Help Needed
CHAPTER NINE Medicating Children
This chapter is divided into seven sections. Section One is an overview that discusses current trends in medicating children, problems the trends cause, and directions for the future. It also discusses developmental issues. Section Two focuses on stimulant medication and the diagnosis of attention deficit hyperactivity disorder (ADHD). Section Three focuses on research on combined interventions and particularly the Multimodal Treatment Study (MTA study) of Children with ADHD. Section Four focuses on children taking mood stabilizers. Section Five focuses on antipsychotics and children. Sections Six and Seven focus on anxiolytics and antidepressants in children, respectively.
SECTION ONE: PERSPECTIVES, DILEMMAS, AND FUTURE PARADIGMS
Learning Objectives
• Understand the problematic increase in psychotropic medications for children despite a dearth of evidence of the effectiveness of these drugs.
• Have a general understanding of the impact of the FDA Modernization Act and the Best Pharmaceuticals Act for Children.
• Be able to state the “developmental unknowns” associated with giving kids psychotropic medications.
Thus far, we have explored the medical model and psychological, cultural, and social perspectives as they relate to psychopharmacology. In this chapter, we demonstrate that using psychotropic medications with children and adolescents raises particular problems and concerns from several perspectives. As discussed in Chapter Three, we frequently see explanations and justifications from the medical model perspective used to reduce childhood disorders to chemical and genetic problems, excluding crucial consideration of environmental traumas, developmental foreclosures, or life stressors.
We explore child and adolescent psychopharmacology primarily from the medical model perspective but complement this approach with information from the other perspectives (psychological, cultural, and social). We set the stage by exploring the current status of the treatment of children and adolescents with mental and emotional disorders. This chapter is structured differently from the others in this book. We begin by discussing the context from the social and cultural perspectives and the problems with prescribing psychotropic medications to children. Then we cover an introduction to stimulants used to treat symptoms of ADHD. Finally, we give the status of their current use since the last edition of the book if that is possible.
Dr. Frank O'Dell, Professor Emeritus of Counseling in the College of Education and Human Services at Cleveland State University, has argued in all his lectures on counseling children and adolescents that the United States is an “anti-kid” society (Personal Communication, 2001). By that he means fewer and fewer therapists and psychiatrists choose to treat or continue to work with children in counseling. To support his argument, O'Dell points out that resources for children, including the number of hospital beds in mental health wards for children, have been shrinking. He believes the rules of managed care companies, dwindling personnel resources, and increasing difficulty in working with parents or guardians and their struggling children all contribute to the current trend. This has been a problem for at least 45 years. The American Academy of Child & Adolescent Psychiatry (AACAP) (2001) summarized the following facts, which support O'Dell's assertion, indicating little has changed:
• There is a dearth of child psychiatrists. Satcher (2001) stated further that many barriers remain that prevent children, teenagers, and their parents from seeking help from the small number of specially trained professionals who are available and that places a burden on pediatricians, family physicians, and other gatekeepers to identify children for referral and treatment decisions (U.S. Department of Health and Human Services, 2001).
• The AACAP's report projected that between 1995 and 2020, the need for child and adolescent psychiatrists will increase by 120%, whereas the need for general psychiatry is projected to increase at 22% for the adult population.
• McCarty, Russo, and Rossman (2011) demonstrated that only 13% of youth with suicidal behaviors and ideation receive mental health services.
• In November 2010, the Coalition for Juvenile Justice estimated that up to 75% of teenagers in the juvenile justice system nationwide have a diagnosable mental disorder, and these numbers continue.
• One in 10 children suffers from mental illnesses severe enough to impair development. Fewer than 1 in 5 children get treatment for mental illness.
The U.S. Department of Health and Human Services (2001) concluded that burgeoning numbers of children are suffering needlessly because their emotional, behavioral, and developmental needs are not being met by the institutions and systems created to care for them. As the number of children and adolescents needing psychological treatment rises and the number of service providers falls, the primary treatment modality becomes psychotropic medications rather than therapy. Imagine if you were a parent of one of these children.
Debner (2001a) reported that in a one-year period, 350 children needing hospitalization were turned away from hospitals in the Boston area. This phenomenon is occurring in most major U.S. cities and is exacerbated by hospitals holding onto children who are ready to be discharged, because there is no suitable placement for them. In another article, Debner (2001b) noted that the chief pediatricians from the five major academic health centers in Massachusetts indicated there is a serious crisis in psychiatric services for youth in the state. The doctors said they and their staffs could not find appropriate therapy and other mental health services for mentally ill children. As a result, many such children deteriorate to the point of crisis. Thomas and Holzer (2006) reported that America suffers from a serious long-term shortage of child psychiatrists that is taking a toll on young people, their parents, and their doctors. It is further recognized that the demand for psychotropic drugs is intense in spite of dangerous side effects.
The Washington Post (2002) published an article about a woman who desperately needed a psychiatric evaluation for her teenage daughter and who left 36 phone messages for various psychiatrists. She received only four replies. All the replies were from practitioners who refused to take the case because they did not treat adolescents. The article further detailed how, more and more, in-network providers (clinicians) prefer not to take patients covered by managed care plans, because reimbursements are so low and restrictions so numerous. The article also highlighted the disparity and arguments between the treating professionals and spokespeople from managed care companies. It is more than fair to say that desperate parents and anguished children are caught in the political policy dilemma over the cost and reimbursement of mental health treatment for children and adolescents.
Since the first edition of this book, there has been a movement to train more primary care physicians in pediatric mental health services to try to address the shortage of pediatric mental health professionals. Aupont et al. (2013) describe a model called Targeted Child Psychiatric Services designed for primary care physicians as well as child psychiatrists. This was associated with improved access to the child psychiatric services that exist, helped identify optimal care settings for patients and helped pediatricians be more likely to accept a patient back after that patient had been under psychiatric care.
Another problematic topic is who dispenses medications in schools. Most states have a policy on this and many states have a Nurse Delegated Medication Administration program (Ryan, Katsiyannis, Losinski, Reid, & Ellis, 2014). Most standardized curricula include trainings of approximately 30 hours with 8-hour updates every two years or so. These are by and large directed by professional nurses (Spector & Doherty, 2007). Nationwide lists of states and their programs can be found at http://www.nasbe.org/healthy_schools/hs/bytopics.php?topicid=4110&catExpand=acdnbtm_catD and http://www.healthinschools.org/health-in-schools/health-services/school-health-services/school-health-issues/medication-management/state-policies-on-administration-of-medication-in-schools.aspx.
THE EXPLOSION OF PSYCHOTROPIC MEDICATION PRESCRIPTIONS FOR CHILDREN AND ADOLESCENTS
With diminishing psychological supports for children and adolescents, using psychotropic medications with them has become the treatment of choice, even though the majority of medications used with them lack FDA “on-label” approval for them (Werry, 1999). Researchers currently estimate that between 7.5 and 14 million children in the United States experience significant mental health problems (Riddle, Kastelic, & Frosch, 2001; Wozniak, Biederman, Spencer, & Wilens, 1997). These statistics vary a little from Satcher (2001), cited earlier; clearly, millions of children in this country require mental health services. Children are increasingly prescribed psychotropic medications as part of their treatment; in many cases, the medications replace the therapy (Jensen et al., 1999; Phelps, Brown, & Power, 2002). Given the explosion in the use of psychotropic medication with children, it is important also to note that this population has been excluded from clinical trials of these drugs. Hence, decisions about juvenile medication obviously rest more on extrapolation of adult data to children and adolescents than on direct research and evaluation of the safety and efficacy of psychotropic medication with children (Riddle et al., 2001; Vitiello & Jensen, 1997).
Coyle (2000) indicated that 80% of all medications prescribed to children and adolescents in the United States have not been studied for the safety and benefit of these populations. As of 2011, The National Institutes of Health indicated that methylphenidate, lithium, all atypical antipsychotics, lorazepam, and amitriptyline were still on the highest priority list of needs in Pediatric Therapeutics of drugs to be studied in pediatric populations.
Even though there is a black box warning related to the risk of increased suicidality in children and adolescents prescribed SSRIs and SNRIs, the use of these psychotropic agents has increased with children and adolescents (Markowitz & Cuellar, 2007). The trend in treating children and adolescents with off-label psychotropic medications, mostly in lieu of counseling and psychotherapy, has triggered concern both in the general public and the mental health community. Coyle (2000), Furman (1993), and Zito (Zito et al., 2000, 2003) argue that there is little or no evidence to support psychotropic drug use with very young children and conclude that such treatment could have harmful psychological, developmental, and physical effects. In a multinational study, American youths were three times more likely to be on an antidepressant medication than their peers in Denmark, Germany, and the Netherlands (Zito et al., 2006). In 2010, the pharmaceutical companies research protocols were really challenged when uncovered pharmaceutical studies on many highly utilized psychotropics were found to be no more efficacious than the placebo. In fact, the second author has personal communications with several psychiatrists in their fourth or fifth decade of practice who question the overall effectiveness of psychopharmacology with patients, especially children (Ramirez, Personal Communication, 2014).
In another multinational study, Zito et al. (2008) found that the annual prevalence of youth taking psychotropic medication was threefold greater in the United States than in the Netherlands and Germany. The atypical antipsychotics represented 5% of antipsychotic use in Germany but 66% in the United States. Interestingly, though, anxiolytics were twice as common in Dutch youth than as in U.S. or German youth.
With proper research, mental health professionals may be able to head off disasters such as aspirin precipitating Reye's syndrome or valproate leading to sudden death in infants (Riddle et al., 2001). Given the lack of knowledge about the long-term and adverse effects of psychotropic medication on children, it is crucial that mental health clinicians be alert to the impact of these drugs on children and advocate for youth when the evidence that such drugs would be helpful is questionable (Ingersoll, Bauer, & Burns, 2004). At this point, we would like to introduce a case that highlights many of the treatment and medication dilemmas children and adolescents encounter.
Phillip is a 7-year-old first-grader from a single-parent home. His mother is on public assistance, and he is the oldest of four boys. Although some of the details of his developmental history are sparse, Phillip began to exhibit impulse control problems at the age of 2 years and 4 months, shortly after his father moved out of the house. He was hyper-vigilant, easily distractible, aggressive with his younger sibling, and frequently irritable. Initially, his mother believed he was going through a stage of rebelliousness, but after several months she became concerned about his behavior and mentioned this to the pediatrician. After a brief examination, the pediatrician indicated that Phillip was likely suffering from ADHD and recommended against medication unless his behavior got too out of control at home. However, she felt he would need a course of methylphenidate/Ritalin, a prescription stimulant, once he began preschool. Phillip's mother accepted this recommendation and planned to have him evaluated when he began preschool. Phillip's behavior improved slightly over the next several months, without therapy or psychotropic medication.
When he began preschool, it took only a few days before all his active symptoms returned. After observing him for several weeks, the teacher recommended to Phillip's mother that he see a physician to be assessed for a stimulant medication. After the evaluation, the physician prescribed 10 mg of methylphenidate/Ritalin daily for Phillip. Methylphenidate/Ritlain is one of the most common stimulants used for symptoms of ADHD in children. It is intended to reduce inattentiveness, distractibility, impulsivity, and motor hyperactivity, with a goal of improved academic productivity. Phillip's symptoms slightly improved over the next eight weeks, but his aggressive behavior toward other children increased. Phillip's mother noticed more unpredictable behavior at home, as well as sleeplessness and restlessness followed by long periods of lethargy. She took him back to his physician, who referred them to a psychiatrist. The psychiatrist, after a three-session assessment, diagnosed Bipolar I (BPI) Disorder, took him off the methylphenidate/Ritalin, and prescribed 50 mg of carbamazepine/Tegretol daily and 0.01 mg of clonazepam/Klonopin. The carbamazepine/Tegretol was used to reduce his manic symptoms. This antiseizure medication has over time been found very effective with Bipolar Disorder (Phelps et al., 2002).
The clonazepam/Klonopin was used to address Phillip's anxious and agitated symptoms. This anti-anxiety medication often relaxes children and reduces anxiety without inducing sleep.
Many of Phillip's symptoms diminished, but his mother noticed both a sluggishness and apathy in him that were new. Over the course of the next year, Phillip's teacher addressed several of his learning and cognitive processing problems. Up to this point, the focus of Phillip's treatment had been psychopharmacologic. No psychosocial interventions were given to Phillip, as is often the case (Phelps et al., 2002). No one seemed to have any awareness or discussion about the optimal level of medication for Phillip, and there was no referral for a psychosocial assessment. As his symptoms worsened, he was evaluated by a psychiatrist schooled in prescribing adult psychotropic medications off label to children. Finally, Phillip's mother took him to see a therapist, who focused on Phillip's attachment issues, his phobic anxiety triggered by sudden loss or the anticipation of sudden loss, and his physiologic symptoms, which the therapist considered powerful side effects of the pharmacologic therapy.
Analyzing the case, Phillip was treated by pharmacology in the medical model method and rational thinking centered on pharmacology dominated the case. The combination of methylphenidate/Ritalin and carbamazepine/Tegretol on Phillip's system was supposed to reduce some of his externalizing symptoms in the constellation of ADHD or Bipolar I disorders, but the psychological aspects of his personality were ignored. Not until much later in the course of his illness did Phillip get some assistance in those domains. Culturally, Phillip's mother had little power in society and was torn between accepting the opinion of the medical experts, and watching the negative impact the medications were having on her son. As mental health professionals, we need to understand the medical psychiatry's rapid efforts to address most disorders of childhood and adolescents with psychotropic medication. Far too often, medicating professionals view talk therapy and other psychosocial interventions as ineffective and second rate. Because medical professionals hold more power in our society than mental health professionals, their medical opinions are frequently given more weight. Today, psychiatrists burdened by enormous caseloads are open to what is known as split-treatment, a joint effort by the mental health professional and psychiatrist to plan and integrate treatment and be vigilant for client manipulation. We must integrate care into a larger model of treatment that addresses each of the four perspectives equally and where mental health professionals' opinions on mental health treatment are given more weight. In addition, the power of pharmaceutical companies must be monitored. Bodenheimer (2000) has documented numerous cases where companies prevented important research findings from being published because they were not favorable regarding the compounds being tested. To what extent may such situations affect clients like Phillip? This will be discussed later in the chapter.
Remember, Phillip was in the 4 to 7 age range when he began treatment. Coyle (2000) comments that there is “no empirical evidence to support psychotropic drug treatment in very young children and that such treatment could have deleterious effects on the developing brain” (p. 1060). Furman (1993) posited that psychiatrists in the United States are recklessly “out of control” in prescribing methylphenidate/Ritalin and other stimulants for children, in contrast to the extreme caution that physicians in almost all European countries use in recommending this treatment approach. With the increasing trend to medicate a younger and younger population (Zito et al., 2000), mental health professionals not only need to understand the impact and therapeutic effectiveness of these medications, but also their limitations and potential for harming children.
THE MEDICATION OF CHILDREN AND THE FEDERAL LAWS
As we have noted in previous chapters, the laws of the land hold great influence over cultural and social paradigms. To a large extent, laws are the result of a dynamic interaction of forces that influence other areas such as socioeconomic status and the fiscal systems of a society. Socioeconomic status and fiscal systems shape laws in very powerful ways, and people with financial resources are able to buy influence with lawmakers. This is nothing new, but bears stating in this chapter. Although recent legislation has been introduced to address the many problems of prescribing psychotropic medications for children, most such laws require only voluntary testing of psychotropic drugs, diminishing any real impact. In this section, we summarize recent laws and comment on them, beginning with a summary in Table 9.1.
TABLE 9.1 Major Emphases of Recent Legislation on Pediatric Pharmacology
|
Law/Rule |
Summary |
|
FDA Modernization Act |
Recognizes rights of children as patients |
|
(Public Law Number 105–115, 1997) |
Sets specific standards for research of pediatric drugs |
|
|
Encourages pediatric labeling |
|
Best Pharmaceuticals for Children Act |
Voluntary pediatric studies of currently marketed drugs |
|
(Public Law Number 107–109, 2002) |
Created list of all pediatric drugs needing documentation |
|
|
Requires timely labeling of pediatric drugs |
|
|
Establishes a mandate to include children of all cultures in studies |
|
|
Voluntary studies of new drugs |
|
Pediatric Rule Bill of 2002a |
Required timely pediatric studies and adequate labeling |
aChild & Family Services Improvement Act: Language on how the use of medications is to be monitored.
© Cengage Learning®
Buck (2000) traced the unfolding need for greater specific labeling of drugs used with patients less than 18 years of age. The burgeoning use of almost all drugs approved for children by the FDA compelled pediatric health care providers to use these drugs off label without a clear knowledge of dosing, administration, or adverse-effect information. In 1992, the FDA took steps to improve both pediatric labeling and research, which resulted in support for building a network of pharmacologic research by the National Institutes of Health (NIH). These efforts began to address the problem, and passage of the FDA Modernization Act (1997) for the first time set specific requirements to tighten regulations relating to pediatric pharmacology. This law encouraged pediatric labeling on drugs used widely with children and adolescents where the lack of labeling might lead to serious misuse. However, the FDA website (2013) warns that users of methylphenidate/Ritalin may have an erection lasting many hours. This from an agency that still cannot conduct pediatric studies that evaluate the full impact of the drug on that population.
This law goes a long way toward recognizing the rights of children as patients, protecting their health, and assisting pediatric providers with essential information. Unfortunately, the law did not go far enough. Many practitioners and lawmakers felt the need for a comprehensive law to mandate pharmacologic research, monitor it, and further protect children.
The Best Pharmaceuticals for Children Act
On January 4, 2002, President George W. Bush signed Public Law Number 107–109, the Best Pharmaceuticals for Children Act (Dodd, 2001), with the anticipation that it would address many of the dilemmas and controversies surrounding the eruption in use of pharmaceuticals for children. This law aims to initiate critical studies with pharmaceuticals already prescribed to a population for whom there exists little research, and it tightens the monitoring and development of new drugs released for children and adolescents. The law seeks to integrate viewpoints on medicating children with the medical, cultural, and social perspectives. Unfortunately, its most powerful provisions regarding the conduct of pharmaceutical companies are voluntary.
The Best Pharmaceuticals for Children Act (BPCA) has 19 sections that can be viewed at http://www.fda.gov/RegulatoryInformation/Legislation/FederalFoodDrugandCosmeticActFDCAct/SignificantAmendmentstotheFDCAct/ucm148011.htm). This law encourages voluntary pediatric studies of already marketed drugs, the so-called off-label psychotropic drugs in widespread use with children, and it creates a research fund for studying these drugs (see http://blogs.fda.gov/fdavoice/index.php/tag/best-pharmaceuticals-for-children-act-bpca/). Both efforts are critical to understanding the effectiveness and efficacy of psychotropic medications for children and adolescents. Further, the law establishes an ongoing program for the pediatric study of drugs, including a list of all drugs for which documentation is needed. This aspect of the law is monitored by the commissioner of the FDA and the director of the National Institutes of Health, who have the power to make written requests to pharmaceutical companies for pediatric studies. The law requires timely labeling changes for pediatric drugs under study.
As of this edition, the status of most pharmaceuticals for children and adolescents remains similar to what it was in 2006. There was the black-box effort with SSRIs and SNRIs, but they are prescribed at rates higher than in 2006 (Cummings & Fristad, 2007) and most other psychotropics are used with children and adolescents to quiet anxiety, agitation, and rage.
