Am
J Psychiatry
Binge
/36:5,
Eating
/979
CLINICAL
Associated
BY RICHARD
Binge
May
with
A. MOSKOVITZ,
eating
has
been
Oral
M.D.,
AURORA
recently
LINGAO,
(1-4)
as a
distinct clinical syndrome with possible neunophysiologic correlates. It is characterized by sudden, uncontrollable episodes of excessive eating, usually ending in physical distress. It may be followed by self-induced vomiting and usually leads to feelings of remorse or self-contempt. Although similar behavior occurs in some patients with anorexia nervosa, the relationship of the binge-eating syndrome to anorexia nervosa is unclean (5). The following case, a typical example of this syndrome, was marked by a dramatic remission of symptoms following discontinuation of an oral contraceptive. It is to our knowledge the first reported case correlating clinical change in symptoms with changes in the EEG. Report
She had taken one combination pill for about 2 years and changed to another, which contained I mg of norethindrone and .05 mg of mestranol, when she was 21. Neurologic examination was unremarkable. Thyroid studies and a glucose tolerance test done before referral were normal. Her initial EEG was remarkable for bifrontal, rhythmic slow and sharp activity. A follow-up EEG I month later was similarly abnormal. A CT scan showed left-sided punctate basal ganglia calcification of undetermined significance. After 8 months of further evaluation and psychotherapy, the patient birth
control
She
reported
single woman was referred for compulsive of3 years’ duration. Since age 21 she had experienced episodic eating binges characterized by a driven, ego-
alien
feeling.
stances
or
several clusters apart, 152.4 despite
She
could
emotions.
identify
The
episodes
no
precipitating
lasted
from
circum15 minutes
acute
fluctuations
of
1.8-2.3
kg
during
our
pills
on a trial
a gradual
binges.
quelae.
Her
mood
and
Dr.
Moskovitz
University
1979:
accepted
is Assistant
of Florida
School
Feb.
Professor, of Medicine,
5,
1979.
contraceptive tivity and
Box
J-256,
of Psychiatry, J. Hillis
Miller
Health Center, Gainesville, Fla. 32610, where Dr. Lingao was a resident when this paper was written. Dr. Lingao is now Psychiatrist, Southwestern State Hospital, Thomasville, Ga. The authors this case.
thank
Dr. Sharda
Karuturi
for her early
0002-953X179/06/072
management
l/02/$00.35
improvement
fitted
in her
with
her
an IUD.
symptoms
over
self-esteem
improved
with
the abate-
Conment
Several reports (1-4, 6) have linked binge eating with abnormal EEGs. The significance of small sharp spikes and 14- and 6-per-second positive spikes, which account for the majority of these abnormalities, has been debated. Two groups of researchers ( I 3) have
reported
encouraging
of
© I 979
results
from
treating
binge
eaters
phenytoin. Rau and Green (4) have reported a correlation between an inventory of soft neurologic signs, including EEG abnormalities, and clinical nesponse to phenytoin. Hypothalamic dysfunction has been suggested (1-3) as a possible etiology for the binge-eating syndrome. Either an inhibitory effect on the ventromedial satiety center or an excitatory effect on the lateral appetitive center of the hypothalamus could lead to hyperphagic behavior. Since oral contraceptives exert at least part of their effect at the hypothalamic level (7), they might influence the emergence of binge eating. The almost exclusive occurrence ofthis syndrome in females, primarily with
We
Department
to discontinue was
and her weight stabilized at 45.4 kg. A EEG 5 months after she stopped taking the oral showed marked reduction of epileptiform acwas only marginally abnormal.
of child-bearing
8,
and
of symptoms,
fect, although been offered request that Jan.
basis
,
and secrecy. occur at any
time of day. The patient would rapidly consume large amounts of food, mostly sweets and starches but also leftovers and other ready-to-eat fare. Each episode would end with marked abdominal distress or sometimes sleep but no vomiting. After each binge, she felt helpless, disgusted, and guilty. Depression accompanied each cluster of binge eating, with insomnia, feelings of defectiveness. and fear of losing control. The frequency and intensity of the binges fluctuated. She could recall no binge-free interval longer than I month since the onset of the episodes. Aside from infrequent headaches, which were rarely severe, she had no other major psychiatric or neurologic symptoms. The patient appeared to function normally in other respects. The only remarkable aspect of her medical history was the use of oral contraceptives continually since age 19.
