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Neurology > Sensory pathways > Flashcards

Sensory pathways Flashcards

1
Q

What is a modality?

A

A type of stimulus (e.g. hot, cold, touch, etc.)
Modalities have specialised receptors, which will transmit information through specific anatomical pathways to the brain.

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2
Q

What are the three main categories of sensory fibres?

A

A-beta (mechanoreceptors of skin, very fast transducting, large, myelinated, transmit innocuous mechanical stimulation such as brush).
A-delta (pain, temperature, fast transducting, myelinated).
C-fibres (temperature, dull pain/aches, itch, slow, unmyelinated).

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3
Q

What type of information do mechanoreceptors transmit to the brain?

A

Touch
Pressure
Vibration
Proprioception (joint position, muscle length, muscle tension)

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4
Q

What type of information do thermoreceptors transmit to the brain?

A

Temperature

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5
Q

What type of information do nociceptors transmit to the brain?

A

Nociception (pain)

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6
Q

Give examples of modified sensory nerve endings specific for different modalities.

A 
Free nerve endings of C-fibres (thermoreceptors and nociceptors).
Encapsulated nerve endings (mechanoreceptors).
Hair cells (auditory).
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7
Q

What are sensory receptors?

A

Transducers that convert energy from the environment into neuronal action potentials.

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8
Q

What is the absolute threshold of a sensory receptor?

A

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

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9
Q

What causes the intensity of a stimulus to be greater?

A

Increased stimulus strength and duration leading to increased neurotransmitter release.

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10
Q

What are TRP channels?

A

Free nerve endings with high thermal sensitivity.
Change in temperature activates a family of transient receptor potential (TRP) ion channels.
Thermoreceptors.

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11
Q

List TRP channels.

A

4 heat activated TRP channels: TRPV1-4.

2 cold activated TRP channels: TRPM8 and TRPA1.

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12
Q

What are the different types of mechanoreceptors?

A

Meissner’s corpuscle- fine discriminative touch.
Merkel cells- light touch and superficial pressure.
Pacinian corpuscle- detects deep pressure, vibration and tickling.
Ruffini endings- continuous pressure or touch and stretch.

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13
Q

Describe the adaptation of tonic receptors.

A

Detect continuous stimulus strength.
Continue to transmit impulses to the brain as long as the stimulus is present.
Keeps the brain constantly informed of the status of the body.
Do not adapt or adapt very slowly.
e.g. Merkel cells- slowly adapt allowing for fine touch to be perceived.

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14
Q

Describe the adaptation of phasic receptors.

A

Detect a change in stimulus strength.
Adapt quickly.
Transmit an impulse at the start and the end of the stimulus, e.g. when a change is taking place.
a.k.a. ‘movement receptors’ or ‘rate receptors’.
e.g. Pacinian receptor- sudden pressure excites receptor, transmits a signal again when pressure is released.

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15
Q

What are somatosensory dermatomes?

A

Each spinal nerve has a specific dermatome on the skin.

Each spinal nerve innervates a certain level in the spinal cord (cervical, thoracic, lumbar, sacral).

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16
Q

What is a receptive field?

A

The region on the skin which causes activation of a single sensory neuron when activated.
Small receptive fields allow for the detection of fine detail over a small area.
Large receptive fields allow the cells to detect changes over a wider area (less precise perception).

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17
Q

Describe the distribution of receptive fields on the fingers.

A

Many densely packed mechanoreceptors with small receptive fields.

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18
Q

What is 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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19
Q

What are the different types of nociceptors?

A

A-delta fibres mediate sharp, intense or first pain. They are myelinated and there are 2 types:

  • type 1: A-delta mechanoheat receptors (noxious mechanical and thermal stimuli).
  • type 2: A-delta mechanoreceptors (noxious mechanical stimuli).

C-fibres mediate dull, persistent or second pain. They are unmyelinated and polymodal (respond to thermal, mechanical and chemical stimuli).

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20
Q

Where are the sensory cell bodies located?

A

In the dorsal root ganglia (body) and trigeminal ganglia (face).

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21
Q

Where is the dorsal horn located?

A

Spinal cord.

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22
Q

What is the dorsal horn organised into?

A

Rexed laminae (I-VII).

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23
Q

Which sensory fibres terminate in laminae III-VI of the dorsal horn (deep)?

A

Innocuous mechanical stimuli- A-beta fibres (and A-alpha).

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24
Q

Which sensory fibres terminate in laminae I-II of the dorsal horn (superficial)?

