Lecture 8.2 Flashcards
(129 cards)
1
Q
What is pain?
A
Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
2
Q
What is acute pain?
A
Acute pain is pain that is of short duration and resolves. It is usually directly related to the resolution or healing of tissue damage.
3
Q
How does acute pain typically resolve?
A
Acute pain typically resolves alongside treatment.
4
Q
What is chronic pain?
A
Chronic pain is pain that persists for longer than would be expected.
5
Q
Why is a strict timeframe (e.g., 1 month) not ideal for defining chronic pain?
A
An artificial threshold for chronicity, such as one month, is not appropriate for defining chronic pain.
6
Q
What is neuropathic pain?
A
Neuropathic pain is pain that arises from damage to, or dysfunction of, any part of the peripheral or central nervous system.
7
Q
What is nociception?
A
Nociception is the process by which noxious stimuli produce activity in the sensory pathways that convey “painful” information.
8
Q
What is allodynia?
A
Allodynia is pain caused by a stimulus that does not normally provoke pain.
9
Q
What is hyperalgesia?
A
Hyperalgesia is an increased response to a stimulus that is normally painful.
10
Q
What is analgesia?
A
Analgesia is any process that reduces the sensation of pain, while not affecting normal touch.
11
Q
What is local anesthesia?
A
Local anesthesia is the blockade of all sensation, both innocuous and painful, from a local area.
12
Q
What is a noxious stimulus?
A
A noxious stimulus is a stimulus that inflicts damage, or would potentially inflict damage, on tissues of the body.
13
Q
What is a primary afferent neuron (PAN)?
A
A primary afferent neuron is the first neuron in the somatosensory pathway. It detects mechanical, thermal, or chemical stimuli at its peripheral terminals and transmits action potentials to its central terminals in the spinal cord.
14
Q
Where is the cell body of a PAN located?
A
All primary afferent neurons have a cell body in the dorsal root ganglion.
15
Q
What is a nociceptor?
A
A nociceptor is a primary afferent, or sensory, neuron that is only activated by a noxious stimulus.
16
Q
Besides sensory experience, what other type of experience is pain?
A
Pain is also an emotional experience.
17
Q
What does pain indicate the awareness of?
A
Pain indicates the awareness of damage or injury.
18
Q
Why is rest important in relation to pain?
A
There is a need to rest until healed.
19
Q
What are the two main types of pain discussed?
A
The two main types of pain discussed are acute and chronic.
20
Q
What are the characteristics of acute pain?
A
Acute pain is characterized by a demonstrable cause, tissue damage, and resolution of pain alongside treatment.
21
Q
What are the characteristics of chronic pain?
A
Chronic pain is characterized by obscure aetiology, longer duration, and a relatively low chance of resolution.
22
Q
What is psychiatric comorbidity, and how common is it in chronic pain patients?
A
Psychiatric comorbidity is the co-occurrence of a psychiatric disorder with another medical condition, and there is a high degree of it in chronic pain patients. Sixty to eighty percent of chronic pain patients have a DSM psychological disorder.
23
Q
What percentage of chronic pain patients also have a DSM psychological disorder?
A
Sixty to eighty percent of chronic pain patients have a DSM psychological disorder.
24
Q
What is notable about the pharmacological management of pain and psychological disorders?
A
There is a significant overlap in the pharmacological management of pain and psychological disorders.
25
What is nociceptive pain most commonly a case of?
Nociceptive pain is most commonly a case of acute pain where a strong, noxious stimulus impacts skin or deep tissue.
26
What sensations characterize nociceptive pain?
Nociceptive pain is characterized by sharp, aching, and throbbing sensations.
27
What happens to acute nociceptive pain after the stimulus is removed?
Acute nociceptive pain resolves after the stimulus is removed.
28
What causes chronic nociceptive pain?
Chronic nociceptive pain is due to inflammation and other mechanisms, which results in extended persistence of pain sensations.
29
What are some examples of conditions that cause nociceptive pain?
Examples of conditions that cause nociceptive pain include bruises, burns, cuts, broken or fractured bones, arthritis or other musculoskeletal disorders, and migraine and tension headache.
30
What are the two neural pathways of nociceptive pain?
The two neural pathways of nociceptive pain are the sensory/discriminatory pathway and the emotional/motivational pathway.
31
What information does the sensory/discriminatory pathway provide?
The sensory/discriminatory pathway, with dorsal horn neurons in the spinothalamic tract projecting to the thalamus and primary somatosensory cortex, informs intensity and location of a painful stimulus.