Received
recommendation
to
hours and occurred in clusters over 2 to S days. The were spaced from several days to several weeks alternating with periods of strict dieting. She was cm tall and maintained her weight at 47.7-48.6 kg
The binges generally occurred in solitude They tended to occur in the evening but could
accepted
the next 2’/2 months. By the end of this time she noted a marked change, with only I episode ofovereating during the following 3 months. This episode, on Thanksgiving, was not accompanied by the usual drivenness and emotional se-
follow-up
A 25-year-old eating abrupt
REPORTS
M.D.
ment
Case
RESEARCH
Contraceptives
AND
described
AND
age,
further
suggests
a hormonal
psychodynamic explanations (5). These considerations our patient stop her medication.
postulate
that
the
marked
improvement
ef-
have
led
also
us
to
in our
patient’s symptoms and the associated improvement in her EEG resulted directly from her discontinuing the use of birth control pills. These assumptions are limited by our omission of blind technique and our failune to rechallenge the patient with her medication. Nevertheless, the subacute time course of her imAmerican
Psychiatric
Association
721
CLINICAL
AND
provement
RESEARCH
suggests
This case neurophysiologic
drome.
that
this was not a placebo
provides further mechanism
It particularly
hypothalamic
excitability
a role
Since
our
with an epileptiform that hen symptoms
of the
lateral
for
I. Green bances
disordered
patient’s
response
CT
Scan
pattern, we from over-
hypothalamus.
to phenytoin.
Variants
BY ROBBIE
and
CAMPBELL,
Although
Genetic M.D.,
it is well
Heterogeneity
PETER
known
that
HAYS,
genetic
136:5,
Ma)’
1979
of compulsive medication. Am
eating disturJ Psychiatry
1974
2. Rau JH, Green RS: Compulsive eating: a neurophysiologic approach to certain eating disorders. Compr Psychiatry 16:223231, 1975 3. Wermuth BM, Davis KL, Hollister LE, et al: Phenytoin treatment ofthe binge-eating syndrome. Am J Psychiatry 434:12491253, 1977 4. Rau JH, Green RS: Soft neurological correlates of compulsive eaters. J Nerv Ment Dis 166:435-437, 1978 5. Nogami Y, Yabana F: On Kibarashi-gui (binge eating). Folia Psychiatr Neurol Jpn 31:159-166. 1977 6. Davis KL, Quails B, Hollister L, et al: EEG’s of ‘binge” eaters (ltr to ed). Am J Psychiatry 131:1409, 1974 7. Kastin AJ, Schally AV, Gual C. et al: Release of LH and FSH after administration of synthetic LH-releasing hormone. J Clin Endocrinol Metab 34:753-756, 1972
The epidemiology of binge eating raises the question of its frequency of association with oral contraceptive use. While none of the authors cited above indicate which of their patients were using these drugs, we would expect, according to chance alone, that some were. It would be interesting to see whether reanalysis of their data shows correlations between oral contraceptive use and either EEG abnormalities or positive
RS, Rau JH: Treatment with anticonvulsant
131:428-432,
symptoms
EEG resulted
J Psychiatry
REFERENCES
effect.
evidence to support a for the binge-eating syn-
suggests
function.
were correlated further suggest
Am
REPORTS
in Schizophrenia
M.B.,
DON
factors
are
B. RUSSELL,
None
M.D.,
of
the
AND
DAVID
subjects
J.
had
ZACKS,
M.B.
epilepsy,
neunologic
syn-
important in the etiology of functional psychoses, it is also clear that a specific overt genetic predisposition is not always necessary for their emergence. Dalen (I) demonstrated two sets of etiologic factors in a series of
dromes, or a history of alcoholism, drug psychosis, more than trivial exposure to illicit drugs other
or than
cannabis.
been
manic
drugs.
patients,
associated
one
with
Subsequently,
set
EEG Hays
mainly
genetic
and
and
brain
anomalies (2) drew
similar
the
other
a series of bipolar manic-depressive patients and on the basis of a series of schizophrenic patients, forward
a similar
hypothesis
about
two
a family
later, put
gree
separate
sets
scans logic
are therefore hypothesis.
suitable
for
testing
the
above
etio-
Method
The scribed
the
subjects
were
35 outpatients
as schizophrenic
psychiatrist
who
by another
who
proposed
had
been
consultant
them
for
de-
and
the
by
study.
