LETIERS
cal problems,
and
the
in relation
symptoms
Mr.
A experienced
no exacerbation
of
to medication
use. Mr. A began treatment with buspironc, S mg/day, which increased to S mg b.i.d. after 1 week. After 2 weeks taking buspironc he discontinued it, believing it ineffective and becoming more anxious. Fluoxetinc, 20 mg/day, was then prescribcd. Four weeks later he described a clearing of the
“fog,” with reduction in associated anxiety. later he reported feeling much better, and initiation
of treatment
improvement
he continued
Three months 8 months after
to experience
in depersonalization
moderate
symptoms
and
marked
some patients although our
with depersonalization patient experienced
et for
disorder. Interestingly, an overall reduction of his
presenting symptoms following treatment with fluoxetine, he emphasized remission of anxiety to which he had admitted only secondarily on initial presentation. One might speculate that this patient’s depersonalization disorder represented a subclinical anxiety disorder that was subjectively unmasked in the course of successful pharmacologic treatment. While this notion contrasts with the suggestion that panic is a lesser form of depersonalization (4), it is consistent with the concept of depersonalization as a dissociative disorder, in which dis-
sociation
serves
of overwhelming
a protective
function
to prevent
the emergence
anxiety.
REFERENCES 1 . Brauer R, Harrow M, Tucker GJ: Depersonalization phenomena in psychiatric patients. Br J Psychiatry 1 970; 1 1 7:509-5 15 2. Nemiah JC: Dissociative disorders, in Comprehensive Textbook of Psychiatry, 5th ed, vol I. Edited by Kaplan HI, Sadock BJ. Baltimore, Williams & Wilkins, 1989 3. Hollander E, Liebowitz MR, Decaria C, Fairbanks J, Falbon B, Klein DF: Treatment of depersonalization with serotonin reuptake blockers. J Clin Psychopharmacol 1990; 10:200-203 4. Hollander E, Fairbanks J, Decaria C, Liebowitz MR: Pharmacologic dissection of panic and depersonalization (letter). Am J Psychiatry 1989; 146:402 CHRISTOPHER G. FICHTNER, M.D. RICHARD P. HOREVITZ, PH.D. BENNE1T G. BRAUN, M.D. Chicago, Ill.
Adverse SIR:
Vascular As briefly
M.D.,
and
viously
been
fluoxetinc
Effects reviewed
associates
With
in the letter
( 1 ) adverse
reported
(Dista
Associated
Fluoxetine
ofJ.A.
Yaryura-Tobias,
vascular
to be associated
effects
with
have
pre-
the withdrawal
with etinc
dysfunction,
the diagnosis treatment
increased tient
great
during
developed
and
neighboring
were
apy
Am]
ever noted
prior
to fluoxetinc
Mr. A, a 38-year-old man, was involved with a diagnosis of both dysthymia and
Psychiatry
149:12,
December
1992
in psychotherassociated char-
month toes
on the
part
of the
apparent
The
bruising
of both
patient
consistent
disorder. Fluoxof 20 mg/day and
to 40 mg/day.
and
two
EDITOR
feet.
pa-
of the
At the same
spontaneous epistaxis times per week, which
pressure. response
to increase
and
dosage,
retifluox-
ctine treatment was discontinued after 3 months. Psychotherapy continued without additional biological treatment. The physical symptoms remitted concomitantly. During this
first
fluoxetinc
trial,
no
association
between
symptoms and fluoxetinc was hypothesized. Fluoxetinc treatment was rcinitiatcd after 8 months
at a dose
of 20 mg/day,
these
approximately
increasing
to 40 mg/day
and then 60 mg/day over a 2-month period. Spontaneous epistaxis and inflammation and bruising of the patient’s toes with infection of the toes reappeared. On this occasion, a dermatobogic consultation was sought and clavulanic acid, 250 mg t.i.d., was prescribed. The infection resolved over 7 days. However, inflammation and bruising consistent with vascular spasm phenomena (acrocyanosis) remained. The epistaxis, times per week, again plied pressure.
at a frequency was controlled
of approximately with externally
two ap-
Further medical evaluation, including hcmatologic and thyroid studies, indicated no abnormalities. Laboratory tests revealed a platelet count of 1 95,000/mm3, a WBC count of 3600/mm3, and a hemoglobin level of 14.1 g/dl. Fluoxetinc dosage was increased to 80 mg/day. With no therapeutic effect noted after 30 days, the fluoxetine was tapered over a 4-week period. Epistaxis as well as aforementioned bruising and inflammation diminished with rcduction
duccd
in dosage
We believe other authors problems
and
disappeared
when
fluoxetinc
was
re-
to 20 mg/day. that this case (2-4) regarding
associated
with
report supports the concerns of potentially significant bleeding
fluoxetinc
treatment.
