PLEASE PAY ATTENTION TO THE CASE STUDY AND SAMPLE ESSAY (Please follow the sample essay to sequence because that is how my instructor wants us to answer the decision questions)
ZERO PLAGIARISM
FIVE REFENCES
To prepare for this Assignment:
- Review this week’s Learning Resources. Consider how to assess and treat clients requiring therapy for pain and sleep/wake disorders.
The Assignment
Examine Case Study: A Caucasian Man With Hip Pain. You will be asked to make three decisions concerning the medication to prescribe to this client. Be sure to consider factors that might impact the client’s pharmacokinetic and pharmacodynamic processes.
At each decision point stop to complete the following:
- Decision #1
Which decision did you select?
Why did you select this decision? Support your response with evidence and references to the Learning Resources.
What were you hoping to achieve by making this decision? Support your response with evidence and references to the Learning Resources.
Explain any difference between what you expected to achieve with Decision #1 and the results of the decision. Why were they different? - Decision #2
Why did you select this decision? Support your response with evidence and references to the Learning Resources.
What were you hoping to achieve by making this decision? Support your response with evidence and references to the Learning Resources.
Explain any difference between what you expected to achieve with Decision #2 and the results of the decision. Why were they different? - Decision #3
Why did you select this decision? Support your response with evidence and references to the Learning Resources.
What were you hoping to achieve by making this decision? Support your response with evidence and references to the Learning Resources.
Explain any difference between what you expected to achieve with Decision #3 and the results of the decision. Why were they different?sessing and Treating Clients With Pain
Complex Regional Pain Disorder
White Male With Hip Pain
BACKGROUND
This week, a 43-year-old white male presents at the office with a chief complaint of pain. He is assisted in his ambulation with a set of crutches. At the beginning of the clinical interview, the client reports that his family doctor sent him for psychiatric assessment because the doctor felt that the pain was “all in his head.” He further reports that his physician believes he is just making stuff up to get “narcotics to get high.”
SUBJECTIVE
The client reports that his pain began about 7 years ago when he sustained a fall at work. He states that he landed on his right hip. Over the years, he has had numerous diagnostic tests done (x-rays, CT scans, and MRIs). He reports that about 4 years ago, it was discovered that the cartilage surrounding his right hip joint was 75% torn (from the 3 o’clock to 12 o’clock position). He reports that none of the surgeons he saw would operate because they felt him too young for a total hip replacement and believed that the tissue would repair with the passage of time. Since then, he reported development of a strange constellation of symptoms including cooling of the extremity (measured by electromyogram). He also reports that he experiences severe cramping of the extremity. He reports that one of the neurologists diagnosed him with complex regional pain syndrome (CRPS), also known as reflex sympathetic dystrophy (RSD). However, the neurologist referred him back to his family doctor for treatment of this condition. He reports that his family doctor said “there is no such thing as RSD, it comes from depression” and this was what prompted the referral to psychiatry. He reports that one specialist he saw a few years ago suggested that he use a wheelchair, to which the client states “I said ‘no,’ there is no need for a wheelchair, I can beat this!”
The client reports that he used to be a machinist where he made “pretty good money.” He was engaged to be married, but his fiancé got “sick and tired of putting up with me and my pain, she thought I was just turning into a junkie.”
He reports that he does get “down in the dumps” from time to time when he sees how his life has turned out, but emphatically denies depression. He states “you can’t let yourself get depressed… you can drive yourself crazy if you do. I’m not really sure what’s wrong with me, but I know I can beat it.”
During the client interview, the client states “oh! It’s happening, let me show you!” this prompts him to stand with the assistance of the corner of your desk, he pulls off his shoe and shows you his right leg. His leg is turning purple from the knee down, and his foot is clearly in a visible cramp as the toes are curled inward and his foot looks like it is folding in on itself. “It will last about a minute or two, then it will let up” he reports. Sure enough, after about two minutes, the color begins to return and the cramping in the foot/toes appears to be releasing. The client states “if there is anything you can do to help me with this pain, I would really appreciate it.” He does report that his family doctor has been giving him hydrocodone, but he states that he uses is “sparingly” because he does not like the side effects of feeling “sleepy” and constipation. He also reports that the medication makes him “loopy” and doesn’t really do anything for the pain.
