Week 4-Pain Catastrophising, Depression and Suicide Flashcards

1
Q

Define Catastrophising

A

The tendency to view the worst consequences of things and events (Pain Catastrophising is the same thing, but pain-specific)

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2
Q

What is the Pain Catastrophising Scale (PCS)? (Sullivan et al., 1995)

A

3 subscales:
Magnification: “I become afraid that the pain will get worse”

Rumination: “I can’t stop thinking about how much it hurts”

Helplessness: “There is nothing I can do to reduce the intensity of pain”

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3
Q

Define Concept Redundancy

A

Pain catastrophising often correlates with
depression, fear of pain, or anxiety. For this reason the concept itself has been challenged, e.g., is possibly redundant (Quartana et al., 2012)

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4
Q

True or False: Cold pressor pain is greater in high- than in low-catastrophising individuals (Sullivan et al., 1995)

A

True!

-Dunk your hand in ice water where you will quickly feel pain and you rate pain ratings during different time intervals

Split the groups based off the PCS i.e., high and low-catastrophising (all healthy)

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5
Q

True or False: Catastrophising explains 7%-31% of the covariance with pain outcomes (Sullivan et al., 2001)

A

True! (This looked at clinical populations and did the cold pressor task again: These points show countless research examples of how pain catastrophising can determine and relate to several clinical outcomes)
* Concurrent pain (Sullivan et al., 1995)

  • Post-surgical pain (Pavlin et al., 2005)
  • Analgesic intake (Jacobsen and Butler, 1996; but see also negative data in Khan et al., 2011)
  • Length of hospitalisation (Gil et al., 1992)
  • Activity intolerance (Sullivan et al., 2002)
  • Return to work (Sullivan and Stanish, 2003)
  • Effectiveness of spinal cord stimulation therapy (Rosenberg et al., 2014)
  • Risk of developing chronic pain, e.g. after knee replacement (Burns et al., 2015)
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6
Q

What was found in the Meta-analysis of pain catastrophising scale (PCS) scores in different syndromes in 220 studies? (Wheeler et al., 2019)

A
  • Stratified the relationship between PC and chronic pain syndromes
  • Healthy people score a mean PCS score of 15 and some chronic pain conditions also fell in the normal conditions.
  • Nociplastic pain (e.g., generalised pain/
    fibromyalgia) is particularly associated
    with high PCS scores.
  • Excellent test-retest reliability (0.8-0.9) for total PCS scores (less so for three factors)
  • No significant effects of age and gender on relationship between pain and PCS.
  • We can conclude therefore that PC is a key component of some chronic pain conditions
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7
Q

What was found in the Meta-analysis of correlations between pain catastrophising and pain severity and disability? (Calderon et al., 2019)

A
  • Meta-analysis of 85 studies revealed
    moderate correlations between PCS and pain severity in knee pain, low-back pain and widespread pain.
  • Positive correlation for all types of pain which means PC levels can predict the severity of pain that different chronic pain populations may have.
  • There is still a difference between those who are high and low-catastrophising
  • ‘Low quality’ in many studies may have
    compromised results.
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8
Q

Decreased conditioned pain modulation in high pain catastrophisers: What was Weissman-Fogel et al’s (2008) study?

A
  • High pain catastrophisers may have low endogenous mechanisms (i.e., pain modulation)

-Applied 1-min heat stimulus before and after a strenuous exercise (40 hand-grips)
CPM

  • We should feel less pain from the heat stimulus after the hand-grips due to pain modulation (double check in recording)

Correlations:
-Pain catastrophising - heat pain
(conditioning stim): r = 0.48, P<0.05 pain catastrophising - muscle pain (test stim): r = 0.31, P<0.05

-Pain Catastrophising - CPM: r = -0.32,
P<0.05

  • It was a negative correlation (high PC = less CPM). PC could be linked to mechanisms in which people experience less pain outcomes (check in recording)
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9
Q

What Evidence on Brain Structure is there?

A

Blankenstein et al., (2010):
-Brain structure: Pain catastrophizing correlates with grey matter density in dorsolateral prefrontal cortex.

-A negative correlation r=-0.67 between thickness of cortical grey matter in DLPFC and PCS in patients with Irritable bowel syndrome (n=11) (higher PCS = reduced thickness) HOWEVER we need better studies as these are relatively small studies + there isn’t perfect replication of these studies.

