Pain Quiz 1

• Pain is an uncomfortable sensory and emotional experience related to actual or potential tissue damage.

Rene Descartes' Model of Pain

• Rene Descartes lived from 1596-1650
• Descartes compared the human body to a machine.
• Pain messages were believed to travel to the brain through hollow tubes.
• This model is considered the 1st model of pain.
• This model is a biomedical one

Gate Control Theory of Pain

• The spinal cord has a "gate" at the top.
• The brain controls the gate by opening or closing it.
• The gate opens if a pain signal becomes strong enough.
• The transmission of nerve impulses, from afferent fibres to spinal cord transmission (T) cells, is controlled by a gating mechanism in the spinal dorsal horn (substantia gelatinosa).
• This gating mechanism relies on the amount of activity in large- and small-diameter fibres.
• Large fibres close the gate and inhibit transmission.
• Small fibres open the gate and facilitate transmission.

Mature Organism Model

• The brain assesses the threat level of stimuli.
• The samples the brain has include:
• Past experiences
• Knowledge of stimulus
• Beliefs of stimulus
• Cultural understanding of the stimulus
• Observed behaviours of others to the stimulus (successful or unsuccesful)
• Stimuli results in altered behaviours and altered physiology
• The best evaluation of all inputs is its output

Neuromatrix Model

• Pain is a multidimensional experience created by specific “neurosignature” patterns of nerve impulses.
• The nerve impulses are generated by a widespread neural network and the "body-self neuromatrix" in the brain.
• Cognitive-evaluative inputs include:
• Tonic Input
• Past experiences
• Phasic Input
• Expectations - Anxiety
• Sensory-discriminative Inputs include:
• Phasic cutaneous input
• Trigger points
• Deformities
• Visceral input
• Visual
• Vestibular
• Other sensory inputs
• Motivational-affective inputs include:
• Biomarkers in blood
• Thoughts on injuries
• Influences from external sources
• Outputs include:
• Pain perception is broken down into:
• Cognitive-evaluative
• Sensory-discriminative
• Motivational-affective aspects
• Action programs
• Involuntary/voluntary action patterns
• Social communication
• Coping Strategies
• Stress-regulation programs
• Cortisol levels
• Noradrenaline levels
• Cytokine levels
• Immune system activity
• Endorphin levels

Fear Avoidance Model

• Activities are avoided based on the fear of increasing pain or re-injury.
• This leads to disuse, depression, disability, and lowered pain thresholds.
• Hypervigilance contributes to avoidance, including:
• Fixation on chronic pain
• Avoidance of movement.
• Recovery happens when injuries do not cause fear.
• Recovering includes:
• Returning to activities
• Those scared to move will not recover as well as those who aren't.

Biopsychosocial Model

• Pain is multidimensional and results from physiological, psychological and social factors.
• Each factor contributes differently.
• People with high self-efficacy had better outcomes.
  • Significant decrease in pain
  • Saying "I can do things despite my pain”
• Thinking more damage has occurred results in more pain.
• Such as how you move, bend, or twist.
• Social factors influence outcomes.
• Family habits can influence how children view pain.
• People that do not see the benefits of an activity will avoid it

Predictive Processing Model

• The brain creates predictions for the causes of sensations that it receives.
• Pain arises from a mismatch between the brain's predictions and the reality that happens.
• The process for an ankle injury involves:
• Sensory input being sent to the brain
• The brain predicting the input (expectation)
• A comparison of the expectation and sensory input.
• The input either confirms danger, and produces pain, or it doesn't
• When raising the heel with no injury:
• Sensory input is sent to the brain
• The brain predicts the input (expectation)
• The expectation is compared to the sensory input.
• This confirms the expectation, and confirms safety, creating no pain output
• When raising the heel with an ankle injury:
• Sensory input is sent to the brain
• There is an error in what is predicted
• A new rule is created because movement is dangerous
• A conformation of danger happens
• Pain is the output
• When raising the heel with no injury initially:
• Sensory input is sent to the brain
• The brain predicts the input (expectation)
• The expectation is compared to the sensory input.
• The expectation equals the sensory input
• This confirms pain will happen