REFERENCES 1. Yaryura-Tobias JA, Kirschen H, Ninan P, Mosbcrg HJ: Fluoxetinc and bleeding in obsessive-compulsive disorder (letter). Am J Psychiatry 1991; 148:949 2. Guyton AC: The systemic circulation, in Medical Physiology. Philadelphia, WB Saunders, 1981 3. Steiner W, Fontaine R: Toxic reaction following combined administration offluoxetine and L-tryptophan five case reports. Biol Psychiatry 1986; 21:1067-1071 4. Aranth J, Lindberg C: Bleeding, a side effect offluoxetine (letter). Am J Psychiatry 1992; 149:412
of
symptoms were such symptoms
treatment.
symptoms
resolved with the application of external Because of an absence of therapeutic
Company, Fluoxetine Hydrochloride, Adverse Reactions, 1989). These researchers subsequently reported eight cases of bleeding in patients diagnosed with obsessive-compulsive disorder and treated with fluoxetinc. We would like to report symptoms in a single paThe No
the second inflammation
Products
tient possibly associated with fluoxetine. recurrent over two trials of medication.
including
of obsessive-compulsive was initiated at a dose
time, the patient developed sporadic at a frequency of approximately two
cence
reduction in associated anxiety. Asked to describe the improvement in his depersonalization symptoms, Mr. A replied that when he reflected on his life events, it seemed that he was “more in them.” This case lends support to the observation of Hollandcr al. (3) that scrotonin reuptake inhibitors may be effective
actcrologic
TO THE
DAVID
Phenelzine
Treatment
of Depression
W. GUNZBERGER, PH.D. DIANE MARTINEZ, M.D. San Antonio, Tex.
in Parkinson’s
SIR: We present the case of a patient treated monoamine oxidase inhibitor (MAOI) phenclzine dopa-carbidopa combination who showed marked ment in both the Parkinson’s disease and depression.
Disease with the and Limprove-
I 71
cal problems,
and
the
in relation
symptoms
Mr.
A experienced
no exacerbation
of
to medication
use. Mr. A began treatment with buspironc, S mg/day, which increased to S mg b.i.d. after 1 week. After 2 weeks taking buspironc he discontinued it, believing it ineffective and becoming more anxious. Fluoxetinc, 20 mg/day, was then prescribcd. Four weeks later he described a clearing of the
“fog,” with reduction in associated anxiety. later he reported feeling much better, and initiation
of treatment
improvement
he continued
Three months 8 months after
to experience
in depersonalization
moderate
symptoms
and
marked
some patients although our
with depersonalization patient experienced
et for
disorder. Interestingly, an overall reduction of his
presenting symptoms following treatment with fluoxetine, he emphasized remission of anxiety to which he had admitted only secondarily on initial presentation. One might speculate that this patient’s depersonalization disorder represented a subclinical anxiety disorder that was subjectively unmasked in the course of successful pharmacologic treatment. While this notion contrasts with the suggestion that panic is a lesser form of depersonalization (4), it is consistent with the concept of depersonalization as a dissociative disorder, in which dis-
sociation
serves
of overwhelming
a protective
function
to prevent
the emergence
anxiety.
REFERENCES 1 . Brauer R, Harrow M, Tucker GJ: Depersonalization phenomena in psychiatric patients. Br J Psychiatry 1 970; 1 1 7:509-5 15 2. Nemiah JC: Dissociative disorders, in Comprehensive Textbook of Psychiatry, 5th ed, vol I. Edited by Kaplan HI, Sadock BJ. Baltimore, Williams & Wilkins, 1989 3. Hollander E, Liebowitz MR, Decaria C, Fairbanks J, Falbon B, Klein DF: Treatment of depersonalization with serotonin reuptake blockers. J Clin Psychopharmacol 1990; 10:200-203 4. Hollander E, Fairbanks J, Decaria C, Liebowitz MR: Pharmacologic dissection of panic and depersonalization (letter). Am J Psychiatry 1989; 146:402 CHRISTOPHER G. FICHTNER, M.D. RICHARD P. HOREVITZ, PH.D. BENNE1T G. BRAUN, M.D. Chicago, Ill.
