Presentation on theme: "Physiology & Psychology of Pain. What is Pain?? Introductory Ideas Sensation of the affected level of unpleasantness Perception of actual or threatened."— Presentation transcript:
Physiology & Psychology of Pain
What is Pain??
Introductory Ideas Sensation of the affected level of unpleasantness Perception of actual or threatened damage Perception based on expectations, past experience, anxiety, suggestions, cognitive factors Acute Chronic Pain is Subjective Simple Spinal Reflex Arc
First Order Neurons Stimulated by sensory receptors End in the dorsal horn of the spinal cord Types A-alpha – non-pain impulses NCV m/sec A-beta – non-pain impulses NCV – 36-72m/sec A-delta – pain impulses due to mechanical pressure Large diameter, myelinated, NCV – 4-30m/sec Short duration, sharp, prickling, localized C – pain impulses due to chemicals or mechanical Small diameter, unmyelinated, NCV -.5-2m/sec Delayed onset, diffuse, aching, throbbing
Neurotransmitters Chemical substances that allow nerve impulses to move from one neuron to another Found in synapses Norepinephrine Substance P Acetylcholine Enkephalins Endorphins Serotonin Can be either excitatory or inhibitory
Descending Neurons Transmit impulses from the brain (corticospinal tract in the cortex) to the spinal cord (lamina) Periaquaductal gray area (PAG) – release enkephalins Nucleus Raphe Magnus (NRM) – release serotonin The release of these neurotransmitters inhibit ascending neurons
Assessment of pain Visual analogue scale Picture McGill pain questionnaire Part I: is used to localize the pain and identify whether the perceived source of the pain is superficial (external), internal, or both. Part II: incorporates the visual analogue scale. Part III: is the pain rating index, a collection of 76 words grouped into 20 categories. Patients are to underline or circle the words in each group that describes the sensation of pain being experienced. Groups 1-10= somatic in nature Groups 11-15= affective Group 16= evaluative Group 17-20= miscellaneous words that are used in the scoring process.
Pain Scales Visual Analog Scale Locate area of pain on a picture McGill pain questionnaire Evaluate sensory, evaluative, & affective components of pain 20 subcategories, 78 words None Severe 0 10
Scoring Add up the total number of words chosen, up to the maximum of 20 words (one for each category) The level of intensity of pain is determined by the value assigned to each word. 1 st word = 1 point 2 nd word = 2 point And so on Pt could have a high score of 20, but have a low- intensity score by selecting the 1 st word in each category.
Submaximal Effort Tourniquet Test In 1966, Smith et al described a method of matching a patients pain using a SETT. The SETT is performed by inflating a BP cuff to above systolic pressure on the pt elevated arm. Once the cuff is inflated, the pt is instructed to open and close the hand or fist rhythmically. A handgrip dynamometer and a metronome can be used for standardization. The pt should continue opening and closing the hand or fist until the cramping sensation that he or she feels matches the pain from the original pathology. The amount of time that elapses from onset to fruition of matched pain is the recorded objective measure. The SETT can be repeated at every tx session to gauge tx progress and is effective in matching all types of pain
Pain Threshold – level of noxious stimulus required to alert an individual of a potential threat to tissue Pain Tolerance – amount of pain a person is willing or able to tolerate
Pain Control Theories Where have we been? Where are we now?
Where have we been? Specificity theory 4 types of sensory receptors – heat, cold, touch, pain A nerve responded to only one type Nerve was continuous from the periphery to the brain Pattern theory A single nerve responded to each type of sensation by creating a code (i.E. Different telephone rings) Gate control theory Melzack & wall, 1965 – the basis for theories today Non-painful stimulus can block the transmission of a painful stimulus
Pain Of all the components of the injury response, none is less consistent or less understood than an individuals response to pain The sensation of pain is a diffuse entity inherent to the nervous system and basic to all people It is a personal experience that all humans endure Acute pain is the primary reason why people seek medical attention and the major complaint that they describe on initial evaluation.
Chronic pain may be more debilitating than the trauma itself and, in many instances, is so emotionally and physically debilitating that it is a leading cause of suicide. Pain serves as one of the bodys defense mechanisms by warning the brain that its tissues may be in jeopardy, yet pain may be triggered without any physical damage to tissues. The pain response itself is a complex phenomenon involving sensory, behavioral (motor), emotional, and cultural components.
Once the painful impulse has been initiated and received by the brain, the interpretation of pain itself is based on interrelated biological, psychological, and social factors. What are the nerve fibers that stimulate pain? Nociceptors. Once these are stimulated, pain impulses are sent to the brain as a warning that the bodys integrity is at risk. The emotional response may be expressed by screaming, crying, fainting, or just thinking that hurts!