However, the pharmaceutical companies continue to challenge the Pediatric Rule on all fronts and now it is 2014 and most important drugs for children have not been studied with a pediatric group. So goes the Pediatric Rule. On October 17, 2002, the U.S. District Court for the District of Columbia ruled that the FDA did not have the authority to issue the Pediatric Rule and has barred the FDA from enforcing it. The Pediatric Rule would have required timely pediatric studies and adequate labeling of all human drugs.
Child and Family Services Improvement Act
The Child and Family Services Improvement Act of 2011 (Public Law 112–34) includes new language that addresses the social-emotional and mental health of children who have been traumatized by maltreatment. State Child and Family Services Plans now have to include details about how emotional trauma associated with maltreatment and removal is addressed. They also have to describe how the use of psychotropic medications is monitored.
A WORD ON CROSS-CULTURAL PERSPECTIVES
Tseng (2003) proposed many variables and differences in prescribing psychotropic medications to children and adolescents from various cultures. He stressed that one must consider not only the physician's attitudes about treating people from different cultures, but also the patients' perspectives on how they feel about psychotropic medications. Thus, the giving and receiving of medications has many implications. This factor is greatly enhanced for children and adolescents, because the physician must not only communicate with the parents about the diagnosis and the psychotropic medications (neither of which may make sense in the parents' worldview) but must also weigh carefully the cultural issues that the family brings to treatment.
Tseng (2003) also addresses the enculturation issues of children. His research has described how not every culture emphasizes the fast-paced and often accelerated approach to growing up that characterizes the United States. Enculturation is defined as a process through which an individual, starting in early childhood, acquires a cultural system through the environment, particularly from parents, school, and so on. Some cultures, such as many Asian cultures, have a laid-back attitude toward babies and toddlers that is more indulgent. Yet later, they show a dramatic shift for these children, who, when they arrive at latency, the developmental period between the ages of 6 and 11 or 12, experience enormous pressure to be diligent and to achieve. Thus, as clinicians treat children and adolescents from all cultures, they need to reconsider cross-cultural adjustment and revise the psychosocial stages of Erikson (1968), which depended on developmental understandings in a particular culture.
With the upsurge in the use of psychotropic medications, it is impossible to monitor the expected and unexpected adverse effects. Given the expanding knowledge of the varying developmental trajectories of children from other cultures, mental health practitioners and psychiatrists need to exercise further caution when prescribing psychotropic medications for these children. Lin and Poland (1995) described in detail the remarkably large interindividual variability in drug responses and side effect profiles. This can be partially accounted for in differences of ethnicity and/or culture apart from physiological pace. Some cultures are very suspicious of medication and may delay the decision for more than a year.
Lin and Poland (1995) have made significant contributions to the understanding of cultural psychiatry and to the fact that genetic factors associated with individual and ethnic backgrounds contribute greatly to responses to medication in children, adolescents, and adults. Kirmayer and Ban (2013) note that cultural differences in self and personhood are equally important. All researchers we reviewed point to variations within the same ethnic group and variations among ethnic groups. This further complicates the integrative dilemma, which is how to view psychopharmacology and cases from the four perspectives outlined in Chapter One as well as consider important developmental lines and levels. Mental health professionals recognize that researchers have much to learn about psychopharmacology with children and adolescents, as shown by the research cited in this chapter. We need to integrate our growing understanding of cultural psychiatry with our limited understanding of how psychotropic medications work in children. The Best Pharmaceutical Act for Children (2002) provided for including in studies children from various racial and ethnic backgrounds. The law calls for studying the impact of medications on children of different cultures.
PSYCHOLOGICAL PERSPECTIVES OF CHILDREN AND ADOLESCENTS
Medicating children and adolescents for all types of psychological disorders is a solution that only reflects partial truth. The overt behaviors and symptom profile for which they receive medication may only mask the deeper psychological wounds of loss, trauma, abuse, sibling rivalry, neglect, sexual abuse, or gender conflict. Furman (2000) has indicated that if mental health professionals carefully examined the overuse of stimulants with children, they would discover a variety of conflicts and problems fueling the hyperactive behavior. These issues could include cruelty in the home, harsh toilet training, neglect, sexual abuse, delay in language development, and more.
Young children cannot address their inner conflicts without the help of a caring therapist and the modality of play therapy, yet far too often they are diagnosed with Bipolar I or ADHD and medicated in an attempt to quickly suppress their active symptoms. There should be far more effort to get the child to a therapist to uncover the underlying cause(s) of the child's anguish, but this requires resources that, at the time of this writing, lawmakers are not giving a high priority.
The American Academy of Pediatrics (2011) for ADHD makes clear that parent and teacher assessments at home and school, respectively, along with clinical review and examination by pediatrician or psychiatrist, often omit psychological assessment of the child by a mental health professional to rule out abuse, neglect, loss, sleeplessness, or other potential causes of hyperactivity or mania. In this protocol (the AAP guidance), the psychology and clinical history of the child are treated as unimportant. Many authors unfortunately support rapid assessment of ADHD children to speed up treatment with stimulant medication.
OPPOSITION TO THE CURRENT TREND OF MEDICATING
Opponents to exclusive medication treatment for ADHD, Bipolar I, and other conditions have pointed out significant regional variations in the amount of psychotropic medications prescribed to children and wide variations in regional diagnostic criteria for ADHD and other conditions (Safer, Zito, & Fine, 1996; Wolraich, Hannah, Pinnock, Baumgaertel, & Brown, 1996). These variances have legislators and mental health advocates from various regions of the country clamoring for more judicious use of psychotropic medications with children, with more careful attention to the range of adverse effects from them, and a more formalized protocol for diagnosing ADHD, Bipolar I, and other conditions. This protocol should go well beyond the traditional oral report from teacher to parent about a child's externalizing behavior. Opponents of psychotropic medication use in children call for a more specific and guided differential diagnosis of these disorders because the symptoms commonly overlap with Oppositional Defiant Disorder, Conduct Disorder, Major Depressive Disorder, various anxiety disorders, and many developmental disorders (American Academy of Child and Adolescent Psychiatry, 2007; August, Realmuto, MacDonald, Nugent, & Crosby, 1996). Many researchers and practitioners still feel that ADHD in particular is a myth and that the explosion in use of the diagnosis renders differential diagnosis impotent (Armstrong, 1997; Furman, 2000). Fur-man (2000) concluded,
I have tried to trace the thinking that followed the discovery of the vastly different approaches in the United States and Europe to the management of the active or overactive child.…This thinking led to the conclusion that ADHD is not a specific disorder or pathological entity but rather a collection of symptoms that could be manifested by a child in distress, a child in conflict within himself and/or with his environment. It has no more specificity than that, and likewise methylphenidate has no specificity in producing its effects Suppressing these symptoms by “subduing” the child with medication hides from all the source of the child's troubles, precludes his being able to obtain mastery of his troubles through understanding, and subjects him to a false label of brain pathology. (p. 141)
Furman, now deceased, indicated that his conclusions were not new but simply ignored.
AN OVERVIEW OF PEDIATRIC AND ADOLESCENT PSYCHOPHARMACOLOGY
By the time this text has been published, only a handful of psychotropic medications will have been approved as on label for the preschool age group. Examples include methylphenidate/Ritalin, amphetamine/Adderall, haloperidol/Haldol, and chlorpromazine/Thorazine (Zito et al., 2003). Methylphenidate/Ritalin is now under great scrutiny (Zaicek, 2009). For preschool-age children, it is aggressive behavior that generally triggers a referral for treatment (Bassarath, 2003). A few more psychotropic medications have been approved for use in older children and adolescents (Kluger, 2003), but those (such as the antidepressant fluoxetine) are hotly debated because of suicidal risk. Table 9.2 lists as many medications as we were able to find with on-label approval for children.
We have mentioned the national dilemma that more children and adolescents demand psychological services each year, yet there are fewer service providers. Concurrent with this expanding problem is the dramatic increase in the use of psychotropic medications off label for a variety of mental and emotional conditions and disorders. Although this is problematic in and of itself, the focus on psychological and interpersonal factors in treating children and adolescents has dangerously diminished. Whereas it used to be common practice for child psychiatrists to choose in each case from among drug therapy—primary drug therapy and secondary counseling, or primary counseling and secondary drug therapy (Kraft, 1968)—today these choices are rarely discussed routinely.
Also note that DSM criteria are primarily normed on adults and are more difficult to apply with children. House (1999) has indicated that over half of the time, children who meet the criteria for one mental or emotional disorder meet criteria for other disorders as well. This multiple nature of children's problems frequently results in a polypharmacy approach and requires careful decisions by the physician and/or treating team (Brown & Sammons, 2002). How carefully those decisions are made varies from setting to setting and clinician to clinician and are more random today (Leslie, 2011).
Researchers do know that the preschool years are one of the key developmental periods for maturation of the brain dopamine system, which is targeted by stimulants (Coyle, 2000). The FDA-approved package insert on methylphenidate/Ritalin warns against its use with children under age 6. Given all the unknowns, many scholars and physicians are concerned about the quality and care and the current explosion of prescribing practices with preschoolers. Mental health professionals do not have enough clear evidence about how preschoolers respond to psychotropic medications, and researchers are very uncertain about the impact of such medications on the development of preschoolers. Let's examine some of the major developmental issues.
TABLE 9.2 Drugs with FDA On-Label Approved Uses in Children
For many of you, this section on human growth and development in children and adolescents is a review. Most texts on development emphasize cognitive, language, moral, and psychosocial developmental paths. We briefly consider these lines of development and include others that are potentially affected by the ingestion of psychotropic medication. Understanding development is further complicated by the construct of developmental lines —the simultaneous occurrence of several aspects of human growth and development.
Although there are dozens of lines of human development, this multiplicity is still not a focus for mental health professionals outside of developmental studies. What should be common knowledge for mental health professionals is still peripheral to their training. For example, the Council for the Accreditation of Counseling and Related Educational Programs (CACREP) requires only one human development course for a master's degree in school or clinical mental health counseling. There may be dozens of lines of human development. These include physical development, cognitive development, emotional development, sexual development, moral development, spiritual development, kinesthetic development, socioemotional development, gender identity, and role-taking ability. These are just a few of the lines of development to which every person has access, and, for the most part, everyone proceeds through them unevenly.
The sheer number of developmental lines and the fact that most people proceed unevenly through them raise enormous, unaddressed issues for psychopharmacology. We noted earlier that scientists know very little about how brains develop and that many researchers are concerned that psychotropic medications could profoundly damage the brains of children and adolescents when taken long term. Glen Elliott, director of the Langley Porter Psychiatric Institute Children's Center of the University of California at San Francisco, noted that the current use of psychotropic medications on children “has outstripped our knowledge base … we are experimenting on these kids without tracking the results” (Kluger, 2003, p. 51). For example, even when an adolescent truly appears to suffer from Bipolar I Disorder, the sequelae of mood stabilizer side effects such as weight gain and perhaps hair loss are likely to be more devastating for a person of that age than for an adult—but there is no research on such psychological issues.
Perhaps the greatest problem of studying child and adolescent psychopharmacology from the four integrative perspectives is that whenever the issue of medicating children comes up, the only perspective represented is that of the medical model. A good example is a Time magazine cover story, by Kluger (2003) that basically explores only the medical model perspective, with only minor attention to psychological, cultural, and social issues. The same article presents a diagram showing what parts of the brain are believed to be correlated with different mental or emotional disorders. At no point in the article does the author state that these areas are hypothesized to be correlated with symptoms and there is no evidence that they cause symptoms. This remains true as of the second edition of this book.
As we have noted throughout the book, many symptoms that are psychogenic in origin register in the brain, but this does not mean the symptoms were caused by the brain. This bias toward the medical model perspective leads laypeople to assume that mental/emotional disorders, whether in children or adults, are strictly medical disorders. This assumption is not currently supported by the evidence we have been covering in this book. A full-scale multimodal approach to mental and emotional disorders in children and adolescents considers medication and possible brain pathology as only one part of the story in a very complex interaction of tentative causes and interventions.
Developmental psychopharmacology is a newer area of research that studies brain development focused on brain plasticity (the brain's ability to shape itself to environmental or chemical input) and sensitive periods (during which experience can alter neural representation before hardwiring occurs) (Carrey, Mendella, MacMaster, & Kutcher, 2002). Pediatric psychopharmacology is an equally young enterprise with the first published reports dated in 1937 but by the 1980s the United States had become the world leader in medicating children (Riddle, Walkup, & Vitiello, 2008).
Although these disciplines are examining development strictly from the medical model perspective, its overarching question is, “What happens in the complex process of neural development when an infusion of psychotropic medications is introduced to address particular environmental stressors during periods of accelerated brain development?” Compared to adults, children and adolescents respond to psychotropic medications in different and distinctive ways that have implications for efficacy and safety (Vitiello & Jensen, 1995). The rate at which prescriptions of psychotropic medications have grown for children despite the dearth of research to support their efficacy raises the question “are we doing too much or too little?”
Epstein (2001) posited that active brain growth spurts occur stagewise in correlation with Piagetian types of development. Thus, a child who is making the transition from the sensory motor stage to Piaget's preoperational stage is in a very active brain growth stage (from age 2 to 4 years). Epstein cites Boothroyd (1997), who noted that lexical knowledge and syntactic knowledge grow rapidly until age 4. At about 6 (from age 6 to 8), the next rapid brain growth period parallels Piaget's concrete reasoning stage, where a child begins to think logically about experienced inputs, the concrete operational stage. Epstein discussed the next brain growth period as slow (from age 12 to 14 years), a time of practicing and consolidating new networks in preparation for the next rapid brain growth stage (between ages 14 and 16 years). Psychotropics often are administered to preschoolers in the rapid growth period between ages 2 and 4 years, and to early-latency children between the ages of 6 and 8 years. Mental health professionals do not know enough about the impact of both on-label and off-label psychotropics in these rapid brain growth periods to be administering them to children and adolescents. Bramble (2003) concluded that given the changing nature of pediatric pharmacology and developmental pharmacology, this society needs a rapid expansion of pediatric research and academic inquiry into the impact of psychotropics on children's development. The second author in an extensive review of developmental pharmacology articles found only those supported fully by pharmaceutical companies or ones that cost between $29.50 and $40.00. Almost all recommended the use of a psychotropic as a first-line intervention. Interestingly, the pharmaceutical companies signed documents stating that they had no “conflict of interest.” In addition, the medications being used are only partially successful 40–50% of the time (Rapoport, 2013).
Another problem with pediatric psychopharmacology is polypharmacy : the use of more than one psychotropic simultaneously, a usage that interacts with children's metabolism in a variety of unpredictable ways (Brown & Sammons, 2002). Clinicians who observe children and adolescents under the influence of polypharmacy are often startled not only by the dramatic change in the clients' affective and behavioral state but also by the array of side effects they experience. Tonya, a very aggressive 12-year-old, was placed on olanzapine/Zyprexa (an atypical antipsychotic), sertraline/Zoloft (an SSRI antidepressant), lorazepam/Ativan (an anxiolytic), and valproate/Divalproex (a mood stabilizer). This combination of medications was ostensibly for what appeared to the attending psychiatrist as Bipolar I with severe agitation and aggression in the manic phase. Tonya's symptoms diminished, but her teacher noticed new ones: slurred speech, mild tics, and a constant staring off without responding when addressed. Now, rather than disrupting the class, she slept through it. Although from the perspective of the teacher and other students this was an improvement, was Tonya being helped, or was she merely medicated into submission when she might have been more fundamentally helped with assessment and therapy from a wider interpersonal perspective?
Other developmental considerations include adverse cardiovascular effects. We have many reports of sudden deaths of children and adolescents treated with psychotropic medications, including methylphenidate/Ritalin, TCAs, SSRIs, bupropion/Wellbutrin, lithium, and most neuroleptic medications. Gutgesell et al. (1999) detailed the cardiovascular and electrophysiologic effects of commonly used psychotropic medication, which can be deadly. Although the precise causes of the deaths have not been documented, severe heart spasms (cardiac arrhythmias) and delayed repolarization of the heart rhythm (delayed QTc interval) make the heart muscle vulnerable to possibly lethal changes (such as ventricular tachycardia). These tragedies call on mental health professionals to be vigilant and cautious when prescribing psychotropic medication. With many high-risk medications, cardiovascular monitoring is particularly important. In fact, Wagner and Fershtman (1993) recommended ECG monitoring at baseline and during drug therapy for children and adolescents who are on the medications associated with cardiovascular side effects. Brown and Sammons (2002) argued that the use of most psychotropic medication exceeds data available for efficacy, effectiveness, and safety.
Many concerns also remain related to the physiological impact on children who take psychotropic medication. One is the controversy about the impact of stimulant treatment on brain growth in children (Bell, Alexander, Schwartzman, & Yu, 1982). Researchers have recently learned that methylphenidate and other stimulants decrease blood flow to selected parts of the brain, specifically the cortex area that controls conscious movement (Zeiner, 1995). In a recent study (Castellanos et al., 2002), the research team concluded that developmental trajectories for all brain structures, except caudal, remain parallel for children and adolescents in ADHD patients and controls. This suggested that genetic and early environmental influences on brain development in ADHD are fixed, nonprogressive, and unrelated to stimulant treatment.
However, initial brain scans of patients with ADHD showed significantly smaller brain volumes in all regions than what appeared in the brain scans of the controls. In general, because of brain plasticity (the brain's ability to shape itself), it is possible for children to be highly susceptible to a negative impact on their brain development during one period of development and less so in another period of development (Carrey et al., 2002). Does treatment with psychotropic medications constitute a negative impact? These authors further concluded that researchers are only beginning to understand the long-term effect of psychotropic medication on neuron cell factors and their overall impact on brain development. All these developmental concerns or issues involve potential adverse effects for children and adolescents taking psychotropic medication.
At this point, we cover the different categories of medications used on children and adolescents. We begin the next section with a more thorough treatment of stimulant medications.
Review Questions
• What are some of the main problems with the increase in psychotropic medication prescriptions for children?
• What was the impact of the FDA Modernization Act and the Best Pharmaceuticals Act for Children? Name at least three changes these acts initiated.
• What are the “developmental unknowns” that make prescribing psychotropic medications for children problematic?
SECTION TWO: STIMULANT MEDICATION
Learning Objectives
• Understand the mechanism of action and side effects of stimulant medications.
• Be able to discuss the type of symptoms stimulants seem most helpful for.
Even though stimulants are currently the best-studied psychotropic medication used on children, many issues regarding their use are still unresolved. Because stimulants are prescribed almost exclusively for children, we have included information on them in this chapter. Before discussing some of the controversial issues, let's examine some background and general information on these widely prescribed medications.
The first known stimulant in the West was cocaine. It was isolated in 1859 by a German chemist named Albert Niemann and was given to Bavarian soldiers to decrease fatigue. In 1884 Karl Koller perfected its use as an analgesic during eye surgery. His assistant, a young neurologist named Sigmund Freud, was off visiting his fiance at the time and so missed out on credit for that discovery. Freud had been personally experimenting with cocaine and wrote the paper “Uber Coca” (“On Cocaine”) prior to realizing its addictive qualities (Freud & Carter, 2011). Many people in South American societies still regularly chew coca leaves with little ill effect, because unprocessed leaves are far less dependence inducing than is refined cocaine powder (Siegel, 1989). Efforts to synthesize amphetamine began in 1887, when physicians believed it useful for treating asthma. This belief emerged from the use of an herbaceutical called ma huangin Chinese medicine. Ma huang is discussed more thoroughly in Chapter Ten on herbaceuticals, but for now understand that it is the ingredient ephedra that is central to the story of amphetamines. This ingredient produces the bronchial dilation that relieves the wheezing of asthma.
