Pain
Kevin J. Black
I. Background
A. Pain as a neuropsychiatric phenomenon
Pain is defined as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.” Pain “is always a psychological state” and “is always subjective”.1
As this definition notes, pain is much more than a pure sensory phenomenon. Rather, pain is a very complex phenomenon that involves every level of the nervous system from primary sense organs through association and limbic cortex. In fact, it has been observed that the great irony of pain is that it is primarily mediated by an organ that has no nociceptors (the brain).
Components of pain. Consider the pain felt when a finger comes too close to a hot stove. Listed in the subsequent text are some of the components that contribute to the perception of pain in this situation.
Detection. Sufficient heat activates small diameter nerve fibers in the skin that send signals through the spinal cord and thalamus to primary sensory cortex.
Tissue responses. A burn that produces tissue damage may provoke inflammation or other responses that themselves produce ongoing activation of sensory, including pain, fibers.
Gating. Some pain signals are blocked, for instance, at the spinal cord, before ever reaching the brain.
Attention. Common experience shows that distraction can prevent our noticing an injury in some situations, whereas staring at the burned finger and thinking about it can worsen the perception of pain.
Sensory illusions. Analogous to optical illusions, somatic sensory illusions demonstrate how the brain (mis) interprets the actual physical environment. For instance, an alternating grid of cool and warm metal contacts appropriately spaced can produce the sensation of pain although
the cool contacts themselves are not painfully cold and the warm contacts alone are not painfully hot.
Cognition. Someone who has burned his finger many times may benefit from the knowledge that a burn of a certain severity is not likely to cause permanent damage and that the pain is transient. By contrast, an individual with a severe burn in the past may erroneously predict a higher severity of pain or consequent disability than actually occurs, thereby affecting the degree of attention to the sensation and the affective response.
Emotion. Fear, worry, anxiety, and sadness intensify the perceived severity of pain.
Societal responses. Adults who observe someone incurring a first-degree burn from the stove tend to respond very differently depending on whether the unfortunate party is a 5-year-old or a 35-year-old. After acute painful injury, others’ sympathies are engaged and they may provide help, such as fetching things from across the room. Physicians also respond in various ways, such as provision of medications or certification of disability. Whether these societal responses can be helpful or not depends on the situation.
Importantly, these components of pain allow useful treatment interventions at several levels, from local anesthesia to physical therapy to family therapy.
We rely on patient report for assessment and measurement of pain. Many excellent questionnaires and rating scales are available to facilitate description of pain and monitoring of therapy.
Types of pain. There are numerous types of pain that probably represent distinct mechanisms both at the peripheral (nociceptors) and central (brain) levels. For instance, visceral pain (e.g., duodenal ulcer) differs substantially from acute skin pain (e.g., paper cut). Various other distinctions can be made where different pain syndromes differ qualitatively as well as in spatial and temporal distribution (e.g., migraine, pharyngitis, angina, pleurisy, dysuria, childbirth, and various types of superficial lesions, such as accompany burn, stab, crush, or freeze injuries).
B. Pain as an adaptive response
Pain can be useful. Pain leads us, now, to withdraw a hand that gets too near a hot stove and, later, to stay a little farther from the stove next time we cook. A sunburn may prompt us to move into the shade as it develops and may encourage more liberal use of sunscreen the next time we visit the beach. Pain can keep us from putting too much weight on a sprained ankle. In fact, patients with impaired pain perception risk severe injury.
Pain is not always useful. The examples in the preceding text are of acute pain with a clear, modifiable, external cause. In other situations, pain is less useful. After diagnosis, pain in a cancer patient is not often helpful to the patient.
Similarly, pain that lingers for years after an acute back injury usually does not benefit the patient.
Both patients and doctors often develop maladaptive responses to pain. These responses do not necessarily reflect evil intent on either part; in fact they are often benevolent but misguided responses.
C. Pain is a major public health problem
Back pain alone is one of the five most common reasons for visits to a physician.
Neck pain is estimated to disable over 4% of all adults in Saskatchewan.
Indirect costs such as disability payments and lost work account for about half of the estimated costs of chronic pain.
The annual cost of low back pain in the United States was estimated at $100 billion.
