Somatosensory Function Flashcards

1
Q

Somatosensory modalities: list and define the major somatosensory modalities

A

Somatosensory function: ability to interpret bodily sensations (mechanical, thermal, proprioceptive, nociceptive)

Modality (type of information encoded):

  1. Touch - light touch, pressure, vibration –> mechanoreceptor
  2. Proprioception - joint position, muscle length and tension –> mechanoreceptor
  3. Temperature - thermoreceptor
  4. Pain - noniceptor

All the touch and proprioception information is detected by mechanoreceptors (it all comes from some sort of mechanical stimulus e.g. a deformation is transduced into a string of impulses passing along the axo)

The mechanoreceptors involved in touch and proprioception is NOT a separate entity but is actually the peripheral terminal of the peripheral axon of the primary sensory neurone

NOTE: sensory neurones have their cell bodies in the dorsal route ganglion and it has a centrally directed axon and a peripheral axon that goes into the periphery -­‐ the ends of these peripheral axons are the receptors

Types of Sensory Neurones

Sensory neurons tend to vary in size and conduction velocity

Each group of sensory neurones that carry a particular modality will have their own set of characteristics e.g. size and conduction velocity

  • Aβ-fibres: innocuous mechanical stimulation
  • Aδ-fibres: noxious mechanical and thermal stimulation
  • C-fibers: noxious mechanical, thermal and chemical stimulation
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2
Q

Define the terms: receptor, stimulus threshold, stimulus intensity, adaptation, receptive field, 2 point discrimination, and lateral inhibition

A

Receptor: ’sensory receptors are transducers that convert energy from the environment into neuronal action potentials’’

Stimulus threshold: ’A threshold is the point of intensity at which the person can just detect the presence of a stimulus 50% of the time (absolute threshold)’’

Stimulus intensity: how quickly a neuron fires
Increased stimulus strength and duration = increased neurotransmitter release = greater intensity

Adaptation:
A. Tonic receptors

  • Detect continuous stimulus strength
  • Continue to transmit impulses to the brain as long the stimulus is present
  • Keeps the brain constantly informed of the status of the body
  • e.g. Merkel cells

–Slowly adapt allowing for superficial pressure and fine touch to be perceived

Tonic receptors – do not adapt or adapt very slowly

B. Phasic receptors

  • Detect a change in stimulus strength
  • Transmit an impulse at the start and the end of the stimulus

–e.g. when a change is taking place

e.g. The pacinian receptor

–Sudden pressure excites receptor

–Transmits a signal again when pressure is released

Phasic receptors – adapt quickly

With mechanoreceptors, you have a mixture of slow and fast adapting receptors -­‐ this gives you more information

Receptive fields

‘’The receptive field is 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. Precise perception

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

The lips and tongue are very sensitive because they have high-density innervation with very small receptive fields

Another physiological property of these neurones is that they can code for the intensity of the stimulus

This is coded by the FREQUENCY of the action potentials going down these sensory fibres

The intensity is nothing to do with the amplitude, only the frequency

This means that you can localise touch much better in these areas

2 point discrimination​

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

Somatosensory dermatomes:
C5 -clavicle
C6 - thumb, index finger
T4- the level of nipples
T10- umbilicus

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3
Q

Distinguish between different types of thermoreceptors

A

Thermoreceptors:

  • Aδ- (cold) and C-fibres (heat)
  • Free nerve endings
  • Transient receptor potential (TRP) ion channels (stimuli depends on type of ion channel)
  • 4 heat activated channels:

–TRPV1-4 (capsaicin - used as a topical analgesic because it doesn’t allow other painful stimuli to occur)

•2 cold activated

–TRPM8

–TRPA1 (activated as wasabi - 15 degrees painfull cold)

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4
Q

§Distinguish between different types of mechanoreceptors

A

5 different types (+ hair follicle receptor)

Meissner’s corpuscle - fine discriminative touch, low-frequency vibration

Merkel cells - light touch and superficial pressure

Pacinian corpuscle - Detects deep pressure, high-frequency vibration, and tickling

you have an axonal ending in the middle and it is wrapped around several concentric circles of epithelial cells -­‐ this allows the receptor to be very sensitive to vibration

Ruffini endings: Continuous pressure or touch and stretch

Mechanoreceptors for touch are usually very sensitive -­‐ they have a low threshold of activation

