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Special Aspects of Treatment of Joint Dysfunction

Joint Dysfunction, Part 2



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by William Kaufman, M.D., Ph.D. (1949)
Copyright C 2001 Charlotte Kaufman. Reprinted with permission.
Edited by Andrew W. Saul

(Dr. Kaufman now discusses physical and psychological stresses, allergy, posture, obesity and other factors that may interact or interfere with niacinamide megavitamin therapy for arthritis. This chapter’s three original photographs are not provided here, but may be seen in the original text, available through this website. For ordering information, you may either click here or scroll to the very bottom of this webpage.)

References cited in this chapter are posted at

Four Complicating Syndromes Frequently Coexisting with Joint Dysfunction

It might appear to the reader that the niacinamide treatment of a patient with joint 
dysfunction is a more or less mechanical and uninteresting procedure. However, in 
practice, the treatment of a patient with joint dysfunction is never a mechanical or dull 
routine, since therapy of joint dysfunction and commonly occurring complicating 
syndromes must always be adapted to the special needs of the individual patient. For 
the most part, the treatment of a patient with joint dysfunction is a constantly interesting 
and instructive discipline both for the patient and physician. 

Commonly occurring complicating syndromes coexisting with joint dysfunction must 
often be corrected if the patient is to be able and willing to take niacinamide therapy as 
prescribed, and if he is to feel well ultimately. Even though joint dysfunction improves to 
the level of 96-100 (no joint dysfunction) in response to adequate niacinamide therapy, 
the patient may have continuing articular and non-articular symptoms, of one or more of 
these complicating syndromes, and he may erroneously conclude that the niacinamide 
treatment of his joint dysfunction has failed. On the other hand, whether or not a patient 
is taking niacinamide treatment, when these complicating syndromes are corrected, he 
may have an improved sense of well-being and freedom from articular and non-articular 
symptoms, but it does not follow necessarily that his joint dysfunction is improving, since 
serial re-measurements of his Joint Range Index may indicate that his joint dysfunction 
may be unimproved or worsened. 

In the treatment of a patient with joint dysfunction who has one or more of four 
complicating syndromes frequently coexisting with joint dysfunction, the physician must 
correctly identify the basis of the patient's articular and non-articular symptoms, and 
must institute concurrently the appropriate specific therapy required for the successful 
management of joint dysfunction and any of these four syndromes which the patient 
may have: 

(a) the delayed post-traumatic articular syndrome (see page 79);
(b) the chronic allergic syndromes (page 96);
(c) the sodium retention syndrome (page 114);
(d) the syndrome of psychogenically induced, sustained hypertonia of somatic muscle 
(page 115).

The articular symptoms of any one or any combination of these four syndromes may be 
present in a patient without joint dysfunction, or may be absent in a patient with joint 
dysfunction (with or without clinically obvious arthritis); and may occur in a patient with 
joint dysfunction before niacinamide therapy is instituted, during the course of adequate 
niacinamide therapy, when adequate niacinamide therapy is replaced by inadequate 
niacinamide therapy or upon premature cessation of niacinamide therapy. The articular 
and non-articular symptoms of bodily discomfort of these four syndromes may vary in 
intensity, duration and extensiveness. With each of these syndromes a patient may 
have a steady state of discomfort which persists until the syndrome is successfully 

The four complicating syndromes frequently coexisting with joint dysfunction will be 
described as if each were an independent clinical entity. Often, the successful 
management of any one of these syndromes will not materially influence the clinical 
course of the other untreated coexisting syndromes. At times, however, these 
complicating syndromes may be interrelated, in the sense that when one of the 
untreated complicating syndromes becomes more severe, the other coexisting 
untreated complicating syndromes also become more severe; and in the sense that the 
successful treatment of one of the complicating syndromes may simultaneously amel-
iorate or lessen the intensity of symptoms of the other untreated coexisting complicating 
syndromes. Clinically, it may be very easy, or it may be extremely difficult, to ascertain 
the etiologic basis of the patient's articular and non-articular symptoms. The most 
helpful clues to the etiology of the patient's symptoms are obtained from careful clinical 
study, including a detailed history of the onset and development of symptoms, re-
examination of the patient, an analysis of the food-symptom diary kept by the patient 
(see page 103), and an evaluation of the patient's response to a trial of therapy directed 
toward the amelioration of the symptoms of a given complicating syndrome.

Although from the physician's point of view, the patient's symptoms are subjective 
phenomena, to the patient his symptoms are real and have objective existence. By 
giving verbal expression to his symptoms, the patient is exteriorizing the fact that he 
does not feel well, and implying that if his symptoms could be made to disappear, he 
would feel well.

The physician must give careful consideration to the possible meaning of all the 
patient's symptoms, whether or not they seem to be trivial, atypical or bizarre at the time 
of their recital. The physician should regard the patient's symptoms as direct or indirect 
clues to the nature of the patient's ill health, even if the clinical meaning of these 
symptoms continues to be inapparent. Once the etiology of the patient's symptoms is 
recognized by the physician, it often becomes possible to institute appropriate treatment 
which, in time, ameliorates these symptoms. While the etiologic basis of some 
symptoms may be readily perceived by the physician, the clinical significance of other 
symptoms may remain obscure for a long time or may never be ascertained. Even 
some symptoms which at first hearing appear fantastic to the physician may prove, in 
time, to have a definite clinical basis which can be identified. When the nature of the 
patient's disorder becomes manifest, it is often found that most patients with puzzling 
symptoms were entirely accurate and honest in their reporting of symptoms. It is the 
rare patient who deliberately distorts facts and invents complaints and illnesses, and 
even such a patient by so doing gives valuable clues to the nature of his illness.

In evaluating the clinical significance of articular and non-articular symptoms, it is 
necessary to remember that the patient's prevailing emotional state influences the 
nature of his complaints (29) (182) (242). A patient who is mildly depressed may 
complain at great length about his various symptoms, and may express considerable 
doubt that he will ever get well. On the other hand, a patient who is euphoric will 
complain little or not at all of articular and non-articular symptoms, and his general atti-
tude toward all of his life situations will be optimistic. A patient who has feelings of 
anxiety, guilt, hostility or frustration may find substitute satisfaction in complaining 
bitterly about articular and non-articular symptoms. A patient whose attention is fixed on 
his symptoms will have many complaints excepting when his attention is distracted by 
more interesting matters. A patient with a rigid conception of his own perfection seldom 
will complain of symptoms. Occasionally, a patient unconsciously attempts to gain the 
approval of the physician by exaggerating his favorable response to therapy. On the 
other hand, a patient may use his complaints about poor health to "punish" the 
physician (authoritarian figure) by insisting with evident satisfaction that his health has 
been unimproved or worsened by treatment, when it is obvious from physical 
examination and from the remainder of the patient's story that he has in fact improved 
physically. At times, when a patient has secondary gains from his illness, he seems 
impelled to complain about his symptoms, and even when he has improved as a result 
of treatment and has fewer symptoms, he continues to complain more and more about 
less and less.

(In this section, there is excluded from discussion such severe accidental injuries as 
lacerations of the supporting structures of joints, bone fractures involving joint 
structures, torn articular cartilages causing internal derangement of joints, and 
penetrating joint wounds.)

Without knowledge of the clinical patterns of the delayed post-traumatic articular 
syndrome, the cause of many articular symptoms and signs often remains obscure. 
With knowledge of such patterns, and with knowledge of the patient's physical activities, 
occupation, and emotional tensions, the physician can often identify the basis for the 
patient's troublesome articular symptoms and signs, and can advise the patient how to 
modify his way of living so that in the future he will be less likely to experience such 
symptoms and signs.

The delayed post-traumatic articular syndrome is the consequence of certain types of 
mechanical joint injury: 

(a) articular trauma which is likely to occur in the course of more or less ordinary 
physical activity; 

(b) alterations in the alignment of joints due to certain acquired habits of posture, or 
indirectly due to niacinamide-induced improvement in joint mobility;

(c) psychogenically induced, sustained hypertonia of somatic muscle.

In general, the severity of the patient's delayed post-traumatic articular symptoms 
seems to depend on the following factors: the clinical grade of severity of his joint 
dysfunction; the severity, repetitiveness and duration of the inciting mechanical joint 
injury; the patient's prevailing moods; and his attitudes toward his symptoms and life 

Mechanical joint injury may be well tolerated by persons with the milder grades of joint 
dysfunction, who will have either no clinically discernible articular sequelae or will 
develop relatively mild symptoms and signs of the delayed post-traumatic articular 
syndrome for relatively short periods of time; but mechanical joint injury usually is poorly 
tolerated by persons with the more severe clinical grades of joint dysfunction, who tend 
to develop severe symptoms and signs of the delayed post-traumatic articular syndrome 
which last for relatively long periods of time (97). In general, immediate and delayed 
post-traumatic articular symptoms and signs tend to be more severe in untreated 
persons with joint dysfunction than in persons with joint dysfunction who are receiving 
adequate amounts of niacinamide. A patient with joint dysfunction who is receiving 
inadequate niacinamide therapy is more likely to suffer from the delayed post-traumatic 
articular syndrome than if he were receiving adequate niacinamide therapy. If his 
niacinamide intake is increased from inadequate to adequate levels, even though 
mechanical joint injury continues at the same level as previously, the niacinamide-
induced reparative process will often preponderate over the trauma-induced 
deteriorative process, and the delayed articular post-traumatic syndrome will be 

The immediate effects of a single episode of extremely severe joint injury are well 
understood because of the close temporal relationship between the articular injury and 
the ensuing articular symptoms of discomfort, pain and disability, which may be 
associated with one or more of the following physical signs in the mechanically injured 
joint region: tenderness to palpation, swelling, heat, redness, congestion of the 
superficial circumarticular veins, spasm of somatic muscles operating the injured joint, 
and painful or painless limitation of active and passive articular movement. The delayed 
effects of such severe mechanical joint injury may include a continuance of articular 
discomfort, pain and disability lasting for months or years, and clinically well-defined 
arthritic changes in the injured joints (33) (121) (19) (131).

The immediate effects of a single episode of a less severe grade of mechanical joint 
injury are also well understood, but the delayed effects of such an injury to the joints 
have not been given the clinical attention they deserve. Because there is often an 
asymptomatic period of two to four days between the subsidence of the immediate post-
traumatic articular symptoms and the appearance of the delayed post-traumatic articular 
syndrome, the physician and patient may be unable to perceive the causal relationship 
between the inciting mechanical joint injury and the delayed post-traumatic articular 
symptoms. When the delayed post-traumatic symptoms of joint discomfort, pain and 
disability occur three or four days after the inciting joint injury, there may be one or more 
of the following objective findings in the injured articular regions: tenderness to 
palpation, swelling, heat, redness, congestion of the superficial circumarticular veins, 
spasm of the somatic muscles operating the injured joint, and painful or painless 
limitation of active and passive articular movement. These delayed post-traumatic 
articular symptoms and signs may be more severe and more persistent than those 
occurring immediately after joint injury, and gradually decrease in severity, usually 
disappearing by the tenth to fourteenth day following the inciting injury to the joint. 
Occasionally, the delayed post-traumatic articular syndrome may persist for a month or 
more after a single joint injury, particularly when the patient's joint dysfunction is 
extremely severe, or when the inciting trauma is unusually great. At times, there may be 
no articular symptoms and signs immediately following mechanical joint injury, or such 
immediate articular symptoms as may appear immediately after the injury may seem so 
insignificant to the patient that he disregards them. Sometimes, the only sign of the 
delayed post-traumatic articular syndrome may be increased painless limitation in the 
ranges of movement of the injured joint. Even relatively slight injury, when sufficiently 
repetitive, may lead, in time, to a steady state of articular discomfort, pain and disability, 
and to the appearance of clinically obvious arthritic deformities in the injured joint region 

Sometimes, the cause of delayed post-traumatic articular symptoms may be identified 
only with difficulty after a prolonged period of clinical study. When a patient with joint 
dysfunction suddenly experiences a single isolated episode of joint pain and disability, 
or gradually develops a persistent state of articular discomfort (with or without periodic 
exacerbations) or merely an asymptomatic lowering of the ranges of joint motion, 
careful clinical study may disclose the fact that in the performance of a particular 
physical act either once or repetitively, the patient inadvertently or unknowingly injured 
the affected joints, or may disclose the fact that the patient has developed 
psychogenically induced, sustained hypertonia of somatic muscle of sufficient severity 
to injure his joints. Joints used statically or dynamically in the performance of everyday 
activities may incur mechanical trauma sufficiently severe to cause a single episode of 
articular discomfort, pain and disability, or may incur mechanical trauma sufficiently 
severe and repetitive to cause a steady state of articular discomfort, pain and disability.

When a patient has joint dysfunction of a high clinical grade of severity, his articular 
structures are particularly vulnerable to lesser grades of joint trauma, which may give 
rise to the more severe and persistent symptoms and signs of the delayed post-
traumatic articular syndrome. When a patient is recovering satisfactorily from joint 
dysfunction in response to continuously adequate niacinamide therapy, and a specific 
joint is subjected to a single episode of moderate injury, usually there is temporarily a 
delayed post-traumatic decrease in the range of movement of this joint -with or without 
accompanying symptoms of the delayed post-traumatic articular syndrome - although 
his uninjured joints continue to improve at a satisfactory rate. If the articular injury is 
more or less continuous, the range of movement of the injured joint decreases, and, in 
time, tends to stabilize for as long as the niacinamide-induced reparative process bal-
ances the trauma-induced deteriorative process in the injured joint. At this time, an 
increase in the patient's niacinamide intake does not materially improve the range of 
movement of the continuously injured joint, except in some instances where previous 
levels of niacinamide treatment have been inadequate. However, a decrease in 
niacinamide intake causes the range of movement of the continuously injured joint to 
decrease at a more rapid rate than if adequate amounts of niacinamide were taken con-

The Joint Range Index may or may not be significantly depressed by the post-
traumatically decreased range of movement of a single joint. It is, therefore, necessary 
to analyze the component joint ranges which are measured for the computation of the 
Joint Range Index in order to observe which joints show post-traumatically decreased 
ranges of joint movement and which joints simultaneously have made satisfactory 
improvement in the ranges of joint movement for the period of observation during which 
the patient was ingesting continuously adequate amounts of niacinamide.

It is often possible to identify the type of behavior which caused mechanical injury of 
certain joints from an analysis of the distribution of joints with decreased ranges of 
movement and those with increased ranges of movement, and from knowledge of the 
patient and his physical activities and hobbies at various seasons of the year, and of his 
emotional tensions. For example, when the fingers of the right hand, right wrist and right 
show decreased movement, and the patient has recently returned from a train trip, one 
can establish that the most likely cause of the decreased ranges of movement was the 
carrying of a suitcase. When mechanical articular injury is sufficiently generalized, there 
is a delayed post-traumatic decrease in the ranges of movement of the injured joints 
and in the Joint Range Index even though the patient with joint dysfunction is ingesting 
continuously adequate amounts of niacinamide; however, with cessation of joint injury 
there is usually a satisfactory rise in the Joint Range Index in response to adequate 
niacinamide therapy.

Certain physical activities have been identified as causes of the delayed post-traumatic 
articular syndrome in some patients at various times during this study, and include: 
sawing, planing, hammering, house-painting, weeding, spading, hoeing, spraying, 
hedge-clipping, lawn-mowing, bowling, sailing, rowing, paddling a canoe, fly-fishing, 
driving a car, knitting, crocheting, tatting, wringing of clothes, house-cleaning, cleaning, 
scrubbing floors, waxing floors. In some persons the repetitive performance of a 
physically awkward act may cause joint injury; e.g., the frequent daily use of a desk 
telephone with a short cord, which requires the user to twist his body into an awkward 
position each time he uses the telephone. In some patients, holding the joints in a fixed 
position and carrying moderate weights for relatively short or long periods of time may 
give rise to a delayed post-traumatic cycle of joint discomfort and disability; e.g., 
maintaining one knee and ankle fixed in an awkward position by sitting on the medial 
aspect of the ipsilateral heel, or sitting in a chair with the dorsum of the ipsilateral foot 
twisted behind one leg of the chair; hanging onto an overhead strap in a subway or bus; 
holding a knitting bag, handbag, shopping bag, brief-case, suitcase, or even holding a 
strong dog in leash. Similarly, certain jerky movements requiring the sudden exertion of 
extra muscular force will also give rise to a post-traumatic cycle of joint discomfort and 
disability; e.g., opening a window or drawer that "sticks," or loosening a stubborn jar 
cover with a strong steady twisting movement, or opening and closing a "tight" water 
faucet. Joint trauma may occur during the night when the patient maintains awkward 
sleeping postures for relatively long periods of time, particularly if he simultaneously has 
during sleep psychogenically induced, sustained hypertonia of somatic muscle. Certain 
recently acquired or old methods of walking which the patient habitually uses will cause 
injury to the knee and hip joints and will cause a steady state of symptoms of articular 
discomfort, pain and disability, and signs of impaired mobility of hip and knee joints.

