pain, movement, mood Flashcards
both pain and touch sensory pathway
synapse in thalamus
sensations perceived in primary somatic sensory cortex
contralateral (stimulated on R –> shift to L side)
thalamus
central switch station of brain
sorts out incoming physical signs (2* –> 3* thalamus)
where does pain pathway cross to contralateral side
- pain: spinothalamic pathway (1* cross at dorsal horn in spinal cord)
where does touch pathway cross to contralateral side
- touch: dorsal column pathway (1* crosses in medulla)
touch vs pain
touch nerves send signals more quickly than pain nerves
(feel pierce before pain)
- thicker myelin sheath
somatosensory relays of spinothalamic pathway
1) relay signal to tissue damage, pain sensation
2) signal generated at nociceptors in region of damage
3) nociceptors are free nerve ending. merge into afferent nerve fibre (Ad, C type)
4) fibre carry signal from periphery –> spinal cord
synapse at dorsal horm
5) spinothalamic neruon (2*, receiving neuron) sends long axon to thalamus.
6) thalamus (3* neuron) relay info to cortex (4* neuron)
variety of cortical regions receive pain info
pathway that affects sensory processing
(how do we know the location)
signal travels along topographic lines
reach primary somatosensory cortex (L hemisphere = right body)
signal travels along labeled line
receptor and its primary afferent (1* neuron) labeled because only respond to only 1 type of stimulus
chain of neurons relaying sensory info of particular modality
modalities
modalities represent a class of stimuli (eg lead to somatosensation)
some are non-overlapping (vision and sound)
some are submodalities which overlaps (touch, pain)
unimodal receptors
only 1 adequate stimulus
not have manifold adequate stimuli
polymodal receptor
nociceptors: free nerve endings in the skin are called polymodal nociceptors because they contain multiple receptors and thus respond to various combinations of the above mentioned stimulus.
eg: mechano-heat C fibers
large representation of face compared to trunk on cortical map
relay of info from face region more extensive than from trunk
high density of receptors in face region, more precise sensory experience.
3 factors of sensation
1) location
2) intensity
3) quality
location of sensation
location of receptor (receptive field)
duration of stimulus
intensity of sensation
a) freq code (the more intense the stimulus, more AP per unit time (FREQ)
b) population code (number of receptors excited)
quality of stimulus
nature of stimulus
vision (photo receptors)
mechanoreceptors
chemoreceptors
osmoreceptors
thermoreceptors
proprioceptors (position in space)
nociceptors (noxious stimuli)
what is pain?
unpleasant feeling
felt acutely to warn indiv of the damage and prompt indiv to take remedial measures
- pain that outlast tissue damage/ after tissue recovered does not serve any USEFUL PURPOSE
3 features of pain
1) intensity
2) unpleasantness (subjective)
3) duration (acute vs chronic)
pain pathophysiology
allodynia: pain to normally non-pain stimulus
hyperalgesia: incr pain to noxious stimuli
allodynia explained in 2parts
1) human sensory exp (lower threshold for excitation + POTENTIATES, higher intensity for given stimuli)
2) neural activity (incr AP response per unit time)
- central sensitization (spinal cord)
- peripheral (nociceptors neurons)
spontaneous pain
spontaneous activity in pain pathway especially in nociceptors
central sensitisation
sensitised spinal neurons strongly excited by touch.
