|
Joint Dysfunction, Part 2
Home
|
|
CHAPTER 2
To read
Chapter 3, click this link: http://www.doctoryourself.com/kaufman8.html
To return
to Chapter 1: http://www.doctoryourself.com/kaufman6.html
THE
COMMON FORM OF JOINT DYSFUNCTION
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 http://www.doctoryourself.com/kaufman11.html
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
treated.
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.
DELAYED POST-TRAUMATIC
ARTICULAR SYNDROME
(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
situations.
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
ameliorated.
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
(96).
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-
tinuously.
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
shoulder
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
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
dysfunction.
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.
MISCELLANEOUS TYPES OF
MECHANICAL JOINT INJURY AND THEIR
TREATMENT
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)
(73).
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
therapy.
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
muscle.
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
disappeared.
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
discomfort.
SOME EXAMPLES OF
MECHANICAL JOINT INJURY
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
forefinger.
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
ironing.
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
dysfunction.
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.
CHRONIC ALLERGIC
SYNDRONIES
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
cases.)
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
symptoms.
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
material.
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
psychoneurotic.
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.
TREATMENT OF CIIRONIC
ALLERGIC FOOD SYNDROMES
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
interdicted.
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
again.
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).
SOME EXAMPLES OF FOOD-INDUCED
ALLERGIC REACTIONS
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
investigation:
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
headache.
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
symptomatology.
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
lymphadenopathy.
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
Syndrome.
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.
SODIUM RETENTION SYNDROME
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)
(144).
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.
SYNDROME OF
PSYCHOGENICALLY INDUCED, SUSTAINED HYPERTONIA OF
SOMATIC MUSCLE
GENERAL CONSIDERERATION
OF PSYCHOSOMATIC SYMPTOMS IN JOINT
DYSFUNCTION
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
security.
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
offered.
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).
PSYCHOBIOLOCIC STUDY OF
THE PATIENT WITH JOINT DYSFUNCTION
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
history.
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.
PSYCHOGENICALLY INDUCED,
SUSTAINED HYPERTONIA OF SOMATIC MUSCLE
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.
COMMONLY OCCURRING
SYMPTOMS OF REGIONALLY SUSTAINED
HYPERTONIA OF SOMATIC MUSCLE
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
Muscles.
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
coughing.
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.
COMMONLY OCCURRING
PHYSICAL SIGNS OF PSYCHOGENICALLY INDUCED,
SUSTAINED HYPERTONIA OF
SOMATIC MUSCLE
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
contraction.
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.
TREATMENT OF
PSYCHOGENICALLY INDUCED, SUSTAINED HYPERTONIA OF
SOMATIC MUSCLE
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
supportive.
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
uncomfortable.
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.
SOME EXAMPLES OF
PSYCHOGENICALLY SUSTAINED MUSCULAR
HYPERTONIA AND ITS RESPONSE
TO TREATMENT
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
father.
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 http://www.doctoryourself.com/kaufman11.html
)
To go on to
Chapter 3, click this link: http://www.doctoryourself.com/kaufman8.html
To go
back to Chapter 1: http://www.doctoryourself.com/kaufman6.html
|
