Proc. 4th Congr. Int. College Psychosom. Med.

, Kyoto 1977
Psychother. Psychosom. 31: 38-48 (1979)

The Psychosomatic Theory of Bronchial Asthma

J.J. Gwen
Unit of Psychbiological Research, Department of Psychiatry, University of Leiden,
Jelgersma-Kliniek, Leiden

Abstract. The author discusses the development of the psychosomatic asthma theory as
a paradigm of theory formation in psychosomatic medicine. The first formulation of the
theory was based on clinical and psychiatric observations. It was tested by psychological,
physiological and experimental methods and as a result was reformulated and extended. In
its present form it regards asthmatic breathing as a reaction of a predisposed personality
structure (partly hereditary, partly acquired during a youth situation in which ovcrprotec-
tion by a domineering parent played a large role), to an ambivalent conflict with a key
figure. The resulting frustration is not acted out by aggressive, flight, or depressive behav­
iour, but inhibited; thereby the motoric and verbal discharges are displaced into (substituted
by) a respiratory behaviour pattern, which is characterised by an abnormally forceful
contraction of the abdominal muscles during the expiration. The resulting high intra­
abdominal pressure is transmitted into the thorax where it pushes the posterior membran­
aceous wall of the trachea and large bronchi forward into the lume .v1 thus produces a
long stretched obstruction of the large airways. The passage o. .ne air through the
compressed large air passages under high pressure and low velocity is the mechanism which
causes the typical wheeze and the other manifestations of the asthmatic airway obstruction.
A hypothesis is suggested for the ways in which this psychoneurogenic respiratory
behaviour contributes to the so-called bronchial hyper-reactivity and the secondary develop­
ment of allergies.

Introduction

As a physician and clinical scientist I would like to present my contribution

to this symposium in the form of a concrete example of how a psychosomatic
theory, after having been formulated, can be tested by psychological and
physiological methods and how, in doing so, new facts can be discovered which
can serve as stepping stones for the formulation of a better theory. Thus the
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 The Psychosomatic Theory of Bronchial Asthma 39

theory is fruitful both as a stimulus for further research and as a way to obtain
more and better tested knowledge.
The psychosomatic theory about the etiology of bronchial asthma was
based originally on clinical-medical and psychiatric observations, some of them
long ago, some of them more recent like those described in the monographs of
French and Alexander (11), Groen (16), de Boor (4), Jores and Von Kerekjarto
(21) and others.
In 1955 Bastiaans and Groen (3) formulated the following theory: bronchial
asthma is caused by the interaction of: (1) a predisposing personality, partly
hereditary, partly acquired during a youth situation in which an overprotective
parent (usually the mother) produced in the child an ambivalence against any
‘loving dominance’, experienced also later in life from key figures, and thereby a
difficulty to act out the feelings of combined helplessness, protest, and frustra­
tion in reaction to {2) conflict situations with such key figures, so that the
resulting (3) aggression in words or actions, in weeping or other behaviour is
inhibited and substituted (‘displaced’) by an abnormal pattern of respiratory
behaviour.
Several of the clinical and psychiatric observations, on which the theory was
based, have been confirmed and expanded, e.g. on the effect of suggestion and
placebos in either improving or producing attacks, the therapeutic results of
hypnosis, the production of attacks by certain odours (often non-allergenic)
which have a special meaning for the patient, and the results of separating
asthmatic children from their family environment, even in places where no
special anti-allergic precautions were taken.
In the reviews of Groen (16) and Bastiaans and Groen (3), it was pointed
out that not all emotional events produce attacks. They gave impressive exam­
ples that, for instance, extreme fear as experienced by their patients inside
German concentration camps during World War II, did not produce astlima.
According to them it is a specific emotional situation of ‘feeling oppressed’,
either bodily by an unpleasant feeling in the throat or chest, by exercise, by
cloudy or windy weather, of ‘feeling irritated’ by certain odours or fumes or by
a conflict with a key personality, without being able to express feelings of
frustration or irritation by words or action, which produces the attacks. In the
more recent literature these clinical observations are supported by measurements
of airflow resistance under influence of suggestion, e.g. by the inhalation of
saline vapors of which the patients were told that they have a broncho-con­
strictive action. Conversely it was shown that the airway obstruction in asthmat­
ic children can be relieved by saline inhalations or by ‘psychological’ relaxation.
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 Groen 40

