Pain: Psychological factors and treatments (FSWPK35)
Institution
Erasmus Universiteit Rotterdam (EUR)
Book
Wall
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Pain: Psychological factors and treatments (FSWPK35)
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Content preview
Elective: Pain
Psychological factors and treatments
Practical Course Information
Coordinator: Prof.dr. MJ Wieser
Cursus code: FSWP-K-3.3.14
College year: 2017-2018
Ects: 5
Language: English
Opleiding: Bachelor 3 Psychology
Modules
1. Definition and neurobiological basis of pain
2. Emotional influences on pain
3. Cognitive influences on pain
4. Psychological interventions
Goal
The aim of this course is to increase students' knowledge of a topic, which has gained increased interest
in Clinical Psychology in recent years: Pain and its modulation by psychological factors. The main goal
is for students to learn about recent scientific insights into the neurobiological basis and psychological
models of pain, its modulation by psychological factors, and (psychological) treatment methods.
Contents
Pain is an all-too-familiar problem and the most common reason that people see a physician. Pain is an
adaptive process and serves an important purpose by alerting us to potential tissue damage and injuries
and thereby inducing protective reactions. For a long time, pain was considered as a purely physical
sensation and symptom of an underlying somatic disease. In the last decades, it has become clearer and
clearer that pain is a psycho-biological experience including sensory and emotional components. In this
course, students will be introduced to the biological and psychological underpinnings of pain and
experimental paradigms to investigate pain in the psychological laboratory. The main focus will be on
psychological factors of pain such as the influence of emotions, attention, expectations (placebo-effect).
Other topics of this course include phenomena such as phantom limb pain or chronification of pain and
their underlying neurocognitive mechanisms. Furthermore, diagnostics of pain and different
psychological treatment approaches will be discussed.
Literature
• Mcmahon, S.B. & Koltzenburg, M. (2010). Wall and Melzack’s Textbook of Pain. 5th
Edition. Elsevier, Amsterdam.
• Al’Absi, M & Flaten, M. A. (2016). The Neuroscience of Pain, Stress, and Emotion. Elsevier,
Amsterdam.
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, Topic 1: Definition and neurobiological basis of pain
Preliminary Discussion
Learning Goals
Problem 1.1: Pain and Psychology?
1. What is pain? x
2. What’s the difference between physical and psychological pain?
3. Can the pain intensity differ between people and how can you measure pain?
Problem 1.2: Different shades of pain in the brain
4. Where is pain localized in the brain and how does the pain process work? x
5. What happens if one of the processes gets damaged?
Problem 1.3: Up and down, round and round?!
6. What parts of the body are involved in pain? (pathways) x
7. What are the ascending and descending pathways? x
8. What causes a person to experience more pain than someone else?
Literature
Book 1 : Representation of Pain in the Brain (Apkarian, et al.)
Defining a pain network in the brain
Brain activity can be depicted with different techniques including PET, SPECT, functional magnetic
resonance imaging (fMRI), electroencephalographic (EEG) dipole source analyses and
magnetoencephalographic (MEG) analysis.
There are many differences in cortical and subcortical activation patterns, but a consistent network has
emerged with sensory, limbic, associative and motor areas. Most activated areas are S1, S2, ACC,
insular cortex, prefrontal cortex (PFC) (IC), thalamus and cerebellum. Areas activated by pain receive
direct or indirect nociceptive input.
• S1 & S2: input of somatosensory thalamus
• Cingulate cortex: input of medial thalamic nuclei & lateral thalamic regions
• IC: thalamic nociceptive input
Posterior cingulate areas provide a direct route for the control of motor responses to painful stimuli. The
most common subcortical pain-related activity takes place in the thalamus and cerebellum.
Different nuclei in the thalamus receive nociceptive input from the dorsal horn, the cerebellum receives
spinal connectivity. Some studies suggest activity in the nucleus accumbens and amygdala. PAG is also
active.
