Theories of pain PDF

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Early theories: Specificity theory & Pattern theory. Gate-control theory. Neuromatrix theory. Psychosocial models of pain: Fear avoidance & Social communication
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Psychology of Pain

Lecture 2: Theories of Pain Overview of lecture  Early theories - Specificity theory - Pattern theory

 Gate-control theory  Neuromatrix theory  Psychosocial models of pain - Fear avoidance - Social communication

Why do we need theories? Conceptual theories can explain, predict effects of pain and aid development of treatment.

What needs to be explained? •Injury and pain are variable (not always a 1:1 connection) •Innocuous stimuli may produce pain (difference between sensory pathways firing and you experiencing pain) •Pain location different from damage location (things that shouldn't be painful are painful) eg. Very light touch produces pain experience •Pain may persist in the absence of injury •Nature & location of pain changes with time •Pain is not single but multidimensional (Melzack & Wall, 1996)

Case study- for discussion o James is a 45 year old shop assistant who experienced chronic back pain for the past 3 years. The pain occurred following the lifting of a heavy object, and resulted in 6 months off work. o He received a combination of massage therapy and NSAIDs. He says that being active

makes his pain worse, and he exhibits slow movements and displays guarding behaviour. o He reports he has good support at home; his wife takes time off work to help out, especially when the pain is bad and he is unable to move. o He says that the pain gets him down regularly, he is irritable and has problems sleeping at night. He worries about the future and whether he will become permanently disabled. Pain is more than just a biological condition: Biophysical overview: Lifting a heavy object. Resulting back pain Emotional aspect: Feeling down, irritable, depression Social component: Wife helps him- helps to reinforce avoidance/habitual behaviour. He isolates himself- feels down so probably doesn’t want to interact with others or go to work. Pain is a disease: not just a symptom- pain persists after an injury (10% of the time). Also, Allodynia, feel immense pain even from a weak stimulus (eg. A feather brushing against an arm feels very painful).

Early theories Early Biomedical Models - Historically, 19th and 20th century models of nociceptive processing followed the traditional biomedical model of disease (pain and tissue injury directly linked). Can generally be divided into two general perspectives (Gatchel, 2007).

Specificity theory - Generally stated that there were unique receptor mechanisms and pathways that transduced and transmitted specific painful information from the periphery to the spinal cord and then to the brain.

•Descartes (1664): specific pain system We detect information around us, tells us about our environment. Theory says that there is a specific pain pathway. Eg. There is a touch sensation. The cold pain sensation pathway is different for hot pain. So separate sensations= separate pathways.

•Müller’s ‘doctrine of specific nerve energies •nerves represent information collected from senses

•Von Frey’s cutaneous senses theory- one of the earliest and best known of the modern specificity theorists (See Finger, 1994). •touch, cold warmth, pain project to the brain •there are pain receptors and touch receptors - His work revolved around the identification and description of mechanical and thermal receptive fields on the skin- suggest that specialised never endings were involved in the transduction and transmission of painful information.

•Problems with assumptions •multiple receptors exist below sensory spots •no specific receptor type for each modality •psychological experience not related to single receptor Shown now that the theory is incorrect, there are multiple pathways. This theory doesn’t account for a top-down effect. The brain CAN modulate the info coming in.

Pattern theory - Pattern response. Nociceptive information was not primarily due to activation of specific receptors and pathways but rather was due to the pattern of responses in afferent systems (conducting or conveying from the periphery toward a central point). It was the stimulus intensity and the processing of the pattern of responses that determined the perceptual response to the nociceptive input, namely, pain.

•Peripheral pattern theory (Weddell, 1955) •excessive peripheral stimulation produces a pattern of nerve impulses that results in pain. Multiple sensory inputs- combination/profile of these inputs that will determine how you experience pain. •some assume general patterning, and don’t consider specific nature of inputs (Weddell)

•Central summation (Livingstone, 1943) •pathological stimulation of sensory nerves produces increased activity in SC circuits; can be triggered by non-painful stimuli. This theory starts to tap into the psychological effects of pain- not explained by the specificity theory. •what is the evidence? Although these two general perspectives had limitations, many issues and potential

explanations related to pain and suffering remained elusive.

