Suppressed anxiety as a symptom in Parkinson’s disease: thoughts on causal connections and psychotherapy

Mark Hurni

Summary: It is true that the scientific literature sees psychological factors like anankastic personality, withdrawal or (masked) depression in Parkinson’s disease, but does not further analyse the connections. Such are established by means of concrete experiences with the disease and the (psycho-) therapy and associated with the findings of medical investigations. Finally the question remains unanswered what is the (overwhelming) cause of anxiety, that results in freezing of the motor system. A prenatal event is not excluded.

James Parkinson already expressed the conjecture that anxiety and shock played a role in the aetiology of the disease that he described (Parkinson 1817). To date this hypothesis has not found any scientific confirmation, but at least it is being increasingly recognised in clinical practice that psychological factors considerably influence the course of Parkinson’s disease (Marsden et al. 1981, Birkmayer and Riederer 1985, Cleeves et al. 1986, Ellgring et al. 1993, Ludin 1995). Here one may name the frequency of depressive and anxiety states in Parkinson’s patients (Ellgring et al. 1990, Stein et al. 1990, Liu et al. 1997, review in Cummings J.L. 1992 and  Richard et al. 1996), which cannot be explained by the physical disability alone (Gotham et al. 1986, Ellgring et al. 1993, Hubble and Venkatesh 1995, Cole et al. 1996, Strehl and Birbaumer 1996), or the stress-induced alteration in motor performance, which manifests itself in freezing and the paradoxical kinesia (Schwab and Zieper 1965, Marsden et al. 1981, Ludin 1995). Nevertheless medical research has not hitherto concerned itself further with the psychological connections. Although there are differing reports of improvement in symptoms due to psychotherapy in Parkinson’s disease (Routh et al. 1987, Ellgring et al. 1990, Peseschkian 1990, Leplow et al. 1994), so far there has clearly been only one controlled therapeutic study to confirm these positive changes in motor performance and social skills  (Mohr et al. 1996, Müller et al. 1997). Thus the patients of a behavioural therapy efficiency study showed better precise motor skills after a period of therapy of only three months, a reduction in resting tremor and an improvement in posture and gait and in their handling of critical situations (Mohr et al. 1996). While these improvements were not lasting (Mohr et al. 1997), they could hardly be expected to be, since a three-month therapy is doubtless too short to have a causal effect. Longer lasting studies are necessary for this, as are experiments with different forms of therapy.

However, it might be useful to keep the psychological aspect in mind, not only for therapy but also in research into aetiology. It has been shown that anxiety and helplessness as consequence of traumatic experience induce depletion of noradrenaline in the locus coeruleus (Peterson et al. 1993, Birbaumer and Schmidt 1996) and that the absence of noradrenaline causes neurochemical changes that promote the reduction of the dopamine content in the brain (Fornai et al. 1998) and can lead to increased cell degeneration (Cohen 1983). This insight and personal experience have led me to put forward the hypothesis that anxiety and helplessness in combination with a rigid defence mechanism produce oxidative stress and thus are to be regarded as at least additional causative factors of the disease.

Experience

I was  41 years old  in 1990 when the disease began, with a slowing of handwriting that was appreciable only subjectively, and developed gradually over the following years with increasing akinesia, a small degree of rigidity and no tremor. After a tentative diagnosis in 1992, there followed in 1993 the diagnosis of Parkinson’s disease. On the assumption that the disease must be connected with the emotional stress that I was experiencing in professional and interpersonal situations, I immediately began a course of classical (client-centered) psychotherapy. Professionally I continued to be fully committed, although I needed more and more time for recreation. Three years later, however, there ensued a collapse, with physical symptoms of stress, total loss of the voice and tremor which forced me to reduce my work-rate. After the therapy so far had delivered no tangible results, I began Integrative Body Psychotherapy (IBP).