All this work confirms that the air passages can be narrowed and typical
asthmatic wheezing produced by socio-psychogenic influences, especially those
giving rise to unexpressed emotional conflict situations. Ikemi et al. (19) have
supported the theory of ambivalence towards an overprotective mother by
clinical and psychiatric observations under the Japanese system of education, in
which the parents might easily be tempted to overprotect their children. In the
following we will concentrate on the work carried out in the Netherlands to test
the psychosomatic asthma theory by physiological and psychological methods.

Experimentally Produced Psychogenic Attacks

New support for the psychosomatic theory came from demonstrations by

Dekker and Groen (6) that the experimental exposure of a group of patients to
emotional situations which had special meaning for them induced asthmatic
attacks which were indistinguishable from attacks which occurred after the
inhalation of allergens or 'spontaneously’. For these studies the patients were
asked to tell freely in what life situations they had experienced attacks. These
situations were then reproduced as far as possible in the laboratory, and the
production of asthmatic wheezing and the reaction of the vital capacity regis­
tered. These experimental ‘psychogenic’ attacks were indistinguishable from
spontaneous attacks; they reacted, in the same way as ‘spontaneous’ or allergen-
induced attacks, to isoprénaline or multergan. It should be stressed that under
these laboratory conditions some patients reacted to both allergic and psychic
stimuli. This indicates that a division of asthmatic patients into ‘psychogenic’
and ‘allergenic’ groups is not justified.
An interesting finding in these studies was the observation that modifica­
tions of the original ‘asthmatogenic’ situation still produced attacks. Patients
who developed attacks when looking at a goldfish in a bowl subsequently
developed attacks after looking at a toy goldfish or even at the empty bowl.
In the course of further work it was discovered that 2 patients who had
experienced positive reactions to the inhalation of nebulised allergens, after a
number of trials, began to react with attacks when only the control solution, in
which the allergens were dissolved, was inhaled, even when every precaution was
taken to exclude contamination of the apparatus by the allergen. On continuing
the tests, asthmatic attacks occurred in these patients in the same environmental
setting, after the inhalation of pure oxygen and even when only a glass mouth­
piece was put into their mouths which was not even connected with the
apparatus.
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 The Psychosomatic Theory of Bronchial Asthma 41

