pain Flashcards
nociceptive pain
Pain from actual or threatened damage to non-neural issue - due to the activation of nociceptors
Nociplastic Pain
Pain that from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain.
Neuropathic Pain
Pain caused by a lesion or disease of the somatosensory nervous system
Acute Pain
Pain that is temporarily related to injury and that resolves during the appropriate healing period. It is usually short-lived.
- Easily described- sharp, stinging, pulling
- Specific location
- Specific aggravating and easing factors
Chronic Pain
Chronic pain is any pain that lasts beyond the expected period of healing or exists for more than three months.
- Difficult to describe
- May move locations
- Difficult to pin point things that make it better and worse
maladaptive
serves no purpose
becomes a limiter to someones life
pain catastophising - pain related fear- hypervigilance avoidance - disuse, depression, disability
does pain reflect the state of the tissues?
the more acute the more likely pain experienced is a reflection of their tissues
chronic pain is more likely to not be a result of the tissues
noxious stimuli
Events that damage or threaten to damage tissues and that activate specialised sensory nerve endings called nociceptors.
Stimuli adequate to activate nociceptors are not the same for all tissues.
pheriphery- detectors- sensory
SKIN- Thermal, mechanical and chemical
JOINTS- Mechanical -rotation/torque beyond the joint’s normal range of motion and chemical
MUSCLES- Mechanical -blunt force, stretching, crushing and overuse and chemical
VISCERAL SYSTEM- Mechanical (distension, traction on the mesentery) and chemical (released from inflamed or ischemic organs, inhaled irritants).
brainstem
Rostral ventromedial medulla (RVM)
in the brainstem determines whether nociceptive information is prioritised in the dorsal horn of the spinal cord.
It can enhance nociception following injury but failure to resolve after tissue healing can lead to chronic pain ‘locked in’.
brainstem
Descending modulatory system
Antinociceptive (Good cop)
* Norepinephrine, serotonin
Pronociceptive (Bad cop)
A genetically driven imbalance in the antinociceptive and pronociceptive activity within the RVM probably involving 5-hydroxytryptaminergic and norepinephrinergic mechanisms may represent a possible pain endophenotype
Distraction
using a cognitive task, high working memory load (HWML) Vs low working memory load.
HWML showed significant less activity at the spinal cord and significantly less pain. (Sprenger et al 2012)
networks that link sensors to the hub, brain to the periphery
brain stem
spinal cord
centeral sensitisation
nociceptors
activation spinal cord
Nociceptors are continuously active in our everyday behavior (subconsciously and consciously) as a way of protecting us.
Activation must reach a threshold to travel to the brain and be interpreted as pain. This threshold may be equated to the “pain control theory” melzack & wall 1965
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Central Sensitisation
Where nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways.’ (Woolf 2011 p1)
Seen in the short-term with tissue damage (hyperalgesia) and in the long-term with chronic pain conditions (Woolf and Salter 2000).
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what info is added at the brain (hub)
- Past experience (Memory)
- Personality
- Beliefs
- Attention
- Fear/Worry
- Mood
- Thoughts
2
Neuromatrix Theory
Pain is a multi dimensional experience produced by a characteristic “neurosigniture” patterns of nerve impulses generated by a widely distributed neural network “neuromatrix” within the brain.
They can be triggered by sensory inputs but can be generated independently of them (Melzack 2005)
Protectometer
SIMS
- SAFETY messages in me SIMs (DOWN- desensitise)
- Supportive family and friends, useful knowledge, fitness and mobility, hope, positive attitude/expectation, positive past experience, resilience, acceptance, healthy and balanced diet, love and friendship.
Protectometer
DIMS
- DANGER message in me DIMs (UP- sensitise)
- Low expectation, poor sleep, reducing movement and activity, negative attitude, worry, perceived injustice, bad past experiences, no hope, fear, low mood, lack of support, lack of knowledge or incorrect messages, loss of identify or role (job, family role), poor health of tissues, poor diet, loneliness and isolation
neurosigniture 1
Pain perception
needs to be routine activation often bilaterally of
* Primary and secondary somatosensory cortices
* The posterior, mid and anterior insula
* Anterior cingulate
* Pre frontal cortices
neurosigniture 2
Activation of subcortical areas such as
- Hypothalamus
- Amygdala
- Hippocampus
- cerebellum
neurosigniture 3
COGNITIVE, EMOTIONAL AND CONTEXTUAL INFLUENCE
neurosigniture 4
pain experience
PAIN EXPERIENCE – ‘Cerebral Signature’ of pain that is bespoke for an individual and requires activity within multiple brain regions
insula cortex
INSULA CORTEX is the most consistently activated region during painful experiences (Tracey 2011).
pain gate theory by melzack and wall (1965)
- non-painful input closes the nerve gate to painful input
- and prevents pain sensation from reaching the CNS.