In the 1920s, a Chinese pharmacologist working for Eli Lilly (K. K. Chen) was working to isolate and synthesize ephedra from ma huang. He succeeded in synthesizing a compound so structurally similar to ephedra that it was named ephedrine. Although this could be taken orally, the goal for asthma treatment was a compound that could be inhaled. Gordon Alles succeeded in developing another variation of the molecule that could be delivered in an inhaler. Called Benzedrine, this variation was successful in treating asthma. Aside from treating asthma, it also seemed to induce euphoria. People soon realized they could open the inhaler and ingest the contents for what became known as “the amphetamine rush.” This also became a popular pastime on college campuses during exams. Amphetamines were experimented with to manage a number of disorders, and one of their early uses was treating children for what was described as “overactivity.”
Werry has asserted that research in psychopharmacology for children began with publication of Bradley's (1937) paper on how amphetamine seems to calm overactive children and help children with learning disabilities. The only other noteworthy investigations of the same period were studies on the effects of antihistamines on children (Connors, 1972). These works are thought to be the only primary contributions to child psychopharmacology until very recently (Werry, 1999).
Bradley's work reemerged in the 1960s after psychiatry began moving away from a psychodynamic model toward the biological model dominant today. Psychiatrists at that time were not well trained in the statistical methods that were becoming the norm in evaluating medications. They turned to psychologists for assistance. The psychologists emphasized the need to look at medication effects on learning and academic performance (Werry, 1999). Such research has, until very recently, remained focused primarily on stimulant medication.
Research in pediatric psychopharmacology received an unintentional boost in the 1960s with the creation of a diagnosis called Minimal Brain Dysfunction (MBD). MBD was one of the several precursors to the current ADHD diagnosis. MBD was treated with stimulant medications such as methylphenidate. Although later discarded because it was too vague, the MBD diagnosis did much to lead to the development of a norm for a methodology with which to evaluate the effects of drugs, and particularly stimulants, on children.
In World War II, German, British, American, and Japanese soldiers all used amphetamines, a practice still common in the U.S. Air Force to help pilots keep alert on bombing missions (Knickerbocker, 2002). After World War II, the Japanese had such huge surpluses of amphetamines that they marketed them to civilians. These drugs were advertised for the elimination of drowsiness and repletion of spirit. Researchers estimate that by 1948, 5% of the Japanese population between the ages of 15 and 25 was dependent on amphetamines.
After World War II, it became evident that amphetamines have appetite suppressant qualities, and chemists tried to tease these out from the reinforcing properties that were connected to abuse. However, most of these initial efforts (such as methylphenidate/Ritalin) failed, and then the drugs were simply marketed as amphetamines.
The amphetamine molecule is a simple and highly malleable molecule that acts as the chemical template for over 50 pharmacologically active substances (Grilly, 1994). Amphetamine is basically made of two compounds (isomers) labeled “L” and “D“ amphetamine. D-Amphetamine is more potent and was marketed as Dexedrine. A minor modification in this molecule yields methamphetamine marketed as Methedrine. Other variations of the amphetamine molecule can produce MAO inhibitors. Modifying amphetamine to dimethoxy-methylamphetamine (DOM) produces a psychedelic compound similar to mescaline, and further modification produces the empathogen methylene-dioxymethamphetamine (MDMA, street name “ecstasy”). The latter was a promising psychotherapeutic compound until criminalized (Eisner, 1994). The therapeutic effects revolved around chemically induced states of empathy, euphoria, and well-being that facilitated insights that were then to be integrated into clients' normal awareness (Stevens, 2009).
Table 9.3 outlines stimulant medications used to treat ADHD in children.
TABLE 9.3 Stimulant Drugs Used to Treat ADHD in Children
Mechanisms of Action in Amphetamines
Amphetamines exert almost all their effects by causing the release of norepinephrine and dopamine from the synaptic vesicles into the synaptic cleft. There are different mechanisms for amphetamines to act as dopamine agonists and the number of mechanisms used depends on the type of amphetamine. There are two isomers of amphetamine, “L” and “D.” The “L” isomer amphetamine mechanisms of action include:
• Pure reuptake inhibitor for DA
• No presynaptic activity
• Enhances NMDA receptor response
• Weak block monoamineoxidase
• 80% metabolized
• The classic L-isomer amphetamine is methylphenidate/Ritalin
The D-isomer amphetamine mechanisms of action are similar to those of cocaine and include:
• Reuptake inhibition of DA (inhibit DAT)
• Drug taken into terminal by DAT & depletes vesicles (causes DA transporter to act in reverse) thus releasing DA from the presynaptic neuron
• Enhances NMDA receptor response
• Weak block of monoamineoxidase (MAO)
• Releasing NE from presynaptic neuron
Amphetamine/Dexedrine is the classic D-isomer amphetamine but is less prescribed than Adderall. Mixed amphetamine salts/Adderall includes D-amphetamine.
In a study comparing methylphenidate to cocaine, Volkow et al. (1995) noted that although the mechanisms of action and effects are similar, methylphenidate clears more slowly from the brain, which, they hypothesize, makes it less dependence inducing. Readers are encouraged to think critically about this result, because when a similar mechanism of slow clearance is invoked to defend cannabis (marijuana) as low in dependence-inducing qualities, it is often rejected (De Fonseca, Can-era, Navarro, Koob, & Weiss, 1997). Either the mechanisms discussed decrease the probability of dependence or they do not. Pharmaceutical and political agendas should be separated from this debate so that people can objectively examine the issues. In previous chapters, we have listed the adverse effects of psychotropics being discussed. With ADHD, these effects are interwoven into the complex presentation of the stimulants. We ask you to consider why in the continent of Europe (an area of the world that has about the same population as the United States), stimulant medications are used with children for only about 5 to 8% of the treatment population so treated in the United States. Now let us examine the DSM-5.
According to the DSM-5, the diagnostic criteria for attention-deficit/hyperactivity disorder are
A. Either (1) or (2):
(1) six or more of the following symptoms of inattention have persisted for at least five months to a degree that is maladaptive and inconsistent with developmental level:
Inattention
(a) often fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities
(b) often has difficulty sustaining attention in tasks or play activities
(c) often does not seem to listen when spoken to directly
(d) often does not follow through on instructions and fails to finish schoolwork, chores, or duties in the workplace (not due to oppositional behavior or failure to understand instructions)
(e) often has difficulty organizing tasks and activities
(f) often avoids, dislikes, or is reluctant to engage in tasks that require sustained mental effort (such as schoolwork or homework)
(g) often loses things necessary for tasks or activities (e.g., toys, school assignments, pencils, books, or tools)
(h) is often easily distracted by extraneous stimuli
(i) is often forgetful in daily activities
(2) Hyperactivity: Six (or more) of the following symptoms of hyperactivity impulsivity persisted for at least six months to a degree that is maladaptive and inconsistent with developmental level:
Hyperactivity
(a) often fidgets with hands or feet or squirms in seat
(b) often leaves seat in classroom or in other situations in which remaining seated is expected
(c) often runs about or climbs excessively in situations in which it is inappropriate (in adolescents or adults, may be limited to subjective feelings of restlessness)
(d) often has difficulty playing or engaging in leisure activities quietly
(e) is often “on the go” or often acts as if “driven by a motor”
(f) often talks excessively
Impulsivity
(g) often blurts out answers before questions have been completed
(h) often has difficulty awaiting turn
(i) often interrupts or intrudes on others (e.g., butts into conversations or games)
B. Several hyperactive-impulsive or inattentive symptoms that caused impairment are present before age 12 years.
C. Several inattentive or hyperactive-impulsive symptoms are present in two or more settings.
D. There must be clear evidence of clinically significant impairment in social, or occupational functioning.
E. The symptoms do not occur exclusively during the course of a Pervasive Developmental Disorder, Schizophrenia, or other Psychotic Disorder and are not better accounted for by another mental disorder (e.g., Mood Disorder, Anxiety Disorder, Dissociative Disorder, or a Personality Disorder). (APA, 2013, pp. 59-60)
Source: Diagnostic and statistical manual of mental disorders, 5th ed., (Washington, DC: American Psychiatric Association, 2013).
Both the “Consensus Statement” of the National Institutes of Health (1998) and the “Clinical Practice Guidelines” of the American Academy of Pediatrics (AAP) (2011) recommend careful diagnosis of ADHD and then an appropriate and judicious use of stimulants in combination with other psychosocial treatments to address the symptoms. Epstein et al. (2010) also emphasize that children treated with stimulant medication show improvement in ratings by parents and teachers but not in their level of functioning as measured by grades. Thus they note that mental health services in addition to medication are important.
In terms of assessment most protocols recommend a neurologic exam, a consultation with a psychiatrist or psychologist who specializes in ADHD, behavioral observation reports from parents, grandparents, teachers, and other school personnel. Olfson, Gameroff, Marcus, and Jensen (2003), analyzing national data, reported the increased rates of treatment from 0.9 per 100 children in 1987 to 3.4 per 100 children in 1997. They posited that this increase along with fewer treatments (counseling) per child was attributed to a broader awareness of the diagnosis by special educators, growth of managed behavioral health care, and increased public acceptance of psychotropic medications. But we ask, has the mushrooming of the ADHD diagnosis in children led to improved assessment and treatment?
The answer is mixed. Although some teachers, school administrators, and pediatricians rapidly diagnose ADHD in children, the NIH (1998), the National Institute of Mental Health (NIMH) (1996, 2000), and the AAP (2001) all have developed diagnostic guidelines for ADHD for years. More recently, The American Academy of Child & Adolescent Psychiatry (AACAP) (2007) released a practical, evidence-based practice parameter. In 2011 the same group released a practice guideline with expanded treatment of how to make the diagnosis and how to add psychosocial interventions to treatment (AACAP, 2011). The initial guideline was again updated in 2012. In all cases, these expert societies recommend a careful evaluation by a trained psychiatrist or psychologist in conjunction with teachers, mental health professionals, and family members. They recommend an evaluation period that is not rushed, so the team can rule out other conditions that might be confused with ADHD, and which includes observation and rating scales.
In a 10-year review of rating scales assessing ADHD, Collett, Ohan, and Myers (2003) concluded that DSM IV-based rating scales can reliably, validly, and efficiently measure ADHD symptoms in youth. In this comprehensive review, the authors evaluated the validity and sensitivity of subscales on several rating scales to assess the symptoms of ADHD. The greater use of narrowband rating scales in the assessment of ADHD can supplement and complement clinical interviews and behavioral observations in the evaluation of ADHD in children and adolescents. It is now evident that reliable and valid ADHD rating scales can augment the accuracy and specificity of diagnosis.
In a comprehensive response to the Multimodal Treatment Study (Owens et al., 2003), the authors sought to answer the layered question, “What do we treat in ADHD?” and “Who treats it?” based on the needs of the child and her or his circumstances (Paul, 1967, p. 111). Their findings were remarkable. The children least likely to respond well to a combined treatment of stimulants and milieu therapy were those with depressed parents or caregivers and severe ADHD. Owens et al. (2003) examined several outcome predictors, using nine baseline child and family characteristics. None were predictive, but the two issues discussed earlier along with a lower IQ of the identified child correlated with an outcome less-than-favorable with the combined treatment.
ADHD Efficacy, Effectiveness, and Conundrum
ADHD has been classified as one of the externalization disorders, along with Conduct Disorder and Oppositional Defiant Disorder. As opposed to the other two, stimulant medication has been the treatment of choice for ADHD for about 25 years in the United States (Phelps et al., 2002). In fact, stimulants for ADHD are the most widely researched and used medications in child psychiatry. Evidence indicates significant increase in the use of stimulants for both preschoolers and children despite the fact that the FDA approval is only for children ages 6 and older (Brown & Sammons, 2002; Riddle et al., 2001; Zito et al., 2000, 2003). The data include empirical evidence on safety, efficacy, and adverse effects.
Research demonstrates the beneficial effects of stimulants on symptoms linked with ADHD. These effects include diminished inattention, impulsivity, overactivity (Bennett, Brown, Carver, & Anderson, 1999), improved classroom attention and academic efficiency (DuPaul & Rappaport, 1993), and improved mother–child relationships (Barkley, Karlsson, Strzelecki, & Murphy, 1984). However, with all the benefits cited for the use of stimulants with ADHD, available literature to date has not supported or demonstrated that stimulants enhance school achievement (Phelps et al., 2002). Short-term efficacy studies supported the impact of stimulants on the target symptoms. From this literature, clinicians can conclude that using stimulants with children appropriately diagnosed with ADHD diminish the child's inattention, impulsivity, and hyperactivity, but do not necessarily improve his or her academic achievement. It is very possible that the child will adapt better to the demands of the classroom environment and become less externally driven. However, it would also be interesting to research whether or not stimulants improve performance in children who are not diagnosed with ADHD.
Proponents of stimulant treatment for ADHD are more convinced than ever that the disorder is passed on through heredity via the DRD4 receptor gene and that, as twin studies have suggested, up to 80% of the variance in the trait of hyperactivity/impulsivity is now considered to be based on genetics (Barkley, 1998). Peter Jaska (1998), president of the Attention Deficit Disorder Association (ADDA), is a staunch advocate of stimulant treatment for ADHD and argues that “we cannot and will not turn back decades of scientific research on the biological basis of ADHD, medical research, educational progress, and federal disability legislation, because some people selling books claim that ADHD is a ‘myth’” (p. 1). Both Jaska and Barkley are experts on the biological bases for ADHD derived from the medical model perspective and the resulting medication for treatment, but they seldom address intrapsychic, cultural, or social perspectives of ADHD.
Review Questions
• What are the mechanisms of action and side effects of stimulant medications?
• What types of symptoms are stimulants most useful for?
SECTION THREE: ADHD AND COMBINED INTERVENTIONS
Learning Objectives
• Understand the differences between the initial, two-year, and eight-year follow up of the MTA study group.
• Be able to describe conditions that may be comorbid with ADHD and why this may also be a misdiagnosis.
Interventions with ADHD usually begin with assessing the child or adolescent for oral stimulant medication, because most studies have indicated short-term behavioral improvement related to the symptoms of the disorder when stimulants are used (American Academy of Pediatrics, 2001; Barkley, DuPaul, & Connor, 1999; Phelps et al., 2002). Methylphenidate/Ritalin accounts for 90% of the prescriptions for ADHD (Advokat, Comaty, & Julien, 2014). In the late 1990s studies demonstrated that Adderall (amphetamine/dextroamphetamine) is equally efficacious but methylphenidate/Ritalin is still the leader in medications used to treat ADHD.
As noted, most consensus statements on ADHD treatment recommend psychosocial interventions that assist the family as well as the person diagnosed with ADHD. These approaches include psychotherapy, cognitive-behavioral therapy, behavioral therapy, social skills training, impulse control therapy, parenting skills training, support groups, and family therapy. Each of these approaches alone or in conjunction with stimulant medication can help ameliorate some of the symptoms of ADHD and/or address some of the underlying factors affecting the person with the disorder. The American Academy of Pediatrics (2001) first treatment guideline specifically recommended behavioral therapy as the best adjunct intervention with stimulants to establish targeted outcomes and manage the child's behavior both in the classroom and at home. They also stated that if one stimulant does not work at the highest feasible dose, the physician should recommend another. Clinicians learning about pharmacology may find it helpful to remember that stimulants generally provide only relief of symptoms, thus requiring other treatment modalities and follow-up. In a follow-up to that Bader and Adesman (2010) recommended a list of complementary and alternative treatments for ADHD. Although the American Academy of Pediatrics did not recommend these specifically they did note that essential fatty acid supplementation is well tolerated and modestly effective.
Results of the Multimodal Treatment Study for Children with ADHD (MTA Cooperative Group, 1999) demonstrated initially that stimulant treatment was slightly more effective than behavioral therapy alone, and equally effective to therapy and medication combined. It should be noted that parents preferred the behavioral therapy conditions to the stimulants-alone treatment. As with all treatment approaches for ADHD, the MTA study is not without its critics, who argue for a better match of patient with a treatment strategy tailored and selected for the individual's needs (Green & Albon, 2001). When the selected management (interventions) for a child with ADHD has not met targeted outcomes, clinicians must evaluate the original diagnosis, adjust treatments and medications, and evaluate for coexisting conditions.
Another critic of the MTA study (Leo, 2002) noted that the fanfare surrounding publication of the study “was nothing short of extraordinary” (p. 53). Leo pointed out that ABC News reported that results indicated drug therapy was much better than counseling for ADHD. Leo contends that the MTA study was heavily biased toward medication treatment. He claims the study's authors all had a history of strongly favoring medication, bringing their objectivity into question. He also points out that the MTA study had four groups: one received medication, one received behavior therapy, one received both, and a fourth group received no treatments from the MTA researchers but instead received standard treatment in the community. The most “robust” changes were reported in ratings by teachers and parents of children in the study. The problem with this, according to Leo, is that the investigators preselected a group of parents who believe it is acceptable to medicate children; in fact, in all cases the parents contacted the investigators to enroll children in the study. This fact, according to Leo, points to a bias in the sample.
Edwards (2002)addressed the important follow-up outcomes of studies and interventions in the wake of the report from the MTA Cooperative Group study (1999). He recommended that a specific family-based intervention be used in a mental health setting in conjunction with pharmacologic treatment. He specifically cited Parent Management Training (PMT) as an approach that through cognitive-behavioral coaching helps parents manage their child's difficulties. Whatever the method, more physicians, researchers, and clinicians are recommending family interventions with children and adolescents diagnosed with ADHD. The research in treatment outcomes of ADHD is complicated, and we encourage you to evaluate many strategies and interventions for your clinical work, especially those that include family/parent strategies.
The MTA study was followed up at two years and at eight years. Here is a summary of the findings. At two years, cessation of drug treatment was correlated with significant clinical decline. Continued drug therapy was correlated with moderate decline and initiation of stimulant therapy for those in control group was correlated with significant improvement (MTA Cooperative Group, 2004). So at this point again the cornerstone of treatment seemed to be with the medication. At the eight-year follow up, 33% of the subjects were still on medication (and 83% of them were on stimulants). Improvement was maintained but the group had not “normalized” meaning there were still significant achievement gaps between them and so-called “normal” controls. Thirty percent still met the DSM-IV criteria for ADHD (though one suspects more would meet criteria under DSM-5 because you only need five criteria met rather than six). Overall, medicated children did better in math and reading. There was still a significant test score gap between children in the study and the control group. Also, interestingly, approximately 30% showed signs of antisocial behavior and 25% showed signs of Oppositional Defiant Disorder (Barnard-Brak & Brak, 2011; Sheffler et al., 2009). This is interesting because many specialists felt that the antisocial behavior often comorbid with ADHD was because the ADHD was untreated. It seems that there may be something else to the antisocial behavior because it seemed to persist in so many people despite their long-term treatment for ADHD.
