Skip to main navigation menu Skip to main content Skip to site footer

Psychosomatics in times of evidence-based medicine


Jürg Kollbrunner


For more than thirty years, Jim, a psychotherapist, has been working as a clinical psychologist at a university head and neck clinic in diagnostics and therapy with patients who suffer from communication disorders, psychosomatic dysfunctions or head and neck cancer. In a multidisciplinary team he has researched different functional disorders and published scientific papers and several books. His professional orientation is based on psychodynamics and systemic family therapy, and for decades he has advocated that all matters concerning health and sickness should be understood and treated psychosomatically, too. Besides, for example, megrim, irritable colon, neurodermatitis, dorsalgia and stuttering, affections that seem to be of a pure organic origin should be understood against the background of the sick person’s life story and therapy should be oriented towards that person’s individual goals in life. Jim advocates this approach even in approaching cancer and the therapy for it: in the 1960s psycho-oncological research in the USA revealed interesting results regarding psychosocial factors as a contributory cause in the genesis of cancer. But with the emergence of evidence-based medicine (EBM) in the 1980s, the very thought of such a causal factor in the origin of cancer was disdained, with the unfair argument that, with such an approach, cancer sufferers might be accused of having caused the cancer themselves. The taboo became so strict that today’s psycho-oncologists are forced to view their field of specialty as merely rehabilitative. Likewise, today almost only organ-based theories and therapies are propagated for many diseases with sufficiently demonstrated complex physiological causations. This is compounded by the fact that EBM, with its usually purely quantitative methods, is hardly ever able to identify qualitative factors such as the experience of life events. Together with like-minded colleagues, Jim has advocated for the psychosocial approach and treatment in many oral or written debates with dissenters and journal reviewers. He has never deviated from the position that it is useful to try to understand every grave disease against the background of the individual’s life story.

An unexpected event

Then, three years ago, Jim was bitten by a tick while hiking. Three days later he fell ill with tick-borne encephalitis (TBE). The first phase of this disease, with influenza-like symptoms, lasted only three days. But in the following symptom-free two weeks Jim was confronted with the death of his elderly mother, an event that was not unexpected, but the meaning of which was nonetheless difficult for him to grasp. He participated in preparing the funeral arrangements, but even before the funeral service took place the second phase of TBE began with amphicrania, reduced consciousness and amnesic aphasia. In the middle of the night he became disorientated in bed, no longer being able to distinguish between up and down. In an attempt to distract himself from his severe headache he stood up and tried to turn on the television, but only turned the remote aimlessly in his hands without realising that he needed to press a button. Ellen, his wife, notified the family doctor who recommended immediate hospitalisation.

Several hours after his emergency hospitalisation Jim developed left-sided apraxia with positive Babinski reflex, partial facial nerve palsy, proximal weakness of the arms and hoarseness. Magnetic resonance imaging showed subcortical foci of white-matter gliosis. His condition continued to worsen. He developed micturition disturbance, cardiac decompensation with bradycardia and central sleep apnoea-hypopnoea syndrome with Cheyne-Stokes respiration, which required biphasic positive airway pressure ventilation. For one night and one day his survival was uncertain. But two weeks later – following optimal symptomatic therapy in the intensive care unit and neurological clinic – Jim could be transferred to the rehabilitation clinic. After another four weeks of excellent care by the medical professionals and Ellen, Jim was discharged with only minor residual symptoms, ready for several weeks of out-patient rehabilitation. Eight months after the tick bite, with much gratitude, he stated that he had fully recovered.

Concession or confirmation?

How did this dramatic experience change Jim’s beliefs and attitudes toward psychosomatics? Did he learn that diseases that can be well-explained on a physiological level do not have anything to do with psychology? No. On the road to recovery, when he could think and speak clearly again, he began to wonder why none of his visiting relatives, friends or colleagues raised the question of his psychosocial situation which could have contributed to the disease’s progression. None of them seemed to consider this matter. It was so clear: tick bite – viral disease – danger of death – saved! They considered forces of nature, the fact that Jim had resisted them, and perhaps also the worrying questions “In what state will I find him?” and “How will I react?”

