Module 1 - Pain

Pain Basics

• Pain is triggered by noxious stimuli as an unpleasant sensation, either sensory or emotional.

Types of Pain

• Fast pain is sharp, highly localized, and rapidly perceived.
• Slow pain is diffuse, dull, hard to localize, includes aching/throbbing, has delayed perception while increasing over time.
• Acute pain lasts less than 6 months
• Chronic pain lasts longer than 6 months.
• Productive pain correlates to tissue damage, serving as a warning of injury, it wanes as damage resolves and is accompanied by sympathetic nervous system responses.
• Non-productive pain doesn't warn of injury, has a cause difficult to identify, and is often accompanied by stress and depression.
• Somatic pain arises from somatic structures.
• Visceral pain arises from organs and involuntary body structures.
• Inflammatory pain occurs in the presence of inflammation.
• Neuropathic pain is associated with damage or disease of the somatosensory system.

Aδ and C Fibers

• Both Aδ and C fibers are nociceptive neurons.
• Myelinated Aδ fibers transmit sharp, well-localized pain.
• Unmyelinated C fibers transmit dull, aching pain that is difficult to pinpoint.
• Both travel from target tissue, past cell bodies in dorsal root ganglia, to dorsal horn of the spinal cord, synapsing in specific layers (lamina) onto ascending fibres, travelling primarily to the thalamus and to structures in the brain stem (via the spinothalamic and spinorecticular tract).

Nociception vs. Pain

• Nociception is the readily quantifiable neuronal signals alerting the brain to an injury.
• Pain cannot be quantified and is influenced by circumstances and emotional context.

Physiological Characteristics of Itching

• Puritoceptive itch is generated in the skin when there is inflammation or in response to tissue damage, associated with protection and avoidance of noxious stimuli.
• Neurogenic itch is secondary to organ diseases like renal or liver disorders.
• Psychogenic itch is associated with mental health illnesses.
• Neuropathic itch results from central or peripheral nervous system dysfunction in the absence of physiological stimuli.

Role of Change in Threshold of Nociceptive Neurons

• Release of neurotransmitters helps sensitize high-threshold neurons to easily activated low-threshold neurons.
• Increased sensitivity of nociceptive neurons at the injury site persists during healing, reversing as healing nears completion.

Hyperalgesia and Allodynia

• Allodynia is when something non-painful causes pain, such as walking on a sprained ankle.
• Hyperalgesia is when a small injury causes greater pain, such as banging a sprained ankle.

Productive vs. Non-Productive Pain

• Productive pain serves as a warning of injury, occurring instantly.
• Non-productive pain does not serve as a warning of injury, describing the ongoing pain experience.

Subjectivity of Pain

• When nociceptive information is received, the sensory cortex assesses the circumstances surrounding the injury, as do emotional structures.
• Memory and emotional information combine to provide an assessment of the person's emotional context.
• Sensory, emotional, and memory information is summed with nociceptive signals to allow the brain to decide how to proceed.

Descending Inhibitory Pathways

• Descending inhibitory pathways serve to terminate nociceptive signaling in the dorsal horn of the spinal cord, allowing the brain to conduct necessary activities in the absence of pain, prioritizing survival.

Pain Gate Mechanism

• The substantia gelatinosa, located at the top of the dorsal horn, controls nociceptive signaling.
• The pain gate mechanism is a system within the spinal cord, substantia gelatinosa of dorsal horn, and acts as a gate to control the transmission of pain signals to the brain.
• Neurons within the substantia gelatinosa receive input from both large and small sensory fibres acting as a 'switch' to modulate the transmission of pain signals based on the balance of activity between these fibres.
• Non-painful, large fibre stimulation alters activity of interneurons in substantia gelatinosa, preventing pain signals from travelling to the brain (closing the gate).
• Strong activation of small pain fibres e.g. intense noxious stimuli, "opens" the gate allowing pain signal to travel to the brain.