I was intuitively convinced right from the beginning that my disease must have something to do with anxiety, although I was not aware of this anxiety. However, my stressful experiences had to be an expression of it, and as it soon turned out, the affect was perfectly suppressed. Because I did not want to hinder the psychotherapeutic process, I considered no drug-based therapy for Parkinsonism and continued to do without it as the symptoms worsened. With an average duration of effect of 5 to 10 years in rather slight cases, and also being aware of the fact that these are statistical averages, I found myself too young to take on the risk of loss of efficacy and side-effects. I proceeded on the assumption that oxidative stress (cf. Jenner and Olanow 1998) was the cause of my illness, and that anxiety was playing a significant role in it. As long as this anxiety is not integrated, the oxidative stress continues as a result, which also provides an explanation for the fact that the efficacy of the classical treatment of Parkinsonism with drugs is limited and after a certain time leads to severe oscillations, whose affinity to psychological factors I have already mentioned.

A sort of anamnesis

The therapy showed that I had typical premorbid traits of the Parkinsonian personality (cf. Poewe et al. 1990, Menza et al. 1993, Heberlein 1998, review in Hubble and Venkatesh 1995) with excessive control, conformism, lack of spontaneity, suppressed aggressive impulses, identification with ego ideals, excessive tidiness, dependability, consciousness of duty, industriousness, awareness of normal behaviour and other characteristics mentioned in the literature (cf. Poewe et al. 1991), which is recognised as a defence mechanism. Also traumatising life experiences in childhood (cf. Eatough et al. 1990) and stressful psychological circumstances before the illness appeared (cf. Marsden et al. 1981, Russ and Fischer 1991) were not absent. Alongside the social avoidance behaviour, which was one of my characteristics in early youth as a loner, with hindsight other early experiences appear as premorbid symptoms of the illness. I remember one individual case of blockade and loss of voice with a student colleague twenty years before the disease appeared, and also regular inhibitions of gait as I passed a street café with many people, at approximately the same period. Somewhat later there occurred increased stress accompanied with hyperhidrosis in contact with other people during my studies, and later also in professional life. In addition I had always been a non-smoker, always reacted to alcohol with tenseness rather than relaxation, could never bear hashish and avoided medicines as much as I could, all circumstances that occur in conjunction with the characteristics of the premorbid Parkinsonian personality and are mentioned as possible early warning signs (Bell et al. 1994). About a year before the disease appeared, blockades occurred again, in contact with other people, and there followed a phase of deep depression, which lasted several months. Remarkably I did not permit these inner conflicts to appear on the surface, which highlights the rigidity of the defence, which appears to be the decisive factor for the increased risk (Bell et al. 1994).

Clinically, after eight years of progress of the disease there is fairly strong akinesia, mainly affecting the right side, slight rigidity and a weak tremor, which practically only appears in situations of emotional stress. In addition, at times there occurs almost complete loss of voice. It is noticeable that the symptoms of Parkinsonism increase in the presence of psychological stress to the point of complete freezing, while in the presence of therapeutic measures or other physically relaxing circumstances or situations this reduces to almost normal mobility at least at the gross motor level. The difference in motor system performance is very great and the change can take place in remarkable short spaces of time. To my mind, the causal connection of stress and change of symptoms is clear in this case, although the interference is chiefly with precise motor control, which is independent of the psychological state and probably to be attributed to the loss of nigrostratial cells.

Anxiety and motor activity

By way of illustration I should like to mention a workshop in dance and movement and a course in self defence. Although the dance workshop was led by a somatic psychotherapist, it was not otherwise an activity with a therapeutic goal, unless we want to suggest that the expression of feelings through music (The 5 Rhythmsä according to Gabrielle Roth) is something therapeutic in itself. In this course I found that I had enough strength to last out through five days of dance and movement with healthy participants without significant limitations. However, I could only move to certain emotions (sorrow, anxiety) in a limited way or not at all. Thus I was completely blocked in the expression of anger and rage, and had to leave the cycle and sit down. Surprisingly, however, I had no difficulty subsequently in portraying the feeling of joy and expressing it in dancing with perfect movements.