Back pain has been estimated to consume 2% of the entire gross national product of the Netherlands.
Medical and disability costs of just 95 Irish patients attending a multidisciplinary pain clinic totaled £1.9 million, with £1.5 million attributed to 22 younger, unemployed patients.
II. Prevalence
Exact prevalence of many pain syndromes is hard to determine confidently because of variable definitions and methods.
Acute pain is ubiquitous.
Subacute pain is also very common. Low back pain “on most days for at least 2 weeks” occurs at some point in at least one seventh of the population.
Chronic benign pain (no identifiable dangerous substrate) has been estimated to occur in up to 40% of the population.
Approximately 15% to 20% of women of childbearing age have chronic pelvic pain.
Occurrence of pain appears to be relatively similar in different cultures (with some important differences). However, medical care seeking and disability vary substantially across cultures.
III. Etiology and Pathophysiology
A. Nociception
Pain related to identifiable stimuli begins with stimulation of nociceptors in skin, viscera, and other organs. Small-diameter neurons activated by these nociceptors synapse in the dorsal horn of the spinal cord, where local interneurons can modulate signal transmission to the brain. Pain signals from the dorsal horn proceed to the thalamus through the contralateral spinothalamic tract but also to the medulla, brainstem, and hypothalamus.
B. Central pain anatomy2
Sensory thalamic nuclei pass pain signals to primary and secondary somatosensory (S2) cortex. However, neuroimaging studies have revealed that other brain regions such as anterior cingulate cortex and insula are at least equally involved in the perception of pain. The anterior cingulate, insula, S2 and thalamus are most commonly involved. The posterior insula is needed to represent basic features of pain including intensity,
whereas the anterior insula has a demonstrable role in emotional and learned effects on pain perception. Many investigators have discussed a lateral and a medial pain pathway, the lateral representing more sensory and discriminative processes and the medial pathway subserving affective and cognitive influences. Both pathways can be activated in the absence of nociceptive stimuli, for example by empathy for pain in others.
whereas the anterior insula has a demonstrable role in emotional and learned effects on pain perception. Many investigators have discussed a lateral and a medial pain pathway, the lateral representing more sensory and discriminative processes and the medial pathway subserving affective and cognitive influences. Both pathways can be activated in the absence of nociceptive stimuli, for example by empathy for pain in others.
C. Descending influences
Specific brainstem nuclei reciprocally innervate the dorsal horn and send descending influences that enhance or suppress pain. Abnormal function of these descending pathways has been demonstrated in animal models of sensitization to pain and more recently in a human functional magnetic resonance imaging (fMRI) study of secondary hyperalgesia. Descending modulatory influences of higher centers are harder to study, but recent studies have suggested that thalamus, hypothalamus, amygdala, and limbic and prefrontal cortical areas can all modulate the perception of painful stimuli.
D. Neurotransmitters
Opioid analgesics exert their effects at μ-subtype opioid receptors in the dorsal horn and at other central nervous system (CNS) sites. Cyclo-oxegenase (COX) enzymes are inhibited by nonselective COX inhibitors (such as aspirin) and by selective COX-2 inhibitors. These agents can decrease tissue inflammation in addition to direct central effects. Other neurotransmitters with a significant role in pain perception or treatment include norepinephrine (centrally acting drugs can reduce pain), glutamate (through N-methyl-D-asparate [NMDA] receptors), dopamine (involved in central pain processing), and γ-aminobutyric acid (GABA) (agonists act at GABA receptors in the dorsal horn).
E. Changes in pain pathways in chronic pain
Pain can actually modify the body system that perceives it, sometimes leading to changes that sustain a long-term painful response to an initially transient injury. Chronic pain affects the nervous system at all levels. Patients with chronic pain show increased sensitivity to various visceral and peripheral painful stimuli, and activate pain-related brain nuclei in a different manner than do healthy controls. One fascinating recent study of patients with chronic back pain found a 5% to 11% decrease in brain gray matter volume, most obvious in dorsolateral prefrontal cortex and thalamus, and correlating significantly with duration of chronic pain.
F. Psychological and social contributors to chronic pain
Patient and physician beliefs and expectations about pain are often incorrect and have been shown to affect recovery.