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5
Q

Classification of somatosensory receptors

A
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6
Q

Explain the process of lateral inhibition

A

Cell bodies: body and face

•Cell bodies are in the dorsal root ganglia (body) and trigeminal ganglia (face)

Sensory information - cervical level - cuneate tract - cross over at medulla - medial lemniscus tract - thalamus - tertiary neurons primary somatosensory cortex

Somatosensory from the face - pons - second-order nucleus to trigeminal neurons - the hypothalamus - cortex

Dorsal horn neurons can be divided into two main types:

  • Those with axons that project to the brain (projection neurons)
  • Those with axons that remain in the spinal cord (interneurons)

Lateral inhibition

  • 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 inhibitory interneurons within dorsal horn of spinal cord
  • Facilitates enhanced sensory perception (discrimination)

Lateral Inhibition in Dorsal Column Nuclei

This is a method of improving the resolution of localising the stimulus

In this pathway, lateral inhibition takes place in the gracile and cuneate nuclei

Each axon, as it comes into the nucleus, doesn’t just activate the

next cell in the chain but it ALSO has lateral branches that are INHIBITORY to the neighbouring axons

So each axon, as it comes into the nucleus, excited the next neurone in the chain AND inhibits its

neighbours

This competition between neurones sharpens the resolution

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7
Q

Sensory pathways: explain the ascending pathways transmitting sensory information and somatotopic organisation within the pathway

A
  • Innocuous mechanical stimuli
  • Fine discriminative touch
  • Vibration
  • Aβ fibers 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

Information from the Leg:

  1. Comes in from the leg via the primary sensory neurone
  2. As the axon goes into the dorsal horn it passes straight into the white matter at the back of the spinal cord -­‐ DORSAL COLUMNS
    The fibres coming from the lowest parts of the body will be most MEDIAL in the dorsal columns

As you go higher up the spinal cord, the sensory neurones coming in will project axons that are positioned more LATERALLY in the dorsal columns

  • *LOWER = MEDIAL**
  • *HIGHER = LATERAL**

This arrangement of axons in the dorsal columns are considered as being TWO tracts:

Cuneate Fasciculus -­‐ waist UP
Gracile Fasciculus -­‐ waist DOWN
NOTE: Fasciculus = bundle of axons
3. The information goes up these fasciculi until they get to the MEDULLA
4. In the medulla, the neurones synapse with two nuclei (cuneate and gracile nuclei) which then send axons across the midline (at the decussation)
5. After crossing the midline, the fibres turn upwards and form a new pathway called the MEDIAL LEMNISCUS
6. The medial lemniscus maintains the same position until it reaches the thalamus
7. In the thalamus the axons relay with the third neurone in the chain -­‐ it is one of the thalamic nuclei: VENTRAL-­‐POSTERO-­‐LATERAL NUCLEUS
8. Through this, the information is passed via this third neurone to the primary somatosensory cortex

Information coming from the FACE

  1. The main sensory nerve of the face is the TRIGEMINAL (CN V)
  2. The trigeminal nerve comes into the middle of the pons and it synapses with a second order neuron in the trigeminal cranial nucleus
  3. Then the axon of this second cell crosses the midline and joins the medial end of the medial lemniscus
  4. Because these fibres are more medial within the medial lemniscus, they relay through the ventral-­‐posteromedial nucleus
  5. The axon of the third neurone then relays this information to the face region of the primary somatosensory cortex

Summary of the Central Pathway

  • 1st order neurons terminate in the medulla
  • 2nd order neurons terminate in the thalamus
  • 3rd order neurons terminate in the somatosensory cortex

Decussation in the brainstem

There is a somatotopic arrangement of the pathway right from the start (i.e. lower is more medial) -­‐ this is the basis of localisation, the brain knows where the input is coming from

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8
Q

Ascending pathways 2: pain, temperature and crude touch

A

The spinothalamic (anterolateral) pathway

Pain and temperature sensations ascend within the lateral spinothalamic tract

Crude touch ascends within the anterior spinothalamic tract

1st order neurons terminate in the dorsal horn

The axon of the primary sensory neurone coming from the lower part of the body will carry the information into the dorsal horn and it will synapse immediately with the second order neurone

The second order neurone then crosses the midline goes into the white matter and ascends up the spinothalamic tract

This arrangement occurs all the way up the spinal cord with fibers being added to the spinothalamic tract as you ascend