Definitions from prep work of week 1

• Nociception
• Includes the CNS and PNS processing noxious stimuli.
• This involves tissue injury and temperature extremes
• Which activates nociceptors and their pathways
• It is the neural process of encoding noxious stimuli
• Encoding may be automatic (elevated blood pressure) or behavioural (motor withdrawal reflex).
• Allodynia
• Pain from a stimulus that should not normally provoke pain
• The stimulus leads to an unexpectedly painful response.
• E.g. light feather touch causing pain
• Hyperalgesia
  • Is increased pain from a stimulus that normally provokes it.
  • Includes an increased response at a normal threshold.
  • This is a consequence of perturbing the nociceptive system either peripherally or centrally.
• Neuropathic pain
• Caused by a lesion or disease of the somatosensory nervous system.
• Happens when a health condition affects nerves.
• Nociplastic pain
• Pain that arises from altered nociception and no clear evidence.
• No tissue damage
• The activation of peripheral nociceptors
• Sensitisation
• Increased responsiveness of nociceptive neurons to normal input.
• Either as a response or normally subthreshold inputs
• Heightened sensitivity to stimuli that may occur normally in either the central or peripheral nervous system.
• Central sensitisation
• Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input.
• The increased responsiveness comes from the dysfunction of endogenous pain control systems.
• Peripheral sensitisation
• Increased responsiveness and reduced threshold of nociceptive neurons.
• This happens in the periphery to the stimulation of their receptive fields.
• Multidisciplinary treatment
• Multimodal treatment is provided by practitioners from different disciplines
• E.g. the prescription of an antidepressant by a physician alongside exercise treatment from a physiotherapist
• All professions work separately with their own therapeutic aim for the patient and not communicating with each other.
• Chronic pain
• Pain that continues longer than 3 months since onset.
• Acute pain
• Pain that has lasted less than 3 months since onset.

Sensory Afferents

• Αβ fibres
  • Large diameter
  • Highly myelinated
  • Fast conduction Velocity (>40 ms-1)
  • Low Receptor activation Threshold
  • Stimulates light touch, non-noxious, rapid, sharp sensation.
• Aδ fibres
  • Small Diameter (2-5µm)
• Thinly myelinated
• Fast conduction Velocity (5-15ms - 1)
• Medium Receptor activation Threshold (High and low)
• Stimulates Localized nociception sensation.
• C fibres
  • Smallest Diameter (<2µm)
  • Unmyelinated
  • Slow conduction Velocity (<2ms - 1)
• High Receptor activation Threshold
• Stimulates Slow, diffuse, dull nociception sensation.

Mechanoreceptors

• Mechanoreceptors respond to a change in the environment.
• They convert physical energy of specific stimuli into electrochemical energy.
• Touch
• Parts of the skin respond differently.
• Some sensors are more sensitive than others.
• There are sensors that send different messages, being:
  • Where you're touched
    • How hard you're touched
    • Duration of touch

Nociceptors

• Specialised polymodal neurons are sensitive and high threshold.
• Detects and responds to potentially damaging forms of energy: heat, mechanical, and chemical.
• Nocireceptors respond to a change in their environment and generate an action potential.
• When associated with Cutaneous mechanoreceptors
  • A-Delta
  • Noxious mechanical stimulus (actual tissue damage-Hammer strike, etc)
    • Localised nociception
  • Fast conduction Velocity (5-15m/s)
    • Faster than C fibres
  • Projects through Lamina 1 and 5
    • Sometimes 2- never 3,4
  • It synapses directly with second order neurons
  • C fibres
    • Noxious thermal, mechanical and chemical stimuli -Dull, diffuse, aching, burning and delayed pain
    • Slow conduction (0.2-2m/s)
    • Pain Receptors
    • Projects through Lamina 1,2,5 and 10
    • Often synapse indirectly with second order neurons via interneurons

Homunculus

• The homunculus is a 3D map of the somatosensory cortex.
• Body parts sized according to mapping in the brain
• Larger areas have more nerve endings and therefore heightened sensitivity.
• In the sensory strip of the cortex:
• Sensory information like heat or pain, receives information based on body structure
• Sensory signals are posterior
• Motor signals are anterior

Peripheral sensitisation

• Peripheral sensitisation mechanisms damage to tissue initiates a nonspecific inflammatory response.
• Damage to tissue or nerves in the periphery results in localised release of pro-inflammatory mediators
• Bradykinin, histamine, chemokines and cytokines, nerve growth factor (NGF), adenosine triphosphate (ATP), prostaglandin E2 (PGE2)
• This creates acidic conditions. "Soup” is a super acidic environment
• Constant release of these substances can lower the activation threshold of peripheral nociceptors (i.e. sensitisation).
• They trigger action potentials, thus continually activating the nociceptors.
• Sensitisation
  • Constant release of chemicals lower the activation threshold
  • It triggers inflammatory response without too much damage
• The continued activation of nociceptors over time causes transcriptional changes.
• These changes lead to enhanced excitability maintaining sensitisation.
• Where peripheral nerves become more excitable and fire more easily
• These action potentials can cause a release of excitatory transmitters from other branching terminals of the same axon.
• Which elicits the release of inflammatory mediators from adjacent tissue, then excites adjacent nerve endings.
• Spreading any inflammatory responses with neighboring nerves being excited
• Neighboring nerves can be excited and spread the inflammatory response
• Cardinal signs of inflammation:
• Heat
• Swelling
• Redness
• Pain