When the pain is intense or unexpected, an immediate reflex loop activates the behavioral response by sending instructions to motor nerves to remove the body part from the stimulus. Sticking your finger with a needle Placing your hand on a hot stove These stimulis activate specialized nerve fibers to send signals through a peripheral nerve network Routing the impulses up the spinal cord to the brain
When the afferent impulse reach the spinal cord, a reflex loop is formed within the tract to activate the muscles necessary to remove your hand or finger from the stimulus. The remaining impulses of the reflex continue on to the brain, where they are translated as pain, and you respond by saying ouch! or other choice words. If an individual has knowledge about a potentially painful stimulus, such as receiving an injection, cognitive mechanisms can inhibit the reflex loop and block portions of the behavioral response. As a the painful stimulus increases, so does the conscious effort required to keep from trying to escape from the stimulus.
The emotional component may still be in place as you grimace, make a fist, or think what is this jerk doing to me. The cultural components of pain are almost too complex to define. However, pain perception has been linked to ethnicity and socioeconomic status. Example Italian patents are less inhibited in the expression of pain than are the Irish or Anglo-Saxon patients Ultimately, cultural components can be viewed as any variable that relates to the environment in which a person was raised and how that environment deals with pain and responses to pain.
Pain Process Noxious input or nociceptive stimulus causes the activation of pain fibers. The painful impulse is triggered by the initial mechanical force of the injury (whether sudden or gradual onset) and is continued by chemical irritation resulting from the inflammatory process In subacute and chronic conditions, pain may be continued by reflex muscle spasm in a positive feedback loop or through the continued presence of chemical irritation
The pain response is initiated by stimulation of nociceptors Nociceptors- specialized nerve endings that respond to painful stimuli Mechanical stress or damage to the tissues excite mechanosensitive nociceptors Chemosensitive nociceptors are excited by various chemical substances released during the inflammatory response Chemical irritation of nerve endings may produce a severe pain response without true tissue destruction
Unlike other types of nerve receptors, nociceptors display a sensitization to repeated or prolonged stimulation During the inflammatory process, the threshold required to initiate an action potential is lowered, and the continued stimulation of the chemosensitive receptors perpetuates the cycle
Modulation of Pain Acute pain response begins with a noxious stimulus. IE. A burn or cut externally or internally a muscle strain or ligament sprain After trauma chemicals are released in and around the surrounding tissues. Immediately after the trauma, primary hyperalgesia occurs Lowers the nerves threshold to noxious stimuli and magnifying the pain response
Pain fibers A-delta fibers- a type of nerve that transmits painful information that is often interpreted by the brain as burning or stinging pain C-fibers- a type of nerve that transmits painful information that is often interpreted by the brain as throbbing or aching
After an injury, A-delta and C fibers carry noxious stimuli from the periphery to the spinal cord. The noxious stimuli activates 10-20% of the A- delta fibers and 50-80% of the C-fibers. Triggered by strong mechanical pressure or intense heat, A-delta fibers produce a fast, bright, localized pain sensation. C-fibers are triggered by thermal, mechanical, and chemical stimuli and generate a more diffuse, nagging sensation
After an injury, such as a sprained ankle, an athlete feels Sharp, well-localized, stinging or burning sensation coming from which fibers?? A-delta fibers This initial reaction allows an individual to realise that trauma has occurred and to recognize the response as pain Very quickly, the stinging or burning sensation becomes an aching or throbbing sensation, which indicates activation of which fiber C-fibers A third type of peripheral afferent nerve fiber warrants mention. A-beta fibers, respond to light touch and low intensity mechanical information. Rubbing and injured area These interrupt nociception to the dorsal horn
The brains limbic system aids in integrating higher brain function with motivational and emotional reactions. Contains afferent nerves from the hypothalamus and the brain stem. Receives descending influence from the cortex. This communication is responsible for the emotional response to painful experiences. When an injury occurs, the neural communication between the limbic system, thalamus, RF, and cortex produces reactions such as fear, anxiety, or crying. In short, the limbic system is responsible for the bodys affective qualities of reward, punishment, aversive drives, and fear reactions to pain AKA: motivational-affective system.
The integration of the cortex is an important component in both the ascending and descending aspects of pain modulation. Via axons, ascending pain stimuli are transmitted from the thalamus to the central sulcus in the parietal lobe (somatosensory cortex), where the pain is discriminated and localized. Because of the proliferation of nerve cells and the cortexs functions Consciousness Speech Hearing Memory Thought It is unlikely that the afferent synapses that occur during noxious stimulation affect only one efferent neuron. Thus, many areas of the cortex can be stimulated during a painful experience.
