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The sections to be presented will
cover the clinical manifestations of anorexia nervosa,
bulimia nervosa, rumination, and pica. The foregoing
diagnostic entities have been defined formally as eating
disorders in the Diagnostic and Statistical Manual of
the American Psychiatric Association beginning with
the Third Edition in 1980 and will continue to be so
designated in the Fourth Edition to be published in
the 1990's. Before describing these disorders with the
focus on clinical symptomatology and diagnostic focus
and range it is important to establish certain general
principles in the approach to the patient with an eating
disorder. Increasingly research in the last decade has
uncovered the continuity of basic neurophysiologic structure
and process underlying the regulation of appetite and
eating derived from animal model research extended our
understanding and approach to human clinical eating
disorders. It is important to make a fundamental distinction
between a feeding disturbance (a relatively transient
behavior affecting eating which is clearly derived from
anxieties and conflicts in relationship or self-appraisal
occurring at different epochs of psychosocial development)
and an eating disorder (a psychobiologic regression
characterized by de-differentiation, interference or
distortion of eating manifested by deficits in: a) appetite
regulation; b) food selection or preference; and c)
consummatory behavior). An eating disorder is likely
to be persistent over time with a surrounding context
of habitual attitudes and reactive behaviors that ultimate
affect the patient's nutritional and general medical
status. Individual psychological defenses and family
reactions are usually secondary to the loss of control,
the threat to competency, and perceived physical danger.
Symptoms of the eating disorder may reactivate early
conflicts related to dependence, separation individuation,
and personal autonomy. Very often the significance of
signs and symptoms of the eating disorder depend upon
the complexity of the patient's psychological structure
and where they are in the progression of their psychological
development.
As an example of the foregoing anorexia
nervosa with severe restrictive ingestive behavior
may occur in preadolescence without the emphasis
on body image distortion but rather presenting a
clinical picture of malaise, growth retardation, and
ritual obsessionality with regard to food avoidance
of specific foods. In adolescence the same restrictive
eating pattern is accompanied by exquisite sensitivity
to unusual body experience and preoccupation with body
size and fear of becoming fat, often ritualistic exercise
and calisthenics with more complex mental ideas regarding
calories and their significance as well as intense adolescent
struggles for autonomy and individuality from parental
control. In later adult life the same anorectic restrictive
eating pattern may be associated with difficulties in
the marital situation, infertility from the amenorrhea,
social difficulties, and even in more recent research
findings, suggestions of problematic nurturance of children.
In middle age and later life similar restrictive eating
pattern is accompanied by fears of aging and death often
associated with a depressive or melancholic clinical
disorder, sometimes an association with bereavement
from loss of a spouse, and often accompanied by various
health preoccupations and peculiarities focused on the
"health" qualities of food rather than calories
or effects on body size.
An example of some of the basic
dimensions that we consider in the study of eating disorders
would include the following: Binge eating desire
(a subjective sense and desire that may be characterize
by a hyperphagic component, carbohydrate or rarely an
associated non-nutritive substance desire); binge
eating behavior (this usually is characterized by
rapid rate of eating with gulping of easily ingested
and obtained food, often occurring outside of usual
meal times and occasionally in the middle of the night);
reactive behaviors (these may include fasting,
induced vomiting, ruminatory regurgitation, rumination,
laxative and diuretic abuse, and polydypsia); food
enjoyment (this is the hedonic and reward component
of food intake. Often this component is reduced in eating
disturbances with accompanied depression and diminished
with the predominance of a compulsive and stereotyped
component to eating in the more severe instances of
bulimia); food preference (this refers to the
psychobiologic foundation of food selection; distortions
are seen in the restriction of cuisine and food selections
in anorexia nervosa and in the unusual preference for
carbohydrates seen in bulimia, in pica preference is
predominantly for non-nutritive substances or for singular
foods eaten in a repetitive manner); food preoccupation
(this refers to the ideational component of the
mental preoccupation with food; in anorexia nervosa
one sees the dissociation of mental preoccupation with
food, which may be intense throughout the day and result
in the purchasing, hoarding, cooking and serving of
food to others from actual ingestive behavior. The severe
binge eating desire of the patient with bulimia nervosa
more often than not leads to obligatory binge eating
outside of usual meal times); postprandial state (this
refers to a sense of fullness and unusual body experiences
related to the act of eating both in anorexia nervosa
and in bulimia nervosa. The physiological anlage for
distorted postprandial phenomena may be related to delay
in gastric emptying found in both anorexia nervosa and
bulimia nervosa, decreased bowel time, esophagitis,
and rumination found in approximately 20% of patients
with bulimia nervosa); and associated features
(body image preoccupation and distortion, whivh is especially
prominent during adolescence and young adulthood; mood
variation or overt mood disorder, which may take the
form of an associated overt depressive disorder or severe
demoralization with a persistent eating disturbance).
It is important to define the dimensions
and the extent of the eating disorder. This is often
done by behavioral mapping of the subjective and objective
experiences and behavior of the patient. It is important
to define the acute or chronic status of the eating
disorder, the presence or absence of developmental antecedents,
the level of psychological developmental achievement,
the degree of family integrity, coping style, and resilience.
Psychotherapeutic approaches generally involve clarification
and confrontation, and support and interpretation to
the patient and the family. Our current approaches are
primarily rehabilitative in focus, helping the patient
achieve a degree of cooperative self-regulation in relationship
to eating and food and reasonable understanding of developmental
and family conflicts. Frequently there is a need for
intensive reconstructive psychotherapy, however, this
must be determined on an individual basis.
Detailed psychiatric investigation
should be initiated reviewing the developmental history,
the critical aspects of the family environment and specific
phenomenology of the eating disorder. Assessments of
family coping styles, conflicts, and patient's defenses
in reaction to the eating disorder should be evaluated
for their appropriateness in facilitating a systematic
plan that could lead to treatment goals. A thorough
developmental history including thorough family and
genetic history, careful assessments of associated disorders
such as depression, developmental disorders, adolescent
behavior or personality disorders, and an assessment
by psychological testing emphasizing special research
areas where appropriate such as a more careful assessment
of the body image and issues such as autonomy and self-control.
Nutritional deficits and consequences
should be carefully evaluated and most often measurements
such as body composition, laboratory studies, especially
involving measures of protein sufficiency such as serum
albumin, transferrin, and C3 complement as well as specific
nutritional deficiencies should be assessed carefully.