Aug.
7, 1978:
revised
Jan.
9, 1979; accepted
Feb.
6, 1979.
history
adopted.
All
or
on P.H.) that
relatives;
relatives’
most
accounts.
subjects
similar
obtained
covered
all
histories Patients
from first-
were were
ral classification patients had
height thought
had
of the detailed
schizophrenias recording
had
psychotropic
and
each
patient
second-dc-
supplemented then
two groups; those with and those without tory of major functional psychosis. In the course of a separate investigation
by
divided
into
a family
his-
of the natu-
(5), 18 of these of symptoms at the
of the syndrome. Of these 18 subjects, 16 had disorders, 19 had hallucinations (auditory in
12 cases), I I had catatonic symptoms, 15 had delusions that were regarded as primary, and 7 had passivity phenomena. The 7 patients who did not have catatonic symptoms had auditory hallucinations. Of the I I patients who did not have passivity phenomena, 9
had Received
was
phenothiazines
of us (R.C.
from
of etiologic factors in schizophrenia (3). Like EEGs, CT scans are painless and safe, and have been reported to show abnormalities more often among schizophrenics than among controls (4). CT
None
with
One
damage.
conclusions
treated
primary
delusions,
1 had
prominent
catatonic
symptoms, marily of
and 1 had a syndrome that consisted thought disorder, tactile hallucinations, misrecognition , and secondary delusions.
pri-
is Associate Professor, and Dr. Hays is Professor, of Psychiatry, University of Alberta, First Floor, Clinical Sciences Building, Edmonton, Alberta, Canada T6G 2G3. Drs. Russell and Zacks are Consultant Radiologists, University of Alberta Hospital. Address reprint requests to Dr. Hays.
visual CT scans were performed using an EMI head scanfling unit with a water bag. Six images (160 x 160 matrix) were obtained for each patient. The scans were
This project was supported Health Advisory Council.
angled 15#{176} offthe orbitomeatal and number printouts were
Dr.
Campbell
Department
722
by a grant
from
the
0002-953X/79/06/0722102/$00.35
Alberta
Mental
© 1979
American
Psychiatric
Association
line and obtained.
a film recording No sedation
on
J Psychiatry
Binge
/36:5,
Eating
/979
CLINICAL
Associated
BY RICHARD
Binge
May
with
A. MOSKOVITZ,
eating
has
been
Oral
M.D.,
AURORA
recently
LINGAO,
(1-4)
as a
distinct clinical syndrome with possible neunophysiologic correlates. It is characterized by sudden, uncontrollable episodes of excessive eating, usually ending in physical distress. It may be followed by self-induced vomiting and usually leads to feelings of remorse or self-contempt. Although similar behavior occurs in some patients with anorexia nervosa, the relationship of the binge-eating syndrome to anorexia nervosa is unclean (5). The following case, a typical example of this syndrome, was marked by a dramatic remission of symptoms following discontinuation of an oral contraceptive. It is to our knowledge the first reported case correlating clinical change in symptoms with changes in the EEG. Report
She had taken one combination pill for about 2 years and changed to another, which contained I mg of norethindrone and .05 mg of mestranol, when she was 21. Neurologic examination was unremarkable. Thyroid studies and a glucose tolerance test done before referral were normal. Her initial EEG was remarkable for bifrontal, rhythmic slow and sharp activity. A follow-up EEG I month later was similarly abnormal. A CT scan showed left-sided punctate basal ganglia calcification of undetermined significance. After 8 months of further evaluation and psychotherapy, the patient birth
control
She
reported
single woman was referred for compulsive of3 years’ duration. Since age 21 she had experienced episodic eating binges characterized by a driven, ego-
alien
feeling.
stances
or
several clusters apart, 152.4 despite
She
could
emotions.
identify
The
episodes
no
precipitating
lasted
from
circum15 minutes
acute
fluctuations
of
1.8-2.3
kg
during
our
pills
on a trial
a gradual
binges.
quelae.
Her
mood
and
Dr.
Moskovitz
University
1979:
accepted
is Assistant
of Florida
School
Feb.