Affect theory •Pain as a sensory modality is not new idea •pain influences all sensory events; has motivation and emotion qualities (Marshall, 1894). Emotions play a role in pain felt

•Pain considered opposite of pleasure •But sensory aspect of pain often seen as primary & emotional aspect as secondary or as a response to pain- but emotion is not just a consequence, they’re co-existing ‘Quality of the soul’- pain is an emotion in contrast to a pure sensory event. Livingston (1943, 1998) was one of the first to expose the weaknesses of specificity theory and argue for pain as a subjective state that arises from activation of aversive networks in the brain. The failure of these unidimensional sensory and affective models to explain much of what was observed experimentally and clinically (Beecher, 1959) and the inadequacy of treatments based on these models served as the impetus for a more complex, integrative model. In particular, the seminal gate control theory of pain postulated by Melzack and colleagues (Melzack & Casey, 1968; Melzack & Wall, 1996).

Gate-control model of pain- Melzack and Wall (1965) Old theories don’t really consider top-down effects eg. Placebo effects. Melzack and Wallrevolutionised pain theories. Gatchel (2007)- Melzack and Wall (1965) sought to combine the properties of the specificity theories with the best features of the pattern response theories and the affective-motivational view in order to generate the most inclusive gate control theory of pain. The gate control theory of pain had to account for a number of facts such as the following: (1) the variable relationship between injury and pain; (2) non-noxious stimuli can sometimes produce pain; (3) the location of pain and tissue damage is sometimes different; (4) pain can persist long after tissue healing; (5) the nature of the pain and sometimes the location can

change over time; (6) pain is a multi-dimensional experience; and (7) there is a lack of adequate pain treatments. (p. 165) o Proposes that there are 5 stages that compose the mechanism by which noxious signals enter the spinal cord from the periphery and then proceed to higher level brain areas 1. First stage consisted of the small diameter peripheral nerve fiber transmission of signals to cells in the spinal cord (lots of different types, Aβ, Aδ and C)- noxious and nonnoxious. 2. Second stage included facilitatory interneurons in the region of the spinal cord to account for the fact that cells in the spinal cord can show prolonged after discharge (continued production of nerve impulses after the stimulus that caused the activity has been removed) following the arrival of a signal from the peripheral nerve (Wall, 1960). 3. Focuses attention on a group of additional peripheral fibre inputs to the spinal cord that could be involved in pain processing. 4. Includes inhibitory interneurons to account for the fact that post-synaptic inhibition was likely to occur in the spinal cord. 5. Inclusion of a descending modulatory system to account for the finding that there was an inhibitory influence from the brainstem to the spinal cord. 6. Inclusion of a loop system, assumption that ascending signals to the brain engage and influence descending modulatory systems. 7. Image below illustrates loop system:

Peripheral afferent fibres

•Peripheral afferent nerve fibres signal both noxious and non-noxious (touch) stimulation -Distinction between peripheral nervous system and CNS (spinal cord, brain). Peripheral senses detected by various sensors- transmit these signals to the CNS to carry out an effect/response. There are different types of fibres that input the info to the spinal cord: •Aβ fibres are low threshold stimulated by touch (non-noxious, not harmful) •Aδ and C fibres are stimulated by injury, more extreme trigger required (noxious stimuli- could lead to harm); Aδ relate to sharp, first pain; C relate to dull, second pain. Aδ transmitted faster due to myelination- hence sharp pain. •Noxious and non-noxious differentiated time of trigger A noxious stimulus is “an actually or potentially tissue damaging event.”