Joint trauma may occur also when a patient with joint dysfunction (with or without 
clinicallv obvious arthritic deformities) has mental tensions which are exteriorized 
through psychogenically induced, sustained hypertonia of somatic muscle. Although 
such a patient may erroneously believe that he is completely relaxed, the coapting 
pressures exerted continuously against articular surfaces, and the accompanying 
tensions on periarticular structures often cause continuous joint trauma for as long as 
this sustained somatic muscle hypertonia persists. When psychogenically induced, sus-
tained hypertonia of somatic muscle is present and the patient uses his joints in 
everyday activities, there is joint trauma in excess of what would have occurred in the 
performance of these activities in the absence of sustained hypertonia of somatic 
muscle. Psychogenically induced, sustained hypertonia of somatic muscle in persons 
with the more severe grades of joint dysfunction may cause articular swelling, redness, 
increased congestion of the superficial circumarticular veins, increased heat, spasm of 
the somatic muscles operating the joints, stiffness, and limitation in the ranges of active 
and passive joint movement. In time, repetitive joint trauma from this source will favor 
the appearance of clinically obvious arthritic deformities. Ordinarily, the patient is 
unaware of his mental tensions and his psychogenically induced, sustained hypertonia 
of somatic muscle, although he is very aware of his symptoms due to the delayed post-
traumatic articular syndrome.

Many persons with joint dysfunction (with or without clinical or radiographic evidence of 
arthritic changes in joints) may be unaware of any articular discomfort or disorder until 
joint trauma gives rise to the delayed post-traumatic articular syndrome. The anxiety 
and mental tension developed by such patients as a result of this articular discomfort, 
pain and disability (particularly when a steady state of articular discomfort is reached)
often create secondary psychogenically induced, sustained hypertonia of somatic 
muscle which is sufficiently severe to perpetuate joint injury and its sequelae.


Treatment of the delayed post-traumatic articular syndrome should be directed toward 
preventing the joint traumata which produce this syndrome and toward giving the patient 
relief from whatever delayed post-traumatic articular symptoms he may have. Since 
joint injury may be caused by ordinary or unusual, essential or non-essential daily 
activities, it is not always possible to prevent articular trauma, even when the physical 
act producing joint injury is known. However, once the causation of mechanical joint 
injury is recognized, the patient should be advised how to keep joint injuries to a 
minimum in the performance of his essential everyday physical activities. A patient who 
understands the temporal and causal relationship between the mechanical joint injuries 
of everyday activities and the symptoms of the delayed post-traumatic articular syn-
drome is likely to modify his activities so that mechanical injury to his joints will be 
minimal and, when possible, to avoid those unessential physical activities which may 
actuate the delayed post-traumatic articular syndrome.

Many patients erroneously believe that "exercise loosens the joints." It is often 
necessary to demonstrate to a patient that after exercise his Joint Range Index and the 
ranges of movement of his exercised joints are depressed, sometimes for days or 
weeks. In patients who have the lesser clinical grades of joint dysfunction, such delayed 
post-traumatic depression of joint ranges may not be sufficiently severe or prolonged to 
warrant the interdiction by the physician of all unessential physical exercise. However, 
in patients who have the more severe clinical grades of joint dysfunction, such delayed 
post-traumatic depression of the joint ranges may be sufficiently marked and prolonged 
to impede satisfactory joint recovery in response to niacinamide therapy. For each 
patient, where possible, physical exercise should be adjusted so that the resultant joint
injury will not materially impede satisfactory niacinamide-induced recovery from joint 

Although physically strenuous exercise may give some patients with the more severe 
grades of joint dysfunction temporary benefit through transient release of 
psychogenically induced, sustained hypertonia of somatic muscle, the joints are not 
benefited by such exercise. It may be desirable to permit a patient with unresolved 
mental tensions to continue to enjoy his strenuous physical exercise, since the 
advantages of obtaining transitory relief from sustained hypertonia of somatic muscle 
may outweigh the disadvantages of actuating the post-traumatic articular syndrome. 
However, in time, with satisfactory psychotherapeutic resolution of his emotional 
tensions, the patient usually is relieved of his psychogenically induced, sustained 
hypertonia of somatic muscle, and consequently does not have the urgent need for 
seeking emotional release through excessive physical activity.

The more niacinamide-induced recovery a patient has had from his initial clinical grade 
of joint dysfunction, the better he will be able to tolerate the articular trauma of his 
everyday activities. The substitution of inadequate for adequate niacinamide therapy, or 
the premature cessation of adequate niacinamide therapy, tends to make the delayed 
post-traumatic syndrome more severe. Continuously adequate niacinamide therapy 
helps to minimize the symptoms and signs of the delayed post-traumatic articular 
syndrome but does not prevent their occurrence.

The use of plain or enteric coated aspirin (0.3 to 0.6 g per dose) or enteric coated 
sodium salicylate (0.6 g per dose) distributed as needed during the day - in a person 
having no intolerance for these drugs - often gives the patient relief from his localized or 
generalized post-traumatic articular symptoms. Rarely, for the relief of articular pain, it is 
necessary to give additionally codeine (0.030 to 0.060 g per dose) or demerol (0.100 to 
0.150 g per dose), as required. Procaine hydrochloride infiltration of an injured joint 
region has not been used (33) (211), nor were intravenous procaine hydrochloride 
injections used (63).

Relative rest of the injured joints tends to hasten recovery from the delayed post-
traumatic articular syndrome, provided that there is daily movement of the joint, without 
weight-bearing, through the fullest possible ranges of active and passive movement. 
When the delayed posttraumatic articular syndrome occurs in a given joint region, it is 
often helpful to apply massive hot, wet, Epsom salt dressings (for 30 minutes 3 or 4 
times daily) to a large region, including and surrounding the injured joint. Moist heat 
seems to be more efficacious than dry heat, although it is often more convenient to use 
dry heat (heating pad, or heat from an electric incandescent bulb). With the use of moist 
or dry heat special care must be taken not to burn the patient. Certain types of massage 
administered to injured articular regions may be helpful in giving some patients 
subjective relief from localized post-traumatic articular symptoms. A patient who injures 
his joints and develops generalized delayed post-traumatic articular symptoms may 
have temporary relief from these symptoms by soaking in a tepid bath for 20 or 30 
minutes. In selected instances, a suitable type of body massage following the bath may 
give additional benefit.


Posture. Certain types of posture in sitting, standing; walking and working cause 
mechanical joint injury, regardless of the patient's clinical grade of joint dysfunction, 
whether or not he is receiving adequate niacinamide treatment. Often there is a 
correlation between the patient's posture and his symptoms of bodily fatigue and joint 
discomfort, pain and disability, and therefore the physician must constantly analyze the 
patient's static and dynamic postures and make appropriate suggestions for the 
correction of faulty posture. A few commonly occurring types of static and dynamic 
postural abnormalities are described below, together with suggestions for their 
treatment. No general discussion of posture is included, since a number of excellent 
descriptions of what constitutes good posture are available in the literature (33) (84) 

It was observed that many patients who were making satisfactory recovery from severe 
or extremely severe joint dysfunction in response to adequate niacinamide therapy 
(even those who had reached the level of slight joint dysfunction or no joint dysfunction) 
had continuance or worsening of symptoms referable to hip and knee joints and to the 
muscles of their lower extremities, and that objectively, recovery of movement in hip and 
knee joints lagged behind recovery of movement in other moveable joints. When it was 
recognized that these patients were continuing to use habitually the abnormal posture 
described below, even though therapeutically increased ranges of joint movement 
permitted more efficient walking posture, appropriate suggestions were made for the 
correction of improper postures. When the patient taking adequate niacinamide therapy 
adopted these suggested changes in walking posture, he experienced some immediate 
relief from his symptoms and, in time, when the recommended posture became 
habitual, he usually became entirely free from symptoms referable to his hip and knee 
joints and to his lower extremity muscles, and the rate of recovery in the ranges of hip 
and knee joint movement was accelerated. Now that patients are routinely advised, as 
described below, to modify improper walking posture at the outset of niacinamide 
therapy, the continuance or accentuation of this pattern of articular and muscular 
symptoms of the lower extremities is seldom seen, and recovery of movement in hip 
and knee joints parallels that of other joints in response to adequate niacinamide 

This commonly occurring postural abnormality of standing and walking results chiefly 
from sustained hypertonia of the quadriceps muscles, associated with various degrees 
of cocontraction (sustained hypertonia) of the flexor and adductor muscles of the thighs. 
At first this postural abnormality may occur only as an unconsciously adopted 
accompaniment of unresolved emotional problems, which initiate psychogenically in-
duced, sustained hypertonia of somatic muscle. In time, such postures and the 
sustained hypertonia of somatic muscle may become habitual, whether or not the 
patient continues to have unresolved emotional problems. In the standing position, the 
patient's muscles contract more forcefully than necessary to maintain his stance 
efficiently. In addition, the patient usually has increased pelvic tilt and increased lumbar 
lordosis, and holds his head in a forward position which accentuates the 
thoracicocervical curve. Any dorsal kyphosis the patient may have seems to become 
more prominent as a result of this abnormal posture. Often in this posture the patient's 
abdominal muscles become so lax that his abdomen becomes pendulous (6). In 
walking, the person with sustained muscular hypertonia tends to maintain the poor 
standing posture described above. In forward progression, he tends to inhibit the natural 
swinging movement of the arms. With each consecutive step, the ipsilateral trunk-thigh 
muscles elevate the thigh sufficiently to permit pendulum-like swinging of the entire 
ipsilateral lower extremity as a more or less rigid unit, with little or no associated knee 
movement. Upon simultaneous palpation of the anterior and posterior thigh muscles of 
the patient as he walks, it is possible for the physician to detect a high degree of 
cocontraction of antagonists and protagonists of the hip and knee joint movement 
without palpable relaxation of these thigh muscles during walking. It is tiring for the 
patient to stand and walk in the manner described above. He also experiences a sense 
of resistance to walking which he describes as dragginess, heaviness, weakness, 
unsteadiness and stiffness of the lower extremities. He may have pain, discomfort and 
stiffness in the muscles of his thighs, back and neck; there are often associated 
symptoms of discomfort, pain and disability in the hip and knee joints. In addition, the 
patient may have pain and discomfort in the joints of his lumbosacral region, in his 
upper thoracic spine, and in the cervical spine. He may have noticed that over a period 
of time he has become "round-shouldered," that it is hard for him to straighten up, and 
that his "stomach" has become more prominent. When such a posture is habitual for 
many years, the patient with joint dysfunction suffers from the steady state of the post-
traumatic articular syndrome, and is likely to develop arthritic changes in the various 
joint regions subjected to excessive mechanical trauma, resulting in part from improper 
alignment of joints, and in part from continuously sustained hypertonia of somatic 

Such a patient is shown how to modify 'his gait so that he consciously lifts his feet, 
raising and flexing each knee alternately with each successive step, instead of walking 
stiff-kneed. He may notice at once that walking in this way is relatively effortless and 
comfortable as compared with his usual gait, which caused his lower extremities to feel 
draggy, heavy, weak, unsteady and stiff, and his thigh muscles to feel painful and 
uncomfortable. With this correction in gait, simultaneous palpation of anterior and poste-
rior thigh muscles will indicate that there is alternately well-coordinated contraction and 
relaxation of the opposing thigh muscles. When, in addition, the patient learns to hold 
himself as tall as possible in standing, walking and sitting, he may lose his pelvic tilt, 
lumbar lordosis and anterior neck flexion. The patient must practice the therapeutically 
suggested alterations in posture so that ultimately he habitually uses those static and 
dynamic postures which cause the least injury to his joints, and as a result he will no 
longer be troubled with symptoms from this type of improper p05ture. When a patient 
has marked limitation in ranges of movement of hip and knee joints before niacinamide 
therapy is instituted, he is unable to correct his gait in the manner suggested. When 
niacinamide-induced recovery permits sufficient increase in hip and knee movement, 
this correction of gait is possible. Occasionally, irreversible arthritic joint changes are 
present which make this improvement in posture mechanically impossible. 

Sacro-iliac Joint Strains. A patient with a history of recurrent sacro-iliac strains is given 
certain suggestions concerning posture which are often helpful in preventing 
recurrences of such strains: he should avoid twisting his trunk in the performance of any 
physical act while standing with his trunk bent at an angle of 35 to 55 degrees with his 
thighs, since this maneuver is frequently the cause of sacro-iliac strain. He should not 
"cross his knees" when sitting. He should not stand asymmetrically with most of his 
body weight resting on one foot. He should sleep on a non-sagging bed.

High Heels. Women who wear high-heeled shoes are likely to have postural back 
strains caused by compensatory lumbar lordosis, pelvic tilt, flexion of the neck and slight 
bending of the knees - all of which are necessary to maintain balance in the erect 
posture when high heels are worn. Some women wearing high-heeled shoes may have 
a steady state of back fatigue, discomfort and pain from such postural strains, while 
others may have these symptoms only when they are on their feet a great deal, or when 
they carry unaccustomed weights. Symptoms from postural strain are accentuated by 
the alternate wearing of high-heeled and low-heeled shoes. Women are advised to wear 
slippers and shoes having heels of uniform height, preferably low or medium heels.

Lifts. Often patients who were obliged to wear lifts continuously on their shoes to 
alleviate hip and knee discomfort prior to adequate niacinamide therapy found during 
niacinamide-induced recovery of joint mobility that discomfort of hip and knee joints 
increased in severity. However, when the lifts were removed, this discomfort 

Obesity. The excess weight of the moderately overweight patient increases mechanical 
injury of the weight-bearing joints (hips, knees, ankles, small joints of the feet). The 
excess weight of the markedly overweight patient causes more severe mechanical 
injury of these joints and, in addition, during standing and walking the patient has 
postural strain from balancing his heavy, often pendulous abdomen, and develops 
associated articular symptoms of fatigue, discomfort and pain in various portions of his 
back. Adequate weight reduction is part of the treatment of such patients with joint 
dysfunction, and a prerequisite for this is often the successful resolution of the patient's 
emotional problems (23) (138).

Painful Feet. A patient with painful feet may adopt awkward bodily postures which 
subject many joints of the body to excessive mechanical injury.

It is not uncommon to find that considerable foot pain is caused by the wearing of shoes 
which have unevenly worn heels or projecting irregularities of the insoles. A patient who 
habitually dorsifiexes his toes while wearing shoes, often develops considerable 
discomfort of the feet and legs. When such a patient is made aware that he habitually 
dorsiflexes his toes, he can eventually break himself of this habit, and he will be free 
from discomfort from this source.

During the course of adequate niacinamide therapy, a patient with joint tilt, 
dysfunction may develop considerable pain and discomfort in the ball of the foot and in 
one or more of the four small toes of the feet even though he has continued to wear 
footgear (shoes, slippers, socks or stockings) which was comfortable previously. When 
one foot is significantly longer than the other, the foot pain experienced during 
niacinamide therapy may be more severe in the longer foot, or present only in the 
longer foot.

As part of the progressive retrograde changes of untreated joint dysfunction, over a 
period of years many patients develop in the four small toes mild, moderate or marked 
deformities, consisting of partial flexion of the interphalangeal joints, and partial 
extension of the corresponding metatarsophalangeal joints; thus, one or more of the 
four small toes of each foot are "curled" to various degrees. Where there is a significant 
disparity in the length of the two feet, the "curling" of the toes of the longer foot is the 
more pronounced than that of the shorter foot. Such "curled" toe deformities are much 
more common in women than in men, presumably because the higher heels and 
narrower toe caps of women's shoes are additional factors which mechanically favor the 
formation of "curled" toes. With niacinamide-induced articular improvement, there is a 
gradual "uncurling" of the deformed toes, with virtual lengthening of the feet which is 
particularly prominent on weight-bearing. Consequently, footgear of a size entirely 
comfortable prior to niacinamide-induced joint reconstitution becomes painfully short, 
with resultant injury to the feet. When such an injury has taken place, the patient often 
complains of pain, burning, throbbing and swelling in the ball of the foot. These 
symptoms usually are most severe on the plantar surfaces of the second, third and 
fourth metatarsophalangeal joints. Examination reveals redness, swelling, heat and 
exquisite tenderness to digital pressure on the ball of the foot. There may be swelling, 
pain and redness of the interphalangeal joints of the four small toes. The skin of the 
dorsolateral surfaces of the fourth and fifth toes near the interphalangeal joints may be 
irritated, swollen, painful and reddened from rubbing against the lining of the shoes, and 
at times there may be, in addition, secondary infection. Callusing of the skin of the ball 
of the foot, and corns in the rubbed areas on the toes are commonly found.

