Shyness

 

Shyness

Dr Jonathan Haverkampf, M.D.

 

The world as one sees it

Shyness itself is not a medical condition. It is a subjective perception, which is triggered by a complex set of emotions. One actually has to see oneself as being shy. If an individual does not perceive oneself as shy, then there is no shyness. This may sound counterintuitive, but even if one is very introverted and prefers to spend all day reading a book, one does not have to experience shyness. It depends on where one sees oneself in a social context. Only if one’s expectations are different from present reality, one may experience negative emotions, which may lead to a sense of shyness.

 

Shyness is not social anxiety

Social anxiety, unlike shyness, is a psychiatric diagnosis and it is present if certain criteria are met.

 

Manifestations of shyness

Shyness means feeling apprehension and discomfort around other people. Quite frequently, there is concern about what other people think about oneself. Minor details of one’s outward appearance, voice or behavior are focused on repeatedly. This constant analyzing of other people’s opinions and thoughts about oneself is often associated with low self-esteem, depressed thoughts, anxiety and setting high standards for oneself. One becomes very self-conscious in the presence of other people rather than being really self-aware. One’s own unrealistic expectations about the outcome of a situation may make it even more difficult. It is quite often the fact that shy people often expect too much rather than two little in social settings. Romantic Hollywood movies with love on first sight or rousing boardroom speeches that completely turn the destiny of a company are not what usually happens in the real world. Most social interactions are much more mundane, which does not make them less important. To see this can be quite liberating to a shy person.

 

Unfamiliar situations

Shyness is most likely to occur during unfamiliar situations, although not always. Unfortunately, situations remain unfamiliar if shy people avoid them. Shyness may fade with time, but avoiding unfamiliar situations. Usually shy individuals want contact to other people and relationships, which makes them struggle against shyness. However, this often makes the problem worse. By focusing on shyness as a problem within oneself self-esteem and self-confidence can further be lowered.

 

Social Skills

Developing social skills may help, but it may not take care of the underlying problems. Especially if there is low self-esteem, there is a risk the newly learned social skills merely cover up a problem further down below. This can have a negative effect on one’s self-esteem and self-confidence in the long-run because deeper down the individual does not believe the image he/she is projecting into the world.

Learning communication skills can be helpful in giving shy individuals more confidence. Behavioral traits in social situations such as smiling, easily producing suitable conversational topics, assuming a relaxed posture and making good eye contact, may not be second nature for a shy person. It may also be worthwhile to explore other communication channels. The internet, for example, has helped shy people become more active in a dating environment. Exchanging a number of messages and photos first, makes the other person less unknown, which helps the shy person be less intimidated and self-conscious.

Communication training can improve the situation as the individual learns to more easily interact with others and receive valuable feedback in return. Focusing on an exploration of one’s values, interests and aspirations can facilitate communication by raising one’s confidence in talking about certain issues. If one sees meaning and value in a topic, it is far easier to converse about it.

 

Predisposition for Shyness

There is some evidence for a genetic predisposition for shyness. Some research has indicated that shyness and aggression are related—through long and short forms of the gene DRD4, but this is merely a working hypothesis. Further, it has been suggested that shyness is related to obsessive-compulsive disorder. However, because of the numbers of factors involved and the difficulties in linking a basic cell mechanism to a group of thoughts and behaviors, this remains speculative.

A long form of the serotonin transporter promoter region polymorphism (5-HTTLPR) seems to be somewhat correlated with shyness in grade school children. [1] Interestingly, a connection between this form of the gene and both obsessive-compulsive disorder and autism has been shown in previous studies. [2] The dopamine D4 receptor gene (DRD4) exon III polymorphism, had been the subject of studies in shyness and aggression and “novelty seeking” traits.

 

Medication

Substances from the class of antidepressants known as selective serotonin reuptake inhibitors (SSRIs) can be used to treat shyness in individuals who feel inhibited in their daily life because of low self-esteem and psychological symptoms, such as depression or loneliness. They can often be a valued support in combination with psychotherapy. As the individual can better communicate with his or her environment they may no longer be needed after a while. They are generally viewed as non-addictive and can be discontinued relative easily, but to solidify and maintain any positive changes they should be taken for at least a year, and especially in cases of social anxiety longer, if they are well tolerated.