We spoke with one interventionist who provides a learning/coaching service to children with ADHD (Joyce Kubik, Personal Communication, April 2003). Kubik not only conducts specific skill-building training/coaching for ADHD children but also conducts support groups for parents. She also gives workshops for teacher in-service programs. Her overall message is that children with ADHD are capable of developing specific learning strategies that will lead to improved academic learning and success. She outlines these specific skills in her book S.C.O.P.E.: Student Centered Outcome Plan and Evaluation (Kubik, 2002). The central theme of her work is to help parents and teachers find ways to help students with attention difficulties. The American Academy of Child & Adolescent Psychiatry (2001) stated,
Research also should include the role of school and community-based professionals, as well as primary care clinicians, in delivering treatment services. Little is known about how short or long-term effectiveness varies as a function of the school and community-based professional involvement. … They should consider child and family outcomes and cost-effectiveness of care. Linking outcomes to service parameters is an important step in encouraging practice in system change. (p. 10)
In this summary statement, you can recognize aspects of the multimodal model that forms the basis of this book in analyzing and evaluating interventions with children and adolescents diagnosed with ADHD. It calls for more comprehensive research on the multiple factors that contribute to ADHD in children and adolescents and initiates the process to improve research on outcomes with this disorder.
The American Academy of Pediatrics (2001) also stressed that evaluation for ADHD should include an assessment for coexisting or comorbid conditions. The literature on ADHD identifies several psychological and developmental disorders that coexist in children with ADHD (Biederman, Mick, Faraone, & Burback, 2001; Phelps et al., 2002; Spencer, Biederman, & Wilens, 2002). These disorders included conduct and oppositional defiant disorders, mood disorders, anxiety and depressive disorders, mental retardation, learning disabilities, tics, substance abuse, and medical conditions. Researchers have estimated that among children with ADHD, the prevalence rate of Oppositional Defiant Disorder is up to 35%, Conduct Disorder up to 26%, anxiety disorders up to almost 26%, and depression up to 18% (AAP, 2001). It is more difficult to estimate comorbidity rates of Bipolar Disorder, substance abuse, and tics. Most authors who discuss comorbidity and ADHD tend to discuss the issue from a pharmacologic perspective rather than a counseling perspective (Levy & Hay, 2001; Solanto, Arnsten, & Castellanos, 2001). This is a burgeoning and complex conundrum in the treatment of ADHD. We encourage you to be alert to the great variability in children and adolescents diagnosed with ADHD and to assess for other conditions or factors.
Susan L. Andersen (2005) studied stimulants and the developing brain. She found that the effects of stimulant drugs during different stages have unique short-term, acute effects that also influence their long-term effects. Chronic, pre-pubertal exposure alters the expected developmental trajectory of brain structure and function and results in a different topography in adulthood. She also discovered that the timing of exposure (childhood vs. adolescence), the age of examination after drug exposure (immediately or delayed into adulthood), and sex influenced observable effects. Hopefully this can provide new treatment options for ADHD.
Mental health clinicians should be able to recognize the evidence recommending cautious use of stimulants with children and adolescents diagnosed with ADHD, and should remain alert to the potential for overdiagnosis or misdiagnosis of the disorder and the extensive range of comorbid/coexisting conditions. Phelps et al. (2002) summarized issues surrounding comorbidity of ADHD, ODD, and CD related to the evidence that when two or more of these disorders occur together, the prognosis is more guarded. They also addressed the hypothesis that ADHD occurs first in the child and the symptoms of impulsivity and inattention interact with the psychosocial issues of family turmoil, parental problems, and abuse factors to trigger ODD and/or CD. Clinicians need to be alert to the range of symptoms of several disorders when assessing and evaluating symptoms of impulsiveness and hyperactivity. These conditions could emanate from psychological family and environmental factors. Although the debate continues about the effectiveness of stimulant medication with ADHD, Greenhill (1998) and NIH (1998) concluded that stimulants used for ADHD children and adolescents
1. Produce moderate to marked short-term improvement in motor restlessness, on-task behavior, compliance, and academic performance.
2. In studies of six months or longer, children fail to maintain academic improvement or improve social problem-solving skills (Greenhill, 1998, p. 53).
Recently, atomoxetine/Strattera, a nonstimulant and a selective norepinephrine reuptake inhibitor (SNRI) has demonstrated some promising results in reducing ADHD symptoms (Brown University, 2002). It was approved for use in children ages 6 and older in 2003 and for maintenance treatment of ADHD in children and adolescents in 2008. Atomoxetine/Strattera is metabolized primarily through the CYP2D6 enzymatic pathways. It demonstrates an adverse event percentage of between 3.5 and 7% (poor metabolizers) in clinical trials. These adverse events include gastrointestinal problems, irritability, insomnia, aggression, and dizziness. As a nonpsychostimulant, atomoxetine/Straterra has potential as an alternative to the stimulants now used with ADHD. As with any new medication, only time and continued research will tell if atomoxetine will improve on the side effect profile of stimulant medications.
In a very sad and disappointing statement, the status of the treatment of ADHD has not changed in seven years since the first edition of this text.
• Children, adolescents, and adults are being diagnosed at accelerated rates.
• The first and second course of treatment is pharmaceuticals.
• Efforts by the FDA, legislation like the Best Pharmaceuticals for Children Act have been marginalized.
• Limited assistance for the poor, Medicaid, wards of the county or state, orphans and other children, and adolescents with restricted access to quality medical care.
• A belief still that life is better through pharma— just watch TV since the Health Care Act passed in 2009.
• Society's intolerance for anxious, agitated, and aggressive children.
• Large metropolitan school systems' inability to understand the impact of bullying on students with disabilities.
So with little progress, more children take the drugs and some experience improvement whereas many others graduate to more potent pharmaceuticals.
Review Questions
• What were the differences between the initial findings of the MTA study and the two-year and eight-year follow up?
• What does the eight-year follow-up tell us about antisocial behavior and ADHD treatment?
• What conditions may be comorbid with ADHD and why may these be a case of misdiagnosis?
SECTION FOUR: MOOD STABILIZERS AND BIPOLAR I DISORDER IN CHILDREN
Learning Objectives
• Be able to think critically about the problems of putting children and adolescents on medications tested on adults.
• Be able to articulate alternatives to so-called mood stabilizing medications for children.
The DSM-5 (American Psychiatric Association, 2013) provides the following diagnostic criteria for Bipolar Disorder, Single Manic Episode:
A. Presence of only one Manic Episode and no past Major Depressive Episodes. Note: Recurrence is defined as either a change in polarity from depression or an interval of at least two months without manic symptoms.
B. The Manic Episode is not better accounted for by Schizoaffective Disorder and is not superimposed on Schizophrenia, Schizophreniform Disorder, Delusional Disorder, or Psychotic Disorder Not Otherwise Specified.
Criteria for Manic Episode
A. A distinct period of abnormality and persistently elevated, expansive, or irritable mood, lasting at least one week (or any duration if hospitalization is necessary).
B. During the period of mood disturbance, three (or more) of the following symptoms have persisted (four if the mood is only irritable) and have been present to a significant degree:
(1) inflated self-esteem or grandiosity
(2) decreased need for sleep (e.g., feels rested after only three hours of sleep)
(3) more talkative than usual or pressure to keep talking
(4) flight of ideas or subjective experience that thoughts are racing
(5) distractibility (i.e., attention too easily drawn to unimportant or irrelevant external stimuli)
(6) increase in goal-directed activity (either socially, at work, or school, or sexually) or psychomotor agitation
(7) excessive involvement in pleasurable activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments).
C. The symptoms do not meet criteria for a Mixed Episode.
D. The mood disturbance is sufficiently severe to cause marked impairment in occupational functioning or in usual social activities or relationships with others, or to necessitate hospitalization to prevent harm to self or others, or there are psychotic features.
E. The symptoms are not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication, or other treatment) or a general medical condition (e.g., hyperthyroidism).
Source: Diagnostic and statistical manual of mental disorders (5th ed., Text Revision, pp. 123–125). Washington, DC: American Psychiatric Association, 2013.
We have seen in the past decade an increasing interest and shift in focus from Conduct Disorder (CD) and Oppositional Defiant Disorder (ODD) to Bipolar I Disorder in children and adolescents (Kusumaker, Lazier, MacMaster, & Santor, 2002; Milkowitz et al., 2014). We illustrated this in the case of Phillip at the beginning of this chapter. Although in our Chapter Eight discussion of mood stabilizers we focused on Bipolar I Disorder, in this chapter we use the more general BPI, because that is the construct common to the literature on children and adolescents. Many diagnostic scholars tell us the prevalence of BPI is growing, especially in preadolescent children, with almost no gender differences (Bland, 1997; Hirschfeld et al., 2003; Zarate & Tohen, 1996). The case for increased incidence is still undecided.
In the Diagnostic and Statistical Manual of Mental Disorder, 5th Edition (DSM-5; American Psychiatric Association [APA], 2013), BPI is the basis of a new category, Bipolar and Related Disorders. BPI is the centerpiece of this section, which also includes Bipolar II Disorder, Cyclothymic Disorder, Bipolar Disorders related to substance use or medical conditions, and other specified and unspecified Bipolar and Related Disorders. In order to stem the tide of BPI misdiagnoses in children, Disruptive Mood Dysregulation Disorder was introduced to the DSM-5 section on Depressive Disorders. The jury is still out on whether this will reduce the false diagnosis of BPI in children (Margulies, Weintraub, Basile, Grover, & Carlson, 2012) or, for that matter, how we should treat Disruptive Mood Dysregulation (Jairam, Prabhuswamy, & Dullur, 2012).
There is considerable controversy regarding the appropriateness of a BPI diagnosis in children. Questions regarding the appropriateness of such a diagnosis are founded on the idea that criteria for BPI may overlap with criteria for developmental issues; other disorders usually diagnosed during infancy, childhood, or adolescence (e.g., what the DSM-5 calls Neurodevelopmental Disorders); and other problems known to affect people of all ages (e.g., depressive, anxiety, substance use, and impulse-control disorders) (Chang, 2008). Further, there are currently no pediatric diagnostic guidelines for BPI in children, and it is inappropriate to use the DSM criteria for BPI because they were normed on adults (Kowatch et al., 2005; Sahling, 2009).
One of the most problematic issues is assuming that any type of irritability or acting out is somehow related to the invalid notion of a “bipolar spectrum.” Differentiating between irritability (very common in children and adolescents) and symptoms of BPI is an ethical imperative for clinicians, particularly those working in foster care or with other children and adolescents who have no one to advocate for them (Banaschewski, 2009; Sahling, 2009). Although published studies using functional brain-scanning technologies to investigate early-onset BPI are few, some show brain anomalies similar to those that correlate with adult BPI (Frazier et al., 2005). Only longitudinal studies will answer the question regarding how predictive such anomalies are for the development of BPI because brain scans can only suggest endophenotypes that are related to vulnerability to a disorder (Jackson, 2006).
The problems with the exponential increase in diagnosing pediatric bipolar disorder are many. In many children, rapid mood swings can be normal. The treatment guidelines (Kowatch et al., 2005) admit that “no one can say for sure what these children will look like when they grow up” (p. 214). This is a disturbing statement because BPI, properly diagnosed, is thought to be a chronic disorder. The authors of the treatment guidelines admit that the DSM symptoms for adult mania are problematic when used for children, but then they recommend continuing to use them. Overall, the treatment guidelines fail to draw distinctions between normal children and those really afflicted with BPI (Sahling, 2009).
Currently, the DSM-5 diagnostic criteria for Bipolar Disorder are used for children and adolescents without any major modifications and the features providing the best distinction between ODD, CD, ADHD, and BPI are the presence of a flight of ideas, grandiosity, and the episodic nature of the grandiosity (Carlson, 1996; Kusumaker et al., 2002). As we summarize the literature on BPI in children and adolescents, we learn that it is difficult to diagnose, more clinicians are recognizing its prevalence at an earlier age of onset, three tentative developmental theories are linked to it (McMahon & DePaulo, 1996), and more clinicians are using antimanic medications to treat BPI in both children and adolescents.
Soutullo et al. (2005) concluded that there is an overdiagnosis of Bipolar Disorder in the United States when compared to several countries like Spain, Turkey, India, Brazil, Switzerland, Denmark, and Finland. This difference may be attributed to a relative lack of data, differences in diagnostic criteria, different levels of recognition of child and adolescent psychiatry as a true specialty in Europe, clinician bias against Bipolar Disorder, an overdiagnosis in the United States, and/or a true higher prevalence of BD in the United States. It sounds like the same case with ADHD.
Viesselman (1999) addressed the general symptoms of BPI as expansive mood, inflated self-esteem, decreased need to sleep, talkativeness, flight of ideas, distractibility, psychomotor agitation, and excessive involvement with pleasurable activities. Phelps et al. (2002) addressed the fact that BPI youth often are incorrectly diagnosed as having Schizophrenia; thus, BPIs are difficult to discern in children and adolescents because many present with an agitated depressed mood rather than mania (Weller, Weller, & Fristad, 1995). Lewinsohn, Klein, and Seeley (1995) stated that pediatric clients with BPI present with more psychomotor agitation, elevated mood, increased verbalizations, inflated self-esteem, distractibility, and a decreased need for sleep. Duffy (2010) detailed with great specificity the potential genetic markers for children who might be vulnerable to inherit Bipolar I.
The treatment of choice for BPI in children and adolescents is the mood stabilizers covered in Chapter Eight. These drugs include lithium/Eskalith, Lithobid, valproate/Depakote/Depakene/Divalproex), carbamazepine/Tegretol, oxcarbazepine/Trileptal, and olanzapine/Zyprexa. Many scholars already cited in this chapter argue against indiscriminate use of these medications with pediatric populations without further study and argue for more complete awareness of the dynamics affecting the child.
Riddle et al. (2001) discussed the finding that the older antiepileptic drugs had been well researched as mood stabilizers in adults but not in pediatric populations. Campbell, Kafantaris, and Cueva (1995) have studied lithium/Eskalith, carbamazepine/Tegretol, and valproate/Divalproex used for children with nonspecific aggression and found lithium/Eskalith was superior to placebo and to the other antiepileptic drugs in reducing aggression. One very important note: Eberle (1998) found that one type of adverse event of using valproate with girls is that of polycystic ovarian disease, which can have profound consequences for females.
In the early 21st century, children and teens are 40 times more likely to be diagnosed with Bipolar Disorder than they were in the late 20th century (Miller & Barnett, 2008). As noted above there is evidence that this is due to diagnostic inflation and not an epidemic-level increase in the disorder. Geller et al. (2012) compared lithium/Eskalith, valproic acid/Divalproex, and risperidone/Risperdal in a trial called Treatment of Early Age Mania (TEAM). The response rate for risperidone/Risperdal was significantly higher (68%) than for lithium/Eskalith (36%) or valproic acid/Divalproex (24%). Advokat et al. (2014) note that quetiapine/Seroquel and aripiprazole/Abilify are as effective as risperidone/Risperdal. As noted in the chapter on antipsychotics though, these drugs come with severe side effects like weight gain and disruption of metabolic functions that can lead to type 2 diabetes.
In our clinical work of over 40 years, we have found that the comorbid substance use disorders were a major missing piece in several cases with children and adolescents. These clients were diagnosed with ODD, CD, or BPI and seemingly did not improve with psychotherapy or psychotropic interventions. The missing link and confounding variable was their hidden polysubstance abuse or dependence, which exacerbated some symptoms and masked others. The links in the literature show how the onsets of BPD, ADHD, CD, or ODD become significant risk factors in diagnosing substance use disorders. It should be noted that any attempts to procure research papers on pediatric or child papers on the research topics of developmental pharmacology, ADHD, BP I, and pharmaceuticals related to these disorders published in 2013 or 2014 were sponsored by pharmaceutical companies and cost $39.00.
The following case may provide additional understanding of these complex variables.
Nicole, a 14-year-old Caucasian girl currently living in a foster home, had just been referred to a Severe Emotional Disturbance (SED) unit in her school system. Nicole had a history of acting out, impulsivity, distractibility, conduct, and learning problems from a very early age. Initially, Nicole was referred to a specialist for her impulsivity and distractibility both at home and in preschool at the age of 4.
During the assessment, the clinician suspected a mood disorder but seemed to have more evidence for ADHD. He recommended a daily course of amphetamine salts/Adderall with behavior management therapy at home and school, focused on specific age-appropriate behaviors. At the time of the evaluation, he did not notice Nicole's intermittent scratching of her genital area. Over the next six months, Nicole showed little improvement in her symptoms and behaviors as a result of the amphetamine salts/Adderall and the milieu behavioral therapy. In fact, some of her behaviors worsened: she attacked other children, was cruel to animals, and was overtly curious about male and female genitals. After nine months, the psychologist consultant at the school recommended another neuropsychiatric evaluation and an outside therapist who would address some of Nicole's apparent psychological conflicts along with her behavior.
The second psychiatric evaluation yielded a change in diagnostic perspective. This time, the psychiatrist diagnosed BPI and prescribed valproic acid/Divalproex and a low dose of lorazepam/Ativan, an anxiolytic. The new therapist, a female, stopped the behavior therapy and began to treat Nicole with a combination of play therapy and insight-oriented therapy. The play produced associations to remote possibilities of earlier sexual abuse and abandonment, and the insight therapy captured her already highly critical superego (obsessive thought patterns and preoccupation with sexual act) and her deep affection for the rituals of the Catholic Church. Nicole remained on this treatment regimen for about two-and-a-half years. During treatment, she never really settled down in class or at home, but her behavior and attention were slightly more manageable. (We have all had cases where there is just enough improvement from the medication to raise expectations even if the client seems not to be making progress in many important areas of her life.) Later, Nicole developed a passion for reading 7 to 10 books a week that she got from the local library. On her trips back and forth to the library, she befriended some older boys (ages 10 to 13) who offered her street stimulants at a very low cost. Nicole welcomed the friendship and experimented with the drugs (stimulants, soapers, cocaine), but was gangraped by the boys one Saturday afternoon. Overwhelmed by this horrific sexual trauma, Nicole did not speak of it to anyone. She also immediately stopped associating with the boys. Her response to this event was alternately to withdraw into a cocoonlike isolation and to become aggressive with people.
She verbally assaulted teachers and foster parents and attacked her friends and other students. She was unreachable and totally out of control. She stopped attending her therapy sessions with the counselor, but she continued to seek street drugs.
Puzzled and frustrated, the school crisis team recommended an additional psychiatric evaluation and assessment for Nicole and possible hospitalization. This triggered a series of episodes in which she ran away, had several foster and specialized school placements, a brief stay at a juvenile detention facility, one abortion, and two attempts at drug rehabilitation for her dependence on stimulants, cocaine, and now alcohol. Somehow Nicole survived and is now in an SED classroom with a specialized social worker as an aide. She is on olanzapine/Zyprexa for psychotic mania, sertraline/Zoloft for depression and anxiety, low doses of valproic acid/Divalproex for violent and aggressive outbursts, and zolpidem/Ambien as needed for sleep. In essence, at 14, Nicole was loaded with psychotropic medications (polypharmacy). She was referred to a new female therapist, with whom she rarely spoke; when she did, she mentioned missing her former, caring play therapist, one of the most stable objects (people) in her life. Although Nicole did attend her class regularly and her behavior was quite manageable, her teachers reported very little learning progress and a total inability to interact with her classmates. Her therapist echoed much of the same descriptions, but voiced marginal hope when she and Nicole engaged in drawing or other forms of play therapy or discussed issues related to an all-loving versus all-punishing God. The concluding remarks in her individual educational plan (IEP) at school read, “No change, few academic gains, impulsive/aggressive behavior stabilized, little socialization, continues in counseling.”