•2nd order neurons terminate in the ventral posterior lateral (VPL) nucleus of the thalamus

The information from the LOWEST parts = LATERAL and HIGHER parts = MEDIAL

The spinothalamic tract follows the same line all the way to the brainstem

In the thalamus, it relays through the ventral posterolateral nucleus and the third neurone goes up to the primary somatosensory cortex

So, for pain and temperature information coming from the body, decussation occurs at the SAME LEVEL as the information coming into the spinal cord

Nociceptive Information from the FACE

  • It comes via the trigeminal nerve (CN V)
  • It goes into the trigeminal ganglion at the level of the pons
  • Then something strange happens:
  • The axon goes DOWNWARDS in the brainstem alongside the trigeminal nucleus
  • It eventually synapses with a secondary neurone in the trigeminal nucleus at the level of the MEDULLA (not the pons where it entered the brainstem)
  • This occurs because the trigeminal nucleus is actually a large column of grey matter that extends from the midbrain to the medulla
  • The trigeminal nucleus is divided into areas and each area serves a different modality
  • The area of the trigeminal nucleus that deals with touch is in the pons (so touch neurones from the face synapse at the level of the pons)
  • The area of the trigeminal involved in nociception is found at the level of
  • So the pain/temperature axons come into the pons and they have to travel down alongside the trigeminal nucleus before it finds the correct neurone to synapse with
  • The axon of the second neurone then crosses the midline and joins the medial end of the spinothalamic tract
  • It then synapses with the ventral posteromedial nucleus in the thalamus and then it is relayed on to the primary somatosensory cortex
  • NOTE: the lower part of the trigeminal nucleus, which deals with nociception, is in the medulla but for some reason it is called the spinal trigeminal nucleus
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9
Q

Pain receptors

A

General notes:

What is pain? ‘’An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.’’

A nociceptive stimulus is one that is potentially harmful or unpleasant

NOTE: a stimulus is something that you can measure objectively, but a sensation like pain isn’t real, you can’t measure it

Pain has been conjured by the brain based on the nociceptive information that has been presented to it

Pain has emotional coding to it

Nociception and pain tend to be used interchangeably but there is a distinction to it

Pain Receptors

Pain has special receptors -­‐ NOCICEPTORS

IMPORTANT NOTE: even if you stimulate the mechanoreceptors with a very high intensity, you will NEVER FEEL PAIN

You will only feel pain if there happen to be nociceptors in the same part of the body

IT IS ONLY NOCICEPTORS THAT CAN PRODUCE THE SENSATION OF PAIN

  1. Polymodal -­‐ there are different types of nociceptor that respond to different types of stimuli
  2. Free Nerve Endings -­‐ in terms of structure they are much simpler than mechanoreceptors, usually just free axonal endings of sensory neurones
  3. High Threshold -­‐ higher activation threshold than touch receptors
  4. Slow Adapting -­‐ this is good because if there is a potentially harmful stimulus then you want to be constantly reminded of it so you do something about it

Sensory Neurones

There are TWO types of sensory neurone that carry nociceptive information:

  • Aδ fibers mediate sharp, intense or first pain

–Type 1: noxious mechanical

–Type 2: noxious heat

  • Fast adapting
  • Produces pain fast -­‐ alerts you to the potential of some harmful scenario
  • FAST CONDUCTING -­‐ but still no where near as fast as touch neurones

C neurone

  • Produces a dull, aching pain
  • The role of C neurone mediated nociception is to remind you of the injury so that you guard this part of the body
  • SLOW conducting -­‐ unmyelinated
  • C-fibres mediate dull, aching or second pain
  • –Noxious thermal, mechanical and chemical stimuli (polymodal)

Receptive Fields

Receptive fields of nociception neurones tend to be much LARGER than the ones for touch

The nociceptive pathway is phylogenitally much older than the touch pathway

The receptive fields are large because you don’t need to be able to localise the pain minutely as you can do with touch

The method of coding intensity is the same as with touch neurones -­‐ the higher the intensity the greater the frequency of impulses

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10
Q

Anterior spinal cord 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
  • Retained light touch, vibration and 2-point discrimination due to intact dorsal columns

Bilateral pain and temperature loss

Normal light touch, vibration and 2-point discrimination sensations

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11
Q

Sensory and emotional pain pathways

A

Affective Pain Pathway

As well as the straight-­‐forward ascending pathway going to the primary somatosensory cortex, there must be other pathways going to other parts of the brain