 

Psychotherapy

Psychotherapy can help uncover some of the conflicts and emotions underlying the anxiety and fears in the presence of unknown others. Often there are issues from one’s personal history that add difficulties and fears. If they are dealt with, the shyness can become much less or even disappear. Imagining situations and developing a good communication skill set can go a long way. Ultimately, the explorations of one’s values, interests and aspirations can relieve stress, psychological pressure and help one avoid situations that are more harmful than beneficial, such as unwanted relationship constellations or work situations that lack meaning. (Re)establishing a sense of the inner compass can work miracles in cases of shyness.

According to research, early intervention methods that expose shy children to social interactions involving teamwork, especially team sports, decrease their anxiety in social interactions and increase their self-confidence later on. One possible reason is that a greater set of skills in communicating information, such as emotions and needs, to other people, allows for more variation and better adaptation to different communication situations and environments.

 

Being Oneself

Shyness can seem to be a part of one’s personality. The difference between this and anxiety is fluid. The important question is whether we are really dealing with shyness or heightened sensitivity and insight, which can also be central to creativity. The key is to find out what the person values and finds important and how the individual can lead a more fulfilling and happier life, which frequently resolves the subjective problems with shyness in the process.

 

References

 

[1] Arbelle, Shoshana; Benjamin, Jonathan; Golin, Moshe; Kremer, Ilana; Belmaker, Robert H.; Ebstein, Richard P. (April 2003). “Relation of shyness in grade school children to the genotype for the long form of the serotonin transporter promoter region polymorphism”. American Journal of Psychiatry. 160 (4): 671–676. doi:10.1176/appi.ajp.160.4.671.PMID 12668354.

[2] Brune, CW; Kim, SJ; Salt, J; Leventhal, BL; Lord, C; Cook Jr, EH (2006). “5-HTTLPR Genotype-Specific Phenotype in Children and Adolescents with Autism”. The American Journal of Psychiatry. 163 (12): 2148–56. doi:10.1176/appi.ajp.163.12.2148. PMID 17151167.

 

 

Dr Jonathan Haverkampf, M.D. trained in medicine, psychiatry and psychotherapy and works in private practice for psychotherapy, counselling and psychiatric medication in Dublin, Ireland. The author can be reached by email at jonathanhaverkampf@gmail.com or on the websites www.jonathanhaverkampf.com and www.jonathanhaverkampf.ie.

This article is solely a basis for academic discussion and no medical advice can be given in this article, nor should anything herein be construed as advice. Always consult a professional if you believe you might suffer from a physical or mental health condition. Trademarks belong to their respective owners. No checks have been made.

 

Sleep Disorders and Medication

 

 Sleep Disorders and Medication (2)

 

Sleep Disorders and Medication

Dr Jonathan Haverkampf, M.D.

 

Sleep problems affect many people. Especially in our complex and fast paced world remaining thoughts or emotions from the day can occupy us at night. Dealing with stress effectively, such as prioritizing the activities in one’s life in line with one’s values and interests, can improve sleep considerably. The mental health diagnostic manual DSM-IV defines insomnia as difficulty initiating sleep or maintaining sleep.

Several mental health conditions can also cause sleeplessness. Major depression, PTSD, trauma, anxiety, bipolar disorders, psychosis and many more can cause insomnia. Many organic diseases can also cause insomnia, as can sleep apnea and chronic pain syndromes. In some cases, where no other reason can be found, an idiopathic insomnia may itself be a mental health problem.

The first step is to identify whether there is a sleep problem that requires treatment. People who sleep seven to eight hours usually do not have a problem with lack of sleep. In the case of paradoxical insomnia, although one believes to have a sleep problem, electrophysiological measurements show no sign of a sleep disturbance.

The second step is to identify if there is inadequate sleep hygiene. If there are behaviors that are not conducive to good sleep, they should be addressed first. Some behaviors increase arousal, such as consuming caffeine or nicotine in the evening or at night. Various drugs, legal and illegal, can affect one’s sleep greatly. Intense thoughts or emotions can also disturb one’s sleep, as do day-time naps or significant irregularities in the daily sleep-wake schedule.

