An Interview with Jan Roth
Written by Jan Soukup
Somatoform dissociation has always been on the margin of my interest. A short time ago I asked myself, why? I knew that the classical hysterical symptoms described by Breuer and Freud were somatoform. I heard that somatoform dissociation was the typical symptom in traumatized WWI soldiers. And when I asked Czech psychiatrists and psychologists what they thought of when they hear the word “dissociation”, all of them talked about conversion/somatoform symptoms. So why did I never find it as interesting as the psychoform symptoms? Was it because it is so well “known” and not so “innovative”? Or because there has never been clear evidence of how somatoform dissociation is connected to trauma? Or because the field of conversion symptoms is viewed as belonging to neurologists rather than explorers of psychology? Or – because patients with somatoform symptoms are believed to be difficult to treat and not to profit much from psychotherapy? It was difficult for me to say. But my view changed after I read articles by Paul F. Dell, and Ellert Nijenhuis, and attended a presentation by Professor Jan Roth, a leading Czech neurologist, who spoke about psychogenic movement disorders. I asked Prof. Roth for an interview, and he agreed. I was curious to understand the issue of somatoform disorders from neurologist’s point of view.
An interview with Prof. Jan Roth, MD, PhD
What does your work look like?
I’ve worked for 25 years as a neurologist specializing in so-called movement disorders, i.e. diseases and disorders of basal ganglia and its connections. These manifest themselves as movement disorders – lack of ability to move, slowing down (which is usually connected to Parkinson's disease), or abnormal movement disorders, as is trembling, chorea, dystonia, myoclonus and tics. The basal ganglia disorders have also a strong neuropsychological aspect, as they are connected to the limbic system and mesocortical system. And practically each patient with basal ganglia disorder exhibits some psychopathology – sometimes very discrete and subclinical, at other times dominating the whole clinical picture. But at this time I am the head of Movement Disorders Center and my main focus is Huntington disease, a disorder that has nothing to do with dissociation
Where did you first come into contact with so-called psychogenic or functional disorders?
This is an interesting question. I believe I first met such disorders before I even knew it, in the military. There the young guys, especially from ethnic minority groups, who were under stress and pressure, disconnected from their families and living in a group environment, would fall into trance or a fugue during which they did not perceive what was happening around them, and did not move. It looked like a catatonic stupor – and maybe it is a catatonic stupor to some extent. But I see it as a severe stress reaction to the army environment, which is completely strange to their personalities. They were taken to the psychiatrist and soon recovered
Later on, when I started to work as a neurologist I saw that many of the patients presented with unexplainable problems, causes of which could not be found, even after repeated examinations and investigations. I was curious about what was the matter with these people,. So I asked around and I found that every single doctor had similar experiences. This was not solely in neurology, but in the fields of internal diseases, gastroenterology, pneumology, otorhinolaryngology, rheumatology, etc. It represented at least 10% of all patients that come to our outpatient centers. Perhaps we should not call it psychogenic, because by this we already impose our interpretation of the problem – but let's say a functional disorder of movement. Someone might say dissociative, but again by that we might imply a base or a cause to something that does not even have to be dissociation.
Could you tell us more about the process of diagnosing psychogenic movement disorders (PMD)?
One of the problems is that psychiatrists believe that, according to their classification, PMD or a dissociative movement disorder is something where you have to rule out all possible organic causes to the condition. But this is not true. PMD is a positive diagnosis, it has its diagnostic criteria that have to be determined, and it is not necessary to rule out everything before we can say it could be a PMD. It has many specific symptoms that must manifest themselves and that are very neurological: the symptom cannot be interpreted from the point of view of physiology or pathophysiology, it is inconsistent in time, there is usually a sudden outset, sometimes a considerable placebo-effect, the symptom-appropriate medical treatment is usually ineffective, etc..