Neuropathic vs. Chronic Pain

• Neuropathic pain arises from nerve damage within the nervous system, causing abnormal pain signals, and feels like electric shocks, pins and needles, or burning sensations, and can be triggered by light touch or temperature changes.
• Chronic pain stems from various sources that includes muscles, joints, or organs, feels like a dull ache, soreness, or throbbing, and can be triggered by movement or specific activities related to the affected area.

Wind-Up

• Spinal neurons subjective to repetitive or high-intensity nociceptive impulses become progressively and increasingly excitable.
• This occurs even after the stimulus is removed.

Pain Transmission Pathway

• Damaged cells in peripheries release neurochemicals and substances (e.g. histamine, substance P, prostaglandins) into the tissue where they stimulate.
• Nociceptors depolarize, sending an action potential from the damaged area in the periphery, along the first order neuron, into the spinal cord where it synapses.
• Two types of first order neurons exist: fast and slow fibres
• The first order neuron synapses with a second order neuron in the dorsal horn of the spinal cord
• The action potential arriving in the dorsal horn releases neurochemicals, stimulating the second order neuron to depolarize, which then travels along the second order neuron, crossing to the opposite side of the spinal cord, then heads upwards towards the brain via the spinal thalamic tract.
• The second order neuron synapses in the thalamus of the brain with the third order neuron.
• They then travel to multiple areas of the brain such as cortex, cortical regions.

Pain Gateway & Modulation

• The substantia gelatinosa (SG) is an anatomical region in the dorsal horn of the spinal cord, is moving forwards = pain gateway, where action potentials go into the SG and synapse in different laminae.
• Termination of primary neuron and activation of secondary neuron occurs in SG, forming the gate.
• PAG - peri acuductal grey, is an anatomical region within the midbrain that's stimulated by the arrival of the second action potential from the spinal thalamic tract.
• The PAG then sends a descending action potential signal back down the spinal cord via another tract, synapsing in the dorsal horn where it releases neuromodulating chemicals to dampen transmission through the SG.
• This decreases the amount of first order action potential transmission through the SG, meaning fewer action potentials come up the spinal thalamic tract = less pain arrives at brain, less pain when passed onto higher orders in the cortex, forming the ascending excitatory pathway.
• Endogenous opioids (endorphins) are main neuromodulating chemicals released by PAG to dampen down conduction, closing the gate to reduce pain to the brain.

