Hijos en el Hijo 185

The coping strategies reviewed in this tool kit reflect those that are used in ours and others’ cognitive behavioral therapy (CBT) approaches for managing adult Attention-Deficit/Hyperactivity Disorder (ADHD). We all have our different takes on things and those areas of special emphasis, but there is a great deal of overlap in and agreement about the coping skills that are beneficial for adults with ADHD.

Numerous studies of the different CBT programs designed for adults with ADHD have indicated that it is an effective treatment option. Results indicate improvements in symptoms of ADHD, as well as coexisting mood and anxiety. CBT generally does not tar-get the symptoms of ADHD per se, that is, inattention, hyperactivity, and impulsivity—

but rather how these symptoms affect daily functioning. It is the medications used to treat ADHD that are used to treat specific symptoms. In fact, most (but not all) participants in the clinical outcome studies of CBT for adult ADHD were on a stable dose of medications but continued to have some coping difficulties.

While we have provided a good overview of the coping strategies involved in CBT for adult ADHD, we have not yet discussed medication treatment. This section will review the basics of pharmacotherapy, including the role of medications and the different types of medications commonly prescribed. Various other questions and concerns about their use (and misuse) will be discussed.

It should be noted that there are a variety of other treatment options for adult ADHD that you might encounter. Medications and CBT for adult ADHD have a firm scientific foundation for their use. Other treatments vary in the amount and strength of the sup-porting evidence. A review of the different options is beyond the scope of this tool kit, but we suggest that interested readers refer to Ramsay’s (2010) book length review of nonmedication treatments for adult ADHD for more information.

Why Should I Consider Medications for ADHD?

Medications are the most widely studied treatment modality for ADHD. They have been shown to help children with “hyperkinetic syndrome” (the diagnostic term for ADHD that was used in the early 20th century) since 1937, although most treatment studies date back about 50 years when methylphenidate (Ritalin^®) was first investigated. In the intervening time period, there have been thousands of articles published on the effects of different medications for the treatment of ADHD. The majority of these studies involved children and adolescents, although a large number of clinical trials of medications for

164 The Role of Medications

adults with ADHD have been published over the past 25 years. So the first reason to consider medications is that they work.

Another reason to consider medication treatment is based on what we know about the ADHD brain. In a nutshell, it doesn’t work as efficiently as a non-ADHD brain does.

There are lots of studies using different methods (neuropsychological testing, neurode-velopmental assessments, observations of behavior, neuroimaging, etc.), and most of them point to significant differences in how people with ADHD process information and control their behavior. In the early part of the 20th century, it was assumed that there was some sort of brain defect or brain damage (captured in the diagnostic terms

“minimal brain damage” and “minimal brain dysfunction”) present—but this hasn’t turned out to be the case. Scientists at the time thought the disorder came from “lesions”

or “malformations” in parts of the brain controlling movement, but there was no evi-dence for this.

In the mid-1900s, the neurochemical theory of psychiatric disorders came into favor, and it was hypothesized that chemical imbalances led to the various conditions seen by mental health practitioners. In those days, it was noted that there were differences in the metabolism of dopamine and norepinephrine seen in children with ADHD and that medications that increased these neurotransmitters, like the stimulants, were shown to have a beneficial effect on ADHD symptoms. For the ensuing several decades, the pre-vailing wisdom was that these neurotransmitter deficiencies were the cause of ADHD and that medications worked by restoring a sufficient supply of these chemicals, not unlike treating scurvy, a vitamin C deficiency, by giving citrus fruits. The vitamin defi-ciency analogy, while appealing, is simply not accurate to describe the neurobiological basis of ADHD.

Over the past 25 years, a more sophisticated understanding of the mechanisms of ADHD has emerged. This model suggests that the neural circuits underlying our execu-tive functioning (including the ability to process information, to hold information in working memory, to inhibit motor behavior, and to plan complex actions over long periods of time) are not sufficiently or properly synchronized in people with ADHD.

This leads to inefficient problem solving and to excess energy consumption in order to accomplish routine daily tasks. In addition, the brain’s reward circuits also seem to be underpowered, leading ADHD people to feel bored easily, to crave rewards, and to seek stimulation or excitement more frequently than other people.

These newer models of the brain enable us to explain how medications can be helpful to people with ADHD. In essence, they enable neurotransmission to take place in a more energy-efficient fashion, so that brain functions like information processing, problem solving, working memory, focusing/concentrating, staying on task and sitting still are all improved with ADHD medications. Another way these medications work is that the underpowered reward circuits of the ADHD brain are better at their job—hence people stay on task longer and don’t get as bored as easily as they usually do.

A final reason to consider using medication for ADHD is when other nonmedical approaches have been tried, but ADHD symptoms continue to impair functioning and to cause suffering. Over the past several decades, studies have shown that combined treatment (that is, medication along with psychosocial intervention) usually produces the best results in terms of symptom remission and functional outcomes. This makes perfect sense since these approaches work differently (“bottom up” for medications and

“top down” for psychosocial treatments), and a synergy of effects can result by apply-ing a “bio-psycho-social” approach. This is not to suggest that it’s wrong to avoid usapply-ing medications—many people prefer to tackle their ADHD without relying on them. It’s simply to say that there is good evidence showing how the combination approach is often the best way to achieve the most optimal results.