Hubbard, CS., et al., (2014):
-Analysed correlations between grey matter thickness and PCS in migraine patients (n=17) and healthy controls (n=18).

-Medial PFC showed a negative correlation with PFC in migraine patients and a positive correlation in healthy controls.

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10
Q

What Evidence on Brain Function is there? (Seminowicz & Davis, 2006)

A

-Brain activation patterns in high- and low pain catastrophisers of healthy P’s

-Brain activation patterns for both mild
and high pain are exaggerated in various
pain processing structures in individuals
with high PCS scores compared to low PCS scores in areas such as the DLPF, STG etc.,

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11
Q

What was found in the Meta-analysis of studies analysing correlations between brain activation during pain stimulation and pain catastrophising? (Galambos et al., 2019)

A

-Meta-analysis of 10 functional MR studies, mostly involving healthy people giving pain stimulation in the scanner.

-The results indicate a connection between pain catastrophizing and brain areas tightly connected to higher levels of pain perception (somatosensory cortices, anterior insula, anterior cingulate cortex and thalamus) and/or modulation (e.g., the dorsolateral prefrontal cortex).

-Pain catastrophizing might be related to salience detection, pain processing, and top-down attentional processes.

-PC is related to some sort of pain processing in the brain which can lead to worse pain outcomes.

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12
Q

What is the Genetic underpinning of pain
catastrophising? (Trost et al., 2015).

A
  • Heritability of pain catastrophising was investigated via a twin study with 53 mono-zygotic, relative to 53 dizygotic (non-
    identical but same sex-important as there are sex differences in pain) twins
  • Cold pressor test was utilized.
    – Pain catastrophising and pain showed positive heritability indices, and heritability and pain catastrophising together explained 37% of variance in pain tolerance threshold.
    -More consistencies in identical twins so there is some element of genetic heritability
  • Replication : A recent twin study (Burri et al., 2018) confirmed a 36% heritability of pain catastrophising.
  • This supports a biological mechanism for PC with a genetic component
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13
Q

What are the 3 Main Theories of pain
catastrophising?

A
  • Attentional model: catastrophising as an increased attentional bias to pain
  • Communal coping model : catastrophising maximises the probability that distress will be managed within social/interpersonal context (i.e., a way of communicating pain and obtaining health)
  • Fear avoidance model: NOT a model of how catastrophizing affects pain experience, but a model of the cycle of chronic pain
  • FA model attributes a significant role (and negative consequence) to pain catastrophizing as a factor promoting the generation and maintenance of chronic
    pain cycle.
  • See Sullivan et al. (2001) ON CANVAS, Quartana et al. (2009), Leung (2012) see slide notes for additional reading about these theories

-Empirically testable

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14
Q

What is the Attentional Model: Catastrophising-attention links in
patients?

A
  • Pain patients are hypervigilant to pain, manifesting e.g., in scanning the body during anticipation of somatosensory stimuli.
  • Fibromyalgia syndrome patients (soft tissue pain at multiple sites of the body) show higher pain intensity, vigilance to pain, and pain catastrophising than chronic back pain patients. (Crombez et al., 2004).

– Correlation study in 64 fibromyalgia and 46 chronic back patients using PCS, Pain Vigilance Questionnaire - catastrophising mediated the relationship between vigilance and pain (Crombez et al., 2004).

  • This is great as Fibromyalgia is a hard condition to treat but we have 2 clear mechanisms i.e., vigilance and PC
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15
Q

What is the Hypervigilance to pain cues in the environment in chronic pain? (AM)

A
  • FMS patients show exaggerated neural
    responsiveness and increased pain rating for even non-pain scenes – showing enhanced vigilance (Fallon et al., 2015)
  • EEG study, patients compared to healthy
    (matched controls) observing two categories of image (painful and non-painful images matched).
  • Patients demonstrated greater PCS scores.
  • Augmented late positive potential (LPP)
    component (associated with processing
    complex/emotional content of images) was
    seen in patients in response to both pain and non-pain pictures (hypervigilance)
  • Their level of PC and hypervigilance is changing their brain responsiveness (which is an objective measure)
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16
Q