Professor, of Medicine,
5,
1979.
contraceptive tivity and
Box
J-256,
of Psychiatry, J. Hillis
Miller
Health Center, Gainesville, Fla. 32610, where Dr. Lingao was a resident when this paper was written. Dr. Lingao is now Psychiatrist, Southwestern State Hospital, Thomasville, Ga. The authors this case.
thank
Dr. Sharda
Karuturi
for her early
0002-953X179/06/072
management
l/02/$00.35
improvement
fitted
in her
with
her
an IUD.
symptoms
over
self-esteem
improved
with
the abate-
Conment
Several reports (1-4, 6) have linked binge eating with abnormal EEGs. The significance of small sharp spikes and 14- and 6-per-second positive spikes, which account for the majority of these abnormalities, has been debated. Two groups of researchers ( I 3) have
reported
encouraging
of
© I 979
results
from
treating
binge
eaters
phenytoin. Rau and Green (4) have reported a correlation between an inventory of soft neurologic signs, including EEG abnormalities, and clinical nesponse to phenytoin. Hypothalamic dysfunction has been suggested (1-3) as a possible etiology for the binge-eating syndrome. Either an inhibitory effect on the ventromedial satiety center or an excitatory effect on the lateral appetitive center of the hypothalamus could lead to hyperphagic behavior. Since oral contraceptives exert at least part of their effect at the hypothalamic level (7), they might influence the emergence of binge eating. The almost exclusive occurrence ofthis syndrome in females, primarily with
We
Department
to discontinue was
and her weight stabilized at 45.4 kg. A EEG 5 months after she stopped taking the oral showed marked reduction of epileptiform acwas only marginally abnormal.
of child-bearing
8,
and
of symptoms,
fect, although been offered request that Jan.
basis
,
and secrecy. occur at any
time of day. The patient would rapidly consume large amounts of food, mostly sweets and starches but also leftovers and other ready-to-eat fare. Each episode would end with marked abdominal distress or sometimes sleep but no vomiting. After each binge, she felt helpless, disgusted, and guilty. Depression accompanied each cluster of binge eating, with insomnia, feelings of defectiveness. and fear of losing control. The frequency and intensity of the binges fluctuated. She could recall no binge-free interval longer than I month since the onset of the episodes. Aside from infrequent headaches, which were rarely severe, she had no other major psychiatric or neurologic symptoms. The patient appeared to function normally in other respects. The only remarkable aspect of her medical history was the use of oral contraceptives continually since age 19.
Received
recommendation
to
hours and occurred in clusters over 2 to S days. The were spaced from several days to several weeks alternating with periods of strict dieting. She was cm tall and maintained her weight at 47.7-48.6 kg
The binges generally occurred in solitude They tended to occur in the evening but could
accepted
the next 2’/2 months. By the end of this time she noted a marked change, with only I episode ofovereating during the following 3 months. This episode, on Thanksgiving, was not accompanied by the usual drivenness and emotional se-
follow-up
A 25-year-old eating abrupt
REPORTS
M.D.
ment
Case
RESEARCH
Contraceptives
AND
described
AND
age,
further
suggests
a hormonal
psychodynamic explanations (5). These considerations our patient stop her medication.
postulate
that
the
marked
improvement
ef-
have
led
also
us
to
in our
patient’s symptoms and the associated improvement in her EEG resulted directly from her discontinuing the use of birth control pills. These assumptions are limited by our omission of blind technique and our failune to rechallenge the patient with her medication. Nevertheless, the subacute time course of her imAmerican
Psychiatric
Association
721
CLINICAL
AND
provement
RESEARCH
suggests
This case neurophysiologic
drome.
that
this was not a placebo
provides further mechanism
It particularly
hypothalamic
excitability
a role
Since
our
with an epileptiform that hen symptoms
of the
lateral
for
I. Green bances
disordered
patient’s
response
CT
Scan
pattern, we from over-
hypothalamus.
to phenytoin.
