to be perceived.

PHASIC:
Pacinian receptor
Sudden pressure excites receptor
Transmits a signal again when pressure is released

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15
Q

Which regions of spinal cord innervate skin

A

Cervical (not C1)
Thoracic
Lumbar
Sacral

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16
Q

Differentiate dermatome and receptive field

A

Dermatome is an area of skin supplied by 1 spinal nerve

Receptive field is region on the skin which causes activation of a single sensory neuron when activated

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17
Q

T/F A large receptive field allows cells to detect changes over smaller areas.

A

F:
Small receptive fields allow for the detection of fine detail over a small area. Precise perception

Large receptive fields allow the cell to detect changes over a wider area (less precise perception)

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18
Q

Name a site of small receptive fields

A

The fingers have many densely packed mechanoreceptors with small receptive fields

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19
Q

Define two point discrimination

A

Minimum distance at which two points are perceived as separate
Related to the size of the receptive field

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20
Q

What do the dermatomes look like on the leg

A

From an anterior view: Inward diagonal (inferomedially) from L1 in groin region through to L5 across the shin and S1 on the ankle and outside of foot

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21
Q

Site of large receptive fields

A

Back

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22
Q

What types of fibers do nociceptors have

A

Adelta mediate sharp, intense or first pain.

They are MYELINATED. There are two types.

Type 1= Aδ… noxious mechanical

Type 2 : Aδ- noxious heat

And c fibres also transmit pain, but mediate dull, persistent or second pain. Unmyelinated
Respond to thermal, mechanical and chemical stimuli (polymodal)

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23
Q

Where are the cell bodies of sensory afferent neurons located

A

dorsal root ganglia (body) and trigeminal ganglia (face)

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24
Q

How is the dorsal horn of the spinal cord organised

A

Rexed Laminae (I-VII)

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25
Q

Where do innocuous mechanical stimuli fibers terminate within the dorsal horn?

A

Aβ-fibers (&Aα) terminate in lamina III-VI (deep)

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26
Q

Where do noxious mechanical stimuli fibers terminate within the dorsal horn?

A

Pain and temperature – Aδ and C-fibers terminate in lamina I-II (superficial)

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27
Q

What is the main neurotransmitter in the dorsal horn that the fibers release

A

Glutamate main excitatory neurotransmitter

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28
Q

Function of interneurons within dorsal horn

A

Interneurons connect between different laminae and between adjacent peripheral inputs (lateral inhibition)

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29
Q

What is lateral inhibition

A

When a receptive field can overlap with another receptive field (difficult to distinguish between 2 stimulus locations )

Lateral inhibition occurs in the dorsal horn, in which interneuons prevent overlap from 2 receptive fields, allowing pinpoint accuracy. It prevents messages 2 overlapping receptive fields being transmitted to the second order neuron

THE DIFFERENCE BETWEEN ADJACENT INPUTS IS ENHANCED BY LATERAL INHIBITION

http://www.d.umn.edu/~jfitzake/Lectures/DMED/SensoryPhysiology/GeneralPrinciples/LateralInhibition.html

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30
Q

What are the three important brain areas for somatosensory perception

A

Primary somatosensory cortex (postcentral gyrus)

Secondary somatosensory cortex (in parietal operculum, head of the lateral sulcus)

Posterior parietal cortex is for spacial awareness of the body (kind of relates to the WHERE dorsal stream)

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31
Q

Differentiate noxious and innoxuous

A

Harmful and non harmful

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32
Q

What info does dorsal column pathway transmit

A

Fine discriminative touch

Vibration

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33
Q

How does sensory information get to the dorsal column

A

Aβ fibers enter via the dorsal horn (into DEEP lamina and enter the ascending dorsal column pathways

(strangely it’s actually more anterior even though called deep, but deep into anterior horn compared to where the spinal dorsal root enters)

34
Q

What information is conveyed along the cuneate tract of the dorsal column

A

fine touch and vibration ipsilaterally from upper limbs and body (above T6) travel

anything below travels in the GRACILE TRACT

35
Q

How is the body represented in the dorsal column nuclei in the brainstem (ie. cuneate nucleus and gracilis nucleus)

A

There is a topographic representation of the body in the brainstem dorsal column nuclei

36
Q

Where to gracilis and cuneate tracts synpase

A

These first order neurons synapse in the gracile and cuneat nuclei in the medulla!

(YOU MUST be able to identify the tracts and nuclei of those tracts on an image of the medulla, see slide 25 on new ppt.)