Cardiac function should be measured carefully including
EKG and holter monitor before exercise of any significant
degree is allowed for the patient. If possible some
assessment of measures of activity and physical strength
should be done since patients lose their self-perceptive
objectivity regarding their levels of activity and their
actual physical reserve capacity. Often in severe anorexia
nervosa 24-hour cortisol levels are extremely elevated
easily distinguishing this disorder from Addison's disease
among other clinical differential signs such as apparent
over activity rather than fatigue and relentless pursuit
of thinness as opposed to worry and concern over declining
body habitus and strength.
In summary the eating disorders
constitute a group of syndromes (anorexia nervosa, bulimia
nervosa, pica, and rumination) characterized by a psychobiologic
regression leading to disturbances in appetite regulation,
food preference, and consummatory behavior often with
associated disregulations in mood, activity, self-perception,
and neuroendocrine function. Attempts to cope with these
disorders often lead to exaggerated ineffective and
often destructive psychological defenses for the individual
patient and futile reactions by the family.
Since 1980, with the formulation
of the Diagnostic and Statistical Manual III in psychiatric
practice, formal criteria for anorexia nervosa have
existed. Currently with the revision of the aforementioned
manual the basic definitions involve refusal to maintain
body weight over a minimal normal weight for age and
height (for instance a weight loss leading to maintenance
of body weight 15% below that expected, or failure to
make expected weight gain during a period of growth
leading to body weight 15% below that expected), intense
fear of weight or becoming fat even though underweight,
disturbances in the way in which one's body weight,
size, or shape is experienced (for instance, the person
claims to feel fat even when emaciated, believes that
one area of the body is too fat even when obviously
underweight), and in females absence of at least three
consecutive menstrual cycles when otherwise expected
to occur (secondary amenorrhea); a woman is considered
to have amenorrhea if menses occurred only following
hormone administration.
Patients with anorexia nervosa frequently
present with a history of weight fluctuations and shifts
in appetite regulation. Often the most dramatic symptom
is an abrupt or gradual shift in food selection (cuisine).
This occurs in the direction of lower calorie foods
and a shift in the absolute number and variety of foods
that are eaten. Often this constriction of cuisine is
accompanied by a variety of rationalizations for it
such as the fear of fat, reduction in calories, vegetarianism,
and various food fads. There is a shift in the consummatory
pattern (ingested intake style and day and night eating
habits). The patient is often seen to eat very slowly
and to cut food into small pieces. Often meals are prepared
by the patient in an aesthetically pleasing manner and
served to others while the patient does not a morsel.
Patients suffer from a number of
postprandial complaints such as after eating bloating
and a feeling of fullness. Such complaints in recent
years have been shown to be objectively related to delayed
gastric emptying and slowed bowel motility, most likely
on the basis of lowered metabolism, dehydration, and
possibly due to disrupted bowel hormonal controls.
Often patients show disturbances
of mood in the direction of depression, agitation, and
anxiety. Relatives complains of the patient's snappiness
and irritability.
In the history obtained from the
patient with anorexia nervosa there is often evidence
in a small number of patients of an actual history of
mild obesity. The later often forms a central core of
defense and resistance that aids the patients rationalization
for the reduction of food intake and the vigilant maintenance
of a thin body habitus. The patient's body mental representation
of the body which consists of their mental visualization,
self-evaluation, and actual body sensations is markedly
distorted. Although difficult to objectively demonstrate
patients subjectively feel that they are extremely large
and fat even though seen to be emaciated by others.
They depreciate themselves in rating the aesthetic value
of their body image and they complain of numerous unusual
body sensations such as enlarged shoulders, arms, thighs,
hips, and abdomen, although these cannot be objectively
seen or measured.
There are a number of reactive behaviors
such as occasional vomiting of an induced, ruminatory
regurgitation, or rumination type (often in the service
of reducing calories). Occasionally laxative or diuretic
abuse and polydypsia are present also as part of contraweight
maneuvers secretly engaged in by the patient patient.
Anorexia nervosa in the past has
been characterized as a relentless pursuit of thinness:
A fixed idea connected to the pursuit of a prepubescent
body habitus taking the female patient away from the
intensity and conflicts surrounding the increased body
size, growth, and psychological changes of puberty later
adolescence, and young adulthood.
Our recent more sophisticated understanding
of eating disorders views anorexia nervosa as a restrictive
eating disturbance occurring throughout the lifecycle.
Clinical cases have been reported as young as age six
and into the geriatric age range. Psychological concerns
often vary depending upon the stage of development.
Thus prepubescent cases are reported with more equal
incidence distribution of females to males (75/25%)
often accompanied by an obsessional and depressive clinical
picture and growth retardation. Female preponderance
(95/5%) occurs throughout adolescence and young adulthood
with the percentage of males increasing toward the middle
age level and in atypical cases predominating in the
geriatric age level. Restrictive eating disorder in
children tends to occur with a cognitive picture of
rejection and avoidance of both solid food and liquid.
Often the child has a phobic avoidance of the notion
of taking in food and a fear of swallowing or choking.
Sometimes this has been based on a traumatic incident
preceding the anorexia but often occurs in the nature
of an anxiety episode followed by phobic avoidance.
Because of the decreased fat percentage in prepubescent
children there can often be a precipitous loss of weight
and compromise of fluid and electrolyte status necessitating
early hospitalization, bedrest, and supportive approaches
to nutrition while psychiatric treatment is being initiated.
Also of particular interest both
in childhood cases of anorexia nervosa and in the childhood
history of adolescent and young adult patients are early
shifts in appetite regulation, food finickiness, shifts
in food selection, a history of unusual weight fluctuations,
and a locus of body image sensitivity such as early
injuries or congenital abnormalities. The symptoms of
anorexia nervosa are often minimized by the patient.
Professional attention usually results from pressure
by the family, spouse, school, or employer. First noticed
very often is unusual behavior related to food in addition
to the restriction of food selection and quantity of
food, unusual food related behaviors such as food hoarding,
changed food handling, or slowing in rate of eating.
Sometimes the patients seek nutritional
knowledge but one is often amazed by the numerous rationalizations
for limiting their cuisine including fears of the toxic
aspects of food, and a panople of contemporary health
concerns. Increased motoric activity amounting to several
hours per day of exercise is frequently found (a portion
of this genetic activity may be innovatively concealed).
The actual type of activity often include walking, stretching,
and calisthenics which although intense do not truly
represent a high level of kinetic work due to the patient's
real weakness and loss of strength due to muscle deterioration.
On the surface patients may state that their grades
in school continue to be excellent but on careful inquiry
one finds that their actual efficiency of studying is
reduced and there is a degree of cognitive dulling with
the need to put in many more hours of study to obtain
the same results obtained previously.
