Serotonin-norepinephrine reuptake inhibitors, also known as SNRIs, are a new class of drugs used to relieve depression and anxiety. Has your physician suggested any of the following medications? These are the most commonly prescribed SNRI medications for anxiety:
- Effexor (venlafaxine)
- Pristiq (desvenlafaxine)
- Cymbalta (duloxetine)
SNRI vs SSRI
Similar to selective serotonin reuptake inhibitor (SSRIs), SNRIs increase the levels of specific neurotransmitters. They are called SNRIs because they increase both serotonin and norepinephrine. The reason norepinephrine is thought to be important is because it is known to be involved in the stress response, which forms the basis of anxiety reactions. Toward the end of his interview with Anxiety.org, Dr. Bruce McEwen addresses how stress can impact an individual.
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How do SNRIs work?
SNRIs increase levels of both serotonin and norepinephrine. A variety of neural systems use norepinephrine as a neurotransmitter, and both the amygdala and the hippocampus are affected. Research has also shown that norepinephrine has influences on the thalamus and prefrontal areas of the cortex.3 In addition, it regulates systems in the body involved in heart rate, breathing, and blood flow to the muscles.
As with SSRIs, it is the longer-term effects of SNRIs that are helpful with anxiety. The immediate effect of SNRIs, like SSRIs, is sometimes to increase anxiety, so they, too, may need to be started gradually. Anxiety reduction occurs after a week or 10 days.
With both SSRIs and SNRIs, you should not assume that they are correcting some “chemical imbalance” that causes anxiety. When considering how a medication works, keep in mind that a drug that’s very good at reducing anxiety isn’t necessarily changing the underlying processes that create anxiety in the brain. Just because a medication relieves a problem doesn’t mean it corrects the cause of the problem.
Aspirin provides a helpful analogy.1 Imagine that you crack a tooth on hard candy and subsequently develop an abscess in the tooth. As a result, you experience a toothache and a low-grade fever. If you take aspirin and both the toothache and fever disappear, it would not be correct to assume that your difficulties were due to a shortage of aspirin in your system.
Like SSRIs, SNRIs are thought to work by promoting neuroplasticity in the brain. After a week or so, the higher levels of norepinephrine and serotonin may stimulate neurons to remodel themselves and their circuits in a variety of ways that promote increased flexibility. So it seems that SNRIs may make the circuitry in the brain more capable of being modified. This means you will have more success changing your brain to resist anxiety. Evidence suggests that SNRIs may work best when taken in combination with psychotherapy.2
Common SNRI Side Effects
Always be aware of the possible side effects that come with any medication. Common side effects associated with SNRIs are:
- Dry mouth
- Nausea
- Nervousness
- Insomnia
- Drowsiness
- Dizziness
- Headache
- Sexual response difficulties
- Loss of appetite
- Agitation
Because SNRIs also target norepinephrine receptors as well as serotonin receptors, SNRIs tend to have more side effects than SSRIs. Talk with your doctor about any possible side effects that you may be experiencing. Different medications affect you uniquely and you may need to try different ones before you find one with fewer side effects.
Other articles in this series include:
Part 1: Medication As Part Of Your Anxiety Treatment
Part 2: The Pros And Cons Of Anti-anxiety Medication
Part 3: SSRI Fact Sheet
Sources
1. Coplan, Jeremy D., and R. Bruce Lydiard. “Brain circuits in panic disorder.” Biological Psychiatry 44, no. 12 (1998): 1264-1276.
2. Saskia de Maat, Jack Dekker, Robert Schoevers, Gerda van Aalst, Cecile Gijsbers‐van Wijk, Marielle Hendriksen, Simone Kool, Jaap Peen, Rien Van, and Frans de Jonghe. “Short Psychodynamic Supportive Psychotherapy, antidepressants, and their combination in the treatment of major depression: a mega‐analysis based on three Randomized Clinical Trials.” Depression and anxiety 25, no. 7 (2008): 565-574.
3. Thomas Frodl, Johanna Scheuerecker, Veronika Schoepf, Jennifer Linn, Nikolaos Koutsouleris, Arun LW Bokde, Harald Hampel et al. “Different effects of mirtazapine and venlafaxine on brain activation: an open randomized controlled fMRI study.” Journal of Clinical Psychiatry 72, no. 4 (2011): 448.
Catherine Pittman, Ph.D, is the Chair of the Psychology Department at Saint Mary’s College in Notre Dame, Indiana, and is a practicing clinical psychologist. As a professor at Saint Mary’s College in Notre Dame, Indiana, Dr. Pittman teaches courses on Abnormal and Clinical Psychology, and also supervises students working on their senior theses. In addition, she has a private practice at Roseland Counseling in South Bend, Indiana. She enjoys working with individuals with anxiety disorders because more is understood about the causes of anxiety in the brain than about other disorders. She also provides therapy to those coping with depression, bipolar disorder, brain injury, and post-traumatic stress disorder.
Dr. Pittman began her studies of anxiety as she earned her Ph.D. in clinical psychology at Northern Illinois University in 1989, and has been treating individuals with anxiety disorders since that time. She also completed over 10 years of postdoctoral work with the Brain Injury Treatment Program at Memorial Hospital in South Bend, Indiana. Dr. Pittman recognized that, although the research on the neurological basis of anxiety has resulted in a great deal of knowledge about the causes of anxiety, this knowledge was not readily accessible to therapists or individuals coping with anxiety. She has endeavored to promote increased understanding of the causes of anxiety in the brain through her classes, presentations, articles, and books. Her most recent book, coauthored with Elizabeth Karle, is Rewiring the Anxious Brain,and can be purchased on Amazon.