Brain processing of the multidimensionality of pain
Somatosensory cortex is important for perception of sensory features, such as the location and duration
of pain, whereas the limbic and paralimbic areas (such as ACC and IC) are more important for the
emotional and motivational aspects of pain. Involvement of the ACC is required to produce aversive
learned behaviour for the noxious stimuli. There is a connection discovered between the intensity of
painful hot stimuli, and IC activation. IC is also important for pain affect.
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, • Large unilateral IC lesions increase pain perception;
• Focal posterior IC lesions lead to central pain, and specific defects in acute pain perception;
• Anterior IC example of subjective strength of painful stimuli.
The prefrontal pain-induced activity is more related to the cognitive aspects of pain perception than
directly on the pain sensation or affect.
The orbital frontal-accumbens-medial thalamus network is involved in the affective perception of pain,
the dorsal frontal cortex acts as top-down controller that modulates pain and is therefore limited to the
scope of suffering. The cerebellum plays a role in the modulation of instinctive and somatic nociceptive
reactions.
How do we distinguish location and quality of pain?
Every pain experience is unique, individuals can distinguish malicious harmful heat cold. There is
evidence that the neural activity in the place of the S1 pain could identify. There is found that S1
nociceptors neurons have receptive fields/ontvangingsvelden discrete so that different neurons respond
to painful stimuli in different areas on the skin. The IC also takes part in locating pain.
Strigo et al. found that the two types of different types of activation caused pain in the IC, S1, motor
cortex and PFC.
Laterality of pain representation
Distinct brain responses to nociception and to subjective perceived pain
• Ventral stream: is for determination of intensity
• Dorsal stream: is for determination of localization
Figuur 1. Ventrale en Dorsale stroom.
Green: dorsal, Purple: ventral.
Relative to the subjective rating of perceived pain, the IC reactions should be divided into two areas:
• Nociceptive areas
• Pain-perception areas
Temporal sequence of cortical activity during pain perception
The first brain activity through pain comes from the S2 and IC. The first pain is to direct threat to be
reported get back directly, the second pain attracts more long-lasting attention and motivates
neuroendocrine responses to minimize damage and recovery to optimize. There are also blood flow
techniques used to study differences in brain activity. Casey et al., found that the activation pattern
differed for repeated painful temperature stimuli. The scan differed immediately after the stimulus or if
3
, the pain all of 40 seconds was present. Parts of the ACC and amygdala reacted according to a predictable
pattern. The thalamus, basal ganglia, part of the IC and associated motor areas were then activated; the
perception part of the IC, together with the higher frontal and parietal areas was activated.
The brain’s role in modulating pain
Descending projections from the cerebral cortex 'feed into' the modular systems and additional pain
modulation may also take place in the cortex.
Opiates in the Brain
Opiate reactions are studied by means of two approaches: rate of the metabolic function of the brain as
a response to pharmaceutical agents/intermediaries and a direct measurement of receptors.
Acquisition of data over time (as the radiotracer binds to specific receptors together with appropriate
kinetic models) allows quantification of receptor sites and enzyme functions in human subjects.
Figure 1. Temporal sequence of brain areas activated when participants rates the magnitude of pain perceived for a thermal
painful stimulus.
Fentanyl has a inhibiting effect on measurements of pain related neural activity. Dynamic changes in
the activity of the endogenous opioid system and -opioid receptors are examined: reductions in vivo
availability of -opioid receptors reflect an activation in this neurotransmitter system, this was the
subject of surveillance in the ACC, PCF, IC, thalamus, basal ganglia ventral (nucleus accumbens and
ventral pallidum), amygdala and PAG.
An area in the dorsal ACC is associated with suppression of the affective quality of pain. It may be that
the brain opiate-system is damaged with chronic pain.
Another addition to the variability of -opioid receptors binding, and the capacity to activate this
neurotransmitter system, is described as a function of General polymorphism of catechol O-
methyltransferase (COMT) enzyme.
Dopamine and pain
Dopamine plays a part in pain modulation: weakens nociceptive reaction in animals.
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