The common core physical symptoms
and signs in anorexia nervosa include amenorrhea (usually
of more than three months duration), abdominal discomfort
and constipation, bradycardia, cold intolerance, agitation
and hyperactivity, pervasive sense of lethargy, insomnia,
dry skin, brittle hair and nails, and often musculoskeletal
pain. Dental abnormalities are often seen with increased
caries due to the vulnerability to the teeth caused
by decreased salivation seen in restrictive anorexia
nervosa. Unusual cases of foot drop, peripheral neuropathy,
and a Wernicke Korsakoff-like syndrome have been reported
in patients due to possible thiamine deficiency. The
thermoregulatory deficit primarily manifested by cold
intolerance often is correlated with the rapidity and
extent of weight loss and in recent studies has been
shown to correlate to some degree with brain atrophy
shown by increasing cerebral ventricular size. Breast
atrophy and muscle wasting as well as susceptibility
to fractures (due to osteoporosis secondary to amenorrhea)
especially of the spinal column are not unusual consequences.
The skin may be covered by light downey hair (lanugo
hair) the significance of which is not clear but may
be related to both heat preservation and a shift to
prepubertal status in the hypothalamic pituitary hormonal
axis. Cardiovascular signs and symptoms such as palpitations,
bradycardia, and hypotension are a reflection of cardiac
atrophy and alternations in cardiac metabolism resulting
in changes in both myoneural transmission and work efficiency
of the heart secondary to the malnutrition. Hypokalemia
due to vomiting and laxative abuse in some patients
may also add to cardiac complications. In recent years
increasing numbers of patients have been studied with
co-existing diabetes mellitus and anorexia nervosa.
These patients are often exceedingly difficult to treat
due to the exacerbation of the eating symptoms by the
shifts in endocrine and metabolic status related to
the diabetes. Conversely up to 30% of diabetic patients
may show some type of either restrictive or bulimic
eating disturbance which does not reach the level of
a clinical disorder.
The clinical picture of anorexia
nervosa often presents with a challenge in differential
diagnosis and certainly the following conditions should
be considered: Hyperthyroidism, hypothyroidism, adrenal
insufficiency, hypopituitarism, inflammatory bowel disease,
and CNS or occult neoplasm. Hyperthyroid patients may
show weight loss and hyperactivity but also have increased
food intake, hyperthermia, heat intolerance, and increased
serum thyroid hormones. Hypothyroidism mimics anorexia
with symptoms of weakness, constipation, bradycardia,
hypothermia and cold intolerance. However, hypothyroid
patient often show weight gain, hypo activity, and increased
serum TSH.
Adrenal insufficiency may cause
bradycardia, hypotension, lethargy, decreased oral intake,
however it also causes hyperpigmentation, and decreased
intertriginous hair (hyperkalemia, low serum cholesterol).
Rarely pituitary dysfunction will cause amenorrhea but
there will also be a secondary hypothyroidism, adrenal
insufficiency, or changes in prolactin if caused by
a mass lesion.
Inflammatory bowel disease and other
causes of gastrointestinal dysfunction may be clinically
similar to some manifestations of eating disorders but
may be diagnosed by abnormal diarrhea and by laboratory
and clinical indications of inflammation.
Chronic illness such as tuberculosis
and malignancies may cause cachexia but these are not
accompanied by the desire for thinness and distorted
body image and are usually characterized by other specific
clinical signs.
The psychological profile of the
patient with anorexia nervosa is often characterized
by an obsessional rigid quality to ideas concerning
not only the restriction of food and perfectionistic
aesthenic body image but also a limited range of affective
expression in relationships to family and inhibitions
in heterosexual development. In preadolescents and children
with anorexia nervosa the cognitive framework is often
a phobic and avoidant attitude toward the intake of
food and fluids accompanied by signs and symptoms of
depression and anxiety. In adolescents there is often
a rejection of sexuality, perfectionism, rigidity in
thoughts, and a pseudoaltruism and over idealism.
Recent historical studies have suggested
that some of the early female saints of the Catholic
church may have had clinical anorexia nervosa accounting
for their propensity for fasting and asceticism. Chlorosis
(the "green sickness" described often in young
women in the 18th and 19th centuries) may have been
in some instances a form of anorexia nervosa accompanied
by anemia (iron deficiency), restrictive eating habits,
and psychological disturbances (interestingly the "green"
designation initially referred to the patient's pubescent
and virginal status).
Finally, recent observations of
food related behaviors in anorexia nervosa have yielded
interesting observations that may help to both define
the patient's clinical status and aid in their nutritional
rehabilitation. Often the patient's food preferences
are restrictive in fat and refined carbohydrates as
well as certain complex carbohydrates such as breads,
cereals, and protein (red meat). The patient frequently
consumes most vegetables and specific fruits in an effort
to control weight gain. Often there is an observable
increase in the amount of non-caloric condiments which
are used to alter the flavor of food, possibly to make
it less appealing (cinnamon, mustard, vinegar). In addition
there may be an increased desire for diet drinks, coffee,
and tea.
The physical experience with food
finds the anorectic cutting the food into small pieces,
often shifting the food around in order to arrange it
in novel patterns on the plate. The patient eats slowly
with prolonged chewing time before swallowing. Sometimes
there is a preference for small containers of food and
often food is "tossed away" to avoid consumption.
Although the patient with anorexia nervosa does not
usually induce vomiting very often food is spit out
of the mouth secretly and discarded and on occasion
ruminatory regurgitation and actual mechanical or chemically-induced
vomiting does occur.
Clinical research has shown that
patients later presenting as normal weight bulimics
with a past history of restrictive anorexia nervosa
are likely often to have complicated co-diagnostic problems
such as current depressive disorder and a more extensive
eating disturbance.
The most recent criteria for bulimia
nervosa consist of the following major features: recurrent
episodes of binge eating (rapid consumption of a large
amount of food in a discrete period of time usually
less than two hours); at least three of the following
1) consumption of high calorie easily ingested food
during a binge, 2) inconspicuous eating during a binge,
3) termination of such eating episodes by a abdominal
pain, sleep, social interruption, or self-induced vomiting,
4) repeated attempts to lose weight by severe restrictive
diets, self-induced vomiting, or use of cathartics or
diuretics, and 5) frequent weight fluctuations greater
than ten pounds because of alternating binges and fasts;
awareness that the eating pattern is abnormal and fear
of not being able to stop eating voluntarily; depressed
mood and self-depreciating thoughts following eating
binges; and bulimic episodes not due to anorexia nervosa
or any known physical disorder.
The actual syndrome of bulimia nervosa
defined a patient who suffers from powerful and intractable
urges to over eat and seeks to avoid the fattening effects
of food by inducing vomiting or abusing purgatives.
