In light of preoperative and postoperative mortality and morbidity, continued advancement in pain and anxiety management would benefit millions. Although significant strides have been made in the past few decades, it is imperative that research and development continue. This article discusses types of pain and anxiety, the relationship between pain and anxiety, the physiology of pain and anxiety, and current trends in pain and anxiety management.
The current management of pain and anxiety continues to evolve much as it has throughout its history. Beyond advances in pharmacology and technology, changes in societal views have historically influenced how we address these conditions. Discussing how cultural views have shaped medical management may help in understanding the continued evolution of treatment. Historically, the management of pain has evolved through many different societal and medical influences. Meldrum elaborates on how pain contributes to philosophic, political, and religious ideology and has defined the suffering of individuals throughout human history. As the oldest medical problem and the universal physical affliction of humankind, little of its physiology has been understood until very recently.
In the 17th century, European physicians treated pain most often with opium, particularly laudanum, which was a mixture of opium in sherry. Yet pain was often seen as a medical necessity or diagnostic aid. Pain was used to relieve evil spirits or to amputate diseased limbs. It was a valued sign of the patient’s vitality and of the effectiveness of treatment. Physical suffering was inevitable; the meaning, rather than actual pain, was what mattered to the physician. Pain was also attributed to serving as a counterirritant to disease.
The necessity of pain was questioned in medical opinions of the 1800s. Although the skilled surgeon took pride in his ability to operate quickly, the utility of sedation for long procedures was readily apparent. Dr William T.G. Morton, an American dentist, demonstrated the use of ether in 1846 to perform a dental extraction. The advent of anesthesia created much medical and societal controversy. Debates began over the ethics of operating on an unconscious patient and that the relief from pain might actually impede healing. Religious writers called anesthesia a violation of God’s law. It wasn’t until 3 decade later that anesthesia gained widespread acceptance.
Today the treatment of pain has changed dramatically; yet pain and its management or lack thereof continues to be one of the main obstacles in establishing routine dental care. It is estimated that as many as 75% of adults experience some degree of dental fear and that up to 10% may possesses a dental phobia that prevents them from seeking treatment in all but the most dire of circumstances. Neglect and procrastination result in conditions necessitating surgical treatment leading to increased perioperative and postoperative pain, which reinforces the pattern of treatment avoidance.
Pain management is important from a public health perspective as well. The American Society for Pain shows that pain results in more than 50 million lost workdays each year, worth an estimated $100 billion in the United States. Currently, approximately 20 million Americans experience jaw and lower facial pain (temporomandibular joint disorder [TMD/TMJ]) each year. Furthermore, as the population ages, we can expect that rates of acute and chronic pain will increase in elderly individuals.
Types of pain and anxiety
The International Association for the Study of Pain defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It is a subjective experience. Nocioception is defined as the neural processes of encoding and processing noxious stimuli. It is one of the pathophysiologic processes that produces pain. Although we appreciate that pain very often has a physical cause, it also has a psychological component that by itself may produce pain via psychosomatic pathways.
Pain is classified into acute versus chronic pain, with further differentiation based on pathophysiology, etiology, and/or the affected area. Acute pain is usually self-limiting and resolves within a few weeks. It tends to be nocioceptive in nature as pertaining to a disease, injury, or other form of tissue damage. It commonly occurs in trauma, during the postoperative period, and in acute medical illnesses. Acute pain can be further classified into somatic and visceral pain. Somatic acute pain that arises in the superficial structures has a sharp or throbbing sensation. Somatic pain arising from deeper musculoskeletal sources tends to be a dull aching, less localized throb. Conversely visceral pain is from damage or disease of an internal organ or its surroundings. Visceral pain can be dull and diffuse in nature, sharp and localized, or referred based on the specific etiology.
Chronic pain describes a condition that last longer than a month to years. Its nature is largely neuropathic, but has nocioceptive components. Neuropathic pain tends toward paroxysmal lancating episodes with residual burning and throbbing. It tends to be associated with a hyperpathic state. Most forms of chronic pain are associated with a musculoskeletal disorder, or peripheral or central lesions. Musculoskeletal pain is nocioceptive, whereas peripheral and central lesions are neuralgic in nature.
