Journal of Psychosocial Nursing and Mental Health Services

Psychopharmacology 

Are You Ready for Change?

Barbara J. Limandri, PhD, PMHNP, BC

Abstract

Under the direction of the Journal's new Psychopharmacology Section Editor, a different approach will be taken: psychotropic drugs will be classified based on their neurobiological mechanism of action in the brain. This approach focuses on how the drug acts on brain cells and neurotransmitters involved in the specific symptoms presented by patients. The current article introduces the approach and will help clinicians think about medications as they relate to the neurobiological functions they are trying to correct. [Journal of Psychosocial Nursing and Mental Health Services, 56(2), 11–13.]

Abstract

Under the direction of the Journal's new Psychopharmacology Section Editor, a different approach will be taken: psychotropic drugs will be classified based on their neurobiological mechanism of action in the brain. This approach focuses on how the drug acts on brain cells and neurotransmitters involved in the specific symptoms presented by patients. The current article introduces the approach and will help clinicians think about medications as they relate to the neurobiological functions they are trying to correct. [Journal of Psychosocial Nursing and Mental Health Services, 56(2), 11–13.]

Exploring psychotherapeutic issues and agents in clinical practice

Every new year we are faced with the challenge of change, resolving to make changes in our lives. This year the Journal of Psychosocial Nursing and Mental Health Services has passed the baton for this column from Laura Leahy, DrNP, APRN, FAANP, to me. In reviewing the columns during the previous column editors' terms, I am humbled by the breadth and depth of coverage in psychopharmacology and challenged to maintain that practical scholarship while introducing some change.

One change I will offer is one that Robert Howland, MD (2014), introduced as an alternative system of classifying psychotropic drugs by relevant mechanism of action and neurobiological activity. There are at least two benefits to this system: (a) stigma about specific drugs is decreased, and (b) a more efficient way of learning is presented. Let's look at a few examples.

Clinical Examples

Example 1

A client indicated he continued to have severe nightmares and admitted he was not taking the prescribed prazosin because he did not have high blood pressure. The clinician explained to him in a simple manner how prazosin blocked the alpha-adrenergic receptors thereby decreasing his reactivity to stimuli, especially at bedtime when he was hypervigilant. His previous prescriber told him that prazosin was helpful with nightmares, but the pharmacist told him it was for hypertension. Feeling too embarrassed to tell the pharmacist he had nightmares, the client simply avoided the medication.

Prazosin is approved by the U.S. Food and Drug Administration to treat benign prostatic hyperplasia and hypertension, but it is also frequently used off-label to treat nightmares associated with posttraumatic stress disorder (Stahl, 2013). Prazosin is effective with all those conditions because it blocks alpha-1 norepinephrine (adrenergic) receptors, especially in the limbic region of the brain (even more specifically in the amygdala) which, when activated, stimulates the stress response, including hypervigilance, fear, and anxiety during the sleep cycle. The initial prescriber was wise to use this medication with the client but did not adequately explain how and why it was useful. What seemed to be medication nonadherence was simply the client not fully understanding the medication and feeling embarrassed by the nightmares that he was not able to use the pharmacist's assistance. By taking more time in the beginning with a client to explain his/her symptoms and how the pharmacodynamics of the medication can bring relief will serve to build a collaborative and attentive relationship with the client.

From the clinician's perspective initially, it requires more patience and perseverance to learn the details of neurophysiology and functional neuroanatomy, but once learned it is easier to understand how drugs affect behavior simply by knowing what neurotransmitters are involved and in what manner (i.e., agonist or antagonist). Because many nursing programs do not offer detailed content in neurophysiology of mental disorders, psychiatric–mental health nurses may feel discouraged with this approach at first. One mission for this column, therefore, is to describe drugs in terms of their neurobiological activity, neurotransmitter effects, and pharmacokinetics with recognition of the need for neurophysiology review.

