sensory pathways Flashcards
define somatosensory function and types
ability to interpret bodily sensation mechanical, thermal , proprioceptive (movement) and noxious (potentially harmful BUT not always painful)
comparison of sensory nerve axons
axons of sensory nerve have different terminals- thermo and nociceptors have free nerve endings, mechanoceptors have enclosed nerve endings
types of sensory nerves with speed, myelination and diamater
A beta fibres are for unharmful mechanical stimuli- have greatest diameter, speed and are myelinated A delta fibres are for potentially harmful mechanical and themal stimuli- also myelinated C-fibres are for potentially harmful mechanical, thermal and chemical stimuli- not myelinated, have smallest diameter and speed
define sensory receptors
transducers that convert energy into action potentials
thermoreceptors- fibres involved and comparison
A delta and C fibres- use free nerve endings both fibres detect coldness, only C fibres detect heat
thermoreceptors- sensitivity to temp and ion channels
minute changes in temp. can be detected, but sensitivity to temp is different in different parts of the body, depending on the ion channels present- i on channels are called transient receptor potential (TRP) ion channels, activated by heat (TRPV1-4, channel that detects capsaicin as well) or by coldness (TRPM9/A1)
mechanoreceptors- comparison (1 similarity and types)
all A beta meissners corpuscle receptors detect low frequency vibraion and very fine touch merkel cells detect light touch eg brush pacinian corpuscles detect deep pressure, high frequency vibration or tickling ruffini endings detect stretch and continuous pressure
nociceptors- commonality and types of fibres for diff types of pain
they are free endings sharp pain (eg pin) and excessive coldness detected by A delta fibres dull aching pain and excessive heat detected by C fibres
define stimulus threshold
point of intensity where person can detect the stimulus half of the time- if stimulus given 4 times, person detected it twice
stimulus intensity- what does it depend on
depends of stimulus strength and duration, which affects amount of NT released
adaptation via tonic receptors+ example
these detect continuous stimulus strength- if you sat on chair, they initially send burst of impulses to brain, and then continue to do so, keeping brain constantly informed they adapt slowly eg merkel cells
adaptation via phasic receptors + example
not like tonic receptors- detects CHANGE in stimulus strength, sending impulses when change taking place eg pacinian recepto transmit impulse during sudden pressure, then another once pressure gone
define receptive field compare fields in different areas
area of skin where stimulus activates a SINGLE sensory neurone arm has small receptive fields to detect fine detail fingers have even smaller receptive fields, so many mechanoreceptors in a small area back has large receptive fields ie less precise detection of stimulus as mechanoreceptors spread out
explain two point discrimination, what it depends on and how its carried out
minimum distance at which two points are perceived by body as separate- clinically important to assess dorsal column depends on receptive field- in hands distance should be much smaller two ends of a paper clip are placed on an area of skin- if they are placed on different fields, 2 points of touch are perceived, if they re placed in one field (eg back), 1 point of touch perceived
cell bodies in body and and face and pathway
cell bodies are either in dorsal root ganglia (for body) or trigeminal ganglia (for face) info from lower limb goes to lumbar region via primary neurone and goes up via GRACILE FASCICULUS, info from upper limb goes to cervical region and goes up to medulla via CUNEATE FASCICULUS info then goes to gracile and cuneate nuclei, secondary neurone forms and crosses over at medulla to form medial leminiscus, which goes up to thalamus, which then goes to somatosensory cortex via tertiary neurone
whart is median leminisicus
area of myelinated axons called internal arcuate fibres, which are axons of the gracile and cuneate nucleus
pathway for face
primary neurrone goes to trigeminal nucleus, which goes up to thalamus via secondary, then somatosensory cortex via tertiary
dorsal horn neurones and location of different nerve types
projection neurones- have axons that go to brain interneurons- have axons that stay in spinal cord A delta and C fibres are in superficial part of spinal cord, A beta are in deep part of spinal cord