At the same time I found that I could move almost without major motor problems to those emotions that were difficult or impossible for me to express by myself, if the course leader or a member of the group demonstrated the rhythm for me by dancing it. As soon as I was left to my own devices again, however, although I saw a dozen or so fellow group members moving, I was completely blocked myself. I realised then that I didn’t know what was right, as it were the permission, the impulse for the movement was lacking.

This experience was confirmed to some extent in a self defence course (Impactä). Even the very glimpse of aggression shown by the attacker in the exercises blocked me on the first weekend of the course and completely inhibited my ability to defend myself. The effect of this did not leave me all week - and I persisted in the stress-induced psychological and motor blockade. Only the therapeutically conveyed realisation that I had to make this energy my own enabled me the following weekend of the course to release myself from the paralysis, which to the amazement of all present was expressed physically and not least audible and visibly in the voice. It is interesting about this experience that it is similar to the frequently observed “freezing” in Parkinson’s disease, which is recognised as having an affinity with stress and has been compared by well-known authors to the “playing dead reflex” which can be employed as a coping strategy by certain animals alongside the fight or flight reaction (Birkmayer and Riederer 1985). Also, the fact that this shock reaction in animals is resolved by intensive trembling (Levine 1997), could be an indication of its relevance for Parkinson’s disease. In any case a certain parallel between posttraumatic stress and Parkinson’s disease cannot be denied (Van der Kolk 1996).

The Therapy

But not even body psychotherapy can work miracles, and although I attended a psychotherapy session at least weekly, and in addition began training in integrative body psychotherapy, which involves a great deal of self-awareness, a year went by with short term improvements of the condition and motor performance, it is true, but also with the realisation that the defence mechanism, which clearly plays a decisive role in the illness, was completely preventing lasting changes. The physical work, which mainly consists of breathing and relaxation techniques, had no effect, because I so efficiently cut off the affects, that although I was able to complete all the exercises, I felt nothing at all apart from the sporting exertion. Simultaneously I intellectualised and rationalised everything radically, with the result that access to the isolated feelings was not possible and I perceived neither emotions nor physical sensations. Although I supported the work with all the resources at my disposal - especially intellectual resources, the question of resistance to therapy arose. Only dismantling the defence opened way to experience the changes in the affective states and their connection with the changes in the motor inhibition, even though anxiety itself could not yet be experienced in the process.

Parallel to the dismantling of the defence, the stress conditions grew stronger, without my becoming emotionally aware of the anxiety, however. At the same time motor performance grew worse as a whole. I withdrew completely for certain periods of time, apart from the attempts at therapy. I certainly felt alone, while both on the telephone and especially in personal contacts, I immediately lost my voice, showed psychological and physical stress symptoms, my whole body trembled, I suffered from depressed breathing and as a result deteriorated noticeably in motor performance. But also the effect of the therapy became clearer, since the oscillations between psychological depression and inhibition of social skills and motor performance and therapy-induced sense of well-being became greater. However, I could not hang on to these successes of the therapy and within hours I fell back into the old pattern of stress and blockade.

My experiences show clearly the connection between affect and motor activity (cf. Birkmayer and Riederer 1985). The insights that can be derived from it make it possible for the therapy to adapt to the conditions of the disease and to improve its efficacy. In the foreground of this is access to the feelings, and especially to anxiety and effective experiencing of it, from which I expect that it will replace its somatic manifestations. A hard task for the stamina is set by the fact that a temporary worsening of the condition through the dismantling of the defence must be taken as part of the bargain. However I am confident that the temporary improvements achieved in the symptoms will gradually lengthen, and that it will be possible to make them permanent, as has been reported also in the course of treatment of a 58-year-old female patient (Peseschkian 1990).

