Pain 1

• Pain involves the brain, spinal cord, and peripheral nerves

Omega 3 Fatty Acids

• Often taken as NHPs for inflammation treatment.
• Theorized to inhibit the arachidonic acid-conversion pathway.

Acute Pain

• Is normal physiology and serves as a warning mechanism.

Assessing Pain as a Symptom

• LATERSNAPS: location, associated symptoms, timing (onset, duration, etc.)
• Ask about the mechanism of injury or pain onset using "how did it start?".
• Determine the severity using "How bad is your pain?".
• Use a scale of 0-10 to quantify pain.
• Use a faces tool for pediatric patients to assess pain.
• Look for associated signs and symptoms (s&s) like fever.
• Determine if the pain is radiating, and check for referred pain.

Nervous System Communication

• The nervous system (NS) includes the central nervous system (CNS) and the peripheral nervous system (PNS).
• The CNS consists of the brain and spinal cord.
• The PNS consists of nervous tissue outside the CNS and the enteric nervous system (ENS).
• The PNS includes sensory information in the afferent division
• Motor commands come from the efferent division

Sensory Receptors

• Special sensory receptors monitor smell, taste, vision, balance and hearing.
• Visceral sensory receptors monitor internal organs.
• Somatic sensory receptors monitor skeletal muscles joints and skin surface.
• Examples: Ruffini's endings, Pacinian corpuscles, Krause's end bulbs, Meissner's corpuscles, Merkel disks, root hair plexus

Afferent Pathway

• This involves sensory information from the PNS to the CNS.
• It starts at the sensory receptor in a specific body part and ends in the CNS's somatosensory cortex.
• The sensory impulse must be strong enough to reach a threshold to initiate an action potential.
• If the impulse is not strong enough, there is no action potential and no pain message.
• Nociceptors (in skin, bones, blood vessels, visceral organs) lead to the 1st order neuron (PNS).

PNS to CNS Communication

• Nociceptors use A or C nerve fibers of the PNS, leading to the 1st order neuron then to the spinal nerve and the dorsal root and ganglion.
• Posterior horn synapse ('substance P' neurotransmitter) leads to the 2nd order neuron.
• This neuron decussates (crosses over) and ascends the spinal cord's white matter column via the 'spinothalamic tract' (lateral).
• This tract goes to the thalamus ('relay station') and synapses with a 3rd order neuron.
• It ends up at the somatosensory cortex in the brain for localization.

Sensory Homunculus

• Maps the cortex region per anatomical body part based on innervation numbers.
• Somatosensory association areas link the sensation to previous experience.

Stimuli and Pain Awareness

• Large stimuli can trigger many or all receptors resulting in high awareness of pain.
• Examples include trauma (tissue tearing), pressure receptors, free nerve endings, and temperature changes.

Non-Pharmacological Techniques

• Decrease inflammation & sensation through ice in the PNS
• Alleviate the trigger: massage and physiotherapy in the PNS
• Change the sensation through distraction/behaviour modulation in the CNS via CBT and activities

Pain Terminology

• Location:
  • Visceral pain is deep and organ-related.
  • Cutaneous pain is superficial and surface-related.
  • Referred pain is due to body surface innervated by the same spinal nerve/nerve plexus + interneuron communication.
• Reflexes include withdrawal reflex.
• Chronic pain is persistent pain.
• Neuropathic pain is persistent nerve irritation and is difficult to treat:
  • Allodynia (pain caused by a non-painful stimulus)
  • Hyperalgesia (hypersensitivity to a painful stimulus)
  • Paresthesias ('pins & needles')
  • Can occur with decreased perfusion of a nerve, positional.
• Phantom pain is neuropathic pain post amputation:
  • The spinal cord neurons are still active despite the lack of stimulus (no nociceptor) and interneurons are still communicating pain.
  • Often leads to chronic pain.

Dermatomes

• Cutaneous segments are serviced by the same spinal nerve.
• Used in clinical assessment to determine sensory and motor pathways.

Reflexes

• Flexor 'withdrawal' reflex involves stimulus (sharp pain) leading to reflex to withdraw without cerebral control.
• Activation of a sensory neuron (afferent), interneuron (at level of stimulus in CNS), and automatic activation of a motor neuron (efferent) for response by the effector; awareness.

Acute versus Chronic Pain

• Acute pain lasts less than 10 days.
  • Self-limiting.
  • Endogenous modulators are secreted and can persist, improving SNS responses.
  • Innate protective mechanism and appropriate treatment is often effective.
• Chronic pain lasts more than 6 months.
  • It likely travels along C fibres.
  • It involves neurogenic inflammation.
  • It can be an outcome of under-treated acute pain, chronic inflammatory disorders.
  • Is not self-limiting.
  • Endogenous modulators are absent.
  • SNS responses are not active.
  • It is a destructive mechanism that is not beneficial to the host and yields other dysfunctions (insomnia, anxiety, anorexia, depression, etc.).
  • Treatment requires many modalities (e.g., CBT).

Endogenous Neurotransmitter Modulators

• Are 'neuromodulators' and use an efferent pathway.
• Endogenous opioid peptides include endorphins, enkephalins, and dynorphins.
• Serotonin & norepinephrine:
  • Released from the CNS (hypothalamus, limbic system, reticular formation).
  • Use a descending pathway.
  • Bind opioid receptors (mu, kappa, delta) to inhibit substance P.
• Substance P: excitatory CNS neurotransmitter that propagates pain input.

Pain Gate Theory

• Pain signals can be interrupted in the substantia gelitanosa of the spinal cord acting as a "gate".