The patient is advised to stay off his feet for several days, to immerse his lower 
extremities in hot Epsom salt solution up to the mid-calf region for 30 minutes three or 
four times a day, and to obtain footgear correctly fitted to his "new" foot size, measured 
to his foot size when he is in a standing, weight-bearing. position. At any time the 
wearing of footgear that is too small will cause a recurrence of this type of foot 


CASE U, No.178, female, age 43, housewife, married.

This patient, who had slight dysfunction (Joint Range Index 88.1) without arthritis, 
complained when first seen that she had had daily, for a number of years, pain, swelling 
and stiffness in the joints of her hands, more marked at all times in the right hand than 
in the left hand. She was unable to attribute her discomfort and disability to any specific 
act which might have injured her joints. Her articular symptoms were always much 
worse on Wednesdays and Thursdays, and by the following Monday were noticeably 
better, although she was never completely free from joint discomfort.

Upon questioning, it was found that for many years she ironed every Monday for about 
five hours continuously. When she was asked to demonstrate her method of ironing, it 
was observed that she exerted strong and persistent pressure in gripping the handle of 
the iron tightly with the fingers of her right hand, and exerted a strong downward 
pressure with her right wrist as she moved the iron back and forth. The left hand 
grasped the edge of the garment tightly between thumb and forefinger as she stretched 
the cloth in the course of her ironing. She stated that three or four days after ironing, her 
chief discomfort in the right hand was in the wrist and in all of the joints of the thumb 
and fingers. In her left hand, pain was limited to the wrist and the joints of the thumb and 

Since there seemed to be a causal relationship between the method of ironing and the 
patient's joint symptoms, she was advised to distribute her ironing through the week so 
that she would do no more than one hour of ironing on any one day. She was also 
instructed to use no more than the minimal muscular force necessary to perform her 

After a month of such a program, she was free from articular pain, swelling and stiffness 
for the first time in many years. For three years she has had no difficulty referable to the 
joints of her hands and wrists, even though she continues to do the same amount of 
housework and ironing.

This patient had a post-traumatic pattern of persistent articular pain and disability 
resulting from repetitive episodes of mild joint trauma occurring every 7 days, with cyclic 
exacerbations of articular difficulties for 3 or 4 days after joint trauma was sustained.

CASE V, No.452, female, age 61, invalid, married.

When first seen, this patient had extremely severe joint dysfunction (Joint Range Index 
52.2) and severe rheumatoid arthritis, as well as a post-traumatic pattern of immediate 
and delayed articular pain, discomfort and disability resulting from a single episode of 
mild joint trauma.

She had performed what was for her the unusually difficult task of addressing 20 
envelopes for Christmas cards, holding the pen in her right hand. Ordinarily, her 
husband would have performed this service for her, but he was away on a business trip, 
and she did not wish to ask anyone else to relieve her of this obligation. When she 
completed her writing, she experienced uncomfortable cramps, fatigue and unusual 
stiffness in her right hand, which lasted for about 30 minutes. She was free from further 
unusual discomfort in her right hand until four days later, when she suddenly 
experienced severe, persistent articular pain and increased stiffness in the joints of her 
right thumb, first and second fingers, and, to a slightly lesser extent, in the joints of the 
fourth and fifth fingers. Her pain, articular swelling and stiffness persisted at a severe 
level for four days, with gradual subsidence of the delayed post-traumatic articular 
syndrome over a period of one month, which corresponded to her first month of 
niacinamide therapy. At the time of her second office visit, there was no evidence of the 
delayed post-traumatic articular syndrome.

CASE W. This 65-year-old woman accidentally cut the digitorum profundus tendon of 
her right forefinger 16 years before the photographs of Figure 35 were taken. At the 
time of the initial examination her Joint Range Index was 71.5, indicating moderate joint 

Since the accident, the right forefinger could be flexed to a limited extent, and was 
moved during the course of her daily work, but not to a sufficient degree to be useful in 
the performance of household tasks. Thus, the right forefinger was not exposed to the 
more severe mechanical joint in-juries of housework and psychogenically induced, 
sustained hypertonia of somatic muscle. This patient was extremely right-handed, and 
grasped her various household implements with great force, probably because she did 
not have full use of her right forefinger.

There was no clinical evidence of impairment of innervation or circulation to the right 
forefinger. Sensations of heat, cold, pain, light touch, vibration, motion and position 
were normal in all the digits of the right hand. All the digits of the right hand were equally 
warm, and of the same color (210).

Because the interphalangeal joints of the right forefinger had been subjected to little 
mechanical injury, they had no articular deformities. However, the joints of other digits of 
the right hand were markedly deformed, presumably because of repetitive mechanical 
joint injury incurred by the tight grasping of household utensils, and by psychogenically 
induced, sustained hypertonia of somatic muscle. There was marked limitation of 
movement of the interphalangeal joints of the deformed digits, but not of the 
interphalangeal joints of the right forefinger.

Certain food-induced articular and non-articular allergic symptoms which are described 
below may obscure partially or completely a patient's subjective appreciation of 
improvement in response to adequate niacinamide therapy, even though objectively 
satisfactory improvement in joint function is demonstrated by continuously rising values 
of the Joint Range Index on serial re-measurements of joint ranges. While these allergic 
reactions usually do not include any significant degree of limitation in ranges of joint 
movement, they may be responsible for considerable articular pain and discomfort, in 
addition to other symptoms of bodily discomfort. It is, therefore, of considerable 
importance in the medical management of a patient with joint dysfunction to distinguish 
between the symptoms of aniacinamidosis, which are ameliorated in time by adequate 
niacinamide therapy, and allergic syndromes which are ameliorated in time only by 
elimination of the offending allergen, or by hyposensitization to the offending allergen.

Although many diverse clinical manifestations of food allergy may occur in persons with
joint dysfunction, three syndromes occur frequently in response to the ingestion of an 
offending food or foods: (a) Allergic Pain Syndrome (223) (167) (221), (b) Allergic 
Fatigue Syndrome (223) (167) (152) (153), (c) Allergic Mental Syndrome (223) (167) 
(151) (152) (153) (220) (40) (166) (213) (31) (165). These syndromes are described 
below. (Rarely, the allergic pain syndrome occurred when there was an active dental or 
tonsillar focus of infection, and was alleviated when the source of infection was 
eradicated. Only three examples of such benefit were observed in this series of 455 

These syndromes may occur separately in various degrees of severity and chronicity, or 
in any combination, and may be associated with a number of allergic symptoms not 
specifically included in the description of these syndromes. Clinical manifestations of 
these allergic syndromes may appear almost immediately after the ingestion of an 
offending food material and may continue for a few hours or a few days; or they may 
appear after a latent period of 12-76 hours following the ingestion of the allergen, and 
continue for as long as two weeks, gradually decreasing in severity during this interval. 
The daily ingestion of an offending food or food material produces a more or less steady 
state of allergic symptoms, with some exacerbation of these symptoms soon after the 
ingestion of this food.

Clinical proof that a suspected food is responsible for a patient's allergic symptoms is 
obtained (a) when such symptoms disappear when the offending food material is 
completely excluded from his diet for a sufficient period of time (2-3 weeks), and (b) 
when there is a recurrence of the initial pattern of allergic symptoms upon ingestion of 
the offending food material soon after he has become symptom-free as a result of 
abstinence from the allergenic food for a sufficient period of time; i.e., before abstinence 
from the food has been sufficiently prolonged for hyposensitization to have occurred.

(In addition to these three syndromes of allergic food reaction, offending foods have 
caused in patients with joint dysfunction the following types of allergic symptoms, which 
could be produced by the ingestion of the offending food, and could be eliminated by 
complete avoidance of the offending food:

Skin: Hives, angioneurotic edema, chronic pruritus, chronic skin lesions
Mucous membranes: Angioneurotic edema, canker sores.
Eyes: Chronic conjunctivitis.
Head: Cephalgia, including migraine.
Respiratory tract: Sneezing, postnasal drip, vasomotor rhinitis, recurrent sore throats, 
recurrent colds, sinusitis, asthma.
Gastro-intestinal: Nausea, vomiting, abdominal pain and cramps, heartburn, water 
brash, diarrhea, bilious attacks.)

While the ingestion of any food material can produce allergic symptoms in allergic 
persons, certain foods (chocolate, citrus fruits, tomato, pineapple, whole wheat, corn, 
milk, eggs and nuts) seem to be the most frequent offenders in the production of the 
allergic syndromes described below.

An oral threshold dose of an offending food is defined as the smallest quantity of that 
food which, when ingested not oftener than once every two weeks, will produce allergic 
symptoms in a person sensitive to this food. An oral sub-threshold dose of an offending 
food is defined as that amount ingested not oftener than once every two weeks which 
will produce no clinically discernible allergic reactions in a person sensitive to this food. 
However, if sub-threshold doses of a single offending food are eaten daily by a person 
who is sensitive to this allergenic food in threshold doses, in a few days or weeks there 
may be precipitated a clinically obvious allergic reaction, which probably represents the 
summation of clinically inapparent allergic reactions which have reached an intensity 
exceeding the threshold for the production of allergic symptoms.

If sub-threshold amounts of several offending foods are eaten on the same day, an 
allergic reaction to these may occur, even though such foods when eaten separately on 
different days do not give rise to a clinically apparent allergic reaction. It has been noted 
that single sub-threshold doses of different offending foods ingested on consecutive 
days may precipitate a clinically obvious allergic reaction.

In many persons with severe food allergies, the amount of the offending food which 
precipitates clinically significant allergic reactions is so small that every trace of this food 
must be eliminated from the patient's diet if he is to have relief from his allergic 

When an offending food is eliminated from the diet for a sufficiently long period of time, 
the tolerance gained with clinical hyposensitization may be excellent and apparently 
unlimited; or it may be moderate and easily broken down, either by too frequent 
ingestion of the food in small or moderate amounts, or by the single ingestion of an 
excessive quantity of this food; or, the tolerance may be so slight that it may be easily 
broken down by the single ingestion of a very small amount of the offending food 

Whether or not the patient has a personal or family history of allergy, at any time he 
may become sensitized to any food and have any pattern of food-induced allergic 
symptoms, which may vary in severity, chronicity and extensiveness from time to time 
(158) (159) (160).

Transient sensitization to certain foods has been observed in many patients with upper 
respiratory infections ("colds") who have a continuance of their acute coryza, malaise 
and lymphadenopathy as a result of a practice widely used in the treatment of "colds," 
particularly, during the early days of the "cold," namely, the ingestion daily of a quart or 
more of such liquids as citrus fruit juices, pineapple juice, tomato juice, milk and choco-
late milk. When a person with a limited tolerance for these food materials takes these 
liquids in larger quantities than usual for him, his oral threshold dose is exceeded, and 
an allergic tissue reaction is produced which resembles that of "infectious colds." Often, 
this food-induced allergic reaction prolongs "cold-like" symptoms for several weeks. 
However, when the patient eats his usual diet and takes 8 to 10 glasses of water daily 
instead of large quantities of the above fluids, this food-induced allergic reaction is 
avoided and the patient recovers much more rapidly from his "cold."

Cyclic food resensitization is likely to occur when certain foods in season are eaten daily 
in ordinary or excessive amounts; e.g., tomatoes, citrus fruits, pineapple, strawberries, 
peaches, melon, corn; and hyposensitization is likely to occur when these foods are not 
in season, and the patient excludes them from his diet, or limits the amounts ingested. 
To avoid cyclic resensitization, an allergic patient is advised to vary his diet as much as 
possible throughout the year, and not to have too frequent or excessive ingestion of any 
one food (158) (159) (160).

Sometimes a patient with pollinosis will observe during his hay fever season that his 
reactions to known allergenic foods tend to be more severe, and that certain foods, 
which he could ingest with impunity at other seasons, give rise to allergic food reactions. 
Conversely, the ingestion of certain foods during his hay fever season may worsen his 
symptoms of pollinosis.

Extremes of environmental temperature occasionally increase the severity of the 
patient's reaction to the ingestion of an allergenic food.

A given food may cause allergic symptoms only when the patient is emotionally 
disturbed; or, a person who reacts to the ingestion of an allergenic food may react more 
violently if this food is ingested at a time when he is emotionally disturbed. Many 
patients suffering from severe allergic symptoms have considerable secondary anxiety 
concerning their allergic ailment, and often associated psychosomatic symptoms are so 
severe that they dominate the clinical picture, and the patient is considered to be 

Excessive ingestion or excessive retention of dietary sodium tends to make the allergic 
reaction to allergenic foods more severe (99).

In women, a cyclic variation in the allergic pattern has been noted, so that clinical 
evidence of food allergy may occur only during the two weeks before, but not during the 
two weeks after, the menstrual period; or, food-induced allergic symptoms may be 
present throughout the month, but accentuated during the two weeks before the period 
(223) (167).

Allergic Pain Syndrome. In certain allergic persons, the ingestion of a threshold amount 
of an offending food material causes primarily mild, moderate or severe generalized 
pain in somatic muscle, tendon, periosteum, and periarticular and articular structures. A 
patient experiencing the allergic pain syndrome avoids all unnecessary physical 
exertion, since ordinary physical activity causes him pain and discomfort. Physical 
examination may disclose tenderness to palpation of somatic muscle, tendon, 
periosteum and periarticular structures. When the blood pressure cuff is inflated during 
the measurement of blood pressure, the patient may spontaneously complain of severe 
pain in the muscles of his arm. Somatic muscle is hypotonic and feels flaccid. Active 
and passive movement of joints may cause articular pain. The pain of this syndrome is 
usually not alleviated by the ingestion of aspirin, and if the patient is allergic to aspirin, 
the ingestion of this drug may even be responsible for the initiation and continuance of 
his allergic pain syndrome. Body massage usually worsens his pain and discomfort. In 
persons having the allergic pain syndrome, relatively slight mechanical joint injury will 
evoke severe and prolonged symptoms and signs of the delayed post-traumatic 
articular syndrome.

Allergic Fatigue Syndrome. In certain allergic persons, the ingestion of a threshold 
amount of an offending food material causes primarily extreme muscular fatigue, which 
is often associated with cervical lymphadenopathy (rarely, generalized 
lymphadenopathy), lymphocytosis and hypothermia (although occasionally there is a 
moderate elevation in temperature). Physical activity intensifies this allergic fatigue, but 
prolonged rest does not relieve the patient's symptoms of fatigue.

Allergic Mental Syndrome. In certain allergic persons, the ingestion of a threshold 
amount of an offending food material causes primarily mental symptoms, including 
mental fatigue, depression and confusion. The person may complain of disagreeable 
"mental fogginess or haziness," "a feeling of partial anesthesia," or a "feeling of being 
drugged." Thought processes are slowed. The patient may have unwarranted irritability, 
unreasonableness, temper tantrums, loss of memory, inability to concentrate, 
restlessness, sleepiness (although occasionally insomnia is noted). The patient’s mental 
inertia may be so severe that he finds it difficult to make decisions about even 
uncomplicated matters. He vacillates, procrastinates, and has trouble in carrying out 
even the simplest plans that he has made. He may require long naps during the day 
and may sleep long hours at night without relief from such mental fatigue. He knows 
that "something is wrong" with him, and he can describe his pattern of mental 
symptoms, although usually he is reluctant to do so because such symptoms have been 
made light of by his family and friends. A patient may refuse to discuss his pattern of 
allergic mental symptoms with the physician at the time of the initial visit, fearing that 
such symptoms are indicative of mental disease (insanity). He often complains that "life 
is not worth living” feeling this way.

The allergic patient with this mental syndrome may be secondarily disturbed because 
his family and physicians consider him to be a chronic grumbler and complainer. He 
feels emotionally insecure because he has been unable to obtain therapeutic relief from 
his allergic symptoms. Often such a person, with the tentative diagnosis of 
"psychasthenia," "neurasthenia," "nervous exhaustion," "psychoneurosis," or 
"psychosomatic fatigue," is referred to a psychiatrist, who, after studying the patient, be-
lieves that the patient's problems are psychosomatic in origin, not realizing that food 
allergy has created a somatopsychic disorder, which can be corrected by the removal of 
the offending food material from the patient's diet, but not by psychotherapy.

