In 1977, George Libman Engel (December 10, 1913 – November 26, 1999), an American internist and psychiatrist who spent most of his career at the University of Rochester Medical Center in Rochester, NY and gave a seminal contribution to medicine via the formulation of the biopsychosocial model,1 criticized the dominant medical culture of those days. He said that biomedical dogma requires that all disease, including “mental” disease, be conceptualized in terms of derangement of underlying physical mechanisms. He added that this allows only two alternatives in medical doctors’ behavior and approach: the reductionist, which says that all phenomena of disease must be conceptualized in terms of physicochemical principles; and the exclusionist, which says that whatever is not capable of being so explained must be excluded from the category of diseases. The reductionists concede that some disturbances belong to the spectrum of disease, categorizing these as mental diseases. The exclusionists regard mental illness as a myth.
Let’s translate into practice the consequences of the above-mentioned reductionist and exclusionist approaches based on the following clinical history:
John is a 35-year-old man treated for a diagnosis of panic disorder with paroxetine (Paxil) for five years. Two months ago, John decided to decrease and discontinue paroxetine because he had been in good health for three years. A few days after discontinuation of paroxetine, John presented flu-like symptoms, fatigue, dizziness, confusion, and mild rapid mood swings. He first thought he had the flu because of the winter season and because many colleagues at work had it, but when after two weeks he still presented with these symptoms he decided to go to the general practitioner.
Here the exclusionist enters the scene. The GP reassured John that this was flu and when John pointed out that everything began just a few days after paroxetine discontinuation, the GP said that these symptoms were not capable of being so explained, thus they must be excluded from the category of mental disease and simply considered a flu. The GP suggested John take non-steroidal anti-inflammatory drugs for a few days. Since after two further weeks John still had flu-like symptoms, fatigue, dizziness, confusion, moderate rapid mood swings, and also nightmares and tachycardia, he decided to ask for a consultation with the psychiatrist who had prescribed him paroxetine the first time.
Here the reductionist enters the scene. The psychiatrist conceded that antidepressant discontinuation syndrome has been documented in the medical literature and that the symptoms described by John might belong to this spectrum of disease. However, stating that discontinuation syndromes are rare and symptoms are short-lasting, the psychiatrist excluded the possibility that it was discontinuation and explained John’s symptoms as the initial phase of a relapse of panic disorder. Thus, the psychiatrist suggested that John go back on paroxetine to eliminate the symptoms. John went back on paroxetine and in two days the symptoms were gone. He informed the psychiatrist of this rapid improvement and the psychiatrist suggested that he not discontinue paroxetine again.
In 1977, George Libman Engel proposed an alternative to the reductionists and the exclusionists. He suggested that medical doctors, and psychiatrists among them, need a biopsychosocial model. Its scope is determined by the historic function of the physician to establish whether the person soliciting help is “sick” or “well” — and if sick, why sick and in which ways sick — and then to develop a rational program to treat the illness and restore and maintain health.
Let’s translate this concept into practice once again using John’s history, which I invented although it resembles the clinical history of many patients I visit daily.
Let’s imagine that John is not convinced by the psychiatrist’s opinion, and instead of going back on paroxetine, he decides to consult another psychiatrist that he found mentioned on a web page about paroxetine and problems related to its discontinuation (for instance, this one). This second psychiatrist listens to John’s history and agrees with John that he is “sick,” and that there is a link between the discontinuation of paroxetine and the symptoms that occurred. This psychiatrist asks John if he agrees to be assessed via an interview which was developed to assess withdrawal after discontinuation of antidepressants and lets the psychiatrist know more about these symptoms (Cosci et al. 20182). John agrees to be interviewed. Thereafter, the psychiatrist, taking into account his clinical evaluation and the results of the interview, gives his feedback to John. The psychiatrist tells John that the symptoms that occurred are withdrawal symptoms, that they are due to the discontinuation of paroxetine and they are well-known in the literature (for example, Fava et al., 20153; Cosci & Chouinard, in press4). In addition, the psychiatrist tells John that “withdrawal” is a general term which, in reality, includes three different well-known and well-described syndromes. These three syndromes are: new withdrawal symptoms, rebound, and persistent post-withdrawal disorder (Chouinard & Chouinard, 20155).
- New withdrawal symptoms consist of symptoms which were not present before the beginning of the antidepressant treatment and were not present before reduction or discontinuation. They can be both unspecific or specific serotonin-related symptoms. Among the unspecific serotonin-related symptoms, nausea, headaches, tremor, sleep disturbances, decreased concentration, anxiety, irritability, and depression are common. Among the specific serotonin-related symptoms, flu-like symptoms, electric shock sensations, and confusion are common. These symptoms are usually short-lasting — that is, they last no more than six weeks — and spontaneously reversible, thus the best to do for patients is to wait until the symptoms fade away.
