Assessing and Treating Clients With Pain

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Chronic pain and its treatment

This chapter will provide a brief overview of chronic pain conditions associated with different psychiatric disorders and treated with psychotropic drugs. Included here are discussions of the symptomatic and pathophysiologic overlap between disorders with pain and many other disorders treated in psychopharmacology, especially depression and anxiety. Clinical descriptions and formal criteria for how to diagnose painful conditions are only mentioned here in passing. The reader should consult standard reference sources for this material. The discussion here will emphasize how discoveries about the functioning of various brain circuits and neurotransmitters - especially those acting upon the central processing of pain - have impacted our understanding of the pathophysiology and treatment of many painful conditions that may occur with or without various psychiatric disorders. The goal of this chapter is to acquaint the reader with ideas about the clinical and biological aspects of the symptom of pain, how it can be hypothetically caused by alterations of pain processing within the central nervous system (CNS), how it can be associated with many of the symptoms of depression and anxiety, and finally how it can be treated with several of the same agents that can treat depression and anxiety. The discussion in this chapter is at the conceptual level, not at the pragmatic level. The reader should consult standard drug handbooks (such as Stahl's Essential

) for details of doses, side effects, drug interactions,Psychopharmacology: the Prescriber's Guide and other issues relevant to the prescribing of these drugs in clinical practice.

What is pain?

No experience rivals pain for its ability to capture our attention, focus our actions, and cause suffering (see for some useful definitions regarding pain). The powerful experience ofTable 10-1 pain, especially acute pain, can serve a vital function - to make us aware of damage to our bodies, and to rest the injured part until it has healed. When acute pain is in origin (i.e., originatingperipheral outside of the CNS) but continues as chronic pain, it can cause changes in CNS pain mechanisms that enhance or perpetuate the original peripheral pain. For example, osteoarthritis, low back pain, and diabetic peripheral neuropathic pain begin as peripheral pain, but over time these conditions can trigger central pain mechanisms that amplify peripheral pain and generate additional pain centrally. This may

Table 10-1 Pain: some useful definitions

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explain why research has recently shown that chronic pain conditions of peripheral origin can be successfully targeted for relief by psychotropic drugs that work on central pain mechanisms.

Many other chronic pain conditions may start and never have a peripheral causation to thecentrally pain, especially conditions associated with multiple unexplained painful physical symptoms such as depression, anxiety, and fibromyalgia. Because these centrally mediated pain conditions are associated with emotional symptoms, this type of pain has until recently often been considered not to be "real" but rather a nonspecific outcome of unresolved psychological conflicts that would improve when the associated psychiatric condition improved; therefore, there was not a perceived need to target this type of pain. Today, however, many painful conditions without identifiable peripheral lesions and that were once

Figure 10-1. . Detection of a noxious stimulus occurs at the peripheralActivation of nociceptive nerve fibers terminals of primary afferent neurons and leads to generation of action potentials that propagate along the axon to the central terminals. A fibers respond only to non-noxious stimuli, A fibers respond to noxious mechanical stimuli and subnoxious thermal stimuli, and C fibers respond only to noxious mechanical, heat, and chemical stimuli. Primary afferent neurons have their cell bodies in the dorsal root ganglion and send terminals into that spinal cord segment as well as sending less dense collaterals up the spinal cord for a short distance. Primary afferent neurons synapse onto several different classes of dorsal horn projection neurons (PN), which project via different tracts to higher centers.

linked only to psychiatric disorders are now hypothesized to be forms of chronic neuropathic pain syndromes that can be successfully treated with the same agents that treat neuropathic pain syndromes not associated with psychiatric disorders. These treatments include the SNRIs (serotonin-norepinephrine reuptake inhibitors: discussed in on antidepressants) and the Chapter 7 2 ligands (anticonvulsants that block voltage-gated calcium channels or VSCCs: discussed in Chapter

on mood stabilizers and in on anxiety disorders). Additional psychotropic agents acting8 Chapter 9 centrally at various other sites are also used to treat a variety of chronic pain conditions and will be mentioned below. Many additional drugs are being tested as potential novel pain treatments as well.

Since pain is clearly associated with some psychiatric disorders, and psychotropic drugs that treat various psychiatric conditions are also effective for a wide variety of pain conditions, the detection, quantification, and treatment of pain are rapidly becoming standardized parts of a psychiatric evaluation. Modern psychopharmacologists increasingly consider pain to be a psychiatric "vital sign," thus requiring routine evaluation and symptomatic treatment. In fact, elimination of pain is increasingly recognized as necessary in order to have full symptomatic remission not only of chronic pain conditions, but also of many psychiatric disorders.

"Normal" pain and the activation of nociceptive nerve fibers

The nociceptive pain pathway is the series of neurons that begins with detection of a noxious stimulus and ends with the subjective perception of pain. This so-called startsnociceptive pathway from the periphery, enters the spinal cord, and projects to the brain ( ). It is important toFigure 10-1 understand the processes by which incoming information can be modulated to increase or decrease the perception of pain associated with a given stimulus, because these processes can explain not only why maladaptive pain states arise but also why drugs that work in psychiatric conditions such as depression and anxiety can also be effective in reducing pain.

