Pain

To be read in conjunction with 'Applying Psychology to Health' by Philip Banyard, and Health Psychology by Sarafino (2nd Edition)

Nature and Symptoms of Pain

DESCRIPTION AND CATEGORIES OF PAIN

Two main categories of pain

1. Acute - is a relatively brief sensation, usually less than six months duration - usually a response to a specific trauma - forms the basis for danger warnings and subsequent learning.

2. Chronic - lasts more than six months - exists beyond the time for normal organic healing The pain begins to impair other functions Patients may begin to experience learned helplessness and hopelessness this leads to the classic signs of depression (lethargy, sleep disturbance, weight loss) May quit work and adopt a self imposed invalid existence.

Categories of Chronic Pain

*Chronic recurrent pain -- benign condition consisting of intense pain alternating with pain-free periods. eg, Migraine, Tension headaches, Endometriosis

* Chronic intractable-benign pain -- benign condition where pain is persistent with no pain free periods, although the pain may vary in intensity eg low back pain.

* Chronic Progressive Pain --malignant condition where pain is continuous and increases in intensity as the organic condition (disease) worsens eg. Cancer and rheumatoid arthritis

THE PHYSIOLOGY OF PAIN

The organic (disease) side of the pain continuum

This involves some stimulus to the bodies pain receptors and transmission of the pain experience through special nerve pathways to the brain.

Pain Receptors

These are bare sensory nerve endings that network throughout all organs and tissues of the body (except the brain)

They respond to many types of stimuli eg extremes of temperature, lacerations, or anything that is potentially damaging to the tissue.When actual injury occurs, Bradykinin (the most potent pain producing chemical/enzyme known) is released from the damaged cells. This bradykinin attaches to the pain receptors (free nerve endings) causing them to transmit pain impulses.

Neural Pathways in Pain

These painful impulses travel to the central nervous system through two different fibres

1. The fibers that transmit impulses quickly are called A-delta fibres. The types of sensations they carry are localised, sharp, pricking, brief sensations.

2. The fibres that transmit impulses more slowly are called C fibres. The types of sensations they carry are dull, burning, aching, longer lasting sensations.

Both these fibres send impulses by releasing a transmission agent called Substance P. Both fibres (A-delta and C) follow a similar pathway up the spinal cord until they reach the Brain.C fibres end in the lower regions of the forebrain whereas a-delta fibres go straight onto the motor and sensory areas of the cortex.

The lower regions of the forebrain do not assess the pain signals as dramatically as the motor and sensory areas of the cortex. The cortex provides immediate attention for the sharp localised pain signals, whereas the c fibres carrying dull aching pain signals are assessed more from an emotional/motivational perspective in the forebrain.

What is Chronic Pain?

Canadian woman who felt no pain (Melzack and Wall, 1988) See p154 (Banyard)

Good thing? -- Not really - led to an early death.

Congenital Analgesia

Pain is literally a lifesaver, alerting the brain to physical harm. "Pain is the body's smoke alarm," says Robert Coghill, a neurophysiologist at the National Institutes of Health. Victims of congenital analgesia, a rare condition that leaves them unable to feel pain, hurt themselves without knowing it, bending their joints to the point of tearing ligaments, or walking on a damaged bone until it breaks. They usually die by the time they are in their 30s from injuries they never felt, their bodies scarred from head to toe.

Episodic Analgesia

Serious injury (e.g. loss of limb) - little pain felt.

See 6 characteristics (Banyard p155) (Melzack and Wall 1988).

  1. The condition has no relationship to the severity or the location of the injury.
  2. No simple relationship to circumstances - occurs in battle or at home.
  3. Victim fully aware of injury but feels no pain
  4. Analgesia is instantaneous
  5. Analgesia lasts for a limited time
  6. Analgesia is localised, pain can be felt in other parts of the body (arm blown off is not felt, but injection is!)