Communal coping model of catastrophising: What is the Supporting Evidence? PART 1

A
  • CCM model attributes catastrophising as a mechanism to communicate pain and enable social support.
  • High-Catastrophisers display facial expressions of pain longer for than non-catastrophizers in the presence of observer but not when alone (Sullivan et al., 2004).
  • Perhaps this is some sort of mechanism where PC is related to some communicative mechanism to obtain help.
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17
Q

Communal coping model of catastrophising: What is the Evidence for support? PART 2

A
  • Measuring the correlation between PCS scores and intensity of facial pain expressions displayed during cold-pressor test (Sullivan et al., 2006).
  • Forty subjects were exposed to CPT (1 min) and were videotaped. Trained observers analysed facial expressions during 15-20 s of the CPT. There was a positive correlation r = 0.40, p<0.01 (females) and r = 0.36, p<0.02 (males) between the amount of pain behavior exhibited (facial expressions) and pain catastrophising score (i.e., high PCS = high PB exhibited)
  • Heightened perception of pain in others and catastrophising (Sullivan et al., 2006).
  • Sixty participants (not trained) rated video clips of 11 subjects undergoing CPT. Higher levels of pain perceptions in others was related to pain perceptions in raters (Correlations between cat. score and inferred pain).
  • PC can be related to levels of empathy which supports the Communal Model as it actually is related to social interactions to pain both for being helped and helping others.
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18
Q

What is the Prosocial (CCM) evidence: High pain catastrophisers attribute stronger
pain to others: role of insula, anterior cingulate (Fallon et al., 2015)

A
  • In this study, high and low catastrophisers (healthy people) rated painful and non-painful scenes whilst brain activity recorded with EEG.
  • High- PCS group rated scenes as more painful, and showed enhanced brain responses in Anterior cingulate cortex and the insula cortex
  • This suggest enhanced empathic reactions in high catastrophisers - prosocial
  • This supports the idea that PC is part of a mechanism promoting prosocial behaviour
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19
Q

Communal coping model of catastrophising: How does the spouse view the patient’s pain? (Burns et al., 2015)

A
  • Burns et al., (2015) employed electronic
    diaries to record PCS, pain and partners’
    responses every 3 hours for 14 days:

– pain was stronger when the spouse was
present (Communal coping model i.e., opportunity to receive help)

– within-person increases in pain catastrophising were positively associated
with spouse reports of patient pain behavior

  • Suggests the Communal coping aspect works as the spouse recognises higher pain behaviour suggesting the importance of PC in the communal coping model
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20
Q

What’s the Fear avoidance model: Role of catastrophizing (Vlayen et al., 2000)

A

-Fear and avoidance can lead us into a cycle of chronic pain (ideally we want to encourage reducing fears by confronting these to recover)

-People who often experience pain will catastrophise pain

-Become more scared of their pain and avoid anything that may worse it

-This can cause people to feel depressed

-The pain experience cycle repeats (check recording to ensure model is accurate)

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21
Q

FA model: What’s the Evidence linking fear of pain to negative outcomes in CP patients?

A
  • People with high level of pain catastrophising avoid strenuous muscle exercise (Sullivan et al., 2002), and disability in low-back pain patients correlates with fear of pain rather than with pain severity (Crombez et al., 1999).
  • Interventions aimed at reduction of fear of movement (graduated performance of feared movements) have shown reductions in activity avoidance and move more (Boersma et al., 2004; Woods et al., 2008).
  • In general, reduced fear of pain and reduced pain catastrophising are associated with lower level of disability (Smeets et al., 2006).
22
Q

Can we do something about pain catastrophising? What’s the Experimental data? (Terry et al., 2015)

A

-There’s nothing wrong with PC, however, it worsens the pain experience for certain populations

-Two groups of healthy people underwent experiment with electrical stimulation
of the foot, producing a (mildly painful) reflex (NFR). Was asked to report the pain intensity

Randomised to one of two groups:
Group 1: Anti-catastrophising statements (statements aimed at reducing levels of catastrophising)

Group 2: Education about mechanisms of pain (was the education well taught though?)

