Week 1 - Lecture 2 - Pain pathways and management Flashcards
What are the conditions for pain?
Strength of Stimulus - the stronger the stimulus, the less the patient is able to tell where the pain is
Position of the Painful Structure - pain is referred distally
Depth from the Surface - more superficial lesioned tissue, the more precise is its
localizing ability
Nature of the Affected Tissue - nerve root versus peripheral nerve
Does a single nerve behave in a “all or none” phenomenon?
YES
- A single nerve behaves in a ‘all or none’ phenomenon
- Action potentials occur completely or not at all
- A strong stimulation does not produce a stronger impulse
- A strong stimulation may produce a higher frequency of firing impulses
- Nerve injury results in the sprouting of new terminals as part of the normal process of peripheral nerve regeneration
- New extensions may be hyperexcitable and exhibit abnormal electrical discharges
What is referred pain? Why does that happen?
- WHAT: an error in perception by the sensory cortex in the brain as to the source of the painful stimulus (i.e., felt elsewhere than its true site)
- WHY: cutaneous, visceral, and skeletal muscle nociceptors converge on a common nerve root of the spinal cord, but brain interprets as cutaneous (higher proportion)
Uneven distribution of free nerve endings, leading to confusion in perception of where pain actually is.
Example: pain in left arm from heart attack.
What are dermatomes?
an area of skin in which sensory nerves derive from a single spinal nerve root
What is the difference between a dermatome and a myotome (key muscle)?
A myotome is the group of muscles that a single spinal nerve innervates. Similarly a dermatome is an area of skin that a single nerve innervates.
Explain the link between a dermatome and pain.
- Projects more distally than the key muscle (myotome)
- Dermatome and key muscles develop from the same segment
- Any structure within a particular segment can refer pain to the same dermatome of that segment
- It may refer along the whole length of the dermatome or only part of it
- Pain is generally referred in a distal direction, thus the structure at fault will be located proximal to where the patient feels the pain
What is root pain?
- Irritation of nerves and nerve roots
- Deep, sharp and well localized
- All root (radicular) pain is referred, but not all referred pain is root pain
- L3 nerve root = knee pain, but so does Hip OA.
What is acute pain?
- Results from injury or disease that causes, or can cause, tissue damage
- E.g., infection, trauma, metabolic disorder progression, degenerative disease
- Protects against further tissue damage
- 3 to 6 weeks
What is subacute pain?
- Similar to acute pain occurring later in the process
- Continues to protect against damage
- 6 weeks to 3-6 months
What is chronic pain?
- Persists beyond the normal time expected for healing of injured tissue
- Associated with structural and functional changes in the central nervous system
- No longer a symptom or protective
- over 3-6 months
What are the different stimulus or sources of pain?
- Chemical Sources
- Substances that are released with tissue injury (space occupying)
- Ie inflammation. Histamines,
- Mechanical Sources
- Normal Stress on Abnormal Tissue
- eg. Movement with a patient just out of cast (normal/small ROM)
- Abnormal Stress on Normal Tissue
- Not necessary for pathology to be present for pain to be produced
- •eg. Bend finger back and hold it.
- Normal Stress on Abnormal Tissue
Fill in the blanks.
What is upregulation and sensitization?
Nociceptive system is usually very quiet
When injury activates the system, a relatively innocuous stimuli can trigger pain perception
- Events that were not painful before become painful
***1. Cortical reorganization >
- Central sensitization
- Peripheral sensitization
What is the difference between nociceptive pain and neuropathic pain?
Nociceptive pain: normal pain response
Usually aching or throbbing and well-localized, time limited (resolved once the tissue heals), responds well to analgesics
Neuropathic pain: nerve damage (e.g., abnormal firing, increased signal to brain)
Tingling, shock-like or burning pain, usually chronic and responds poorly to conventional analgesics
Name a few types of neuropathic pains and explain what it is.
Hyperalgesia: increased pain from a stimulus that normally provokes pain = more pain
Allodynia: pain due to stimulus that does not normally provoke pain > now = earlier pain
What is neuropathic pain?
- A direct consequence of a lesion or disease affecting the somatosensory system
- Often experienced in parts of the body that otherwise appear normal
- Generally chronic, severe and resistant to over-the-counter analgesics
- May result from various causes that affect the brain, spinal cord and peripheral nerves, including:
- Complex Regional Pain Syndrome (II) > post injury, response altered,
- Diabetic Neuropathy
- Phantom Limb Pain
- Post-Stroke
- There is almost always an area that has a sensory deficit and within it is the area of maximum pain
- Pain may be spontaneous or evoked (e.g., allodynia, hyperalgesia, hyperpathia)
- Often the stimulus/response relationship is unclear
- The quality of the pain is described as burning, electric shock, shooting and dysesthesia (abnormal)
- *
What are the known mechanisms of neuropathic pain?