Anxiety is a state of worry and nervousness that occurs in a variety of mental disorders, usually accompanied by compulsive behavior or attacks of panic, a vague unpleasant emotion that is experienced in anticipation of some misfortune. There are several different types of anxiety with differing treatments. Nonetheless, anxiety itself as it pertains to medical or surgical treatment is often a healthy, if not ideal response. Nonpsychiatric physicians need to be able to distinguish between normal anxiety and phobias. Conditions such as generalized anxiety disorder and posttraumatic stress disorder may necessitate psychiatric treatment as part of long-term care. A preliminary evaluation of anxiety involves evaluating the objective consequences of the patient’s heightened state. For example, is the patient’s anxiety leading to neglect of care or endangerment of the patient and medical staff? Are there functional and physical manifestations of stress that interfere with daily and long-term function? Anxiety that obstructs personal, social, or professional life or presents with physical signs and symptoms, such as chest pain or shortness of breath, or suicidal and homicidal thoughts requires further workup and should not be dismissed as a necessary complication of treatment.
Physiology of pain and anxiety
Physiologically, pain begins with the activation of the first-order nocioreceptor of unmyelinated c fibers and a-delta fibers. These neurons synapse with second-order neurons in the dorsal horn of the spinal cord. Second-order neurons include afferent, interneuron, sympathetic, and reflex neurons. Afferent branches then cross the midline to the contralateral spinothalamic tract and ascend to the thalamus. In the thalamus, second-order synapse with third-order neurons then send axons to synapse in the anterior cingulate and post-central gyrus of the cerebral cortex. Within the cortex, pain is processed, localized, and associated with emotions. During nocioreception, chemical mediators are released peripherally and in the dorsal horn. These neurotransmitters can modulate the sensation of pain. The main excitatory peptides are substance P (subP) and calcitonin gene–related peptide (CGRP), which increase sensitization of nocioreceptors. Continued stimulation of these receptors results in modulation of pain. Peripheral nocioreceptors decrease their threshold, and increase their frequency of firing to the same stimuli with continued firing after the stimulus is removed. Prostaglandins resulting from tissue damage directly activate nocioreceptors. SubP and CGRP also cause degranulation of mast cells, vasodilatation, and formation of leukotrienes, resulting in neurogenic inflammation. Centrally, excitatory neuropathies result in sensitization of second-order neurons, receptor field expansion, and hyperexcitability of neurons.
The initial stimuli for anxiety can be a physical challenge or a perceived threat. This threat may be conscious or subconscious and results in stimulation of the amygdala. The amygdala modulates the response by attaching emotional significance to the stimuli. Feelings of agitation and anger accompanying the stimuli aid in creating and maintaining a memory of the event. The stress response begins with the release of corticotropin-releasing factor, which helps activate autonomic, immune, and endocrine stress responses. The hormonal sequence eventually leads to the release of epinephrine and glucocorticoids, which subsequently activate the sympathetic system. The amygdala also stimulates the midbrain and brain stem causing many of the physical symptoms associated with anxiety.
Physiology of pain and anxiety
Physiologically, pain begins with the activation of the first-order nocioreceptor of unmyelinated c fibers and a-delta fibers. These neurons synapse with second-order neurons in the dorsal horn of the spinal cord. Second-order neurons include afferent, interneuron, sympathetic, and reflex neurons. Afferent branches then cross the midline to the contralateral spinothalamic tract and ascend to the thalamus. In the thalamus, second-order synapse with third-order neurons then send axons to synapse in the anterior cingulate and post-central gyrus of the cerebral cortex. Within the cortex, pain is processed, localized, and associated with emotions. During nocioreception, chemical mediators are released peripherally and in the dorsal horn. These neurotransmitters can modulate the sensation of pain. The main excitatory peptides are substance P (subP) and calcitonin gene–related peptide (CGRP), which increase sensitization of nocioreceptors. Continued stimulation of these receptors results in modulation of pain. Peripheral nocioreceptors decrease their threshold, and increase their frequency of firing to the same stimuli with continued firing after the stimulus is removed. Prostaglandins resulting from tissue damage directly activate nocioreceptors. SubP and CGRP also cause degranulation of mast cells, vasodilatation, and formation of leukotrienes, resulting in neurogenic inflammation. Centrally, excitatory neuropathies result in sensitization of second-order neurons, receptor field expansion, and hyperexcitability of neurons.