MENTAL STATUS EXAM
The client is alert, oriented to person, place, time, and event. He is dressed appropriately for the weather and time of year. He makes good eye contact. Speech is clear, coherent, goal directed, and spontaneous. His self-reported mood is euthymic. Affect consistent to self-reported mood and content of conversation. He denies visual/auditory hallucinations. No overt delusional or paranoid thought processes appreciated. Judgment, insight, and reality contact are all intact. He denies suicidal/homicidal ideation, and is future oriented.
Diagnosis: Complex regional pain disorder (reflex sympathetic dystrophy)
Select what the PMHNP should do:
Savella 12.5 mg orally once daily on day 1; followed by 12.5 mg BID on day 2 and 3; followed by 25 mg BID on days 4-7; followed by 50 mg BID thereafter
Amitriptyline 25 mg po QHS and titrate upward weekly by 25 mg to a max dose of 200 mg per day
Neurontin 300 mg po BEDTIME with weekly increases of 300 mg per day to a max of 2400 mg if needed
Decision Point One
Savella 12.5 mg once daily on day 1; followed by 12.5 mg BID on day 2 and 3; followed by 25 mg BID on days 4-7; followed by 50 mg BID thereafter
RESULTS OF DECISION POINT ONE
·
Client returns to clinic in four weeks
· Client comes into the office to without crutches but is limping a bit. The client states that the pain is “more manageable since I started taking that drug. I have been able to get around more on my own. The pain is bad in the morning though and gets better throughout the day”. On a pain scale of 1-10; the client states that his pain is currently a 4. When asked what pain level would be tolerable on a daily basis, the client states, “I would rather have no pain but don’t think that is possible. I could live with a pain level of 3.”. When questioned further, the PMHNP asks what makes the pain on a scale of 1-10 different when comparing a level of 9 to his current level of 4?”. The client states that since using this drug, I can get to a point on most days where I do not need the crutches. ” The client is also asked what would need to happen to get his pain from a current level of 4 to an acceptable level of 3. He states, “If I could get to the point everyday where I do not need the crutches for most of my day, I would be happy.”
· Client states that he has noticed that he frequently (over the past 2 weeks) gets bouts of sweating for no apparent reason. He also states that his sleep has “not been so good as of lately.” He does complain of nausea today
· Client’s blood pressure and pulse are recorded as 147/92 and 110 respectively. He also admits to experiencing butterflies in his chest. The client denies suicidal/homicidal ideation and is still future oriented
Decision Point Two
Continue with current medication but lower dose to 25 mg twice a day
Discontinue Savella and start Lyrica (pregabalin) 50 mg orally BID
Discontinue Savella and start Zoloft (sertraline) 50 mg daily
Complex Regional Pain Disorder
White Male With Hip Pain
Decision Point One
Amitriptyline 25 mg po QHS and titrate upward weekly by 25 mg to a max dose of 200 mg per day
RESULTS OF DECISION POINT ONE
· Client returns to clinic in four weeks
· Client comes to the office still using crutches. He states that the pain has improved but he is a bit groggy in the morning
· Client’s pain level is currently a 6 out of 10. The PMHNP questions the client on what would be an acceptable pain level. He states, “I would rather have no pain but don’t think that is possible. I could live with a pain level of 3.” He states that his pain level normally hovers around a 9 out of 10 on most days of the week before the amitriptyline was started. The PMHNP asks what makes the pain on a scale of 1-10 different when comparing a level of 9 to his current level of 6?” The client states, “I’m able to go to the bathroom or to the kitchen without using my crutches all the time. The achiness is less and my toes do not curl as often as they did before.” The client is also asked what would need to happen to get his pain from a current level of 6 to an acceptable level of 3. He states, “Well, that is kind of hard to answer. I guess I would like the achiness and throbbing in my right leg to not happen every day or at least not several times a day. I also could do without my toes curling in like they do. That really hurts.”