- Ectopic impulse generation
- Response to activity in adjacent nerves
- Changes in sensitivity
- Peripheral (3 types)
- Central
- Chemical property changes
- Neuroanatomical reorganization
What are ectopic impulses?
Stimulation independent
Neuroma – high density of regenerated nerve endings
Friction between nerves and rigid structures (e.g., musculoskeletal)
Sustained compression
****Not sure why D image is there
What is ephatic-coupling?
A mechanism in which neurons, that would otherwise operate in isolation, communicate via extracellular electrical signals
Within the same peripheral nerve
Explain the two different types of ephatic coupling.
Physical Proximity
Action potentials traveling down a motor nerve can trigger impulses in a sensory nerve, where unmyelinated
Chemical
Noradrenaline responsive fibres triggered by sympathetic activation
What is peripheral sensitization?
Increased afferent nociceptor input to the CNS
Increasing pain signals that could occur through:
- Spontaneous firing, not requiring a signal
- An easier threshold to reach
- Increased firing frequency
1st afferent has been modified in sending of AP’s, Gate keeper cells cant keep up, causes increased signal, and more pain results in the brain.
What are chemical mediators?
Trauma> Inflammatory Response>
Chemical Influence on Afferent Neuron Impulse
What is the mechanism of reduce response threshold?
Chemicals released in response to tissue trauma will bind to ion channels in the membrane to alter permeability and excitability
Indirect influence through 2nd messenger system
(altered pH of the tissue)
Inhibition of after-hyperpolarization
**in general = Prevents hyperpolarization from occurring causes more easily secondary firing of AP/neuron
What is the mechanism of recruit silent nociceptors?
A large portion of A(delta) and C fibers are insensitive in normal, non-injured, non- inflamed tissues
No firing in ~ 1/3 of nociceptive specific neurons
Injury releases inflammatory mediators to trigger their sensitivity to mechanical stimuli
Mediators cause increase in positivity, more and more over time = silent nociceptors turned on,
Inability to turn off again to chronic pain (simulated tissue damage)
What is the mechanism of phenotype change?
Altered neuron type (nerve (arrow) pain fibre)
- Non-nociceptive to nociceptive
Transcription changes occur within the cell
Stimulation now interpreted as pain
- Once was perceived as light touch/vibration
Type of afferent can actually change cellular makeup to become painful source.
Explain the chemical property changes mechanism. (central sensitization)
Chemicals release from nociceptive afferents induce changes in properties of spinal cord neurons
WDR (wide dynamic range) and NS neurons change firing patterns with non-noxious stimuli
NS fire like WDR when central sensitization occurs
Reduced threshold firing
***WDR: wide dynamic range- tends to be more sensitive because they respond to multiple signals - tends to fire faster
NS: neuro specific neurons
Explain the neuroanatomy reorganize mechanism (central sensitization).
Reorganization of the cortical sensory map.
Sprout nerves to connect to pain pathways
Changes their interpretation
Continual stimulation of A(delta)and C fibres leads to Aβ fibre changes
- Now binding to same sites, enhancing pain response to something like light touch
Explain the enhanced withdrawal reflex
RECIPROCAL INHIBITION
Collateral branches of the afferent fibres synapse on inhibitory interneurons that suppress the activity of motor neurons innervating antagonist muscles
CROSS EXTENSOR RESPONSE
If the stimulated part is a limb, the response includes extension of the opposite limb
Explain the vicious cycle model.
A simple model
- An abnormality in structure, posture, movement or stress results in pain that reflexively leads to muscle hyperactivity
- Increased sensitivity of muscle spindle afferents
- Increased muscle stiffness
- Increased muscle metabolite production
- Spasm or fatigue = further pain, dysfunction
Explain the pain adaptation model.
More complex – pain does not arise from the muscle itself
- —Increased inhibition of agonist motor units
- +++Increased facilitation of antagonist motor units
- —Overall reduced maximum force output of agonist
What are some examples of physiological/quantitative?
Pressure
- Apply pressure against the skin and increase pressure until the individual reports that it is painful
Monofilaments (measure for allodynia > experience pain with the lower stimulus)
- Wires with increasing thickness that are pressed against the skin until wire bends
- Greater wire thickness requires greater pressure to bend wire