Most often the patient has, in addition, a morbid fear
of becoming obese. Usually there are a minimal average
of two binge eating episodes a week for at least three
months. In addition to the use of self-induced vomiting,
laxative, or diuretics patients may also engage in reactive
strict dieting or fasting and vigorous exercise in order
prevent weight gain.
Although this is predominantly a
disorder of women in the age of 12 to the mid-20's,
often the bulimia nervosa pattern of behavior may persist
into early middle age and up to 10% of cases are seen
in males. Rarely have instances of bulimia nervosa been
reported in childhood although recently a number of
atypical cases have been described involving hyperphagic
behavior and self-induced vomiting in children predominantly
in reaction to parental loss, abandonment, or childhood
bereavement.
Over three-quarters of patients
with bulimia practice self-induced vomiting and a modal
of frequency of binge eating and vomiting episodes is
usually ten per week. Close to one-quarter of the patients
with bulimia will abuse laxatives on a daily basis,
often in amounts several hundred times the suggested
recommended daily dose. Other behaviors such as the
chewing and spitting out of food, diuretic abuse, occasional
use of enemas, purposeful contamination of food, hoarding,
and kleptomania with respect to food have also been
described.
Bulimic patients have a dietary
chaos with fragmentation of their meal schedule,
long periods of fasting between meals a virtual absence
of consumption of normal meals. Binge episodes occur
outside of normal meal times frequently in early mornings,
late afternoons, or in the middle of the night. Middle
of the night binging may be a pattern with an equal
frequency of occurrence in males. There may also a correlation
with sleep disturbance and later onset of obesity. Often
the patient consumes rapidly large amounts of carbohydrates,
sweets, and easily prepared high calorie foods to the
point of abdominal distension and discomfort. Although
there is no agreed upon criteria, severe binges may
be from 2,000-20,000 calories in one sitting.
Dietary chaos, binge eating, and
abnormalities in food selection lead to long periods
of true anorexia (such as morning anorexia following
middle of the night binging), reactive fasting, and
a tendency to increased meal size due to the rebound
phenomena of prolonged periods of not eating punctuated
by the binges. Recently it has been shown that although
the patients with bulimia nervosa are usually of normal
weight they may experience episodes of increased serum
free-fatty acids and ketones which resemble a starvation
state. Despite their normal weight and usually high
normal body fat percentage, patients with bulimia nervosa
present with a number of clinical abnormalities including
oligomenorrhea and amenorrhea and specific nutritional
deficits such as iron deficiency, hypokalemia resulting
from the episodic vomiting, hyperamylasemia (specifically
increased serum salivary isoamylase) which may be related
to both the binging and vomiting as well as an abnormal
cephalic phase of eating.
Patient with bulimia may show metabolic
alkalosis, hypochloremia and hypokalemia. Parotid gland
swelling appearing as puffy cheeks is usually due to
acinar hypertrophy rather than hyperplasia. As a result
of the self-induced vomiting by placing the fingers
down the throat, patients with bulimia often have erosion
on the dorsal surface of the hand usually near the metacarpal
phalangeal joint of the second and third digit (Russell's
sign). Dental abnormalities are often prominent with
dental erosion on the lingual surface of the teeth from
the vomiting, as well as periomyolysis and other abnormalities
of the teeth and gums. Often when referring for dental
examination it is important that the examining dentist
be made aware of the bulimic disorder since this is
often concealed.
Bulimia should be differentiated
from hyperphagia which is defined as an excessive ingestion
of food beyond that needed for basic energy requirements.
Ingestion in hyperphagia may occupy unusual amounts
of time and eating may be obligatory and disrupt normal
activity. In contrast bulimia usually occurs surreptiously
in defined episodes and is terminated by abdominal pain,
guilt, or sleepiness. Hyperphagic conditions may occur
in association with central nervous system disorders
such as neoplasms, the Klein-Levin Syndrome (a bulimic-like
syndrome occurring in adolescents characterized by moderate
obesity, lethargy, and hypersomnia), Frohlichs syndrome,
Parkinson's Disease, genetic disorders including Prader-Willie
Syndrome (deletion of the long arm of chromosome 15),
and in associated major psychiatric disorders such as
depression, depressive phase of bipolar disorder, seasonal
affective disorder, certain phases of schizophrenia,
and in reaction to antidepressants and neuroleptics.
Often a typical patient with bulimia
has been found to be a single, Caucasian female in her
early 20's often well educated and slightly above average
weight for height. Results often show these individuals
are more vulnerable to anxiety, depression, impulse
behavior, mood fluctuation, confused sex role identity,
poor self-esteem, and severe food and weight preoccupations
in response to a cultural norm of thinness. Patients
with bulimia nervosa often have histories in early childhood
of either deprivation or over protection. The deprivational
histories often lead to conflict surrounding attachment
and loss with eating in response to mood sensitivity
leading to relief of either depression, anxiety, or
loneliness. Bulimic patients who have been over protected
or over stimulated as children, often have vivid memories
of their childhood conflicts and describe subjectively
a feeling during binging of both recapitulating the
earlier sense of security and also some degree rebelling
against the limitations of what others regard as rational
and healthy eating.
Binge eating occurs in individuals
when alone, not only due to the opportunistic situation
but also subjectively due to the desire to alleviate
a dyshoric mood state. The compulsive postprandial regurgitation
after a period of time not only serves as a contra weight
behavior but also takes on an acquired meaning related
to the satisfaction of asserting self-control by "purging"
the body of negative feelings. Investigations of the
developmental line of eating and the neurobiology of
appetite and eating may provide data to further define
bulimia as a disorder in a broader psychobiologic context.
There may be an early developmental
and neurobiologic linkage between mood regulation, bonding
and attachment, and appetite regulation that underlies
the particular linkages in the clinical manifestations
of bulimia nervosa. Specific food related behaviors
in bulimia involve both polyphagic and carbohydrate
specific desires during a binge. However, when not in
a binge or binge/purge cycle a bulimic patient may eat
cereal, cakes, cookies, ice cream, peanut butter, pasta,
and potato chips, thus showing a much broader range
of calorie rich foods and not demonstrating the restriction
of cuisine seen in anorexia nervosa. The bulimic patient
often consumes easily purged foods to control weight
gain and craves foods that satisfy taste desires usually
sweet or salty. Eating rate is increased and often there
are large bites of food with a lowered chewing to swallowing
ratio. Food hoarding and kleptomania that is food related,
occurs quite frequently as well as unusual food related
behaviors such as contaminating food in order to avoid
eating it, eating and binging of uncooked or unprepared
food. When out of control bulimic patients often disrupt
daily school and work activities to wander from store
to restaurant to store purchasing food, binging, storing
food in the car, and regurgitating. One might regard
such behavior as "obligatory," to the extent
that it preempts or capriciously interrupts important
scheduled activities.