Carlen et al (1978) - Israeli soldiers - Yom Kippur War. Loss of arm - 'bang', 'thump' or 'blow'. Melzack, wall and Ty (1982) - 37% of accident victims reported the experience of episodic analgesia.

 


Fibromyalgia: Pain Without Injury

There is a major problem of faulty logic in the way this highly disabling condition is being perceived. The pain of fibromyalgia is not usually fazed by modern therapies and when you look at the tissues that hurt, you won't see any evidence of injury or disease. It's pain without tissue pathology. Just because you can't see the pain, some might say that the pain is not real, the usual assumption being that it is "psychological." That's the faulty logic often employed. Pain does not require obvious tissue disease to be real and excruciating.

The occurrence of body-wide pain in the absence of tissue damage, as in fibromyalgia, interferes with all aspects of a person's life and undermines their credibility. The problem is that normal activities can be exhausting, sleep is disturbed, the ability to concentrate is impaired, gastrointestinal function is often abnormal, persistent headaches are common, and the unrelenting pain that no one can see is often detrimental to their personal and professional lives--as it creates a "credibility gap."


Neuralgia - sharp pain along a nerve pathway. Causalgia - burning pain Both develop after wound or disease has ended. Triggered by a simple stimulus e.g. breeze or vibration. Physiological cause of headaches not known. Melzack and Wall (1988) report that migraine causes dilation of blood vessels, not the other way around! Pain out of proportion to the injury Some cancers produce little pain until they are advanced. (Serious illness, little pain). Kidney stones are not serious, but produce excruciating pain. Purpose of pain See three points p156

  1. Prevents serious damage. If you touch something hot, you are forced to withdraw your hand before it gets seriously burnt.
  2. Teaches one what to avoid
  3. If pain is in joints, pain limits the activity, so no permanent damage can occur.

but pain can become the problem, and cause people to want to die.

Phantom limb pain Melzack (1992) 7 features p157

The body that never was New Scientist 3rd June 2000

  1. Phantom limb feels real. Sometimes amputees try to walk on their phantom limb.
  2. Phantom arm hangs down at the side when resting. Appears to swing in time with other arm, when walking.
  3. Sometimes gets stuck in awkward position. If behind the patients back, then patient feels obliged to sleep on stomach.
  4. Artificial limb appears to fit like a glove. See artificial limb as part of their body.
  5. Phantom limbs give impression of pressure and pain
  6. Even if phantom limb is experienced as spatially detached from the body, it is still felt to belong to the patient.
  7. Paraplegic people experience phantom limbs. They can even experience continually cycling legs.

Not just the cut nerve endings (neuromas) sending messages to the brain, because cuts made along the neural pathways only produce a temporary relief from pain.

Melzack believes - brain contains a neuromatrix of the body image - neurosignature - like a hologram.

Connections to this neuromatrix - sensory systems, emotional and motivational systems. It is the emotional and motivational systems that cause the phantom limb experience.

Neuromatrix pre-wired - young amputees experience phantom limb pain.

People born without limbs also experience phantom limb pain.

Theories of pain

Specificity theory

Pain and touch sensors on the skin are wired to a pain centre in the brain. This theory is biological and does not account for any psychological factors in the pain experience. Pain receptors carry the painful sensation directly to the brain, and any emotions displayed as part of the experience are merely reactions to the initial pain stimulus.This theory does not account for pain when there is no organic basis for the pain. For example, cannot account for a footballer playing till the end of a match unaware that he may have a broken ankle until the game is over. In this case there is an organic basis for pain but it is not felt until the person gives time to focus attention on the painful area.

Problem (Melzack and Wall, 1988). Even though the senses can be in contact with pain, we do not feel it; and Vice versa - gentle touch can trigger a painful reaction (Neuralgia and Causalgia).

Neurography - an attempt to map nerve cells with specific areas of the body.

Chery, Croze and Duclaux (1980)

  1. onset of pain not connected with the activity in the specialised nerves.
  2. Painful stimuli (e.g. chemicals, pressures, heat) produce different patterns but subjects could not tell the differences.