The initial stimuli for anxiety can be a physical challenge or a perceived threat. This threat may be conscious or subconscious and results in stimulation of the amygdala. The amygdala modulates the response by attaching emotional significance to the stimuli. Feelings of agitation and anger accompanying the stimuli aid in creating and maintaining a memory of the event. The stress response begins with the release of corticotropin-releasing factor, which helps activate autonomic, immune, and endocrine stress responses. The hormonal sequence eventually leads to the release of epinephrine and glucocorticoids, which subsequently activate the sympathetic system. The amygdala also stimulates the midbrain and brain stem causing many of the physical symptoms associated with anxiety.
Pain and anxiety relationship
The correlation between anxiety and pain continues to be debated. Intuitively, we know that uncontrolled pain may exacerbate present and future states of anxiety. Yet, the causal relationship between anxiety and increased pain is less clear. Indeed, many clinicians view increased pain in anxious patients to be a subjective increase in perceived pain versus nocioreception, discounting patient discomfort as either psychosomatic or psychiatric. Often, higher than normal levels of anxiety may be overlooked by medical staff in the preoperative area.
To gain insight into the relationship between anxiety and pain, Kain and colleagues conducted a study to determine if postoperative pain could be predicted based on preoperative anxiety. Their research examined women undergoing abdominal hysterectomy and included evaluations on patients’ state and trait anxiety, coping mechanisms, and level of stress. Patients completed the State-Trait Anxiety Inventory preoperatively and both the McGill Pain Questionnaire and the Visual Analogue Scale (VAS) postoperatively. Their results showed positive correlations between the level of anxiety and postoperative pain. Based on their findings, Kain and colleagues suggested using postoperative anxiety-reducing strategies as an adjunct to postoperative analgesics. In a subsequent study, Kain and colleagues examined patients who underwent similar surgical procedures. The patients were divided into 2 groups: one group received an anxiolytic and the other group received a placebo. The research demonstrated that pain was significantly decreased in the anxiolytic group for 1 week postoperatively.
Ploghaus and colleagues measured neural activity in subjects who were given visual cues before receiving thermal stimuli. Patients were given time to associate high-intensity cues with high thermal activity and low-intensity cues with low thermal activity. Subsequently, high-intensity cues were given with low thermal stimulation. The results demonstrated higher anxiety, stronger pain, and hippocampal involvement with preliminary evidence of neural representation of pain and anxiety. Ploghaus and colleagues surmise that hippocampal involvement from increased anxiety results in pain intensity amplification.
However, not all studies support a closed relationship between anxiety and pain. In a subsequent study, Kain and colleagues examined 70 women who received abdominal hysterectomies. Two groups were formed: one group was given an anxiolytic and the other was given a placebo. The results showed no statistical correlation between reduced anxiety and postoperative pain beyond the pharmacologic effect of benzodiazepines combined with anesthesia. These conclusions contradicted Kain and colleagues’ previous studies. The investigators noted that previous results correlating reduced anxiety to decreased postoperative pain were for minor surgical procedures and may not be applicable to patients with major surgery.
Large prospective, double-blinded, randomized studies would be helpful to determine if a physiologic causality exists between anxiety and increased pain. Nonetheless, psychiatric and psychosomatic manifestation of increased pain from heightened anxiety is well established. Many health care providers intuitively understand this correlation between psychological and physical health. This understanding coupled with humanitarian motivation should influence our treatment of anxiety from a holistic approach to address the emotional needs of our patients.
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