PHYS: Somatic Sensations (inc. Pain and Temperature) Flashcards
exteroception, proprioception, interoception
- exteroception: info abt external world (mechanoreceptors, thermoreceptors, nociceptors) - type of somatic sense
- proprioception (kinaesthesis): info abt position of body in space (type of somatic sense)
- interoception: info re: homeostasis e.g. BP, hunger, thirst (type of visceral sense)
3 ways to activate a mechanoreceptor
- stretch
- tethered: proteins act as elastic strings, press on ion channels and cause them to open
- indirect gated
how is a mechanoreceptor activated?
- translation: stimulus causes physical change in receptor shape > change in membrane potential
- transduction: spike region generates AP if stimulus is large enough
- transmission: conducting region sends message to brain via AB sensory fibres
how does the location of a skin mechanoreceptor determine its function?
- located deeper (pacinian + ruffini) = bigger receptor field size = more crude/delocalised touch and vibration
- superficial (merkel + meissner’s) = smaller size = finer touch
meissner’s corpuscle:
- structure
- location
- function
- adaptivity
- barrel-shaped, encapsulated, connected to AB sensory fibres
- dermal papillae (non-hairy/glabarous skin)
- fine/light touch
- rapidly adapting (FAI)
pacinian corpuscle:
- structure
- location
- function
- adaptivity
- onion ring, encapsulated, connected to AB sensory fibres, large RF
- deep dermis (hairy + non-hairy skin)
- deep pressure + vibration
- VERY rapidly adapting (FAII)
merkel’s discs:
- structure
- location
- function
- adaptivity
- small receptive field, unencapsulated, connected to AB sensory fibres
- upper dermis
- low frequency vibration (Braille), indentation, pressure, texture, VERY FINE DETAIL
- slow adapting (SAI)
ruffini endings:
- structure
- location
- function
- adaptivity
- large receptive fields, encapsulated, connected to AB sensory fibres
- dermis
- detect stretch/tension
- slow adapting (SAII)
describe fast vs slow adapting receptors, including their alternative names
- fast (phasic): only fire APs @ onset and offset of stimulus - good for detecting changes
- slow (tonic): fire as long as the stimulus is present - good for sustained stimuli
types of fast/slow adapting receptors
- FA I (meissners - small RF): only respond @ offset and onset
- FA II (pacinian - large RF): fire during quick changes
- SA I (merkel’s - small RF): fire APs throughout duration of stimulus
- SA II (ruffini - large RF): more sparse APs throughout stimulus
3 types of proprioceptors
- cutaneous mechanoreceptors (Ruffini endings)
- joint receptors (Ruffini endings + pacinian corpuscle)
- muscle spindles + Golgi tendon organs
muscle spindles
- structure
- afferent fibres
- efferent fibres
- encapsulated proprioceptive structures containing intrafusal muscle fibres, parallel w/ muscle fibres = muscle stretch causes receptor stretch
- afferent: stretch detected by type 1a (Aa = fast adapting) and type II (AB = slow adapting) sensory fibres
- efferent: initiate stretch reflex (muscle contraction) to maintain posture and coordination via gamma motor neurons - e.g. patellar jerk
Golgi tendon organs
- location
- afferent fibres
- efferent fibres
- attached to tendons
- afferent: type 1B sensory fibres detect muscle stretch (type of Aa fibre)
- efferent: alpha motor neurons initiate INVERSE stretch reflex (muscle relaxation) to prevent injury and overstretching
why does pain exist (short term and long term)?
- short-term pain = withdrawal from source prevents further damage
- also a social signal to alert others to danger
- long-term pain = promotes behaviours e.g. sleep and inactivity = recovery
what are nociceptors?
- what do they detect?
- where are they located?