-Pain report of pain intensity decreased after an anti-catastrophising intervention but reflex activity was the same

  • Objectively, the pain was probably the same, but the way they were experiencing it and rating it were different dependent on the intervention.
23
Q

Applications: How can we reduce pain catastrophising? (review by Wideman and Sullivan, 2011)

A
  • Cognitive Behavioural Therapy: 10 sessions of thought monitoring and cognitive restructuring were associated with reductions in pain catastrophising, and pain in half of chronic headache patients, and this effect continued after 1 year (Thorn et al., 2007) (impressive that 50% had a reduction: However CBT is more expensive compared to medication).
  • Neurophysiology education: teaching patients pain science and physiology has been shown to reduce catastrophising (rumination) and pain severity (Moseley et al., 2004; Meeus et al., 2011).
  • Graded activity and graded exposure
    (consider in relation to the Fear-Avoidance-
    Model): Decreases in disability and pain
    after exposing patients in a graded manner
    to movements and activity confirmed.
    Reductions in disability were related to decreased pain catastrophising irrespective
    of the type of graded intervention (George
    et al., 2010). Therefore when we think about reducing pain-related fear, we need to target reducing PC.
24
Q

What’s the Significance of depression in chronic pain: Context (check recording)

A
  • Depression predicts increased health costs in pain patients Engel et al. (1996)

– Analysed data from 1059 back pain patients, and computed a multivariate regression between total costs and various
independent variables including depressive symptoms.

– Total health care costs predicted by the presence of depression symptoms in the first month of the initial primary care visit.

25
Q

What’s the Prevalence of depression in chronic pain patients?

A
  • About 15% prevalence of depression in chronic pain patients in communities (e.g., Gureje et al., 2008)
  • 40-60% in patients treated in specialised pain centres have depression (based on a review of 9 epidemiological studies: Banks & Kerns, 1996)
  • Having more than one pain is a strong predictor of depression (e.g., Gerrits et al., 2014; Gureje et al., 2008) (this includes pain severity too)
26
Q

What are the Directional links between chronic pain and depression?

A
  1. Depression causes pain (option 1)
    Bidirectionally (option 3)
  2. Chronic pain causes depression (option 2)

Intervening variables mediate the links between pain and depression:
* pain catastrophising
* helplessness
* impaired sleep

  • NOTE: We shouldn’t stigmatise CP patients regarding PC because they are allowed to view pain differently and have more negative perceptions considering their circumstances.
27
Q

What’s the evidence backing the idea that Depressed people feel more chronic pain?

A

Old’ hypothesis of depression–pain relationship:
– Pain (e.g., low-back) represents a bodily manifestation of depression (Psychosomatic. Somatisation = tendency of depressed people to show a number of somatic complaints

  • 80% of depressed people experience abdominal pain, low-back pain, musculoskeletal pain, pain in joints and neck (Stahl, 2002) (These are NOT CP Patients)
  • Shared symptoms of chronic pain and depression: impaired sleep, feelings of helplessness…
28
Q

Depression predicts chronic pain in later years: What’s the Longitudinal evidence?

A
  • Leino and Magni (1993) evaluated presence of depression and different types of pain in a sample of metal industry workers (longitudinal study – baseline to 5 and 10 years later).
    – Depression at time baseline and after 5 years predicted the level of musculoskeletal pain at 10 years follow-up.
  • Longitudinal study found that people with depression at baseline were shown to be more likely to develop musculoskeletal pain 8 years later (OR = 2.14) (Magni et al., 1994)
  • These studies didn’t do a good job at controlling the confounding factors e.g., poverty: poor diet, greater stress, less exercise which could account for these results.
29
Q

What was the Study which measured Inducing depressed mood in healthy people and its impacts on experimental pain (Tang et al., 2008)

A

-Tang et al., (2008) utilised a bag holding task (duration measure) to consider pain tolerance and pain intensity ratings.

-A musical presentation was used to induce
changes in mood.

-People reported lower levels of pain tolerance and a higher rating of pain when hearing music designed to make people sad.

-This supports the hypothesis that depression can ‘cause’ pain

-Consider: Pain induced by holding a shopping bag – controlled method? (holding a bag isn’t experimentally valid)

30
Q

What was the Study which measured Inducing depressed mood in healthy people and its impacts on experimental pain (Berna et al., 2010.)

