WHAT IS THE PAIN?

Pain is not just a sensory modality but an experience.

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Pain as defined by the International Association for the Study of Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
IASP Task Force on Taxonomy. Classification of Chronic Pain, Second Edition. IASP Press; 1994.  

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This definition recognizes the interplay between the objective, physiological sensory aspects of pain and its subjective, emotional, and psychological components.

Approximately 20% of primary care patients experience chronic pain, and pain screening is intended to improve the quality of pain management by systematically identifying patients with pain in clinical settings, but currently there is no commonly accepted gold standard for clinically important pain.

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One of the most common reasons for seeing a physician, chronic pain is estimated to affect 20% of the world’s population
Lancet. 2011;377

None of the currently available treatments pharmacological, surgical, physical, complementary, or psychological are adequate to mitigate the problem of low back pain in the majority of patients.

Chronic pain is a complex phenomenon that is influenced by genetic, neurophysiological, psychosocial, and behavioral factors. Pain as the fifth vital sign or 6th if you count pulse Ox:

The inclusion of pain level as a vital sign had no impact on pain management, which remained unchanged before and after the implementation of pain as the fifth vital sign and using pain as the fifth vital sign alone is not sufficient for improving pain care, and that other measures to improve evaluation and tx of pain are needed.  

Annually, pain is estimated to burden the U.S. economy with $ 100 billion in direct costs and $ 61 billion in productivity losses. These losses, which amount to a mean of 4.6 hours weekly, are largely due to diminished performance at work
JAMA 2003;290: 2443.

Opiates and other strong analgesics have long been known to numb psychological as well as physical pain, but new evidence suggests that even mild over the counter drugs like acetaminophen may relieve psychological discomfort, such as the stress of social rejection.

The investigators further suggest that acetaminophen may prevent violent behavior, as many studies have shown that being rejected can trigger aggressive and antisocial behavior, which could lead to further complications in social life If acetaminophen reduces the distress of rejection, the antisocial behavioral consequences of rejection may be reduced as well.

Physiology

Pain is an unpleasant sensory or emotional experience associated with actual or potential tissue damage.  

Pain is a blend of the physical and nonphysical components and varies depending on whether the pain is acute or chronic in nature and with the pt in whom the pain is occurring.

Pain is thought to be an evolutionary protective mechanism, by creating anxiety and limiting activity, pain serves to forewarn of physiologic excess and to prevent tissue damage and organ dysfunction.  

Pain is a complex integration of noxious stimuli, affective traits and cognitive factors.   Remember that “pain is what the pt says it is”.   The multifaceted, complex nature of pain poses numerous challenges for the clinician engaged in treating pt’s suffering from painful conditions.

A person’s expectations about pain might affect how much discomfort he or she experiences.
Pain. 2012;153: 1074-1081

When participants viewed a needle prick, as opposed to a cotton swab touch, their unpleasantness ratings and pupil dilation responses were higher provides empirical evidence of the common advice not to look at the needle prick when receiving an injection.

No two pt’s will have the same experience of pain, each person who experiences pain does so in a unique, individual way, even if the physical injury is identical to that afflicted upon another.  

There are no lab tests or objective diagnostic tools to detect the presence of pain, to assess the intensity of pain, or even to determine the source of pain.

Opium is made from the dried juice of the opium poppy Papaver somniferum, with morphine being the principal alkaloid of opium.   Understanding the sometimes striking individual differences in pain response can be elusive, suggested differences can be explained by a biopsychosocial model of pain that includes genetic, social, and psychological factors.

Abundant evidence shows that pain and tissue damage are poorly related, and there are significant differences among individual patients and their perception of pain that extend beyond pathology psychosocial factors consistently account for significant variance in pain reports among these patients and too many patients focus on the pain, lie around, become increasingly sedated on medications, and get into a downward spiral that can affect every aspect of their lives.

Patients can become socially isolated, start doing less and less, and may even gain weight and some really should get out, get some physical exercise, and get their mind off the pain.

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Essentially, all surgical patients will experience postoperative pain, but the intensity of it varies among patients, and a study suggests that this variability is largely determined by genetics.

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The ABCB1 gene codes for the P-glycoprotein 1 MDR1, an important central nervous system efflux transporter of opioids; functional impairment of MDR1 by 1 of the more than 100 known ABCB1 polymorphisms could result in an increased concentration of opioids in the brain.

Single-nucleotide polymorphism SNP c. 3435C/ T rs1045642 in exon 26, which has an allelic frequency close to 50% in Caucasians, significantly modifies MDR1 activity, and therefore might modulate pain intensity; mildly negative social encounters the kind often experienced in day-to-day living can induce stress analgesia and reduce a person’s sensitivity to physical pain
Pain. 2010;151: 372-377.

Doctors who are aloof, distracted, who don’t make eye contact, or who are generally unresponsive to patients may provoke an analgesic response that may cause the patient to report less pain, with insufficient pain control a possible result. No effect of positive interactions was a surprise.

A study based on FDG-PET imaging suggest that arthritic pain has a strong emotional component that is not present with experimental pain conditions induced by heat application
Arthritis Rheum 2007;56: 1345-1354.