As the spinothalamic tract projects towards the primary somatosensory cortex, it gives off collateral branches (all the axons do this) to various other structures

The main structures that the spinothalamic tract projects to are:

Brainstem o Thalamus

o Hypothalamus

Limbic structures

The input to the brainstem is mainly to the reticular formation

The input to the thalamus is mainly to the intralaminar nuclei

These two areas are part of the reticular activating system -­‐ this is the system that maintains your consciousness

The purpose of these collateral inputs from the spinothalamic tract is to increase your level of arousal and to make sure that you are aware of any potentially harmful situations

The information passing through the hypothalamus and limbic structures result in signalling of the unpleasantness of the stimulus

Until all these structures have analysed the input, the nociceptive input is not a mood-­‐changing thing -­‐ it isn’t emotional at all

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12
Q

Explain how nociceptive input can be gated by peripheral and central mechanisms

A

There are a couple of pathways that can reduce the amount of pain that you feel:

  1. Central Inhibition Pathway
  2. Peripheral Inhibition Pathway

Both these pathways affect the system in the dorsal horn

  • The focus of the central inhibition pathway is the periaqueductal grey matter (the grey matter surrounding the cerebral aqueduct)
  • Cells in this area have an enormous input from other parts of the brain
  • If brain activity gets to a certain level, these cells send impulses down various pathways through the brainstem and it eventually gets to the dorsal horn at each level
  • These descending axons synapse with an interneurone and activate it
  • These interneurones affect the synapse between the first and second-­‐order neurones
  • The interneurones release ENKEPHALIN which is INHIBITORY

This means that the intensity of the activity feeding into the spinothalamic tract is reduced -­‐ if the interneurone activity is high enough, it could prevent the synapse from working all together

So the higher the level of activity going on in the brain, the more likely you are to have activity in the central inhibition pathway and hence the more likely you are to reduce the amount of information going down the spinothalamic tract hence the less pain you feel

We have this because although it is good to be aware of harmful things, there are situations where it is beneficial to focus on other things aside from the pain e.g. soldier who has been wounded on the battlefield

NOTE: enkephalin is an opioid -­‐ so when we give patients morphine we are essentially mimicking this inhibition system

Peripheral Inhibition

This also works at the level of the dorsal horn

  • RED fibre is the C-­‐fibre that is carrying nociceptive information
  • This C-­‐fibre enters the dorsal horn and activates a projection neurone -­‐ the projection neurone axon then goes across the midline and joins the spinothalamic tract

YOU ALSO GET INPUT FROM NON-­‐NOCICEPTIVE NEURONES ()

  • Axons of these non-­‐nociceptive neurones will go straight to the dorsal columns but they do have a collateral branch that is capable of activating an inhibitory interneurone which can reduce the activation of the projection neurone and hence reduce the activity going up the spinothalamic tract
  • This is why if you have something that hurts like an insect bite, rubbing the area will make it hurt less
  • By rubbing the area you are increasing the activity going down the non-­‐ nociceptive fibre and hence you get increased activation of the interneurone and increased inhibition of the projection neurone
  • This can be used as low level stimulation for something like back pain or even childbirth
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13
Q

Somatosensory pathology: summarise the mechanisms of somatosensory disruption

A

Nociceptive Dysfunction

If there is pathway disruption then the nociceptive information can’t get up to the brain and so you don’t feel pain

This leads to trouble because if you can’t feel pain then you don’t know which part of the body is damaged

Examples of Loss of Pain:

Charcot Joints -­‐ peripheral neuropathy that affects the input coming from inside the joints. If these inputs are damaged then you have nothing to tell you that you’re using your joints inappropriately -­‐ this leads to joint deformities

You can also get exacerbation of pain

One of the ways this can happen is wind up in the dorsal horn

If someone has had chronic pain (e.g. cancer), certain peripheral nerves coming into the spinal cord will have been carrying high levels of input for a long time

The cells in the dorsal horn can then change and lower their sensitivity or their synapses can change, which means that the information going into the spinothalamic tract is increased so this can actually increase the level of chronic pain

Chronic pain is very difficult to treat in some situations

You can get neuropathic pain where the nervous system itself is somehow damaged so it works abnormally

You can also get psychogenic chronic pain where there is no demonstrable physical cause -­‐ this is probably because areas within the brain that normally analyse nociceptive input are abnormal

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