Central Sensitisation

• Increased outputs from primary afferent terminals increases the excitability of the postsynaptic neurons.
• Either directly or through activation of secondary mechanisms.
  • 1: Development of or increases in spontaneous activity
  • 2: Reduction in the activation threshold by peripheral stimuli
  • 3: Increases responses to suprathreshold stimulation
  • 4: Enlargement of receptive fields
• State of hyper excitability in the CNS
• This includes the dorsal horn of the spinal cord and the brain.
• Central Sensitisation results in:
• The body responding to input from injured or inflamed sites (a sensitive CNS)
• There is a amplified response from regions adjacent to and remote from the injured site ("smudging")

Definitions

• Hyperalgesia: Painful stimuli that was always painful has become more painful.
  • Weight bearing on ankle sprain
  • Decreased pain threshold
  • Increased pain in response to suprathreshold stimuli
  • Spontaneous pain
• Allodynia: Is when non-painful stimuli becomes painful.
  • Slightest twist hurts when it shouldn't
• Somatic Pain.
• Immediate pain that comes because of a reaction to a rapid mechanical stimulus.
• Such as a blow to the body
• OR a extreme hot stimulus
• OR chemical irritation.
• It is usually short duration
• And associated with a withdrawal reflex
• Neuropathic Pain
  • Also known as nerve pain.
  • Happens from injury to the somatosensory nervous system.
• This can be negative signs and symptoms (uncomfortable but not painful)
• Tactile hypoesthesia
• Abnormal sensory response in which sensation is reduced.
• Pinprick hypoalgesia
• Loss of vibration sensation
• There can be positive signs and symptoms
• Paresthesia
• Numbness, tingling, pins and needles
• Dysesthesia
• Abnormal physical touch sensation without outside cause
• Paroxysmal pain Skin redness and warmth and attacks of severe pain in various parts of the body.
• Peripheral mechanisms of neuropathic pain (Ectopic Impulse) Peripheral sensitisation mechanisms are peripheral changes.
• Ectopic impulse generation Messages are firing ectopically
  • The nervous system can get wound up
  • Like a wiring problem
• Those with ectopic impulse generation are safe for them to do things but will hurt a lot
• In injured primary sensory neurons, the diagram shows how changes in sensitivity can lead to action potentials
• In intact primary sensory neurons, messages can still fire without presence of danger
• Central mechanisms of neuropathic pain (e.g., disinhibition) involve:
• Increased glutamate levels
• Synaptic efficacy (plasticity or live wiring)
• Axonal Sprouting
• Disinhibition (+ apoptosis of interneurons)
• Occurs when dorsal horn neurons are more susceptible to activation by excitatory inputs including non-nociceptive A-fibres
• This triggers or maintains central sensitisation
• This happens after nerve lesions

Nociplastic Pain

• Nociplastic pain is third mechanistic pain descriptor apart from nociceptive and neuropathic pain
• Defined as:
• Pain that arises from altered nociception.
• No clear evidence of actual or threatened tissue damage.
• The activation of peripheral nociceptors
• AND disease or lesion of the somatosensory system
• This term is intended for clinical and research use.
• To identify individuals with hypersensitive pain in regions with normal tissues.
• With or without any signs of neuropathy
• The nervous system is plastic when applied in context to Nociplastic pain
• If someone like Bill has nociplastic pain
  • The pain must be shown clearly
  • Bill’s nervous system is adapting and becoming more sensitive
  • It is more sensitive at the ankle
  • And where signals hit the spinal cord
  • And more sensitive at the brain

Self-Report Questionnaires

• Are the most common tools in assessing psychological factors of chronic pain
• Self-Report Questionnaires are beneficial because:
  • Are efficient for data collection.
  • Meaning they can be completed before appointment.
  • Have Normative values for comparison.
  • Can locate patient population to assess whether they've improved or worsened
  • Are Comprehensive
  • And cover more ground than an interview.
  • Assist with diagnosis’
  • Through using screening tools.
• Though there are limitations:
  • Cannot be used for further assessment
    • Only confirms clinically significant change when pre-post treatment

Challenges with Self-Report Questionnaires

• Validity
• Language challenges, or fine motor-skills hinderances, creating concentration barriers
• Some clients may find filling out questionnaires frustrating
• They may also: Affect rapport
• For unexplained reasons
• And can not be used as a substitute for a good clinical interview.
• Self-Report Questionnaires include
• Depression Anxiety Stress Scale (DASS)
• Pain Catastrophizing Scale (PCS)
• Pain Self-Efficacy Questionnaire
• Brief Pain Inventory
• Tamps Kinesiophobia Questionnaire