Bulimic patients may have a history
of sexual abuse in childhood with severe developmental
psychopathology resulting in a co-diagnosis of borderline
or self-defeating personality disorder. A more chaotic
clinical picture may result magnifying the eating disturbance
and exaggerating psychological defensiveness and resistences
to treatment. One sees very frequently a family history
in immediate relatives of alcoholism, depression, and
upon careful inquiry one obtains histories of both bulimic
and restrictive eating disorder especially in female
relatives.
Early developmental history is often
reported as unremarkable, however more recently careful
studies are being undertaken to look at early maternal
nurturant behaviors and styles within the family. It
is possible that the influences of parental models of
eating peer group influences, and certain cultural pressures
may by an important element in shaping the development
of feeding and providing antecedent determinants of
bulimia nervosa. Diagnostic clarification will enable
us to fully understand and classify clinical subtypes
of bulimia nervosa. Multiple factors are involved in
both the etiology and persistence of the disorder, further
studies are needed to evaluate treatment protocols (pharmacologic,
individual and group psychotherapy, behavioral interventions,
and nutritional approaches) on the basis of long term
clinical course.
Pica is defined as a pathological
craving for either a food item or its constituents or
substances not commonly regarded as food. The psychiatric
diagnostic nomenclature emphasizes repeated non-nutritive
ingestion for a period of time which emerges as a habitual
mode of response for the patient. We may view pica in
a developmental context, such as determining the age
level of a patient, their physiologic state, and the
level of cognitive and intellectual development and
also relate pica to sociocultural and historical patterns
that may determine the actual food selections of a people
or a region.
Physiologic studies in animals had
shown that pica may result from specific nutrient deficiencies
or be part of a nutrient specific appetite.
Analogously the same pattern has
been inferred in humans. Nutrient deficiencies and medical
consequences such as iron deficiency, lead intoxication,
growth and cognitive impairment, and intestinal obstruction
are frequently associated with idiosyncratic dietary
habits. Additionally pica may be seen in the deteriorating
phase of certain schizophrenic patients as well as being
frequently observed among the mentally retarded and
in the developmental chaos of autistic children. The
most prominent incidents of pica occurs in association
with iron deficiency in a fascinating array of clinical
phenomena. Some examples will follow.
A 43-year-old female who developed
anemia secondary to menorrhagia began to show the eating
of ice (pagophagia) frequently several ice trays of
ice cubes per day. Therapy with oral iron abolished
the pica within three weeks.
A 53-year-old female who had a partial
gastrectomy 15 years prior to evaluation had demonstrated
an esophageal web receiving mechanical dilatation to
relieve dysphagia. Her hemoglobin was 7. The patient
developed craving for tomato seeds which was rather
relentless and constituted a good deal of her eating
behavior throughout the day. Parental iron treatment
abolished the pica.
A 33-year-old female who developed
anemia secondary to carcinoma of the ascending colon
developed pagophagia (ice cube eating) which was abolished
by oral iron and blood transfusions.
A 48-year-old female developed cautopyreiophagia
(ingestion of ashes of 15 burnt match books daily).
Her hemoglobin was 6.5 grams and her serum iron was
14. This patient had gastrointestinal bleeding due to
a lesion in the cecum and adenocarcinoma of the left
lobe of the liver. Iron therapy, surgery, and transfusion
abolished the pica.
Early cases of pica dealt with pregnant
women who ate clay and were mildly anemic. There were
problems interpreting the data from these studies since
there were often cultural traditions related to fertility
and assuring the safe birth of a child. Current explanations
of pica center around developmental studies where
pica is viewed as possibly a vestigial instinct, psychodynamic
theories related to early maternal deprivation and parental
conflict, need state hypothesis that purpose
a nutritional deficit and homeostatic compensation,
sociocultural determinants that involve ethnic
traditions and beliefs related to rights of passage,
health, and fertility, consequences of erratic reinforcement
in a chaotic unstructured environment, and neurobiologic
bases of food selection and ingestive behavior data
resulting from animal investigations (iron deficiency
leading to pagophagia, pica resulting from labrynthine
stimulation, and pica and iron deficiency related to
decreased dopamine receptor neurotransmission as an
etiologic factor in spontaneous pica).
In children factors such maternal
deprivation, joint family structure, parental neglect,
child beating, impoverished parent-child interaction,
and disorganized family structure have been implicated
in those children who develop pica in association with
anemia in contrast to children with anemia without pica.
It has also been shown that a significant
number of children who demonstrated persistent pica
later developed alcoholism. Some additional evidence
implicated gastrointestinal distress and a type of gastrointestinal
"malaise" which persists after the physiologic
cause has been removed. In the later situation pica
may persist as a result of physiologic conditioning.
In children ages eighteen to thirty-six
months old pica may be considered normal with an incidence
of greater than 50%. However, persistence of excessive
hand to mouth movement as in pica is abnormal in children
older than three. In the past there have been a racial
association of double the percentage of incidence of
pica in black children 1:6 compared with a Caucasian
cohort. Pica has been associated with diets that are
not only low in iron but also zinc and calcium in comparison
to control diets. In the mentally retarded there are
changes in incidence of pica with IQ, the use of medication,
and manifestations of behavioral and appetite. The majority
of patients with pica are moderately under weight. Pica
appears to increase as the IQ increases. There is also
an increased incidence of pica in patients with CNS
congenital anomalies and associated medical problems
such as diabetes, deafness, and seizures.
Pica seems to increase in incidence
in patients taking neuroleptic which may be related
to diminished postsynaptic dopamine receptor changes.
In the retarded behavioral problems associated with
pica may include stereotyped behavior, hyperactivity,
self-abuse, food related abnormal behaviors including
eating off the floor and chewing of objects. Pica may
also coexist with rumination, hyperphagia, and anorexia.
Geophagia, sociocultural factors
and developmental considerations all have been significant
in determining the type of pica. Lead poisoning continues
to be a hazard in young inner city children residing
in homes that remain with lead base paint have an incidence
of excessive blood level bordering on 20%. The persistence
of hand to mouth movements in young children, especially
from age 18 months to three years, results in the ingestion
of lead based paint. Lead may also enter the blood stream
by inhalation of particulate lead from automobile fumes
and from nearby factories which use lead based materials.
Greater environmental sensitivity to protection of the
population has slowly but definitely reduced the foregoing
hazards. Elevated blood levels had multiple effects
on cognition (including learning impairment and behavior,
diminished attention span and impulsive behavior) when
whole blood levels reach 70 dB micrograms per dl an
insidious onset of anorexia apathy and poor coordination
may occur. Neurologic complications of chronic lead
poisoning may present as mental retardation, convulsive
disorders, peripheral neuropathy, behavioral disturbance,
or any combination thereof. Reduction in exposure is
the cornerstone of prevention in a lead intoxication
treatment program and active consultation with medical-social
service departments is clearly indicated.