Treatment of insomnia should also always include psychotherapy. It can help reduce the worries about and consequences of sleeplessness, and thereby break the vicious cycle of insomnia. Feeling less anxious about the ability to get a goodnight’s sleep often improves one’s sleep. Cognitive therapy, CBT, but also psychodynamic approaches can be helpful.

There are several over-the-counter sleep aids available, often with questionable effectiveness. Nonprescription drugs, such as sedating antihistamines, protein precursors, and a host of other substances can work in individual cases, but they are often not strong enough even in cases of moderate insomnia. L-Tryptophan has been withdrawn from the market after it was linked to outbreaks of eosinophilia. Melatonin may help some individuals, although the placebo should not be underestimated.

Most hypnotics are approved by the U.S. Food and Drug Administration (FDA) only for short-term use. The z-drugs zolpidem (Stilnoct®, Ambien®, Ambien CR®, Intermezzo®, Stilnox® and eszopiclone (Lunesta®), as well as the melatonin-receptor agonist ramelteon (Rozerem®) are exceptions.  The z-drugs are by their function related to the benzodiazepines and are also considered potentially addictive if taken regularly. This means that if they are stopped one’s sleep might be worse for a while. There could also be an additional increase in anxiety and, at least theoretically, panic attacks. Benzodiazepines and z-drugs should not be used while driving a car or operating heavy machinery, and the longer lasting ones can lead to a hangover in the morning and drowsiness during the day.

If the insomnia has lasted for a while and is expected to reoccur for at least a couple of weeks, sleep inducing antidepressants should be considered first choice. Mirtazapine (Remeron®) is often a good option, which in clinical experience is more sleep inducing at lower doses (15mg) than at higher doses (45mg). Second-generation antipsychotics, such as Olanzapine (Zyprexa®) are also used, but it seems there should be some other symptom or reason that justifies their use because of the potentially more serious die-effects. If the insomnia is combined with some types of obsessive thoughts or even Tourette’s syndrome, for example, sleep inducing second-generation antipsychotics may be a logical choice.

Psychotherapeutic treatment of insomnia is discussed in my other articles, but medication as a supportive measure seems warranted in some cases, especially if a modern antidepressant can help the patient maintain a job or a relationship, while using therapy to explore the reasons of the sleep disturbance.

Listed below are some substances that are used to treat insomnia.

We will start with the group of benzodiazepines and then move on to the pharmacologically closely related z-drugs, which should usually be preferred to the former, if they are used at all.

 

Benzodiazepines

The most commonly used class of hypnotics for insomnia are the benzodiazepines. Benzodiazepines are not significantly better for insomnia than antidepressants. [1] While they have an important role in anxiety and panic attacks, especially in the time interval until an antidepressant works, their role in the treatment of insomnia should only occur in niche cases, and only over a short internal. The z-drugs, which also work on the benzodiazepine receptor should be preferred, if at all necessary. In clinical practice, the risk for dependency seems higher if the benzodiazepines are used as sleeping pills than if they are used in acute anxiety attacks.

Benzodiazepines all bind unselectively to the GABA-A receptor. There is some indication that certain benzodiazepines (hypnotic benzodiazepines) have significantly higher activity at the α1 subunit of the GABA-A receptor compared to other benzodiazepines (for example, triazolam and temazepam have significantly higher activity at the α1 subunit compared to alprazolam and diazepam, making them superior sedative-hypnotics – alprazolam and diazepam, in turn, have higher activity at the α2 subunit compared to triazolam and temazepam, making them superior anxiolytic agents). Modulation of the α1 subunit is associated with sedation, motor impairment, respiratory depression, amnesia, ataxia, and reinforcing behavior (drug-seeking behavior). Modulation of the α2 subunit is associated with anxiolytic activity and disinhibition. For this reason, certain benzodiazepines may be better suited to treat insomnia than others.

  • Triazolam (Halcion®)
  • Temazepam (Restoril®)
  • [Alprazolam (Xanax®)]

and others may be useful as an insomnia medication that stays in the system longer. For instance, they have been effectively used to treat sleep problems such as sleepwalking and night terrors. However, these drugs may cause sleepiness during the day and can also cause tolerance.

