Letters

Media

Coverage

Versus

Fluoxetine

as the

to the Editor

of Suicidal

Cause

Ideation

in patients

already

suffering

is known about electrical enwise normal heart.

the publication of an article by Martin H. Teicher, and associates ( 1 ) on six case reports of patients who experienced suicidal ideation with fluoxetine treatment, the media have paid close attention to the phenomenon. Stories concerning the fluoxetine defense for violent crime and suits brought concerning suicidal ideation have been reported. The

from

a cardiac

abnormalities

condition, appearing

but little in an oth-

SIR: Since

M.D.,

following with

case reflects

fluoxetine

some

during

this

of the difficulty time

in treating

of intense

media

patients

attention.

Mr. A was a 49-year-old man who was HIV asymptomatic. He was first seen psychiatrically plaints of anxiety. On examination he showed

positive but with cornevidence of anhedonia, feelings of guilt, depressed mood and thoughts of death for the past 6 months. Recent losses included the death of his mother 6 months earlier. He was doing well mcdically but refused to take zidovudine because he heard that it had serious side effects. A regimen of fluoxetine, 20 mg every morning, was begun, and within a week the patient returned, stating that he had stopped the medication. He claimed that the medication made him feel “horrible on the inside” but he had no idea what the cause could be until he saw the news on a local channel which covered a story of a woman who had made suicide attempts and who attributed this to fluoxetine. He claimed that his symptoms began before the broadcast and that he knew they were the same. Convinced that the fluoxetine was the cause of this “horrible” feeling, he became fearful ofthe medication, stating that he did not want to kill himself (which by now he was convinced he would do if he continued the medication).

,

This case reflects some of the difficulties that the recent media coverage may cause. The patient had already shown a meluctance to take medication because of the side effects that he was told might occur. He was also unable to state what the feeling was, instead stating that it sounded like what he saw on television. It is unfortunate, given the need to document

information such

on adverse

confusion

concerning

effects

of the psychotropic

the

etiology

was

agents,

that

present.

REFERENCE I . Teicher MH, preoccupation

1990;

Glod C, Cole JO: during fluoxetine

Emergence treatment.

147:207-210

CONSTANTINE

Carbamazepine-Induced SIR:

of intense suicidal Am J Psychiatry

Carbamazepine

Atrioventricular is currently

widely

IOANNOU, Brooklyn,

M.D. N.Y.

Block

used

in neurology

and is now more and more recommended for lithium-resistant and rapid cycling patients. Carbamazepine-induced cardiac electrical conduction disorders have previously been reported

572

Ms. A, 63 years old, had been treated for a unipolar affective disorder with periods of mood-noncongruent psychotic features for the past I 0 years. All previous heart evaluations, including ECGs, had been normal. She was admitted to the hospital for a depressive psychotic episode and slight signs of confusion. Neuropsychological tests suggested features of organic brain disorder. CT scan showed calcifications in basal ganglia and slight cerebellar atrophy. ECG showed bilateral temporal theta waves with irritative features. Carbamazepine, 100 mg b.i.d., was introduced and brought a progressive improvement. She was followed up for 3 years as an outpatient and showed sustained clinical stability and even improvement on neuropsychological tests. After 3 years, Ms. A presented an effort dyspnea. ECG was normal but the treadmill stress test showed a second-

degree

atrioventricular

block,

and

episodes

of third-degree

atrioventricular block with ventricular escape were docurnented on Holter monitoring. No symptoms of intoxication were found. Carbamazepine was stopped and dyspnea disappeared. Because her psychiatric condition rapidly worsened, carbamazepine was reintroduced with close supervision. After a few weeks, cardiac symptoms reappeared and the drug was definitely stopped. Holter monitoring was normal thereafter, as were ECG, thallium stress test, and echocardiography. ECG never showed conduction defects on follow-up. According to Hewetson et at. ( I ), Steiner, in 1 970, reported that carbamazepine prolongs atrioventricular conduction time in dogs. Meyrignac et al. (2) reported cases of carbamazepine-induced complete atrioventricular blocks. Boesen et al. (3) reported on other abnormalities such as an intermittent complete atrioventricular block, an atrioventnicular block with a functional escape rhythm, and an intermittent asystolia. Others like Benassi et al. (4) and Ladefoged and Mogelvang (5) have reported carbamazepine-induced heart conduction disorders, but in patients with already-known heart disease. Our patient seems to be a rare case of a pure carbamazepineinduced severe heart conduction disorder without previous heart disease. It is interesting also to note that symptoms appeared 3 years after the beginning of the drug treatment without apparent preceding symptoms. The most plausible physiopathogenic explanation for this phenomenon is the chemical structure of carbamazepine (like tnicyclics), with

quinidine-like

effects

on cardiac

conduction

We therefore recommend that dyspnea, cope appearing in a carbamazepine-treated taken seriously, even in the absence of other and an apparently normal heart. ECG is quate to detect conduction defects, and it complemented by a stress test and Hotter is not demonstrative. If carbamazepine

Am

J

Psychiatry

pathways. dizziness, or synpatient should be cardiac symptoms not necessarily adetherefore should be monitoring if ECG is the only drug to

1 49:4,

April

1992

LEUERS

which such a patient then be mandatory.

responds,

a cardiac

pacemaker

should

REFERENCES 1. Hewetson KA, Ritch AES, Watson aggravated by carbamazepine therapy J 1986; 62:497-498 2. Meyrignac C, Berges C, Benhothom Albengres E, Blatrix C: Bradycardie laire induits par Ia carabamaz#{233}pine noauricular

block

induced

by

RDS: Sick sinus syndrome for epilepsy. Postgrad Med

(letter).

cardiac

conduction

disturbances.