Mechanism of Experimentally Induced Attacks

This production of asthmatic attacks by environmental, nonallergic stimuli,

under controlled laboratory conditions, gave new impetus to the research into
the mechanism by which these attacks are brought about.
More than 75 years ago, Talma (26) made two clinical observations which
unfortunately have been overlooked by many modern authors, (a) During the
attack the expiratory wheeze is exactly identical when heard through the
stethoscope at different places over the thorax, over the trachea and at a
distance. This must mean that the wheeze is not produced by an obstruction of
the small air passages, but by a centrally situated narrowing of the trachea and
(or) the major bronchi, from where it is conducted both upwards and down­
wards. (b) Many asthmatics, when asked to demonstrate ‘how they wheeze’,
during an attack, and also some normal individuals, can produce the typical
expiratory wheeze at will; apparently wheezing, and the obstruction of the
respiratory passages by which it is caused, can be produced by a voluntary
effort!
50 years later Dekker and Groen (7) discovered that this voluntary effort
acts through an active contraction of the abdominal, thoracic and cervical
musculature during the expiration, which (as the diaphragm is relaxed) produces
a high positive pressure in the thorax and neck. The positive intrathoracic
pressure thus produced, is many times higher than normal. It compresses the
trachea and the larger bronchi, mainly by pushing the membranaceous part of
the posterior wall of the trachea and larger bronchi forward into the lumen, and
it is this long stretched narrowing of the large air passages which is the seat of
the asthmatic obstruction during the expiration. The experimental asthmatic
dyspnoea, in other words, is caused primarily by an abnormal breathing pattern
of the ‘voluntary’ striated muscles of ventilation. The same abnormal breathing
pattern can be ascertained by observing patients while they wheeze ‘spontane­
ously’ and by palpation of the abdominal and scalcni muscles. That this abnor­
mally forceful expiration actually produces a compression of the trachea and
major bronchi has been demonstrated in the first place by observing patients
during ‘spontaneous attacks’ through the bronchoscope and by radiologic in­
vestigation after filling the bronchi with lipidol. In subsequent investigations
Dekker and Ledeboer (8) taught healthy people and asthmatic patients to
‘wheeze’. When the subjects had acquired sufficient practice in this voluntary
wheezing, frontal, transverse, and oblique short-time x-ray exposures were made
of the changes in diameter of the trachea and the main bronchi during a normal
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and during a voluntary ‘wheezing’ expiration. Similar studies were done on

asthmatic patients during quiet breathing, during wheezing at request, and
during a ‘spontaneous’ attack.
It could be thus demonstrated that during a voluntarily induced ‘asthmatic’
expiration in normal subjects a considerable narrowing of the lumen of the main
bronchi and the trachea was produced. An identical narrowing of these main
airways was seen during voluntary wheezing expirations in patients with asth­
matic bronchitis and emphysema. Exactly the same type of narrowing of the
cervical and thoracic trachea of the major bronchi was found in patients during
severe ‘spontaneous’ attacks of asthmatic and during attacks provoked by
inhalation of histamine and house dust. These observations were confirmed, for
instance, by Gandevia (12) and Tammeling and Sluiter (27).

Direct Measurement of Intrabronchial Pressure during Wheezing

By physiological studies Dekker el al. (5) showed that all the changes in pressure and
airflow velocity of an asthmatic attack are also present during a voluntary expiration
accompanied by wheezing in a normal individual.
In two individuals they measured the intrabronchial and intra-oesophageal pressures by
means of polyethylene catheters introduced in a large bronchus and in the oesophagus,
respectively. In addition the airflow velocity was registered by means of a pneumotachog­
raph. It could thus be concluded that during a voluntary wheezing expiration an important
impediment to the air flow must have been situated between the point of measurement and
the mouth, thus confirming the roentgenological observation of a long stretched narrowing
of the larger bronchi and trachea. In 1965 Bruderman and Groen (unpublished) confirmed that
asthmatic patients, while they were free of attacks, could reproduce the expiratory
wheeze at will; during the manoeuvre these authors registered intrathoracic pressure and
airflow velocity and showed that the curves were indistinguishable from those obtained
during so-called spontaneous asthmatic attacks in such patients. Independently Dekker et al.
(10) showed by physical sound analysis that the ‘spontaneous’ asthmatic wheeze is indistin­
guishable from the wheeze produced at will.
From these studies there can be little doubt that the main mechanism in the causation
of the asthmatic bronchial obstruction is a passive compression of the trachea and major
bronchi, caused by a too forceful use of the accessory muscles of ventilation, especially the
abdominal and scaleni muscles during the expiration. In other words asthma is a respiratory
neurosis. Whereas a voluntary wheezing expiration can be started and stopped at will, the
wheezing expiration during a spontaneous attack takes place (or stops) ‘automatically’. It
has become a different type of automatic ‘reflex’ breathing.
In addition to bronchocompression, three other mechanisms may contribute to the
airway obstruction in asthma: spasm, swelling of the mucous membrane by oedema and
hyperaemia and plugging by mucus. It will be a matter for further research to ascertain what
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their quantitative contribution to the total airway resistance in the bronchial tree is. Further
research will also have to elucidate how far down the compression of the main airways
continues into the middle size bronchi, and also how much obstruction of the small air
passages by the secretion and aspiration of mucus into the bronchioli enhances the effect of
the positive thoracic pressure on the main bronchi. Meanwhile the compression theory has
already elucidated some very simple facts, for example why positive pressure breathing or
pursed-lip breathing, singing (16) or playing a flute or clarinette (24) do away with the
wheeze! The same holds for the effect o f ‘relaxing’ breathing exercises, whether by yoga or
other systems. The elucidation of what is wrong with the asthmatic breathing offers a simple
explanation of how these breathing therapies work.