Special types of pica and their
medical complications include paper pica which may lead
to mercury poisoning and a particular group of signs
and symptoms with low serum iron and zinc in association
with geophagia in Turkish children who may manifest
hypogonadism, hepatosplenomegaly, and dwarfism.
Bezoar is derived from the Persian
word signifying "antidote." These were concretions
from the alimentary canal of animals and were thought
to have both medicinal and magical properties. Clinically
bezoars can be characterized as tricho (hair), phyto
(plants), and gastro- (mineral or chemical substances).
Tricho and phyto bezoars account for over 90% of reported
clinical cases. Certain occupational situations (painters
who swallow shellac, asphalt workers), medical procedures
and treatments (contrast radiography and medically prescribed
special diets) may predispose to bezoar formation.
A case example might involve a 17-year-old
female in whom a hair ball was found to take up almost
the entire stomach and gastrostomy was required for
removal. Further clinical evaluation might find that
this young woman had trichotillomania and trichophagia.
Other factors to consider might be psychosocial tension
and conflict in the family as well as the possibility
of an obsessional or delusional disorder of some type.
Another example might be discovery
of a trichobezoar in a young child exhibiting trichophagia
along with iron deficiency and possible irritation and
hemorrhage of the gastric mucosa. Fecal impaction has
been described in two school age children resulting
from sand eating. Pica may also result from iron deficiency
secondary to celiac disease. Medical complications resulting
from pica such as intestinal obstruction, intestinal
perforation, dental complications, hyperkalemia associated
with geophagia, hypokalemia with anemia and parisitosis
must always be considered. For instance a significant
number of children with toxocariasis have a history
of pica. Younger patients and children with pica should
be routinely screened for parasitism and other possibly
orally transmitted diseases.
Radiographic findings may assist
in diagnosis of pica and an abdominal flat plate may
visualize chips of lead paint, radiolucent paint particles
of clay or foreign objects. In intestinal perforation
pneumoperitoneum may be seen especially after the ingestion
of a sharp object. A radiopaque foreign body may be
visualized and a barium swallow may be useful in determining
whether a large gastric mass is bezoar, leiomyoma or
carcinoma. In rare situations maternal pica of lead
based material may result in the birth of infant with
radiographic findings of congenital lead poisoning.
Parotid hypertrophy occurs frequently
with starch eating. As noted above many delusional and
psychotic patients should be screened clinically for
pica. Kraeplin was one of the first to document an extraordinary
array of inedible materials consumed by psychotic patients
and felt that this behavior might be a "vegetative"
sign of psychosis: "A perversion of the appetite."
For instance an interesting syndrome of nicotinism and
myocardial infarction was described in a psychotic delusional
patient who repeatedly ate tobacco.
The clarification of the role of
iron deficiency as an etiologic factor in spontaneous
pica is ongoing. Current ideas center around the possibility
of a central nervous system neurochemical iron dependent
appetite regulation. Investigations, however, have linked
decreased brain iron specifically to decreased dopamine
2 receptors and the consequent reduction of several
CNS dopamine driven behaviors. This suggests that there
may be a role for the linkage of iron depletion to a
dopaminergic component in the psychobiology of food
selection.
Mechanisms which ensure variety
of food selection and avoidance of possibly dangerous
or none nutritive foods may be impaired in pica. Pica
in man is indeed a complex behavior with multiple determinants
ranging from demands of tradition and acquired tastes
in the cultural context to presumptive neurobiologic
mechanisms (iron deficiency, CNS neurotransmission,
physiologic conditioning).
Clinical consequences of pica may
have broad epidemiologic implications as in lead intoxication
and geophagia in children leading to severe impairment
of intellectual and physical development. Acute and
chronic medical complications may pose surgical emergencies
(intestinal obstruction from bezoars) as well as more
subtle encroaching symptoms of parasitosis intoxications
and resulting nutritional deficits.
Although pica, as a naturally occurring
behavior in animals, has a parent utility in aiding
digestion or overcoming nutritional deficit, its presence
in man appear to be the result of culturally contrived
or pathophysiologic circumstances and any adaptive value
remains obscure. The occurrence of pica in pregnancy,
mental retardation, schizophrenia, and autism suggests
a psychobiologic significance to link a disturbance
in food selection to other complex neuroendocrine mediated
responses.
Treatment approaches have been primarily
preventative, educational, and directed toward modification
of the pica behavior itself. Iron repletion has dramatically
reversed pica for those patients whose clinically symptoms
were more clearly coincident with iron deficiency from
nutritional or covert medical causes. Further investigation
of pica may clarify the normal psychobiology and developmental
progression of food selection.
Rumination, which is an uncommon
disorder may occur from infancy through adulthood, and
is derived from the Latin ruminiare "to
chew the cud." Merycism derived from the Hellenic
is the act of post ingestive regurgitation of food from
the stomach back into the mouth followed by chewing
and reswallowing. The two terms after often used interchangeably.
Rumination is associated with medical complications
such as aspiration pneumonia, electrolyte abnormalities
and dehydration and is considered in the differential
diagnosis of vomiting and failure to thrive in infants
and young children.
From latency through adulthood rumination
frequently has a benign course. Recently, however, it
has been associated with bulimia, anorexia nervosa,
and depression. Past studies have described the disorder
to lack of emotional responsivity in attunement between
mother and child stemming from early maternal depression
and anxiety. Medical disorders such as gastroesophageal
reflux and hiatal hernia also are present in the population
of ruminating children. Applications of formal behavioral
therapy techniques such as aversive conditioning has
been common in the past decade complimenting the more
traditional approaches utilizing a substitute caregiver.
It should be noted that in the psychiatric nomenclature
rumination is designated as a disorder of infancy.
The infant shows a characteristic
position of straining and arching of the back with sucking
tongue movements and the gaining of satisfaction with
the rumination. Diagnostic criteria include repeated
regurgitation without nausea or associated gastrointestinal
illness for at least one month following a period of
normal functioning usually for three months, weight
loss or failure to make expected weight gain occurs
often. Irritability is noted between regurgitations
and hunger is often inferred by the observer. Although
the disorder occurs most frequently after three months
of age it has been reported in as young as a three week
old infant and in rare occasions in the neonatal intensive
care unit. Consequent failure to thrive with malnutrition
may produce severe developmental delays. Interestingly,
rumination has been described in families over four
generations with the theory proposed that children learned
to ruminate by imitation of their parents. The course
of rumination may depend on the age of the patient and
the severity of the complications. Although the infant
may manifest hyperphagia, post ingestive regurgitation
leads to progressive malnutrition (sham eating).