A few patients with joint dysfunction have, in addition to the allergic mental syndrome, a 
primary neuropsychiatric disturbance. In such in-stances, treatment must include 
adequate niacinamide therapy, exclusion of the offending food material from the diet 
and expert psychotherapy.


Skin testing was rarely used in attempting to identify allergenic foods, since false-
negative scratch or intracutaneous skin reactions may be obtained for a given food or 
group of foods, the ingestion of which causes the patient to experience clinically 
important allergic reactions, and falsepositive skin reactions may be obtained for food 
materials, the ingestion of which is clinically well tolerated by the patient (167) (152) 
(153) (151) (158) (159) (160) (81) (150).

Elimination diets, especially the diets of Rowe (167) (171), were used and modified 
empirically as necessary in the attempt to rid the patient of his food-induced allergic 
symptoms. At times, it may be extremely difficult to select a basic elimination diet which 
will accomplish this. When symptoms due to food allergy are not abated in 7 to 14 days, 
the patient is probably allergic to one or more foods in the elimination diet. While an 
elimination diet containing few foods sometimes gives relief from allergic symptoms, the 
too-frequent ingestion of the small number of foods in such a diet favors sensitization of 
the patient to any of the allowed foods. When new foods are added to the patient's basic 
elimination diet after he has been free from his chronic allergic food symptoms for two 
weeks, the patient should keep an accurate food-symptom diary which permits the 
physician to assess the patient's clinical reactions to the ingestion of the newly added 
food materials. If any added food seems to be giving rise to allergic symptoms, its use is 
interdicted. The patient's elimination diet is liberalized as rapidly as possible by the 
addition of those foods which by trial he is able to ingest repeatedly without 
experiencing allergic symptoms. It is possible at any time for an allergic patient to 
become sensitized to foods that formerly he tolerated well, and when symptoms 
suggestive of allergic reaction to the ingestion of foods recur, it is necessary to resume 
the search for offending food materials.

The polypropeptan method (223) of specific desensitization to twelve basic foods was 
given a limited trial, and good results were obtained in some patients. The food-
symptom diary was useful in observing the clinical effects of specific desensitization, 
and the patient's reaction to the subsequent addition of new foods not included in the 
basic list of twelve foods. When the ingestion of new foods caused allergic symptoms, 
and specific propeptans were available for treatment, the patient was desensitized to 
these foods; when specific propeptans were not available, the use of these foods was 

The method of individual food-testing advocated by Rinkel and others (159) (155) was 
not employed.

At times the antihistaminics were employed as palliative measures in the treatment of 
hay fever symptoms and of certain pruritic skin conditions (hives, contact dermatitis). 
The chronic allergic food syndromes described in this volume did not seem to respond 
to treatment with antihistaminic drugs.

While it is tedious and time-consuming for the patient to keep an accurate food-
symptom diary, and for the physician to analyze such a diary, this method of clinical 
investigation has been most helpful in the identification of specific foods causing allergic 
symptoms, and in the evaluation of the patient's response to elimination of allergenic 
foods from his diet. Some patients were unwilling or unable to cooperate in keeping a 
food-symptom diary and in restricting their diet as suggested. About 70% of persons 
who had symptoms suggestive of chronic allergic food syndromes were willing and able 
to cooperate in this exacting program.

The diary is kept in a standard stenographer's notebook, with a central dividing line on 
each page. Each notebook page contains the record of one day only. The diet (including 
all snacks, condiments and food-tasting) and the time of ingestion of each meal are 
noted in sequence in the left-hand column of each page. The patient is instructed to be 
specific in his description of the types of food eaten and, wherever possible, to list the 
ingredients of such mixtures as soups and salads. In the right-hand column, the patient 
lists his complaints, including the time of onset, degree of severity and duration of 
symptoms. A diary which is carelessly kept or has days omitted is not reviewed. It is not 
considered desirable in most instances to study food-symptom diaries which are kept 
for less than one month.

Certain additional information included in the diary is of value in the analysis of the 
patient's allergic and non-allergic symptoms. The patient records his emotional upsets, 
since these may cause reactions to allergenic foods to seem more severe, or may be 
accompanied or followed by psychosomatic symptoms. Any unusual physical activity is 
recorded, since this often actuates a delayed post-traumatic articular syndrome which 
might otherwise be confused with certain types of chronic allergic food reactions. 
Women record the days of menstrual flow, so that any pre-menstrual accentuation of 
allergic or sodium retention symptoms can be detected.

Such a diary gives more objective and accurate information concerning the patient's 
pattern of symptoms than his verbal impressions of how he has felt for a given period of 
time. Through the use of the food-symptom diary, it is possible for the physician to 
analyze accurately the patient's clinical reactions to:

(a) the ingestion of threshold amounts of allergenic foods; 

(b) the elimination of allergenic foods from the patient's diet

(c) the re-introduction of allergenic foods after a period of abstinence, to test the degree 
of clinical hyposensitization to the offending food material, and to detect promptly any 
clinical evidences of resensitization to such foods; and

(d) the daily ingestion of sub-threshold amounts of allergenic foods for a sufficient 
period of time to produce summation effects.

In addition to data relative to allergic syndromes, objective analysis of the food-symptom 
diary yields other clinical information about the patient, and may be helpful in 
differentiating the symptoms of chronic allergic syndromes, delayed post-traumatic 
syndrome, sodium retention syndrome and psychosomatic syndromes. A carefully kept 
food-symptom diary indicates the regularity or irregularity of the patient's living and 
eating habits; the variety or monotony of his diet; his caloric intake; the relative amounts 
of protein, carbohydrate and fat in his diet; the quality and quantity of dietary protein; his 
vitamin and mineral intake; and his caffeine and alcohol intake.

The identification of offending foods is relatively simple when the diary shows days 
when the patient is entirely free from allergic symptoms, and is relatively difficult when 
the diary indicates that the patient is never free from allergic symptoms. When an 
offending food is eaten less often than once a week, the allergic symptoms following the 
ingestion of this food usually appear after a latent period of half an hour to 72 hours 
(usually 12-24 hours) and usually last from 4 hours to 4 days. When the patient's diary 
reveals that he is never without allergic symptoms, the only clues to the identity of the 
offending food material are obtained by noting variations in the intensity of symptoms. 
Slight intensification of symptoms usually follows soon after the ingestion of an 
offending food, and slight diminution in the intensity of allergic symptoms is noted when 
such offending food material is absent from the diet for a day or more. It is in such 
instances that the use of elimination diets or polypropeptan therapy is most helpful in 
alleviating the steady state of allergic symptoms. Once the patient has become 
symptom-free, the effects of the addition of new foods can be ascertained from a study 
of the food-symptom diary.

When analysis of the food-symptom diary suggests that the patient is having food-
induced allergic symptoms, recommendations are made that the suspected allergenic 
food material be completely eliminated in all forms from the patient's diet. The patient 
continues to keep his food-symptom diary so that the effects of restriction of suspected 
allergenic food materials can be observed. Specific dietary advice is always given to the 
patient so that, after exclusion of suspected foods, his diet is adequate in protein, 
calories and minerals. When milk and milk products are excluded from his diet for any 
prolonged period of time, suitable calcium preparations are administered to offset the 
resulting dietary loss of calcium. Patients who habitually use large amounts of salt in the 
diet or who seem to have symptoms resulting from excessive sodium retention are 
asked to limit their salt intake.

When a patient is allergic to many foods, usually only a few of the allergenic foods 
which cause his symptoms can be identified upon analysis of the first month's diary. 
Even when a few of the offending foods are eliminated from his diet, the subsequent 
food-symptom diary often shows one or more of the following alterations in the pattern 
of allergic symptoms:

(a) a lessening in intensity of symptoms, (b) longer intervals of freedom from such 
symptoms, (c) the elimination of certain allergic symptoms but not of others; e.g., the 
allergic pain syndrome may be eliminated, but allergic pruritus may persist. Such 
changes in the patient's allergic symptomatology may be noted usually within two or 
three weeks after the exclusion of the chief offending foods from his diet, although 
occasionally benefits may be noted from the exclusion of allergenic foods as early as 
the third or fourth day. Eventually, when all of the offending foods are eliminated from 
the allergic patient's diet, he becomes symptom-free, and the food-symptom diary may 
be discontinued. Should allergic symptoms recur, he is asked to resume keeping the 
food-symptom diary.

If the offending food is re-introduced into the patient's diet after several months of 
abstinence, his reaction to the ingestion of this food may be of the original intensity, or 
less severe, or absent, depending upon the degree of hyposensitization to the offending 
food which occurred in the time during which this food was excluded from the patient's 
diet. In most persons, in order to achieve complete clinical hyposensitization to the 
offending food, it may be necessary to exclude this food for a year or longer. Rarely, 
even with prolonged exclusion from the diet, there is no demonstrable clinical 
hyposensitization to an offending food (150) (167) (219).

When it has been demonstrated that a patient has become clinically hyposensitized to a 
single ingestion of a food which formerly caused allergenic symptoms, he is instructed 
to have this food infrequently, in amounts limited to average servings, in order not to 
become resensitized to this food (160) (199). He is advised not to have this food more 
than once a month for six months; for the next six months, not to have the food more 
often than once every two weeks; and thereafter, not to have the food more often than 
every fifth day. If at any time there is a recurrence of symptoms due to ingestion of this 
food, it must be excluded from the diet to permit clinical hyposensitization to take place 

Sometimes, a patient wants to find out for himself whether he is really allergic to a given 
food, or whether it is his "imagination" or an idea of the doctor's. When he ingests the 
allergenic food before hyposensitization has occurred, he has his usual allergic 
symptoms. However, he will not have allergic symptoms in response to the ingestion of 
this food if he has become hyposensitized.

Although suggestion may play a part in the production of the allergic patient's symptoms 
and in his relief from symptoms following the exclusion of allergenic foods from his diet, 
the reaction of truly allergic persons, who are markedly sensitive to a given food, is 
predominantly due to bodily changes produced by the ingestion of allergenic food 
materials. This becomes strikingly clear when such a patient inadvertently and 
unknowingly ingests an allergenic food material, and subsequently develops his typical 
pattern of allergic symptoms (233) (22) (61) (93) (151) (152) (153) (184).

Although a patient may complain that a diet which eliminates certain offending foods is 
monotonous, analysis of his diet when his choice of foods is unrestricted is likely to 
show little or no variety in his daily menus. An emotionally well-adjusted person is 
usually able to tolerate dietary restrictions without developing anxiety, even though 
essential or favorite foods may be interdicted. Sometimes a person who has developed 
excessive guilt in response to certain life situations seems to welcome food restriction, 
since symbolically this constitutes punishment for his real or fancied sins.

Certain patients are unable to cooperate adequately in the investigation and treatment 
of their allergic food syndromes because of their emotional disorders; e.g., a patient 
may develop considerable anxiety in response to dietary restriction of important or 
unimportant foods, perhaps because deprivation of food symbolizes a threat to his 
security and re-activates old, unresolved conflicts, and he will drop treatment; or, a 
patient who has secondary gains from the continuance of his allergic symptoms may 
protest that he will "do anything to feel well," but he impedes in every possible way the 
efforts of the physician to work out a solution to his allergic problems. Treatment of the 
chronic allergic food syndromes of such patients will not be successful until the basic 
emotional disorder has been corrected by psychotherapy (218).


CASE AA. This case history demonstrates the clinical effects of the ingestion at different 
times of various amounts of an offending food, to which the patient was moderately 
allergic, and subsequent hyposensitization resulting from abstinence from this food for a 
sufficiently long period of time.

A 52-year-old widow complained of severe headaches recurring cyclically every Sunday 
for many years, and occasional milder headaches at other times. These headaches had 
not been modified by her uneventful "change of life," which occurred when she was 46 
years old. Every Sunday morning she awoke with a violent, throbbing bitemporal 
cephalgia (headache) associated with photophobia, nausea and vomiting. The severe 
headache persisted for 24 hours, and was succeeded by dull head discomfort persisting 
for as long as 48 hours. No previous medical measures had prevented the cyclic 
recurrence of her headaches or had given her appreciable relief from the pain and 
associated discomfort of this type of cephalgia.

She was asked to keep a food-symptom diary for one month. This record revealed that 
every Saturday night she ate as many as fifteen pieces of chocolate candy during the 
course of a weekly bridge game, although at other times during this month she did not 
eat chocolate. On the basis of her food-symptom diary, it was suspected that chocolate 
was the chief offending food material. Upon advice, she eliminated chocolate 
completely from her diet for two weeks, during which interval, for the first time in 10 
years, she was free from her usual Sunday headaches and associated symptoms. As a 
confirmatory test, she re-introduced chocolate into her diet, and reported that ap-
proximately 12 hours after the ingestion of 10 pieces of chocolate candy she 
experienced her usual severe cephalgia with associated nausea and vomiting.
Thus, it was confirmed clinically that chocolate was the offending food: 

(a) by the absence of her headaches upon the exclusion of chocolate from her diet, and 

(b) by the reappearance of her usual severe cephalgia upon re-introduction of a given 
amount of chocolate into her diet before clinical hyposensitization had taken place.

The patient cooperated over a period of many months in a sequential clinical 

1) to determine the smallest oral dose of chocolate which would cause her usual 
headache; i.e., the amount of chocolate that was the threshold oral dose for the 
production of her usual allergic symptoms:

When she had abstained from chocolate for two weeks and was free from her usual 
headaches during this interval, the smallest amount of chocolate ingested at one time 
which produced her usual headaches after a latent period of approximately 12 hours, 
was four squares of a popular chocolate bar.

2) to determine that oral dose of chocolate ingested once every two weeks which was 
sub-threshold for the production of her allergic symptoms; i.e., the amount of chocolate 
ingested once every two weeks that was insufficient to cause her headaches:

When she had abstained from chocolate for two weeks and was free from her usual 
headaches during this interval, she was able to eat three squares of chocolate once 
every two weeks for three successive two-week periods without precipitating her usual 

3) to demonstrate that in time the ingestion of sub-threshold doses of chocolate under 
certain conditions caused the appearance of her allergic symptoms.

When she had abstained from chocolate for two weeks and was free from her usual 
headaches during this interval, the daily ingestion of one square of chocolate for four 
successive days caused no clinical symptoms until the fifth day, when she awakened 
with her usual severe headache.

For the next two-week period, she abstained from chocolate and was free from her 
usual headaches during this interval. Then she ate three squares of chocolate on one 
day, without experiencing any clinically apparent allergic reaction. When she repeated 
the same oral dose of chocolate four days later, she developed her usual severe 
headache on the following day.

In this instance, it would appear that eventually the threshold necessary for the 
production of her allergic symptoms was exceeded as a result of the summation of 
clinically inapparent allergic reactions following the repetitive ingestion of sub-threshold 
amounts of the offending food.

When chocolate was excluded in all forms from this patient's diet for one year, during 
this time she was completely free from headaches, and became sufficiently 
hyposensitized so that she could eat four or five pieces of chocolate candy daily for 
weeks at a time without experiencing headaches or other allergic symptoms.

CASE BB. This case history demonstrates the occurrence of the Allergic Fatigue 
Syndrome and the Allergic Pain Syndrome following the ingestion of an offending food 
to which the patient was severely allergic, and subsequent hyposensitization resulting 
from abstinence from this food for a sufficiently long period of time.

This 36-year-old physician experienced for more than 8 years severe and persistent 
generalized periosteal pain, excessive and persistent fatigue that was not relieved by 
rest, and recurrent afebrile attacks of swollen lymph nodes. These symptoms at 
irregular intervals reached such intensity that periodically he had to take to bed for a 
week or more, until there was some remission in his symptoms. 

On two occasions 9 and 10 years ago, he experienced two distinct severe episodes of 
classic acute infectious mononucleosis. Although his heterophile antibody test was 
strongly positive during the two acute attacks of infectious mononucleosis, it was 
negative subsequently. However, for at least 6 years, stained smears of his peripheral 
blood revealed the presence of atypical lymphocytes resembling those usually found in 
infectious mononucleosis (154).

He was studied over a period of many years by internists, allergists, hematologists and 
psychiatrists. Chronic afebrile brucellosis was excluded through a battery of tests (74). 
Skin testing indicated that he was allergic to a variety of inhalants and foods. Over a 
period of several years he was desensitized to various pollens and house dust with 
relief of his seasonal hay fever, but with no relief of his presenting symptoms of pain, 
fatigue and recurrent swollen lymph glands. The elimination from his diet for several 
years of a number of foods to which he showed strongly positive skin reactions (milk, 
eggs, wheat, nuts, lettuce, legumes) did not appreciably alter his chronic illness. It was, 
therefore, believed that his food allergies did not contribute to his chronic 

The psychiatrists doubted that his symptoms were the expression of serious 
maladjustments to life situations or hypochrondriasis, although they noted moderate 
anxiety about his health. The consensus of his attending physicians was that he had a 
chronic recurrent type of infectious mononucleosis. He was advised to "take it easy, to 
adopt a philosophical attitude" toward his illness, and take it in his "stride."