32
What information does the emotional/motivational pathway provide?
The emotional/motivational pathway, with neurons in the spinobulbar tract projecting to brainstem nuclei, thalamus, and the limbic system, informs emotional and motivational aspects of the pain experience.
33
When is the subjective experience of pain formed?
The subjective experience of pain is formed only when information from both the sensory/discriminatory and emotional/motivational pathways combine.
34
What causes neuropathic pain?
Neuropathic pain is due to damage to, or dysfunction of, any part of the central or peripheral nervous systems.
35
What sensations characterize neuropathic pain?
Neuropathic pain is characterized by burning, stabbing, buzzing, or electric shock-like sensations.
36
What are some examples of conditions that cause neuropathic pain?
Examples of conditions that cause neuropathic pain include postherpetic neuralgia, which is a complication from shingles, painful diabetic neuropathy, sciatica, and phantom limb pain.
37
What is notable about some conditions, like lower back pain, in regards to pain types?
Some conditions, like lower back pain, may include both nociceptive and neuropathic components.
38
How does neuropathic pain affect normal transduction and conduction in peripheral afferent neurons?
In neuropathic pain, normal transduction and conduction in peripheral afferent neurons are hijacked to maintain nociceptive signaling in the absence of a relevant stimulus.
39
Where can this hijacking of normal transduction and conduction occur?
This hijacking can occur peripherally at primary afferent neurons, at central neurons in the dorsal horn of the spinal cord, and in numerous brain regions.
40
What are the two mechanisms of neuropathic pain?
The two mechanisms of neuropathic pain are segmental central sensitization and suprasegmental central sensitization.
41
What is central sensitization?
Central sensitization is increased responsivity to pain receptors in the central nervous system.
42
What is segmental central sensitization?
Segmental central sensitization is when peripheral injury is combined with central sensitization at the spinal cord segment receiving nociceptive input from the damaged area of the body.
43
What is a consequence of segmental central sensitization?
A consequence of segmental central sensitization is that the experience of pain continues after tissue damage is resolved.
44
What is suprasegmental central sensitization?
Suprasegmental central sensitization is when plastic changes in brain sites within the nociceptive pathway result in sensitization in these areas. This can occur following peripheral injury or in the absence of identifiable triggering events.
45
What conditions is suprasegmental central sensitization implicated in?
Suprasegmental central sensitization is implicated in fibromyalgia and pain in major depressive disorder and anxiety.
46
What condition results from nerve damage from shingles?
Postherpetic neuralgia results from nerve damage from shingles. It results in burning pain in nerves and skin long after the shingles rash or blisters have healed.
47
What are the symptoms of Painful Diabetic Neuropathy?
Painful Diabetic Neuropathy, which is nerve damage in the periphery due to high glucose levels, causes numbness, tingling, pain, or sensory problems in hands or feet.
48
What is Phantom Limb Pain?
Phantom Limb Pain is the sensation of pain in a limb or organ that has been amputated.
49
What is Sciatica and what are its common causes?
Sciatica is pain that radiates from the lower back down the leg along the sciatic nerve, most commonly due to a herniated disk or bone overgrowth that puts pressure on lumbar spine nerves.
50
What type of syndrome is Fibromyalgia?
Fibromyalgia is a chronic, widespread pain syndrome of no known cause.
51
What is the estimated prevalence of Fibromyalgia in Australia?
In Australia, the estimated prevalence of Fibromyalgia is 2-4% of the population.
52
What is the estimated global prevalence of Fibromyalgia?
Globally, the estimated prevalence of Fibromyalgia is 2.2% of the population.
53
Which gender does Fibromyalgia tend to affect more?
Fibromyalgia tends to affect women more than men, with 75-90% of cases occurring in women.
54
When is the peak incidence of Fibromyalgia?
The peak incidence of Fibromyalgia is in middle-aged women.
55
What are the characteristics of Fibromyalgia?
Fibromyalgia is characterized by fatigue, nonrestorative sleep, tenderness at multiple sites where ligaments, tendons, and muscle attach to bone, and significant psychiatric comorbidity.
56
Is Fibromyalgia a defined disorder in the DSM-5?
Fibromyalgia is not a defined disorder in the DSM-5.
57
What DSM-5 disorder will all Fibromyalgia patients satisfy the criteria for?
All Fibromyalgia patients will satisfy the criteria for Somatic Symptom Disorder.
58
What are the criteria for Somatic Symptom Disorder?