Examining this case from our four perspectives yields some important insights and omissions. Nicole did receive a more extensive assessment early on and participated in behavioral therapy first, which is recommended by the literature (AAP, 2001; Kusumaker et al., 2002; Phelps et al., 2002) followed by art therapy and insight therapy when the behavioral therapy failed. It is critical to note that the second therapist helped Nicole discuss psychological and cultural issues and learned about the pressure from her complicated feelings about her upbringing in the Catholic Church and her deep awareness of her self-critical feelings and thoughts.
As is so often the situation with a foster child, other social and cultural pressures intervened, such as drug abuse, negative and exploitive peer relationships, and sexual trauma. It is not clear whether Nicole ever experienced sexual or physical abuse earlier in her life. The most recent team is faced with an early adolescent girl with a long history of psychotropic and psychotherapeutic treatments whose life is further complicated and traumatized by rape and drug dependence. Given the assumption that the significant others in her life—case managers, foster parents, teachers—feel she is out of control, the attending psychiatrist then addressed her range of symptoms and conflicts with a polypharmaceutical strategy. This approach numbs and tranquilizes Nicole so she is more appropriate in her various living environments but fails to address the boiling issues, anguish, and conflicts from the other aspects of her life. Treatment for Nicole should begin by recognizing the extreme complexity of her life space and developing a treatment plan and approach to gradually help her titrate off some of her medications while addressing in counseling the complex issues of abuse, drug dependence, abandonment, and loss of self that so plague her. She will need a very extended and interpersonal treatment approach if she is to recapture hope and resiliency in her life. We also would speculate about the accuracy of her diagnosis, because of the interplay of her conflicts and varying presenting problems and lack of empathy in her counseling.
Review Questions
• What are some of the problems of putting children and adolescents on medications tested on adults?
• What alternatives do we have to so-called mood stabilizing medications for children?
SECTION FIVE: CHILDREN AND ANTIPSYCHOTIC MEDICATION
Learning Objectives
• Know the diagnoses for which typical and atypical antipsychotics are being used in children.
• Be able to discuss the problems with this practice.
Schizophrenia with adolescent onset has been noted since the earliest descriptions of the disorder. Readers will recall Emil Kraepelin's initial diagnosis of a patient as having “dementia praecox,” which means “youthful insanity.” As Russell (2001) notes, given that the disorder has been linked with adolescents through the evolution of its diagnostic forms, one might think there would be ample treatment literature regarding these populations, but there is not. Childhood-onset schizophrenia (prior to age 12) is even rarer than adolescent onset. It is estimated that maybe 1 child in 10,000 would suffer this before the age of 12 (Remschmidt, 2002). The differential diagnosis must include substance-use disorders, depressive disorders with psychotic symptoms, and what DSM-5 calls other neurodevelopmental disorders like Autism Spectrum Disorder (Androutsos, 2012). Even when criteria are met it is very difficult to diagnose schizophrenia in a child. The Child Psychiatry Branch at the National Institute of Mental Health (NIMH) conducted a longitudinal study of childhood onset schizophrenia. Outpatient screening accurately diagnosed 55% of the 121 cases. However, inpatient observation including medication-free observation ruled out 96 children with alternative diagnoses. Outpatient screening only accurately diagnosed 62% of this same group. The conclusion the researchers drew was that inpatient, unmedicated observation was the most accurate way to diagnose these children (Gochman, Miller, & Rapoport, 2011).
In a review of controlled studies of antipsychotic agents to treat Schizophrenia, Campbell, Rapoport, and Simpson (1999) found only one controlled study of the use of these agents with adolescents and one report on their use with children younger than age 12. Therefore, Russell (2001) notes, until more research is conducted clinicians must extrapolate from adult studies to children and adolescents, which poses many risks. Although he comments this is not cause to adopt a nihilistic attitude, it does call for clinical skepticism. Russell maintains it may be true that people with early-onset Schizophrenia have more severe forms of the disorder, but this has yet to be determined conclusively and it does not mean pharmacologic treatment will not be effective. Further, early-onset Schizophrenia seems to have more severe negative symptoms, making the atypical antipsychotics a better choice if the children can tolerate the adverse drug effects (Botteron & Geller, 1999).
Although few data are available regarding the use of antipsychotics with childhood psychoses, in the 20th century the neuroleptic haloperidol/Haldol was used because it tended to be less sedating (Andreasen, 2000). Because of the potential for Parkinsonian-like symptoms, this medication was often prescribed with an anti-Parkinsonian agent such as benztropine/Cogentin. Ernst et al. (1999); Phelps et al. (2002); and Riddle et al. (2001) also addressed the use of the “atypical” newer neuroleptics for children diagnosed with tics, behavioral problems in autism, psychotic illness, and nonspecific aggression. In 2004, Toren et al. (Toren, Ratner, Laor, & Weizman, 2004) did a benefit-risk assessment of atypical antipsychotics in treating schizophrenia and comorbid disorders in children. They found the atypicals seemed to work better than neuroleptics and now it seems that neuroleptics like haloperidol/Haldol are only used if the patient does not respond to an atypical. Of the atypical, risperidone/Risperdal and olanzapine/Zyprexa seemed to improve cognitive functions and inhibit suicidal behavior. Madaan, Dvir, and Wilson (2008) noted that the FDA concluded there was enough support for using atypicals in children and approved two atypicals for childhood schizophrenia.
As we noted in Chapter Seven, evidence is mounting that atypical antipsychotics are also correlated with increased risk for diabetes and hyperglycemia and that this risk includes children and adolescents (Koller, Cross, & Schneider, 2004). Research by Correll et al. (2009) confirmed these mounting suspicions. The study concluded that use of aripiprozole, olanzapine, quetiapine, and risperidone for 12 weeks all produced weight gain, and varied in lipid and metabolic parameters. The authors called for more careful monitoring of the child's health before using an atypical. Whatever medication a clinician chooses, Russell (2001) emphasizes the need for multimodal treatment that includes psychosocial interventions such as individual and family therapy, psychoeducational counseling, and social skills training.
A more common problem is raised by Pappadopulos et al. (2002) in a study that examines the range of off-label prescribing of atypical antipsychotics for aggression. These authors state that although in theory doctors seem to agree about optimal prescribing practices, in the “real world” there is wild disparity in the prescriptions written. Apparently, even the agreement between researchers and front-line doctors can be influenced by staff pressure, limited staff resources, managed care limits on inpatient stays, and the movement away from physical restraint.
Another problem that requires further debate and research concerns the notion that Schizophrenia is a wide spectrum of early-onset disorders manifesting in a variety of the disorder called “schizotaxia,” which refers to a genetic predisposition to Schizophrenia (Meehl, 1962). Tsuang, Stone, and Faraone (2001) advocate treating Schizophrenia prophylactically. These authors maintain that the theoretically genetic predisposition toward Schizophrenia may be associated with reversible problems and may improve the child's quality of life. Despite this strong medical model perspective, they admit that psychosocial interventions may also work. They conducted a six-week trial of risperidone (prescribed at low levels) in six subjects identified as schizotaxic. They reported that five of the six reported increased cognitive abilities during the trial as well as greater enjoyment of social activities. Obviously, there is no way to determine the amount of placebo effect until a double-blind, placebo-controlled trial is done.
Great caution needs to be exercised here, as the implications are that asymptomatic children might be given antipsychotics in the hope that their diagnosis as schizotaxic is correct. The antipsychotic market currently amasses $5 billion a year, and many fear that the theory of schizotaxia is just another way of bending the parameters of diagnosis to help pharmaceutical companies profit from a new market. Currently, no diagnostic system in the world identifies adolescents in the phase before onset as ill, so this approach would have ramifications for the diagnosis. Ideally, the issues surrounding the politics of research and publishing described in Chapter Two, need to be more adequately addressed before any further medicating of asymptomatic populations. As Frances (2013) noted, preventive psychiatry could only work if we know the etiology of a disorder and have a safe and effective treatment for the disorder. We have neither where schizophrenia is concerned.
In Chapter Seven, we discussed neuroleptics and their affinities for different CNS receptors, their pharmacokinetics, and pharmacodynamics. Marriage (2002) spoke to our inability to predict the response of an individual patient (child or adolescent) to a typical or atypical neuroleptic. He addressed the enormous response variation, especially with adolescent males, Asians, Native Americans, and people suffering from various forms of organicity. For children or adolescents exhibiting symptoms of psychosis, the long-term prognosis is poor (Phelps et al., 2002), and we need to learn a great deal more about the adverse side effects of both the typical and atypical medications (Riddle et al., 2001). Given the outcome of Olfson et al. (2006) National Trends Study, which indicated that children treated with second-generation medication (atypical antipsychotics) included descriptive behavior disorders (37.8%), mood disorders (31.8%), pervasive developmental disorders or mental retardation (17.3%), and psychotic disorders (14.2%), we are again reluctant to endorse atypicals as a treatment of choice for childhood psychosis.
Review Questions
• What are some of the conditions for which children are being put on antipsychotic medications?
• What are the main drawbacks to this practice?
SECTION SIX: ANTIANXIETY MEDICATIONS AND CHILDREN AND ADOLESCENTS
Learning Objectives
• Understand particularly how anxiolytic medications are used with children who have school anxiety.
Despite the high prevalence of anxiety disorders in children (10 to 20%), very few controlled medication trials have been conducted. In DSM-5, Obsessive-Compulsive Disorder (OCD) and Post Traumatic Stress Disorder (PTSD) have been given their own categories. Children's anxiety disorders, Separation Anxiety Disorder, Selective Mutism, Specific Phobia and Generalized Anxiety. In the late 20th century, Brown and Sawyer (1998) concluded that regarding anxiolytic medication with children, “few published empirical studies support their long term efficacy for children and adolescents” (p. 83). Bernstein and Shaw (1997) noted that psychotropic medications should not be the sole intervention but should be used as an adjunct to counseling. Interventions that facilitate active mastery are important, to prevent symptoms returning after discontinuation of medication. Little has changed and almost 20 years later anxiety disorders in children are first best treated with non-pharmacological therapies like behavior therapy, cognitive-behavior therapy, and internalizing prevention programs. House (1999) noted that children's disorders can be generally grouped as externalizing (like acting out against others) and internalizing. Internalizing often results in anxiety symptoms. Young children with anxiety disorders are more likely to be depressed and to exhibit temperamental inhibition and sleep problems (Doughert et al., 2013).
The 2013 article of Rapp et al. will guide our complex study of anxiety disorders. The DSM-5 and earlier versions have really not assisted our journey to discover effective treatments for children and adolescents suffering from anxiety disorders (AD). It is the second author's opinion that there have been too many changes in the DSM related to AD since 1980. Our focus needs to shift to treatment with safe and effective outcomes. Bernstein, Borschardt, and Perwien (1996) viewed these changes as placing at risk a decade of research on childhood anxiety disorders, although Phelps et al. (2002) supported elimination of some categories of childhood anxiety disorders from DSM III-R as a research-based simplification of the categories. Although prevalence rates vary for current anxiety disorders with children and adolescents (Botteron & Geller, 1999; Garland, 2002), incidences of Generalized Anxiety Disorders (GAD), and Separation Anxiety Disorder (SAD) are frequently thought to require both psychopharmacologic and psychotherapeutic interventions. Currently, although almost all the drugs are used off label, SSRIs such as paroxetine/Paxil, fluvoxamine/Luvox, fluoxetine/Prozac, citalopram/Celexa, and sertraline/Zoloft are prescribed for children and adolescents with anxiety disorders. Advokat et al. (2014) noted that fluoxetine/Prozac may be the best medication if medication is necessary. The current concern over safety of these medications for children and adolescents applies to their use in anxiety disorders as well as in depression. One of chronic side effect of SSRIs recognized in children is a behavioral activation (Riddle et al., 1991), like an increased agitation different from a mania. As noted earlier the Food and Drug Administration (2003) issued a Public Health Advisory stating that use of SSRIs and similar types of antidepressants with depressed children and adolescents may be linked to increased suicide rates. How this will affect use of these antidepressants for anxiety disorders remains unclear. Rapp, Dodds, Walkup, and Rynn (2013) continued to use SSRIs in their combined treatment approaches with children diagnosed with GAD, SP, and SAD. Their study gave very high marks to Cognitive-Behavioral Therapy (CBT) in conjunction with a psychopharmacological approach.
In a review of the literature on anxiolytic medications used in pediatric populations, Livingston (1995) noted mixed results with benzodiazepines and said that in cases where studies show initial results, the results fail to be significant in replications of the studies. Livingston notes that if children are going to be placed on these medications, prescribers need to “start low and go slow” (p. 248). Recall from Chapter Six, benzodiazepines such as alprazolam/Xanax and diazepam/Valium have an inhibitory impact on the CNS at the GABA receptor complex. As Advokat et al. (2014) note these drugs usually cause cognitive impairments and so are not recommended except in the case of short-term medical procedures (e.g., dental procedures).
SCHOOL ISSUES, ANXIETY, AND CHILDREN
A relevant law when addressing anxiety in children is the Individuals with Disabilities Education Act (IDEA). Services to children are provided under a number of provisions in this act, and often many DSM anxiety disorders can be used to qualify a child for services. The diagnostic categories of DSM do not automatically correspond to the eligibility categories in IDEA. The interested reader can go to http://www.ed.gov/offices/OSERS/IDEA/the_law.xhtml for a listing of the relevant diagnoses. IDEA services focus on disability conditions that interfere with a child achieving academically or vocationally.
Anxiety disorders have been used to qualify a child for special services. A key symptom is fears associated with personal or school problems that persist over a period of time and adversely affect educational performance. Anxiety disorders are one of the most common childhood disorders and may impair a child's life even if symptoms are below the threshold for a DSM diagnosis. For example, some studies show “subclinical” anxiety to be highly correlated with reading difficulty (Bernstein & Shaw, 1997). Currently, studies are underway to measure the impact of bullying on anxiety (Twemlow, Fonagy, Sacco, & Brethour, 2006).
Developmental differences exist in the presentation of the anxiety disorders. For example, younger children with Separation Anxiety Disorder have far more symptoms than older children. In adolescents, somatic complaints and school refusal are more common than in younger children. Conversely, older children with GAD show more symptoms than younger ones. This is probably caused by cognitive differences, because older children have more mental tools with which to craft their worries.
Interestingly, in several studies with benzodiazepines, the medicated groups did no better than placebo controls. Two studies did yield significant differences among school refusers and children with selective mutism and social phobia. In one study, the school refusers did better than controls when given Tofranil/imipramine, a tricyclic antidepressant. The other study, on selective mutism and social phobia, showed that the experimental subjects did better than controls when given Prozac.
A related childhood disorder is Separation Anxiety Disorder. Here, the anxiety is aroused by separation from familiar people (usually parents) or leaving home. The reaction is excessive and may include fears that something will happen to the parents or to prevent reunification. Somatic complaints are also common. The distinction must be made between developmentally normal separation anxiety and this disorder. If refusal to go to school is thought to be due to Separation Anxiety Disorder, the child will go if accompanied by the parent. Although benzodiazepines and antihistamines have been used to treat this (Wozniak et al., 1997), exposure-based interventions and relaxation are likely to be more effective.
Another subthreshold condition is shyness. It is consistently correlated with adult and childhood anxiety disorders. Although common (90% of people report feeling it at some time in their lives), it can be debilitating as the person gets older. Shy men marry later and become parents later than their counterparts who are not shy. Although shy women marry and become parents at ages comparable to their counterparts who are not shy, they are less likely to attend college or work outside the home. Social phobia is a severe manifestation of shyness that afflicts about 5% of children. It delays social and emotional development. The overwhelming fear of doing or saying something embarrassing or humiliating keeps such people from eating, drinking, or writing in public or engaging in everyday conversations.
Although children generally outgrow shyness, they do not outgrow Social Phobia. Children with social phobias are usually depressed and lonely and almost always solitary. They may show extreme anxiety in situations where they feel they are being evaluated by others. The onset of Social Phobia is usually in adolescence and without treatment, the course is often chronic. There is high comorbidity with depression, other anxiety disorders, and substance abuse to self-medicate. As with other childhood anxiety disorders, the recommended treatments include rehearsal, imagery, and drug treatment with antidepressant compounds. Behavior therapy has a 70% success rate for both children and adults, with systematic desensitization and exposure being the common treatments. Although more children and adolescents are being prescribed SSRIs and SNRIs for shyness and Social Phobia, there is literature supporting the practice. Rapp et al. (2013) continued to use SSRIs as the pharmacological treatment of choice in their protocols with some success and marginal adverse effects in the pediatric population. They reported on one study that used pregabalin (Lyrica) with promising results with a pediatric population. There are too many adverse effects to pregabalin.
Review Questions
• How could anxiolytics be helpful to children with school anxiety?
SECTION SEVEN: ANTIDEPRESSANTS AND CHILDREN AND ADOLESCENTS
Learning Objectives
• Understand why the black-box warning on antidepressants for children is important.
• Be able to suggest the type of monitoring necessary if a child is on an antidepressant.
• Know the “placebo problem” especially in reference to children and antidepressants.
Many reports have appeared on an increased incidence of MDD in children and adolescents. Although more studies on this have begun, there is always error in the epidemiologic methods used to gather such data, so such reports are far from conclusive (Ingersoll & Burns, 2001). As McClure, Kubiszyn, and Kaslow (2002b) noted, many approaches are used for diagnosing and treating mood disorders in children, only a few have any empirical support. It does seem that when identified, childhood or adolescent depression is characterized by high rates of comorbidity with conduct, anxiety and attention deficit disorders, impaired social and vocational functioning, increased rates of substance abuse, eating disorders, and higher risk for completed suicide (West, 1997). Given that, it is important to consider all treatments that may be helpful when a child or adolescent does manifest symptoms of depression.
Depression (unipolar) can be very difficult to discover, discern, and diagnose in children and adolescents. In children, the symptoms manifest themselves as hyperactivity, impulsivity, and aggressiveness. Grief and loss may trigger enuresis, sleeplessness, nightmares, and extreme stubbornness, depending on the age of the child (Brown & Sammons, 2002; Riddle et al., 2001; Ryan, 2002; Viesselman, 1999). In fact, Ryan (2002) noted that depressive illnesses in children and adolescents can be protracted, recurrent, and continue into adulthood.
Newer research in to the complexities of antidepressant action can help neurologists and clinicians better understand developmentally important age differences in the nervous system. Researchers are beginning to see that developing animals differ from older ones in serotonin-mediated responses. Very-early-onset stress may compromise later adaptive capacity of some of these systems (Goldman-Rakic & Brown, 1982). Juvenile depression may also differ substantially from adult depression regarding the role of noradrenergic mechanisms and thus in the responsiveness to compounds that target norepinephrine. Practitioners need to be alert to warnings such as those by Coyle (2000), who noted there is “no empirical evidence to support psychotropic drug treatment in very young children and that such treatment could have deleterious effects on the developing brain” (p. 1060).
Tricyclic Antidepressants in Children
Overall, the results have not supported data found in adult studies regarding the efficacy of tricyclic antidepressants in treating juvenile depression (Cohen, Gerardin, Mazet, Purper-Ouakil, & Flament, 2004; Rosenberg, Holttum, & Gershon, 1994). The weight of currently available evidence suggests that TCAs as a group are indistinguishable from placebo, except in side effects (Kutcher et al., 1994; Puig-Antich et al., 1987). The highest response rate in a study is about 44%. In addition, a significant risk arises of serious cardiac problems in developing bodies. The same conclusions hold true for the TCA derivatives such as desipramine/Norpramin and nortriptyline/Trazodone. Both have been fairly well studied, and researchers have failed to show significant therapeutic differences from placebo but did show a high number of adverse side effects. In addition, both still carry the risk of cardiovascular complications.