Asthma Induced by Exercise and Hyperventilation

In the last years an increasing number of studies have been devoted to

exercise-induced asthma (18, 20). Some patients notice themselves that exer­
cise, be it brisk walking, climbing stairs or running, may produce wheezing. By
exposing unselected patients to physical exercise on a treadmill or bicycle
ergometer, it has been found that a considerable number of asthmatics develop
this wheezing experimentally. The characteristics of this airway obstruction after
induced exercise, notably a diminution of the forced expiration volume (FEV)
during 1 sec and of peak expiratory flow rate (PEFR) are exactly those of a
spontaneous asthmatic attack. The phenomenon is the more remarkable because
many patients who have low FEV, and PEFR before the test, show an improve­
ment of these parameters during the exercise, sometimes to normal values, which
however is followed by a drop, a few minutes after the exercise is stopped. It is
difficult to explain this mechanism by the allergic theory ; it has been equally
difficult to correlate the airway obstruction with the effects of the exercise on
blood pH - Pco2, PQ , distension of the lungs, swelling of the mucosa or mucus
secretion and most investigators regard the cause of exercise-induced asthma as
unknown (1 ,2 , 13-15, 25).
One need not be a respiratory physiologist but only a good observer of
behaviour and muscular activity to notice that a wheeze after exercise is absent
or present, dependent on the use of the abdominal muscles during the expira­
tion. It is surprising that so many investigators who have described the great
variability, in airflow resistance in asthmatic patients, ascribe this to ‘bronchial
instability’ or spasm of the air passages, without considering that the bronchial
tree is situated within the thoracic cage and therefore subject to different
degrees of compression, depending on the pressure relationship within the cage!
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 Groen 44

In 1946 Herxheimer (18) was the first to draw attention to the fact that
many asthmatics develop their attacks after hyperventilation, and that this can
be reproduced experimentally. His observations did not draw immediate atten­
tion but have since been confirmed by several clinicians and respiratory physiol­
ogists. In 1949 we described the case of a girl who developed her first attack of
asthma after running after a street car under emotional circumstances. Bastiaans
and Groen (3) have demonstrated an emotional basis in other cases of exercise-
induced asthma.
Since then we have seen patients who have alternative attacks of hyper­
ventilation and typical asthma (they called them attacks of ‘breathing’ or
‘wheezing’) and we have also seen hyperventilation change ‘spontaneously’ into
typical asthma. Occasionally one can watch the development of typical asth­
matic attacks in a patient who is asked to hyperventilate for the measurement of
his maximum breathing capacity.
The fact that hyperventilation, a typically neurogenic disturbance of the
ventilation, can develop into asthmatic bronchial obstruction, forms both
clinical and experimental support for the neurogenic pathogenesis of the asth­
matic attack.