A

Pain and temperature- A-delta and C-fibres.

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25
Q

What is the main excitatory neurotransmitter released from the presynaptic neurones in the dorsal horn?

A

Glutamate.

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26
Q

What is the role of interneurons in the dorsal horn?

A

Connect between different laminae and between adjacent peripheral inputs to modulate pain and transmit mechanical stimulation throughout the dorsal horn.
Lateral inhibition.

27
Q

What is lateral inhibition?

A

A receptive field can overlap with another receptive field.
Difficult to distinguish between 2 stimulus locations.
Lateral inhibition prevents the overlap of receptive fields.
Facilitates pinpoint accuracy in localisation of the stimulus.
Mediated by interneurons within dorsal horn of spinal cord.
Facilitates enhanced sensory perception.
The difference between adjacent inputs is enhanced by lateral inhibition.

28
Q

What are the central sensory structures of the brain and where are they located?

A

SI: primary somatosensory cortex- in postcentral gyrus.
SII: secondary somatosensory cortex- in parietal operculum.
Posterior parietal cortex: spatial awareness of the body.

29
Q

What are the ascending pathways?

A

Dorsal column system- touch and proprioception.

Spinothalamic (anterolateral) pathway- pain, temperature and crude touch.

30
Q

What sensory modalities does the dorsal column system transmit?

A

Innocuous mechanical stimuli such as fine discriminative touch and vibration, proprioception.

31
Q

Describe the pathways in the dorsal column system.

A

A-beta fibres enter via the dorsal horn and enter the ascending dorsal column pathways.
Information conveyed from lower limbs and body (below T6) travel ipsilaterally along the gracile tract.
Information conveyed from upper limbs and body (above T6) travel ipsilaterally along the cuneate tract.

32
Q

Where do first order neurones of the dorsal column system terminate?

A

In the medulla.

33
Q

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

A

In the gracile nucleus.

34
Q

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

A

In the cuneate nucleus.

35
Q

Where do the second order neurones of the dorsal column system decussate?

A

In the caudal medulla.

Form the contralateral medial lemniscus tract.

36
Q

Where do axons of the second order neurones in the dorsal column system terminate?

A

In the thalamus- in the ventral posterior lateral nucleus.

37
Q

Where do third order neurons in the dorsal column system terminate?

A

In the somatosensory cortex- from the VPL, project to somatosensory cortex.
Size of somatotopic area is proportional to density of sensory receptors in that body region (somatosensory homunculus).

38
Q

What are the 2 pathways within the spinothalamic tract?

A

Pain and temperature sensations ascend within the lateral spinothalamic tract.
Crude touch ascends within the anterior spinothalamic tract.

39
Q

Where do first order neurones of the spinothalamic tract terminate?

A

Dorsal horn.

Primary afferent axons terminate upon entering the spinal cord.

40
Q

Where do second order neurones in the spinothalamic tract decussate?

A

Immediately in the spinal cord (dorsal horn) to form the spinothalamic tract.

41
Q

Where do the second order neurones of the spinothalamic tract terminate?

A

In the ventral posterior lateral nucleus of the thalamus.

42
Q

What are the key differences between the dorsal columns and the spinothalamic tract?

A

Spinothalamic tract transmits information about pain, temperature and crude touch, with second order neurone decussation in the spinal cord.
Dorsal columns transmit information about light touch, vibration and proprioception, two-point discrimination, with second order neurone decussation in the brainstem (medulla).

43
Q

What is the gate control theory of pain (1965)?

A

A gate control system modulates sensory input from the skin before it evokes pain perception and response.
Pain response in dorsal horn can be modulated by activating A-beta fibre- innocuous mechanical stimulation, e.g. brush.
1: Myelinated A-beta fibres are activated.
2: These signals flood the pathway and stimulate the substantia galatinosa in the dorsal horn of the spinal cord.
3: The gate swings closed.
4: The C (small, nociceptive) fibre signals are stopped at the gate and the pain signals are not transmitted to the thalamus.
5: Analgesia is achieved.

44
Q

What is an anterior spinal cord lesion?

A

Blocked anterior spinal artery causes ischaemic damage to the anterior part of the spinal cord.
Spinothalamic tract damage causes pain and temperature loss below the level of the lesion.
Retained light touch and vibration sensation due to intact dorsal columns.

45
Q

What is pain?

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
Sensory and emotional component to pain.

46
Q

What are the different types of pain?