- FREE nerve endings
- polymodal: can detect thermal, mechanical, chemical stimuli that are painful
- located everywhere except CNS
4 types of sensory neuron fibres (lvl of myelination + function)
- Aa: heavily myelinated (proprioception + motor)
- AB: myelinated (touch, pressure, vibration)
- Adelta: little myelinated (sharp/fast pain, temperature)
- C: unmyelinated (temperature, slow pain, itch)
how is pain felt as ‘ouch’ vs ‘groan’
- Adelta fibres are myelinated so signals are quicker = quick ouch sensation, readily localised b/c all afferent fibres reach the thalamus and somatosensory cortex (NEOSPINOTHALAMIC - SYNAPSE LAMINA I)
- C fibres are unmyelinated so signals are slower = groan sensation, more poorly localised b/c fibres end in lower brain regions (PALEOSPINOTHALAMIC - SYNAPSE LAMINA II AND III)
2 types of A delta receptors
- mechanical: mediate fast pain response to mechanical stimuli e.g. pin prick
- thermal: mediate fast pain response to noxious temps, mostly cold
(both have high threshold b/c only respond to painful stimuli)
4 types of C-fibres
- nociceptive (peptidergic and non-peptidergic)
- silent
- itch (e.g. histamine)
- non-nociceptor
silent C-fibres
- sensitive to heat but not mechanical stimuli - can be unsilenced by chemical stimuli e.g. capsaicin
non-nociceptor C-fibres
- respond to pleasurable touch and cooling stimuli
2 divisions of the spinothalamic tract
- anterior: crude touch, pressure, itch
- lateral: pain, temp, sexual sensations
spinothalamic tract pathway
- 1st order sensory neurons synapse w/ 2nd order neurons in the dorsal horn
- 2nd order neurons decussate contralaterally in spinal cord and synapse w/ 3rd order neurons in thalamus (ventral posterior nucleus) > somatosensory cortex
sensory pathway from face and head (trigeminal pain/temp pathway)
- 1st order neurons: three branches (V1, V2 and V3) of trigeminal nerve > synapse w/ 2nd order neurons in spinal trigeminal nucleus
- 2nd order neurons: decussate in trigeminal lemniscus (brainstem) and synapse in ventral posteromedial nucleus of the thalamus
- 3rd order neurons: travel via the internal capsule to the primary somatosensory cortex within postcentral gyrus
how does sensitisation work during tissue injury?
- nociceptors adapt in response to multiple components of the ‘inflammatory soup’
- increased chance of activation and electrical activity > hyperalgesia/allodynia
- primary hyperalgesia
- secondary hyperalgesia
- allodynia
- primary: pain hypersensitivity in immediate region of injury
- secondary: pain hypersensitivity in surrounding area of injury
- allodynia: non-noxious stimuli is perceived as painful e.g. warm water on a sunburn
gate control theory
- AB (touch) fibres can inhibit C and A-delta fibres (nociceptive) b/c AB fibres are myelinated = quicker
- i.e. this is why pain is reduced when you rub the area
how do descending pathways inhibit synaptic transmission in the dorsal horn? (pain modulation)
- descending inhibitory neuron releases enkephalin > acts on u-opioid receptors on 1st order neuron coming into dorsal horn
- reduces release of excitatory neurotransmitters e.g. glutamate to slow pain transmission
- originates from PAG
why does chronic pain (>3 months) occur
- in response to persistent injury, nervous system has increased plasticity > enhanced pain signalling, hypersensitivity and reduction in threshold
- no physiological purpose unlike acute pain
types of pain
- nociceptive: visceral or somatic (deep or superficial)
- neuropathic: central or peripheral
- inflammatory: tissue inflammation or hypersensitivity
congenital insensitivity vs erythromelalgia
- insensitivity: loss of nav1.7 function
- erythromelalgia: gain of nav1.7 function (blockage of blood vessels in lower extremities > hyperinflammation)
examples of neuropathic pain
- complex regional pain syndrome: develops after injury, surgery, AMI, starts in a limb
- post-herpetic neuralgia: viral origin e.g. shingles/HIV
- back/spinal injury
- diabetic neuropathy
which drug blocks NMDA receptor activity?
- ketamine
which neurotransmitter is responsible for sensitisation in the dorsal horn?
- glutamate
- also microglial activation > release BDNF > shift in gradient of pain transmission neurons > more excitability
phantom limb pain
- following amputation, nerves that would normally innervate the missing limb can cause pain
- can arise for peripheral, spinal, central mechanisms
referred pain and what might it be caused by?
- when pain in visceral structures radiates to cutaneous areas and sensation arises from body surface
- may be due to 1st order neurons converging on 2nd order neurons of the same spinal cord region > dorsal horn neurons become hypersensitive > interpreted as coming from the skin
thalamic pain
- caused by vascular injury to thalamic neurons (responsible for sensory processing)
- damaged neurons can initiate excruciating pain signals w/o nociceptive stimulation > referred to contralateral side
- unresponsive to conventional analgesics so anticonvulsants have to be used
DCML pathway
- 1st order – dorsal root ganglion to medulla (decussate here)
- 2nd order – medulla to thalamus
- 3rd order – thalamus to primary somatosensory cortex