Sensory Pathways Flashcards
What is a sensory modality?
A type of stimulus (e.g hot, cold, touch).
Modalities have specialised receptors, transmit information through specific anatomical pathways to the brain.
What are the types of receptors and their modalities?
Enclosed nerve endings:
Mechanoreceptors - touch, vibration, pressure and proprioception (joint position, muscle length, muscle tension)
Free nerve endings:
2) Thermoreceptor - temperature
3) Nociceptor - nociception (pain)
What are the different classifications of sensory fibres?
Abeta - large fast conducting myelinated sensory fibres involved in transmitting innocuous mechanical stimulation.
Adelta - myelinated fast conducting sensory fibres but not as fast as Abetas because the have a smaller diameter. Involved in transducting pain and temperature. Nociceptors and thermoceptors
C - slow transducting, no myelination. Involved in the slower aching pain, (temperature and itch).
Together they build up a peripheral nerve
Describe the sensory nerve endings
Individual axons within sensory fibres have modified terminals depending on the modalities.
C fibres unmyelinated with free endings - for heat
Abeta myelinated with nerve endings encapsulated in
layers of connective tissue - mechanoreceptors
Define sensory receptors?
They are transducers - convert energy from the environment into neuronal action potentials
Define absolute threshold?
The level of stimulus that produces a positive response of detection 50% of the time. If the stimulus is strong enough it will generate a generator potential that will illicit a train of action potentials
What happens if you give a stronger stimulus? What happens if you increase the stimulus strength and duration?
A larger generator potential is produced which cause a train of AP with increased frequency and duration –> more neurotransmitter is released
Increased stimulus strength and duration = increased neurotransmitter release = greater intensity
Describe the thermoreceptors?
TRP ion channels - transient receptor potential (TRP) ion channels.
Free nerve endings with high thermal sensitivity.
There are 4 heat-activated channels (TRPV1-4) and 2 cold activated TRP channels (TRPM8, TRPA1)
What are the different kinds of mechanoreceptors?
Meissner’s corpuscle - fine discriminative touch, low frequency vibration
Merkell cells - light touch and superficial pressure
Pacinian corpuscle - detects deep pressure, high frequency vibration and tickling
Rufini endings - continuous pressure or touch and stretch
What are tonic receptors?
They detect continuous stimulus strength - don’t adapt or adapt very slowly.
They continue to transmit impulses to the brain as long as the stimulus is present which keeps the brain constantly informed of the status of the body.
Merkel cells - slowly adapt allowing for fine touch to be perceived. Stroking
What are phasic receptors?
Detect a change in stimulus strength - adapt quickly They transmit impulses at the start and at the end of the stimulus.
Pacinian receptor - sudden pressure excites receptor which transmits a signal again when pressure is released.
What are the receptive fields?
Region on the skin which causes activation of a single sensory neuron when activated. There are different sizes of receptive fields.
Small receptive fields allow for the detection of fine detail over a small area. Precise perception (arms). The fingers have many densely packed mechanoreceptors (with small receptive fields)
The back has large receptive fields that allow the cell to detect changes over a wider area (less precise perception)
See slides for diagrams of receptive fields
What is two point discrimination?
Minimum distance at which two points are perceived as separate - related to the size of the perceptive field.
See slide for diagram
Describe the dorsal root
See diagrams on slide
Cell bodies are in the dorsal root ganglia (body) and trigeminal ganglia (face). After the DRG the sensory fibres enter the dorsal horn.
Describe the dorsal horn
It is organised into Rexed Laminae (I-VII). See slides
Innocuous mechanical stimuli - Abeta fibres terminate in lamina III-VI (deep)
Pain and temperature stimuli - Adelta and C fibres terminate in lamina I-II (superficial)
There are two main types of dorsal horn neurones:
1) Those with axons that project to the brain (projection neurones)
2) Those with axons that remain in the spinal cord (interneurones - connect different laminae)
What is lateral inhibition?
Receptive fields can overlap making it difficult to distinguish between 2 stimulus locations. Lateral inhibition prevents the overlap of the receptive fields and facilitates pinpoint accuracy in localisation of the stimulus.
Mediated by inhibitory interneurones within the dorsal horn of the spinal cord.
The difference between adjacent inputs is enhanced by lateral inhibition
Facilitates enhanced sensory perception (discrimination)
Describe the gate control theory
Inhibition of primary afferent inputs (C fibres/Adelta fibres PAIN) before they are transmitted to the brain.
See diagram - Abeta fibre can stimulate a inhibitory interneurone that can inhibit the projection neurone going to the brain.
Label the central sensory structures of the brain
See diagram
SI - primary somatosensory cortex (in postcentral gryus)
SII - secondary somatosensory cortex (in parietal operculum)
Posterior parietal cortex = spatial awareness of body
What is the dorsal column system?
Transmits the innocuous mechanical stimuli (vibration, fine discriminative touch)
Abeta fibres enter via the dorsal horn and enter the ascending dorsal column pathway.
Information conveyed from the lower limbs and body (below T6) travel ipsilaterally along the gracile tract. Above T6: ipsilaterally along the cuneate tract. See diagram
Describe the 1st order neurones - DC
They teminate in the medulla:
Fibres in the gracile tract first synapse in the gracile nucleus.