- excited wide dynamic range neuron (grey column of spinal cord) along spinothalamic pathway –> sensation of pain
- potentiate freq of pain signal
peripheral sensitisation
nociceptor terminals become more sensitive to the same quantity of the chemical mediators
potentiates pain intensity
inhibitory neuron function
excitation of Ab fiber 1* (touch) will inhibit spinal-thalamic tract neuron 2* (pain)
rmb: pain crosses at dorsal column
possible MOA of allodynia
1) degeneration of inhibitory neuron
2) inhibitory neuron is now activatory neuron. phenotypic alteration
3) spinal thalamic tract becomes sensitised, more easily excitable. tissue damaged, more neurotransmitters, incr freq so there is decr in threshold
neurochemicals involved in sensitisation
CGRP
5HT
ATP
Sub P
glutamate
drugs that inhibit neurochemicals that are involved in sensitisation
1) aspirin (NSAID, inhibit COX, block PG prod)
2) acetaminophen (reduce COX, antagonist TRPV receptor)
3) ubrogepant (CGRP RA)
eg of allodynia
sprained ankle
neuropathy (nerve damage)
surgery (trauma and nerve damage)
sunburnt
- affects 1* nociceptive neurons and spinal neurons (interneuron)
types of pain modulation
- decr pain: regulate signal along pain pathway, stress, morphine, context , PAG
- enhance pain: anxiety
methods to modulate pain
1) descending - stimulates PAG, stimulate interneuron to inhibit transmission
2) segmental modulation
PAG (periaquefuctal grey) and pain inhibition pathway
in midbrain
1) neurons in prefrontal cortex can activate PAG regions
2) medulla (in nuclues raphe magnus)
3) excites another neuron in spinal cord (interneuron = produce enkephalin)
4) inhibits transfer of signal to spinothalamic neuron (opioid receptors on axons of C, Ad fibers) : 5HT, enkephalin
- inhibit sub P
1st —-INHIBITED—-> 2nd order (spinothalamic neuron)
morphine and enkephalin
morphine mimics enkephalin
binds to opioid receptors of axons (pain 1*)
- segmental modulation of pain
(gate theory)
stimulate large diameter afferents (Ab, touch)
excite inhibitory interneuron
decr transmission of pain signal in spinal cord
- gate closed = local analgesic effect at spinal cord
- descending pathway
stimulate mid-brain PAQ
activate nucleus raphe magnus –> stimulate interneuron in spinal cord
release opioids (endorphin, 5HT, NA, enkephalin)
- inhibit the presynaptic form releasing sub P
- inhibit the post synapse of 2* neuron from transmitting signals.
types of movements generated
1) reflexes - involuntary, withdrawal
2) rhythmic motor patterns (require vol initiation and termination) : walk, breathe, swim
3) voluntary - goal directed
cortex – voluntary movement
premotor area and primary motor cortex
(left brain controls right muscle)
brain stem (rhythmic motor patterns)
from mid brain –> medulla
brainstem and cortex influence execution of behaviour (via neurons that send long axons from site of origin –> spinal cord)
spinal cord
reflexes, site of motor neurons to control muscle activity
sensorimotor cortex contains
somatosensory cortex (parietal) vs somatomotor cortex (frontal lobe)
neurons in basal ganglia
dopamine neurons
degeneration leads to Parkinson’s disease
interacts with cortex and affects initiation & selection of motor program
damage to basal ganglia
1) disorder of movement - tremor, rapid flicking, dystonia, bradykinesia (slow) eg PARKINSON’S
2) disorder of posture - rigidity
parkinson’s marked by 3 features
tremor
rigidity
bradykinesia
descending control of efferent
corticospinal brainstem pathways for voluntary motor function
descending spinal tract system that originate from cortex/ brainstem
upper motor neurons travel in corticospinal tract
synapse in spinal cord (lower motor neurons)
contact with skeletal muscle (contraction)
steps for voluntary movements
1) knowledge where body is in space (relative to obstructions)
2) where it intends to go
3) selection of a plan to get there (diff ways,selects fastest/ safest)
4) plan held in memory until the appropriate time
5) instruction to implement the plan
1) knowledge where body is in space
mental body image generated by SOMATOSENSORY proprioceptive and visual inputs to
posterior parietal cortex (converge info – relative idea of where you are at)
1) knowledge where body is in space
mental body image generated by SOMATOSENSORY proprioceptive and visual inputs to
posterior parietal cortex (converge info – relative idea of where you are at)
- proprioceptor stimulated
2) where it intends to go and what to do
anterior frontal lobes
abstract thought, decision making, anticipate consequences for action
weight factors, risk vs benefits
3) selection of a plan and held till execution
premotor cortical areas
cerebellum – coordinate movement
basal ganglia – decision, selection
4) implementation
go command implemented by primary motor cortex
in participation of basal ganglia and cerebellum
“rhythmic motor movement”