I believe the diagnosis of PMD should always be made by a neurologist, and he should consult others when he is not sure. It should never be made by a psychiatrist, because the psychiatrist is less aware of physiological movement patterns, what means inconsistent in time, and all the other manifestations that make the criteria of a PMD, since these criteria are based on movements patterns and characters and on observation of it. Misdiagnosis is very likely to end up in a circle of repeated examinations to rule-out any thinkable causes and the risk of making the problem chronic and terrifying is heightened.
Could you describe a typical case of a patient with PMD?
Typically the patient is a younger adult, more often a woman, presenting with neurological symptoms such as psychogenic non-epileptic seizure. The manifestation could be very similar to real epileptic seizure, but there are some discrepancies for the experienced neurologist. Psychogenic non—epileptic seizures are very common. It has been said that up to one quarter of epileptic seizures are non-epileptic. Very often epileptic and non-epileptic seizures combine together, and about 20% of admissions to neurological wards for “seizures” are due to psychogenic episode. Other typical neurological symptoms are disordered walk, trembling, twitching or twisting of certain parts of the body. So a typical case could be a young woman, about 30 years old, who comes to us unable to walk, she has twitches of the whole body, her knees buckle, she is heavily handicapped by that, she may be on disability pension for some other reason or on industrial disability for this problem, which can start, as the woman says: “exactly on May 25, 2005 I woke up, went out of the house and suddenly I stopped walking”. This abrupt beginning is quite typical. You find no signs of organic impairment of the brain, there is no hemiparesis, nothing you could explain. She may have a specific facial expression, so called “facies martyrea“ (i.e. an expression of a martyr), or, on the other hand “la belle indifference”, which is a completely indifferent or disinterested facial expression (it could even be a quiet smile). And it often seems that the person does not ask for help (but this not the rule), they just sit there, unable to walk, have this disinterested expression, as if they had no emotions around the fact they cannot walk.
Apart from the typical abrupt outset, it can happen that there is a complete remission for some period of time, and then it starts over again (but it is not always the case). Usually the symptom does not get worse progressively, even though the person may say so. But when you see it in two or three years, the symptom is of the same intensity, but the manifestation may have changed dramatically. Twisting movements change into paresis, or a heavy disorder of walking accompanied by strong involuntary movements changes into a wheelchair-bound presentation where the involuntary movements are not present at all. Commonly you find in these patients profound inconsistencies. For example, a woman when she tries to walk collapses helplessly, but when she sits on a chair, she can hold her legs up or displays she has strength in her legs. Another example, is when you ask a patient who has involuntary movements of an arm to move her the other arm in a given manner, either it is not possible, because she is unable to concentrate on one regular and one irregular movement, or the involuntary movement of the arm disappears. Alternatively if you ask her to tap your hand and change the speed, the speed of trembling of the ill arm also changes. So this is what we call inconsistencies.
What you can see very often in these patients is distraction. When you observe the symptom, it is very noticeable, and when you point out the symptom, it usually gets stronger. And then, when you do not observe the patient or she has the feeling she is not being observed, the problem is much smaller or even disappears. We can look out of the window to see how the patient walks away from our department, or we follow him outside, and the symptoms look very different. And sometimes – and I think I have luck in this – I meet my patients with heavy movement disorders outside in a tram and they just do not have the symptom at all. And then it is really difficult to tell – is it malingering or is it PMD?
How do you understand the etiology of the PMD? You said you cannot find any serious trauma..
Contemporary imaging methods, like fMRI or PET show that the disordered psychogenically-induced movement originates in the very same brain areas as normal movement, which means the modulation of the movement is wrong, not the neural circuit - it is also identical. “Hardware” is ok; the problem lies in the neural feedback and modulation (“software”). A patient with twisted leg may feel it is in the right position, when he does not see it, and feel it is twisted when you put it in the right position.
Thank you Dr Roth for giving us your neurological point of view of somatoform symptoms.
After my interview with Dr Roth, I was left wondering several things, including:
- How do we as students of trauma and dissociation understand the etiology of PMD?
- What are the ways to cooperate with neurologists who may be less familiar with psychologically processes and what can we offer from our knowledge on trauma and dissociation?
- How do we engage in psychotherapy with this group of patients and what are the expected outcomes?