The criteria for Somatic Symptom Disorder include worry, which is disproportionate and persistent thoughts about the seriousness of one's symptoms, anxiety, which is persistently high levels of anxiety about health or symptoms, and time, which is excessive time and energy devoted to these symptoms or health concerns. It also includes one or more physical symptoms such as widespread, persistent, and difficult to pinpoint pain, tiredness and weakness, dizziness, numbness, or paralysis, nausea, vomiting, or diarrhea, and dyspnea.
59
Are the symptoms of Fibromyalgia progressive?
The symptoms of Fibromyalgia are chronic and debilitating, but not necessarily progressive.
60
Which areas of the brain are associated with pain?
The thalamus is associated with pain.
61
Which areas of the brain are associated with fatigue?
The striatum, spinal cord, and nucleus accumbens are associated with fatigue.
62
Which areas of the brain are associated with concentration and anhedonia?
The prefrontal cortex and nucleus accumbens are associated with concentration and anhedonia.
63
Which areas of the brain are associated with sleep and appetite?
The hypothalamus is associated with sleep and appetite.
64
Which areas of the brain are associated with mood and anxiety?
The amygdala and orbitofrontal cortex are associated with mood and anxiety.
65
What is the comorbidity rate between depression/anxiety and pain?
The comorbidity rate between depression and anxiety with pain is 30-60%.
66
What are the bidirectional relationships between pain and depression/anxiety?
Pain is a predictor of the onset and persistence of major depressive disorder and anxiety, and major depressive disorder and anxiety are predictors of pain.
67
What are the effects of comorbidity between MDD/ANX and pain?
Comorbidity between major depressive disorder or anxiety and pain results in a much greater impact than either alone. It worsens disability, decreases active coping, and decreases favorable response to treatment and satisfaction.
68
How does the prevalence of MDD relate to the number of pain sites?
Prevalence of major depressive disorder is lowest in no pain, intermediate in one pain site, and highest in multiple pain sites.
69
How does the prevalence of ANX relate to the number of pain sites?
Prevalence of anxiety is lowest in no pain, intermediate in one pain site, and highest in multiple pain sites.
70
What type of medication is used for neuropathic pain?
Antidepressants are used for neuropathic pain.
71
What approach is used for treatment selection?
A symptom-based approach is used for treatment selection, where each symptom is matched with brain circuits and neurotransmitters that may mediate those symptoms, and this information is used to select a corresponding drug treatment.
72
What is the most commonly prescribed medication for pain?
The most commonly prescribed medications are antidepressants.
73
What are the different types of antidepressants used?
The different types of antidepressants used include tricyclic antidepressants, selective serotonin reuptake inhibitors, or serotonin-norepinephrine reuptake inhibitors.
74
Is it clear which antidepressant to use first?
There is a question mark over which antidepressant to use first.
75
Is the mechanism of action for antidepressants in neuropathic pain certain?
The mechanism of action for antidepressants in neuropathic pain is uncertain.
76
How does the onset of analgesia compare to the onset of antidepressant effects?
Analgesia is achieved faster and at lower doses than the onset of any antidepressant effect, which takes about six weeks.
77
Is there a correlation between antidepressant effects, mood, and pain?
There is no correlation between antidepressant effects, mood, and pain.
78
Do antidepressants provide analgesia in those with and without MDD?
Antidepressants provide analgesia in those with and without major depressive disorder.
79
According to Saarto & Wiffen (2007), how effective is amitriptyline at reducing pain compared to placebo?
According to Saarto & Wiffen (2007), active treatment with up to 150mg/day of amitriptyline is more effective at reducing pain compared to placebo.
80
According to Saarto & Wiffen (2007), how effective is venlafaxine at reducing pain compared to placebo?
According to Saarto & Wiffen (2007), venlafaxine is more effective at reducing pain compared to placebo.
81
According to Saarto & Wiffen (2007), what is the NNT for SNRIs and TCAs?
According to Saarto & Wiffen (2007), the NNT for serotonin-norepinephrine reuptake inhibitors is 3.1, and the NNT for tricyclic antidepressants is 3.6.
82
According to Saarto & Wiffen (2007), what is the NNH for amitriptyline and venlafaxine?
According to Saarto & Wiffen (2007), the NNH for amitriptyline is 6, and the NNH for venlafaxine is 9.
83
According to Saarto & Wiffen (2007), are TCAs or SNRIs better tolerated?
According to Saarto & Wiffen (2007), tricyclic antidepressants are less well tolerated than serotonin-norepinephrine reuptake inhibitors.
