Sensory Pathways: Lecture Flashcards
How are sensory receptors formed?
Individual axons of sensory nerves have modified terminals
What are two broad categories of terminal type?
Free ends - Thermoreceptors, Nociceptors
Enclosed – Mechanoreceptors
What are the four classifications of sensory fibres?
Aa - Fastest, Proprioception (Muscle)
Ab - Fast, Mechanoreceptors - Innocuous physical (Skin)
Ad - Quite fast, Thermo and Nociceptors
C - Slow, Aching pain, thermo and Itch
(Noxious mechanical, thermal and chemical stimulation)
What do Thermoreceptors consist of?
A delta and C type sensory fibres
Transient Receptor Potential (TRP) Ion channels that respond to temperature
What are some Subsets of Transient receptor potential channels?
Heat Responsive
TRPV 1-4
Cold Responsive
TRPM8
TRPA1
What are four types of mechanoreceptors?
Meissner’s Corpuscle - Fine, discriminative touch, Low frequency, Vibration
Merkel Cell - Light touch, superficial pressure
Pacinian Corpuscle - Deep pressure, High Frequency vibration, tickling
Ruffini Endings - Continuous Pressure or touch, stretch
What is the absolute threshold of a stimulus?
Point of stimulus intensity where it is detected 50% of the time.
Higher intensity = more APs because detected more often, more neurotransmitter release
What are two types of receptor in regards to adaptation?
Tonic Receptors - Very Slow or No adaptation, respond for stimulus duration
e.g. Merkel cells respond as long as touch persists
Phasic Receptors - Fast Adapting, respond to CHANGE in stimulus strength
I.E At start and End of GP, e.g. Pacinian Corpuscle respond when pressure applied and released
What is a sensory field?
Area of skin that activates SINGLE Neuron when stimulated
What is two point discrimination?
Minimum distance at which two point can be perceived as separate when stimulus applied, the smaller the sensory field (e.g hands) the smaller this distance is, compared to places like back.
What is a dermatome?
Area of skin innervated by a single spinal nerve
Where are the sensory cell bodies of the face and body?
Dorsal Root ganglia - Body
Trigeminal ganglia – Face
What are the features of the dorsal horn?
Contains Projection Neurones and Interneurones
Divided into Rexed Laminae (I-VII)
Pain and temperature fibres (A delta and C) terminate in lamina I-II (Superficial)
Innocuous mechanical stimuli fibres (A beta and A alpha) terminate in laminae III-VI (deep)
Glutamate is the main excitatory transmitter for projection neurones
What is the purpose of the interneurones in the dorsal horn?
Lateral inhibition – increase the resolution of a stimulus and allow for greater localisation by inhibiting the lateral fibres to the main fibre
What are the features of the dorsal columns?
Both dorsal columns transmit innocuous mechanical stimuli through second order nuclei
Below T6 lower limbs ipsilateral gracile (The medial dorsal column for the legs)
Upper limbs ipsilateral cuneate tract (The lateral dorsal columns for the arms)
Where do second order sensory fibres terminate?
2nd order CROSS IN MEDULLA - Form contralateral medial lemniscus tract - terminate in Ventral posterior lateral nucleus
Lower limbs are lateral - topographic representation
Where do third order sensory fibres terminate?
3rd order neurones from VPL project to somatosensory cortex
Primary somatosensory cortex in postcentral gyrus
Secondary somatosensory cortex in parietal operculum
Where do pain, crude touch and temperature sensory fibres travel?
Travel through spinothalamic (anterolateral) tracts
First order terminate in dorsal horn, second order desscutate immediately and ascend contralateral.
Second order terminate in Ventral posterior lateral nucleus in thalamus
Crude touch is mediated by A delta fibres (Free nerve ending).
What can loss of only certain sensations suggest?
Area of spinal cord lesion, injury, disease etc can be tested Specific loss of sensation e.g sensation not pain and temp can suggest only dorsal horn affected.
What is the definition of pain and how is it transmitted?
Pain - Unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
Transmitted between neurones via Glutamate synapses
Sensory component - Spinothalamic tract (To thalamus and cortex)
Emotional component - Spinoreticular tract (To hypothalamus and Amygdala)
What is the ‘pain signature’?
Brain activity in: Cortex: SI SII Insula cortex Anterior cingulate cortex Prefrontal cortex
Amygdala
Cerebellum
Brainstem
What is the gate control theory?
The gate control theory proposes that stimulating fibres with non-noxious physical sensation facilitates inhibitory interneurones in the dorsal horn (Usually via Ab fibres) – reducing the chance of a painful stimuli being projected to the brain, therefore reducing the intensity of the pain felt
What is descending pathway inhibition?
Occurs in Periaqueductal Grey (PAG), via Monoamine inhibition of pain (Noradrenaline more so than Serotonin) preventing nociceptive processing. High conc of mu opioid receptors in PAG and RVM allow the areas to release endogenous opioids to bring about analgesia.
Placebo Analgesia can occur through activation of descending inhibition pathways
What is primary hyperalgesia?
Peripheral Sensitization – Often occurs due to inflammation, chemical mediators such as Histamines bind to the nociceptors and can either depolarize them or lower the threshold of a stimulus needed to depolarize them. This leads to more frequent generator potentials and a greater intensity of pain.
It can also cause primary allodynia when non noxious stimuli can now trigger generator potentials.
What is secondary hyperalgesia?What is secondary hyperalgesia?
It is Central Sensitization
NMDA receptors activate, this allows Ca2+ in, increases synaptic strength, reduces inhibitory influences, increasing pain sensitivity.
Persistent NMDA activation causes neural plasticity and chronic pain.
Causes allodynia and hyperalgesia and can increase receptive field size
What are the three neuropathic pain clusters? How is neuropathic pain placed into ‘phenotypes’?
Sensory loss
Thermal hyperalgesia
Mechanical hyperalgesia
Pain placed into phenotypes over what noxious and non-noxious stimuli cause it and its intensity.
What treatments are given for neuropathic pain?
Despite effect of endogenous opioids, exogenous have little effect
SNRI (serotonin noradrenaline reuptake inhibitors) and TCA antidepressants effective
SSRI not very effective, suggest noradrenaline more important in descending inhibition
Some suggestion that Noradrenaline is inhibitory to pain and serotonin stimulatory (or inhibitory to thermal sensation)
Describe Neuromodulation in chronic pain patients
Non-invasive primary motor cortex stimulation (transcranial direct current stimulation, tDCS)
Look at:
Activation of endogenous analgesic systems in the brain
PAG
Anterior cingulate cortex
Analgesic mechanisms unclear – however gives insight into which personalised medicines are more likely to effective for each patient.