 

Sensory Decision Theory

This theory relies heavily on the psychological perception of a painful stimulus.

Painful stimuli is perceived according to the individuals cognitive processes eg

* perceptual habits

* beliefs

* expectations

* costs and rewards

* memory of previous pain experiences

Therefore this theory espouses that individual characteristics and situational factors affect pain. It allows for the need to focus on the painful area in order to become aware of the pain signals eg footballer.

Pattern theories

Pain conducting nerves are shared with other sensory nerves- pattern of activity from the nerve cells dictates how the pattern is interpreted.

Three types of cells:

  1. Nociceptive cells -respond to pain
  2. another class that respond to intense stimuli and weak stimuli
  3. Respond to touch, not pain.

Gate Control Theory

Proposed by Melzack and Wall in the 1960's
Gate opened or closed by 3 factors (Banyard p160)

  1. Activity in the pain fibres - opens the gate
  2. Activity in other sensory nerves - closes the gate
  3. Messages from the brain - concentrating on the pain or trying not to think about it

Conditions that open or close the gate

 

Conditions that open the gate

Conditions that close the gate

Physical conditions

Extent of the injury Medication
  Inappropriate activity level Counterstimulation, eg massage

Emotional Conditions

Anxiety or worry Positive emotions
  Tension Relaxation
  Depression Rest

Mental conditions

Focusing on the pain Intense concentration or distraction
  Boredom Involvement and interest in life activities

Painful impulses from the pain receptors only reach the brain if the "gate" is open.

Three variables control this gate

1.A-Delta fibres (sharp pain)

2.C fibres (dull pain)

3. A-Beta fibres that carry messages of light touch

Special neurons located in the grey matter of the spinal cord make up the gate This gate has the ability to block the signals from the a-delta and c-delta fibres preventing them from reaching the brain.

The special neurons in the spinal cord are inhibitory ie they keep the gate closed. These special neurons make a pain blocking agent called enkephalin. This is an opiate substance similar to heroin which can block Substance P the neurotransmitter from the C fibres and the A-delta fibres and this keeps the gate closed.

C-Fibres and A-Delta fibres obstruct (inhibitory) the special gate neurons and tend to open the gate. A-beta fibres are irritable (excitatory) to the special gate neurons and tend to keep the gate closed.

If impulses in the C and A-Delta Fibres are stronger than the A-beta Fibres the gate opens. A-delta fibres are always stronger.

Specialised nerve impulses arise in the brain itself and travel down the spinal cord to influence the gate. This is called the central control trigger and it can send both obstructive and irritable messages to the gate sensitizing it to either C or A-beta fibres.

e.g. if the central control sensitizes the gate to C fibres it is more likely to open. If it sensitises to A-Beta fibres it is more likely to close.

Hence cognitive processors influence the transmission of pain

Cognitive processors that open the gate:

* Anxiety

* Tension

* Depression eg persons having surgery

* focusing on pain

Cognitive processors that close the gate

* Happiness

* Optimism

* Distraction

* Concentration eg footballer, soldiers.

In summary whether or not pain impulses are received by the brain is dependent on a combination of the following

1.The strength of the C fibre impulses (opening the gate)

2. The strength of the A-beta fibre impulses (closing the gate)

3. The central control trigger's sensitization of the gate to C or A-beta Fibres (to either open or close the gate)Eg rubbing area after a bump reduces the pain by stimulating the a-beta fibres of light touch to close the gate. (Theoretically)Gate control theory is the most comprehensive and widely accepted theory at present.

Evidence on the Gate-Control Theory

Reynolds (1969) found that rats electrically stimulated in the periaqueductal gray area were able to tolerate pain (a clamp applied to their tails). Morphine works by acting directly on the periaqueductal gray area. It is thought this area works by sending signals down from the brain in order to close the gate.