Jim experienced the situation differently. Apart from a deep sense of gratitude for the help he received, he was mindful of the fact that the tick-born encephalitis virus (TBEV) was indeed a cause of his severe disease, but not the only one. Epidemiological facts suggest that other influences affect whether a viral infection remains harmless or leads to such dramatic consequences as meningoencephalitis or even meningoencephalomyelitis. In fact, 85-90% of persons infected with the TBEV recover after several days of the disease’s initial harmless phase or don’t even realise that they have been infected. Only 10-15% develop TBE.

Between natural and empirical science

What is the reason for such different outcomes? The quantity of the virus that is absorbed is not decisive, as severe disease progression has also been documented following low-dose TBE infections [1]. Experts emphasise that “the basis of the disease severity is largely unknown” [2], and call this “a most intriguing question” [3]. Some assume genetic backgrounds to be the determining factor, for example a mutation of the gene CCR5 [3]; others see the reasons as more likely to be found in factors regarding the host’s immunity. In TBE patients with encephalitis, levels of interleukin-10 are lower than in those with the milder meningitis [4], and the fact that the production of immunosuppressive cytokines increases under psychological stress has been known for a long time [5]. Animal experiments revealed that mice with different susceptibilities responded with qualitative differences to a TBE infection. The more resistant mice had lower virus reproduction and cytokine production but produced more neutralising antibodies and also survived longer [2]. The observation that the production of natural killer cells increases in TBE patients at the time of hospitalisation but, unlike with other infections, drops to normal values after a short period of time points in the same direction [6]. Perhaps timely protection against an excessive immune response (which can be self-destructive) lets the disease progress in a less harmful manner. But whatever biochemical processes are involved in determining the disease’s progression to be more or less harmful, the question concerning the nature of the gatekeeper that operates the “switch” has so far not been answered. Broadening the approach to take the patient’s personal life story and living situation into consideration is the only way that promises new answers. Since the 1990s it has been uncontested that the human experience can have a causal influence on the onset and progression of a disease via psycho-neuro-immuno-endocrinological processes, particularly in the form of acutely experienced psychosocial stress.

Jim suspected from an early stage what unusual stressors he had experienced and led to him being extremely vulnerable in the months and weeks prior to his infection. He was relieved when, a few days after his hospitalisation while he was still unable to speak properly, he heard from Ellen that he had been released from his duties of lecturing at the university for the rest of the semester.

What happened?

One to two years before his retirement Jim began to reflect on how he would like to shape the third phase of his life. He loved his work as a psychotherapist and scientist. To him his work was the second most important thing in life after living together with Ellen and the children. He had no special unfulfilled wishes for the future. Would he want to accept new tasks in his occupational field? Would he develop new hobbies? Would he experience feelings of emptiness or boredom? Then he noticed a job advertisement: “Wanted: A university lecturer to lecture two hours a week on the topic of ‘Introduction to social psychology’.” This was an incredible opportunity, because more than thirty years ago, as an assistant, Jim lectured on the exact same topic at the same university for five years. He always remembered this experience fondly, particularly the interactive times when he succeeded in motivating the students for exciting group work and experiments. Without hesitation Jim applied for the new, old role and was accepted. His predecessor carefully prepared him for the challenge with helpful information about the newest developments in the field and the teaching material, the student body (up to two hundred students), the new localities and the multimedia technology. He was looking forward to the start of the adventure. However, the employment contract sent to him lay on his desk at home for several days before he signed and returned it.

Jim started his new adventure with much enthusiasm, which the students noticed and appreciated. But a kind of disillusionment already arose after the third double lesson. He realised that he had underestimated the scope of the teaching material that was new to him. The textbook Mann’s “Sozialpsychologie” [7] he had used thirty years ago had 240 pages and a weight of 250 grams; the new powerful textbook with the same title, by Aronson et al. [8], comprises 685 pages and weighs two kilograms. Jim had to realise that he had to learn and understand the new content himself first, before he could present it to the students. This required a lot of time. The struggle with multimedia teaching technology had to be overcome, but Jim experienced painful disillusionment with the motivation of the students. It seemed to him most students were less interested in the exciting content of social psychology than in storing the facts they needed to know for the examination. Once, after having initiated a highly current discussion – concerning the line between freedom of expression and vilification using the example of the low-budget film “Innocence of Muslims” – he walked along the auditorium with his headset microphone and two further microphones in his hands searching for discussion partners. Out of over a hundred students he found three who felt brave enough and wanted to speak a bit.