The Behavioural Approach to Asthmatic Breathing

The psychosomatic theory was originally built on observations carried out

within the framework of psychodynamic psychology. The early authors were
interested in the development of emotional attitudes of the child and in its
behaviour during conflict and ambivalence towards authority and key personal­
ities. In the modem behaviour psychology of asthma, the accent is not on the
feeling states of the patient but on his breathing behaviour. This is regarded as a
response to certain environmental stimuli. As no patient is born with asthmatic
breathing, asthma is considered as a form of acquired behaviour which develops
as the response of a certain innate disposition or motivation of the organism to
certain stimuli. In the light of modern learning theory, asthma can therefore be
fruitfully regarded as a learned response. Whether it arises from an uncondi­
tioned stimulus by coupling with a conditioned stimulus through a classical
Pavlovian mechanism or whether it is caused by instrumental conditioning, or
both, has not yet been decided.
From the early work of Dekker et ai (9), 2 patients were described, who,
after having experienced asthmatic attacks induced by the inhalation of specific
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 The Psychosomatic Theory of Bronchial Asthma 45

allergens, later developed attacks when they inhaled an ‘empty’ control solution,
pure oxygen or even when the mouthpiece of the nebulizer was put into their
mouth. These patients, therefore, were examples of classical conditioning in
which the inhalation of an allergen had been the unconditioned stimulus. On the
other hand 2 other patients, described by Dekker and Groen (6), had attacks
when they looked at a goldfish in a bowl (to which they were not allergic) and
one of them later developed attacks while she was looking at a toy goldfish and
even at the empty bowl. These and other examples given by the authors speak in
favour of an instrumental process as the cause of asthmatic conditioning.
The question of how the asthmatic response can be reinforced seems a
puzzle at first sight. Why should patients continue to utilize a form of breathing
which is both subjectively unpleasant and objectively serves no useful purpose?
In this respect asthma can be compared to hyperventilation, enuresis, certain tics
or writing cramps or certain forms of so-called hysterical behaviour. A presum­
able answer is that, in most cases subconsciously, these forms of behaviour are
enforced as an avoidance reaction under the influence of strong anxiety from
which the patients want to escape. In the case of asthmatic breathing this
anxiety is supposed to be the fear of suffocation, which makes patients gasp for
breath during the inspiration and press out the air during expiration. Any
situation in which the patient feels oppressed may recall this fear of suffocation
or (after conditioning) of developing another attack.
Another explanation might be that during childhood when the asthmatic
breathing started, it did serve a useful purpose, because it was rewarded by the
attention of the mother, which the child did not succeed in attracting by crying
or otherwise. In this respect it is interesting to recall a hypothesis which
Bastiaans (unpublished) has offered to explain the well-known development of
asthma in children who have suffered from infantile eczema. Until recently these
babies were, on medical advice, tied to their cots to prevent them from
scratching. Children in such, for them, frightening situations first cry to draw the
attention of their parents or nurses to untie them, but this had no success. In
their effort they try other respiratory movements and in doing so develop the
‘abdominal pressure’ respiration which produces the wheeze. Whereas the
mother or nurses did not react to the crying, the wheeze induced them to release
the child and take it to them. This course of events is an example of instrumen­
tal conditioning. Once the association is established between this form of
respiratory behaviour and the reward by being released from a frustrating
situation, it can be reinforced by similar experiences of obtaining relief by
wheezing from other oppressive situations. It is even possible that wheezing,
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 Groen 46

even at a later age, is further reinforced by the reward of attention from key
figures (doctors among them) as suggested by Khan et al (22, 23).

In the Netherlands van der HaI (17) has used a simple approach, based on the work.of
Talma (26) and Dekker and Groen (6, 7). He taught asthmatic children and their mothers to
wheeze at will and showed them that they could also stop this voluntarily induced wheeze.
He then ordered the mothers to practise this voluntarily produced and ‘cured’ breathing a
few times every day. He did not use a control group but mentions that this method greatly
reduced the anxiety for the attacks in both the children and their parents and that it
diminished the frequency of the attacks in almost all his cases.

A few other recent case reports in the literature suggest that behavioural
methods, applied to both patients and key figures in the patients family, show a
definite promise in improving the therapeutic results.