During the meat shortage in 1944, for a period of several months this patient had a 
"spontaneous" remission from his illness. He was astonished and delighted to feel well 
for the first time in more than 8 years. However, he did not realize at the time that this 
period of freedom from symptoms corresponded exactly to the interval during which he 
ate no beef. (Previous skin-testing to beef had given a negative reaction both by the 
scratch and intracutaneous methods.) After several months of a beef-free diet, he ate 
his first beef-containing meal, and immediately there was a recurrence of his Allergic 
Pain Syndrome and Allergic Fatigue Syndrome and lymphadenopathy. Following the 
ingestion of this beef-containing meal, there was for 10 days no appreciable decrease in 
the intensity of his allergic symptoms.

This patient was advised to abstain from beef except for a test meal of beef to be taken 
once every 6 months. After 6 months of abstinence from beef, he was symptom4ree 
until he ingested a beef-containing test meal, which again caused a recurrence of his 
allergic symptoms, this time lasting only 3 days.

For another six-month period of abstinence from beef, he was symptom-free, until he 
ingested his next beef-containing test meal, which was followed by an allergic reaction 
lasting only 36 hours. After the next beef-free and symptom-free six months, the 
ingestion of a beef-containing test meal caused a recurrence of his allergic symptoms 
lasting only 8 hours. Finally, after 6 months more of abstinence from beef and freedom 
from allergic symptoms, the next ingestion of a test meal of beef caused no subjectively 
discernible allergic reaction.

During the 2 ½ years in which he abstained from beef (save for single test meals of beef 
every 6 months) there was a progressive clinical hyposensitization to beef, as indicated 
by a gradual decrease in the intensity and severity of the beef-induced allergic 
reactions. Future study will indicate whether or not clinical hyposensitization is 
sufficiently complete so that beef may again be introduced into his diet in moderate 
amounts at weekly or bi-weekly intervals without causing re-sensitization to beef and a 
recurrence of this patient's Allergic Pain Syndrome, Allergic Fatigue Syndrome and 

CASE CC. This case history demonstrates the occurrence of the Allergic Mental 
Syndrome in response to the ingestion of an offending food, and the absence of this 
syndrome upon exclusion of the offending food from the diet.

This 19-year-old college girl had an excellent academic record for her freshman and 
sophomore years, being in the first 10 per cent of her class scholastically. Early in the 
first semester of her junior year, she noticed for the first time that she was foggy 
mentally and forgetful, and that it was difficult for her to concentrate on her studies, as a 
result of which she fell behind in her required class work. After a few weeks, her mental 
fatigue became so severe that she frequently overslept in the morning, missing classes. 
There was no lessening in the intensity of her mental fatigue as a result of extra sleep, 
and she often felt "drugged" on awakening. Frequently she was so sleepy in the 
afternoon that she had to take long naps.

In an attempt to overcome her deficiencies in her school work, she gave up all social 
activities, no longer having "dates" or going to the movies; instead, she devoted all her 
time to study. She became emotionally upset when she realized that course material 
that should have been easy for her to master, was not; and that she could not recall 
things which she had learned and understood well at an earlier time. She was failing in 
her school work, and had received notice from the Dean's office that she was taking 
excessive class cuts.

Before Thanksgiving she was advised by the Dean to consult a psychiatrist in order to 
determine the cause of her recent scholastic inadequacies and the cause of the recent 
changes in her personality which had been noted by instructors.

When she was first seen, she volunteered that she was afraid she was losing her mind. 
Her history revealed that during the last semester of her sophomore year she took a 
course in nutrition and decided to improve her protein intake by adding eggs to her diet, 
in spite of the fact that previously she had disliked eggs and always avoided eating 
them. Accordingly, during the first semester of her junior year, she forced herself to eat 
one or two eggs daily.

Upon questioning, it became apparent that her troubles in college began soon after the 
introduction of eggs into her diet. In view of this, she was asked to stop the ingestion of 
eggs and all egg-containing foods. She was also asked to keep a food-symptom diary 
(which proved to be unnecessary, since within 2 weeks after the exclusion of eggs from 
her diet, she again felt mentally alert, was free from the disagreeable fogginess and 
sleepiness, and was able to do her school work easily and efficiently). In spite of her 
poor scholastic showing during the beginning of the first semester, she was able to 
complete the first semester of her junior year with a B-plus average.

This patient has not been significantly desensitized to eggs or egg-containing foods 
after two years of abstinence from these foods.

CASE DD. This case history demonstrates the occurrence of the Allergic Pain 
Syndrome in response to the ingestion of a number of offending foods to which the 
patient was severely allergic, and the absence of this syndrome upon exclusion of the 
offending foods from the diet.

Since the age of 10, this 35-year-old housewife had not been free at any time from 
generalized subcutaneous edema and severe bone, joint and muscle pain. These 
symptoms were cyclically increased in intensity during the 10-day interval preceding her 
periods, and also seemed to be aggravated by weather changes. She did not complain 
of physical or mental fatigue, and had no mental symptoms save for premenstrnal 
tension. Her basal metabolic rate was within the normal range. She had been studied 
and treated by many physicians over a period of many years without obtaining even 
slight relief from her symptoms. Most of the physicians thought she had some form of 
chronic "rheumatism," and in addition that she suffered from hypochondriasis.

Physical examination disclosed that she had moderate joint dysfunction, which 
responded satisfactorily to the. subsequent institution of therapy with adequate amounts 
of niacinamide, but her syndrome of subcutaneous edema and pain was not materially 
affected by this treatment.

The premenstrual accentuation of her subcutaneous swellings and pain and 
premenstrual tension were controlled by a moderately low-sodium diet throughout the 
month, supplemented by 1 g of enteric coated ammonium chloride three times a day 
after meals and at bedtime, which was administered daily for the two weeks preceding 
her periods. Because her symptoms of pain persisted, even though her Joint Range 
Index increased satisfactorily over a period of time in response to niacinamide therapy, 
and even though the premenstrual accentuation of her symptoms was prevented by a 
low-sodium diet, an allergic cause for her symptoms was sought and found.

Analysis of her food-symptom diary over a period of several months indicated that she 
was severely allergic to wheat, eggs, pork and nuts. When these foods were excluded 
from her diet for 3 weeks, she became completely free from subcutaneous edema and 
bodily pain for the first time in her life that she could remember.

Adequate niacinamide therapy caused satisfactory improvement in the Joint Range 
Index, but did not alleviate the Allergic Pain Syndrome. Salt restriction alleviated only 
the symptoms due to the salt-retention syndrome. Exclusion of allergenic foods from the 
diet relieved the Allergic Pain Syndrome. Thus, in order for this patient to feel well, it 
was necessary to institute the proper medical treatment for three separate clinical enti-
ties: joint dysfunction, sodium retention syndrome and food-induced Allergic Pain 

CASE EE. This case history demonstrates the occurrence of the Allergic Fatigue 
Syndrome in response to the ingestion of a number of offending foods to which the 
patient was severely allergic, and the absence of this syndrome upon exclusion of the 
offending foods from the diet.

This 20-year-old male, a college senior, complained for 3 years of persistent physical 
weakness and exhaustion. He also had at times swollen neck glands. Although he was 
so tired at times that he was unable to attend classes, he had no difficulty in mastering 
his course work, and his scholastic record was excellent.

Over a period of several years, studies in the college Health Service gave no positive 
evidence for active tuberculosis, brucellosis or infectious mononucleosis as a cause of 
his fatigue. Physical examination showed that he had a slight grade of joint dysfunction, 
and that his muscles were hypotonic and weak. His joint dysfunction responded to 
adequate treatment with niacinamide, but his physical fatigue and weakness and his 
muscle hypotonia did not improve.

A study of his food-symptom diary showed a daily ingestion of chocolate and tomato-
containing foods. Clinical proof was obtained that chocolate and tomato were the chief 
offending substances. Within 10 days after eliminating these foods from his diet, he had 
complete relief from his physical fatigue and muscle hypotonia. Subsequently, there 
were no recurrences of his symptoms, save when occasionally he "forgot" and ate the 
offending foods.


Certain patients have complaints of bodily discomfort which disappear when the sodium 
content of the body is decreased by appropriate therapy, and recur whenever excessive 
sodium retention recurs. It is believed, therefore, that these symptoms are the result of 
excessive retention of sodium in the body, whatever the cause of this may be (216) 

It is well known that excessive sodium retention (as well as chloride and water retention) 
occurs cyclically in women who have premenstrual tension, and that excessive 
ingestion of sodium in the diet or in medicaments accentuates premenstrual tension. 
Any or all of the following symptoms and signs may occur in a mild or severe form 
starting 10-14 days before the onset of the period, and usually subside during the period 
or immediately thereafter: gradual enlargement, swelling and bloating of the body so 
that garments become uncomfortably tight; a gain of 2-5 pounds in weight, which is lost 
soon after the period begins; myalgia, arthralgia, backache, cephalgia (including 
migraine), nausea, sensations of intestinal bloating, pelvic discomfort, labial itching; 
emotional instability (including nervousness, touchiness, crying spells, irritability, 
quarrelsomeness, dopiness and depression); excessive fatigue, inability to concentrate, 
impaired memory, clumsiness, insomnia, hyperkinesis, erratic behavior, increased 
sexual desire. There may be noticeable edema of the face and various portions of the 
body. The breasts are usually enlarged and tender to palpation, and somatic muscle 
and periosteum are likely to be tender to digital palpation.

In most other clinical forms of sodium retention the symptoms and signs are less severe 
and less extensive than those found in severe premenstrual tension, and consist chiefly 
of arthralgia, nervousness, insomnia, dizziness and increased blood pressure (65) (142) 
(143) (190) (222) (128). Sodium retention of a degree sufficient to cause symptoms may 
occur in persons who are ingesting excessive amounts of sodium. However, some 
persons have a significant degree of sodium retention with even a moderate intake of 
sodium. Reduction of excessive amounts of sodium in the body by appropriate therapy 
gives complete relief from the above symptoms, and in some persons there may be a 
decrease in blood pressure as a result of salt restriction.

With excessive sodium retention, there may be an accentuation of symptoms due to 
coexisting complicating syndromes (the delayed post-traumatic articular syndrome, 
chronic allergic food syndromes, and psychosomatic syndromes). When the sodium 
content of the body is decreased by therapy, there is a decrease in the severity of the 
symptoms due to sodium retention, and usually a decrease in the intensity of symptoms 
of the coexisting complicating syndromes.

The symptoms and signs of excessive sodium retention (64) (88) (139) are usually 
controlled when the patient limits the amount of salt in his diet, drinks 8 to 10 glasses of 
water daily and, when indicated, takes enteric coated ammonium chloride tablets (1 to 3 
g,  t.i.d. p.c. and h.s.)

Although severe sodium chloride restriction has been known to cause symptoms which 
are usually alleviated by the administration of salt (175) (28), no patient in this series 
who was treated for the sodium retention syndrome developed such symptoms.



Either before treatment for joint dysfunction was undertaken or subsequently, most 
patients included in this study suffered at one time or another from a variety of transient 
or persistent, mild, moderate or severe symptoms of bodily discomfort, which were 
interpreted as being collateral to primary mental tension (43) (235) (203) (49). 
Psychosomatic symptoms occurring during the course of treatment of joint dysfunction 
often caused the patient much subjective discomfort, and obscured his appreciation of 
improvement in joint dysfunction in response to adequate niacinamide therapy, even 
though satisfactory improvement in joint dysfunction was demonstrated objectively by 
continuously rising values of the Joint Range Index as determined serially during the 
course of adequate niacinamide therapy.

In most instances, the existence of psychosomatic illness (where symptoms of bodily 
discomfort are caused, intensified or perpetuated by mental influence) can be validated 
when the symptoms of bodily discomfort are consonant with the emotional problems of 
the patient (235) (50) (110) and disappear upon satisfactory discharge of the inciting 
mental tension; and when, upon careful clinical investigation, no evidence can be found 
for co-existing somatic disease which could produce such symptoms (237). In some 
instances, symptoms of bodily discomfort initiated by mental tensions may persist as 
habit patterns even when the inciting mental tensions are adequately discharged. In the 
treatment of a patient with such symptom-producing non-purposive habit patterns, the 
patient must be re-educated before these mechanisms of habitual behavior can be 
extinguished (100) (122).

It is not uncommon to find in a person with psychosomatic symptoms the coexistence of 
clinically significant asymptomatic or symptom-producing somatic disease. Symptoms of 
primarily somatic disease may or may not be similar to symptoms of a coexisting 
psychosomatic illness. When the symptoms due to concurrent somatic disease and 
psychosomatic illness are similar or identical, the relative relief obtained from removal of 
the psychosomatic component by psychotherapy may be such that the patient 
temporarily feels greatly benefited. If the patient and physician are satisfied with such a 
therapeutic result, serious somatic disease may be overlooked until it produces such 
symptoms and signs that its presence cannot be ignored, and by this time, the somatic 
disease process may not be amenable to any form of therapy.

While patients differ in the degree of susceptibility to externalization of their mental 
tensions through psychogenic symptoms of bodily discomfort, any patient may develop 
psychosomatic symptoms either transiently or persistently if the mental stresses to 
which he is exposed are for him sufficiently severe, sufficiently prolonged, or sufficiently 
repetitive (111) (110) (2) (3).

Once psychosomatic symptoms occur, patients differ in their ability to become free from 
such symptoms, either spontaneously or through directed therapy. It is well known that 
symptom-producing alterations in visceral function and in somatic muscle tone are the 
usual accompaniments of many emotional states, such as anxiety, fear, panic, 
resentment, hostility and rage (27) (241) (133) (55). In acute and subacute emotional 
states, symptoms of bodily discomfort produced by psychogenic alterations in visceral 
function often preponderate, while in chronic emotional states, symptoms of bodily 
discomfort produced by psychogenically sustained hypertonia of somatic muscle 
preponderate. In acute, subacute and chronic emotional states, the patient's collateral 
emotional response to the unpleasant sensory concomitants of psychogenically altered 
bodily function produces a heightening of his total emotional tensions and an increase in 
the severity, extensiveness and duration of his psychosomatic symptoms (29) (182). 
When these psychogenic symptoms of bodily discomfort become severe enough, they 
often serve to deflect the patient's attention from his primary mental tension and anxiety 
to his collateral somatic dysfunction. Thus, temporarily he may feel relieved, and may 
not be disturbed consciously by his primary mental tension, although in time he may de-
velop secondarily considerable mental tension and anxiety concerning his continuing 
psychosomatic symptoms and their possible meaning to his health and his future 
security. Before instituting treatment of the patient with psychosomatic symptoms, the 
physician should try to evaluate the part played by the psychosomatic symptoms in the 
maintenance of the patient's biodynamic homeostasis, and the emotional resources 
which the patient could muster to deal with his basic emotional problems if his 
psychosomatic symptoms were prematurely removed by ill-advised psychotherapy.

A patient who is usually well-adjusted may have psychosomatic symptoms only when 
he is suffering from an acute or subacute tensional situation, but a severely 
psychoneurotic patient may never be entirely free from reciprocally interacting 
psychogenic symptoms of bodily discomfort and mental tensions. In some patients the 
severity, extensiveness and subjective awareness of psychosomatic symptoms may 
seem directly proportional to the severity of the existing mental stress, while in others no 
such direct relationship obtains. In some patients, exposure to any degree of mental 
stress always seems to call forth the same fixed pattern of psychosomatic symptoms 
and mental tensions. Psychosomatic symptoms may be absent, or present at low levels 
of intensity, extensiveness and psychic awareness when the patient's chronic 
psychoneurosis is compensated, and are usually present at high levels of intensity, 
extensiveness and psychic awareness when the psychoneurosis becomes 
decompensated. Usually, the more aware the patient is of his psychosomatic 
symptoms, the less aware he is of his primary mental tensions; indeed, if he is aware of 
any mental tensions at all, he usually attributes these to his intense concern about his 
presenting psychosomatic symptoms and their meaning to his health and future 

A patient with joint dysfunction (with or without obvious arthritic deformities) who also 
has a compensated psychoneurosis will tolerate a more or less steady state of 
reciprocal emotional and psychosomatic discomfort which he considers to be normal for 
him. The continuance of his troublesome symptoms and the secondary gains he derives 
from his chronic compensated psychoneurosis may in time afford him a considerable 
degree of emotional security and satisfaction. It is only when his psychoneurosis be-
comes decompensated that such a patient will develop intolerable anxiety and 
intolerable psychosomatic symptoms, and when his psychoneurosis again compensates 
either spontaneously or through psychotherapy, he will revert to his original steady state 
of tolerable emotional and psychosomatic discomfort, and he may feel that he has been 
cured and is normal again. Frequently the treatment of psychogenic syndromes of 
bodily discomfort is rendered difficult by the unwillingness of the patient with such syn-
dromes to cooperate in an investigation of the mental and emotional factors which are 
etiologically related to his presenting psychosomatic illness.