Variants
BY ROBBIE
and
CAMPBELL,
Although
Genetic M.D.,
it is well
Heterogeneity
PETER
known
that
HAYS,
genetic
136:5,
Ma)’
1979
of compulsive medication. Am
eating disturJ Psychiatry
1974
2. Rau JH, Green RS: Compulsive eating: a neurophysiologic approach to certain eating disorders. Compr Psychiatry 16:223231, 1975 3. Wermuth BM, Davis KL, Hollister LE, et al: Phenytoin treatment ofthe binge-eating syndrome. Am J Psychiatry 434:12491253, 1977 4. Rau JH, Green RS: Soft neurological correlates of compulsive eaters. J Nerv Ment Dis 166:435-437, 1978 5. Nogami Y, Yabana F: On Kibarashi-gui (binge eating). Folia Psychiatr Neurol Jpn 31:159-166. 1977 6. Davis KL, Quails B, Hollister L, et al: EEG’s of ‘binge” eaters (ltr to ed). Am J Psychiatry 131:1409, 1974 7. Kastin AJ, Schally AV, Gual C. et al: Release of LH and FSH after administration of synthetic LH-releasing hormone. J Clin Endocrinol Metab 34:753-756, 1972
The epidemiology of binge eating raises the question of its frequency of association with oral contraceptive use. While none of the authors cited above indicate which of their patients were using these drugs, we would expect, according to chance alone, that some were. It would be interesting to see whether reanalysis of their data shows correlations between oral contraceptive use and either EEG abnormalities or positive
RS, Rau JH: Treatment with anticonvulsant
131:428-432,
symptoms
EEG resulted
J Psychiatry
REFERENCES
effect.
evidence to support a for the binge-eating syn-
suggests
function.
were correlated further suggest
Am
REPORTS
in Schizophrenia
M.B.,
DON
factors
are
B. RUSSELL,
None
M.D.,
of
the
AND
DAVID
subjects
J.
had
ZACKS,
M.B.
epilepsy,
neunologic
syn-
important in the etiology of functional psychoses, it is also clear that a specific overt genetic predisposition is not always necessary for their emergence. Dalen (I) demonstrated two sets of etiologic factors in a series of
dromes, or a history of alcoholism, drug psychosis, more than trivial exposure to illicit drugs other
or than
cannabis.
been
manic
drugs.
patients,
associated
one
with
Subsequently,
set
EEG Hays
mainly
genetic
and
and
brain
anomalies (2) drew
similar
the
other
a series of bipolar manic-depressive patients and on the basis of a series of schizophrenic patients, forward
a similar
hypothesis
about
two
a family
later, put
gree
separate
sets
scans logic
are therefore hypothesis.
suitable
for
testing
the
above
etio-
Method
The scribed
the
subjects
were
35 outpatients
as schizophrenic
psychiatrist
who
by another
who
proposed
had
been
consultant
them
for
de-
and
the
by
study.
Aug.
7, 1978:
revised
Jan.
9, 1979; accepted
Feb.
6, 1979.
history
adopted.
All
or
on P.H.) that
relatives;
relatives’
most
accounts.
subjects
similar
obtained
covered
all
histories Patients
from first-
were were
ral classification patients had
height thought
had
of the detailed
schizophrenias recording
had
psychotropic
and
each
patient
second-dc-
supplemented then
two groups; those with and those without tory of major functional psychosis. In the course of a separate investigation
by
divided
into
a family
his-
of the natu-
(5), 18 of these of symptoms at the
of the syndrome. Of these 18 subjects, 16 had disorders, 19 had hallucinations (auditory in
12 cases), I I had catatonic symptoms, 15 had delusions that were regarded as primary, and 7 had passivity phenomena. The 7 patients who did not have catatonic symptoms had auditory hallucinations. Of the I I patients who did not have passivity phenomena, 9
had Received
was
phenothiazines
of us (R.C.
from
of etiologic factors in schizophrenia (3). Like EEGs, CT scans are painless and safe, and have been reported to show abnormalities more often among schizophrenics than among controls (4). CT
None
with
One
damage.
conclusions
treated
primary
delusions,
1 had
prominent
catatonic
symptoms, marily of
and 1 had a syndrome that consisted thought disorder, tactile hallucinations, misrecognition , and secondary delusions.
pri-
is Associate Professor, and Dr. Hays is Professor, of Psychiatry, University of Alberta, First Floor, Clinical Sciences Building, Edmonton, Alberta, Canada T6G 2G3. Drs. Russell and Zacks are Consultant Radiologists, University of Alberta Hospital. Address reprint requests to Dr. Hays.
visual CT scans were performed using an EMI head scanfling unit with a water bag. Six images (160 x 160 matrix) were obtained for each patient. The scans were
This project was supported Health Advisory Council.
angled 15#{176} offthe orbitomeatal and number printouts were
Dr.
Campbell
Department
722
by a grant
from
the
0002-953X/79/06/0722102/$00.35
Alberta
Mental
© 1979
American
Psychiatric
Association
line and obtained.
a film recording No sedation
on