The notion of central control and descending inhibition of pain is based on the bodys ability to use and produce various forms of endogenous opiates. Each having a distinct function and a specific receptor affinity. The enkephalins are found throughout the central nervous system, but particularly in the dorsal horn. Thus, the aggregation of noxious stimuli may cause both presynaptic and postsynaptic control of nociception in the dorsal horn via enkephalin release
Review of the process of Pain Transmission Much decision making in the tx of pain can be based on the understanding of the physiological and chemical interaction that occurs after trauma. In simple terms, pain transmission appears to be fairly straightforward. The acute pain response is initiated when substances are released form injured tissues, causing a noxious stimulus to be transmitted via A-delta and C fiber to the dorsal horn
Pain Theory: Historical Perspectives Theories regarding the cause, nature, and purpose of pain have been debated since the dawn of humankind. Most early theories were based on the assumptions that pain was related to a form of punishment. The word pain is derived from the Latin word poena meaning fine, penalty, or punishment.
The ancient Greek believed that pain was associated with pleasure because the relief of pain was both pleasurable and emotional. Aristotle reassessed the theory of pain and declared that the soul was the center of the sensory processes and that the pain system was located in the heart
The Romans, coming closer to contemporary thought, viewed pain as something that accompanied inflammation. In the 2 nd century, Galen offered the Romans his works on the concepts of the nervous system. However, the views of Aristotle weathered the winds of time. In the 4 th century, successors of Aristotle discovered anatomic proof that the brain was connected to nervous system Despite this, Aristotles belief prevailed until the 19 th century, when German scientist provided irrefutable evidence that the brain is involved with sensory and motor function
Specificity Theory of Pain Modulation Modern concepts of pain theory continue to advance from the ideas of Aristotle. However, controversy still exists as to which theories are correct. The theories accepted at the turn of the century were the specificity theory and the pattern theory, two completely different and seemingly contradictory views
The specificity theory suggests that there is a direct pathway from peripheral pain receptors to the brain. The pain receptors are located in the skin and are purported to carry pain impulses via a continuous fiber directly to the brains pain center The pathway includes the peripheral nerves, the lateral STT ( spinothalamic tract) in the spinal cord and the hypothalamus (the brains pain center) This theory was examined and refuted using clinical, psychological, and physiological evidence by Melzack and Wall in They discussed clinical evidence describing pain sensations in severe burn patients, amputee patients, and patients with degenerative nerve disease.
These syndromes do not occur in a fixed, direct linear system Rather in the quality and quantity of the perceived pain are directly related to a psychological variable and sensory input. This theory had been previously addressed by Pavlov, who inflicted dogs with a painful stimulus, then immediately gave them food. The dogs eventually responded to the stimulus as a signal for food and showed no responses to the pain
The psychological aspect of pain perception was later addressed by Beecher, who studied 215 soldiers seriously wounded in the Battle of Anzio, finding that only 27% requested pain-relieving medication (Morphine). When the soldiers were asked if they were experiencing pain, almost 60% indicated that they suffered no pain or only slight pain, and only 24% rated the pain as bad. This was most surprising because 48% of the soldiers had received penetrating abdominal wounds. Beecher also noted that none of the men were suffering from shock or were insensitive to pain because inept intravenous insertions resulted in complaints of acute pain.
The conclusion was drawn that the pain experienced by these men was blocked by emotional factors. The physical injuries that these men had received was an escape from the life-threatening environment of battle to the safety of a hospital, or even release form the war. This relationship suggests that it is possible for the central nervous system to intervene between the stimulus and the sensation in the presence of certain psychological variables. No physiological evidence has been found to suggest that certain nerve cells are more important for pain perception and response than others; therefore, the specificity theory can be discounted.
Contemporary Pain Control Theories Although both the specificity and pattern theories of pain transmission were eventually refuted, they did provide some lasting principles that are still present in contemporary pain modulation theories The strengths of these 2 theories, plus findings obtained through additional research, were factored together to for the basis of the current perspective regarding pain transmission and pain modulation. Still, there is much to be learned and studied before the exact mechanisms of pain transmission and perception are understood.
Pattern Theory of Pain States that there are no specialized receptors in the skin. Rather, a single generic nerve responds differently to each type of sensation by creating a uniquely coded impulse formed by a spatiotemporal pattern involving the frequency and pattern of nerve transmission.
An analysis of the words elements Spatio- the distance between the nerves impluses temporal- the frequency of the transmission An example of this type of coding can be found with most institutional phone systems. A call from inside a university has a different ring from an outside call. Although this theory was closer to being neurological correct there were still shortcomings Melzack and Wall refuted this theory as well, based on the physical evidence of physiological specialization of receptor-fiber units. Plus this theory failed to account for the brains role in pain perception.
