Am J Psychiatry 163:8, August 2006
LETTERS TO THE EDITOR
ceitfulness, oppositionality, and defiance. Besides mood
lability, distractibility, and acts of self-harm, there was no
evidence of depression or mania. The patient refused
mood stabilizers and atypical antipsychotics because of
the possibility of weight gain.
Doses of topiramate started at 25 mg once in the morn-
ing for 5 days and then increased to 25 mg twice daily. Af-
ter 15 days taking 50 mg/day, the patient’s dose of topira-
mate was increased to 25 mg in the morning and 50 mg at
bedtime. For the next 7 days, she was administered a dose
of 75 mg/day and had no behavioral outbursts. She be-
came more cooperative with staff and did not require re-
straints. The staff noted a significant improvement in her
disruptive behaviors as well.
Although her mania was much improved, she contin-
ued to display some emotional lability and distractibility.
Therefore, her disruptive behavior symptoms improved
independently and more significantly than her mood-re-
lated symptoms. She had CGI improvement ratings of 2 for
mania and 1 for overall illness. Despite her reports of poor
concentration and transient hyperactivity, there was no
evidence for these or other side effects, such as weight
gain or difficulties with verbal communication.
As illustrated, topiramate monotherapy may be effective in
treating disruptive behavior disorders, independent from its
therapeutic effect for mania that is possibly related to its effi-
cacy in decreasing impulsivity in binge eating disorder, bor-
derline personality disorder, and pathological gambling dis-
order in adults. Because of a favorable side effect profile,
including possible weight loss, medication compliance may
be less of a problem. Further randomized controlled studies
of adjunctive and monotherapy topiramate treatment are
needed. Future studies should assess aggression as an out-
come measure with the Overt Aggression Scale.
1. Barzman DH, DelBello MP, Kowatch RA, Warner J, Rofey D,
Stanford K, Rappaport K, Daniels JP, Strakowski SM: Adjunctive
topiramate in hospitalized pediatric patients with bipolar dis-
orders. J Child Adolesc Psychopharmacol 2005; 15:931–937
DREW H. BARZMAN, M.D.
MELISSA P. DELBELLO, M.D.
Binge Eating Associated With Internal Carotid
TO THE EDITOR: Prevalence rates of DSM-IV binge eating dis-
order and intracranial aneurysm have been estimated at 1%
(1) and 2%–5% (2). To our knowledge, there has been no re-
port of comorbidity of these two conditions. We describe a
case of a patient with internal carotid artery aneurysm pre-
senting with symptoms similar to binge eating disorder.
“Mrs. A,” a 32-year-old married woman with two chil-
dren, presented at a psychiatric clinic in Jan. 2003 with de-
pressive symptoms and uncontrollable binge eating epi-
sodes that had been recurrent for 2 months. She became
fixated with her body weight and waist circumference.
Psychosexual stressors from her husband’s extramarital
affairs were also identified. Neither compensatory behav-
ior nor a history of anorexia was elicited.
Despite alleviation of her depressed mood and preoccu-
pation with body weight following treatment with paroxet-
ine (30 mg/day) and weekly psychotherapy for 4 months,
her binge eating episodes persisted. She was then lost to
follow-up for several months. Subsequently, she relapsed
and presented with the following at her visit in Jan. 2004:
binge eating episodes, overconcern with waist circumfer-
ence, depressed mood, decreased self-esteem, psychomo-
tor agitation, episodic headaches, blurred visions, in-
creased body weight (from 47 kg to 54 kg in 4 months), and
increased severity of stress from marital conflict. There was
no identified temporal relationship between her head-
aches and hyperphagia episodes. Similar to prior pharma-
cotherapy, fluoxetine doses (40 mg/day) were effective in
reducing her symptoms of depression and body image dis-
tortion rather than controlling her binge eating impulse.
Her physical examination revealed no negative findings
except galactorrhea. Neither papilledema nor other focal
neurological sign was identified at neurological examina-
tion. Her serum level of prolactin was within normal range
(8.27 ng/ml). A magnetic resonance image of her pituitary
disclosed an engorged vessel from the right internal ca-
rotid artery A1 segment compressed on the right optic ch-
iasma and hypothalamus (Figure 1). An angiography
showed a wide-based aneurysm (maximum width: 5 mm;
height: 4 mm) at the supraclinoid segment of the right in-
ternal carotid artery. Her blurred vision and headaches
subsided after microsurgical decompression. She did not
suffer from any binge eating episode or body image dis-
tortion during the postoperation follow-up for 20 months.
An association between bulimia and central nervous system
lesions and increased intracranial pressure has been reported
previously (3). To our knowledge, Mrs. A is the first reported
case of internal carotid artery aneurysm presenting with a
binge eating disorder. The disproportional treatment re-
sponses and evidence for focal neurological signs suggest the
necessity for organic workup. It is advisable to perform de-
tailed physical assessment, endocrinological evaluation, and
possible neuroimaging studies in patients with binge eating
disorder who have unexpected responses to traditional treat-
ment strategies. Furthermore, our case report may provide ad-
ditional evidence of a neurological basis of binge eating disor-
der. One limitation to this report is that it lacks analysis of the
potential neural substrates for binge eating disorder.
FIGURE 1. Coronal View of T2-Weighted (TR: 400 msec, TE:
120 msec) Image of Brain MRI Revealing Engorged Vessel
Rising From the Right Internal Carotid Artery A1 Segment
With Compression on the Right Optic Chiasma and Hypo-
Am J Psychiatry 163:8, August 2006
LETTERS TO THE EDITOR
1. Hans WH, Daphne VH: Review of the prevalence and incidence
of eating disorders. Int J Eat Disord 2003; 34:383–396
2. Pfohman M, Criaddle LM: Epidemiology of intracranial aneu-
rysm and subarachnoid hemorrhage. J Neurosci Nurs 2001;
3. Krahn DD, Mitchell JE: Case report of bulimia associated with
increased intracranial pressure. Am J Psychiatry 1984; 141:
LINEN LIN, M.D.