Goal for new classes of analgesics for arthritic pain that specifically target the medial pain system  under cingulate cortex, thalamus, and the amygdala brain regions known for the role in processing fear and emotions.

Osteoarthritis (OA) is recognized as one of the most prevalent chronic musculoskeletal diseases worldwide
World Health Organization, 2002

The joints typically affected are located in the hands, knees, hips, and spine with varying degrees of joint deformity and swelling and usually beginning when adults are in their 40s, it is estimated that 9.6% of men and 18% of women >60 years of age are affected with symptomatic OA.

Since age is a significant risk factor in its development, it is predicted that OA will be the fourth leading cause of disability by 2020 In fact, the prevalence of knee OA has been reported to be 44% in those who are 80 years old or greater.

The yearly global economic burden of OA measured by direct and indirect costs is in the tens of billions of dollars annually.

Pain is recognized as one of the hallmark symptoms in knee OA and is the primary reason why patients seek medical attention; It is a significant determinant of functional impairment and disability, even more so than radiographic findings.

Therefore, it is necessary to consider other factors which may be involved in the maintenance of pain when it cannot solely be explained by peripheral nociceptive factors.

As such, alterations in the central nervous system (CNS) may be implicated and understanding the role of central sensitization in pain modulation is important in conditions such as chronic knee OA since its treatment requires an approach that differs from the treatment of pain in a peripheral context.

Duloxetine is a serotonin and norepinephrine reuptake inhibitor (SNRI) with central nervous system activity. Its analgesic efficacy in central pain is putatively related to its influence on descending inhibitory pain pathways.

The analgesic efficacy of duloxetine has been demonstrated in four distinct chronic pain conditions; these include neuropathic pain associated with diabetic peripheral neuropathy, fibromyalgia, chronic low back pain, and osteoarthritis knee pain (OAKP).

Three separate randomized, double-blind placebo-controlled trials have demonstrated that a clinically meaningful decrease in pain severity occurs at about 4 weeks relative to placebo, patients receiving duloxetine report better improvements in physical functioning relative to placebo, duloxetine is safe and effective when used adjunctively with nonsteroidal anti-inflammatory drugs, and  that there are no new safety signals beyond what has been observed in other indications.

Both ascending nociceptive and descending modulatory pathways are involved in pain perception. Ascending nociceptive pathways carry pain signals from the periphery to the brain more specifically, transduction occurs with the activation of peripheral nociceptors (C and Aδ-fibers) through stimulation of peripheral nerve endings which creates an electrical signal, a potential pain impulse, that is conducted to the spinal cord.

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Ascending nociceptive pathways transmit/conduct noxious stimuli from the peripheral regions of the body to the brain. Descending modulatory pain pathways alter the processing of pain signals. Chronic pain, like that associated with knee osteoarthritis (OA), results in changes in the central nervous system, which likely reflect alterations in supraspinal modulation of nociception, and include increases in excitatory and decreases in inhibitory modulation pathways. In the descending modulatory pain system, the neurotransmitters 5-hydroxytryptamine (5-HT) and norepinephrine (NE) modulate pain signals. 5-HT both inhibits and facilitates the perception of pain. 5-HT inhibits pain via the descending inhibitory arm of the descending modulatory pathway and facilitates the perception of pain via the descending facilitatory arm of the descending modulatory pathway. NE inhibits the perception of pain via the descending inhibitory arm of the descending modulatory pathway. NE does not seem to be involved in the facilitatory aspect of pain perception in the descending modulatory pathway

The signal is then transmitted to central nerves in the spinal dorsal horn where peripheral nociceptors synapse with dorsal horn neurons. This is the first stage at which a pain signal can be modulated: either amplified or inhibited. Modulation of the signal is accomplished by neuronal, glial, and endocrine factors in the dorsal horn. Inhibition of the pain signal is referred to as gate control theory and this theory has been updated to reflect the notion that pain in itself is a multidimensional experience involving a distributed neural network, or neuromatrix.

Various neurotransmitters and neuromodulators are involved in the gating process. Both substance P and glutamate are involved in the amplification of pain signals whereas gamma aminobutyric acid (GABA), glycine, endocannabinoids, endorphins, monoamines, and neurosteroids are linked to the inhibition of pain signals. Through ascending pathways, the signal is then conducted further until it reaches the brain.

A painful sensory input is not perceived as painful until it reaches the brain. This is the stage at which the signal is processed by various cortical and subcortical regions responsible for the overall experience and interpretation of pain for an individual. The brain is not only implicated in the interpretation and experience of pain, but it can also modulate pain signals.

Pain signals are also modulated via descending pathways. These pathways travel down from the brain to subcortical nuclei within the mid-brain until they reach the dorsal horn of the spinal cord and can either amplify or attenuate pain signals.

Two essential neurotransmitters involved in the attenuation of pain signals are serotonin (5-HT) and norepinephrine (NE). While 5-HT can both amplify and attenuate pain signals, NE only has an attenuation effect. In addition to 5-HT and NE, opioids and GABA are involved in the inhibition of pain signals whereas glutamate and aspartate are involved in their amplification.

Chronic pain, similar to pain associated with knee OA, results in changes in the CNS, which likely reflect alterations in supraspinal modulation of nociception, and include increases in excitatory and decreases in inhibitory modulation pathways.

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