Chronic use

With chronic use, the sleep inducing effect of the benzodiazepines often goes away, while the risk of tolerance increases quite quickly if they are used as hypnotics. Chronic users of hypnotic medications have more regular nighttime awakenings than patients suffering from insomnia who are not taking hypnotic medications. [2] Hypnotics should be prescribed for only a few days at the lowest effective dose and avoided altogether wherever possible, especially in the elderly. [3] Between 1993 and 2010, the prescribing of benzodiazepines to individuals with sleep disorders has decreased from 24% to 11% in the US, coinciding with the first release of nonbenzodiazepines. [4]

Common Side Effects

The benzodiazepine and nonbenzodiazepine hypnotic medications have a number of side-effects such as day time fatigue, changes in reaction time potentially leading to motor vehicle crashes and other accidents, cognitive impairments and falls and fractures. Elderly people are more sensitive to these side-effects. [5]

Some benzodiazepines have demonstrated effectiveness in sleep maintenance in the short term but in the longer-term benzodiazepines can lead to tolerance, physical dependence, benzodiazepine withdrawal syndrome upon discontinuation, and long-term worsening of sleep, especially after consistent usage over long periods of time. Benzodiazepines, while inducing unconsciousness, actually worsen sleep as—like alcohol—they promote light sleep while decreasing time spent in deep sleep. [6] A further problem is, with regular use of short-acting sleep aids for insomnia, daytime rebound anxiety can emerge. [7]

Although there is little evidence for benefit of benzodiazepines in insomnia compared to other treatments and evidence of major harm, prescriptions have continued to increase. [8] This is likely due to their addictive nature, both due to misuse and because—through their rapid action, tolerance and withdrawal—they can “trick” insomniacs into thinking they are helping with sleep. There is a general awareness that long-term use of benzodiazepines for insomnia in most people is inappropriate and that a gradual withdrawal is usually beneficial due to the adverse effects associated with the long-term use of benzodiazepines and is recommended whenever possible. [9]

 

Z-Drugs

  • Zolpidem (Ambien®, Intermezzo®)

They often work quite well, but some patients wake up in the middle of the night. Zolpidem is now available in an extended release version, Ambien CR®. This helps prolong the effect of the medication. The FDA has approved a prescription oral spray called Zolpimist®, which contains zolpidem, for the short-term treatment of insomnia brought on by difficulty falling asleep.

  • Eszopiclone (Lunesta®)

Studies show people sleep an average of seven to eight hours. Because of the risk of impairment, the next day, the FDA recommends the starting dose of Lunesta® be no more than 1 mg.

  • Zaleplon (Sonata®)

Zaleplon stays active in the body for the shortest amount of time. That means patients can try to fall asleep on their own. Then, if they are still not asleep at 2 a.m., they can take it without feeling drowsy in the morning. However, if one tends to wake during the night, this might not be the best choice.

 

Melatonin-receptor agonist

  • Ramelteon (Rozerem®)

This is a sleep medication that works differently than the others. It works by targeting the sleep-wake cycle, not by depressing the central nervous system. It is prescribed for people who have difficulty falling asleep. Rozerem® can be prescribed for long-term use, and the drug has so far shown no evidence of abuse or dependence.

 

Antidepressants

  • Mirtazapine (Remeron®)
  • Doxepine (Silenor®)

This tricyclic antidepressant is approved for use in people who have trouble staying asleep. Silenor® may help with sleep maintenance by blocking histamine receptors. Dosage is based on health, age, and response to therapy. Caution is required with all the tricyclic antidepressants as they can prolong the QT interval and have a number of other potentially severe side-effects.

  • Trazodone (Desyrel®)

 

Antipsychotics

Certain antipsychotic drugs like Olanzapin (Zyprexa®) also have a sedative effect and they are sometimes used in slow doses as sleep medication. However, because of the rare but potentially severe side-effects of neuroleptics, even in the second generation, they should not be used as sleep medication without any other rational for using them.