Research has demonstrated that TCAs (and MAOIs) have not revealed greater efficacy than that for placebo, and their adverse side effect profile is extensive, including reports of sudden cardiac death (Birmaher, 1998; Brown & Sammons, 2002; Kye et al., 1996; Riddle, Geller, & Ryan, 1993; Werry, 1999). There is little support if any for the routine use of TCAs as a first line of treatment in children and adolescents. Therefore, it is disturbing that millions of prescriptions for desipramine and related compounds have been written for young people under age 18 (Goleman, 1993). Sommers-Flanagan and Sommers-Flanagan (1996) recommended that such prescriptions be reserved for special cases where other treatments have proven ineffective or intolerable and that a thorough physical (including cardiovascular exam) should be conducted before beginning the medication. TCAs should be used in children only under the following conditions:
• Full informed consent of patient and parent
• A history of lack of response to more appropriate treatments
• Full disclosure of side effect profile
• Disclosure of cardiotoxicity of these compounds
• When trials of more effective, available pharmacotherapies (SSRIs) have failed
Also, TCAs should be used with extreme caution, because the noradrenergic system (on which TCAs operate) does not fully develop until early adulthood (Goldman-Rakic & Brown, 1982). This evidence has not changed.
As noted, the FDA (2003) has currently issued a Public Health Advisory cautioning about a possible link to the use of certain SSRI antidepressants in pediatric populations and increased suicide rates. The antidepressants in the advisory are listed in Table 9.4.
TABLE 9.4 Antidepressants Listed in 2003 FDA Public Health Advisory
|
Generic Name |
Brand Name |
|
Fluoxetine |
Prozac |
|
Fluvoxamine |
Luvox |
|
Citalopram |
Celexa |
|
Escitalopram |
Lexapro |
|
Mirtazapine |
Remeron |
|
Nefazodone |
Serzone |
|
Paroxetine |
Paxil |
|
Sertraline |
Zoloft |
|
Venlafaxine |
Effexor |
|
Bupropion |
Wellbutrin |
© Cengage Learning®
As noted, the SSRIs currently are used with children and adolescents for anxiety and depression. Fluoxetine/Prozac has received FDA approval for use in pediatric populations, and fluvoxamine/Luvox is approved for treating OCD in children (Brown & Sammons, 2002). All other SSRIs are prescribed as off label to children with depression as of this writing. Children and adolescents encounter the same adverse effects as when the SSRIs are employed with anxiety disorders. These compounds are more effective in children but not as effective as in adult samples. GlaxoSmithKline pled guilty to criminal charges for promoting paroxetine for use in the pediatric age-range for the treatment of depression (Hensley, 2012).
It is important to note that adolescent girls are particularly vulnerable to depression when entering puberty (Phelps et al., 2002; Silberg et al., 1999). Clinicians should be sensitive to gender, family history of depression, impacting life events, loss, or death when assessing children for depression. Current trends and preliminary understandings of the research suggest that in addressing childhood depression, the clinician must consider both psychotherapy and medication (Badal, 1988, 2003). Ryan (2002) indicated that 30 to 40% of children do not have a sufficient response to the first SSRI treatment.
There is almost no literature on the effects of SSRIs on infants and preschoolers (McClure, Kubiszyn, & Kaslow, 2002a); however, evidence shows SSRI prescriptions are on the increase for this age group (Zito et al., 2000). The majority of researchers looked at the effects of fluoxetine (Prozac) on older children and adolescents, which has shown mixed results (Emslie et al., 1997). Some studies looking at the effects of paroxetine on children and adolescents are also promising (Findling et al., 2000; Keller et al., 2001), but more double-blind, placebo-controlled studies need to be done. Juveniles with a family history for manic or hypomanic symptoms are at higher risk for SSRI-induced manic or hypomanic episodes. If children or adolescents are treated with SSRI medications, treatment should be cautious and should observe the following conditions:
• SSRIs are used in addition to supportive psychotherapy or counseling to deal with psychological issues.
• SSRIs should be supported by education regarding the symptoms, the medication, and what relief the medication is to provide.
• Effective treatment involves parents or caregivers as much as possible.
• Effective treatment includes use of a depression scale (HAM-D or BDI-II) if the child is old enough to take one, to monitor symptoms.
• The acute phase of treatment should take place over 8 to 12 weeks followed by maintenance of 4 to 6 months.
McClure et al. (2002a) conclude that when medication is warranted, the SSRIs are the medication of first choice. Jureidini et al. (2004) disagree, however. They recently reviewed and critiqued seven published randomized, controlled trials of newer antidepressants for depressed children. These researchers found that pharmaceutical companies paid for the trials, the benefits of the drugs were small, and the adverse effects were downplayed, and they concluded antidepressant drugs could not be confidently recommended as a first-line treatment option. This is only one meta-analysis, but it points to the need for validity in published data and full disclosure of biases resulting from funding sources or researchers. Karger (2013) concluded that SSRI and even SNRI treatments for pediatric populations were/are too risky and this is from an international perspective. He stated that the SSRIs were more effective with anxiety disorders. Studies have been more compromised in pediatric populations with depression. Also, Craighead, Miklowitz, and Craighead (2013) summarized the work of Dr. Du of Shanghai who indicated that his studies demonstrate that SSRIs are safer in adolescents than in children. Dr. Du encouraged universal efforts of prevention to address the 17–20% of children who are depressed in all of our cultures.
From an integrative perspective, it is important to review all literature as it comes in, as well as review the researchers and the funding sources to check for possible bias. At the time of this writing, a new government-funded study of SSRIs and children was completed but not officially released in a peer-reviewed journal. The study was the Treatment for Adolescent with Depression Study (TADS), sponsored by the National Institute of Mental Health (NIMH). When we called NIMH to get a copy of the study, we were told the study needed to be peer-reviewed and the results would not be released until that process was complete. Nevertheless, Time magazine (Lemonick, 2004) and The New York Times (Harris, 2004) reported (without benefit of peer review) that the study supported the use of the medications with children. When we asked the NIMH representative how the popular press would have gotten the results to report before the peer review, she said she didn't know. Until a peer review of the study is concluded, the writers have no basis for these conclusions other than their own opinions of the study. Without including the results of peer review, readers are likely to come away with a “sound byte” interpretation of the results that may not be accurate. Readers can access the latest results of drug trials on the NIMH website http://www.nimh.nih.gov/studies/2mooddisordersdep.cfm. We did not try for the results in 2014.
As we noted in Chapter Five, the placebo effects of compounds and the place and type of placebo in studies has yet to be explicated. According to Fisher and Fisher (1997), “A probe of the available scientific reservoir of pertinent studies does not reveal any serious evidence that antidepressants do more for childhood depression than do placebos” (p. 308). An earlier overview of studies by Thurber, Ensign, Punnett, and Welter (1995) concluded that the more adequate the experimental methods in each study, the less likely to be found superior to placebo were the drugs tested. Although Fisher and Fisher (1997) noted that the evidence is still limited for the effectiveness of many counseling/psychotherapy approaches to depressed children and adolescents, this does not excuse the prescribing of compounds for which very little evidence of efficacy and effectiveness exists.
In concluding this section, we remind the reader that clinicians are using off-label psychotropic medication for several other disorders. In each case, the clinician must weigh the benefit versus the potential adverse effects of the drug on the child. We must also speak to the child about his or her reaction and feelings about the medication and request feedback from the parents or guardians about the child's progress or struggles with the psychotropic medications. We believe it is an enormous responsibility to counsel children and adolescents who are on psychotropic medication where little research has been conducted on the efficacy, effectiveness, and safety of the drugs.
In April 2003, the recommendations were published of the Research Forum approved by the American Academy of Child and Adolescent Psychiatry (AACAP) on strategies for psychopharmacological studies on preschool children (Greenhill et al., 2003). The six workgroups of the Research Forum were (1) diagnosis/assessment, (2) research design, (3) ethics/institutional review board (IRB), (4) preschool protocol modifications, (5) FDA/regulatory industry, and (6) training/public issues. Finally, when our text was reviewed in 2005, most psychiatrists challenged us on our strident positions about pharmaceutical research, medicating children, split-treatment (working together—psychiatrist and mental health professional), and the general tone of our text. Now we wish to extend our empathy to all psychiatrists who work under tremendous pressure to cure the incurable and find the magic pill.
CHAPTER THIRTEEN Psychotropic Medication and the Elderly By Elliott Ingersoll and Laura McIntyre
Psychotropic medication and its use with elderly clients as a population is of particular interest to clinicians due to several unique cultural, psychological, social, and physiological factors. Living longer and better is likely an instinct and human desire as old as time, and can be attributed in part recently to more and better education about health and nutrition as well as to strides made in health knowledge and application through technology. It makes sense to address trends in areas regarding older adults that may influence use of psychotropic medications. Odd as it may seem, at a time when people are living longer than ever and requiring more geriatric psychiatrists (Grossberg, 2010) there are fewer geriatric psychiatry fellowships nationwide (Bragg, Warshaw, Cheong, Meganathan, & Brewer, 2012), and we are starting to fill the gap with other professionals like nurses (Beck, Buckwalter, Dudzik, & Evans, 2011).
Old age is typically a degenerative process of the body and mind that precedes physical death as we know it. As joyless as that sounds, as a construct it seems to also be culturally defined, and varies across cultures. Most developed countries have settled on age 65 as defining of the term elderly; however, as Susan Jacoby (2011) discusses in her book, Never Say Die: The Myth and Marketing of the New Old Age (2011), we are now finding ourselves in a storm of marketing and media tempting new categories of older adults to “beat old age” and live as fast, sexy, and exciting as their younger counterparts. “50 is the new 40” and so forth, are common marketing ploys to sell methods to live a higher quality of life the older we get (including better quality through pharmaceuticals). This is all modeled and tested on perfect models of old age, like people in their 60s and 70s. The problem is that most aspiring “oldsters” are in younger old age and not exactly representative of elderly populations such as those that mental health professionals work with in nursing homes. Whether these new standards of “successful aging” become ingrained in society or not, there is a need to address the use of psychotropic medications by clinicians to treat symptoms, behavior, degenerative mechanisms, and illnesses that could be attributed to typical aging or concurrent experiences during the aging process. This is challenging because literature on the use of psychotropic medications in the elderly can be flawed and misleading, for reasons explained in this chapter.
This chapter is divided into five sections. Section One describes DSM-5 changes to delirium and dementia as well as medications to treat the two most common dementias. Section Two examines the state of psychosocial interventions for elderly clients. Section Three discusses pharmacologic treatment of dementia and other issues with psychotropic medications and the elderly. Section Four covers aging and assisted living. Finally, Section Five looks at side effects issues peculiar to the elderly.
SECTION ONE: DSM-5 CHANGES TO DELIRIUM AND DEMENTIA
Learning Objectives
• Be able to describe DSM-5 changes pertaining to Neurocognitive Disorders.
• Understand implications of changes in diagnostic criteria as it pertains to the elderly and clinical assessment and treatment.
• Understand use of etiological subtypes and cognitive domains in DSM-5.
The American Psychiatric Association (APA) has made several across-the-board changes in the DSM-5. Some changes in diagnosis appear to be a general move from attributing causation to a more dimensional perspective, instead highlighting developmental and life-span issues, which include several measures (where there is available data) of gender, race, and culture (including examining life-span functioning issues regarding disorders). Additionally, DSM-5 incorporates the latest research and clinical expertise (including some exploration of biomarkers discussed with etiology, though like genetic testing, this is still an emerging concept), differential diagnoses to distinguish disorders from others comparatively, and examines risks and prognostic factors (American Psychiatric Association, 2013a).
Neurocognitive Disorders (NCDS)
Neurocognitive Disorders (NCDS) are a new addition as the categories in the DSM-5 for what were previously Delirium, Dementia, Amnestic, and other Cognitive Disorders. NCD seems a preferred term anyway, to distinguish dementias not associated with degenerative aging (such as impairment secondary to a medical condition). On the other hand the term dementia will continue to be used in some settings. As we will see, several of the DSM-5 changes are highly significant to working with the elderly adult population and not always for the better.
The word “dementia” is Latin for “madness,” and it seems the editors of DSM-5 attempted, in a way, to reduce some of the stigma that seems to follow the word by replacing the word with two phrases: major neurocognitive disorder (major NCD) and mild neurocognitive disorder (mild NCD). There is no single disease called “dementia” (Gottfries, 1988). Dementias may arise from Alzheimer's disease, Parkinson's disease, Huntington's chorea, and Pick's disease to name a few. Their primary characteristics are declining cognitive function rather than a deficit, as previously utilized in diagnosis. In this sense, it separates them from neurodevelopmental disorders (NDs) in which the defining feature, a cognitive deficit, may be present from birth or developmentally impairing. It should be mentioned here that it is possible to develop an NCD against an existing ND. NCDs are unique in that we do know much more about the etiology of these than any other DSM disorder. Major and mild NCDs are generally distinguished in a subtle but significant way, by severity of cognitive impairment and severity of impairment of independence.
Major NCD concerns more severe impairments and stays consistent with medical terminology for the sake of appropriate treatment plans and to facilitate ongoing research. Major NCD brings together previous diagnoses including dementia and amnestic disorder, but is essentially dementia. The etiology of dementias is more well-known compared to most DSM disorders. The main purpose for a mild NCD category is a matter of debate. Some say it is more for nonmedical mental health professionals working with elderly clients who are still functioning somewhat independently. In this case, it allows for exploration of more effective treatment plans that focus on daily functioning and independence, maintaining and even preventing further decline in cognitive impairments. It could be considered an “early detection and intervention,” system. For some clients it can allow them to make the most of the time they have before suffering a major NCD. For others it can help them maintain or improve functioning and stave off decline. That said, mild NCDs may be an early stage of a later major NCD. As Frances (2013) pointed out, the biggest problem with this new category of mild NCDs is that you are going to be creating millions of patients who may be suffering from nothing more than normal aging and for whom medications can only deliver side effects. He maintained that including mild NCD is basically giving a diagnostic label to a normal part of aging. He wrote that “I would heartily endorse MND if there were a treatment for it or if it provided a really good way of predicting the future. But there is no treatment and little predictive power … accepting mental aging makes more sense than diagnosing it …” (p. 180). Truth be told, we have no effective treatments for the dementias and to medicate more people is at this point in time reckless.
Etiological subtypes (which again, utilize the term dementia when appropriate) for major NCD and mild NCD include Alzheimer's disease, Frontotemporal lobe degeneration, Lewy body disease, Vascular disease, Traumatic brain injury and Substance or medication-induced dementias, HIV infection, Prion disease (e.g., bovine spongiform disorder), Parkinson's disease, Huntington's disease, as well as other causes.
MEDICATIONS FOR ALZHEIMER'S DISEASE AND PARKINSON'S DISEASE
The majority of medication for dementia is for Alzheimer's type dementia (AD), the most common type. AD is a cortical dementia as well as a progressive neurodegenerative disease that involves the irreversible loss of cholinergic neurons. It comes in two variations, an early-onset familial form that seems mostly genetic and a far more common late-onset form that is less rooted in genetics (or may not be at all due to genetic vulnerability) (Balin & Hudson, 2014). In 2013, AD is thought to cost the United States over $200 billion annually (Alzheimer's Association, 2013). Although we still do not know the full etiological picture for this dementia, the predominant problem is what are called neuritic senile plaques (NSP) and neurofibrillary tangles (NFT). NST are composed of beta-amyloid deposits that are key to the neuron death. NFT are made of modified tau protein. Genetic analyses have identified mutations in several genes that result in increased production and deposit of beta-amyloid. The beta-amyloid accumulates due to what is thought to be a problem between production and removal of beta-amyloid. The hypothesis of etiology derived from these findings is called Amyloid Cascade Hypothesis (Hardy & Higgins, 1992) and has been the most popular theory of etiology for 20 years (Balin & Hudson, 2014). The main alternate hypothesis centers on tau protein. Tau protein normally binds and contributes to the structure of microtubules (components of cytoskeleton of eukaryotic cells). An AD tau is hyperphosphorylated (meaning a biochemical site related to signaling mechanisms is saturated). This is what leads to the NFTs which disrupt neuronal transport and lead to cell death (Massoud & Gauthier, 2010). The ultimate strategy would be to develop a neuroprotective agent to modify the effects of beta-amyloid or a medication to flush it from the system before it builds to dangerous levels. Thus far, all we have are drugs to treat symptoms, not underlying causes. The symptoms are far more than cognitive decline. They include behavioral disorders, movement difficulties, mood and anxiety symptoms and what can only be described as radical personality changes.
CAN ALZHEIMER'S DISEASE BE PREVENTED?
Before we address medications, it is important to clarify whether there are any preventative efforts clients can engage to preclude AD. Popular lore is full of stories about being physically active, mentally active, using ginkgo but are they true? There is mounting evidence that the hippocampus is one of the last brain structures to fully mature and the first to be affected by AD. Could it be that environmental exposures during early life could influ-ence later-life onset of AD? Studies have suggested education, complexity of occupation, and an engaged lifestyle have protective effects (Carrillo et al., 2013). Exercise has also been associated with a reduced risk of dementia (Ahlskog, Geda, Graff-Radford, & Petersen, 2011). Exercise was linked to vascular health which was thought to have been preventative but the clinical trials to prevent AD with vascular health are contradictory. The first studies used blood pressure medication to see if that slowed cognitive decline. Three studies have shown that proper use of antihypertensive agents in hypertension and after a cerebrovascular event is associated with a reduction in the incidence of cognitive impairment (Tzourio et al., 2003). The recently completed HYpertension in the Very Elderly Trial (HYVET) study, however, showed that treatment of people over 80 is associated with a reduction in vascular problems but not cognitive impairment (Peters et al., 2008).
Well what about lifestyle? Worldwide, lower levels of education, physical inactivity, suffering from depression, and smoking were all correlated with AD risk (Barnes & Yaffe, 2011). In the United States physical inactivity, depression, smoking, and hypertension had the highest correlations with AD. Other risk factors include sleep-disordered breathing. DSM-5 (APA, 2013) lists three sleep apneas that may be risk factors for AD: Obstructive Sleep Apnea, Central Sleep Apnea, and Sleep-Related Hypoventilation. The influence of diet is more controversial as some studies suggest that omega-3 fatty acids (Schaefer et al., 2006) or adherence to the “Mediterranean diet” could reduce one's risk of AD. However, in a State-of-the-Science Conference held by the National Institutes of Health (NIH) in 2010 there was not sufficient evidence found to say that these diet variables could decrease the risk of AD (Daviglus et al., 2011).
