Chapter Two - Pain and Management Flashcards

1
Q

There are 3rd order neurons to several areas of the brain. What are their roles?

A
  • Planning
  • Sensory discrimination
  • Memory
  • Emotion
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2
Q

Describe the Gate Control Theory.

A

Possible brain modulation, not just a passive system• Includes descending pathways

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3
Q

What are endorphins?

A

Endogenous opioids released within the brain and spinal cord

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4
Q

What is the Neuromatric Theory?

A

Varied dimensions that overlap to create a unique experience

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5
Q

What are the four components of pain?

A

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

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6
Q

What is referred pain? Why do we have it?

A

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)

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7
Q

What is the difference between segmental and extrasegmental referred pain?

A

SEGMENTAL: pain referred to a structure within the same dermatome

EXTRASEGMENTAL: pain referred to >1 dermatome (multiple levelsàsevere)

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8
Q

In one sentence, what is a dermatome?

A

An area of skin in which sensory nerves derive from a single spinal nerve root

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9
Q

Where does the dermatome project? Where can pain refer alon a dermatome? In what direction, usually?

A

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

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10
Q

What is root pain? Is all root pain referred? Is all referred pain root pain?

A

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

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11
Q

What is acute pain? Give examples. What is its role?

A

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

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12
Q

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.

What kind of pain is this?

A

Acute pain

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13
Q

What is subacute pain? What is its purpose?

A

Similar to acute pain occurring later in the process

Continues to protect against damage

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14
Q

Similar to acute pain occurring later in the process

Continues to protect against damage.

What kind of pain is this?

A

Subacute pain.

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15
Q

What is chronic pain? What is it associated with? Does it have a role?

A

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

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16
Q

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.

What kind if pain is this?

A

Chronic

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17
Q

Give two kinds of stimulus or source of pain, and one example for each.

A

Chemical Sources

• Substances that are released with tissue injury (space occupying)

Mechanical Sources

  • Normal Stress on Abnormal Tissue
  • Ex: movement with a patient just out of a cast
  • Abnormal Stress on Normal Tissue
  • Not necessary for pathology to be present for pain to be produced

•Ex: bend finger back and hold it

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18
Q

Fill out this graph:

Mechanical pain / Chemical pain

Frequency of pain

Effect of Altered Position or Movement

Quality of the Pain

Heat, Redness and/or Swelling

Effect of Rest

Irritability

Effect of Anti- Inflammatory Meds

Effect of Exercise or Manual Therapy

A

Mechanical pain / Chemical pain

Frequency of pain : intermittent / constant

Effect of altered position or movement: Pain increases or decreases with certain positions or movements / pain not altered by position or movement (worsens)

Quality of the pain : sudden, sharp twinges / pulsating, throbbing

Heat, redness and or swelling: None/ Common (signs of inflammation)

Effect of rest: Better after prolonged rest/ stiff and sore after prolonged rest

Irritability : Low to moderate / Moderate to high

Effect of anti-inflammatory meds: no effect (need for relief of the mechanism) Better

Effect of exercise or manual therapy: Effective / often not effective (thermal modalities)

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19
Q

How can upregulation and sensitization happend?

A
  • 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
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20
Q

What is nociceptice pain? What are its characteristics?

A

Nociceptive pain: normal pain response
• Usually aching or throbbing and well-localized, time limited (resolved once the tissue heals), responds well to analgesics

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21
Q

What is neuropathic pain? What are its characteristics?

A
  • Neuropathic pain: nerve damage (e.g., abnormal firing, increased signal to brain). It is a direct consequence of a lesion or disease affecting the somatosensory system
  • Tingling, shock-like or burning pain, usually chronic and responds poorly to conventional analgesics
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22
Q

What is hyperalgia?

A

Hyperalgesia: increased pain from a stimulus that normally provokes pain

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23
Q

What is allodynia?

A

Allodynia: pain due to stimulus that does not normally provoke pain

24
Q

What could cause neuropathic pain? Explain and give examples.