 

Over-the-Counter Sleep Aids

Most of these sleeping pills are antihistamines. They generally work well but can cause some drowsiness the next day. They are generally considered safe enough to be sold without a prescription. However, if combined with other drugs that also contain antihistamines, like cold or allergy medications, one could inadvertently take too much.

 

Sleep medication can have a number of side-effects. In 2007, the FDA issued warnings for prescription sleep drugs, alerting patients that they can cause rare allergic reactions and complex sleep-related behaviors, including “sleep driving.” Medication should in the case of a sleeping disorder always be the last option. Better sleep hygiene and psychotherapy/counselling should come long before it and be the first choice. No sleeping pill can take away worries about the job or one’s relationship or correct for drinking coffee in the evening or sleeping next to one’s laptop.

 

References

[1]   Buscemi, N.; Vandermeer, B.; Friesen, C.; Bialy, L.; Tubman, M.; Ospina, M.; Klassen, T. P.; Witmans, M. (2007). “The Efficacy and Safety of Drug Treatments for Chronic Insomnia in Adults: A Meta-analysis of RCTs”. Journal of General Internal Medicine. 22 (9): 1335–1350. doi:10.1007/s11606-007-0251-z. PMC 2219774Freely accessible. PMID 17619935.

[2]   Ohayon, M. M.; Caulet, M. (1995). “Insomnia and psychotropic drug consumption”. Progress in neuro-psychopharmacology & biological psychiatry. 19 (3): 421–431. doi:10.1016/0278-5846(94)00023-B. PMID 7624493.

[3]   “What’s wrong with prescribing hypnotics?”. Drug and therapeutics bulletin. 42 (12): 89–93. 2004. doi:10.1136/dtb.2004.421289. PMID 15587763.

[4]   Kaufmann, Christopher N.; Spira, Adam P.; Alexander, G. Caleb; Rutkow, Lainie; Mojtabai, Ramin (2015). “Trends in prescribing of sedative-hypnotic medications in the USA: 1993–2010”. Pharmacoepidemiology and Drug Safety. 25: 637–45. doi:10.1002/pds.3951. ISSN 1099-1557. PMID 26711081.

[5]   Glass, J.; Lanctôt, K. L.; Herrmann, N.; Sproule, B. A.; Busto, U. E. (2005). “Sedative hypnotics in older people with insomnia: Meta-analysis of risks and benefits”. BMJ. 331 (7526): 1169. doi:10.1136/bmj.38623.768588.47. PMC 1285093Freely accessible. PMID 16284208.

[6]   Tsoi, W. F. (1991). “Insomnia: Drug treatment”. Annals of the Academy of Medicine, Singapore. 20 (2): 269–272. PMID 1679317.

[7]   Montplaisir, J. (2000). “Treatment of primary insomnia”. Canadian Medical Association Journal. 163 (4): 389–391. PMC 80369Freely accessible. PMID 10976252.

[8]   Carlstedt, Roland A. (13 December 2009). Handbook of Integrative Clinical Psychology, Psychiatry, and Behavioral Medicine: Perspectives, Practices, and Research. Springer. pp. 128–130. ISBN 0-8261-1094-0.

[9]   Authier, N.; Boucher, A.; Lamaison, D.; Llorca, P. M.; Descotes, J.; Eschalier, A. (2009). “Second Meeting of the French CEIP (Centres d’Évaluation et d’Information sur la Pharmacodépendance). Part II: Benzodiazepine Withdrawal”. Thérapie. 64 (6): 365–370. doi:10.2515/therapie/2009051. PMID 20025839.

 

Dr Jonathan Haverkampf, M.D. MLA (Harvard) LL.M. trained in medicine, psychiatry and psychotherapy and works in private practice for psychotherapy, counselling and psychiatric medication in Dublin, Ireland. The author can be reached by email at jonathanhaverkampf@gmail.com or on the websites www.jonathanhaverkampf.com and www.jonathanhaverkampf.ie.

This article is solely a basis for academic discussion and no medical advice can be given in this article, nor should anything herein be construed as advice. Always consult a professional if you believe you might suffer from a physical or mental health condition. Trademarks belong to their respective owners. No checks have been made.

