Lecture 4 - Psychology of Pain

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Lecture 4 - Psychology of Pain by Mind Map: Lecture 4 - Psychology of Pain

1. What is Pain?

1.1. Clinical Pain - pain that requires some form of medical treatment.

1.2. Costs of Pain - $500-$635 billion annually. Equal to $2000 for every person in the US.

1.3. Experiencing pain is the most common reason people seek medical treatment. It is experienced by 1/3 of the population. 25% of people in nursing homes experience pain. Pain is experienced more by women than men.

1.4. Pain is the 5th vital sign of illness, along with blood pressure, pulse, temperature, and respiration.

2. Types of Pain

2.1. Acute Pain - sharp, stinging pain that is short-lived (seconds to a few months). It is usually related to tissue damage, e.g. burns, fractures, or overused muscles. It generally subsides when general healing occurs.

2.2. Recurrent Pain - episodes of discomfort interspersed with periods in which the individual is relatively pain free, that recur for more than 3 months. E.g. periodic migraines or non-cardiac chest pains (experienced by 10% of school children).

2.3. Chronic Pain - pain that lasts 6 months or longer (past healing period). It may be continuous/intermittent, or moderate/severe, and felt in any part of the body. It lowers QoL and increases vulnerability to infections. It affects 10% of the population.

2.4. Hyperalgesia - condition in which a chronic pain sufferer becomes more sensitive to pain over time. It may facilitate recuperative behaviours. It is a normal adaptation during sickness.

3. Measuring Pain

3.1. Psychophysiological - Electromyography (EMG) assesses the amount of muscle tension. Indicators of Autonomic Arousal - measures of heart rate, breathing rate, and blood pressure.

3.2. Behavioural - Pain Behaviour Training Programme (Fordyce, 1982) observes behaviours such as time spent in bed and requests for pain killers. Pain Behavioural Scale rates occurrence of vocal complaints, facial grimaces, awkward postures, and mobility. Pain Response Preference Questionnaire - asks how you want to be treated by a spouse. Children's Anxiety and Pain Scale - pain and fear in children. E.g. Wong Baker Faces.

3.3. Self-Report - simplest and preferred method. E.g. Pain Rating Scales (numerical ratings or diary), Visual Analogue Scale (pain as horizontal or vertical line), and McGill Pain Questionnaire - where is your pain? What does it feel like? Any changes over time? How strong is the pain?

4. Physiology of Pain

4.1. Begins with sensory receptors in the skin converting a physical stimulus into neural impulses. The PNS will relay the signal to your brain, where it is registered and interpreted.

4.1.1. Pain Receptors: Free Nerve Endings - sensory receptors found throughout the body that respond to temperature, pressure, and painful stimuli. Nociceptors - specialised neuron that responds to painful stimuli.

4.1.2. Neural signals from Free Nerve Endings are routed to the CNS via Fast and Slow Nerve Fibres: Fast NF - large, myelinated nerve fibres that transmit sharp and stinging pains at about 15-30 metres per sec. They service the skin and mucous membranes. They are stimulated by strong pressure and extreme temperatures. Slow NF - small, unmyelinated NF that carry dull ahcing pains at about 0.5-2 metres per second. They serve all body tissues except the brain. It acts as a warning system, e.g. putting your foot in bath. Stimulated by chemical changes in damaged tissue. After leaving the skin, Fast and Slow Fibres group together as nerves to form sensory tracts. These funnel info up the spinal cord to the back of the brain, where they synapse with neurons in the substantia gelatinosa. In spina cord they link with sensory nerves that carry touch, pressure, and movement sensations to the thalamus. On its way to the thalamus, the fast pathway triggers neural activity in the reticular formation (the brains mechanism for arousing the cortex in response to important messages and reducing awareness for unimportant stimuli). Once in the thalamus, incoming messages are routed to the somatosensory area of the cerebral cortex, the area that receives input from all the skin senses. The amount of somatosensory cortex alloted to various regions of the body determines our sensitivity to that region. E.g. face has more than back. The internal organs are not mapped on this so it is hard to pinpoint visceral (internal) pain and it often becomes referred pain. E.g. the Monoculous is the model that represents sensitive parts of our body. Referred Pain - pain manifested in an area of the body that is sensitive to pain but caused by disease or injury in an area of the body that has few pain receptors.

5. Neurochemistry of Pain

5.1. The brain is capable of stopping pain through a descending neural pathway: Anterior Cingulate Cortex --> Periaqueductal Grey Area --> Neurons in Medulla --> Substantia Gelatinosa of Spinal Cord. This pathway uses serotonin to activate enkephalin containing spinal neurons which inhibit pain information coming from substance P fibres.