lateral inhibition- what it prevents and how
two receptive fields can overlap, making it difficult to distinguish two different stimuli lateral inhibition prevents this overlap to have better sensory perception, done by inhibitory interneurons
pathway for touch and propriception- dorsal column pathway
A beta fibres enter dorsal horn and go up via gracile or cuneate tract (lower or upper) to medulla via primary neurones, synapse to become 2ndary in gracile or cuneate nucleus, and ONLY THERE to they change side to form the contralateral medial leminiscus tract 2ndary neurones then end in VENTRAL POSTERIOR LATERAL NUCLEUS of thalamus
pain and temp localisation vs innocuous stimuli (eg propriception)
pain and temp localisation not as precise
pain, temp vs crude touch
pain and temp go up via LATERAL spinothalamic tract, crude touch (touch that is not well localised) via ANTERIOR spinothalamic tract
quantitative sensory testing- what it’s dependent on
a psychophysical assessment ie dependent on persons situation- some who has had alcohol will not respond the same, whereas the neurconduction study is completely objective
use of quantitative sensory testing and anterior spinal cord lesion DIAGRAM
tests both ascending pathways if anterior spinal artery block, anterior part is damaged (red part anterior, as looking at cord from above in pic), so pain and temp loss occurs below level of lesion (at higher levels, fibres can still cross) dorsal column still intact ie light touch (dorsal in posterior part)
types of nociceptors
a delta fibres needed for sharp or first pain- type 1 harmful mechanical, type 2 harmful heat C fibres mediate dull, aching or second pain (second pain is pain after the initial burst)- thermal, chemical or mechanical
neurotransmitter in nociception
glutamate is used for pain
components of pain and tracts involved
sensory part of pai n carried via lateral spinothalamic tract, also an EMOTIONAL component carried via spinoreticular tract
controversy of brain
fMRI has shown the regions of brain eg amygdala, cerebellum, brainstem and cortex involved in pain, but important to realise pain is subjective, so MRI alone cannot determine whether someone has felt pain
gate control theory
inhibition of sensory input before they go to brain- impulse sent by Abeta fibre goes to interneuron, and C-fibre impulse is blocked, decreasing pain
descending control pathway
key area is periaqueductal gey- monoamines like serotonin and noradrenaline can inhibit spinothalamic tract- opioids do this as well
types of pain and causes
nociceptive pain is due to stimulation of nociceptor- can be to ligaments, bones, organs and skin, often from arthritis, fractures and burns neuropathic pain is due to damage to somatosensory system- due to sciatica, chemotherapy, post-surgery mixed pain often seen in low back pain and osteoarthritis
peripheral vs central sensitisation
peripheral- thresholds to peripheral stimuli decrease AT sit of injury due to inflammatory mediators central sensitisation- thresholds to peripheral stimuli NEXT to site of injury decrease due to plasticity of interneuron, which expands receptive field
hyperalgesia and allodynia DIAGRAM
allodynia- pain from a stimulus that normally is not painful hyperalgesia- even more pain from a stimulus that normally provokes pain, either primary (at site) or secondary (near site) graph shifts left- allodynia is shaded red (normally causes no pain)
diagnosing neuropathic pain- the three steps
three steps- firstly must be injury to somatosensory system, secondly must be pain in region that corresponds to part of somatosensory system that is damaged, and thirdly symptoms correspond to damage- these symptoms obtained via questionnaire
effectiveness of SSRIS in treating neuropathic pain patients
SSRIs (seretonin selective reuptake inhibitors) not effective compared to TCA’s/opioids, as seretonin can be harmful for chronic pain (unlike noradrenaline which can control chronic pain)
conditioned pain modulation
idea that pain can inhibit pain- if pain measured on one arm, then pain stimulated in another arm and pain retested in 1st arm, pain sensation may go down
descending control of pain in chronic pain patients
affected in patients with chronic pain ie areas like PAG are impaired
neuromodulation ifn chronic pain patients
motor cortex stimulated by non-invasive method, activating the PAG, which can reduce pain