SUSAN SHUR-FEN GAU, M.D., PH.D.
MING-BEEN LEE, M.D.
Facilitation in Inducing Folie a Deux Through
TO THE EDITOR: Folie a deux is a psychotic disorder charac-
terized by a shared delusion that is instigated by a psychotic
inducer and a healthy recipient (1). We describe an unusual
case in which the psychosis in the recipient appeared only af-
ter the most influential member of the family adapted the
psychotic ideas of the inducer.
“Mr. G” was a 23-year-old man with no history of psychi-
atric disorder. He was hospitalized with a paranoid delu-
sion that his brother-in-law was a Mafia leader who had
plans to murder him. Mr. G also heard voices telling him to
kill himself or he would be subjected to torture. Conse-
quently, he tried to strangle himself in the hospital.
Additional history revealed that Mr. G’s sister developed
similar symptoms prior to his hospitalization and that she
had been in close contact with him during that time. Their
mother was aware of her daughter’s delusional ideas.
While the mother did not believe in the delusions, she
provided her daughter with unconditional support and
even checked her house for surveillance equipment with-
out asking questions. The mother felt an obligation to
maintain family cohesion, even if her actions contradicted
her own comprehension of reality. Therefore, she avoided
any confrontation with her daughter out of fear the
daughter might commit suicide, which is what an uncle
did several years previously.
Subsequent to his sister’s delusions, Mr. G’s first psy-
chotic symptoms appeared when he realized that his
mother was fully supportive of his sister’s beliefs. Notably,
his psychosis exacerbated only after his mother’s visits on
the psychiatric ward, and his attempt to strangle himself
occurred after a visit from her. He received intensive treat-
ment with doses of diazepam (30 mg/day) as well as indi-
vidual and family psychotherapy that focused on reality
testing of both the patient and the family.
It became apparent that the mother played a major role
in the family and had indirectly supported Mr. G’s psycho-
sis. Following intervention to clarify the mother’s influence
on Mr. G, she changed her attitude and denied explicitly
the existence of his delusions. Consequently, Mr. G began
to improve rapidly. After six sessions of family psychother-
apy, he was free of psychosis and could be discharged.
It is generally accepted that a dyad composed of a charis-
matic psychotic inducer and an induced person with depen-
dent character traits is necessary for the development of
shared psychosis (2). To our knowledge, the case presented
here is the first documented case in which the pathogenic in-
fluence of a noncharismatic psychotic inducer was enhanced
by a healthy charismatic family leader who was fully support-
ive of psychotic ideas without sharing those ideas. This case
introduces the possibility that a psychotic inducer does not
have to be a dominant person in a family. On the other hand,
it does emphasize the role of a family leader in transmitting
an induced psychosis (3).
1. Mickaud R: Translation of Lasègue and Farlet’s paper of 1877.
Le folie à ou folie communiquée. Am J Psychiatry 1964;
2. Howard R: Induced psychosis. Br J Hosp Med 1994; 51:304–
3. Latan B: The psychology of social impact. Am Psychol 1981;
IGOR SALGANIK, M.D.
SHINKARENKO EVGENY, M.D.
PERELROYZEN GALINA, M.D.
near Hadera, Israel
TO THE EDITOR: Fear-associated freezing/immobilization is a
well described, adaptive, defensive behavioral phenomenon
that is common in many species of animals and occurs during
conditions of natural threat or fear. Although freezing behav-
ior has been assessed in humans utilizing stress/anxiety par-
adigms in the laboratory (1), no study, to our knowledge, has
explicitly examined the prevalence of freezing or immobiliz-
ing behaviors in a clinical sample.
In our study, we used the NIMH Panic Questionnaire (2), a
self-report instrument designed to elicit detailed, syndrome-
specific information in patients with panic disorder, to obtain
information regarding panic-related, freezing/immobilizing
behavior. The frequency (“never,” “rarely,” “sometimes,” “al-
ways”) and severity (“mild,” “moderate,” “severe,” “extreme”)
of 44 panic attack symptoms were obtained in a mixed treat-
ment- and community-based sample of 1,118 people who
met self-reported DSM criteria for panic disorder. In our anal-
ysis, we focused on a single item that determined whether the
subjects were actually immobilized during a panic attack.
Among the participants, 198 (18%) reported “always” being
immobilized during panic attacks. Fifty-three percent of the
participants reported varying frequencies of immobilization
panic (“sometimes” [N=405] and “rarely” [N=188]). Thus, 71%
of the participants reported lifetime episodes of immobiliza-
tion panic. Notably, subjects with positive lifetime histories of
immobilization panic were 2.3 times (95% confidence inter-
val [95% CI]=1.73–2.95, p<0.001) and 1.6 times (95% CI=1.21–
2.09, p<0.001), respectively, more likely to suffer from dis-
abling chronic anxiety and sleep panic attacks relative to
panic disorder patients who had never experienced immobi-
lization panic. Moreover, panic disorder patients who had ex-
perienced immobilization panic were 2.4 times (95% CI=
1.64–3.57, p<0.001) more likely to also experience work im-
pairment relative to panic disorder patients who did not re-
port immobilization panic. This latter finding is noteworthy
because work absenteeism is increased in panic disorder pa-
tients relative to nonpanic disorders in primary care settings.
Data presented in this report indicate that immobilizing/
freezing behaviors are common, yet clinically underappreci-
ated, events during panic attacks. The fact that patients with