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Descending pain inhibition
- The non-nociceptive myelin neurones pass up and connect to the somatosensory cortex of the brain.
- The SSC stimulates neurones in the periaqueductal gray area of the mid brain
- which stimulates cells in the medulla, such as the nucleus raphe magnus.
- Pain is then supressed through the release of serotonin and nor-adrenalin,
- this stimulates the inhibitory neurone in the posterior horn
- and blocks ascending pain impulses
types of pain
- somatic superficial - skin - sharp fast pain - localised brief
- somatic deep - deep layers of skin/ muscles - burning aching slow pain- diffuse long lasting
- visceral - caused by lack of o2, inflammation - organs - dull ache slow pain - can cause nausea sweating/reffered
detection of pain
- free nerve endings register damage
- 1st order neurons synapse with 2nd order neurons
2 main nerve fibre types
Aδ fibre
1. mechanical - sharp pricking, fast pain
2. thermal and mechanothermal - slow burning, cold sharp, pricking
B fibre
polymodal - hot and burning sensation, cold, slow deep pain
differences between peripheral and centeral sensitisation
peripheral
* substance P feedback loop
* presynaptic 1st order neurons sensitised
centeral sensitisation
* post synaptic neurons 2nd order sensory neurons sensitised
* many other factors involved in spinal hyperactivity
how does info ascend the spine
spinothalamic tract decusses
Sensory pathways
lead into the spinal cord then up the spinal cord through the brain stem up into the brain.
Motor pathways
bundles of axons in a consecutive array of neurons creating a pathway of motor information to move in the other direction
concious vs unconcious sensory receptors
Conscious: reach cerebral cortex
* Conciously aware of things that arrive at the somatosensory cortex
Unconscious: does not reach cerebral cortex
* Proprioceptive information goes to brain stem, cerebellum ect.
1st, 2nd, 3rd order neurons
- First order neuron
○ Sensory cell body in dorsal route ganglion - Second order neuron
○ Cell body in dorsal horn or brain stem - Third order neuron
○ Cell body in the thalamus projecting to the somatosensory cortex
sensory homunculous where is it found
- Somatosensory cortex
- Post-central gyrus
- Parietal lobe
sensory homunculous what is it?
a map along the cerebral cortex of where each part of the body is processed
LHS spinal cord injury - sensation loss?
(If the spinal cord injury is LHS, the loss of sense would be felt on the RHS due to the cross/dessecation)
spinothalamic
info
* pain, temp, touch, pressure
2nd neuron crossover point
* spinal cord
projection to somatosensory cortex?
* yes
effect of injury in spinal cord
* loss of function opposite side
dorsal column
info
* fine touch, vibration, concious proprio
2nd neuron crossover point
* medulla
projection to somatosensory cortex?
* yes
effect of injury in spinal cord
* loss of function same side
spinocerebellar
info
* unconcious proprio
2nd neuron crossover point
* it doesnt
projection to somatosensory cortex?
* no
effect of injury in spinal cord
* loss of function
concious
pyramidal - direct
unconcious
extrapyramidal - indirect
pyramidal motor pathway
- Interneurons at spinal level but upper neurons project down the spine and control motor neurons at the spinal level
- Direct
- Conscious
extrapyrimidal
Extrapyramidal
1. Upper motor neurons are in the brain stems nuclei no (higher control aswell)
2. No well defined direct connection from motor cortex to lower motor neurons
* Indirect
* Mostly subconscious
pyramidal direct pathway
- UMN- cortical cell body of the motor cortex (some will decussate and descend the spine)
- Often an interneuron
- Lower motor neuron- sends info out through the ventral root
Extrapyramidal pathways unconscious
- Modifies movements: Modulatory actions on LMN
- Rubrospinal- fine motor control upper limb
- the start of the tract are in the red nucleus in the brain - Tectospinal- control neck muscles, head&eye coordination, visual/auditory feedback
- Vestibulospinal- balance
- Reticulospinal- motor functions, autonomic functions, pain modulation
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pain gate
- Neural gate (spinal cord level – Substantia gelatinosa) modifies pain perception
- Gate receives input from Peripheral nerve fibres
- Descending central influences from the brain mediated by behavioural state (attention), emotional state (anxiety), past experiences and self-efficacy
- Large and small fibres
- Output from the gate sends information to an action system resulting in pain perception
- The more the gate is open, the greater perception of pain
3
factors responsible for opening the gate
- Physical factors (injury, activation of large fibres)
- Emotional factors (anxiety, worry, tension, depression
- Behavioural factors (focus on pain, boredom)
3
Factors Responsible for closing the gate
- Physical factors (medication, stimulation of small fibres)
- Emotional factors (positive mood - happiness, optimism, relaxation)
- Behavioural factors (distraction, engagement in other activities)