© 2012-2017 Christian Jonathan Haverkampf. All Rights Reserved.

 

 

 

 

 

Depression and Medication

Depression and Medication (2) 

 

Depression comes in a multitude of flavors. Traditionally a distinction has been made between the reactive or neurotic depression on one end, which has been seen as largely environmentally induced, and the endogenic depression, which was largely seen as driven by biology. We now know that all three factors of biology, psychology and environment interact together in leading to the symptoms of depression.

 

The Circularity of Depression

Due to the plasticity of the brain, which regulates its morphological and chemical balance all the time, environmental influences can affect the circuitry and the functioning of the brain. Since the biology of the brain determines our thoughts and actions, it influences our environment, which again has a feedback on the brain. Thus, all effect depends on communication inside the brain and between the brain and the environment, and vice versa. This plays an immense role in the etiology and the symptoms of depression. It also explains why a combination of medication and psychotherapy in the majority of cases has the best outcome. Medication should be thought of in many cases of depression, except for the lighter reactive versions, while psychotherapy is always indicated if an individual suffers from depression. A condition that relies largely on communication deficits to be maintained, can also be cured through the ‘talking cure’, psychotherapy.

 

The Combination of Psychotherapy and Medication

Depression should in any case be treated with a combination of psychotherapy and medication if it is serious enough. Psychotherapy in most cases takes a few months to work, and medication, while also requiring a few weeks to work, will in many cases get results quicker than psychotherapy alone. In less severe cases, especially when it is a reaction to obvious external factors, psychotherapy alone may do. Medication can especially provide relief before the effect of psychotherapy, which is more geared towards the long-run, takes hold. While medication cannot make life more meaningful per se, it can improve an individual’s mood, which usually leads to more positive thoughts, a more positive outlook on the world, a decrease in ruminations, less anxiety and improved sleep – and appetite if that is desired.

 

Suicidal Ideation

Suicidality needs to be kept in mind in any form of depression and the mainstream opinion has shifted towards addressing these thoughts rather than avoiding talking about them out of fear that it might trigger them. Since the stability of the therapeutic relationship and communication itself are important tools in relieving depression, one should not be too anxious about naming issues that seem relevant.

A concern was that since the activating effect in several antidepressants can occur before the antidepressant affect, the risk for suicide might increase because a patient who still feels depressed becomes more active. However, the clinical experience is that the opportunity to talk about feelings and thoughts openly in a secure relationship reduces the urge towards self-harm.

 

Interests and Values

As I have outlined in another article on depression, facilitating the idea of a future the patient has some control over is often an important step in treating depression. This often means identifying values, interests and aspirations, which can provide greater motivation and a good feeling about the future, should be allowed enough space. There can be sadness about lost opportunities, but this usually subsides in the face of having a clearer direction in life and a greater promise of happiness, if one pursues the things one truly values and aspires to.

 

Medication

Unfortunately, the perfect medication does not exist. But this is also not to be expected since each antidepressant has a unique profile of effects, positive and negative, which can still be influenced largely by the unique biology of the patient. The following antidepressants are the most common ones. Using a single antidepressant (monotherapy) is usually to be preferred over polypharmacy. However, especially in more severe and treatment-resistant cases of depression, combinations may have to be explored, such as combining venlafaxine and mirtazapine (“California rocket fuel”) to yield an especially potent antidepressant and activating combination, which can even improve sleep (at lower to medium doses of mirtazapine).

Selective serotonin reuptake inhibitors (SSRIs)

The selective serotonin reuptake inhibitors (SSRIs) are the most common used antidepressants because of their relative safety and low side-effect profile. Unfortunately, in the beginning the indiscriminate use of the SSRI Prozac® against ‘everything’ from workplace problems to the stress of unhealthy living lead to a backlash in the media, which unfortunately made many patients avoid all medication out of fear to become emotionally flat or experience a change in one’s personality, which has not been shown so far in any convincing way.

