Neuro 7: Sensory pathways Flashcards
What is a sensory modality
Type of stimulus (hot cold etc)
How does information about such modalities get to brain
Modalities have specialised receptors which transmit inforatmion through specific anatomical pathways
Outline the receptors detecting following modalities:
- Touch Pressure Vibration and Proprioception (joint position, muscle length, muscle tension)
- Temperature
- Nociception
- Mechanoreceptor
- Thermoreceptor
- Nociceptor
Classify sensory fibres
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
T/f peripheral nerves contain one type of sensory fiber
FALSE: different fiber types containing information about different modalities present in peripheral nerve
Differentiate the nerve endings for the receptors of different modalities
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
Define sensory receptor
Sensory receptors are transducers that convert energy from the environment into neuronal action potentials
Define absolute threshold
The absolute threshold is the level of stimulus (stimulus strength) that produces a positive response of detection 50% of the time
Put in correct sequence
Neurotransmitter release
Generator potential
action potential
Generator potential
action potential
Neurotransmitter release
What is the consequence of a longer and stronger stimulus
Larger Generator potential,
larger action potential (and threshold potential reached for longer), increased Neurotransmitter release and greater intensity of feel
What type of channels do thermoreceptors have
On which fibres are thermoceptors present
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
4 different types of mechanoreceptors and what they fire based on
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)
Differentiate tonic and phasic receptors
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!
Given an exampe of a tonic and phasic receptor
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
Which regions of spinal cord innervate skin
Cervical (not C1)
Thoracic
Lumbar
Sacral
Differentiate dermatome and receptive field
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
T/F A large receptive field allows cells to detect changes over smaller areas.
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)
Name a site of small receptive fields
The fingers have many densely packed mechanoreceptors with small receptive fields
Define two point discrimination
Minimum distance at which two points are perceived as separate
Related to the size of the receptive field
What do the dermatomes look like on the leg
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
Site of large receptive fields
Back
What types of fibers do nociceptors have
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)
Where are the cell bodies of sensory afferent neurons located
dorsal root ganglia (body) and trigeminal ganglia (face)
How is the dorsal horn of the spinal cord organised
Rexed Laminae (I-VII)
Where do innocuous mechanical stimuli fibers terminate within the dorsal horn?
Aβ-fibers (&Aα) terminate in lamina III-VI (deep)
Where do noxious mechanical stimuli fibers terminate within the dorsal horn?
Pain and temperature – Aδ and C-fibers terminate in lamina I-II (superficial)
What is the main neurotransmitter in the dorsal horn that the fibers release
Glutamate main excitatory neurotransmitter
Function of interneurons within dorsal horn
Interneurons connect between different laminae and between adjacent peripheral inputs (lateral inhibition)
What is lateral inhibition
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
What are the three important brain areas for somatosensory perception
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)
Differentiate noxious and innoxuous
Harmful and non harmful
What info does dorsal column pathway transmit
Fine discriminative touch
Vibration
How does sensory information get to the dorsal column
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)
What information is conveyed along the cuneate tract of the dorsal column
fine touch and vibration ipsilaterally from upper limbs and body (above T6) travel
anything below travels in the GRACILE TRACT
How is the body represented in the dorsal column nuclei in the brainstem (ie. cuneate nucleus and gracilis nucleus)
There is a topographic representation of the body in the brainstem dorsal column nuclei
Where to gracilis and cuneate tracts synpase
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.)
Where do second order neurons of the touch and proprioception pathway decussate
2nd order neurons arise from the gracile/cuneate nuclei and then decussate in the cuadal medulla
Which tract is formed from the decussation of secondary neurons from the touch and proprioception pathway
The contralateral medial lemnisucus tract
Where do 2nd order neurons of the touch and proprioception pathway terminate
i. for the body
ii. for the face
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
Where do 3rd order neurons of the touch and proprioception pathway terminate
They come from the ventral posterior lateral nucleus (for body) or VPM (for face) of the thalamus and project to somatosensory cortex
What is meant by the somatosensory homunculus
Size of somatotopic areas (in the somatosensory cortex) is proportional to density of sensory receptors in that body region
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
F: Pain and temperature localisation not as precise
How does sensory information int the pain, temperature and crude touch pathway get into the dorsal horn
Via Adelta (not Abeta). So A delta fibres pass from the periphery and into the superficial lamina of the dorsal horn
Differentiate the fibres mediating crude touch and fine touch
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
Where do first order neurons terminate in the pain, temperature and crude touch pathway
They terminate in the dorsal horn.