While it is not the purpose of this volume to describe all types of psychosomatic 
symptoms observed in the group of patients treated for joint dysfunction, in this section 
consideration will be given to articular and nonarticular psychosomatic symptoms 
arising directly or indirectly from psychogenically induced, sustained somatic muscle 
hypertonia, and appropriate suggestions for the management of this syndrome will be 

In planning appropriate treatment for psychogenically induced, sustained hypertonia of 
somatic muscle, the physician should try to understand the basis of the patient's 
psychosomatic symptoms m terms of the interactions of endogenous and exogenous 
operational factors which made the patient the person that he is, predisposing him to his 
illness, initiating his psychosomatic disorder, and causing his illness to persist (168).


In the clinical analysis of the patient's health problems (236) (66) (235) (239) (100) (117) 
(157), coexisting psychic, somatic psychosomatic and somatopsychic phenomena were 
regarded as dynamic, interrelated and integrated manifestations of the functioning 
human psychobiologic unit. However, certain techniques were primarily employed in the 
study and treatment of psychic aspects of disease, and other techniques were primarily 
employed in the study and treatment of somatic aspects of disorders. Combinations of 
these techniques were used to identify, study and treat (a) psychosomatic disorders, in 
which symptoms of bodily discomfort are collateral to primary mental disorders, and 
usually disappear when aberrant mental functioning is corrected, and (b) somatopsychic 
disorders, in which mental disorders are collateral to primary somatic disorders, and 
usually disappear when aberrant somatic physiology is corrected.

The clinical study of each patient was performed unhurriedly in order to give the patient 
adequate time to express his complaints fully, and to give the examiner sufficient time to 
collect the necessary clinical data, and, upon reflection, to make the necessary clinical 
correlations, and to evolve a reasonable plan of treatment for the patient. Throughout 
the clinical study, without appearing to do so, the physician continuously observed and 
evaluated the verbal and somatic reactions which exteriorized some of the patient's 
emotional responses during the elicitation of the history, during various procedures of 
the physical examination, and during the summary of the patient's health problems and 
the recommended therapy.

As an approach to the understanding of the patient's emotional and psychological 
problems, during the course of the initial interview, information was obtained, 
sometimes by indirection, concerning many matters which were independent of joint 
dysfunction but were often responsible for the evolution and persistence of the patient's 
presenting attitudes, moods, sentiments, conflicts and psychosomatic symptoms. Such 
information included data concerning the patient's childhood, family problems, home life, 
educational background, social background, religious background, emotional 
background, worries and plans concerning the future, his work experience, adjustments 
to various life situations (including his illness), the patient's interpretation of the cause 
and significance of his symptoms and illness, the persons he has known or heard of 
who have similar symptoms, and any apparent temporal relationship between the 
occurrence of emotionally upsetting events and the onset of his symptoms. The patient 
was encouraged to summarize what he considered to be his "good and bad points," and 
the 'best and worst periods" of his life. An attempt was made to assess his attitude 
toward his failures and successes, toward his mental and physical handicaps, toward 
his "sacrifices" for the benefit of other members of his family, and toward ailing 
members of his family. It was often helpful to know the patient's schedule of activities 
during an average day and week, and during weekends, holidays and vacations, since 
he may have symptoms only at certain times: at home, at work, in church, on a 
vacation, on weekends or holidays, when meeting or visiting certain individuals.

It is important to keep in mind that persons with the more severe grades of joint 
dysfunction who have psychogenic articular and non-articular symptoms often have 
repressed resentment, hostility, rage and aggressive-ness which are chiefly exteriorized 
by localized or generalized sustained hypertonia of somatic muscle (89). In the older 
age groups particularly, psychogenically induced, sustained hypertonia of somatic 
muscle is caused by fear of economic insecurity, of losing dominance in a family or 
business group, of having a ''serious'' illness (e.g., cancer, strokes, loss of mental fac-
ulties), and fear of dying (170).

It was the writer's aim to gather the raw material of the history by haviug the patient tell 
his story in a natural way, with only such comment or questions from the physician as 
were needed to indicate that the physician was sympathetically interested in the 
patient's problems, and to explore those portions of the medical history about which the 
physician wished to obtain more information. During the elicitation of the history, and 
subsequently, the greatest care was taken not to suggest to the patient the existence of 
clinical problems either by interrogation, comment or implication.

It was found that one of the most fruitful sources of information about the patient's 
emotional makeup was his behavior in the doctor's office. Often, his emotional reactions 
to the discussion of events, circumstances or persons were exteriorized by his 
mannerisms, by changes (or lack of appropriate changes) in his facial expression, by 
alterations in his voice, posture, color, neck artery pulsations, respirations; by 
aerophagia, by sweating, by crying, by his asides and by his gait. The patient's attitude 
toward the physician and his assistant sometimes gave valuable clues to certain of the 
patient's emotional problems. At times, clues to an emotionally charged situation were 
obtained during the interview; e.g., when the patient in the rnidst of a sentence "forgot" 
what he was going to say and couldn't "recall" it; when a patient abruptly terminated 
discussion of a given subject and was unwilling to resume such a discussion; when a 
patient made a spontaneous and revealing statement, followed by a prolonged 
discourse intended to correct any "false impression" the examiner may have received 
from the patient's initial statement; when a patient asked question after question about 
non-personal or personal medical matters or digressed, talking at great length about 
emotionally neutral subjects in order to avoid an emotionally painful topic of discussion; 
when a patient exaggerated or minimized the importance of certain matters in his life 

At times, a knowledge of patterns of symptom-language and a knowledge of 
fundamental dynamic patterns of certain psychosomatic disorders were helpful in 
interpreting the meaning of the patient's psychosomatic complaints and in facilitating the 
analysis of his central emotional problem (235).

The interpretation of symbolic body language is a valuable, but not infallible, guide for 
the physician in the identification of a patient's emotional reaction to some problem 
which he is facing. For example, psychogenically induced, sustained hypertonia of 
epicranial muscles which results in headache may indicate that the patient is faced with 
a situation for which there seems to be no satisfactory solution; increased jaw muscle 
tension may be the sign of determination to perform some difficult or unpleasant task; 
painful sustained muscle tension of the tongue and throat muscles may indicate that the 
person has something he wants to say, but can't; pain in the neck may symbolize the 
patient's preparedness for defensive or aggressive action; pain in the left pectoral 
muscle may be present when the person has sustained a loss; pressure in the anterior 
portion of the chest may indicate that the person is sad, grief-stricken or guilty; 
vaginismus may indicate a defensive reaction against having sexual relations; pain in 
the right upper extremity may indicate a repressed desire to strike someone; while 
unilateral thigh and leg pain may indicate that the person wishes to kick someone.

When one elicits data of a personal nature, allowance must be made (even in a non-
psychotic patient) for differences between reality and the consciously or unconsciously 
revised account which the patient gives the physician. Properly interpreted, such 
conscious or unconscious revision may be more indicative of the patient's emotional 
problems, prevailing moods and goal-direction than any "true" statement.

After the history was elicited and rapport established, the patient was routinely asked if 
he wished to talk about any additional matters. It was found that frequently a patient 
took advantage of this opportunity to reveal those personal, and often most troublesome 
problems, which he had refrained from mentioning earlier in the interview.

Next, the physical examination and routine laboratory studies were performed.
During the physical examination, no comment was made by the physician which might 
cause the patient anxiety. At no time during the physical examination was the patient 
led to believe that the examiner was unduly interested in any one part of the 
examination, or was giving unusual attention to any one part of the patient's body. The 
patient's apparent reaction to the physical examination was noted.

When the clinical study of the patient was completed, the findings were related factually 
in terms which the patient could understand. Care was taken not to suggest to the 
patient physical, emotional or mental disorders which he did not have. He was told how 
his health compared with what is judged by present-day standards to be "average good 
health" for his age and sex. He was given an opportunity to ask questions, and when 
necessary those points which were not clear to him were amplified and rephrased.
When correctable disorders were found, if these seemed to be of sufficient clinical 
importance, appropriate therapy was prescribed. When remediless disorders existed, 
the examiner always tried to apprise the patient of such findings in a manner which 
would give rise to the least amount of anxiety and, whenever possible, palliative 
measures were employed to make the patient more comfortable, to retard the progress 
of his disorder, or to prevent complications of disease (41). A patient with a remediless 
disorder was often comforted by the thought that even though there was not an 
efficacious treatment for his disease, medical progress was such that in time new 
discoveries might offer him or other sufferers a remedy for the correction of his disorder.

The objectives of the recommended program of medical therapy were outlined for the 
patient, and the expected response to such therapy was described. If special laboratory 
studies or additional clinical studies were recommended, the reasons for desiring them 
were explained to the patient.

Clinical study of the patient continued when he returned for necessary re-examinations, 
and the physician's initial impressions and conclusions concerning the patient and his 
health problems were modified as necessary upon further reflection, or when new 
clinical data became available. The clinical management of joint dysfunction was carried 
on as previously described, and concurrently other health problems which the patient 
presented were given appropriate treatment.


Although symptom-producing, localized or generalized hypertonia of somatic muscle 
may be caused by any etiologic agent which maintains the central excitatory state of the 
motoneurones innervating the somatic muscle region at their discharge level (36) (194), 
it is most commonly caused by psychogenically induced, sustained hypertonia of 
somatic muscle. Psychogenically induced, sustained hypertonia of somatic muscle 
gives rise to protean clinical manifestations, which may occur in persons with or without 
joint dysfunction, and with or without obvious arthritis. The localized or generalized 
patterns of symptoms resulting from such sustained hypertonia of somatic muscle at 
times may simulate well-known somatic disease patterns, although at other times they 
may not be typical of any known somatic disease. The patient who experiences articular 
and non-articular symptoms as a result of psychogenically induced, sustained 
hypertonia of somatic muscle often seeks medical advice because he mistakenly 
believes that he is seriously ifi with a somatic disease, and often develops considerable 
anxiety about the possible meaning of his illness (60) (232) (224) (75).

The syndrome of psychogenically induced, sustained hypertonia of somatic muscle may 
or may not occur in association with other psychogenic syndromes.

Localized or generalized psychogenically sustained postural hypertonia of somatic 
musculature often symbolizes the preparedness of the human psychobiologic unit for 
aggressive or defensive action against extrinsic or intrinsic noxious factors, with 
sulficiently strong concurrent central inhibition to prevent such completion of the 
required goal-directed action as would permit, at least temporarily, a satisfying 
discharge of both the prevailing somatic and psychic tensions (215) (241) (122) (133) 
(55). In this sense, psychogenically sustained hypertonia of somatic musculature is 
operationally a compromise adjustment of the human psychobiologic unit, and 
represents part of the dynamic pattern of somatization of unresolved conflicts, 
repressions, resentments, and indecisiveness. Psychogenically sustained somatic 
muscle hypertonia may in time become habitual as the adaptive response to even the 
most trivial threat to the patients emotional security, and may include substitutive 
behavior of various types, replacing inhibited goal-directed action. Even when the 
initiating psychic tensions responsible for the creation of the sustained somatic muscle 
hypertonia have been adequately discharged, the retention of hypertonic muscular habit 
patterns may result in a steady state of bodily discomfort which the patient in time 
comes to regard as being normal for him. Such a patient will complain only of 
exacerbations of his bodily discomfort when an old emotional or psychic tension is 
revived, or when he is exposed to a new emotional or psychic stress (25).

Psychogenically induced, sustained hypertonia of somatic muscle, when sufficiently 
intense, prolonged or repetitive, may cause the following symptoms and physical signs: 
fatigue, stiffness, aching, soreness, pain, paresthesias, limitation of joint movement, 
joint traumatization (including the evolution of the delayed post-traumatic articular 
syndrome), and, rarely, muscle spasm and muscle tremor. The symptoms and signs of 
psychogenically induced, sustained hypertonia of somatic muscle may vary from time to 
time in extensiveness, intensity, duration, repetitiveness, and are likely to be more 
severe when the environmental temperature is low than when it is high. In general, the 
more severe the patient's psychic tensions are, the more likely he is to experience 
irradiation of extensiveness, increased severity and increased awareness of symptoms 
of bodily discomfort and physical signs resulting directly or indirectly from 
psychogenically induced, sustained hypertonia of somatic muscle. Once symptom-
producing, sustained hypertonia of somatic muscle has been initiated by psychogenic 
influence, it may be maintained through psychogenic influence and/or through self-
exciting lower neuronal reflex arcs actuated by stimulation of afferent end organs within 
the substance of the contracting muscle itself and within the tendinous origins and 
insertions of the contracting muscle (137) (55) (242).

The validity of the concept that sustained hypertonia of somatic muscle may cause 
symptoms of discomfort has been established by others who used special techniques of 
study, including electromyography and procaine injections into the symptom-producing 
contracting muscles (242) (243) (217). In patients studied by the writer, the presence of 
sustained hypertonia of somatic muscle was inferred from characteristic symptoms and 
signs which were present when a sufficient degree of muscular hypertonia was present, 
and which were absent when this degree of sustained hypertonia disappeared.


Skull Muscles (242). A patient with psychogenically induced, sustained hypertonia of the 
epicranial muscles may complain of sensations of pulling, heaviness, soreness, 
tightness, "tight band around the head," scalp discomfort on combing the hair, small 
painful areas of the scalp, crawling sensations, or headache. These symptoms may 
occur unilaterally or bilaterally, and may be limited to the occipital, temporal, parietal or 
frontal regions, or to any combination of these regions.

A patient with psychogenically induced, sustained hypertonia of jaw muscles may 
complain of aching or pain in the teeth, gums, temporomandibular joints, jaw muscles, 
and may be aware of clicking sounds or full sensations in his ears. He may find it 
difficult to open his jaws widely. A person with complete upper and lower dentures may 
complain "even my false teeth hurt," and a person with partial dentures often complains 
that he is unable to get a comfortable denture. Patients with sustained hypertonia of jaw 
muscles often have extensive clinical and x-ray studies of teeth, sinuses and 
temporomandibular joints, which are usually negative.

A patient with psychogenically induced, sustained hypertonia of facial muscles may 
complain that his face feels swollen, mask-like, frozen, stiff, tender or tight. He may 
have burning, crawling, or tingling sensations in the face. A patient who frowns 
constantly may complain of feeling pressure, discomfort or fullness in the region of the 
bridge of the nose and glabella. Symptoms referable to sustained contraction of the 
orbicularis oris and orbicularis oculi muscles are described below, under Sphincter 

A patient with psychogenically induced, sustained hypertonia of tongue muscles may 
complain that his tongue feels sore, "stiff as a board," tired, or "1ike a piece of raw 
meat." Limited to the anterior and lateral aspects of the tongue there may be lingual 
pain, burning, tingling, abrasions (with or without secondary infection).

Neck Muscles (242). A patient with psychogenically induced, sustained hypertonia of 
neck muscles may have in the back of his neck, unilaterally or bilaterally, aching, pain, 
tightness, drawing sensations, pulling or burning sensations, with or without radiation of 
pain or discomfort upward toward the base of the skull and downward toward the upper 
thoracic spine. He may have stiffness and limitation of neck movement. With severe 
posterior neck pain there may be reflexly sustained, symptom-producing contraction of 
epicranial and facial muscles. Rarely, sustained hypertonia of anterior and posteri9r 
cervical muscles may cause symptoms suggestive of cervical radiculitis or of the 
scalenus anticus syndrome.