In the ruminating adolescent bulimia
and affect disorder may be present. Rumination in adults
has been associated with gastric carcinoma and anemia.
More frequent medical complications occur in the retarded
often with the mortality rate as high as 12-20%.
A possible differential diagnosis
of two vomiting syndromes of infancy may contrast nervous
vomiting from infantile rumination. Nervous
vomiting: the nature of the vomiting is involuntary,
visceral, purposeless, with age of onset as early as
the newborn. Mothering is attentive but dysynchonic
and increases rather than relieves tension. Typical
circumstances of nervous vomiting occur during the baby's
responsiveness to environmental stimulation and successful
management often lessens excessive stimulation alleviating
the tension producing quality of the mother-infant interaction.
In contrast infantile rumination
often appears voluntary, behaviorally based, a form
of self-stimulation and occurs after three months of
age. The mother is frequently emotionally distant and
one notes little reciprocal interaction and attunement.
Typical circumstances of the vomiting occur in the absence
of environmental stimulation when the infant is often
alone and management frequently involves increasing
environmental stimulation with substitute caregivers
who satisfy the infant's needs by efficient and empathic
mothering with appropriate reciprocity and attunement.
From a psychodevelopmental perspective
rumination may be viewed as a type of voluntary self-feeding
compensating for an inadequate mother-infant relationship.
It may then become a defensive habit pattern with both
functional autonomy and a pleasurable self-reinforcing
effect. Rumination has occurred in infants with disorders
including reflux esophagitis, hiatal hernia, malabsorption
and malnutrition, failure to thrive, prematurity, severe
bronchopulmonary dysphagia, growth failure, autism,
grand mal epilepsy, tuberous sclerosis, heroin withdrawal,
barbiturate withdrawal, severe parental object loss,
and severe infection. Repetitive self-stimulatory behavior
(head banging, body rocking, and genital and anal/fecal
play) resistent to maternal interruption has been observed
in ruminating infants.
In young children the persistence
or appearance of rumination is often preceded by a tendency
to rumination in infancy and is characterized by intensity
and frequency changes correlated with emotional arousal.
In adolescents the appearance of rumination is often
associated with anorexia nervosa, bulimia, anxiety,
and depressive disorders and iron deficiency. Rumination
in adults may be chronic, or the individual episode
is postprandial without nausea, effortless, and predominantly
involuntarily in appearance. It may appear occur spontaneously
after a hastily eaten meal causing embarrassment or
may appear seemingly voluntarily and pleasurable. The
symptomatic presence of active ruminatory behavior varies
from as little as six months in duration to a lifetime.
Patients may complain of food returning to the mouth,
belching, precordial distress (possibly due to esophagitis),
indigestion, halitosis, and excessive dental deterioration.
Interesting cases of rumination
have been noted in the past such as using the rumination
as a sham eating technique and utilizing ruminatory
behavior to eat and dispose of foods contraindicated
medically (fatty foods and meat) which have a strong
palatability or preference for the patient. As an example
a patient with gallbladder disease would regurgitate
and extrude fatty foods after enjoying eating them preventing
their absorption which might lead to an attack of cholecystitis.
The presence of specific psychiatric
disorder in adult ruminators is unclear, however there
are reports of associations with anxiety, atypical personality,
affective disorder, and neuroaesthenic traits. Although
some would see the persistence of ruminatory behavior
in adulthood as a relatively benign trait, this is questionable
since medical complications such as aspiration, and
severe dental complications may occur. There may be
a subgroup of normal weight bulimic patients with primary
ruminatory behavior which antedates their bulimic symptoms.
These patients are more likely to be polyphagic during
binge episodes rather than demonstrating the more usual
specific carbohydrate preference. Ruminatory behavior
shifts to actual regurgitation during adolescences to
promote weight control. Such ruminators may not show
the pattern of impulsive behavior, affective disturbance,
or the family history of alcoholism seen in other patients
formally diagnosed as bulimic. There may be, in fact,
two adult subgroups of ruminators one group with minimal
psychiatric problems and a second group with an associated
eating disorder such as anorexia nervosa or bulimia.
Since patients are often reticent about their ruminatory
illness the diagnosis of psychiatric disturbance may
go undetected.
Ruminatory behavior is prevalent
in the institutionalized retarded, often from 2-5%.
Frequently individuals with pica also exhibit rumination.
CNS lesions such a microcephaly, dilated ventricle,
cerebral palsy, apnea, an infantile spasms may be associated
with ruminatory behavior. Features such as predominant
self-abuse and other food related behaviors such as
pica, hyperphagia and anorexia, as well as medical complications,
have been associated with ruminatory behavior in the
retarded. The later patients seem to utilize the rumination
in a self-stimulating manner to relieve internal tension
states blocked from social release because of marked
communication deficits and inability to seek out external
stimulation.
Clinical example might include a
10-year-old boy who lost weight and started ruminating
following institutionalization and separation from family.
Treatment by increasing environmental stimulation abolished
the rumination demonstrating that prompt social stimulation
and reinforcement may abort or terminate the ruminatory
disorder often related to institutional adjustments.
There are a number of theories regarding
the etiology of ruminatory disorder. A behavioral focus
would see the rumination as a habit pattern which is
enhanced by reinforcement such as attention and food,
certain conditions may serve to maintain the rumination
as an operant behavior. A habitual response characteristic
of rumination is suggested by, at times, its seeming
voluntary quality, frequent waxing and waning with environmental
stress, and extinction in response to a aversive stimuli.
There are a number of lines of evidence
linking rumination with mood disturbance (affective
disorder). Infants and children with rumination often
appear sad and withdrawn. For instance, a ruminating
child may develop features of anaclitic depression due
to the absence of a satisfactory love object and an
attuned and reciprocal interaction with mother. Numerous
descriptions have been presented describing the emotional
unavailability of a mother to her child because of maternal
depression as well as her feelings of rejection toward
an unwanted infant. The child may suffer a significant
human object loss of the primary caregiver. Thus the
infant or child is understimulated with consequent development
of a ruminatory disorder.
An animal experimental model of
this type of object loss leading to ruminatory behavior
has been observed in primates. There is also a subgroup
of children for whom human object loss may be a manifest
onset condition for the appearance of ruminatory behavior.
In fact, a careful review of the literature reveals
that human object loss is the most frequent psychosocial
onset event associated with rumination. A pleasurable
self-stimulating component of ruminatory behavior may
serve as a defense against the pain of human object
loss. Protest, despair, withdrawal which are generally
associated with human object loss may also be developmentally
specific clinical features in the symptom context of
rumination following such loss.