A

-Berna et al., (2010) Used mood music + matched congruent statement to induce depressed or neutral mood conditions in an
fMRI study with experimental (thermal) pain and asked for pain ratings + brain response)

-Healthy P’s

-Pain in depressed (compared to neutral) mood was associated with increased activations in subgenual anterior cingulate
cortex (sACC), and left hemisphere (ipsilateral) amygdala, posterior insula,
thalamus, precuneus, and caudate. They also rated higher levels of pain unpleasantness.

  • Objectively, inducing a depressed mood, affects their pain experience (i.e., more pain), which supports the causal relationship of depression causing pain.
31
Q

Depressed people may feel experimental pain less than healthy people: What was found in the Meta-analysis of experimental pain studies? (Thompson et al., 2016)

A

-Using clinical depression, rather than mood induction, yields different results.

-No difference between depressed and healthy people in pain tolerance thresholds
or pain ratings.

-In contrast, pain thresholds (the point where you start to feel pain) were higher in depressed people than in healthy controls.

  • Debunks the theory that pain is caused by depression and tells us that these previous models don’t translate directly to those with chronic pain (which makes sense as it’s not the same as experimental pain).
32
Q

How does Chronic pain act as a cause of depression? (Gerrits et al., 2014)

A
  • Intuitively, pain impacts QoL and could therefore CAUSE depression.
  • Evidence shows that depression frequently develops after the onset of a chronic pain condition and the onset latency is associated with pain severity and number of pain loci.
  • Average onset of depression lagged the onset of pain condition by 11.7 months (Gerrits et al., 2014).
  • Onset of depression related to the number of pain locations, pain severity and pain in the head, abdomen and joints.
  • This research replicates effects of multiple
    pains on likelihood of developing depression (Gureje et al., 2008).
  • Tells us that CP has some causal factor that can cause us to develop depression.
33
Q

What are the Bidirectional relationships between pain and depression?

A

-Is depression a consequence of chronic pain, vice versa, or both?

-Feldman et al. (1999) asked 109 CRPS patients to complete daily diaries of pain, mood and social support during 28 consecutive days.
-The time-lagged cross-correlation analysis showed that the strongest relationship was between pain causing depression, anxious and angry mood (pain-to-depression). However, the reversed relationship (depression contributing to pain) was also significant. A good example of bi-directionality.

34
Q

What is Pain catastrophising as an intervening factor?

A
  • Pain catastrophising often correlates with depression – concept redundancy
    (Quartana et al., 2012)?

Evidence suggests an independent contribution of pain catastrophising to
depression (Richardson et al., 2009):
-65 low-back patients, pain > 6 months
-BCPI = baseline chronic pain intensity
-PCS = Pain catastrophizing scale
-CPAQ = chronic pain acceptance
quest.

*PC was related to depressive symptoms but in a specific way but not in a redundant way as for example, CPAQ is not related to depressive symptoms.

35
Q

Pain catastrophizing as an intervening
factor - could we use pain catastrophizing to target vulnerable groups? (Fallon et al., 2021)

A
  • During COVID lockdown, people with
    chronic pain scored higher on many measures of negative impact. They also
    exhibited greater PCS scores.
  • Self-reported change in mood (anxiety + depressed mood) was shown to be related to increased pain severity in patients.
  • Pain catastrophizing mediated the
    relationship between mood-increased pain
    severity in lockdown (High PCS were most sensitive to this relationship).
  • Mood, and potentially PCS specifically,
    could be used to identify vulnerable patients who will see larger exacerbation of
    symptoms in times of crises.
36
Q

What’s the link between Helplessness and Depression in Chronic Pain? (Palomino et al., 2007)

A

-80 fibromyalgia patients completed a battery of questionnaires measuring symptoms. Helplessness (a subscale component of PCS) was also captured.

The 2-factor model:
-Helplessness is related to interference and loss/inability to engage in life activities – another potential intervening factor.
-However, only helplessness was shown to mediate relationship between pain and depression.

  • PC and helplessness might be an important factor between the relationship between depression and pain.
37
Q

How is Sleep an intervening factor?