5.1.1. Substance P - secreted by pain fibres in the spinal cord and stimulates cells to send pain signals to the brain.

5.1.2. Periaqueductal Grey Area of the Midbrain - activates Enkephalin, when this is stimulated, pain is reduced almost immediately. The analgesia (pain relief) continues even after stimulated is discontinued. Enkephalins - naturally occurring opiates found in nerve endings of cells in the brain and spinal cord. They bind to opioid receptors to deaden pain sensations. They synapse with slow fibres and regulate how much substance P is released, if substance P is not released, or it is released in small quantities, an incoming pain message will be reduce or blocked.

5.1.3. Recent fMRI studies have shown that the dorsal anterior cingulate cortex has been involved in the cognitive modulation of pain and areas of self-regulation. Studies have shown that chronic pain patients are often deficient in self-regulatory skills such as self-control.

5.2. Stress-Induced Analgesia - pain relief that results from the body's production of endorphins as a response to stress.

5.2.1. Endorphin - a natural opioid powerful enough to produce pain reflief comparable to that of morphine and other opiates.

6. Genes of Pain

6.1. Several rare but serious pain disorders are caused by mutations in a gene called SCN9A.

6.1.1. SCN9A - encodes instructions for sodium channels that help nerve cells that relay painful sensations in the body's tissues to the CNS. There are two disorders caused by faulty alleles of these gene: People suffer intense pain because their sodium channels open too easily or cannot close. People are completely unable to feel pain because SCN9A produces a protein which cannot function.

6.2. COMT - one of several enzymes involved in the metabolism of certain neurotransmitters (dopamine, epinephrine, and norepinephrine). It influences the severity of pain and the length of physical and psychological recovery from a traumatic event that has caused musculoskeletal pain, e.g. whiplash.

6.3. Twin studies have reported heritability of about 50% for different pain traits. E.g. variation in how people respond to painful stimuli: Mediating anxiety and depression (linked to prevalence and experience of pain) Affecting individual sensitivity to painful stimuli.

7. Gate Control Theory (Melzack & Wall, 1965)

7.1. There is a neural 'gate' in the spinal cord which regulates the experience of pain. Incoming sensations that signal pain are modulated in the spinal cord as they are conducted to the brain. They are subject to modification under the influence of descending pathways from the brain.

7.2. There is an existence of neural structures in the spinal cord and brainstem that function like a gate, swinging open to increase the flow of transmission from nerve fibres, or swinging shut to decrease the flow.

7.2.1. Gate Open - signals arriving stimulate sensory neurons called transmission cells. These relay signals upward to reach the brain and trigger pain. Activity in the slow pain system tends to force the gate open.

7.2.2. Gate Closed - signals are blocked from reaching the brain and no pain is felt. Activity in the fast pain system tends to close the gate.

7.3. Central Control Mechanism - descending neural pathway by which the brain shuts the gate

7.3.1. A central control mechanism in the brain accounts for the influence of thoughts and feelings on the perception of pain. Through this mechanism, anxiety or fear may amplify the experience of pain, whereas the distraction other activities can dampen the experience of pain.

7.4. The mechanism for opening and closing the gate is in the substantia gelatinosa of the spinal cord.

7.5. Also proposed that a widely distributed network of brain neurons determine a person's perceptual experience by further processing messages reaching the brain. This network of cells (the neuromatric) seem to operate even in the absence of sensory input, placing greater emphasis on the role of the brain in pain experience.

8. Psychosocial Factors in the Experience of Pain

8.1. Age

8.1.1. The overall prevalence of pain amongst older people was 52.9%, which the majority of these reporting pain in multiple locations.

8.1.2. It was also higher in older women, older people with obesity, older people with musculoskeletal conditions, and depressive symptoms.

8.1.3. Pain is associated with decreased physical capacity. Older adults with pain had weaker muscle strength, slower walking speed, and poor overall function.

8.1.4. Pain is also influenced by levels of complaining and social comparison. Adults who reported that their parents had experienced pain were more likely to report pain themselves. Older adults are more vigilant to their health status as they feel vulnerable.

8.2. Gender

8.2.1. Women report more frequent episodes pf pain. These gender differences are already apparent by adolescence.

8.2.2. Certain analgesics may be more effective for women.

8.3. Socioeconomic Status and Stress

8.3.1. People at LSES have greater morbidity and mortality across many diseases.

8.3.2. They experience more stressful life events, more stressful environments, and fewer psychological resources.

8.4. Culture and Ethnicity

8.4.1. The experience of pain is shaped by the meanings that we attach to events. E.g. in some cultures, tattooing and body piercings are perceived as normal and bring great honour.

8.4.2. Pain responses of patients are divided into two culturally related categories. Stoic - grin and bear. Less expressive, turn inwards, and withdraw socially when feeling discomfort. They perceive pain a a private and personal experience. Emotive - verbalise and express pain. Prefer having others around them to respond to their pain and discomfort, and validate it.

8.4.3. Arthritis was higher for non-Hispanic blacks than non-Hispanic whites. Yap women - pregnancy is easy and they got on with it. Spanish word for labour means 'sorrow', they report higher levels of pain.