Maternal mood disorder may lead
to both a genetic factor present in the infant and secondarily
to deprivational consequences to nurturance due to the
mother's depression both contributing to increased risk
for the infant for both mood vulnerability and ruminatory
disorder. There may be a subgroup of infants and children
with rumination who in fact have an affective disturbance,
rejection sensitivity, passivity and increased incidence
of psychiatric disorder. Ultimately diagnostic procedures
for measuring biologic state and trait markers for affective
disorders might be useful in further defining the relationship
of rumination subgroups to other specific psychiatric
disorders.
Prospective followup of ruminators
noting whether a greater than normal incidence of affective
or other psychiatric disturbance occurs would clarify
this linkage. Biological determinants link rumination
with gastroesophageal reflux. In infant and child ruminators
diminished lower esophageal sphincter pressure has been
found. There may be two subgroups of ruminators one
with significant gastrointestinal problems such as reflux
or hiatal hernia and another with no significant gastrointestinal
structural difficulties.
Reflux has been associated with
Sandifers Syndrome. This is a disorder of interest to
psychiatrists because the patient who displays head
cocking (abnormal movements of the head and neck) and
unusual postures may be misdiagnosed as having a tic
or dystonic disorder. In fact, the abnormal postures
occur during gastroesophageal reflux in a child with
a hiatal hernia. Often surgical repair of the hernia
abolishes reflux terminating the abnormal movements
within several days.
In several patients with hiatal
hernias and rumination it has been noted that the rumination
often terminated after surgical repair of the hiatal
hernia. It has been suggested that rumination should
be viewed as part of an extended syndrome of the presentation
of gastroesophageal reflux. The role neuropeptides (including
opioids in rumination) remains to be precisely defined.
There may be a role for peptide hormones such as vasoactive
intestinal peptide (VIP), CCK, gastrin, and motilin.
Opioid containing neurons innervate the circular muscle
and it has been shown that an opioid agonist may totally
inhibit postingestive rumination in adults which along
with other pharmacologic blocking interventions suggests
a central or peripheral opioid mechanism in rumination
characterized by opioid receptor insensitivity or a
reduction in endorphinergic neurotransmission. Studies
in sheep have demonstrated ruminant stomach motility
to be controlled by opioid inhibitory and stimulating
neurotransmission in the central nervous system. A similar
opioid mediating system is important in the regulation
of attachment and the response of separation distress
in mammals. It is possible that the deficiency of attachment
and occurrence of separation may diminish endogenous
opioid activity and provoke ruminatory behavior in infancy.
Rumination and vomiting have been reported during the
post natal withdrawal phase in infants born of narcotically
addicted mothers.
The etiology of rumination is unclear.
Physiologic, psychodynamic, and behavioral theories
have been suggested. Rumination is best seen as a psychobiologic
disorder in which psychological and physiological abnormalities
combine in varying degrees to produce the ruminatory
behavior. Rumination may be on a continuum where the
patient might have maximal gastrointestinal pathophysiology
such as severe reflux with hiatal hernia and minimal
psychological concomitants or the converse where the
patient might have minimal gastrointestinal pathophysiology
or reflux but severe psychopathology or psychosocial
stress.
Proponents of biological theories
believe that the psychological factors definitely influence
rumination. Multiple stresses in children can produce
similar symptomatic behaviors. For the child irritability
and discomfort may result in feeling overwhelmed, anxious,
or depressed or may be manifest as severe reflux with
esophagitis. Inferred reflux esophagitis treated either
medically or surgically may result in a feeling of well
being and a termination of rumination.
Psychodynamically oriented treatment
using a substitute caregiver may reduce rumination for
two reasons. First, the child receives increased stimulation
which aids in trust of an attachment. Second, this additional
care is effective because the child is held upright
during the period of stimulation diminishing both reflux
and esophagitis. The esophagitis which subsides augments
lower esophageal sphincter pressure further diminishing
reflux. Diminished esophagitis results in reduced psychological
tension promoting feelings of well being of both the
infant and mother.
Maternal anxiety may promote secondary
physiologic changes in a child. For example, a mother
feeling overwhelmed by a stressful stimulation or feeling
anxious secondary to a child's persistent vomiting and
weight loss may exhibit increased motoric tension. This
is transmitted to the child who becomes tense and developed
a more rapid heart rate. The increased autonomic response
may alter neuroendocrine controls producing lower esophageal
sphincter relaxation and increased reflux. Thus the
tendency of the child to ruminate may be increased by
an anxious mother. Psychiatric disorder has been associated
with both reflux and esophageal contractility abnormalities.
Transmitted maternal stress could result in infant gastroesophageal
contractile dysfunction promoting reflux and rumination.
Two biopsychosocial sequences of
rumination in an infant may be formulated. One involving
the predominance of interactive maternal child psychopathology
and the other involving the predominance of gastroesophageal
abnormality. A close interrelation occurs between mother
and infant with various pathophysiologic and emotional
stresses. Diagnosis and treatment based on evaluation
of both the psychological state of the mother and the
infant's gastrointestinal function is indicated.
In summary rumination is an uncommon
disorder occurring from infancy through adult life.
Its consists of regurgitating and then reswallowing
partially digested food. It may result in considerable
morbidity in infants and young children. Adult ruminators
may have a benign course with embarrassing involuntary
reflux or may have an associated eating disorder such
as bulimia or anorexia or a mood disturbance such as
depression.
Biologic theories of etiology associate
rumination with gastroesophageal reflux, hiatal hernia
and delayed gastric emptying. Psychological theories
discuss infants who have severe failure to thrive and
often appear depressed. Severe disincrinty between mother
and infant and maternal psychopathology consisting of
anxiety, depression, and inability to adequately nurture
the child may be present. Behavioral ideas discuss self-reinforcing
aspect of the ruminatory behavior. Finally theories
of neuropeptide and opioid regulation cause central
and peripheral deficits of endorphenergic neurotransmission
and receptor sensitivity. Rumination associated with
interactive psychopathology may in fact be an affective
disorder variant.
Treatment approaches emphasize pharmacologic
or surgical treatment of reflux, psychological treatment
of the infant-mother disincrinity (with the use of substitute
caregivers), and behavioral treatment at times using
aversive stimuli (lemon juice, pepper sauce) or positive
social reinforcement in response to the stereotype ruminatory
behavior. Since rumination may have a biologically or
psychologically predominant context a biopsychosocial
theory and sequence are the best approach for diagnosis
and treatment. Therefore a multiple disciplinary approach
to diagnosis and treatment that uses available treatment
modalities is imperative to treatment this disorder
comprehensively and effectively.
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