Inputs Aδ, C, Aβ

Spinal cord

Spinal Cord •Peripheral afferent nerve fibres enter spinal cord where cells in the dorsal horn respond to both •Nociceptive (harmful/potentially harmful)-specific and wide dynamic range cells deliver impulses to projection neurons (transmission cells; T cells) in spinal cord that then send information to the brain. o Peripheral input- spinal cord- set of fibres in spinal cord region, some are nociceptive specific cells and wide dynamic range cells- project to T cells- which transmits this info to the brain so the T cells quite important.

Spinal cord Inputs Aδ, C, Aβ

T

Interneurons •Cells in spinal cord (dorsal horn) send additional impulses after input •If impulses repeated at regular intervals, after-discharge becomes prolonged Some signals can go straight to T cells, others stimulate interneurons- these can also affect T cells. More signals or greater frequency= more likely to fire up to the brain.

Spinal cord Inputs INT

T

Excitatory & inhibitory interneurons •Interneurons can be either inhibitory (decrease likelihood of transmission cells firing) or excitatory (increase likelihood of firing). •Transmission is dependent on a balance of activity between them Explains some pain conditions: eg. If something wrong with inhibitory interneurons- could lead to the lightest touch feeling extremely painful since the experience of pain is not suppressed.

Spinal cord Inputs

INT

T +

Gate control system Gates control system is modulated by a central control system (brain) Control Centre

(touch) Inputs (pain)

Gate Control System + + INT - T +

Action System

All these signals within the spinal cord, can be modulated by the brain. It receives input from the brain, the spinal cord can change its sensitivity due to input from the brain- this explains the effect of expectation. (Top-down influence).

Appraisal of Gate Control •Highlighted importance of spinal cord in modulating incoming nociceptive information •Acknowledged psychological factors are important in pain •More a model of acute pain than chronic pain (limitation?) •Implications •Injury affects afferent nerve fibres •Central changes can produce changes in pain experience, and include hypersensitivity to pain

Contemporary approaches •Separate modalities

•A & C fibre pain; touch and cold fibres •Spinothalamic tract = pain pathway •Central sensitization (central modulation) •Sensory, motivational & cognitive processes occur in parallel

Modern Approaches to pain

Modern neural-theories of the pain •Neuromatrix theory (Melzack, 1999) •Pain disrupts homeostasis; activates neural, hormonal and behavioural processes to return body to homeostasis •Body perceived as a unity (self); produced by CNS suggesting genetically built-in matrix of neurons for whole body that produces nerve-impulse patterns (sensations); but modifiable (e.g., experience) - ‘Matrix’ stems from pattern theory- multiple pathways, peripheral/central interactions.

- Gat c helRJ ,2007:Proposes that pain is a multifaceted experience that is produced by a characteristic neurosignature of a widely distributed brain neural network (body-self neuromatrix). - Integrates cognitive-evaluative, sensory-discriminative and motivational-affective components proposed by Melzack and Casey (1968). Output patterns of the neuromatrix engage perceptual, behavioural and homeostatic systems in response to injury and chronic stress. Pain is the consequence of the output of the widely distributed brain neural network rather than a direct response to sensory input following tissue injury, inflammation etc.

- Development of this hypothetical system stems primarily from reports and research in patients with spinal cord injuries and in patients that experience phantom limb and phantom limb pain. This theory therefore speculates that no actual sensory input is required to produce experiences of the body.

•Price (1999): Pain matrix – pattern of brain responses, partially specific to pain •Kucyi & Davis (2015; in press): Dynamic Pain Connectome

Psychological accounts of pain •Cognitive aspects •Interruptive function of pain (Eccleston & Crombez, 1999) •Role of the ‘self’ & schema enmeshment (Pincus & Morley, 2001)

•Behavioural •Fear avoidance model (Vlaeyen & Linton, 2000)

•Social context •Social communication model of pain (Craig, 2009) •Biopsychosocial approach to pain communication (Hadjistavropoulos et al., 2011)

Fear-avoidance model

Some people are prone to develop a pain-related fear catastrophizing (excessive worrying)much more vigilant to signs of pain/bodily sensations- lead to misinterpretation of injury even though chronic pain is not due to injury- so probably withdraw, avoidance and lead to long-term depression (a vicious cycle). Gatchel (2007): Pain catastrophizing= exaggerated negative orientation toward

A role for psychological resilience?