- Rebound consists of the return of symptoms which were present before the beginning of the antidepressant treatment but were not present before reduction or discontinuation. The symptoms are more intense than the ones that occurred before the beginning of the treatment. For example, if a person undertook antidepressant therapy to treat anxiety, after the reduction or discontinuation of the antidepressant therapy anxiety is back and is more intense than before the treatment. In addition, rebound symptoms occur rapidly after the reduction or discontinuation of the antidepressant treatment, are transient since they can come and go, and are reversible — which means that if the patient goes back to the antidepressant treatment or if the patient waits until they fade away they will really disappear. Rebound is commonly associated with a psychological belief to be in need of the drug which can erroneously drive the patient to go back to the antidepressant. These symptoms are short-lasting, that is they last no more than six weeks, and spontaneously reversible, thus the best to do for patients is to wait until the symptoms fade away.
- Persistent post-withdrawal disorder consists of the return of the original symptoms which were present before the beginning of the antidepressant treatment but were not present before reduction or discontinuation. These symptoms present both with greater intensity and together with new symptoms that the patient has never suffered before. For example, if the antidepressant therapy was taken to treat depression, depression rapidly recurs after the reduction or discontinuation of the antidepressant treatment, it is more intense than before the antidepressant treatment and is associated with other non-depressive symptoms, such as for instance panic. These symptoms persist longer than six weeks and they might be partially or totally reversible. Being so long-lasting, the patient usually benefits from adequate pharmacological or psychotherapeutic support.
Thereafter, the psychiatrist informs John that he currently presents new withdrawal symptoms and encourages him not to go back on paroxetine but to manage these symptoms, making a few sessions with a psychologist who will provide more information on withdrawal and on how to manage it in daily life. The psychiatrist schedules a follow-up visit in one month. At the follow-up visit, John has only mild fatigue and informs the psychiatrist that he has concluded the sessions with the psychologist and feels well.
Just a brief conclusion, since I already told a long story. The exclusionist and the reductionist were not able to help John since they based their evaluation on a biomedical model which needs physicochemical or biological probationary evidence to allow the doctor to recognize an illness and formulate a specific diagnosis. Thus, the exclusionist missed the diagnosis by denying withdrawal syndrome (and, as a consequence, gave the wrong treatment) and the reductionist made the wrong diagnosis by confusing withdrawal with relapse of the original disease, thus, once again, suggesting the wrong treatment. In both cases, they based their interventions on the biomedical model and prescribed medications.
The second psychiatrist was able to help John since he based his evaluation on a biopsychosocial model. The second psychiatrist listened to John’s history, observed John to identify possible signs of illness, assessed him via a specific interview and, taking into account his clinical evaluation and the results of the interview, told John that he was sick because of withdrawal from paroxetine, and suggested to him what to do to improve — that is, to not go back on paroxetine, since it was clear that paroxetine had triggered the current withdrawal syndrome, and to run a psychological intervention aimed at educating John on what was going on and how to manage the daily symptoms.
Withdrawal syndromes which occur after dose reduction or discontinuation of antidepressants are iatrogenic psychiatric disorders, that is, psychiatric disorders triggered by a pharmacological treatment. Since the majority of psychiatric disorders cannot be recognized and diagnosed on the basis of physicochemical or biological probationary evidence, despite numerous attempts by neuroscientists to provide us with evidence, similarly withdrawal syndromes, for their nature of being psychiatric disorders, cannot be recognized, diagnosed, and treated on the basis of the biomedical model. However, antidepressant withdrawal is no longer an unknown disorder since knowledge on this topic has grown enough to be translated into practice. As proposed by George Engel, medical doctors, including psychiatrists, can observe and listen to their patients and develop a program to treat withdrawal and restore health. According to what I have seen in my clinical practice, what Engel proposed in 1977 is still in 2019 the approach that works and produces health!
- Engel, George. The need for a new medical model: a challenge for biomedicine. Science. 1977;196(4286):129–136. ↩
- Cosci F, Chouinard G, Chouinard VA, Fava GA. Riv Psichiatr. 2018;53(2):95-99. doi: 10.1708/2891.29158. ↩
- Fava GA, Gatti A, Belaise C, Guidi J, Offidani E. Psychother Psychosom. 2015;84(2):72-81. ↩
- Cosci F, Chouinard G. The monoamine hypothesis of depression revisited: could it mechanistically novel antidepressant strategies? In Neurobiology of Depression, edited by de Quevedo JL, Carvalho AF, Zarate CA. Elsevier, in press. ↩
- Chouinard G, Chouinard VA. Psychother Psychosom. 2015;84(2):63-71. ↩
Mad in America hosts blogs by a diverse group of writers. These posts are designed to serve as a public forum for a discussion—broadly speaking—of psychiatry and its treatments. The opinions expressed are the writers’ own.