Example 2

After a thorough assessment, the clinical team determined a client has borderline personality disorder manifested by labile moods; chronic self-harm urges usually provoked by disappointments in relationships; depressed mood unresponsive to many trials of selective serotonin reuptake inhibitors and serotonin norepinephrine inhibitors; impulsive behaviors including rage, reckless behaviors, and sexual excesses; and difficulty settling into an occupation or role identity. In addition to beginning a dialectical behavior treatment (DBT) program, the client was referred for medication evaluation. She identified her most problematic symptoms as difficulty falling asleep, constant anger, fluctuating mood, and other individuals being upset with her impulsivity. She agreed that she acted without thinking and did not like suffering the consequences, especially when they involved disrupted relationships. One impulsive behavior that others wanted her to stop, but she did not see as a problem, was cutting on her body. She identified this behavior as relieving pain, even though she has required stitches at times and has many scars. All medications she has tried in the past made her feel numb, caused poor sexual response and desire, and did not seem to make a difference in her mood.

The client was shown a picture of the brain (3D Brain found in the iTunes® App Store), and the practitioner explained that the serotonin and dopamine circuits that ran from her limbic area (emotional brain) through the anterior cingulate and dorsolateral prefrontal cortex likely were not firing regularly, contributing to acting without thinking based on erratic emotions. The client believed this description fit with what she experienced, and asked what she could do. The practitioner indicated GABA was the neurotransmitter that regulated nerve firing and allowed the serotonin and dopamine nerves to fire more smoothly, for which two different medications could be recommended. One medication took a long time to titrate (lamotrigine) and worked well with few side effects. The other medication helped with mood and impulsivity (lurasidone) with the less likely side effect of movement problems and possibly drowsiness but no sexual side effects. The client liked the idea of something that made her drowsy if she could take at bedtime only, but she was still concerned that it was not going to help as much with the impulsivity. She decided to try the lurasidone for a few weeks and was willing to consider adding lamotrigine later if necessary.

Several weeks later, the client stated that she appreciated the practitioner taking her seriously, asking her what she wanted to change, and showing her pictures of her brain, affirming this was a problem with her brain and not that she was a bad person. Lamotrigine was added, and after approximately 6 months, lurasidone was tapered once the client's mood leveled. She then continued with lamotrigine only. The client was able to fully participate in the DBT program to learn coping and self-regulation skills even though she struggled considerably the first 3 months. The most important element was creating the collaborative environment for medications and psychotherapy to work adjunctively, with the client showing improvement over time.

It is important to note that there are no anti-borderline medications, and both medications were offered as off-label use. However, they addressed the neuropathology that the client's symptoms demonstrated. Lamotrigine is a gaba-ergic that enhances the inhibitory neurotransmitter, GABA. Lurasidone is a third-generation serotonin dopamine antagonist that briefly blocks D2 receptors at the striatum frontal cortex circuit and blocks the serotonin 5-HT2A somatodendritic receptors, thereby causing the release of dopamine in the dorsolateral pre-frontal cortex (Stahl, 2013).

New Direction

My hope is that this newly described approach to the column will be of interest to our readers and offer a fresh perspective. As we enter this new year, I invite readers to suggest potential topics for future columns at jpn@slackinc.com.

References

  • Howland, R.H. (2014). A proposed system for classifying psychotropic drugs. Journal of Psychosocial Nursing and Mental Health Services, 52(12), 13–15. doi:10.3928/02793695-20141118-05 [CrossRef]
  • Stahl, S. (2013). Stahl's essential psychopharmacology (4th ed.). New York, NY: Cambridge University Press.
Authors

Dr. Limandri is Professor Emerita, Linfield College, School of Nursing, McMinnville, Oregon.

The author has disclosed no potential conflicts of interest, financial or otherwise.

Address correspondence to Barbara J. Limandri, PhD, PMHNP, BC, Professor Emerita, 9136 SW 36th Avenue, Portland, OR 97219; e-mail: limandribj@gmail.com.

10.3928/02793695-20180122-03

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