There are several planned and ongoing prevention trials for AD that focus on different populations including asymptomatic individuals and presymptomatic individuals with genetic risk factors. The Anti-Amyloid Treatment for Asymptomatic AD Trial (A4 Trial) is to be conducted by the National Institute on Ageing (NIA). This will study clinically normal beta-amyloid positive individuals who will receive an anti-amyloid therapy for a 3-year period. The therapeutic agent for this trial is solanezumab/Alzforum which is basically an antibody directed at the beta-amyloid peptide. One trial of solanezumab/Alzforum funded by Eli Lilly with over 2000 patients, half of whom received solanezumab/Alzforum intravenously every 4 weeks for 18 months failed to show improvement in the primary outcomes (Doody et al., 2014). As we will see this is a variation on initial work done with cannabis compounds. A hypothetical biomarker model of AD is gaining credence. Amyloid imaging and cerebrospinal fluid (CSF) total tau (t-tau) and p-tau, and structural MRI to determine how close in time a particular person is to relevant cognitive events. For example, one recent study concluded that a reduction in the CSF levels of one type of beta-amyloid (beta-amyloid 42) is an early upstream marker of AD (Buchhave et al., 2012). With prevention research raising as many questions as answers, we will not turn to medications to treat the symptoms of AD (remembering there is no cure at this time).
ACETYLCHOLINESTERASE INHIBITORS
Acetylcholinesterase inhibitors (AChE-Is) are the most common drugs used to treat Alzheimer's disease (AD). The most common are donepezil/Aricept, rivastigmine/Exelon, and galantamine/Razadyne. For the most part, these agents have similar efficacy (Molino, Colucci, Fasanaro, Traini, Amenta, 2013; Tan et al., 2014). All these drugs bind to the enzyme (acetylcholinesterase) that breaks down acetylcholine (Ach) much in the same way MAO inhibitors attach to monoamine oxidase to prevent the breakdown of norepinephrine. The side effects include gastrointestinal distress, abdominal cramping, and in some cases anorexia. The main limitations to these medications is that there is only modest improvement at best and in all cases, if the patient lives long enough, the disease process will overtake what the medication can do. A newer treatment for AD is memantine/Namenda, which is an NMDA receptor antagonist that acts on the Glutamate (Glu) system. The homeostasis of the Glu system is very delicate so NMDA antagonists (as mentioned in the chapters on mood stabilizers and antipsychotics) are hard to titrate. More research is needed before we can draw general conclusions on this compound.
Donepezil/Aricept is a piperidine derivative that reversibly inhibits acetylcholinesterase (remember from Chapter Five that not all inhibitors are reversible—e.g., MAO Inhibitor?). Birks and Harvey (2006) did a meta-analytic review of donepezil/Aricept efficacy across 24 trials with almost 6000 participants. Their findings showed significant improvement versus placebo at 24 weeks and 52 weeks on several measures related to cognition. They concluded that people with symptoms anywhere from mild to severe treated for periods of 12, 24, or 52 weeks experienced benefits in cognitive function. Positron Emission Tomography (PET) scans evaluated acetylcholinesterase (AChE) activity in 14 people with AD before and after treatment with donepezil/Aricept. The results showed modest inhibition of AChE with treatment, mostly in the cingulate cortex and this correlates with tests of executive function. As in all areas we have covered in this book, there are some who question the way efficacy is reported in donepezil/Aricept studies. Killin, Russ, Starr, Abrahams, and Della Sala (2014) noted that the effect size of donepezil/Aricept on cognition is larger in industry-funded trials than in independent trials. This is not explained by the longer duration of the industry-funded trials, suggesting perhaps the studies that are industry funded are methodologically designed to inflate the significance. There seems to be consensus that donepezil/Aricept is helpful but there is also consensus that it should not be given until symptoms develop. It is not a prophylactic.
Rivastigmine/Exelon is a carbamate derivative that reversibly inhibits both AChE and butyrylcholinesterase (BuChE). It is the only acetylcholinesterase inhibitor that also inhibits BuChE. BuChE is widely distributed in the central nervous system and might play a role in the function of acetylcholine neurons and neuronal degeneration. It is not clear how BuChE inhibition relates to rivastigmine/Exelon's efficacy. Birks, Grimley Evans, Iakovidou, Tsolaki, and Holt (2009) evaluated nine trials with almost 5000 subjects and found rivastigmine/Exelon at 6 to 12 mg daily is associated with significant improvement versus placebo. Winblad et al. (2007) studied the transdermal formulation and found it had similar efficacy to the tablets but with a 2/3 reduction in reports of nausea. Adler, Muller, and Articus (2014) also found that the transdermal formulation decreased caregiver burden and increased treatment adherence.
Galantamine/Razadyne is a tertiary alkaloid drug that reversibly inhibits AChE. It also binds to the nicotinic Ach receptors enhancing Ach function. The relevance of that to its efficacy though is at this time unclear. Cusi et al. (2007) reviewed 10 trials with almost 7000 participants with mild to moderate AD. The results suggest galantamine/Razadyne was significantly better than placebo. There was not a significant dose-response effect, doses above 8 mg daily were consistently significant. Comparative studies of these three AChE inhibitors led to conflicting results, which makes it hard to recommend one over another. Massoud and Gauthier (2010) recommend using tolerability of the compound as a guide as to which one to use. More recently Tan et al. (2014) found cognitive effects of all drugs to be significant. Memantine/Namenda (described next) was included in this study and the authors concluded there were more dropouts with AChE than with memantine/Namenda (which works via a different mechanism).
Memantine/Namenda is an N-methyl-D-aspartate (NMDA) receptor antagonist. Studies have shown that increased glutamate may lead to excitotoxicity and play a central role in AD (Sucher, Awobuluyi, Choi, & Lipton, 1996). By blocking the glutamate receptor the theory is that this will decrease the excitotoxicity. Massoud and Guthier (2010) summarized findings on the drug. In six trials with moderate-to-severe cases data showed significant benefits versus placebo at 6 months on measures of cognition. A trial comparing memantine/Namenda with donepezil/Aricept showed additional benefits in patients with moderate-to-severe symptoms. As noted, Tan et al. (2014) found that there were fewer dropouts with memantine/Namenda.
The other most common neurodegenerative disease is Parkinson's disease (PD). It occurs in about 1% of people 65–69 years old worldwide. PD is characterized by a progressive loss of dopamine (DA) neurons in a unique combination of brain regions, particularly the substantia nigra. As with Alzheimer's we can only treat the symptoms and in many cases the disease process will overtake what we can do with medication. The primary drugs used to treat PD all try to make up for the loss of DA neurons. Several DA agonists are used to treat PD including levodopa/Carbadopa, apomorphine/Apokan, lisuirde/Revenil, and pramipezole/Mirapex. The most common is levodopa/Carbadopa. Most agonists bind at D1 or D2 receptors. DA receptor stimulation in the dorsal striatum is the primary mechanism by which the drugs partly alleviate the motor features that are associated with PD. PD also affects 5-HT and NE neurotransmitters that may account for PD-related depression (Brichta, Greengard, & Flajolet, 2013). Levadopa is a precursor to DA and thus stimulates the production of DA in the brain. It is sometimes given with levodopa/Carbadopa to ease side effects like nausea. Unfortunately as time goes on each dose becomes less effective. Catechol-o-methyltransferase (COMT) inhibitors (like tolcapone/Tasmar) can help extend the effectiveness of levodopa/Carbadopa and prolong its effects but these medications may have severe side effects on the liver. In addition, there are side effects to levodopa, including induced dyskinesias (drug-induced abnormal movement). Newer therapies being investigated to treat these are glutamate and adenosine receptor antagonists (Blandini & Armentero, 2012).
Other drugs that have modest anti-Parkinsonian actions are amantadine/Symmetrel and memantine/Namenda. As noted memantine/Namenda is an NMDA antagonist and we described its actions above. Amantadine/Symmetrel is actually an antiviral and its mechanism of action in PD is unknown. Amantadine is actually an antiviral agent that has modest anti-Parkinsonian action. We do not know its mechanism of action but Advokat, Comaty, and Julien (2014) suggest it may “… alter dopamine release or reuptake, or it may have anticholinergic properties” (p. 569).
Given that the AChE-Is have been called “cognitive enhancers” and since “cognitive enhancement” has frequently been linked (if only in popular thought) with stimulants, what about treating symptoms of dementia with stimulants? The idea is not a new one and psychostimulants including caffeine and amphetamines have been used to treat various aspects of dementia and related problems from the early 20th century to the present (Rasmussen, 2008). In 1984 Loew posed the question as to whether stimulants might be a neglected option in treating what was then referred to as senility. Roccaforte and Burke (1990) reviewed the limited literature of the effects of stimulants on cognition, motivation, and depression. They concluded that the extant literature was promising enough to require more study. Galynker et al. (1997) did a pilot study to evaluate the effect of methylphenidate/Ritalin on the negative symptoms of dementia. Dementia from AD and vascular dementia were treated. They concluded that in both types of dementia, negative symptoms appeared responsive to methylphenidate/Ritalin. Padala, Burke, Bhatia, and Petty (2007) presented four cases of apathy that were treated with a regimen of methylphenidate/Ritalin. They noted significant improvement in apathy, motivation, and persistence. Following up on that, Padala et al. (2010) noted that methylphenidate/Ritalin was effective in treating apathy and depression in a 12-week treatment study. It is also interesting that in the Padala study no one dropped out due to adverse effects. Finally Rahman and colleagues (2006) tried to reduce abnormal risk-taking behavior in people with frontotemporal dementia using methylphenidate/Ritalin. They concluded that methylphenidate/Ritalin was effective in “normalizing” decision making in the test subjects without impairing other aspects of cognition.
There have been attempts to understand the relationship of caffeine to cognition and whether it could serve to decrease dementia symptoms. In a meta-analysis Santos, Costa, Santos, Vaz-Carneiro, and Lunet (2010) found that caffeine may serve as a mild neuroprotective agent but the differences in methodology made it difficult to conclude anything with certainty. Biessels (2010) concluded the same thing stating that there are not enough studies now to make anything more than general statements. Referencing the Cardiovascular Risk Factors, Aging and Incidence of Dementia (CAIDE) study, Eskelinen (Eskelinen & Kivipelto 2010; Eskelinen, Ngandu, Tuomilehto, Soininen, & Kivipelto, 2009) noted that coffee drinking may be associated with a decreased risk of AD and that this may be mediated by the caffeine and/or other mechanisms like the antioxidant capacity of coffee.
A lesser-known research area is studying the neuroprotective properties of cannabis as well as the use of cannabis to ease some symptoms of dementia. Marchalant, Baranger, Wenk, Khrestchatisky, and Rivera (2012) suggested that because cannabinoids can positively affect age-related processes like neuroinflammation, neurogenesis, and memory, epidemiologic studies should be done on long-term, chronic cannabinoid users to assess their risk for developing AD compared to the general population. Aggarwal and Carter (2010) note that information (or misinformation as the case may be) disseminated by governmental organizations would lead most readers to the conclusion that cannabis has no benefits for the brain and nervous system. This is not the case at all. There are many peer-reviewed studies that support the hypothesis that the cannabinoids in marijuana have neuroprotective properties and can be used to treat neurotoxicity and neuroinflammation. Cannabis may limit the formation of neuritic plaques in the brain and perhaps slow the process of AD. Eubanks et al. (2006) reported that delta 9-THC, both in the test tube and in computer models, inhibited acetylcholinesterase (AChE—the enzyme that breaks down Ach) and prevents AChE amyloid plaque collection. They concluded that “THC is a considerably superior inhibitor of amyloid-B-peptide aggregation …” (p. 773). Other studies have shown that cannabidiol (CBD) and a synthetic cannabinoid (WIN-55, 212-2) can prevent brain cell death caused by exposure to amyloid plaques in animal models (Marchalant, Rosi, & Wenk, 2007; Marchalant et al., 2009).
In another study, Marchalant, Cerbai, Brothers, and Wenk (2008) reported that the number of activated microglia (active in immune defense) increase during normal aging. Stimulation of endocannabinoid receptors reduced the number of microglia in the hippocampi of young rats. The same holds true for older rats and if researchers get clearance to do human studies we may find that stimulation of the cannabinoid receptors could provide clinical benefits in age-related diseases like AD. Finally, Iuvone et al. (2004) demonstrated that CBD exerts a combination of neuroprotective, antioxidative, and antiapoptotic effects against beta-amyloid toxicity. At the time of this writing, it seems that the biggest barriers to research are all legal related to the federal criminalization of cannabis. As researcher Gary Wenk (2014) noted, if you are not connected to the only legal, grant-funded marijuana farm at the University of Missouri, it gets very expensive very quickly to conduct independent research as the time you put in just for legal clearance is itself a significant obstacle. As state decriminalization of marijuana expands, perhaps the federal prohibition will end, at least enough to allow unfettered, scientific research to resume.
Review Questions
• What are some general changes to the DSM-5 that could benefit the elderly as a population?
• What are the changes to Delirium and Dementia in DSM-5?
• What are the primary drugs to treat Alzheimer's disease and how do they work?
• What are the primary drugs used to treat Parkinson's disease and how do they work?
• What are alternatives and/or preventative treatments for dementia?
SECTION TWO: THE STATE OF PSYCHOSOCIAL INTERVENTIONS FOR ELDERLY CLIENTS
Learning Objectives
• Describe several psychosocial interventions to treating elderly clients.
• Understand the need for further research and valid data to expand literature on nonpharmaceutical approaches.
Functioning of elderly people in a clinical context is clearly affected by social and coping skills and support. Looking through an integral lens at treating for mental health disorders, including organic disorders, we know that exploring all facets and dimensions of a client's experiences seems the most thorough way to diagnose and treat if needed, and also to decide if medication could be helpful, when psychosocial interventions can help or whether a combination would be more appropriate. There is growing evidence that psychosocial interventions can empower elderly clients to adapt to a variety of concerns unique to them psychosocially, and also adjust to illnesses and mental health disorders such as depression or cognitive impairments that are often correlated with aging. Proper clinical assessment of older clients' psychosocial experiences and changes they are experiencing is important for clinicians, as is empathically trying to understand the clients' belief systems.
Frank (2014) notes that depression in elderly people has been underreported for decades. Major Depressive Disorder (MDD) affects up to 20% of people older than 65. The point prevalence for MDD in people with Mild Cognitive Impairment (MCI) is approximately the same as in those without MCI (Polyakova et al., 2014). The elderly as a population represent 12% of the population but account for 20% of completed suicides. Males aged 75 and over have the highest rates of suicide in industrialized societies and in many countries suicide rates rise with age (Cattell, 2000). Some psychotropic medications are more highly correlated with suicide as hypnotics and benzodiazepines may increase the suicide risk almost 10-fold (Carlsten & Waren, 2009). Additionally, men account for 81% of suicides of people aged 65 and older. When assessing for later life depression, risk factors are female gender status, unmarried status, stressful life events, lack of social support, and concurrent medical illnesses. All of this is important when considering effective treatments. Many older clients have substantial comorbid conditions such as heart failure, diabetes, and cancer. Chronic disease is a risk factor for developing depression. Some clinicians estimate that antidepressants seem to have equivalent efficacy in younger and older adults but be reminded this may be only about 50% and many older people are not going to tolerate the side effects for a limited return (Nelson & Devenand, 2011). Others note that when you add in cognitive impairment the antidepressant efficacy drops to 40% at best (Thase, Entsuah, & Rudolph, 2001). This is not just a medical question though. Whereas therapeutically our ethical commitment is on the side of life, it behooves all clinicians working with this population to really think through their own perspective on suicide. Is it always bad? Wrong? If so, why? Too often these existential questions are glibly overlooked exacerbating an already difficult situation when the client thinks the clinician is clueless about suffering, the meaning of life, and the quality of life.
Particularly because the elderly may not respond to medication, psychosocial interventions are important. One such intervention is Problem Adaptation Therapy (PATH). PATH involves the same therapeutic factors thought to be effective in most theories of psychotherapy including relationship and client strength factors but more specifically PATH focuses on the client's ecosystem. This includes the client, the home, and the caregivers if relevant. PATH incorporates environmental adaptation tools and invites participation from caregivers, hence this is more specific and focused than just supportive therapy (Kiosses, Arean, Teri, & Alexopoulos, 2009). PATH is an intervention conducted at the home to reduce depressive symptoms and disability in elderly clients with cognitive impairments and disability. Kiosses, Arean, Teri, and Alexopoulos (2010) found that PATH was more efficacious than Supportive Therapy (ST) in decreasing depressive symptoms in elderly clients.
Interpersonal Psychotherapy (IPT) is recommended for elderly clients as a treatment for depression and is shown to be significant in improving general mental and social functioning when used in place of general medical practitioner care. Like its name suggests, it is an intervention that focuses on interpersonal efficacy and functioning. It also uses techniques that focus on communication, to increase social support and puzzle out symptoms. A modified version is Interpersonal Psychotherapy for Mild Cognitive Impairment (IPT-MCI), which includes the client and a caregiver in sessions to promote a richer relationship between them. This can be especially helpful for “old-old” clients who may be experiencing more cognitive and medical issues, and with whom medication may be less effective and have more adverse side effects.
Problem-Solving Therapy for Mild Executive Dysfunction (PST-MED) is a 12-week session for ambulatory elderly clients, which teaches a five-step problem-solving model. The model is taught over the first five weeks of treatment and then the last seven sessions are dedicated to refining problemsolving skills (Alexopoulos et al., 2011; Arean et al., 2010). Participants set treatment goals, discuss and evaluate different ways to reach them, create plans and evaluate how well the plans worked. The results suggest that this not only assisted with planning but also reduced depressive symptoms in a considerable number in subjects with depression and cognitive dysfunction (Arean et al., 2010).
Cognitive Behavioral Therapy (CBT) has been shown to be a very effective treatment for depression in older adults (Doubleday, King, & Papageorgiuo, 2002) after screening for specific cognitive impairments, sensory impairments, and disability. Generally, even with a wider variability of measurable cognitive ability and considering decline of some cognitive abilities in later life, older people can be memory-trained and do well on sustained-attention tasks. According to McKeith et al., (1999), “‘fluid intelligence' (the ability to acquire and manipulate new information, i.e., ‘wit') declines with age whereas ‘crystallized intelligence' (the cumulative product of information acquired as a result of fluid intelligence, i.e., ‘wisdom') does not.” Though research is still emerging, CBT can be utilized with a variety of issues pertaining to elderly people but may need some modifications as we currently see in other psychosocial interventions.
Group therapy is an effective treatment option for older adults, especially those who do not respond favorably to psychotropic medications or individual therapy. Though it has some inherent challenges like accessibility, group therapy can be empowering and transforming for elderly clients when they can socialize with other older adults and share age-related issues (Sochting, O'Neal, Third, Rogers, & Ogrodniczuk, 2013). There are many modalities of group therapy with music group therapy being one of the more effective. Group music interventions are noninvasive and inexpensive ways to reduce symptoms of depression. These approaches also work with clients suffering from mild-to-moderate dementia. Because of the nature of the brain and what might be called musical intelligence (even if that is just the part of the brain shaped by the music you have listened to all your life), musical memories persist longer than some types of memories making this an evocative treatment approach. Chu and colleagues (2014) collected data on participants' prior musical experience, training (if any), and preferences. Other members of the team collected responses to dependent measures and took salivary cortisol samples as a measure of stress reduction. Although the cortisol levels pre and post were not significant, depressive symptoms were significantly decreased and cognitive functioning significantly delayed.