Compensation (on average) prolongs disability. In one study of patients with back pain, the average time off work was 14.9 months for strain injuries incurred at work, versus only 3.6 months for strain injuries incurred away from work.
IV. Diagnosis and Differential Diagnosis
A. Diagnostic evaluation
1. Medical history
Typical medical historical elements include the following:
Onset, location, quality, severity
Timing of pain, associated features, activities that aggravate or relieve the pain
Psychiatric history
Substance use history
Past medical and surgical history, family history, review of systems
Additional useful information includes the following:
Patient’s fears
Patient’s expectations from the doctor for diagnostic workup and treatment
Social history including work history (in children, school attendance), presence of current litigation or disability applications, social supports
Quantification of pain severity
A simple bedside question is “please rate the severity of your pain from zero (no pain) to ten”.
More comprehensive pain measures are available as described in reference 3.
2. Physical examination
This will be guided by the specific pain complaints (e.g., pelvic pain vs. headache) and includes routine mental status examination. For select patients one can include additional steps, such as quantification of function or observation without patient’s awareness (e.g., in the waiting room).
3. Diagnostic laboratory, neurophysiologic and imaging studies
Whether or which laboratory studies are performed depends on the specific pain complaints. Generally such procedures should be limited to assessing for specific hypothesized diagnoses that fit the history and examination, especially dangerous or highly treatable disorders.
4. Placebo challenge
Placebo response is generally not a helpful diagnostic tool because healthy individuals have robust and physiologically mediated responses to placebos, for example in studies of tooth extraction or appendectomy pain. Therefore the positive predictive value of placebo response is low (American Pain Society Position Statement).4
B. Differential diagnosis
Pain in cancer patients is common and a major determinant of quality of life, and is often discussed separately from other pain syndromes. A useful distinction for diagnosis and treatment of other pain syndromes is acute versus chronic pain. Because neuropsychiatrists are less often involved in the management of acute pain or cancer pain, after a brief summary the remainder of this chapter will focus on chronic pain.
V. Cancer Pain and Acute Pain
In cancer and terminal illness, the goal of pain management is usually relief of suffering and there is less concern for long-term side effects.
A large part of medical education and training is devoted to diagnosis and management of acute illness.
In both these settings, several risks of opioid medication are minimized, and these are often the most appropriate treatment. Despite substantial educational efforts, studies continue to find that pain is often undertreated in both cancer care and acute medical care settings.
The American Pain Society recently published guidelines for management of acute pain and cancer pain.5
VI. Chronic pain
A. General principles
Change of emphasis—As pain becomes chronic, the approach to patient management must change from what is useful in the acute pain setting.
Curative to rehabilitative—The following quote admirably describes this shift in emphasis: “An analogy to other chronic diseases must be drawn. A diabetic has an incurable condition but patients with diabetes can minimize the effects of the disease by making the right choices—eating properly, foot care, etc. Conversely, they can jeopardize their health and increase chances for diabetic complications by making poor choices. Similarly, those with chronic pain can make choices to magnify their painful experience or mitigate it. To use a phrase from a family practitioner friend of mine: The pain is there—misery and suffering are optional.… We (medical professionals) must act as guides to help each patient live a good life despite experiencing chronic pain as opposed to living in misery with it.”6 Patients taught that it is okay to return to work before pain completely remits are more likely to have successful treatment outcomes.
Sensory to functional—The focus must shift more to what the patient is able to do than exclusively on the presence and severity of pain.
Diagnostic to surveillance—After initial diagnostic workup indicated by the history and physical examination, the risk–benefit ratio increases quickly for repeated or invasive diagnostic studies, but continued observation is appropriate for new symptoms or signs that may clarify management.
Subspecialty to collaborative—Care must be coordinated by a single physician to avoid mixed messages and unintentional drug interactions, yet collaboration with psychology, physical therapy, psychiatry, anesthesiology, and neurosurgery can be extremely helpful.
Collaboration with the patient—One of the most important aspects of managing chronic pain is establishing reasonable treatment goals on which the patient and physician can agree. Identifying and specifically addressing patients’ expectations and fears are important.
Chronic use of opioid analgesics raises the risk–benefit ratio because of the development of physiologic tolerance.Related posts:
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