8.4.4. Pain Tolerance - how much pain we take - doesn't differ across cultural groups.

8.4.5. Pain Threshold - how much we will tolerate until we complain - does differ across cultural groups.

8.4.6. Cautions - different languages have different amount of words for pain. E.g. in English there are 4 basic ways to describe pain (ache, sore, hurt, and pain). But in Japanese, there are only 3. And, Thai people have only 2.

8.5. Pain Prone Personality?

8.5.1. Acute and chronic pain sufferers show elevated scores on two Minnesota Multiphasic Personality Inventory scales. Hysteria - tendency to exaggerate symptoms and use emotional behaviour to solve problems. Hypochondriasis - tendency to be overly concerned with health and over-report body symptoms.

8.5.2. People who are anxious, worried, fearful, and depressed report more pain. Depression is more prevalent amongst lower back pain sufferers. Patients undergoing dialysis for initially reported symptoms of depression were more likely to develop severe pain.

8.5.3. Some researchers belief that differences in coping are telling to personality types. Treatments should match a patient's coping style. Researchers have identified three subtypes of pain patients: Dysfunctional Patients - high levels of pain because they feel they have little control over their lives. They are inactive. They feel that their illness is their identity. Interpersonally Distressed Patient - receive little social support and feel other people in their lives do not take them seriously. This is most people. Adaptive Copers - report lower levels of pain and distress but continue to function at a high levels.

9. Social Learning

9.1. Social and cultural factors can lead to the social construction of an illness.

9.2. The social environment shapes an individual's pain experience by a way of operant conditioning. The expression of pain serves as an adaptive function by capturing the attention of others and triggering caregiving and helping behaviours.

9.2.1. Fordyce's operant conditioning model of pain - suggests that chronic pain sufferers receive social reinforcement for pain behaviours from the attention they receive from family and friends. Pain Behaviours - actions that are response to pain, such as taking drugs, grimacing, or taking time or work/school.

9.2.2. We learn this in childhood. Children whose parents disregard their pain behaviour may grow up to be more stoic in their approach to pain.

10. Treating Pain

10.1. 2008 expenditure on pain management and drugs in the US alone was $20 billion dollars, expected now to be $30 billion.

10.2. Eclectic/Cafeteria Approach - treatment is tailored to each case and patients are taught several pain management techniques.

10.3. Pharmacological Treatments

10.3.1. Opioid Analgesics - formally called narcotics (Greek - numbness). These are agonists that act on specific receptors in the spinal cord and the brain to reduce the intensity of pain messages or brains response to pain messages. E.g. morphine - binds to receptors in the PAQ, the thalamus, and cells at the back of the spinal cord.

10.3.2. Non-Opioid Analgesics - aspirin and ibuprofen. They reduce pain without sedation, reduction of inflammation, and reduction of temperature when fever is present. They relive pain by blocking a chemical chain reaction that is triggered when tissue is injured.

10.4. Surgery, Electrical Stimulation, and Physical Therapy

10.4.1. Counter-Irritation - stimulating one area of the body to reduce pain in another.

10.4.2. Transcutaneous Electrical Nerve Stimulation - brief electrical pulses applied to nerve endings under the skin to produce numbness.

10.5. Cognitive Behavioural Therapy

10.5.1. A multidisciplinary pain-management programme that combines cognitive, physical, and emotional interventions.

10.5.2. Provides explanation about differences in acute and chronic pain, mechanisms of gate control therapy, and contributions of mental distress.

10.5.3. Cognitive Interventions - enhance a patient's self-efficacy and control over pain. Targets cognitive errors in thinking Catastrophizing - overestimate distress and discomfort caused by an experience. Focus excessively on the negative and use more pain medication. fMRI studies have shown this is associated with enhanced neural activity in the anterior cingulate cortex and the amygdala. It also intensifies pain due to effects on blood pressure reactivity and muscle tension. Overgeneralising - pain will never end and will ruin their lives. Leads to depression. Victimisation - victim of their illness. Experience of injustice. Loss of ideal self. Self-blame Dwelling on the pain

10.5.4. Cognitive Distractions - diverting attention can reduce pain intensity by 30-40%. E.g. playing video games diminished pain by up to 40% (Hoffman, 2007)

10.5.5. Cognitive Reappraisal - reinterpret pain-related sensations. Involves self-regulation in a logical and realistic way.

10.6. Sensory Focus and ACT

10.6.1. Attending directly to painful stimulus without trying to change it. People who score high on anxiety seem to be effective at this.

10.7. Guided Imagery

10.7.1. Component of Lamaze training (childbirth).

10.8. Meditation

10.8.1. Reduce pain intensity ratings by 40% (Zeidan, 2009).

10.8.2. Four areas of the brain affected - primary somatosensory cortex (processes pain), anterior insula (heart rate and blood pressure), anterior cingulate cortex (emotional responses), and prefrontal cortex (command centre)