Other newer nonpharmacological interventions include aromatherapy (Thorgrimsen, Spector, Wiles, & Orrell, 2003), where aromatherapy showed benefit for people with dementia in one small trial. Also there are multisensory therapies, some using a therapeutic PARO robot. Paro is designed to look like a baby seal and was developed by a Japanese industrial automation pioneer Takanori Shibata. It has shown success in elevating mood in facilities where live animals would not be possible. Paro is equipped with five sensors: tactile, light, audition, temperature, and posture sensors with which it can perceive people and its environment. It can respond to sensory input by things like blinking, wagging its tail, and turning in the direction of a voice (Sabanovic, Bennett, Chang, & Huber, 2013). Research attempting to support significant efficacy over pharmacological interventions is also emerging, such as a Penn State College of Medicine pilot study that studied rates of psychotropic drug prescriptions for clients with dementia over 60 years of age in long-term care involved in a Group-based Creative Expression Storytelling Program compared to similar clients in a standard care activity program. The study attempted to explore whether there is a correlation between using the group-based creative program and reduced prescribing of psychotropic medications for clients with dementia (Houser, 2012).
The need to recognize psychosocial interventions as effective in treating a variety of aging issues often seems outweighed by a tendency to overdetermine symptoms in older adults. A number of noncognitive symptoms can be classified under such diagnoses as dementia without a full clinical evaluation, which could lead to nonpharmaceutical interventions as a primary approach. This often leads to diagnosis and treatment (not to mention how clients will understand their symptoms, which could be conflicting for them) using the medical model of disease rather than a more integrative approach to treatment, as well as inappropriate prescribing. Psychosocial interventions could be imagined as a valuable part of multidisciplinary preventative health programs for elderly people and that as people live longer, there are many promising and emerging alternatives to typical primary and secondary clinical treatments.
Review Questions
• Describe several psychosocial interventions for the elderly.
• Why should clinicians consider psychosocial interventions as a primary approach to treatment with the elderly as opposed to pharmacological approaches?
• What are the advantages of clinicians using an integral lens when considering treatment or utilizing preventative, multidisciplinary programs to care for older adults?
SECTION THREE: PHARMACOLOGIC TREATMENT OF DEMENTIA: FROM THE 20TH CENTURY AND INTO THE 21ST CENTURY
Learning Objectives
• Understand trends of psychotropic medication use and why it is relevant to the elderly.
• Describe several commonly prescribed psychotropic medications clinicians utilize to treat elderly clients.
• Describe several drawbacks to available literature regarding psychotropic drugs.
Psychotropic medications are very commonly prescribed for elderly clients (many are now saying over-prescribed) in both community based and managed care (which includes several settings such as geriatric units, acute care geriatric units, and nursing homes). It is not only important for clinicians working with aging adults to be aware of rates of prescription, but important to gauge the accuracy of the literature available regarding pharmacological treatment. Whether benefits outweigh the risks of those treatments is of particular significance to clinicians working with elderly clients. In general, psychotropic prescription rates are increasing. Trends for elderly population in outpatient and in managed care settings show a high rate of psychotropic medication use, especially for women and clients in institutions. It should be noted that geriatric patients being treated for mental illness are more likely to have comorbid disorders and more likely to be overmedicated (Laroche, Charmes, Nouaille, Picard, & Merle, 2006; Procyshyn, Barr, Brickell, & Honer, 2010). Advokat et al. (2014) state emphatically “The elderly are frequently prescribed medication that they do not need or that cause them significant problems either because of extensions of expected pharmacological effects or through adverse interactions with other medications. Inappropriate medication use in the elderly is a major functional and safety issue …” (p. 556). The other big problem is, like many overmedicated children, the elderly are increasingly likely to be on multiple psychotropic medications. Sabzwari, Qidwai, and Bhanji (2013) warn that increasing polypharmacy with psychotropic medications seems to be correlated with increased risk for iatrogenic (preventable harm arising from medical treatment) error.
One problem in nursing homes is that patients are inappropriately medicated more because of staff distress than patient need. Zuidema, Jonghe, Verhey, and Koopmans (2011) looked at staff distress and the nursing home environment and their effects on psychotropic drug use. They found that both staff distress and negative aspects of the nursing home environment were positively correlated with more drugs being used for the patients. Human beings it seems have a healthy denial of death (one can't ruminate on it all day) that merges with an unhealthy “blind eye” turned toward how poor most nursing home environments really are. If you doubt this ask yourself how you felt the last time you visited a nursing home. If you haven't visited one recently, why not? Why not go “hang out” and talk with residents? In Oberlin Ohio, a unique quality of life program allows graduate students from a local music academy live rent free in nursing homes and pay for room and board by doing concerts and tending to the instruments there. It is innovative programs like this that will bridge the distance we have created between our elderly and the rest of our society.
One solution to polypharmacy in nursing homes was proposed by Smeets et al. (2013) in the form of a program with the acronym PROPER (PRescription Optimization of Psychotropic drugs in the Elderly nuRsing home patients with dementia). This was a multicenter cluster randomized, controlled, pragmatic trial using parallel groups with a duration of 18 months with 4 six-monthly assessments. The intervention consisted of structured and repeated medication review supported by education and continuous evaluation. It involved pharmacists, physicians, and nurses. There were three parts to this: (1) preparation and education, (2) conduct, (3) evaluation and guidance. The ongoing (at the time of this writing) trial is expected to decrease overmedication simply by making it an object of awareness for all involved. Simple as this sounds it makes sense. We always tell our students that all psychotherapy is helping clients make aspects of themselves and their lives objects of awareness. The same holds true for ethical practice in any profession.
COMMONLY PRESCRIBED PSYCHOTROPIC MEDICATIONS IN ELDERLY POPULATION
According to the Centers for Disease Control (CDC) the highest rate of suicide deaths for males and females is in the 50–54 age group with about 20 suicides per 100,000. The next highest is the 54—59 age group, and adults 65 and older have a suicide rate of about 15 per 100,000 but for males alone it is 32 per 100,000. For males 85 and older the rate jumps to approximately 47 suicides per 100,000 people (CDC, 2014). Older adults prefer to receive their mental health treatment from their primary health care provider but Advokat, Comaty, and Julien warn that may not be the best approach. As Frances (2013) noted, general practitioners often do have strong relationships with their patients but are not specifically trained in psychiatry and especially geriatric psychiatry. Team approaches can be useful but often are too expensive given the shortage of professionals to treat the elderly. In studying patients with depression older than age (Reynolds et al., 2011), the team cautioned that adding an antidepressant to a cognitive enhancer like donepezil/Aricept requires careful weighing of risks and benefits. This again points to the increase in complexity when treating comorbid conditions. Efficacy has also been demonstrated for escitalo-pram/Lexapro, and duloxetine/Cymbalta (Dolder, Nelson, & Stump, 2010). Of course there are downsides too. Some researchers have found SSRI use in the elderly is correlated with increased risk of falls (likely due to dizziness) (Sterke, Ziere, van Beeck, Looman, & van der Cammen, 2012).
We know Anxiety Disorder continues to be a problem in old age (Blay & Marinho, 2012). We have already touched on the concern that certain anxiolytics (benzodiazepines) can be problematic in the elderly as they are correlated with higher suicide rates and falls. We also know that elderly patients coming to emergency rooms are more likely to be prescribed benzodiazepines (Spanemberg et al., 2011). Although many books on psychopharmacology do not ask the obvious question, we will. If benzodiazepines are so problematic for elderly clients why prescribe them? Whereas many clients prefer benzodiazepines to SSRI antidepressants (and they do have more efficacy for anxiety than SSRIs), in several studies, long-term use of benzodiazepines in elderly clients is associated with poorer outcomes in anxiety and sleep (Beland et al., 2010; Nordfjaern, 2013), psychomotor impairment (Bulat, Castle, Rutledge, & Quigley, 2008), and increased risk of falling (Quigley, Barnett, Bulat, & Friedman, 2014). In some cases patients may be taking these because these were the only drugs available when they were first treated for anxiety. In other cases some people may get genuine benefits and in others tolerance and dependence may be a reason the patients request for the medications. Many recommend new guidelines like not using benzodiazepines for more than 30 days or limited prescriptions to those benzodiazepines like alprazolam/Xanax that have shorter half-lives (Lindsey, 2009).
The behavioral and psychological symptoms of dementia (BPSD) include delusions, apathy, depression, agitation, and irritability. The most difficult of these for caregivers are delusions, agitation, and irritability (Fauth & Gibbons, 2014). The Omnibus Budget Reconciliation Act (OBRA) of 1987 was legislation that aimed to combat misuse of psychotropic medications as well as protect clients in long-term care/nursing homes from unnecessary “physical or chemical restraints imposed for purposes of discipline or convenience” (Omnibus Budget Reconciliation Act, 1987). Additionally, the Health Care Financing Administration (HCFA) regulates nursing homes that use Medicaid and Medicare programs and has created a set of guidelines and regulations to further OBRA in an attempt to reduce inappropriate prescribing.
Atypical antipsychotics have been used more than neuroleptics recently because it was thought that the EPS in neuroleptics is too problematic for the elderly. Well that concern is now being replaced with concern over the atypicals as the severity of their side effect profile becomes more known and problematic (Gurevich, Guller, Berner, & Tal, 2012). In addition in 2005 the FDA issued a black-box warning against the use of atypicals for BPSD in the elderly (FDA, 2005). The warning stated that “Of a total of seventeen placebo controlled trials performed with olanzapine (Zyprexa) aripiprazole (Abilify), risperidone (Risperdal), or quetiapine (Seroquel) in elderly demented patients with behavioral disorders, fifteen showed numerical increases in mortality in the drug-treated group compared to the placebo-treated patients” (p. 1). In some ways given the severe side effects of the atypical antipsychotics it is hard to believe they would not cause some level of damage. Despite the warning and the controversy that surrounds it, treatment of BPSD with atypicals continues though may be declining for another reason. The Centers for Medicare and Medicaid Services (CMS) have always targeted excessive use of antipsychotics in the absence of an appropriate diagnosis or necessity. Beginning in May 2012 an initiative called Partnership to Improve Dementia Care initiated training and research on humane methods to deal with BPSD. The use of atypical antipsychotics will continue to be part of the CMS quality review of facilities (Advokat et al., 2014).
We are still in need of better research with more representative sampling for medicating elderly clients. As early as 1997, Satlin and Wasserman lamented that the literature regarding pharmacological treatment of the elderly is fallible for a variety of reasons, including:
• Many studies utilize younger-old clients, 55–65 years of age to represent a population of people in trials receiving antidepressant therapy when a larger population of older people are actually the ones receiving them.
• Many subjects in studies are the picture of health when many older adults are actually suffering from physiological illnesses. The advantage of this in research is clear but it is not a true representation.
• Many studies are inclusive of clients with only mild/moderate symptoms.
Finally, discussing prescription rates for the elderly seems to merit concern about compliance with psychotropic medication prescribing, but there are two sides to the coin. Elderly clients may be unwitting targets for misleading, dangerous, and even fatal attempts to keep them in compliance with taking drugs pushed on them with tempting direct-to-consumer (DTC) advertising, still legal in the United States. Most DTC drug advertisements zone is on seniors to sell expensive, newer drugs that promise seniors they will treat, but not cure, their ailments. With physicians being coerced, the FDA being laissez-faire regarding ads backing up claims and “Big Pharma” valuing profit over lives, seniors are at a disadvantage and are at risk (Lurie, 2005).
This leads us to a short summary of the primary ethical issues in geriatric psychiatry that must be examined in case of elderly clients being treated with psychotropic medication. The first issue is autonomy versus family or group centrism. Does a medication provide more autonomy for the client? If so does that offset the risk of adverse effects. Even individuals who desire autonomy must sometimes accept that they will require help from family or other caregivers. This raises the ethical concern of who can be told what about medications. Rabins and Black (2010) note that “… in the absence of objections raised by the elder, there is implicit agreement that the involvement of family members is ethically appropriate … however since this contradicts regulations in the USA (HIPPA) and the principle of autonomy … judgment and caution should be exercised” (p. 268). Another issue is care-giving, which straddles the autonomy family centric dilemma. One of the biggest conflicts is when the provider has therapeutic relationships with the provider of care and the recipient of care. If those parties have conflicting goals, consideration should be given to drawing in another professional so that each party has their own clinician/advocate.
Another important concern for nonmedical and medical mental health professions is elder abuse. The elderly are a vulnerable group at increased risk for abuse. According to Lachs and Pillemer (2004), there are three main elements of abuse: harm, a trust relationship, and intent. Clinicians are charged with assessing whether abuse may have occurred and this requires the clinician to make judgments that require ethical considerations. Rabins and Black (2010) give an example of questioning intent when a caregiver becomes frustrated and makes a verbal statement that harms the ill person. They ask, if the perpetrator of harm is suffering from exhaustion and poor judgment? This, they say can be as incapaciting temporarily as dementia can be long-term. Note that careful and repeated consideration of challenging situations and regular discussion is the best approach. This leads to the ethical imperative for the care-giver: self-care. We know that caregivers of people with dementia take psychotropic drugs (benzodiazepines and antidepressants) more frequently than caregivers of patients without dementia (Camargos et al., 2012). This is attributed to the particular stress of caring for someone suffering from dementia. Can clinicians help caregivers find resources that allow for them to renew their energies after long periods caring for a loved one? This is also an ethical imperative for medical and nonmedical mental health professionals.
Another important ethical imperative in working with the elderly is surrogate decision making. Cognitive impairment disrupts decision-making capacity and the ability to consent to medical procedures and other relevant choices. For medical procedures, decisions should be made by a caregiver or substitute whom the patient has previously chosen and identified in advance (preferably through the appropriate legal documents). There are two legal standards for surrogate decision making. The first is “. substituted judgment used if the patient's wishes are known to the surrogate or ‘best interest', used if the patient's wishes are not known” (Rabins & Black, 2010, p. 270). The use of advance directives can be one way of maximizing a client's autonomy. These document a person's values and wishes from general to specific ways. There can be many reasons people do not execute such directives: lack of education, cultural norms, or just the healthy denial of existential givens like illness and dying that all of us have. The final ethical imperative Rabins and Black (2010) cover is end-of-life issues. The older we get the more we should intentionally make our end-of-life wishes known but, as Jacoby (2011) points out, when 80 is the new 50 why rush things? There is also a large body of research that illustrates that people who have advance directives change their minds after developing a life-threatening illness. If that person has appointed a durable power of attorney that person can act in “best interest.”
Review Questions
• What do prescription rates look like in general? For elderly people?
• What are some commonly prescribed psychotropic drugs for older adults?
• Why should we take literature regarding pharmacological treatment of the elderly with a grain of salt, as clinicians?
• What are the primary ethical issues to consider when working with elderly clients?
SECTION FOUR: AGING AND ASSISTED LIVING
Learning Objectives
• Describe several challenges to elderly clients living in managed care/assisted living settings.
• How has legislation attempted to change inappropriate prescribing?
Deinstitutionalization in the late 1960s was prompted by the federal government, ending Medicaid payment for state psychiatric hospitals and institutions for the treatment of mental health. Their point was twofold: to end poor conditions in these facilities and throw the cost back onto states for such care. Theoretically, better functioning and independence to help former patients adapt to community living should have been a focus of treating people with mental disorders, though many psychiatric patients were instead dumped into various other settings like nursing homes and geriatric units. Inappropriate prescribing of psychotropic drugs in managed care settings is a recent concern along with issues of abuse, social stigma, and the unique needs of the elderly with regards to side effects of psychotropic medications (discussed in the next section of this chapter). Assisted living carries risks like abuse, stigma, inadequate care, and improperly trained staff. In many instances even when staff are trained the staff to patient ratio is rarely optimal. For the most part we know that direct care staff (trained or not) are far more comfortable than assisted living administrators in dealing with resident's mental health needs. Whereas administrators are more often concerned about liability (such as getting sued for not chemically restraining a resident who may fall or otherwise injure himself) the direct care staff are more focused on the resident (Dakin, Quijana, & McAlister, 2011). If there are not enough direct care staff, prescribed psychotropic drugs that have differential or adverse side effects for older adults in managed care facilities may not even be noticed, let alone monitored properly. Between 35 and 53% of assisted living clients were receiving one or more psychotropic medications, but only 45% of nursing home nurses had proper psychiatric training (Lindsey, 2009).
Review Questions
• What are the obstacles for older adults needing treatment in assisted living settings?
• What are the significant legislative attempts made to combat issues of abuse and inappropriate prescribing of psychotropic medications in nursing homes? What else can be done?
SECTION FIVE: SIDE EFFECTS PECULIAR TO THE ELDERLY
Learning Objectives
• Describe various side effects peculiar to the elderly as a population.
• Understand the implications of adverse side effects for the elderly.
Older adults are especially prone to adverse side effects and can be more frail and sensitive to side effects that may be more tolerated by their younger counterparts. Age-related physiological changes can cause differences in pharmacokinetics and pharmacodynamics, as well as cause adverse side effects and exacerbate both existing psychiatric disorders and concurrent medical problems. People older than 70 are 3.5 times more likely to be admitted to hospitals due to adverse side effects than their younger counterparts, and the risk for these reactions rises drastically with the number of medications they are taking as well as with their age (Lindsey, 2009).
PSYCHOTROPIC SIDE/ADVERSE EFFECTS IN ELDERLY CLIENTS
As you can tell from this chapter, there is still debate about which medications cause the most problematic side effects for elderly clients. Given that most Americans, and especially the elderly, are on more than one medication, it becomes difficult to discern which medications or combinations of medications are responsible for which adverse events. It is interesting that in reviewing side effects in the elderly in studies conducted in the United States, the benzodiazepines come in for far more criticism than other classes of psychotropic medications. Studies conducted outside the United States more often implicate multiple classes of psychotropic medications as well as nonpsychotropic medications. For example, one research team in Brazil (de Paula, Bochner, & Montilla, 2012) found that antibiotics were as or more likely to cause falls. Another study in Australia concluded antidepressants, anxiolytics, hypnotics, and antipsychotics (or a combination) are all associated with falls and fractures in females but not males (Vitry, Hoile, Gilbert, Esterman, & Luszcz, 2010). This may relate to the extreme and confused nature of U.S. policies on any drugs that may be potentially abused. It is also of interest that social use of alcohol is far more accepted in European societies and in the United States. Even though alcohol use among the elderly can be a problem, many elderly people have moderately enjoyed a cocktail at the end of the day and all of a sudden something like moving into assisted living is supposed to end this (ask yourself how many bars you've seen in assisted living facilities).
There are also multiple dermatologic adverse effects that the elderly may be more susceptible to. Adverse Cutaneous Drug Reactions (ACDRs) are the most frequent adverse events in patients receiving psychotropic medications (Mitkov, Trowbridge, Lockshin, & Caplan, 2014). Whereas some of these are benign and easily treated, others (like Stevens—Johnson syndrome) can be life-threatening. For the benign reactions, clinicians will want to weigh the risks of discontinuation versus taking the patient off the medication if they are suffering from suicidality or suffering from severe symptoms (Bliss & Warnock, 2013). Common ACDRs include pruritus (an unpleasant sensation in the skin that provokes itching), which can be caused by anti-depressants, mood stabilizers, and antipsychotics. Exanthematous reactions are an idiosyncratic, T-cell mediated, delayed hypersensitivity reactions that can cause extreme, red macules (flat discolored area) and papules (a solid, discolored elevation of the skin). Urticaria (hives) and angioedema (swelling similar to hives but under the skin) are the second most common ACDRs. Fixed drug eruptions (lesions that appear within hours of taking the medication and can be mild to severe) and photosensitivity vary in severity and can be caused by antidepressants, mood stabilizers, and antipsychotics. Alopecia (hair loss) is associated with various antidepressants, mood stabilizers, and antipsychotics. These are just some of the more common dermatologic reactions and the interested reader should go to Bliss and Warnock (2013) for a complete list.