A

May result from various causes that affect the brain, spinal cord and peripheral nerves, including:

• Complex Regional Pain Syndrome (II)

  • Diabetic Neuropathy
  • Phantom Limb Pain
  • Post-Stroke

Often experienced in parts of the body that otherwise appear normal

Generally chronic, severe and resistant to over-the-counter analgesics

25
What are the two areas usually found in neuropathic pain?
There is almost always an area that has a sensory deficit and within it is the area of maximum pain
26
How could neuropathic pain be desribed by the patient?
Pain may be spontaneous or evoked (e.g., allodynia, hyperalgesia, hyperpathia) The quality of the pain is described as burning, electric shock, shooting and dysesthesia \*\*Often the stimulus/response relationship is unclear
27
Name the three known mechanisms for neuropathic pain
Known mechanisms include: Ectopic impulse generation Response to activity in adjacent nerves Changes in sensitivity
28
Describe the ectopic impulses theory
Stimulation independent Neuroma – high density of regenerated nerve endings Friction between nerves and rigid structures (e.g., musculoskeletal) Sustained compression
29
Describe the "response to adjacent nerves" theory. What is the main mechanism called? What are the two ways that this mechanism can happend?
Ephatic-coupling * A mechanism in which neurons, that would otherwise operate in isolation, communicate via extracellular electrical signals * Within the same peripheral nerve Two ways: 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
30
What is enhanced mechanosensitivity? What are the two main types of sensitization?
Increased chemical concentrations are not necessarily enough to illicit activity, but do increase sensitivity Pressure or stretch may elicit an action potential (stimuli not typical for generating a response) Peripheral sensitization (or primary) – peripheral nerve endings Central sensitization (or secondary) - spinal cord and brain centers
31
Describe peripheral sensitization. What are the three ways in which the increase could happend?
* Increased afferent nociceptor input to the CNS. Peripheral sensitization causes the amount of pain that you feel to be out of proportion to the extent of your injury * Increasing pain signals that could occur through: * Spontaneous firing, not requiring a signal• An easier threshold to reach * Increased firing frequency
32
In peripheral sensitization, what is the role of the chemical mediators after a trauma?
Trauma Inflammatory Response Chemical Influence on Afferent Neuron Impulse
33
What are the three pathways that peripheral sensitization could go through?
• Trauma triggers an inflammatory response – chemicals to affect afferent pathways Reduced response thresholds Recruitment of silent nociceptors Phenotype change
34
Describe the reduced reponse threshold pathway of peripheral sensitization.
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
35
Describe the recruit silent nociceptors pathway of peripheral sensitization.
* A large portion of Ad 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 increase +ve, more and more +ve over time) Inability to turn off againàchronic pain (simulated tissue damage)
36
Describe the phenotype change pathway of peripheral sensitization.
* Altered neuron type (nerve -\> pain fibre) * Non-nociceptive to nociceptive The actual type of afferent nerve can change cellular makeup to become a more painful source It occurs at the cellular levels Transcription changes occur within the cell Stimulation now interpreted as pain • Once was perceived as light touch/vibration
37
What is central sensitization? What is it initiated by?
* An aspect of neuroplasticity (i.e., brain changes with experience) * Describes the changes at the cellular level which support neuroplastic changes in * Spinal cord * Supraspinal centres Your getting changes in your brain from the peripheral nociceptors Describes the changes at the cellular level… Spinal cord Supraspinal cord • Initiated by high activity levels the in peripheral nociceptors leading to activity- dependent increases in excitability of nerves in the spinal cord
38
What are the two mechanisms of central sensitization called?
Chemical property changes Neuroanatomical reorganization
39
Describe the chemical property changes pathway of central sensitization.
Chemicals release from nociceptive afferents induce changes in properties of spinal cord neurons Wide Dynamic Range (WDR) and NS neurons change firing patterns with non-noxious stimuli NS fire like WDR when central sensitization occurs Reduced threshold firing, increased rate of firing WDR: wide dynamic range- tends to be more sensitive because they respond to multiple signals - tends to fire faster NS: neuro specific neurons
40
Describe the neuroanatomy reorganiszation pathway of central sensitization.
Reorganization of the cortical sensory map Sprout nerves to connect to pain pathways Changes their interpretation Continual stimulation of Ad and C fibres leads to Aβ fibre changes
41
Why as clinicians should we be aware of sensitization?
BAD NEWS * The nervous system changes in response to pain * It becomes more sensitive to pain * What may be considered “excessive” pain behaviours may actually reflect sensitization of the nociceptive system GOOD NEWS • The nervous system changes in response to experience or intervention