A
  • Consistent evidence shows impaired sleep in chronic pain patients. Specifically, insomnia, delayed onset of sleep, night awaking, daytime sleepiness etc.
    e.g., Meltzer et al. (2005); Menefee et al. (2000: review)
  • Sleep disturbances may lead to painful states: Moldofsky et al. (1975) analysed sleep EEG in 10 fibromyalgia syndrome
    patients.
    – 7 out of 10 patients showed abnormal alpha-delta sleep patterns.
    – In 6 healthy controls, similar abnormal sleep patterns were shown and induced by auditory stimulation (i.e., ensured they didn’t enter deep sleep).
    – Disturbed sleep was followed by musculoskeletal pain in healthy controls.
38
Q

What was the impact of disturbed sleep and pain in normal subjects?

A

Sleep disturbances in normal subjects induces a hyperalgesic state: (Kundermann et al., 2004)
-Healthy subjects, two nights of sleep deprivation and two nights of normal sleep.
Quantitative sensory testing (QST) was applied to measure sleep deprivation effects on pain and innocuous thermal processing.

-Sleep deprivation decreased the cold and heat pain thresholds, but did not change
the warm/cold thresholds (shows it can impact on pain processing specifically)

Haack and Mullington (2005):
Long-lasting sleep reduction increases pain symptoms and decreases optimism in healthy subjects: analysed day-to-day changes in psychological state during 12 days of reduced sleep (4 hours) in comparison to controls undergoing normal sleep (8 hours).

-Sleep reduction induced progressive decreases in optimism-sociability (link to
depression), and increased reports of pain (back, stomach, muscle) (now imagine if this was a CP patient!)

  • We can see how prolonged changes in sleep affects your mood and physiological threshold
39
Q

What are the Bidirectional interactions between pain and sleep?

A

-Affleck et al. (1996) analysed sleep quality, pain intensity and attention to pain using portable computer questionnaires administered automatically over 30 days in 50 fibromyalgia patients (longitudinal study).

-A night of poor sleep was followed by a significantly more painful day (sleep&raquo_space; pain path) (t = -3.22, P<0.001).

-A more painful day was followed by a night of poorer sleep (t = -2.10, P<0.05) (pain&raquo_space; sleep path).

  • Supports the idea of a bidirectional interaction of cycle between pain and sleep.
40
Q

What is Suicide behaviour like in chronic pain patients?

A
  • Chronic pain patients are at increased risk of suicidal ideation, attempts and committed suicides, (~2-3 times increased risk) compared to general population
  • 20% lifetime prevalence of suicidal ideation in chronic pain patients
  • 5-14% prevalence of suicide attempts in
    chronic pain population (Tang & Crane, 2008)
41
Q

What are the Different types of Suicidal Behaviour?

A

SI = suicide ideations (thinking about death) – passive behaviour
SP = suicide planning (thinking about suicide) – active
SA = attempted suicide
SC = completed suicide (difficult to research)

  • Prevalence of suicidal behaviour in chronic pain (updated review in Fishbain et al., 2014)

SI: prevalence 8-41% in chronic pain
SA: prevalence 14-38%
SC: only 1 study; history of chronic pain was confirmed as a contributory factor

42
Q

What are the General and pain-specific risk factors of suicide? CHECK IN LECTURE

A

Tang and Crane (2006) offered the first systematic review of general and pain-specific risk factors of suicide in chronic pain patients. They identified elevated risk and also considered the nature of specific risk factors for CP patients.

General risk factors:
* family history of suicide
* individual history of a suicide attempt
* presence of co-morbid depression

Pain-specific risk factors:
* location of pain
* high pain intensity
* long duration of pain
* presence of co-morbid insomnia

43
Q

What are the General Risk Factors of Suicide? (Racine, 2018)

A
  1. Sociodemographic characteristics (gender, employment status)
  2. Personal and family history (history of suicide, adversities in families)
  3. Psychological disorders (depression, anger)
  4. Consumption habits and medication use
44
Q

What are the Pain-Specific Risk Factors of Suicide? (Racine, 2018)

A
  1. Type of chronic pain syndrome
  2. Chronic pain characteristics (duration, severity, comorbidities)
  3. Physical factors (sleep)
  4. Health-related quality of life (mental health)
  5. Psychosocial factors (pain catastrophising, burdensomeness)
45
Q

What Evidence is there for the General Risk Factors of Suicide?