Gate Control Theory Implies a non-painful stimulus can block the transmission of a noxious stimulus. Is based on the premise that the gate, located in the dorsal horn of the spinal cord, modulates the afferent nerve impulses.
The SG (substantia gelatinosa) acts as a modulating gate or a control system between the peripheral nerve fibers and central cells that permits only one type of nerve impulse (pain or no pain) to pass through. Serving in a capacity similar to that of a switch operator in a railroad yard, the SG monitors the amount of activity occurring on both incoming tracts in a convergent system Opening and closing the gate to allow the appropriate information to be passed along to the T cell. Impulses traveling on the fast, non-pain fibers activity in the SG. Impulses on the slower pain fibers exert an inhibitory influence. When the SG is active, the gate is in its closed position and a non-painful stimulus is allowed to pass on to the T cell.
Example: Bumping the head The initial trauma activates the A-delta and, eventually, C fibers Rubbing the traumatized area stimulates the A- beta fibers, which activate the SG to close the spinal gate Thus inhibiting transmission of the painful stimulus
Placebo Effect Placebo stems from the Latin word for I shall please Used to describe pain reduction obtained from a mechanism other than those related to the physiological effects of the tx. Linked to psychological mechanisms All Treatments have some degree of placebo effect Most studies involving TM involving the use of a sham TM (ultrasound set at the intensity of 0) and an actual treatment have shown levels of pain in each group.
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.
Two main categories of pain 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.
Chronic Pain Characteristics of Symptoms last longer than 6 months Few objective medical findings Medication abuse Difficulty sleeping Depression Manipulative behavior Somatic preoccupation
Categories of Chronic Pain *Chronic recurrent pain -- benign condition consisting of intense pain alternating with pain-free periods. eg, migraine, tension headaches, endometriosis.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.
Categories of Chronic 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.
Congenital Analgesia A well-known case of congenital insensitivity to pain is a girl referred to as 'miss C' who was a student at McGill university in Montreal in the 1950s. She was normal in every way, except that she could not feel pain. When she was a child she had bitten off the tip of her tongue and had suffered third-degree burns by kneeling on a radiator.
Congenital Analgesia When she was examined by a psychologist (Charles Murray) in 1950 she did not feel any pain when she was given strong electric shocks or when exposed to very hot and very cold water. When these stimuli were presented to her she showed no change in heart rate, blood pressure or respiration. She did not remember ever having coughed or sneezed, and did not show a blinking reflex. She died at the age of 29 as a result of her condition.
Congenital Analgesia Although during a post-mortem there were no obvious signs of what had caused the analgesia in the first place, she had damaged her knees, hips and spine. This damage was due to the fact that she did not shift her weight when standing or sitting, did not turn over in bed and did not avoid what would normally be considered to be uncomfortable postures. This caused severe inflammation in her joints.
Congenital Analgesia Although there is some evidence that this condition may be inherited, there are other causes such as neurological damage. However, some cases cannot be explained in this way. Most people with this condition learn to avoid causing themselves too much harm but, as in the case of 'Miss C, may die as a result of the problems caused by the analgesia.
Episodic Analgesia Serious injury (e.g. loss of limb) - little pain felt. 6 characteristics (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
Episodic Analgesia 6Analgesia is localised, pain can be felt in other parts of the body (arm blown off is not felt, but injection is!)
Episodic Analgesia 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 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."
Pain - Injury 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 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 limbPhantom limb pain Melzack (1992) 7 features 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.
Phantom limbPhantom limb pain 5Phantom limbs give impression of pressure and pain 6Even if phantom limb is experienced as spatially detached from the body, it is still felt to belong to the patient. 7Paraplegic people experience phantom limbs. They can even experience continually cycling legs.
Phantom limbPhantom limb pain 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.
Phantom limbPhantom limb pain Melzack believes - brain contains a neuromatrix of the body image - neurosignature - like a hologram.
Phantom limbPhantom limb pain Connections to this neuromatrix - sensory systems, emotional and motivational systems. It is the emotional and motivational systems that cause the phantom limb experience.
Phantom limbPhantom limb pain Neuromatrix pre-wired - young amputees experience phantom limb pain. People born without limbs also experience phantom limb pain.
Gate Control Theory Proposed by Melzack and Wall in the 1960's
Gate opened or closed by 3 factors 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 conditionsExtent of the injuryMedication Inappropriate activity level Counterstimulation, eg massage Emotional Conditions Anxiety or worryPositive emotions TensionRelaxation DepressionRest Mental conditionsFocusing on the pain Intense concentration or distraction Boredom Involvement and interest in life activities
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
Pain Gate Theory 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.
Pain Gate Theory 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.
Pain Gate Theory 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.
Pain Gate Theory 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.
Pain Gate Theory 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 sensitising it to either C or A- beta fibres.