· Client denies suicidal/homicidal ideation and is still future oriented
· Decision Point Two
· Select what the PMHNP should do next:
·
·
Continue current medication and increase dose to 125 mg at BEDTIME this week continuing towards the goal dose of 200 mg daily. Instruct the client to take the medication an hour earlier than normal starting tonight and call the office in 3 days to report how his function is in the morning
·
· Reduce the dose of Elavil to 75 mg at BEDTIME (dose has been titrated at weekly intervals by 25mg per week). Add on Biofreeze roll-on therapy to his right leg below the knee and into the foot and toes to be used as needed daily for muscle cramping
·
· : Reduce dose of amitriptyline Elavil to 75 mg po orally at BEDTIME and add- on Neurontin (gabapentin) 300 mg po orally at BEDTIME. Schedule a Ffollow-up phone call in 1 week to assess pain contro
Decision PComplex Regional Pain Disorder
White Male With Hip Pain
Decision Point One
Neurontin (gabapentin) 300 mg orally at BEDTIME with weekly increases of 300 mg per day to a max of 2,400 mg if needed
RESULTS OF DECISION POINT ONE
· Client returns to clinic in four weeks
· Client returns to the office today and seems to be in agony. He states that the Neurontin did not help him at all. He also states that he is foggy in the morning. His current pain level is a 9 out of 10. The PMHNP questions the client on what would be an acceptable pain level. He states, “I would rather have no pain but don’t think that is possible. I could live with a pain level of 3.” The client is also asked what would need to happen to get his pain from a current level of 9 to an acceptable level of 3. He states, “I guess I would like this achiness and throbbing in my right leg to not happen every day or at least not several times a day. I also could do without my toes curling in like they do. That really hurts.”
· Clientis denies suicidal/homicidal ideation and is still future oriented. He does seem to be discouraged throughout the interview about his current pain
Decision Point Two
Select what the PMHNP should do next:
Continue current medication and increase dose to 125 mg at BEDTIME this week continuing towards the goal dose of 200 mg daily. Instruct the client to take the medication an hour earlier than normal starting tonight and call the office in 3 days to report how his function is in the morning
Reduce the dose of Elavil to 75 mg at BEDTIME (dose has been titrated at weekly intervals by 25mg per week). Add on Biofreeze roll-on therapy to his right leg below the knee and into the foot and toes to be used as needed daily for muscle cramping
: Reduce dose of amitriptyline Elavil to 75 mg po orally at BEDTIME and add- on Neurontin (gabapentin) 300 mg po orally at BEDTIME. Schedule a Ffollow-up phone call in 1 week to assess pain control
Assessing and Treating Adult Clients with Mood Disorders
A mood disorder describes a psychological disorder which is characterized as a fluctuation of one’s mood, such as a major depressive or bipolar disorder. An estimated 20 million individuals in the United States have depression which comprises of symptoms such as a loss of pleasure in activities, sadness, weight changes, feelings of hopelessness, fatigue as well as suicidal ideation; all of which can significantly impact daily functioning (Mental Health.gov, 2017). According to Park and Zarate (2019) onset of depression in adulthood continues to flourish where an estimated 30 percent of adults have a lifetime risk of experiencing a major depressive episode with a median age of 32.5. The author further indicates screening for depression, a thorough evaluation, and monitoring is necessary to ensure safety and wellbeing (Park & Zarate, 2019). Pharmacotherapy, along with psychotherapy are first-line therapies for effective outcomes (Park & Zarate, 2019). The purpose of this paper is to review a case study, choose the appropriate selection utilizing research, and discuss ethical considerations.