Sustained hypertonia of pharyngeal muscles may cause throat symptoms of tightness, 
soreness or dysphagia. Sometimes the patient will complain of pain limited to the region 
overlying the most lateral portions of the hyoid bone. Sustained hypertonia of intrinsic 
laryngeal muscles may cause the patient to complain of vocal fatigability, hoarseness, 
or poor control of voice (21). A patient with psychogenically induced, sustained 
hypertonia of pharyngeal, external laryngeal and anterior neck muscles may complain of 
a 'clump in the throat that can't be swallowed," and he may try to relieve his throat 
symptoms by repetitive swallowing, by clearing his throat or by brief, non-productive 

Chest Muscles. A patient with or without coronary artery disease who has 
psychogenically induced, sustained hypertonia of chest muscles may complain of 
heaviness, pressure, or pain in his anterior chest. He may complain of pain or pressure 
limited to the left pectoral muscles, and report that these muscles feel bruised, although 
he can recall no antecedent external injury to this region. He may have pain along the 
insertion of diaphragmatic muscle into the thoracic wall, usually on the left side (240). 
Respiratory dysrhythmias (including the hyperventilation syndrome) (46) (209) may be 
associated with such symptoms of chest discomfort.

Abdominal Muscles. Symptom-producing, psychogenically induced, sustained 
hypertonia of abdominal muscles occurs rarely, and causes soreness, tenderness or a 
"bruised feeling" in the contracting muscles.

Thoracic and Lumbar Vertebral Muscles. A patient with psychogenically induced, 
sustained hypertonia of muscles of the thoracic and lumbar spine may complain of 
stiffness, pain, limitation of movement of the spine and, rarely, radicular pain (180).

Extremity Muscles. A patient with psychogenically induced, sustained hypertonia of 
somatic extremity muscles may have discomfort which seems to originate in joints, 
periarticular structures, tendons, muscles, or any combination of these structures. There 
may be limitation of articular movement, stiffness, awkwardness in the use of 
extremities, joint swelling and pain, as well as muscular fatigue, aching, soreness and 
pain. The patient may complain of dysequilibrium in waliiing when sustained hypertonia 
of somatic muscle is preponderanily localized to the right or left side of the body. When 
walking, he may complain of hip and knee pain, and of dragginess, heaviness and 
stiffness of his lower extremities which results from sustained hypertonia of opposing 
co-contracting thigh muscles. Tight crossing of thighs in the sitting position may produce 
immediate or delayed symptoms of discomfort in the thigh muscles at the site of muscle 
compression. A patient in crossing his knees may exert prolonged pressure on the 
common peroneal nerve of the overlying leg, producing paresthesias in the sensory 
distribution of the nerve, and the feeling that the ipsilateral foot is heavy; rarely, 
complete external peroneal nerve palsy may develop from this source. Some patients 
under emotional tension habitually and unconsciously dorsifiex the toes while wearing 
their ordinary footgear and develop discomfort in the foot and anterior region of the leg.

Sphincter Muscles. Psychogenically induced, sustained hypertonia of somatic sphincter 
muscles may cause a variety of symptoms, depending on the sphincter region involved; 
e.g., sustained hypertonia of the orbicularis oculi muscles may give rise to feelings of 
eyestrain, fatigue, discomfort, paresthesias of the lids, excessive blinking, and 
cephalgia. Sustained hypertonia of the orbicularis oris muscle (with or without sustained 
hypertonia of the masseter muscles) may cause labial sensations of tightness, swelling, 
pain, and paresthesias (particularly, tingling). Tight apposition of the inner surfaces of 
the lips against the labial surfaces of the teeth may cause the patient to complain of 
mucous membrane abrasions, with or without secondary infection. Sustained hypertonia 
of the urinary sphincter muscles may result in difficulty in starting the urinary stream. 
Sustained hypertonia of the vaginal sphincter muscles, with or without associated 
sustained hypertonia of other perineal muscles, may give rise to symptoms of 
vaginismus, vaginal paresthesias, dyspareunia. Sustained hypertonia of the somatic 
muscle of the anal sphincter (136), with or without associated sustained hypertonia of 
other perineal muscles, may cause constipation, sensations of incomplete evacuation of 
stool, rectal pain, and may be responsible for hemorrhoidal symptoms in certain 
individuals. Coccygeal pain and discomfort may arise from sustained hypertonia of the 
levator ani and other perineal muscles attaching to the coccyx.


Psychogenically induced, sustained hypertonia of somatic muscle is not regularly 
associated with small or large pupils, tachycardia or bradycardia, excessive sweating, 
dryness of the mouth or ptyalorrhea, muscle tremors, muscle spasm, nausea, diarrhea, 
polyuria, or elevation of blood pressure, although a patient with psychogenically 
induced, sustained hypertonia of somatic muscle who develops acute anxiety may have 
these somatic and visceral symptoms and sigus of vegetative nervous system 
imbalance (55) (133) (26) (241).

In general, with symptom-producing, psychogenically induced, sustained hypertonia of 
somatic muscle, the patient's sitting or standing posture, gait, body movements and 
mannerisms may appear tense, jerky, and not smoothly integrated. He may hold one 
shoulder higher than the other; he may keep one arm close to his body when sitting or 
walking, or he may hold both arms stiffly by his sides when walking. Occasionally he 
may walk with a stoop; more often, he walks stiff-kneed, with increased lumbar lordosis, 
increased dorsal kyphosis, with his neck in partial flexion and his head thrust forward 
(see page 88). Periodically, he may extend, flex and rotate his neck, and rub the back of 
his neck as if to get relief from neck discomfort. A patient may change his sitting position
suddenly, or move his extremities suddenly from one position to another. Another type 
of patient may cross his thighs tightly when sitting and may sit rigidly, in a slouched 
position, with marked flexion of his spine in the thoracic and lumbar regions, without 
moving for long periods of time. One or both fists may be clenched for long periods of 
time. Tight grasping of objects (pens, pencils, knitting needles, papers, books) in the 
hands may be noted in persons with sustained hypertonia of somatic muscle.

The patient's facial expression often tends to be fixed, tense and relatively immobile. 
Smooth, well-integrated and spontaneous transitions from one facial expression to 
another do not readily occur, and transient grimacing or tic-like movements may 
precede changes in facial expression. Each time certain emotionally charged subjects 
are mentioned, the patient may present a stereotyped facial expression, or may blink 
frequently. A steady state of jaw muscle tension may be noted in some patients; in 
others, variations in jaw muscle tension may be noted when the mouth is closed and the 
patient alternately tenses and relaxes his jaw muscles. The patient may swall9w 
frequently, and at times rhythmically, once every 30 to 120 seconds, and have the usual 
consequences of excessive aerophagia (96).

In persons with sustained hypertoma of the orbicularis oris muscles, one may see 
abrasions on the dental surfaces of the lips, with or without secondary infection. There 
may be excessive attrition of the teeth; there may be indentations along the lateral 
margins of the tongue due to prolonged pressure of the tongue against the lingual 
surfaces of the teeth. In many patients, a leukoplakic line can be seen, usually 
bilaterally, on the buccal surfaces of the cheeks along the line of closure of the teeth. 
This may result either from habitual mouth suction, which draws a portion of the buccal 
inucous membrane within the region of closure of the opposing teeth, or from sustained 
contraction of the buccinator muscles which push a portion of this membrane within the 
region of closure of the opposing teeth. Dentures make relatively deep impressions in 
the supporting mucous membrane as a result of the patient's sustained jaw muscle 

The patient may sigh frequently, and show other types of respiratory dysrhythmia. His 
voice may be poorly modulated. The rhythm of his speech may be jerky, there may be 
elision of syllables, and he may stutter (126). He may noisily clear his throat repetitively, 
or have a recurrent, brief, non-productive cough.

Palpation of somatic muscle in the apparently relaxed patient who has psychogenically 
sustained hypertonia may or may not reveal increased somatic muscle firmness. In 
some patients, the very act of palpating somatic muscle causes muscular hypertonicity 
to disappear for a short time after completion of the palpatory maneuver. In others, 
palpation increases the imtial degree of hypertonia. Palpation of hypertonic somatic 
muscle may reveal small, exceedingly tender islands of tissue - trigger spots (217)
- and when these are palpated firmly, there is irradiation of pain to the substance of the 
entire muscle, reflexly to distant muscles, and to the nearest joint. This may be easily 
demonstrated in persons with habitual hyper tonia of the left pectoral muscles, in whom 
radiation of discomfort may be to the left shoulder and arm, and to the left side of the 
neck. Transient psychogenically induced, sustained hypertonia of abdominal muscles, 
which is usually present only in the recumbent position, may be sufficiently marked to 
render abdominal examination difficult. Resistance to alternate passive flexion and 
extension of extremity muscles may be the only physical sign of increased muscle tonus 
in the apparently relaxed patient who shows no evidence of organic central nervous 
system disease. The tendon reflexes are usually increased in amplitude, with a short 
latent period. Rebound contraction is often prominent. Sustained cocontraction in 
opposing muscles may be of sufficient degree to prevent visible reflex response to 
tendon tapping, but not palpable reflex contraction. In patients with sustained muscular 
hypertonia, ankle and patellar clonus, Hoffman and Babinski Sigus were not elicited. 
Occasionally, swaying in the Romberg position was noted when a patient had sustained 
hypertonia of somatic muscle, which was relatively greater in one half of the body than 
the other. Such persons may sway when walking, or may veer n6ticeably to one side.

It may be difficult to examine the palpebral conjunctivae because of marked hypertonia 
of the orbicularis oculi muscle. Because of sustained hypertonia of the orbicularis oris 
muscle (and buccinator muscle), lips may be hard to retract with a tongue blade in 
attempting to expose teeth and gingiva for inspection. In women patients, the introitus 
may be markedly narrowed by spasm of the vaginal sphincter muscles, and if digital 
examination is attempted, the patient will have severe pain and discomfort from this 
maneuver, and pelvic examination will be unsatisfactory. A simple, effective method of 
causing relaxation of the vaginal sphincter muscles is to ask the patient to relax her 
perianal muscles, which simultaneously causes vaginal sphincter muscles to relax. 
Rectal examination may be rendered difficult because of sustained hypertonia of 
muscles of the anal sphincter and pelvic floor. Spasm of these muscles may cause 
rectal examination to be a painful procedure for the patient, even though the gloved 
examining finger is adequately lubricated. Spasm of sphincter muscles may cause 
hemorrhoidal veins to become prominent.


Psychogenic symptoms were exceedingly prevalent in the group of patients studied, 
and for this reason the writer found it necessary to obtain a working knowledge of 
psychiatric principles and treatment, through study of available literature (122) (50) 
(100) (111) (66) (239) (181) (234) (235) (5) (156) (53) (18) (130) (133) (169) (170) (207) 
(124) (125) (4) (9) (13) (94) (237), and through careful evaluation of the effects of psy-
chotherapy on patients whose emotional disorders were exteriorized through 
psychosomatic symptoms. Various methods of treatment of psychogenic syndromes 
were tested and adapted to the special needs of each patient so that he could be 
helped to become accustomed to dealing more directly, more realistically and more 
effectively with his problems of everyday living. The ultimate objectives of reconstructive 
psychotherapy of patients with emotional disorders and psychosomatic symptoms were 
to enable the patient to have, in time, freedom from his psychosomatic symptoms, the 
ability to solve his problems of living with greater efficiency and with more emotional 
maturity, and a sustained feeling of emotional and physical well-being. Sometimes, 
these therapeutic objectives could be attained only when the patient was referred to a 
competent psychiatrist for study and treatment. Sometimes, these therapeutic 
objectives were unattainable whether an internist or psychiatrist managed the patient's 
emotional disorder (83). Usually, the internist could successfully manage the patient's 
psychosomatic problems and attain the desired objectives (235) (156). Some patients 
were helped to resolve their presenting problems and to have relief of psychosomatic 
symptoms in a relatively short period of time; in other persons, the same degree of 
therapeutic success was achieved over a period of several years; and in other 
individuals, no sustained psychotherapeutic progress was maintained, and any benefit 
the patient had was chiefly from supportive psychotherapy.

It is usually possible to manage most of a patient's emotional problems which are 
exteriorized through psychosomatic symptoms, as an integral part of the general 
medical treatment of his joint dysfunction. A patient is most likely to have complete and 
lasting relief from a psychosomatic syndrome when the emotional tensions which 
initiated his psychogenic symptoms and signs are corrected by successful 
reconstructive psycho-therapy. Usually partial or temporary relief from psychosomatic 
syndromes may occur when the emotional tensions of the patient are lessened by 
helpful changes in his external environment or by supportive psychotherapy. In treating 
a patient with psychogenically induced, sustained hypertonia of somatic muscle, it is 
sometimes possible to alleviate collateral psychosomatic symptoms without improving 
the patient's primary emotional disorder (83) (see Case II, page 140), and when the 
patient feels more comfortable physically, he will have relief from his secondary anxiety 
concerning the meaning of his psychosomatic symptoms. Under such circumstances, 
his primary emotional disorder is likely to be more accessible to study and therapy.

Some psychogenic syndromes are collateral to aberrant physiology; e.g., athiaminosis 
(148), aniacinamidosis (206) (214) (127) (32), menopausal syndrome (121) (33), 
starvation (80), adrenal gland hypofunction (47). In most instances of this sort, when 
somatic dysfunction is corrected, the patient will have prompt recovery from collateral 
psychogenic syndromes; when such somatic dysfunction recurs, there will be a 
recurrence of the collateral psychogenic syndromes (208).

The patient with psychosomatic symptoms is usually unaware that there is a positive 
correlation between his emotional reactions to troublesome life situations and his 
symptoms of bodily discomfort, and he is likely to regard his known emotional problems 
and physical symptoms as representing two distinct and unrelated conditions. He 
usually believes that he has his emotional problems "under pretty good control" (169), 
and seeks medical advice for the relief of his symptoms of bodily discomfort. The 
patient's failure to perceive the reciprocal relationship between his emotional and 
psychosomatic problems, and his preoccupation with psychosomatic symptoms seem to 
represent a type of unconscious adaptive adjustment which he has made to his 
emotional disorder so that he can maintain emotional homeostasis. Much supportive 
and preparatory psychotherapy may be required before a patient will be ready to accept 
reconstructive psychotherapy directed toward the solution of his basic emotional 
problems. When he attains sufficient insight into the nature of his presenting emotional 
and psychosomatic problems, he may be enabled to resolve these problems, and when 
he acquires habitually more mature methods of dealing with his problems of everyday 
living, he will have no further need for "protective" psychosomatic symptoms, which, 
consequently, often disappear.

Data concerning the patient's emotional life must be collected and evaluated as 
objectively and dispassionately as any other clinical data. In analyzing a patient's 
emotional attitudes and behavior, the internist must learn to recognize positive and 
negative transference phenomena and to understand their meaning (50) (4) (239). It is 
relatively easy for a physician to tolerate positive transference reactions as being 
"natural and proper," and to use them to good therapeutic advantage. However, it is 
relatively difficult for a physician to tolerate negative transference reactions with equa-
nimity, unless he is prepared to seek the dynamic basis for such emotional behavior, 
and to manage such negative transference reactions so that they will not unduly hinder 
attainment of the desired therapeutic goals. Some-times, negative transference 
reactions are so intense that all attempts at therapy will fail. The physician must also 
become aware of his own positive and negative counter-transference reactions to a 
patient, and must learn to modify these as required by the best interests of the patient.

From information elicited during the course of clinical study, the physician can often 
detect certain basic, repetitive, and emotionally immature patterns in a patient's 
reactions to various life situations. A patient with emotional disorders and 
psychosomatic symptoms often has certain prevailing attitudes and derivative defense 
reactions which cause him to exhibit, without being aware of their existence, certain 
patterns of emotional behavior which are detrimental to him in his interpersonal 
relationships. When mental tensions generated directly or indirectly by such pervasive 
attitudes and their derivative defense reactions become sufficiently severe, the patient 
may complain of symptoms resulting from psychogenically induced, sustained 
hypertonia of somatic muscle or other psychogenic syndromes. The patient's 
awareness of psychosomatic symptoms supersedes his awareness of his primary 
emotional tensions and produces collateral anxiety concerning the meaning of his 
psychosomatic symptoms of bodily discomfort.

Before attempting to treat a person with psychosomatic symptoms, the physician should 
try to understand the background for the development and retention of the patient's 
emotionally immature attitudes. The physician should appreciate what difficulties the 
patient is likely to experience in trying to improve these attitudes and gain emotional 
maturity. Sometimes, by suffering from symptoms or an illness (psychosomatic), the pa-
tient may be making the best adjustment he can to a difficult life situation, and when this 
is so, the physician must realize that the patient may be better off with his symptoms 
and illness than without them, and in such instances psychotherapy should be chiefly 

Psychotherapy of the patient starts when the patient and physician first meet, and 
continues throughout the course of treatment of joint dysfunction and associated non-
psychogenic syndromes. Often, a patient derives positive psychotherapeutic benefits 
when his physical and emotional problems are delimited and a broad program of 
therapy is outlined for him by the physician. Occasionally, during the first visit a patient 
is able to gain insight into the dynamics of his most pressing emotional problems, and 
has considerable relief from some of his most pressing anxieties without any directed 
psychotherapy on the part of the physician other than the sympathetic elicitation of the 
patient's history, the performance of a careful physical examination, and the subsequent 
detailed discussion by the physician of the patient's clinical problems and the proposed 
form of therapy. Sometimes, during the initial clinical study a patient will have almost im-
mediate, and often lasting, relief from psychosomatic symptoms, without insight into the 
dynamics of his emotional problems, from the reassurance that he has no serious 
physical disease and that his symptoms of bodily discomfort are of emotional origin. 
Other patients seem to be uninterested, or disturbed by the objective analysis of their 
state of health, and either refuse to accept therapy as recommended, or prematurely 
discontinue therapy.