What Are the Medications for ADHD? How Do They Work?

Medications for ADHD are divided into stimulants and nonstimulants. The stimulants, in turn, are divided into those derived from amphetamine (e.g., Adderall ^® , Adderall XR ^® , Vyvanse ^® , Dexedrine ^® ) and from methylphenidate (e.g., Ritalin ^® , Concerta ^® , Metadate ^® , Focalin ^® , Methylin ^® , Quillivant ^® , Daytrana ^® ). Amphetamine, first synthesized in Berlin in 1887, was first released in the United States in 1935 as a decongestant inhaler (Ben-zedrine ^® ) and was soon used to combat fatigue and mild depression. It was shown to be helpful for ADHD in the 1960s and has been on the market continuously since then.

Methylphenidate was first developed in 1944, but it was not identified as a stimulant until 10 years later. It was introduced as a treatment for ADHD in the 1960s and for the past five decades has remained the most commonly prescribed medication for ADHD in the United States (See Appendix F).

Methylphenidate has the simpler mechanism of action of the two stimulants. It works by reversibly inhibiting the reuptake of the neurotransmitters dopamine and nor-epinephrine into the presynaptic neuron where they are made and stored. Inhibiting their reuptake causes the neurotransmitters to stay in the synapse for a longer period of time; hence their transmitter action is prolonged and enhanced (see Figure 19.1 ).

Figure 19.1 . Illustration of How Stimulant Medications Work Presynaptic (Transmitting)

• Blocks reuptake of transmitter into vesicle

• Blocks reuptake of transmitter into presynaptic terminal

• Induces release of transmitter when it is absorbed into the presynaptic terminal

• Inhibits Monamine Oxidase (MAO) leading to more presynaptic transmitter Methylphenidate

• Blocks reuptake of transmitter into presynaptic terminal

Reuptake Site

166 The Role of Medications

Amphetamine has this same property, but in addition, it increases the release of dopa-mine and norepinephrine, and it slows down their breakdown inside the neuron, hence it is more complex in its effects than methylphenidate.

Both classes of stimulants have an immediate onset and a short duration of action (in the range of several hours). They are only effective when present in the central nervous system, which explains why they start working very quickly after they are ingested and why their effects wear off at the end of the day. While different stimulant preparations vary in the length of time they work, this is primarily due to the fact that they release the medication over variable periods of time. The duration of action of these compounds in the brain is primarily determined by how quickly the body can clear them out of the bloodstream (which is the function of the liver). Some people absorb and metabolize them quickly, while others do so more slowly. This explains why different doses are given to different patients, and why it’s important to try both types of stimulants at different dosage strengths in order to determine the optimal regimen.

The three main nonstimulants are atomoxetine (ATX), guanfacine, and clonidine.

ATX (i.e., Strattera^®) is a norepinephrine reuptake inhibitor (NRI) and the other two are known as alph2 adrenergic agonists. In the case of ATX, the turnover of norepinephrine in the synapse is slowed down by the reversible blockade of the reuptake mechanism (which is carried out by the norepinephrine transporter). By increasing the functioning of norepinephrine, the neural circuits of attention, inhibition, and executive functioning are enhanced. ATX takes several weeks to build up in the brain, and the duration of each pill is almost 24 hours.

Both clonidine (i.e., Kapvay^®) and guanfacine (i.e., Intuniv^®) have a complex mecha-nism of action. In effect, they improve the symptoms of ADHD by enhancing the neu-rotransmission of both dopamine and norepinephrine, especially in the frontal lobes.

They are “signal boosters” of the neural circuits involved in ADHD even though they don’t affect the release or uptake of the neurotransmitters. They are helpful in reducing hyperactivity, impulsivity, and overarousal and in improving attention. They are also effective in reducing aggression, anxiety, and tics.

What Can I Expect from These Medications? How Will I Know if They Are Working?

These medications are designed to reduce the symptoms of ADHD. The stimulants begin to work immediately, the alpha agonists may take a few days to show effects, and ATX can take up to 8 weeks to reach full effects. There are several ways to determine if they are helping or not. To begin with, it is important to observe whether or not it’s easier to get started on projects, to get things done, to stay focused on tasks, to complete projects, etc., and if so, to estimate how much easier it is to accomplish these things. Second, if you have a specific target behavior you are particularly hoping to see improve, you should be able to measure if things have changed since taking the medication. For instance, if you want to be able to read a book without interruption, it should be easy to time how long you can read without stopping before and after starting the drug. Third, your clinician is likely to ask you to fill out a symptom questionnaire at the time of each medication management visit. The scores on these scales should be decreasing if the medication

is working. Fourth, the opinions of significant others (partner, friend, work colleague) should be polled to see if they can detect a positive change in ADHD symptoms. Lastly, in some cases, an objective test of attention and/or impulse control is used to quantify the functional impact of the medication. While this is not necessary to monitor treat-ment effects, some office visits now include taking a computerized test.