Key Pain Definitions

• Pain: An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.
• Allodynia: Pain due to a stimulus that does not normally provoke pain.
• Analgesia: Absence of pain in response to stimulation which would normally be painful.
• Anaesthesia Dolorosa: Pain in an area or region which is anaesthetic.
• Causalgia: Syndrome of sustained burning pain, allodynia and hyperpathia after a traumatic nerve lesion, often combined with vasomotor and sudomotor dysfunction and later trophic changes.
• Dysesthesia: Unpleasant abnormal sensation, whether spontaneous or evoked.
• Hyperalgesia: Increased pain from a stimulus that normally provokes pain.
• Hyperesthesia: Increased sensitivity to stimulation, excluding special senses.
• Hyperpathia: Painful syndrome characterized by an abnormally painful reaction to a stimulus, especially repetitive stimulus as well as an increased threshold.
• Hypoalgesia: Diminished pain in response to a normally painful stimulus.
• Hypoesthesia: Decreased sensitivity to stimulation, excluding special senses.
• Integrative pain care: Coordinated and evidence-based management which applies both conventional and traditional/complementary approaches by a team, including the person being treated.
• Interdisciplinary treatment: Treatment provided by a multidisciplinary team collaborating in assessment and treatment using a shared biopsychosocial model and goals.
• Multidisciplinary Treatment: Multimodal treatment provided by practitioners from different disciplines.
• Multimodal Treatment: The concurrent use of separate therapeutic interventions with different mechanisms of action within one discipline aimed at different pain mechanisms.
• Neuralgia: Pain in distribution of a nerve or nerves.
• Neuritis: Inflammation of a nerve or nerves.
• Neuropathic pain: Pain caused by a lesion or disease of the somatosensory nervous system.
• Central Neuropathic Pain: Pain caused by a lesion or disease of the central somatosensory nervous system.
• Peripheral Neuropathic Pain: Pain caused by a lesion or disease of the peripheral somatosensory nervous system.
• Neuropathy: A disturbance of function or pathological change in a nerve: in one nerve, mononeuropathy; in several nerves, mononeuropathy multiplex; if diffuse and bilateral, polyneuropathy.
• Nociception: The neural process of encoding noxious stimuli.
• Nociceptive Neuron: A central or peripheral neuron of the somatosensory nervous system that is capable of encoding noxious stimuli.
• Nociceptive Pain: Pain that arises from actual or threatened damage to non-neural tissue and is due to the activation of nociceptors.
• Nociceptive Stimulus: An actually or potentially tissue-damaging event transduced and encoded by nociceptors.
• Nociceptor: A high-threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli.
• Nociplastic Pain: Pain that arises 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.
• Noxious Stimulus: A stimulus that is damaging or threatens damage to normal tissues.
• Pain Threshold: The minimum intensity of a stimulus that is perceived as painful.
• Pain Tolerance Level: The maximum intensity of a pain-producing stimulus that a subject is willing to accept in a given situation.
• Paraesthesia: An abnormal sensation, whether spontaneous or evoked.
• Sensitisation: Increased responsiveness of nociceptive neurons to their normal input, and/or recruitment of a response to normally subthreshold inputs.
• Central Sensitisation: Increased responsiveness of nociceptive neurons in the central nervous system to their normal or subthreshold afferent input.
• Peripheral Sensitisation: Increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields.
• Unimodal Treatment: Single therapeutic intervention directed at a specific pain mechanism or pain diagnosis.

Nociceptive Pain

• Nociceptive Pain, the most common type, is produced by nociceptive stimuli with the potential to cause peripheral tissue damage.
• External damage characteristics:
  • Usually involves trauma to the skin but can extend to underlying issues.
  • Relatively mild.
  • Pain lasts from a few seconds to a few days.
  • Treatment is generally simple interventions.
  • Pain relief uses mild analgesics, e.g. NSAIDS.
• Internal damage characteristics:
  • More severe than external damage
  • Caused by severe trauma, e.g. fractures, surgery or childbirth
  • Lasts longer than external injury lasting days to weeks.
  • Treatment generally involves removing the cause of tissue damage.
  • Management can involved more powerful opioid analgesics.

Neuropathic Pain

• A type of pain caused by an injury/disease of the nervous system.
• It is generally more severe and can last from months to years.
• Treatment is challenging but pharmacological interventions and specialized ongoing therapies can alleviate pain.

Psychogenic Pain

• This is pain that appears to have no underlying pathology e.g. headaches, abdominal pain, back pain).
• It can be debilitating and interfere with ones ability to function normally
• In absence of physical causes, it is assumed that it is a result of a psychological disorder.

Epidemiology of Pain Presentations

• Jennings Paper (VIC):
  • 55% of paediatrics with severe pain did not receive analgesics.
  • The lower the age, the less likely of receiving opioids for pain.
  • Communication (type/severity/aetiology of pain) can be a barrier when dealing with paediatrics with pain
  • It is harder to quantify a child’s pain making you less likely to use opioid medication.
  • Risk of amount of opioid medication administered and lack of training for paramedics can also cause these barriers leaving to a lack of comfort with children.
• Bendall, Simpson & Middleton Paper (NSW):
  • 87% of people received a single analgesic in an acute pain episode
  • Contemporary guidelines indicated polymodal analgesic therapy is best, e.g. fentanyl and ibuprofen together due to different properties.