Disability Depressi on Avoidance Hypervigila nce

injury

A role for psychological resilience?

Pain experience

recovery

Pain-related fear catastrophiz ing

No fear

(Vlaeyen & Linton, 2000)

How come some people can deal with pain? Perhaps ways of thinking/Environmental factors could help people to cope? Effect people to express pain in different ways according to environment. But social component has limitations- real injury leads to pain. Some pain is just excruciating no matter the environment.

Gatchel 2007: Pain and emotion - Pain is ultimately a subjective, private experience, but is invariably described in terms of sensory and affective properties. The affective component of pain incorporates many different emotions, but are primarily negative. Depression and anxiety have received the greatest amount of attention in chronic pain patients; anger has recently received considerable interest as a significant emotion in chronic pain patients. How can emotion affect pain? 1. Emotional distress may predispose people to experience pain 2. Be a precipitant of symptoms 3. Be a modulating factor amplifying or inhibiting the severity of pain 4. Be a consequence of persistent pain, or be a perpetuating factor. Any number of these could be involved in a particular circumstance interacting with cognitive appraisals. Anxiety, Depression, Anger -

Social communication model Pain doesn’t happen alone. As a result of our interactions/our environment.

Pain experience (past experience?)- Pain expression (how you show it) ß affected by the caregiver/people around you.

Questions Noxious and non-noxious differentiated time of trigger- what does this mean? Gat c helRJ ,PengYB,Pet er sML,Fuc hsPN,Tur kDC.( 2007) .Thebi ops y c hos oc i alappr oac ht ochr oni c pai n:s ci ent i ficadv ancesandf ut ur edi r ec t i ons .Ps y c holBul l .133( 4) : 581624.DOI :10. 1037/ 00332909. 133. 4. 581

The Biopsychosocial Model of Chronic Pain o Traditionally, there was a dualistic view point that conceptualised the mind and body as functioning separately and independently. The inadequacy of the dualistic model contributed to a growing recognition that psychosocial factors, such as emotional stress, could impact the reporting of symptoms, medical disorders, and response to treatment.

o George Engel (1977) one of the first to call the need of a new approach to the traditional biomedical reductionist philosophy. Led to development and evolution of the biopsychosocial model- esp being influential in the area of chronic pain. o Biopsychosocial model focuses on both disease and illness. Illness is viewed as the complex interaction of biological, psychological and social factors (Gatchel, 2005). Whilst disease is the objective biological event, illness refers to a subjective experience of selfattribution that a disease is present. Illness= how a sick person and members of his/her family live with, and respond to, symptoms of disability. o This distinction between disease and illness can be reflected between nociception and pain. Nociception= stimulation of nerves that convey information about potential tissue damage to the brain. Pain= subjective perception that results from the transduction, transmission and modulation of sensory information- like more filtered. This input can be filtered through an individual’s genetic composition, prior learning history, current psychological status and sociocultural influences. Patient needs to be conscious to register pain. Nociception can be detected even in the absence of any subjective report Ieg. A surgical incision). Loeser (1982): o Formulated general model that delineated 4 dimensions associated with concept of pain; dimensions of nociception and pain, suffering (emotional responses that are triggered by nociception or some other aversive event associated with it, such as fear or depression) and pain behaviour (things that people say or do when in pain such as avoiding activities or exercise for fear of reinjury) Both Loeser (1982) and Engel (1977) show that to fully understand a person’s perception and response to pain and illness, the interrelationships among biological changes, psychological status and sociocultural context all need to be considered. Any model that focuses on only one of these dimensions will be incomplete and inadequate....