42
What is somatomotor dysfunction?
* Central nociceptive neurons synapse with other, non-nociceptive neurons * Upregulation (prolonged pain)àchanges in motor behaviour
43
What is hyperalsthesia?
Hyperalsthesia = it is almost similar to hyperalgesia but it is stronger
44
What are the three pathways of somatomotor dysfunction?
Enhance withdrawal reflex Vicious cycle model Pain adaptation model
45
Two things can happen during enhanced withdrawal reflex. What are they called and how do they work?
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 (Muscle Stretch Reflex)
46
Describe 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 fatigueàfurther pain, dysfunction
47
What is the pain adaptation model?
• More complex – pain does not arise from the muscle itself
48
As physiotherapists, it is important to note that a pain assessment does not mean we:
• Rely on changes in vital signs only * Decide that a patient does not “look in pain” * Know how much a procedure or disease “should hurt” * List types of pain descriptions assuming it will be one of them * Assume a sleeping patient does not have pain * Assume a patient will tell you when they are in pain
49
What are the purposes of pain assessment?
* Diagnosis * Prognosis * Track changes over time (numeric rating scale) * Assist in clinical decision making – quality and type of pain to determine Rx
50
What are some things you could be looking for during a pain history assessment?
Pain Characteristics – onset, duration, location, quality, intensity, associated symptoms, exacerbating and relieving factors [OPEN ENDED QUESTIONS!] Past and current management therapies Relevant medical and family history Psychosocial history Impact of pain on daily life – work, daily activities, personal relationships, sleep, appetite, emotional state Patient (and family’s) expected goals for treatment * ASK the patient about their pain (consider the ICF model) * Asking about ADL’s and IADL’s * Asking about physical activity, mood, sleep, appetite, energy level * Identify THE PATIENT’S preferred pain terminology * Hurting, aching, stabbing, discomfort, soreness * Use a pain scale that works for the individual * Insure understanding of its use * Modify sensory deficits
51
What are three types of pain assessment?
* Self-report assessments * Behavioural assessments * Physiological/quantitative sensory assessments
52
Give two examples of self-report pain • Visual Analog Scaleassessments.
* Visual Analog Scale * Questionnaires * E.g., McGill Pain Questionnaire (MPQ) * Select a word to describe pain * Each word has a separate score * Includes all dimensions of the pain experience
53
How do you conduct behavioural pain assessments?
• Observation of painful behaviours * Bracing * Guarding * Facial grimacing * Exaggerate pain behaviours – inappropriate to use subjective ratings * Exaggerated in populations with poor communication (e.g., paediatrics, dementia)
54
How do you conduct physiological/quantitative pain assessments (two ways)? Which procedure is more appropriate for which type of neuropathic pain?
Pressure (measure for hyperalgesia) • Apply pressure against the skin and increase pressure until the individual reports that it is painful Monofilaments (measure for allodynia) * Wires with increasing thickness that are pressed against the skin until wire bends * Greater wire thickness requires greater pressure to bend wire
55
The use of drugs in clinical practice encompasses a wide variety of activities including:
* prescribing * compounding * dispensing * administering * advising * selling Restricted by physiotherapy provincial and federal legislation
56
Use of drugs in clinical practice: there are a number of factors at play:
Access to information means patients are more informed and empowered to ask for additional information PTs are primary care providers, and as the first and sometimes only point of contact, PTs are being asked for advice related to OTCs OTCs do not require a prescription, so they are often seen as less risky and many PTs believe their education and experience is either adequate to provide advice or at a minimum, is better than nothing Consumers are expected to make decisions about their self care regarding OTCs and when they do, they assume personal responsibility When physiotherapy health care providers make a recommendation about OTCs, then greater weight gets put behind that advice HOWEVER! The wide margin of safety for OTCs does not preclude harm to patients or exemption from liability for physiotherapists should harm occur
57
Meds and scope of practice: considerations:
Some jurisdictions prohibit administering, recommending and/or selling OTCs (BritishColumbia, Manitoba and Nova Scotia) If your jurisdiction does not prohibit administering, recommending, and/or selling OTCs, this does not mean you should do it just because you can - consider patient interests over your own interests If you do decide to administer, recommend and/or sell OTCs, consider your scope of practice, your personal competence, patient risk, professional liability and appropriateness – collaboration with other health professionals is recommended Always use judgement and apply reasoning - patient safety should be the primary focus