Ann

Neurol

1 987;

22:280-

281 S.

Ladefoged

SD,

MogelvangJC:

syncopes complicating 1982; 212:185-1 86

argues in favor of it being a social phobia. Response to several different treatments, particularly benzodiazepines, suggests that anxiety reduction is a factor in improvement. Although this is an uncommon problem, the disability to which it leads is profound, and the relief after treatment is greatly appreciated. It is hoped that future study will shed more light on the classification and treatment of this interesting disorder.

Total

atrioventricular

carbamazepine

therapy.

block

Acta

REFERENCES

Presse

Med 1983; 12:577 3. Boesen F, Andersen EB, Jensen EK, Ladefoged SD: Cardiac conduction disturbances during carbamazepine therapy. Acta Neurot Scand 1983; 68:49-52 4. Benassi E, Bo GP, Cocito L, Maffini M, Loeb I: Carbamazepine and

Med

with

Scand

1 . Barlow the

DW: The dimensions

Anxiety

Disorders.

of anxiety

Edited

by Tuma

C.G.

Treatment of Generalized mania With Buspirone

SIR:

Treatment Several

ofBowel

authors

have

Obsessions described

With

responded

Mr.

to

individuals

who

suffer

nortriptyline.

a 65-year-old man who presented preoccupied that he would be flatulent in public. He had never been flatulent around other people. The problem had developed 30 years earlier and had progressed with negligible waxing and waning in its course. It was followed by extreme social withdrawal and the loss of a very successful with

A was

the

business

worry

career.

Prior

treatment

with

psychodynamic

psy-

chotherapy, diazepam, chlordiazepoxide, propranolol, and dicyclomine had produced no improvement. Treatment with adinazolam had produced a modest benefit but had to be stopped because of impotence. Trials of fluoxetine, alpmazolam, and clomipramine produced no benefit. After 3 weeks on a regimen of nortriptyline, 10 mg/day, he noticed a “remarkable improvement” never before felt in his life. He was much more comfortable in public, much less preoccupied with being flatulent, and able to triple his activities. At a dose of SO mg at bedtime there was further improvement. The blood level at this dose was 167 ng/dl. These beneficial effects continued unabated after 6 months. This patient’s case and the literature discussed raise the question of how to classify bowel obsessions. The presence of recurrent, intrusive, senseless thoughts suggest that this is a variant of obsessive-compulsive disorder. In Mr. A’s case, the lack of success with two semotonin uptake blockers argues against this hypothesis. The type of incapacity seen in the con-

Am

J

Psychiatry

1 49:4,

April

1992

MaserJD.

in Anxiety

and

Hillsdale,

Anxiety

Disorder

LYKETSOS, Baltimore,

and

M.D. Md.

Tnichotillo-

Nortriptyline

from agoraphobia without panic, or from social phobia, whose incapacity rests in an excessive preoccupation with the sudden loss of bowel control (1, DSM-III-R). Some have called these worries “bowel obsessions” and have suggested that the condition is a variant of obsessive-compulsive disorden (2-4). Case reports have documented successful treatment with clomipramine, doxepin, imipramine, and behavioral techniques (2-4). I am reporting the case of a patient whose symptoms

disorders, AH,

NJ, Lawrence Erlbaum Associates, I 985 2. Jenike MA, Vitagliano HL, Rabinowitz J, Goff DC, Baer L: Bowel obsessions responsive to tricyctic antidepressants in four patients. Am J Psychiatry 1987; 144:1347-1 348 3. Caballero R: Bowel obsessions responsive to clomipramine (letter). Am J Psychiatry 1988; 145:650-651 4. Beidet DC, Bulik CM: Flooding and response prevention as a treatment for bowel obsessions. J Anxiety Disorders I 990; 4:247-256

JUDITH LABRECQUE, M.D. MARC-ANDRE COTE, M.D. PIERRE VINCENT, M.D. Q uebec, Que., Canada

Successful

EDITOR

dition

A, Toulette K, TillementJ-P, sinusale et bloc sino-auricu(Sinus bradycardia and si-

carbamazepine)

TO THE

SIR: To my knowledge there has been no previous report to document the use of buspirone in the treatment of an anxiety disorder with coexistent trichotillomania. Ms. A, a 31-year-old woman, presented with several months of paroxysmal episodes of acute anxiety accompanied by attendant autonomic hyperactivity. This included the occurrence of hyperventilation, palpitations, dyspnea, and paresthesias. The patient also exhibited an uncontrollable urge to pull out hem hair. This occurred over the same period of time and resulted in a section of alopecia. She reported intrusive thoughts of having an underlying disease state, despite reassurances from physicians on 5everal occasions. This state did not appear to meet the criteria for obsessive-compulsive disorder. A previous 2-week trial of alprazolam appeared to be of no benefit. Ms. A was then started on a regimen of buspinone, 30 mg/day p.o. Within 4 weeks, the trichotillomania remitted completely. A significant improvement of anxiety symptoms was noted on the Sheehan Patient Rated Anxiety Scales. Previous studies have documented successful treatment of both obsessive-compulsive disorder and trichotillomania with clomipramine, a strongly serotonergic tricyclic antidepressant ( 1 2). Buspirone, a well-known anxiolytic agent, a S-hydroxy-

,

tmyptamine

agonist,

is also

thought

This agent was shown to facilitate the treatment of obsessive-compulsive studies may offer an explanation in this case.

to affect

serotonin

balance.

the effects of fluoxetine in disorder (3). These of the efficacy of buspirone

REFERENCES 1 . Swedo SE, Leonard HL, Rapoport JL, Lenane MC, Goldberger EL, Cheslow DL: A double-blind comparison of clomipramine and desipramine in the treatment of trichotillomania (hair pulling).N EngI J Med 1989; 32 1:497-501

573