Nociceptive pathway to the spinal cord

Primary afferent neurons detect sensory inputs including pain ( ). They have their cellFigure 10-1 bodies in the dorsal root ganglia located along the spinal column outside of the CNS and thus are considered peripheral and not central neurons ( ). Nociception begins with transduction -Figure 10-1 the process by which specialized membrane proteins located on the peripheral projections of these neurons detect a stimulus and generate a voltage change at their peripheral neuronal membranes. A

sufficiently strong stimulus will lower the voltage at the membrane (i.e., depolarize the membrane) enough to activate voltage-sensitive sodium channels (VSSCs) and trigger an action potential that will be propagated along the length of the axon to the central terminals of the neuron in the spinal cord ( ). VSSCs are introduced in and illustrated in and .Figure 10-1 Chapter 3 Figures 3-19 3-20 Nociceptive impulse flow from primary afferent neurons into the CNS can be reduced or stopped when VSSCs are blocked by peripherally administered local anesthetics such as lidocaine.

The specific response characteristics of primary afferent neurons are determined by the specific receptors and channels expressed by that neuron in the periphery ( ). For example,Figure 10-1 primary afferent neurons that express a stretch-activated ion channel are mechanosensitive; those that express the vanillinoid receptor 1 (VR1) ion channel are activated by capsaicin, the pungent ingredient in chili peppers, and also by noxious heat, leading to the burning sensation both these stimuli evoke. These functional response properties are used to classify primary afferent neurons into three types: A, A, and C-fiber neurons ( ). A fibers detect small movements, light touch,Figure 10-1 hair movement, and vibrations; C-fiber peripheral terminals are bare nerve endings that are only activated by noxious mechanical, thermal, or chemical stimuli; A fibers fall somewhere in between, sensing noxious mechanical stimuli and subnoxious thermal stimuli ( ). Nociceptive inputFigure 10-1 and pain can thus be caused by activating primary afferent neurons peripherally, such as from a sprained ankle or a tooth extraction. NSAIDs (nonsteroidal anti-inflammatory drugs) can reduce painful input from these primary afferent neurons, presumably via their peripheral actions. Opioids can also reduce such pain, but from central actions, as explained below.

Nociceptive pathway from the spinal cord to the brain

The central terminals of peripheral nociceptive neurons synapse in the dorsal horn of the spinal cord onto the next cells in the pathway - dorsal horn neurons, which receive input from many primary afferent neurons and then project to higher centers ( ). For this reason, they areFigure 10-3 sometimes also called dorsal horn projection neurons (PN in , , and ). DorsalFigures 10-1 10-2 10-3 horn neurons are thus the first neurons of the nociceptive pathway that are located entirely within the CNS, and are therefore a key site for modulation of nociceptive neuronal activity as it comes into the CNS. A vast number of neurotransmitters have been identified in the dorsal horn, some of which are shown in .Figure 10-2

Neurotransmitters in the dorsal horn are synthesized not only by primary afferent neurons, but by the other neurons in the dorsal horn as well, including descending neurons and various interneurons (

). Some neurotransmitter systems in the dorsal horn are successfully targeted by knownFigure 10-2 pain-relieving drugs, especially opioids, serotonin- and norepinephrine-boosting SNRIs (serotonin-norepinephrine reuptake inhibitors), and ligands acting at voltage-sensitive calcium2 channels (VSCCs). All of the neurotransmitter systems acting in the dorsal horn are potential targets for novel pain-relieving drugs ( ), and a plethora of such novel agents is currently in clinicalFigure 10-2 and preclinical development.

There are several classes of dorsal horn neurons: some receive input directly from primary sensory neurons, some are interneurons, and some project up the spinal cord to higher centers ( ).Figure 10-3 There are several different tracts in which these projection neurons can ascend, which can be crudely divided into two functions: the sensory/discriminatory pathway and the emotional/motivational pathway ( ).Figure 10-3

In the sensory/discriminatory pathway, dorsal horn neurons ascend in the spinothalamic tract; then, thalamic neurons project to the primary somatosensory cortex ( ). This particular painFigure 10-3 pathway is thought to convey the precise location of the nociceptive stimulus and its intensity. In the emotional/motivational pathway, other dorsal horn neurons project to brainstem nuclei, and from there to limbic regions ( ). This second pain pathway is thought to convey the affectiveFigure 10-3 component that nociceptive stimuli evoke. Only when these two aspects of sensory discrimination and emotions come together and the final, subjective perception of pain is created can we use the word to describe the modality ("ouch" in ). Before this point, we are simplypain Figure 10-3 discussing activity in neural pathways, which should be described as noxious-evoked or nociceptive neuronal activity but not necessarily as pain.