Case Study
A 32-year-old Hispanic American client presents to the initial appointment with depression. Health history, along with medical workup, appears to be unremarkable except for the slight back and shoulder pain due to his occupation. The clinical interview reveals past feelings of being an “outsider” and has few friends (Laureate Education, 2016). There is a decline in daily activities, a weight increase of 15 pounds over two months, along with diminished sleep and the inability to fully concentrate (Laureate Education, 2016). The results of the depression screening administered by the psychiatric mental health nurse practitioner (PMHNP), indicates severe depression with a score of 51 (Montgomery & Asberg, 1979).
Decision Point One
The selections include Zoloft 25 mg orally daily, Effexor 37.5 XR mg orally daily, or Phenelzine 15 mg orally TID. As a healthcare professional treating a client, Zoloft (sertraline) 25 mg is the first choice at decision point one. Selective serotonin reuptake inhibitors (SSRIs) impede the reabsorption of this neurotransmitter; thus, increasing the serotonin levels of the nerve cells in the brain to allow for improvement in mood (Stahl, 2013). SSRIs have been utilized as first-line therapy to treat major depressive disorder due to efficacy, fewer side effects, cost-effectiveness as well as a wider availability (Masuda et al., 2017). The therapeutic dosing range is typically 50 mg-200 mg (Stahl, 2017). However, beginning at 25 mg and gradually titrating the dose, depending on tolerability, is an appropriate health care decision (National Alliance on Mental Illness, 2018b). Therefore, a low dose of Zoloft appears to be the best option in caring for this client.
Effexor (venlafaxine) is classified as a selective serotonin-norepinephrine reuptake inhibitor (SNRI) which impedes the reabsorption of the neurotransmitters serotonin and norepinephrine changing the chemistry in the brain to regulate mood (Stahl, 2013). Bhat and Kennedy (2017) describe antidepressant discontinuation syndrome (ADS) as a “medication-induced movement disorder” along with various adverse reactions such as intense sadness and anxiety; periods of an “electric shock” sensation; sights of flashing lights; and dizziness upon movement (Bhat & Kennedy, 2017, p. E7). These symptoms are often experienced a few days after sudden discontinuation of an antidepressant with a shorter-life (3-7 hours) such as venlafaxine or paroxetine (Bhat & Kennedy, 2017; Stahl, 2017). Moreover, Stahl (2017) indicates venlafaxine is one of the drugs with more severe withdrawal symptoms in comparison to other antidepressants. It may take some clients several months to taper off of this medicine; therefore, Effexor is not the optimal selection at this time.
Phenelzine is classified as an irreversible monoamine oxidase inhibitor (MAOI) which impedes the monoamine oxidase from deconstructing serotonin, dopamine, as well as norepinephrine. Thus, boosting the levels of neurotransmitters in the brain to regulate mood (Stahl, 2017). Park and Zarate (2019) purport the use of monoamine oxidase inhibitors have a higher risk profile; therefore, are not typically utilized unless a newer antidepressant is considered ineffective. Bhat and Kennedy (2017) indicate there is a need for a long taper with MAOIs. Further, this medication may lose effectiveness after long-term use, and it is considered to have habit-forming qualities for some individuals (Stahl, 2017). The initial dose for phenelzine is taken three times a day which research suggests medication adherence is often tricky when the administration is more than once a day (Goette & Hammwöhner, 2016). Stahl (2017) describes certain risk factors comprising of frequent weight gain, interference of certain food products containing tyramine, drug interactions (serotonin syndrome), as well as a hypertensive crisis. When utilizing this medication for treatment-resistant depression, the advance practitioner is aware of the detrimental adverse reactions which may occur. Therefore, phenelzine is not the safest option for this client.
The overarching goal for this male client is to reduce the symptoms related to his major depressive disorder and to eventually achieve remission without relapse where he can maintain normalcy in his life. After four weeks, his depressive symptoms decrease by 25 percent which is progress; however, he has a new onset of erectile dysfunction (Laureate Education, 2016). Sexual dysfunction is a notable side effect of sertraline (Stahl, 2017). Therefore, the clinician will reevaluate the plan of care given this new information. The outcomes were to be expected as the client was started on a low dose of sertraline, and treatment is typically 50 mg to 200 mg. A continuation in progress may require more time, approximately six to eight weeks in total (Stahl, 2017).