The technique of treatment of psychosomatic symptoms as described below is adapted 
to the specific needs of the individual patient with psychogenically induced, sustained 
hypertonia of somatic muscle.

During the course of the initial clinical study, the physician introduces the patient to the 
concept of psychosomatic illness by citing commonplace examples of psychosomatic 
reactions, selected so that they have no direct or immediate application to the patient's 
emotional disorder and so that they illustrate patterns of psychosomatic reactions which 
differ from those experienced by the patient. Usually, the patient accepts the validity of 
the general concept that emotional experiences may be accompanied by symptoms and 
signs of bodily dysfunction, and that these symptoms and signs are an involuntary 
consequence and accompaniment of underlying attitudes. Gradually, the physician 
modifies the discussion so that concepts of psychosomatic illness and treatment are 
described as they relate more directly to the patient's health problems. In order to give 
the patient a new point of departure in thinking of his psychosomatic illness as the 
exteriorization of his emotional tensions, clinical data obtained during the initial study of 
the patient (including his own description of his reactions to various life situations) are 
used to illustrate how his emotional behavior has been conditioned by certain pervasive 
attitudes and the derivative defenses of such attitudes. When this psychosomatic 
relationship is revealed to the patient in an objective manner by the physician, often the 
patient can perceive at once that the explanation of his illness is consistent with his 
subjective experiences and with reality.

The patient is told that his symptoms and signs resulting from psychogenically induced, 
sustained hypertonia of somatic muscle are not imaginary, and usually are not indicative 
of serious somatic disease. His psychosomatic symptoms and signs have physiological, 
anatomical and psychological bases, which are explained to him in simple terms. When 
the patient is seen in the physician's office to exhibit regionally sustained hypertonia of 
somatic muscle, this fact is called to his attention, not to embarrass him, but to make 
him aware that his sustained muscular hypertonia is objectively demonstrable. He is told 
that his symptoms and signs of psychogenically induced, sustained muscular hypertonia 
have deflected his attention from his troublesome initiating emotional tensions to his 
bodily dysfunction, with the result that he has new anxieties concerning the possible 
meaning of his psychosomatic symptoms and signs.

It is often useful in the exposition of the symptomatology of psychogenically induced, 
sustained hypertonia of somatic muscle to illustrate to the patient that considerable 
muscular and periarticular discomfort and pain can be induced by voluntary sustained 
contraction of somatic muscle. This is done through the use of the procedure described 
below, or some variation thereof. The patient is asked to abduct his right upper 
extremity until it is at right angles to the sagittal plane of the body. The palmar surface of 
his hand faces the floor. Without changing this position of the upper limb, the patient is 
asked to flex his wrist maximally and to make a fist. He is then asked to elongate his 
right upper extremity as much as possible, through sustained muscular contraction. 
Usually, within a few seconds of such sustained muscular contraction, he will 
experience discomfort and pain in muscles, tendons and periarticular structures of the 
wrist region, in the muscles of the forearm, and to a lesser extent in the elbow and 
shoulder regions. He will often be astonished that his voluntary muscle contraction can 
produce such discomfort. During the period of voluntary sustained maximal contraction 
of upper extremity muscles, the sites of the patient's uncomfortable or painful 
sensations are tender to digital palpation, and feel tense. When the sustained muscular 
contraction is terminated by voluntary relaxation of the upper extremity muscles, the 
pain in the elbow region promptly lessens in intensity, although there may be some 
residual discomfort, for some time thereafter.

In addition, it can often be demonstrated to the patient that when he fixes his attention 
on a given anatomic region, he may have awareness of sensations which he would 
otherwise not perceive. The patient who has been seated for some time is asked 
whether or not he is conscious of any sensations from his buttocks pressing against the 
chair. Invariably, his initial answer is in the negative. He is then asked to concentrate his 
attention on any sensations which he may feel from his buttocks pressing against the 
chair. Most patients then report that they feel a sensation of increasing pressure on the 
buttocks, which reaches a maximum level of intensity which is often distinctly 

Typical examples are cited to illustrate that mental reactions can cause changes in 
bodily function, and, if these psychosomatic reactions are sufficiently persistent, 
changes in bodily structure. It is explained that persons with psychogenically induced, 
sustained hypertonia of somatic muscle are characterized by exteriorizing their 
emotional tensions through muscular contraction, which symbolically indicates 
readiness to perform certain defensive or offensive acts, together with sufficient 
concurrent inhibition to prevent execution of these acts. Persons with the syndrome of 
psychogenically induced, sustained hypertonia of somatic muscle usually harbor various 
degrees of repressed hostility, resentment, hatred or rage. When these feelings are 
directed against an individual whom the patient feels he should obey, respect, admire, 
love, or be grateful to, he develops guilt feelings which increase his tensions and make 
his symptoms more severe. The patient must understand that it is not unusual or 
"wrong" to have such mixed feelings. When the physician can verbalize some of the 
patient's destructive feelings, or when the patient can talk frankly and freely about his 
specific problems, without fear of censure by the physician, the patient may have relief 
from his emotional tensions.

Many patients are able to accept without resistance the idea that their somatic 
symptoms have a psychogenic basis. However, it is not unusual for a patient to exhibit 
some degree of resistance to the idea that his illness is a psychosomatic one, and the 
physician must be aware of the degree of such resistance, so that he can more 
effectively direct the subsequent course of treatment. When such resistance is mild or 
moderate, it does not interfere with successful treatment of the patient's psychosomatic 
disorder, since gradually the patient is able to find confirmation in his daily experiences 
of the psychosomatic nature of his disorder, and has relief from his psychosomatic 
symptoms when he is able to acquire and utilize habitually more mature attitudes in the 
solution of his problems of everyday living.

When a patient shows marked resistance to the suggestion that his ill-ness is a 
psychosomatic one, discussion of this subject is terminated for the time being by the 
physician with a reiteration of the nature of psychosomatic disorders in general. 
Subsequently, the treatment of such a patient is more or less limited to somatic aspects 
of disorders, and any improvement in the patient's emotional status is more or less 
fortuitous. In time, a number of patients who showed initially marked resistance to the 
concept of psychosomatic illness "discover" that they have certain symptoms or an 
increase in severity of symptoms only when they are exposed to situations which cause 
emotional tensions, and that their symptoms disappear or become less severe when 
they are not exposed to these types of situations. After a patient has made such a 
"discovery," he often becomes more amenable to treatment of his psychosomatic 
symptoms and underlying emotional disorders, provided that the physician is willing to 
let the patient take full credit for having made original and informative observations 
concerning the nature of his psychosomatic problems.

The most substantial relief from psychogenically induced, sustained hypertonia of 
somatic muscle is afforded by successful treatment of the patient's emotional disorder. 
However, certain ancillary procedures have been found helpful in giving the patient 
some relief from his symptoms of psychogenically induced, sustained hypertonia of 
somatic muscle. The patient may find that his symptoms are lessened when he takes a 
vacation; when he can interest himself in hobbies, sports, or in civic, social or church 
activities; or, when there is an external solution to his problems. Patients may be 
benefited when they are helped to schedule periods of work, exercise, rest and 
recreation, so that they can expend their physical and emotional energies without 
developing excessive physical or emotional fatigue. Sometimes, it is necessary to poit 
out to a patient the deleterious effects of indecision, worry and day-dreaming, and to 
assist him to establish better habits of thinking. Generalized muscular relaxation can be 
induced by tepid baths of 20-30 minutes' duration, or by the application of the methods 
of progressive relaxation (87). The local use of dry heat or the use of hot massive wet 
dressings applied for 30 minutes several times during the day are helpful in the 
relaxation of psychogenically induced, sustained hypertonia in certain muscular regions; 
e.g., posterior cervical region, pectoral muscles, shoulders. Some patients may have 
relief from symptoms described above only when they do strenuous physical work. In 
acute tensional situations, the judicious use of medications (e.g., phenobarbital, 
belladonna, dexedrine, aspirin) for a limited period of time may be helpful.


CASE FF. Pain in the Neck. A 63-year-old manufacturer was recovering satisfactorily 
from joint dysfunction in response to adequate niacinamide therapy until he suddenly 
developed, in the back of his neck, severe pain which radiated into his upper thoracic 
spine. After this pain persisted for a week, he sought medical advice. He could recall no 
injury to his cervical spine. Physical examination revealed a decrease in the range of 
lateral rotation of the neck as compared to previous measurements, and tenderness 
and firmness of posterior neck muscles. When asked if anything was disturbing him, he 
stated that a few days before his neck pain started, one of his salesmen had promised 
his best customer delivery of goods at a date which could not be met and at a price that 
was far too low. The manufacturer was sure that he would lose his best customer, and 
was furious with his salesman, whom he planned to fire. "To top it all," he said, "the pain 
in my neck has been so bad I can't even think straight."

The probable relationship between his emotional tensions and the pain in his neck was 
explained to him, and in discussing his problems, it was suggested that he might meet 
with his customer and salesman in order to correct the error. This was done, and a 
satisfactory solution was evolved. The customer accepted the explanation; the 
salesman kept his job; and the manufacturer lost his pain in the neck. Three months 
later, the lateral ranges of neck movement had increased to the level of movement 
which he had before the joints of the cervical spine were injured by psychogenically 
induced, sustained hypertonia of neck muscles.

CASE CC. Painful Hands. A 50-year-old unmarried female office manager was 
recovering satisfactorily from joint dysfunction in response to adequate niacinamide 
therapy, until she developed painful swelling and stiffness of her fingers, which became 
progressively worse over a period of four months. She had not performed any unusual 
physical tasks which might have injured her finger joints. Measurement of the ranges of 
joint movement showed that all her joints had improved excepting her finger joints, 
which showed decreased ranges of movement. Her finger joints were markedly swollen, 
and felt somewhat warm to the touch, but were not red. 

When asked if anything was upsetting her emotionally, she said she was afraid she 
might lose her job. Without consulting her, her superior had employed a young college 
graduate as assistant office manager, and the patient felt that this girl might replace her 
as office manager. She thought the new worker was cold, unfriendly and efficient, and 
was annoyed that the girl had already made several suggestions about improving office 
procedures. As she talked about the assistant office manager, her hands were clenched 
tightly. When asked what she would like to do to the girl, she said promptly, "I'd like to 
shake the living daylights out of her." This confession surprised her.  When it was 
indicated that she looked upon the girl as a threat to her economic and emotional 
security, she realized that this was so. By clenching her hands tightly she was 
symbolically attacking her assistant, but actually she was injuring her hands by 
psychogenically induced, sustained hypertonia of forearm muscles. For temporary relief, 
she was asked to soak her hands in hot epsom salt solution for 30 minutes three or four 
times a day, and to try to avoid consciously clenching her hands. For more lasting relief, 
it would be necessary for her to overcome her intense feelings of hostility toward the 
girl, which came out of her own fear of insecurity.  Probably, she was told, the assistant 
manager also felt insecure in her new position and wanted to please her manager.

A month later this patient reported that her hands gave her no discomfort, and were not 
swollen, although they still felt a little stiff. She had decided to take an interest in the 
assistant office manager and had had lunch with her several times. She thought that the 
assistant was a "swell person." The fact that she had learned that the girl planned to get 
married and leave the job in about a year undoubtedly had a great deal to do with her 
apparent improvement in her previously hostile attitude.

CASE HH. Generalized Sustained Muscular Hypertonia. A 38-year-old assistant factory 
supervisor suffered for years from constant fatigue and from discomfort and pain in his 
muscles and joints, which had not responded to medical treatment. Physical 
examination indicated that he had extremely severe joint dysfunction, and severe 
generalized sustained hypertonia of somatic muscle. He said that he had difficulty at 
work in getting along with his superiors, but not with his subordinates. He complained 
that younger men were promoted over his head, but solaced himself with the thought 
that this was because he had a mind of his own, and "stood up to" his superiors, who 
were "down on" him for this reason. When questioned about his childhood, he related 
that his father was frequently drunk, and was always strict with him, punishing him 
severely for the most trivial offenses. He was an obedient child, but secretly hated his 

It was pointed out to the patient that the hostility he had originally directed against his 
father was unconsciously being directed against all persons in authority. The 
unconscious fear that his subordinates might feel hostile toward him caused him to be 
over-kind to them. When he showed marked resistance to the explanation that his 
psychosomatic symptoms were the result of his basic attitude of repressed hostility 
toward persons in authority, this subject was dropped and treatment for his joint 
dysfunction was instituted. He had strong resistance to niacinamide therapy, and did not 
take his medications as directed - which was interpreted as being another expression of 
resistance to a person in authority - in this case, the physician.

When he returned for a semi-annual recheck examination, he had become much more 
aware of his hostility toward his superiors, and was gradually succeeding in improving 
his attitudes toward them. He had his first promotion in years, which surprised him and 
encouraged him further. He had lost his articular and non-articular symptoms of 
generalized psychogenically induced, sustained hypertonia of somatic muscle, and had 
become completely free from his excessive fatigue and symptoms of severe bodily 
discomfort. His joint dysfunction had not improved because he felt so well that he 
thought it unnecessary to take medications of any sort.

CASE II. Excessive Aerophagia. A 44-year-old, unmarried traveling salesman 
complained of belching, passing much gas rectally, bloating, and a feeling that all the 
food he ate "turned to gas." His symptoms were most severe on weekends, when he 
was at home with his widowed mother. Not uncommonly during the weekend, he would 
wake at 2 A.M. with left upper abdominal pain radiating into his left lower anterior and 
anterolateral chest and lasting for several hours. He would try to get relief by belching 
and by taking antacids, but had little relief from these procedures. Enemas tended to 
make him feel faint and gave him severe abdominal cramps. He was sure that he had 
serious stomach or heart disease, even though serial electrocardiograms, gall-bladder 
and gastro-intestinal studies per-formed over a period of years were negative. He 
denied having emotional problems, would not discuss his relationship with his mother, 
and said that everything in his life was fine excepting for the gas.

In the office, he was observed to have rhythmic aerophagia at 20-second intervals, and 
to belch about every five minutes. His submental muscles were palpably tense, but he 
had no other evidence of psychogenically induced, sustained hypertonia of somatic 
muscle. His distended abdomen was tympanitic to percussion; borborygmi were heard; 
the large intestine could be outlined by palpation. Fluoroscopy showed a large gas 
bubble in his stomach, and relatively little movement of the left leaf of the diaphragm 
with respiration.

The patient was told that symptoms such as he had were usually the result of excessive 
aerophagia, emotionally induced. He showed such marked resistance to the idea that 
his symptoms could be initiated by emotional factors that subsequent discussion was 
confined to an explanation of the dynamics of the production of somatic symptoms by 
excessive aerophagia, and a description of the method of inhibiting his frequently recur-
ring swallowing reflex. He was asked to hold between his teeth, for 20 minutes at a time 
four or five times daily, a cork which was sufficiently large to prevent him from 
swallowing. If he salivated during this procedure, he was not to swallow his saliva but to 
let it drain out of his mouth, catching it in a towel; if he wanted to belch, he might do so, 
without removing the cork from his mouth.

For one month, he used this method of inhibiting his frequently recurring, rhythmic air-
swallowing reflex, and reported that he no longer had trouble with "gas." In the office, at 
this time he was seen to swallow about once every 10 minutes, and did not belch once 
during a one-hour period of observation. The patient was pleased to have been "cured" 
of his trouble, and stated that his "gas" could not have been caused by emotional 
tensions which were unresolved, since he had the same emotional problems which he 
had had for years, which could not be relieved in a satisfactory way as long as a "certain 
person" was alive. He would not discuss this subject further.

Subsequently, he has been seen over a period of several years without any recurrence 
of his excessive aerophagia. When asked about the status of his emotional problems 
from time to time in this interval, he says "No change."

(End of Chapter 2. References cited in this chapter are posted at )

To go on to Chapter 3, click this link:


To go back to Chapter 1:


Andrew W. Saul


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