A

Nociceptive- tissue damage, typically acute (e.g. skin cut- inflammatory mediators are released, sensitising nerve endings).
Muscle- lactic acidosis, ischaemia (e.g. stretching, fibromyalgia).
Somatic- well-localised (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.

47
Q

What is neuropathic pain?

A

Pain caused by a lesion or disease of the somatosensory nervous system.
Pain in area of neurological dysfunction.
Sharp, burning, electric shocks.
Poor response to usual analgesic drugs (e.g. opiates).

48
Q

Give 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)
49
Q

What is allodynia?

A

Pain due to a stimulus that does not normally provoke pain.

50
Q

What is hyperalgesia?

A

Increased pain from a stimulus that normally provokes pain.

51
Q

What is sensitisation?

A

Increased responsiveness of nociceptive neurones to their normal input.

52
Q

What is hypoalgesia?

A

Diminished pain in response to a normally painful stimulus.

53
Q

What is paraesthesia?

A

Abnormal sensation, whether spontaneous or evoked.

54
Q

What is synaptic plasticity?

A

Initiated by NMDA receptor activation.
Ca2+ mediated synaptic plasticity in dorsal horn neurons.
Increased synaptic strength (efficacy).
Reduced inhibitory influences on dorsal horn neurons.
Persistent activation of NMDA receptor can result in central sensitisation and the development of chronic pain (e.g. arthritis).

55
Q

What is descending pain modulation?

A

As well as ascending pathways to the brain there are also descending pathways to the spinal cord.
These are predominantly monoaminergic and have a powerful influence on nociceptive processing in the dorsal horn by either increasing or decreasing neurotransmitter release at this important first synapse in the pain pathway, onto projection neurons.

56
Q

What are the main neurotransmitters involved in descending pain modulation?

A

Serotonin originating from serotonergic nuclei in the medulla.
Noradrenergic neurons originating in the pons.

57
Q

How is the PAG-RVM axis involved in descending pain modulation?

A

One of the descending control pathways originates in the PAG-RVM axis.
The RVM contains serotonergic neurons which project to the dorsal horn releasing serotonin.
This can either inhibit or facilitate pain depending on which receptors are activated.
The 5-HT1a receptors is predominantly inhibitory and the 5-HT3 receptor is predominantly facilitatory on neurotransmitter release.

58
Q

How is the locus cereleus involved in descending pain modulation?

A

The locus cereleus is located in the pons and is the main noradrenergic nuclei involved with descending control of nociception in the dorsal horn.
It is predominantly inhibitory and can be thought of as pain’s braking mechanism, dampening down the response by binding to pre-synaptic alpha 2 receptors on primary afferents and projection neurons, ultimately reducing excitability.

59
Q

How do endogenous opioids increase descending pain inhibition of pain?

A

The PAG and RVM contain high concentration of µ opioid receptors, encephalin and dynorphin.
Endogenous opioids enhance descending inhibition from the PAG-RVM axis.
Reduce pain transmission in the dorsal horn by inhibiting glutamate release, i.e. activation of spinothalamic neurons.
Forms part of an endogenous analgesic system.

60
Q

How does placebo activate descending inhibition of pain?

A

Placebo-induced endogenous analgesia.
Placebo analgesic activates key brainstem sites involved in descending control, reduced following administration of the µ opioid antagonist naloxone.
Spinal cord is involved in endogenous analgesia, which suggests a descending control mechanism of some sort.

61
Q

Why are TCAs or dual noradrenaline and serotonin inhibitors preferentially used over SSRIs in treatment of neuropathic pain?

A

SSRIs such as fluoxetine and citalopram have a low analgesic efficacy.
The noradrenergic component of descending control systems is more important in the inhibition of pain.

62
Q

How do SNRIs enhance descending noradrenergic inhibition of pain?

A

Damage to primary afferent neuron increases excitability of neuron- central sensitisation.
SNRIs like duloxetine, milnanicpran, venlafaxine- bind to pre- or postsynaptic terminal in dorsal horn.
Noradrenaline increased within synaptic cleft and binds to alpha-2 receptor.
Alpha-2 receptor is inhibitory to signalling within neuron.
Increased noradrenaline inhibits activity in neuron- reduces pain.

63
Q

How may tDCs be used in pain modulation?

A

Transcranial direct current stimulation.
Non-invasive brain stimulation.
Changes in cortical excitability in M1 have been shown to reduce chronic pain in fibromyalgia and migraine patients.

Neurology (17 decks)

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