37
Q

Where do second order neurons of the touch and proprioception pathway decussate

A

2nd order neurons arise from the gracile/cuneate nuclei and then decussate in the cuadal medulla

38
Q

Which tract is formed from the decussation of secondary neurons from the touch and proprioception pathway

A

The contralateral medial lemnisucus tract

39
Q

Where do 2nd order neurons of the touch and proprioception pathway terminate

i. for the body
ii. for the face

A

i. for body ….In the ventral posterior lateral nucleus of the thalamus (VPL).
Topographic representation here (where lower extremities are LATERAL (different to dorsal column)

http: //www.d.umn.edu/~jfitzake/Lectures/DMED/SensoryPhysiology/GeneralPrinciples/LateralInhibition.html
ii. for face…. in ventral posteromedial nucleus of the thalamus (VPM)…. this comes from ventral and dorsal trigeminothalamic tract

40
Q

Where do 3rd order neurons of the touch and proprioception pathway terminate

A

They come from the ventral posterior lateral nucleus (for body) or VPM (for face) of the thalamus and project to somatosensory cortex

41
Q

What is meant by the somatosensory homunculus

A

Size of somatotopic areas (in the somatosensory cortex) is proportional to density of sensory receptors in that body region

42
Q

T/f pain and temperature localisation (i.e. in a separate pathway to the touch and proprioception pathway) is more precisely localised than the somatosensory homunculus

A

F: Pain and temperature localisation not as precise

43
Q

How does sensory information int the pain, temperature and crude touch pathway get into the dorsal horn

A

Via Adelta (not Abeta). So A delta fibres pass from the periphery and into the superficial lamina of the dorsal horn

44
Q

Differentiate the fibres mediating crude touch and fine touch

A

Crude- Adelta… free nerve ending
Fine- Abeta… meissners corpuscles

Crude transmitted on contralateral ANTERIOR spinothalamic tract

Pain and temperature sensations ascend within the lateral spinothalamic tract

45
Q

Where do first order neurons terminate in the pain, temperature and crude touch pathway

A

They terminate in the dorsal horn.

46
Q

Where do the second order neurons decussate in the pain, temperature and crude touch pathway

A

They originate in the dorsal horn and decussate in the spinal cord

47
Q

What tract do the 2nd order neurons form following decussation

A

Spinothalamic tract

48
Q

Differentiate between the lateral and anterior spinothalamic tract

A

Pain and temperature sensations ascend within the lateral spinothalamic tract

Crude touch ascends within the anterior spinothalamic tract

ALL FROM CONTRALATERAL SIDE

49
Q

Where to second order neurons of the pain, temperature and crude touch pathway terminate

A

Ventral posterior lateral (VPL) nucleus of the thalamus.

There is a topographic representation of the body in the VPL (lower extremities are lateral)

50
Q

Contrast the site of termination of

i. first order neurons
ii. second order neurons

in the fine touch and proprioception vs pain, temperature and crude touch pathway

A

i. 1st order. FINE TOUCH- terminate in the cuneate/gracile nucleus of the medulla. CRUDE TOUCH/PAIN/TEMP- terminate in the dorsal horn of the spinal cord
ii. 2nd order FINE TOUCH: start in the above nuclei, termnate in the ventral posterior lateral nucleus. CRUDE TOUCH/PAIN/TEMP- begin in dorsal horn and synapse in the ventral posterior lateral nucleus too

51
Q

Outline use of quantitative sensory testing

A

You can test the different modalities using different instruments (eg hot or cold stimulus, vibration).

Different modalities are transmitted via different tracts, though

SO YOU CAN TEST THE INTEGRITY OF ASCENDING PATHWAYS

I.e if they don’t respond to heat stimulus, there may be problem with the lateral spinothalamic tract. If they don’t respond to fine touch, may be a problem with the dorsal column pathways

52
Q

To be clear, what it conveyed by dorsal column vs spinothalamic pathway

A

Dorsal column: fine touch, vibration, 2 point discrimination

Spinothalamic: pain, temperature and crude touch

53
Q

What could be the cause of Anterior spinal cord lesion

A

Blocked anterior spinal artery causes ischemic damage to the anterior part of the spinal cord

54
Q

Consequences of Anterior spinal cord lesion

A

Spinothalamic tract damage causing pain and temp. loss BELOW the level of the lesin

But retains light touch, vibration and 2 point discrimination as dorsal coumn tract unaffected

55
Q

Define pain

A

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

56
Q

Define nociceptive pain

A

ACUTE- Tissue damage i.e cut skin. Inflammatory mediators sensitise nerve endings

57
Q

Outline muscle pain

A

Lactic acidosis, ischaemia, stretching, fibromyalgia

58
Q

Outline Somatic pain

A

Well localised e.g. inflammation or infection

59
Q

Outline visceral pain

A

Poorly localised, deep e.g stomach, colon, IBS

60
Q

Outline referred pain

A

Pain from an interal organ/structure (e.g. angina)

61
Q

Outline neuropathic pain

A

Pain due to dysfunction of the NS

Up to slide 40 of the new ppt. 43:55 of panpto

62
Q

What phenomenon is responsible for chronic pain

A

Central sensitisation

63
Q

Explain central sensitisation

A

Initiated by NMDA receptor activation (remember they allow CALCIUM into the cell). NMDA receptors allow Ca2+ + mediated synaptic plasticity in dorsal horn neurons.