Where do the second order neurons decussate in the pain, temperature and crude touch pathway
They originate in the dorsal horn and decussate in the spinal cord
What tract do the 2nd order neurons form following decussation
Spinothalamic tract
Differentiate between the lateral and anterior spinothalamic tract
Pain and temperature sensations ascend within the lateral spinothalamic tract
Crude touch ascends within the anterior spinothalamic tract
ALL FROM CONTRALATERAL SIDE
Where to second order neurons of the pain, temperature and crude touch pathway terminate
Ventral posterior lateral (VPL) nucleus of the thalamus.
There is a topographic representation of the body in the VPL (lower extremities are lateral)
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
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
Outline use of quantitative sensory testing
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
To be clear, what it conveyed by dorsal column vs spinothalamic pathway
Dorsal column: fine touch, vibration, 2 point discrimination
Spinothalamic: pain, temperature and crude touch
What could be the cause of Anterior spinal cord lesion
Blocked anterior spinal artery causes ischemic damage to the anterior part of the spinal cord
Consequences of Anterior spinal cord lesion
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
Define pain
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage
Define nociceptive pain
ACUTE- Tissue damage i.e cut skin. Inflammatory mediators sensitise nerve endings
Outline muscle pain
Lactic acidosis, ischaemia, stretching, fibromyalgia
Outline Somatic pain
Well localised e.g. inflammation or infection
Outline visceral pain
Poorly localised, deep e.g stomach, colon, IBS
Outline referred pain
Pain from an interal organ/structure (e.g. angina)
Outline neuropathic pain
Pain due to dysfunction of the NS
Up to slide 40 of the new ppt. 43:55 of panpto
What phenomenon is responsible for chronic pain
Central sensitisation
Explain central sensitisation
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
Which two tracts carry information to the brain about pain
Spinothalamic tract and
Spinoreticular tract
Outline the pathway and significance of the spinoreticular tract in the transmission of pain
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
What is meant by the ‘pain matrix’
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
Two ways of pain inhibition
- Gate control theory
2. Descending inhibitory pathways
Outline gate control theory
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)
Outline descending inhibitory pathways
- PAG-RVM axis –> main neurotransmitter is 5-HT (seratonin)…. harmful (facilitates pain)
- LC in the pons –> Noradrenaline (protective)
5-HT is facilitative for pain, so noradrenaline is main NT for reducing pain
How can the inhibition from the descending pathways be increased
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
When would endogenous analgesic system be activated
during bad injuries, such as a leg break
Can descending control systems be targeted for pain relief
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
Why might SSRIs not be useful in pain relief
These drugs would increase the amount of seratonin in the spinal cord (inhibits uptake of it)….
this doesn’t work because seratonin is facilitative
Why could SNRIs be useful in pain relief
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
What is conditioned pain modulation
Measure levels of endogenous descending control…
in patients who had good descending control, there is better efficacy of duloxetine!
Differentiate central and peripheral sensitisatin
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).
Outline neuromodulation
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
What is hyperalgesa and allodynia
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)
How are opioids analgesic
- Centrally acting, they bing to µ receptors on PAG, to increase inhibition from the descending pathways which modulate pain.
- Opioid binding reduces the release of excitatory neurotransmitter release (glutamate) at the dorsal horn
Explain mechanisms of chronic pain
- Loss of descending inhibition (by either reduction of NA pathways, or increase in seratoninergic pathways)
- Central sensitisation to pain occurs, so there reduced electrical thresholds need to be reached in order to transmit pain