Decision Point Two
The present selections include decrease dose to 12.5 daily orally, continue same dose and counsel client, or augment with Wellbutrin 150 IR in the morning. The preference for decision point two is Wellbutrin (bupropion) 150 IR, which is considered a norepinephrine dopamine reuptake inhibitor (SDRI). An SDRI elevates the neurotransmitters dopamine, noradrenaline, and norepinephrine in the brain to achieve an improvement in depressive symptoms (Stahl, 2017). The purpose of utilizing this agent is three-fold: (1) To boost mood (2) To treat the new onset of sexual dysfunction (3) To aid in weight-loss. According to the National Alliance on Mental Illness [NAMI] (2018a), Wellbutrin is a medication administered for major depressive disorder often in conjunction with an SSRI (NAMI, 2018a).
Further, Wellbutrin may be prescribed with an SSRI to reverse the effects of SSRI-induced sexual dysfunction (Stahl, 2017). Dunner (2014) purports combining antidepressants are safe and may enhance efficacy; however, the combination of medications may also be utilized as an approach to reduce the effects of antidepressant pharmacotherapy. Dunner (2014) concurs that bupropion is frequently used with an SSRI or SNRI to alleviate sexual dysfunction. Stahl (2017), findings indicate the most common side effects of bupropion consist of constipation, dry mouth, agitation, anxiety, improved cognitive functioning, as well as weight loss. The client in this scenario has gained 15 pounds over two months; thus, this medication may aid in his desire to lose weight (Laureate Education, 2016). Further, this agent typically is not sedating as it does not have anticholinergic or antihistamine properties yet have a mild stimulating effect (Guzman, n.d).
Decreasing the Zoloft dose from 25 mg daily to 12.5 mg would not prove feasible as the client has reached a 25 percent reduction in symptomology. The treatment for adults is 50 mg-200 mg, taking an approximate six to eight weeks to see the results in some individuals (Stahl, 2017). If the provider is tapering the medication as part of the client’s plan of care, reducing the dose to 12.5 mg would prove beneficial. Research finds that when taking an antidepressant, the neurons adapt to the current level of neurotransmitters; therefore, if discontinuing an SSRI too quickly some of the symptoms may return (Harvard Health Publishing, 2018). Under some circumstances, discontinuation signs may appear, such as sleep changes, mood fluctuations, unsteady gait, numbness, or paranoia (Harvard Health Publishing, 2018). However, the client is experiencing slow and steady progress on his current dose of Zoloft, so no adjustments are warranted.
At this point, positive results have been verbalized with the current dose of Zoloft 25 mg daily, with the exception of the onset of erectile dysfunction, which is a priority at this time. One study finds that comorbid depression and anxiety disorders are commonly seen in adult males with sexual dysfunction (Rajkumar & Kumaran, 2015). An estimated 12.5 percent of participants experienced a depressive disorder before the diagnosis of sexual dysfunction. The author’s findings suggest a significant increase in suicidal behaviors with this comorbidity. Moreover, the study indicates, some men experienced a sexual disorder while taking prescribed medication such as an antidepressant (Rajkumar & Kumaran, 2015). According to Li et al. (2018), cognitive-behavioral therapy (CBT) is a beneficial tool utilized with clients experiencing mood disorders. The implementation of CBT may increase the response and remission rates of depression. However, the option of continuing the same dose and engaging in counseling services is not the priority at this time. It is essential to address this side effect to enhance his current pharmacotherapy and prevent an increase in depressive symptoms.
The continued goal of therapy is to achieve “full” remission of this individual’s major depressive disorder and to enhance his wellbeing. After four weeks, the client returns to the clinic with a significant reduction in depressive symptoms along with the dissipation of erectile dysfunction. However, he reports feelings of “jitteriness” and on occasion “nervousness” (Laureate Education, 2016). This course of treatment has proven successful thus far, and the outcomes are to be expected due to the medication trials.