Then Jim realised that he lagged behind in his own teaching material. Not seldom when students asked additional questions he had to say, “This I don’t know. I will research it.” The strain increased and the employment contract for the next semester already lay on his desk at home. This time he waited even longer before signing it. For the first time in his professional life Jim felt alarmingly stressed. The duty to prepare for his next couple of lectures weighed on him like a ton of bricks. Then came a week-long hiking getaway during which he had his laptop with him. He never opened it … but he was bitten by a tick.

Jim was greatly relieved when, while he was in the rehabilitation clinic, his wife told him that the employment contract for the next semester had been cancelled.


Today, three years after having contracted TBE, Jim considers it as probable that he would not have developed the disease without the excessive professional stress he experienced in the weeks prior to his infection. In other words, he owes it to his illness that he was released – painfully but effectively – from his excessive demands on himself.

The excessive stress he experienced consisted of four elements. Firstly, he underestimated the vast progress in a specialist field over a period of thirty years; secondly, he underestimated the effect of his age on his learning ability; thirdly he underestimated the impact of the change in the students’ learning strategies; and, finally, he underestimated the implications of modern multimedia educational technology, which enables better audibility and visibility of the lecturer, but also translates into an increased distance from the students.


Jim has learned how important it is to respect signs of overstraining himself (for instance, the two-fold hesitation in signing the employment contract), to understand what these signals mean and to intercept such developments at an early stage, even if this results in painfully parting from a tempting task or, in case of an imposed task, in bitter consequences. In addition, perhaps Jim would have been able to avoid some of the confusion in his grieving process for his mother if he had improved or clarified their relationship early enough.

But Jim’s experience also points to a general insight. In the case of both more or less serious diseases therapists should ask their patients about recent changes in their psychosocial environment. For example with the following simple statement and question: “Sometimes the vulnerability to a disease or an accident is increased by unusual occupational or familial stress. Have you experienced unusual or extreme stress in the past few weeks?” With a bit of such attention maybe some repetitions of “somatisations” could be prevented. On the other hand:

“I believe that diseases are keys which can open certain gates for us. I believe there exist certain gates which only disease can open.” (André Gide)

Jim is the author of this article.


Disclosure statement

No financial support and no other potential conflict of interest relevant to this article was reported.


Jürg Kollbrunner, PhD, is a clinical psychologist and psychotherapist.



  1. Hayasaka D, Nagata N, Fujii Y, Hasegawa H, Sata T, Suzuki R, et al. Mortality following peripheral infection with tick-borne encephalitis virus results from a combination of central nervous system pathology, systemic inflammatory and stress responses. Virology. 2009;390(1):139–50. PubMed
  2. Palus M, Vojtíšková J, Salát J, Kopecký J, Grubhoffer L, Lipoldová M, et al. Mice with different susceptibility to tick-borne encephalitis virus infection show selective neutralizing antibody response and inflammatory reaction in the central nervous system. J Neuroinflammation. 2013;10(1):847. PubMed
  3. Kindberg E, Mickiené A, Ax C, Akerlind B, Vene S, Lindquist L, et al. A deletion in the chemokine receptor 5 (CCR5) gene is associated with tickborne encephalitis. J Infect Dis. 2008;197(2):266–9. PubMed
  4. Günther G, Haglund M, Lindquist L, Forsgren M, Andersson J, Andersson B, et al. Tick-borne encephalitis is associated with low levels of interleukin-10 in cerebrospinal fluid. Infect Ecol Epidemiol. 2011;1(1):6029. Published online February 11, 2011. PubMed
  5. Curtin NM, Mills KH, Connor TJ. Psychological stress increases expression of IL-10 and its homolog IL-19 via b-adrenoceptor activation: reversal by the anxiolytic chlordiazepoxide. Brain Behav Immun. 2009;23(3):371–9. PubMed</jrn>
  6. Blom K, Braun M, Pakalniene J, Lunemann S, Enqvist M, Dailidyte L, et al. NK cell responses to human tick-borne encephalitis virus infection. J Immunol. 2016;197(7):2762–71. PubMed
  7. Mann L. Sozialpsychologie. Weinheim: Beltz; 1969.
  8. Aronson E, Wilson TD, Akert RM. Sozialpsychologie. 6. actual. ed. München: Pearson; 2008.