There are several other substances, that work as antidepressants, and all have potential side-effects. Often a substance is used which has a ‘desirable’ side-effect and that deals more effectively with the individual constellation of symptoms:

  • Insomnia: Mirtazapine (Remeron® and many generics) is effective in inducing sleep at lower doses (around 15mg), an effect that seems to wear off once one goes up to 45mg. However, the antidepressant effect of 15mg is usually too small. Especially early on ‘hangovers’ in the morning are not uncommon. Among very common side effects are dry mouth, constipation, increased appetite, as well as somnolence, sedation, sleepiness (which may wear off).
  • Lack of activation: Venlafaxine (Effexor®, Effexor XR®, Lanvexin®, Viepax®, Trevilor®) is a noradrenaline and serotonin reuptake inhibitor (NSRI) and often affectively increases activation. However, one should be careful with patients who might harm themselves (or others) because activation often occurs before the antidepressant effect takes hold. Also, if used in cases of anxiety it may increase the anxiety before reducing it.
  • Co-morbidity with anxiety, panic attacks, OCD: the SSRIs are a good first choice. Venlafaxine seems to be helpful with anxiety, but often it increases anxiety early on, and possibly even medium-term.

Tricyclic antidepressants

Tricyclic antidepressants should not be used to treat symptoms that can be treated with the SSRIs or an NSRI, because of the letter’s better safety profile. It is difficult to imagine there still is an application for MAO inhibitors, except in the rare depression that does not respond to treatment. In the latter cases, my experience is that often medication has not been administered long enough or prescribed in the right dose. Quite frequently there has been no or only inadequate psychotherapy. It is worth remembering that psychotherapy is still and will always be the core treatment for what were a century ago referred to the ‘neurotic’ conditions, such as reactive depression, anxiety, OCD and the like. The reason is that the symptomatology can be traced to problems in interactions, communication and human relationships. Generally, there is better empirical evidence for the usefulness of antidepressants in the treatment of depression that is chronic (dysthymia) or severe.

In any case, it can take weeks for the full effect of medication to be noticed. A 2008 review of randomized controlled trials concluded that symptomatic improvement with SSRIs was greatest by the end of the first week of use, but that some improvement continued for at least 6 weeks.

 

Major depressive disorder

The UK National Institute for Health and Care Excellence (NICE) 2009 guidelines indicate that antidepressants should not be routinely used for the initial treatment of mild depression, because the risk-benefit ratio is poor. The guidelines recommend that antidepressant treatment should be considered for:

  • People with a history of moderate or severe depression,
  • Those with mild depression that has been present for a long period,
  • As a second-line treatment for mild depression that persists after other interventions,
  • As a first-line treatment for moderate or severe depression.

The guidelines further note that antidepressant treatment should be used in combination with psychosocial interventions in most cases, should be continued for at least 6 months to reduce the risk of relapse, and that SSRIs are typically better tolerated than other antidepressants.

 

Non-Responders

Between 30% and 50% of individuals treated with a given antidepressant do not show a response. In clinical studies, approximately one-third of patients achieve a full remission, one-third experience a response and one-third are non-responders. Partial remission is characterized by the presence of poorly defined residual symptoms. These symptoms typically include depressed mood, psychic anxiety, sleep disturbance, fatigue and diminished interest or pleasure. It is currently unclear which factors predict partial remission. However, residual symptoms are powerful predictors of relapse, with relapse rates 3–6 times higher in patients with residual symptoms than in those who experience full remission.

 

“Trial and error” switching

The American Psychiatric Association 2000 Practice Guideline advises that where no response is achieved following six to eight weeks of treatment with an antidepressant, to switch to an antidepressant in the same class, then to a different class of antidepressant. A 2006 meta-analysis review found wide variation in the findings of prior studies; for patients who had failed to respond to an SSRI antidepressant, between 12% and 86% showed a response to a new drug. However, the more antidepressants an individual had already tried, the less likely they were to benefit from a new antidepressant trial. A later meta-analysis found no difference between switching to a new drug and staying on the old medication; although 34% of treatment resistant patients responded when switched to the new drug, 40% responded without being switched.

 

Combination

A combination strategy involves adding another antidepressant, usually from a different class of antidepressants to have effect on other mechanisms. Although this may be used in clinical practice, there is little evidence for the relative efficacy or adverse effects of this strategy.