Decision Point Three
The present selections are to discontinue Zoloft and continue Wellbutrin, change Wellbutrin to XL 150 mg in the morning, or add Ativan 0.5 mg orally TID/PRN for anxiety. The selection for decision point three is to change the Wellbutrin from IR to XL 150 mg in the morning. The first formulation is immediate- release (IR) and the recommended dosing is divided beginning at 75 mg twice daily increasing to 100 mg twice daily, then 100 mg three times a day with the maximum of 450 mg (Stahl, 2017). The second formulation is extended-release (XL), where the administration for the initial dose is once daily taken in the morning; the maximum is 450 mg in a single dose (Stahl, 2017). The peak level of bupropion XL is approximately five hours; therefore, the side effects reported may subside as the absorption rate is slower than the IR dose (U.S. Food and Drug Administration, 2011a). The immediate-release peak level is approximately two hours which may account for the client’s notable feelings of being jittery and at times nervous (U.S. Food and Drug Administration, 2011b). Furthermore, clients are switched to extended-release to improve tolerance and treatment adherence to once-daily treatment (Guzman, n.d). As a mental health provider, caring for this client, changing the formulation is the best decision at this point as well as to continue to monitor side effects.
As mentioned above, Zoloft, an SSRI, can be utilized as a first-line agent for major depressive disorder (Masuda et al., 2017). Using Wellbutrin as an adjunct to the regimen has continued to reduce his symptoms of depression and has alleviated one of his primary concerns which is sexual dysfunction. Therefore, discontinuing Zoloft and maintaining the use of Wellbutrin is not an appropriate option at this time.
Ativan (lorazepam) is a benzodiazepine with anxiolytic, anti-anxiety, and sedative properties. It provides short-term relief of anxiety symptoms or insomnia (U.S. National Library of Medicine [NLM], n.d.). Lorazepam works by enhancing the effect of the inhibitory neurotransmitter GABA, which inhibits the nerve signals, in doing so, reducing the “nervous excitation” (NLM, n.d., para. 1). In some instances, a low dose, 0.5 mg, may be administered short-term to reduce side effects from another medication. Stahl (2017), indicates many side effects will not improve with an augmenting drug. Common side effects consist of confusion, weakness, sedation, nervousness, and fatigue (Stahl, 2017). Further, Ativan has an increased risk for abuse potential as it is known to have habit-forming properties (Stahl, 2017). As a result, administering Ativan would not be in the best interest of the client.
The ultimate goal is to achieve remission of his mood disorder. The medication regimen has proven effective; thus, considering this to be a successful plan of care. Taking both the sertraline and bupropion can exhibit side effects of jitteriness; however, changing to the extended-release may aid in the dissipation of these feelings. The addition of Ativan to relieve side effects, that are perhaps temporary, is against better judgment without first making an effort to change or modify the medication regimen (Laureate Education, 2016).
Summary with Ethical Considerations
Mood disorders affect millions of individuals in the United States on an annual basis. The prevalence of mental illness continues to flourish, impacting one’s quality of life. Initiating treatment, under the guidance of a healthcare professional, is of the utmost importance. Further, an individualized plan of care comprising of education, therapy, medication, and support is crucial for overall health and wellbeing.
The client is a Hispanic American male employed as a laborer in a warehouse (Laureate Education, 2016). It is essential to assess his financial means before prescribing medications. Although one cannot assume the client has financial hardships, having this knowledge will guide in the process of treatment. If the client is without insurance and has to pay out-of-pocket, medication adherence may not be sustainable. Therefore, as a psychiatric nurse practitioner, providing a cost-effective means whether, through generic prescriptions, discount pharmacies, or prescribing a larger quantity may be a necessary option (Barker & Guzman, 2015). Further, the partnership among clients and practitioners is essential; to establish trust and respect as well as understanding cultural preferences while avoiding stereotypes is vital.
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
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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
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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.
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