A Psychological Finding

It has been shown in controlled studies that Parkinson’s patients move more freely and can accomplish motor tasks as quickly as healthy people, if they are given clear hints as to the sequence of movements (Canavan et al. 1989, Linden et al. 1990) and this is part of the clinical experience as are also other movement phenomena in the presence of external stimuli. Thus for example running on a lined floor or passing a ball are mentioned (cf. Canavan et al. 1989, Mohr et al. 1996). In connection with the experience of suppression of aggression, which is also of course a part of the Parkinsonian personality, the idea comes to the fore that this is an expression of complex and extremely rigid coping of a structural weakness, which is characterised by lack of self. Here the confirmation from outside outweighs the impulses from the own self. One of my teachers accurately described the phenomenon as volition deficit syndrome, which creates anxiety and leads to mental blockades, if the external contribution is lacking. The characteristic nature of this phenomenon is that, in the absence of an impulse from outside, the act of will controlled by the head has no motor effect or only a limited effect. Only the affect-accompanied impulse of volition, which includes bodily feeling, conquers the motor blockade. I experienced that in the dance demonstration mentioned above, which enabled me to imitate the movements without inhibition, or in the absence of this external impulse which blocked me completely. However, I also began to experience my own affect-accompanied impulse of volition, which made me able to move almost completely, which I should like to illustrate with an example. In one of the workshops I was struggling to move in a slow rhythm in a duet with a female colleague, when the leader asked the participants to move towards one side of the dance floor. I looked around to see if the other couples were obeying the instruction and saw that that they were doing this only slowly. For this reason I delayed, and when my colleague moved in the indicated direction a little impatiently, I began to offer playful resistance. To my own amazement this impulse freed the inhibition on movement and I could express my resistance in dancing by fluent and uninhibited movements. The others’ hesitation had given me the permission, and the playful resistance was the impulse of my own volition.

It is perhaps not mere chance that Parkinson’s disease generally appears just then when the external sources of impulses and confirmation peter out, through abandonment of a profession, retirement or other processes. Such circumstances are, as is well known, of such a nature to create anxiety or to reinforce it. It remains questionable, what the cause of the volition deficit is and what produces the fears of loss that are necessary to create it. As in most childhood scenarios, circumstances can be reconstructed in my peri and post-natal primary scenario, which are suitable to create anxieties. However it is not possible to observe an traumatic event of such an overwhelming nature that would necessarily have led to radical abandonment of self. Accordingly, one is inclined to inquire into a prenatal cause, since in animal experiments it has been observed that prenatal stress in the mother animal does not just encourage anxious behaviour in the fully grown progeny, but also changes dopamine turnover (Fride and Weinstock 1988, Alonso et al. 1997). This is all the more a reason to suspect direct stress on the foetus, where the vanishing twin syndrome represents one possibility. This is a twin pregnancy in which one foetus dies in the first three month of pregnancy (Huter et al. 1990, review in Landy and Keith 1998). This is the case in a great number of conceptions and is recognised in psychology as a traumatic cause of psychological problems. There is at least a hint of this in the story of my life. At around fourteen years old I had an intestinal obstruction (ileus) and I still remember clearly today the doctor’s statement that its origin went back to my birth. Even though it is not possible to check now what that meant, it cannot be ruled out that here tissue from the dead twin became entangled in the intestine. In the medical literature the death before birth of a twin in a later stage of pregnancy is also known as a high risk for spastic brain damage in the surviving child, and the vanishing twin syndrome has been named as a possible cause in cases of unknown aetiology (Pharaoah and Cooke 1997). Therefore it might well be suitable to create not only psychological conditions for pathological processes but also biological relationships which are of pathological significance in a multifactorial genesis.

Even if we are not willing to go so far as to suppose that psychological factors are causal in the origin of Parkinson’s disease, clinical experience shows clearly that these have a significant effect in the course of the disease. Therefore it is desirable that the psychological connections in Parkinson’s disease be studied further, and further controlled therapeutic studies carried out, which may show, if they continue long enough, not only what psychotherapy has to contribute to the treatment of Parkinson’s disease, but also whether psychological factors also play a role in its aetiology as James Parkinson conjectured.

1998

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