84
What is the main reason for withdrawals from antidepressant treatment?
The majority of withdrawals from antidepressant treatment are related to side effects.
85
What were anticonvulsants originally introduced for?
Anticonvulsants are a series of compounds originally introduced for the treatment of epileptic seizures.
86
Why are anticonvulsants used to treat various chronic pain conditions?
Anticonvulsants have a variety of mechanisms of action; therefore, they are used to treat various chronic pain conditions.
87
What are the most common anticonvulsants used for pain?
The most common anticonvulsants used for pain are carbamazepine, also known as Tegretol, and gabapentin, also known as Neurontin.
88
According to international guidelines, which medication is commonly trialled first?
According to international guidelines, gabapentin is the first medication trialled. It is common to prescribe the maximum tolerated dose, but this is controversial.
89
Is the precise mechanism for neuropathic pain relief by anticonvulsants certain?
The precise mechanisms for neuropathic pain relief by anticonvulsants are uncertain.
90
How do anticonvulsants modify the ability of neurons to fire?
Anticonvulsants modify the ability of neurons to fire at high frequencies. They may enhance GABA inhibition, have a stabilizing effect on neuronal membranes, or act via NMDA receptor sites.
91
How does carbamazepine work?
Carbamazepine is thought to block voltage-sensitive sodium channels, resulting in fewer channels available to open, making neurons less excitatory and less likely to fire.
92
How does gabapentin work?
Gabapentin is thought to affect calcium channels in the central nervous system and peripheral nervous system. It modifies the release of neurotransmitters, which reduces the excitability of nerve cells.
93
How are anticonvulsants administered?
Anticonvulsants are always administered orally, in tablet form.
94
What are some Australian examples of anticonvulsants?
Australian examples of anticonvulsants include carbamazepine (Tegretol) and gabapentin (Neurontin).
95
When are clinical benefits typically seen after starting anticonvulsants?
Clinical benefits from anticonvulsants are typically seen within approximately one week of administration, with maximum benefit after four weeks.
96
How long do the effects of anticonvulsants last?
The effects of anticonvulsants last five to seven hours.
97
What are the common side effects of anticonvulsants?
Common side effects of anticonvulsants include gastrointestinal upset, dizziness, drowsiness, loss of balance or coordination, tremors or jerky movements, gait ataxia, dysarthria, and double vision or eye twitches.
98
According to Wiffen et al. (2014), how effective is carbamazepine at reducing pain compared to placebo?
According to Wiffen et al. (2014), carbamazepine is generally more effective at reducing pain compared to placebo.
99
According to Wiffen et al. (2014), what percentage of patients experienced a 50% reduction in pain with carbamazepine versus placebo?
According to Wiffen et al. (2014), in 5 studies, 70% of patients experienced a 50% reduction in pain with carbamazepine, compared to 12% with placebo.
100
According to Wiffen et al. (2014), what percentage of patients experienced over a 50% reduction in pain with carbamazepine versus placebo?
According to Wiffen et al. (2014), in 4 studies, 60% of patients experienced over a 50% reduction in pain with carbamazepine, compared to 10% with placebo.
101
According to Wiffen et al. (2019), how effective is gabapentin at reducing pain in postherpetic neuralgia compared to placebo?
According to Wiffen et al. (2019), gabapentin is generally more effective at reducing pain in postherpetic neuralgia compared to placebo.
102
According to Wiffen et al. (2019), what percentage of patients experienced at least a 50% reduction in pain intensity with gabapentin versus placebo in postherpetic neuralgia?
According to Wiffen et al. (2019), studies showed a favorable effect of gabapentin in reducing pain intensity by 50%. At least a 50% pain intensity reduction occurred in 33% of patients taking gabapentin, compared to 19% taking placebo.
103
According to Wiffen et al. (2019), how effective is gabapentin at reducing pain in diabetic neuropathy compared to placebo?
According to Wiffen et al. (2019), gabapentin is generally more effective at reducing pain in diabetic neuropathy compared to placebo.
104
According to Wiffen et al. (2019), what percentage of patients experienced at least a 50% reduction in pain intensity with gabapentin versus placebo in diabetic neuropathy?
According to Wiffen et al. (2019), studies showed a favorable effect of gabapentin in reducing pain intensity by 50%. At least a 50% pain intensity reduction occurred in 38% of patients taking gabapentin, compared to 23% taking placebo.
105
According to Wiffen et al. (2014, 2017), what is the NNT for carbamazepine and gabapentin?