↓ thresholds of Ad fibres to peripheral stimuli at an adjacent site to the injury

expansion of receptive field (i.e. secondary hyperalgesia)

Persistent activation of NMDA –> chronic pain (e.g. arthritis)

Glutatmate is the neurotransmitter here

64
Q

Which two tracts carry information to the brain about pain

A

Spinothalamic tract and

Spinoreticular tract

65
Q

Outline the pathway and significance of the spinoreticular tract in the transmission of pain

A

fibres also decussate and ascend the
contralateral cord to reach the brainstem reticular formation, before
projecting to the thalamus and hypothalamus. There are many further
projections to the cortex.

This pathway is involved in the emotional
aspects of pain

Contrasts to lateral spinothalamic tract which is the sensory component

66
Q

What is meant by the ‘pain matrix’

A

fMRI shows areas lighting up when there is activity (bloodflow).

The pain matrix shows that it’s not just the primary somatosensory cortex which is active during pain.

The following areas of cortex are actvie: 
SI 
SII 
Insula cortex
Anterior cingulate cortex 
Prefrontal cortex 

And other structures also active include:
Amygdala
Cerebellum
Brainstem

67
Q

Two ways of pain inhibition

A
  1. Gate control theory

2. Descending inhibitory pathways

68
Q

Outline gate control theory

A

INHIBITION of primary afferent inputs before they are transmitted to the brain through ascending pathway

Activation of A-beta fibres can inhibit pain signals in the dorsal horn by activating inhibitory interneurons which block the signal transmitted by A-delta or C-fibres (which is why rubbing the area after hurting it can reduce pain)

69
Q

Outline descending inhibitory pathways

A
  1. PAG-RVM axis –> main neurotransmitter is 5-HT (seratonin)…. harmful (facilitates pain)
  2. LC in the pons –> Noradrenaline (protective)

5-HT is facilitative for pain, so noradrenaline is main NT for reducing pain

70
Q

How can the inhibition from the descending pathways be increased

A

Basically problem with where the descending pathways are from, our lecturer says PAG and pons, but other document says PAG and RVM.

But either way, ENDOGENOUS OPIODS can increase inhibition that come from descending pathways because

  • PAG and RVM contain high concentration of µ opioid receptors
  • Opioids bind to these receptors, enhancing descending inhibition

Endogenous opioids increase descending pathway inhibition, and opoiods can be given therapeutically too to increase this inhibiton

71
Q

When would endogenous analgesic system be activated

A

during bad injuries, such as a leg break

72
Q

Can descending control systems be targeted for pain relief

A

Opoiods work in the PAG and RVM

Antidepressents can also be used…. antidepressants include SSRI (selective seratonin reuptake inhibitors) and SNRI (selective noradrenaline reuptake inbitors)…. which do you think is more likely to work

73
Q

Why might SSRIs not be useful in pain relief

A

These drugs would increase the amount of seratonin in the spinal cord (inhibits uptake of it)….
this doesn’t work because seratonin is facilitative

74
Q

Why could SNRIs be useful in pain relief

A

Because damage to peripheral nerve could increase excitability, causing central sensitisation.

Giving an SNRI would increase NA, which would bind to A2 receptor which is inhibitory on signalling… so you reduce pain.

E.g duloxetine

75
Q

What is conditioned pain modulation

A

Measure levels of endogenous descending control…

in patients who had good descending control, there is better efficacy of duloxetine!

76
Q

Differentiate central and peripheral sensitisatin

A

Peripheral sensitisation: this image is referring to the inflammatory changes which occur at the nerve endings of C-fibres. Inflammatory mediators such as bradykinin, histamine etc. all bind to receptors and cause the properties of C-fibres to change (i.e. they have a lower activation threshold for painful stimuli which manifests as primary hyperalgesia).

Central sensitisation: this image refers to the changes which occur in the spinal cord during chronic pain. On-going activation of c-fibers causes a form of NMDA receptor mediated synaptic plasticity (similar to LTP in memory). This causes changes in the central processing of adjacent A-delta fibres, which results in the spread of sensitivity away from the injury site on the skin (i.e. secondary hyperalgesia).

77
Q

Outline neuromodulation

A

Non-invasive primary motor cortex stimulation (transcranial direct current stimulation, tDCS)

Activation of endogenous analgesic systems in the brain
PAG
Anterior cingulate cortex

Analgesic mechanisms unclear

78
Q

What is hyperalgesa and allodynia

A

Allodynia: pain due to a stimulus that does not normally provoke pain

Hyperalgesia: increased pain from a stimulus that normally provokes pain
Primary
Secondary

(due to central sensitisation)

79
Q

How are opioids analgesic

A
  1. Centrally acting, they bing to µ receptors on PAG, to increase inhibition from the descending pathways which modulate pain.
  2. Opioid binding reduces the release of excitatory neurotransmitter release (glutamate) at the dorsal horn
80
Q

Explain mechanisms of chronic pain

A
  1. Loss of descending inhibition (by either reduction of NA pathways, or increase in seratoninergic pathways)
  2. Central sensitisation to pain occurs, so there reduced electrical thresholds need to be reached in order to transmit pain