A New Formulation of the Theory

In reviewing the psychosomatic research of the last decades, we would like

to present an improved multifactorial theory, which is based on the develop­
ment, under the influence of a certain emotional state, of a disturbed pattern of
ventilation with resulting compression of the trachea and main bronchi as the
primary event in the asthmatic obstruction of the bronchial tree. Because of the
pressure and flow changes as a result of this compression the mucous membranes
of the large and small bronchi swell by hyperaemia and oedema, and secrete
more mucus, etc., because the high intrathoracic pressure impairs the capillary,
venous and lymph return from the engorged mucosa. Thus to tire compression
are now added two more factors which produce airway obstruction: mucosal
swelling and mucus secretion. Part of this mucus is aspirated during inspiration
from the air passages into the alvoli and bronchioles where, by absorption of
water, the mucus becomes thick and sticky and blocks the lumen. Thus, to the
obstruction by compression of the larger airways is now added a narrowing of
the smaller air passages which manifests itself clinically, among others, by the
development of an inspiratory in addition to the expiratory wheezes.
The swollen, mucus-covered mucosa is unable to clear itself of dust and
bacteria and is therefore less resistant than normal to bacterial infections. What
is more, large molecular substances, which happen to be inhaled under these
circumstances, stick to and dissolve in tire mucus on the hyperaemic mucous
membranes. The disturbed pressure airflow relations in the bronchial tree during
asthmatic breathing also favour these penetrations: large molecular substances
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are aspirated into the mucous membrane by the increased negative pressure
during the inspiration; they are pressed into the mucous membrane by the
increased positive pressure during the expiration.
Of these large molecules two kinds are of clinical importance: (a) viruses,
their enhanced penetration explains the sensitivity of asthma patients to viral
infections of the respiratory tract; (b) other foreign substances, which after pene­
trating into the mucous membranes come in contact with sessile lymphocytes and
plasma cells with formation of antibodies and thereby become allergens.
This is the mechanism by which asthmatic patients can become secondarily
sensitised (‘allergised’) to macro-molecular substances which they happen to
inhale during the attacks. In this hypothesis the inappropriate use of the
voluntary muscles during asthmatic breathing not only produces bronchial
compression, it also creates the circumstances which secondarily favour the
development of an acquired allergic state. This hypothesis explains why later
both the exposure to a situation which has a certain oppressive meaning for the
patient and the inhalation of the substance to which the patient has thus
acquired an allergic sensitivity, can produce further attacks. Both conditions
(whether psycho-neurogenic or allergic) predispose the patients, through
anxiety- and generalisation-reinforcement, to further conditioning of his ab­
normal breathing behaviour.
This reformulated hypothesis may also furnish a clue for the explanation of
the accumulation of eosinophilic cells in the bronchial mucosa of asthmatic
patients. We sugest that this is a tissue reaction to the penetration of the
glycoproteins which are present in mucus into the mucous membrane.
For more extensive discussion and references the reader is refered to the
author’s contribution in: Hill Modern Trends in Psychosomatic Medicine, vol. 3
(Butterworths, London 1975).

R e fe re n c e s

1 Anderson, S.D.; McEnroy J.D.S., and Bianco, S.: Changes in lung volume and airway
resistance after exercise in asthmatic subjects. Am. Rev. resp. Dis. 106: 30 (1972).
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asthmatic patients during and after exercise. Thorax 27: 718 (1972).
3 Bastiaans, J. and Groen, J.J.: Psychogenesis and psychotherapy of bronchial asthma; in
O’Neill, Modern trends in psychosomatic medicine, vol. 1, p. 348 (Butterworths,
London 1955).
4 Boor, C. de; Psychosomatik der Allergie; ins Bes. Asthma Bronchiale (Huber-Klett,
Bern 1965).
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 Groen 48

5 Dekker, E.; Defares, J.G., and Haemstra, H.: Asthmatic wheezing and the check valve
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J.J. Groen, MD, Unit of Psychobiological Research, Department of Psychiatry,

University of Leiden, Jelgersma-Kliniek, Leiden (The Netherlands)
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