Fibres in the cunate tract first synapse in the cunate nucleus.
See diagrams
Describe the 2nd order neurones - DC
They decussate (cross the midline) in the caudal medulla and form the contralateral medial lemniscus tract. Topographic representation
The axons of the 2nd order neurones terminate in the ventral posterior lateral nucleus of the thalamus. (lower extremities terminate more lateral - topographic representation of the body in the VPL)
See diagrams
Describe the 3rd order neurones - DC
3rd order neurones from the VPL project to the somatosensory cortex
The size of somatotopic areas is proportional to density of sensory receptors in that body region (somatosensory homunculus)
What is the spinothalamic (anterolateral) pathway? Pain, temperature and crude touch
There are two pathways in the spinothalamic pathway:
Pain and temperature sensations ascend within the lateral spinothalamic tract.
Crude touch ascends within the anterior spinothalamic tract.
Describe the 1st order neurones - ST
1st order neurones terminate on entering the dorsal horn. The 2nd order neurones decussate immediately in the spinal cord and form the spinothalamic tract.
See diagram
Describe the 2nd order neurones - ST
They terminate in ventral posterior lateral nucleus of the thalamus.
What are the key differences between the dorsal column and spinothalamic tract
Spinothalamic tract - pain, temperature, crude touch.
- Crosses in the spinal cord
Dorsal column pathway - light touch, vibration, 2 point discrimination.
- Crosses in the brain stem
Should be aware that pain is also linked to emotion not just sensory. Spinoreticular tract - terminates parabrachial area then limbic system
What is the pain matrix?
Functional MRI (fMRI) has shown there is a ‘cerebral signature for pain’
1) Cortex:
- SI
- SII
- Insula cortex
- Anterior cingulate cortex
- Prefrontal cortex
2) Amygdala
3) Cerebellum
4) Brainstem
How is quantitative sensory testing used to test the integrity of the ascending pathways?
You what kind of stimulation affects which tract - damage to tract means the stimulation will not be felt.
spinothalamic tract - temperature and pain
dorsal column system - discriminative touch –> 2 point discrimination
Using QST combined with questionnaires is an effect way of diagnosing people with neuropathic pain
How would you know if there was an anterior spinal cord lesion?
Blocked anterior spinal artery causes ischaemic damage to the anterior part of the spinal cord.
Spinothalamic tract becomes damaged –> bilateral loss of pain and temperature below the level of the lesion.
However the dorsal column system remains intact therefore retained light touch, vibration and 2 point discrimination
Describe nociceptors
Aδ fibers mediate sharp, intense or first pain
- Type 1: noxious mechanical (pain)
- Type 2: noxious heat
C-fibres mediate dull, aching or second pain
- Noxious thermal, mechanical and chemical stimuli (polymodal)
Define pain
An unpleasant sensory and emotional experience associate with actual or potential tissue damage, or described in terms of such damage
Define allodynia
Pain due to a stimulus that does not normally provoke pain
Define hyperalgesia
Increased pain from a stimulus that normally provokes pain
See graph
Primary and secondary hyperalgesia
Peripheral sensitisation vs central sensitisation
Peripheral sensitisation:
There are 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 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).
Describe spinal cord nociceptive processing
Adelta and C fibres synapse superficially in the dorsal horn. Rexed lamina I and II.
Nociception is initiated by NMDA receptor activation
Persistent activation of NMDA receptor can result in the development of chronic pain (e.g arthritis)
LOSS of inhibitory influences
Describe descending pain modulation?
Monoamines are released from the brain stem to inhibit spinal cord excitability. (inhibits pain)
1) PAG-RVM (rostral ventromedial medulla) axis - main NT involved serotonin (harmful pain)
2) LC (locus cereleus in the pons) - noradrenaline (protective - inhibits signalling from the dorsal horn)
Placebo can activate descending inhibition in humans
There is a balance between an adrenergic and serotonin effect. See Pharm opiods
How do endogenous opioids affect descending pain modulation?
The PAG and RVM contain high concentrations of u-opoid receptors. Endogenous opiods enhance the inhibition from the PAG-RVM axis.
Reduces pain transmission in the dorsal horn by inhibiting glutamate release
Forms part of the endogenous analgesic system
What drugs can target the descending control systems for pain relief?
Opioids - PAG and RVM. u-opioid receptors
Antidepressants - TCA, SSRI and SNRI (they would work because the inhibit the reuptake of monoamines.)
SSRI are not that effective while TCAs are much more effective. This shows that NA is much more important in the descending control of pain.
How does chronic pain affect the descending control system?
During chronic pain there are changes in descending control systems. Descending noradrenergic pathways are protective and loss of this control is associated with the development of chronic pain. Similarly, there is a shift towards descending facilitation in chronic pain patients.
Descending inhibition is lost in chronic pain patients.
Duloxetine enhances the action of noradrenaline in the spinal cord and conditioned pain modulation provides a means by which to predict who will respond best to the drug (i.e. those which had deficient descending inhibition).