Stimulation to the brainstem is known as stimulation-produced analgesia (SPA). Pain fibres produce substance P, in order for the pain signal to cross the nerve synapse. SPA causes another chemical to block substance P.

The body produces endogenous opioids that act as a natural analgesic. Endogenous opioids can be tested by using naloxone. This drug can counteract the analgesia produced by the endogenous opioids. It is thought the endogenous opioids can be produced by stimulation-produced analgesia (SPA). Naloxone blocks the analgesic effect of SPA so it is thought that endogenous opioids are produced by SPA (Akil et al 1976). Injecting Naloxone into patients after dental treatment increases their pain (Levine et al 1978). Naloxone does not always block SPA, it depends upon where the electrical stimulation is applied within the periaqueductal grey area.

Melzack and Wall conclude:

  1. There are several descending control systems, some are sensitive to naloxone, but others are not.
  2. Many other non-opioid transmitters, such as noradrenalin, acetylcholine and dopamine are also involved in analgesia.

The effect of endogenous opioids on pain may be dependent upon how long the pain lasts. Morphine taken to relieve short episodes of pain, tolerance develops quickly. When morphine is given to patients suffering from long-term pain (e.g. cancer) they do not develop tolerance (Melzack and Wall, 1982).

In times of stress, for example in sport or on the battlefield, endogenous opioids are released (Bloom et al 1985). This will explain why soldiers can fight on with little pain, even though they are severely injured.

Factors affecting pain

  1. Sensations
  2. Emotional reaction - Beecher 1946, 1956 research on the subjectivity of pain. He interviewed soldiers in the battlefield during WW2 - even though they had serious wounds and extensive surgery. they experienced relatively little pain - the psychological experience of being the end of the war for them - they would be going home. He then interviewed civilian patients with less extensive surgery who reported being in considerable pain - this was the beginning of their ordeal. Civilians were more likely than soldiers to request analgesic drugs. Different circumstances alter the meaning of pain therefore the pain must at least be partly subjective.
  3. Cognitive components

Personal and Social Experiences and Pain.

Migraine sufferers display stronger physiological arousal to words associated with pain than non-sufferers (Jamner & Tursky 1987). This demonstrates classical conditioning. The symptoms of the onset of migraine become associated with the migraine, thus causing the pain to be experienced more strongly.

Pain Behaviours

Four types (Turk et al 1985)

  1. Facial/audible expressions of distress
  2. Distorted ambulation or posture
  3. Negative affect e.g. being irritable
  4. Avoidance of activity

Pain can bring secondary gains

Patients who received compensation stayed in hospital longer and took longer to return to work (Block et al 1980).

Attention received from relatives also affects pain behaviour.

Karen Gil et al (1988) observed parents with children who had a skin disease. The doctor had advised the child not to scratch the skin, which was itchy. Parents who gave more attention to the scratching behaviour seemed to be encouraging the behaviour, because scratching increased!

Flor et al 1987) found that patients with spouses who gave attention to pain behaviours also seemed to be encouraging the behaviours!

Block et al (1980) found that patients reported more pain in an interview if they knew their spouse was watching behind a one-way mirror and their spouse was concerned about their pain.

Emotions, Coping Processes, and Pain

Kent (1985) found that dental patients who reported anxiety, also reported higher levels of pain immediately after treatment and reported four times the original level of pain three months later. Low anxiety patients remembered levels that were less than twice the original levels.

Type A stress people tend to suffer more from chronic headache (DeBenedittis et al 1990).

Gannon et al (1987) balanced three groups for gender and age. The three groups consisted of:

Chronic migraine patients

Chronic muscle-contraction patients

Occasional headache patients.

They were given a stressful time by being asked to solve difficult mental arithmetic problems at a rate of one every fifteen minutes. A warning buzzer would go off from time to time indicating a 'drop in performance' (it wasn't really related to performance). Two-thirds of the chronic sufferers experienced a headache as a result of the stress, whereas only a quarter of the occasional headache patients experienced headaches.

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