 

Augmentation

For a partial response, the American Psychiatric Association guidelines suggest augmentation, or adding a drug from an altogether different class of substances. These include lithium and thyroid augmentation, dopamine agonists, sex steroids, NRIs, glucocorticoid-specific agents, or the newer anticonvulsants.

 

Which medication to use?

The medication used needs to be tailored specifically to the individual and the set of effects that are desired and those which need to be voided. However, there seem to be clear favorites overall, which the following list of antidepressant prescriptions in the US in 2010 shows:

Drug name Commercial name Drug class Total prescriptions
Sertraline Zoloft® SSRI 33,409,838
Citalopram Celexa® SSRI 27,993,635
Fluoxetine Prozac® SSRI 24,473,994
Escitalopram Lexapro® SSRI 23,000,456
Trazodone Desyrel® SARI 18,786,495
Venlafaxine (all formulations) Effexor (IR, ER, XR) ® SNRI 16,110,606
Bupropion (all formulations) Wellbutrin (IR, ER, SR, XL) ® NDRI 15,792,653
Duloxetine Cymbalta® SNRI 14,591,949
Paroxetine Paxil® SSRI 12,979,366
Amitriptyline Elavil® TCA 12,611,254
Venlafaxine XR Effexor XR® SNRI 7,603,949
Bupropion XL Wellbutrin XL® NDRI 7,317,814
Mirtazapine Remeron® TeCA 6,308,288
Venlafaxine ER Effexor XR® SNRI 5,526,132
Bupropion SR Wellbutrin SR® NDRI 4,588,996
Desvenlafaxine Pristiq® SNRI 3,412,354
Nortriptyline Sensoval® TCA 3,210,476
Bupropion ER Wellbutrin XL® NDRI 3,132,327
Venlafaxine Effexor SNRI 2,980,525
Bupropion Wellbutrin IR NDRI 753,516

 

The Need for Psychotherapy

In any case, medication should always be combined with psychotherapy. In the less severe forms of depression and those that seem to have an explanation and are “reactive”, medication often shows to be less effective and psychotherapy eventually leads in many cases to a full remission of the symptoms.

 

Dr Jonathan Haverkampf, M.D. MLA (Harvard) LL.M. trained in medicine, psychiatry and psychotherapy (psychoanalytic and CBT)  and works in private practice for psychotherapy, counselling and psychiatric medication in Dublin, Ireland. The author can be reached by email at jonathanhaverkampf@gmail.com or on the websites www.jonathanhaverkampf.com and www.jonathanhaverkampf.ie.

This article is solely a basis for academic discussion and no medical advice can be given in this article, nor should anything herein be construed as advice. Always consult a professional if you believe you might suffer from a physical or mental health condition. Trademarks belong to their respective owners. No checks have been made.

© 2012-2017 Christian Jonathan Haverkampf. All Rights Reserved.

Schizophrenia and Medication

Schizophrenia in virtually all cases requires lifelong treatment, even when symptoms have subsided. Treatment includes better coping skills in everyday life, strategies to reduce stress and become aware of early warning signs of a psychotic episode, psychotherapy to better manage life, and medication. Medication may be life-long, but does not have to be.

Medication for an independent, autonomous life

Treatment with medication (antipsychotics) and psychosocial therapy can help manage the condition. In some cases, hospitalization may be needed. However, medication has drastically reduced the need for hospitalization. Many patients who had to be hospitalized for most of their lives in earlier times can now care for their families or work as highly paid managers in large corporations.

Medication allows people with schizophrenia to lead normal lives. Especially the newer generation of antipsychotics has increased the quality of life significantly, while reducing some of the side-effects of the earlier generation of antipsychotic medication. Still, antipsychotic medication has overall still not reached the low side-effect profiles of newer antidepressants. While tardive dyskinesia has become rarer with the second-generation antipsychotics (SGAs) and is virtually absent in clozapine especially and the potentially lethal malignant neuroleptic syndrome is a very rare phenomenon, they are often associated with side-effects from weight gain (especially olanzapine) to drowsiness (quetiapine). It seems that we are only willing to accept the greater potential side-effects of modern antipsychotics because of the enormous improvement they can bring in a patient’s quality of life.

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