Kinesiophobia

• Is an excessive, irrational and debilitating fear to carry out a physical movement -Due to a feeling of vulnerability to a painful injury or reinjury.
• This is correlated with pain-related interference
  • Which triggers changes in motor activity. -This influences activities related to pain.
• AND pain-related disability management.
• There are two responses to acute pain:
• 1. confrontation
  • Can provide adaptive responses
• 2. Avoidance
  • And is a maladaptive response
• Both of which are determined by fear of pain
• Maladaptive patterns may lead to:
• Reduction in physical activity and social activities
• Or exacerbate the situation through fear and avoidance behaviour
• Also prolonged disability

Self-Efficacy

• Is a person’s self confidence and capacity to function effectively when in pain.
• How someone achieves what they hope to achieve
• Higher levels of self-efficacy has been linked to lower levels of pain
• AND can reduce disability in patients with chronic pain
• Pain related self-efficacy ratings shift to what's possible .
• After which behaviours are modified for low back pain

Catastrophizing

• Identified as a maladaptive cognitive style
• Is characterized by:
  • Inflating the threat value of pain stimulus
  • Feeling helpless when struggling with pain
  • Ruminating on the experience

Depression

• Someone can be diagnosed with it where either depressed, or lack interest in all activities
• You would you need 5 signs:
• A feeling of being depressed
• A feeling of having very little diminished interest or pleasure in daily activities
• Losing or gaining weight while not dieting.
• Changes > 5%
• Both insomnia or hypersomnia can also be a sign
• Being psychomotor agitated or the opposite
• Fatigue or low energy all day almost all the time
• Feeling of helplessness or guilt every day
• Having a hard time focusing
• Thoughts about death or committing suicide
• Those 5 have to have been present for a long period

Locus of Control

• Refers to as person’s main reasons for events that happen
  • Degree to which people believe they have control compared to other elements
• Someone with a heightened internal locus of control value that they are to blame
• When getting an exam back they would praise themself for performing due to their knowledge
• They would blame the teacher too
• Another person that received the same exam but with a heightened external locus of control would do the opposite
  • They'd blame the teacher because they don't the topic enough

Motor System Changes in Chronic Pain

• Alters movement patterns
  • Chronic pain alters someone’s movement styles
    • Becomes altered -Becomes compensated
• Muscle Weakness and Atrophy Prolonged pain leads to the avoidance of moving or straining certain muscle group -Can perpetuate the experience of long term chronic pain
• Joint Stiffness and reduced ROM
• Pain results in the reduction of the capability to move freely. Which results in restricted movement
• Chronic Sensitisation Where prolonged pain becomes central sensitization
  • Causes hypersensitivity to non-painful stimuli to then become painful

Psychological Factors

• Such as anxiety and mood swings commonly impact
• All leading to painful pain conditions
• Can exacerbate pain if the system is overly in use
  • Results in altered behaviours

Sympathetic Nervous System (SNS)

• SNS role is in responding to acute/chronic pain
• Works the same way that a fight or flight response operates
• In acute stress the nervous systems kicks a fight or flights pathway which releases stress-based hormones
• One is Epinephrine and Norepinephrine that come from adrenal glands
• This activation may alter or interfere with pain perceptions As they can heighten the transmission.

Chronic Pain

• Causes HPA axis to activate more often
• Results in less cortisone in the body
• And Cortisol: is the destructive part of muscle Ensures little glucose runs throughout
• Protein inhibits the continual replacement of bone or calcium
• Causes deterioration
  • All happens due to elevated heart rate and perspiration that comes from the adrenal axis system

HPA Axis Alterations

• The body turns the system back on After some initial changes occur in different stress factors occurring The result = a continuous high that causes dysregulation
• HPA dysregulation alters stress hormones All of which causes deterioration or causes new symptoms of pain to increase.

Pain and Disability

• Have Complex relation to disability
• As pain can limit life functions So it’s hard to manage due to pain and its own impacts
• To treat this requires medical care such as:
• Interventions
• Rehab exercises
• Emotional/ social support.

Within Pain, Neuroscience

• central system is affected in some way That is characterized bz the neurons becoming highly active from signals
• Then starts to be more sensitive on non-active fibres as well
• Avoidant fear causes an anxiety or fear to occur of certain problems
• So many avoid new activities

Maladaptive coping Strategies

Maladaptive coping behaviors may come out as a result

• Such as the fear in exaggerated situations
• That may amplify pain and lead to more disability. Also, some psychosocial changes may also occur such as; • Depression, Which has the capacity to disrupt functions • Or even trigger pain responses to get worse
• Social support and helpful activities would have to take place for any major life shift to occur
• Without a steady support system any functional intensity and impairment can worsen