IC3 Flashcards
spinothalamic tract
on tissue damage
receptors activated > primary afferent (1st order neuron) > AP movement through 1st order neuron to 2nd order neuron > spinal cord > dorsal horn (grey matter of spinal cord) > medulla > thalamus > AP received at somatosensory cortex
movement of AP for pain vs touch
pain:
- first-order afferent > second order in the dorsal horn > cross to the opposite side (left to right) > ventrolateral quadrant > thalamus > somatosensory
touch: first-order afferent > second order in dorsal horn > dorsal column (left side) > medulla > long axon crosses to the right side > thalamus > somatosensory
damage to one side might not affect both sensations
contralateral somatosensory cortex
signal starts on the left and ends on the right.
principles underlying sensory processing?
1) relay uses AP as signal to relay information
2) signal travels along topographic lines
- each region have their own set of afferent relays
- relays remain separate even in the cortex (occupy different spaces in the somatosensory cortex, ie somatosensory HOMUNCULUS)
3) signal only travels along labelled line IE only responds to one type of stimulus
4) signal along relay encode for properties of the stimuli
- intensity: more intense = higher frequency of AP
touch allodynia definition
pain due to a stimulus which does not normally provoke pain (PAIN TO A NORMALLY NON PAINFUL STIMULUS)
due to nerve damage altering the characteristics of the pain pathway.
involves sensitisation
define sensitisation
potentiates response of pain pathway to a given noxious stimuli AND decreases threshold for excitation of the pain pathway.
peripheral vs central sensitisation:
peripheral involves first order
central involves second order neurons in the eg spinal cord.
receptors activated by innocuous pressure (touch)
merkel cell
meissner corpuscle
pacinian corpuscle
ruffini ending
what is hyperalgesia
increased pain to a given noxious stimulus.
(pain sensation)
pathophysiology of pain in allodynia
side branch of A beta fibre that enters the spinal cord and (i) makes a synapse on an inhibitory neuron inhibiting the spinothalamic tract AND (ii) direct synapse with the spinothalamic tract directly exciting it.
usually, the inhibition dominates, but scenarios
A) loss of inhibitory neuron
B) hyperexcitability/sensitisation due to the release of various chemicals at the damaged site = second order neuron also becomes hyperexcitable AND DOMINATES OVER INHIBITION
= direct sensitisation of the spinothalamic tract and incite pain.
how does sensitisation work in pathophysiology? state chemicals
chemicals released by injury
causes sensitisation of nociceptors
- decreased threshold to stimulus
- increased response to stimulus
chemicals include CGRP, glutamate, substance P…
receptors eg AMPAR, NMDAR of the spinothalamic tract…
examples of allodynia
sunburnt
sprained ankle
neuropathy
surgery
describe descending pain modulation
morphine, stress, etc
excites neurons in the midbrain periaqueductal gray (PAQ) > signal to nucleus raphe magnus in the medulla > interneuron in spinal cord > inhibits the transfer of signal to spinothalamic neuron (thus blocking the pain).
what is enkephalin
inhibitory neuron released at the synapse between the 1st order neuron and the spinothalamic tract neurone = block transfer of signal.
it is an endogenous morphine-like substance
mechanism of action of morphine
- act on PAQ neurons
- mimic spinal cord enkaphalin
describe segmental modulation in pain modulation
stimulation of large diameter afferents (for touch) excites inhibitory interneuron = decreased transmission of pain signal in the spinal cord.
hierarchal features of motor control
cortex = voluntary movement
brainstem = postural reflexes, rhythmic motor patterns
(cortex and brainstem send LONG DESCENDING AXONS to the spinal cord)
spinal cord = site of motor neurons and control of muscle activity
loss of output = flaccid paralysis (muscles lose tone), final common pathway (lower motor neurons)
pathway of long neurons in motor behaviour
corticospinal pathway
brainstem pathway
damage of cerebellum and effect
involved in coordinating movement
lesions disrupt the coordination of limb and eye movement, impair balance, and decrease muscle tone.
effect of basal ganglia and interaction with cortex
basal ganglia involved in initiation of movement and selection of motor program
neurons in basal ganglia = dopamine neurons.
degeneration = parkinsons disease = movement start slow/wrong choice of movement
= disorder of movement (tremor, flicking/chorea, flailing, twisting, bradykinesia) and disorder of posture (rigidity).
representation of receptors for somatosensation
higher representation (higher density) of the face than the trunk
relay from the face region is more extensive than from the trunk.
= leads to a more precise sensory experience
mechanism of paracetamol in relation to CNS
antagonism of TRPV receptors esp in the spinal cord.
intensity encoding depends on two coding?
1) frequency code: intensity of stimulus correlates with the number of AP evoked in labelled line
2) population code: intensity of stimulus correlated with number of reeptors excited