A

General factors may offer a way to identify chronic pain patients at increased risk:

  • Chronic Pain Patients with family history of suicide attempts were at 7-8 × greater risk of SI or SP than patients with no such history (Smith et al., 2004)
  • Patients who experienced abuse or domestic violence predicted increased rates of SA (Okifuji and Benham, 2011; Fuller-Thomson et al., 2016)
  • Edwards et al. (2006) analysed the contribution of many variables from self-report instruments obtained in 1512 chronic pain patients. Patients were divided
    into groups of no suicidal ideation (no SI), passive SI (thoughts of death) and active SI
    (thought of suicide).
    – Beck Depression Inventory score vs. SI score: r = 0.58 (P<0.001)
    – Catastrophising score of MPI vs. SI score: r = 0.27 (P<0.01)
  • A number of other studies confirmed the role of depression in suicide behavior in pain patients (Racine, 2018)
  • Suicide attempts more frequent in arthritis patients who drank alcohol or took illicit drugs (Fuller-Thompson et al., 2016)
46
Q

Pain-specific factors: What about the types of chronic pain?

A
  • Methodological problems: often small numbers of syndromes (3-4) investigated, cohort sizes not large enough, different methods to measure suicide behaviour
  • Ilgen et al. (2013) analysed 4.8 million of patients records to determine associations between type of a non-cancer pain
    and suicide:
    – back pain, migraine, non-specific pain were the syndromes with the greatest risk of suicide.
  • However, latest review suggests there is not sufficient conclusive data on prevalence of suicidal behavior in specific types of pain (see Racine, 2018)
  • In older people (>65 years), arthritis pain and renal-related pain (together with pain intensity) predicted suicide ideations and
    attempts (Kim, 2015).
  • What we need to ask is why are these related to suicidal behaviour? is it the stigma or the poor outcomes?
47
Q

What’s the link between Pain Severity and Risk of Suicide?

A
  • Ilgen et al. (2010): used data from a national patient care database, and showed that patients with severe pain committed suicide more often than patients with mild pain.
  • Links to duration of chronic pain condition has not been confirmed (Racine, 2018).
  • Number of chronic pain conditions (comorbidities) is another potential factor: Ilgen et al. (2008) - patients with 2-3 chronic pain conditions show 2-3× greater risk of a suicide attempt.
48
Q

Pain-specific factors: What’s the impact perceived mental health quality? Pagano et al. (2004)

A
  • Life quality typically evaluated using SF36 questionnaire for mental health.
  • Patients who perceive their mental health as bad endorse suicide thoughts more compared to those with higher mental health scores (a number of studies, reviewed by Racine (2018).
  • How people view their own mental health is something that we can identify risks and needed interventions for the chronic pain population.
49
Q

Pain-specific: What’s the impact of sleep impairments?

A
  • Sleep impairments are a predictor of suicide behavior in general population
    – Pain-related sleep-onset insomnia has been shown to correlate with intensity of suicidal thoughts (Smith et al., 2004)
  • Relationship between sleep impairment and SI also exists in chronic pain: fibromyalgia (Calandre et al., 2011), migraine (Liu et al., 2015)
  • Pathways via which impaired sleep affects suicidal thoughts are not known –interaction with depression and pain severity possible/likely.
50
Q

Pain-specific factors: What’s the impact of pain catastrophising?

A
  • Pain catastrophising is an independent contributor to suicidal behavior (Racine et al., 2013; Tang et al., 2016; Brown et al.,
    2020)
  • Of three components of pain catastrophizing, two have been found to contribute to suicidal behavior:
    – helplessness correlated with endorsement of suicidal behavior (Racine et al., 2013)
    – magnification predicted suicidal behavior in rheumatoid patients (Shim et al., 2017)
51
Q

What are some Psychological interventions to reduce suicide behaviour in chronic pain patients?

A
  • Health care professionals need to be aware of an increased risk of suicide, and to know about the risk factors in chronic pain
    patients, to assess risk in patients.
  • Ask questions: “Have you been feeling helpless?”
  • Make actions: provide crisis contacts, check family support (Hassett et al., 2014)

Acceptance and Commitment Therapy program (Hayes et al., 2006):
Thwarted efforts to suppress pain is the basis of suffering leading to increased
suicide behaviour
* emphasis on value of life and positive life goals
* mindfulness-meditation components – acceptance of pain (Newton-John, 2014)