According to Wiffen et al. (2014, 2017), the NNT for carbamazepine is 1.7-1.9, and the NNT for gabapentin is 7.
106
According to Wiffen et al. (2014, 2017), what does the NNT for carbamazepine and gabapentin mean in terms of patient benefit?
According to Wiffen et al. (2014, 2017), the NNT means that fewer people need to take carbamazepine compared to gabapentin to experience a benefit in pain reduction.
107
According to Wiffen et al. (2014, 2017), what is the NNH for carbamazepine and gabapentin?
According to Wiffen et al. (2014, 2017), the NNH for carbamazepine is 2.6, and the NNH for gabapentin is 13.
108
According to Wiffen et al. (2014, 2017), what does the NNH for carbamazepine and gabapentin indicate about tolerability?
According to Wiffen et al. (2014, 2017), carbamazepine is significantly less well-tolerated than gabapentin.
109
What is the main reason for withdrawals from anticonvulsant treatment?
The majority of withdrawals from anticonvulsant treatment are related to side effects.
110
What is the primary focus of therapy for pain?
Therapy for pain targets improvements in physical, emotional, social, and occupational functioning rather than pain resolution.
111
What are the most common forms of therapy?
The most common forms of therapy include operant-behavioral therapy, cognitive-behavioral therapy, mindfulness, and acceptance and commitment therapy.
112
How do therapies for chronic pain differ?
Therapies for chronic pain differ in scope, duration, and goals, resulting in distinct patterns of treatment efficacy.
113
What approach does CBT use to target pain responses?
Cognitive-behavioral therapy is the application of a biopsychosocial approach that targets behavioral and cognitive responses to pain.
114
What is the goal of CBT?
The goal of cognitive-behavioral therapy is to develop coping strategies intended to manage pain.
115
What are some common components of CBT protocols?
Common components of cognitive-behavioral therapy protocols include psychoeducation about pain, behavior, and mood, strategies for relaxation, behavioral pacing, behavioral activation, positive event scheduling, effective communication, and cognitive restructuring for distorted and maladaptive thoughts about pain.
116
According to Williams et al. (2019), how does the effect of CBT on pain intensity compare to active controls immediately following treatment?
According to Williams et al. (2019), compared to active control, the overall effect of cognitive-behavioral therapy does not differ significantly from active controls for pain intensity immediately following treatment.
117
What is an active control in this context?
An active control is a treatment designed to change pain behavior, such as physical therapy, education, or a medical regime.
118
According to Williams et al. (2019), how does the effect of CBT on pain intensity compare to active controls at least 6 months after treatment?
According to Williams et al. (2019), compared to active control, the overall effect of cognitive-behavioral therapy does not differ significantly from active controls for pain intensity at least six months after treatment.
119
According to Williams et al. (2019), how does the effect of CBT on disability compare to active controls immediately following treatment?
According to Williams et al. (2019), compared to active control, the overall effect is significantly in favor of cognitive-behavioral therapy compared to active controls for disability immediately following treatment.
120
According to Williams et al. (2019), how does the effect of CBT on disability compare to active controls at follow-up assessment?
According to Williams et al. (2019), compared to active control, the overall effect is significantly in favor of cognitive-behavioral therapy compared to active controls for disability at follow-up assessment.
121
According to Williams et al. (2019), how does the effect of CBT on catastrophizing compare to active controls immediately following treatment?
According to Williams et al. (2019), compared to active control, the overall effect is just significantly in favor of cognitive-behavioral therapy compared to active controls for catastrophizing immediately following treatment.
122
What is catastrophizing?
Catastrophizing is a negative cognitive and mental set related to expected or actual pain experience, including rumination and helplessness.
123
According to Williams et al. (2019), how does the effect of CBT on catastrophizing compare to active controls at follow-up assessment?
According to Williams et al. (2019), compared to active control, the overall effect of cognitive-behavioral therapy does not differ significantly from active controls for catastrophizing at follow-up assessment.
124
Based on the document, how effective are pharmacological agents at reducing pain?
Pharmacological agents are seemingly effective at reducing pain.
125
What are the differential effects of psychotherapy according to the document?
There are differential effects for psychotherapy.
126
What outcomes does psychotherapy improve after treatment?
Psychotherapy improves disability and catastrophizing after treatment.
127
What is the long-term outcome that psychotherapy improves?
Psychotherapy improves long-term outcomes in disability only.
128
What effect does psychotherapy not have, according to the document?
There is no effect of psychotherapy on pain intensity.
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