Adverse SIR:
Vascular As briefly
M.D.,
and
viously
been
fluoxetinc
Effects reviewed
associates
With
in the letter
( 1 ) adverse
reported
(Dista
Associated
Fluoxetine
ofJ.A.
Yaryura-Tobias,
vascular
to be associated
effects
with
have
pre-
the withdrawal
with etinc
dysfunction,
the diagnosis treatment
increased tient
great
during
developed
and
neighboring
were
apy
Am]
ever noted
prior
to fluoxetinc
Mr. A, a 38-year-old man, was involved with a diagnosis of both dysthymia and
Psychiatry
149:12,
December
1992
in psychotherassociated char-
month toes
on the
part
of the
apparent
The
bruising
of both
patient
consistent
disorder. Fluoxof 20 mg/day and
to 40 mg/day.
and
two
EDITOR
feet.
pa-
of the
At the same
spontaneous epistaxis times per week, which
pressure. response
to increase
and
dosage,
retifluox-
ctine treatment was discontinued after 3 months. Psychotherapy continued without additional biological treatment. The physical symptoms remitted concomitantly. During this
first
fluoxetinc
trial,
no
association
between
symptoms and fluoxetinc was hypothesized. Fluoxetinc treatment was rcinitiatcd after 8 months
at a dose
of 20 mg/day,
these
approximately
increasing
to 40 mg/day
and then 60 mg/day over a 2-month period. Spontaneous epistaxis and inflammation and bruising of the patient’s toes with infection of the toes reappeared. On this occasion, a dermatobogic consultation was sought and clavulanic acid, 250 mg t.i.d., was prescribed. The infection resolved over 7 days. However, inflammation and bruising consistent with vascular spasm phenomena (acrocyanosis) remained. The epistaxis, times per week, again plied pressure.
at a frequency was controlled
of approximately with externally
two ap-
Further medical evaluation, including hcmatologic and thyroid studies, indicated no abnormalities. Laboratory tests revealed a platelet count of 1 95,000/mm3, a WBC count of 3600/mm3, and a hemoglobin level of 14.1 g/dl. Fluoxetinc dosage was increased to 80 mg/day. With no therapeutic effect noted after 30 days, the fluoxetine was tapered over a 4-week period. Epistaxis as well as aforementioned bruising and inflammation diminished with rcduction
duccd
in dosage
We believe other authors problems
and
disappeared
when
fluoxetinc
was
re-
to 20 mg/day. that this case (2-4) regarding
associated
with
report supports the concerns of potentially significant bleeding
fluoxetinc
treatment.
REFERENCES 1. Yaryura-Tobias JA, Kirschen H, Ninan P, Mosbcrg HJ: Fluoxetinc and bleeding in obsessive-compulsive disorder (letter). Am J Psychiatry 1991; 148:949 2. Guyton AC: The systemic circulation, in Medical Physiology. Philadelphia, WB Saunders, 1981 3. Steiner W, Fontaine R: Toxic reaction following combined administration offluoxetine and L-tryptophan five case reports. Biol Psychiatry 1986; 21:1067-1071 4. Aranth J, Lindberg C: Bleeding, a side effect offluoxetine (letter). Am J Psychiatry 1992; 149:412
of
symptoms were such symptoms
treatment.
symptoms
resolved with the application of external Because of an absence of therapeutic
Company, Fluoxetine Hydrochloride, Adverse Reactions, 1989). These researchers subsequently reported eight cases of bleeding in patients diagnosed with obsessive-compulsive disorder and treated with fluoxetinc. We would like to report symptoms in a single paThe No
the second inflammation
Products
tient possibly associated with fluoxetine. recurrent over two trials of medication.
including
of obsessive-compulsive was initiated at a dose
time, the patient developed sporadic at a frequency of approximately two
cence
reduction in associated anxiety. Asked to describe the improvement in his depersonalization symptoms, Mr. A replied that when he reflected on his life events, it seemed that he was “more in them.” This case lends support to the observation of Hollandcr al. (3) that scrotonin reuptake inhibitors may be effective
actcrologic
TO THE
DAVID
Phenelzine
Treatment
of Depression
W. GUNZBERGER, PH.D. DIANE MARTINEZ, M.D. San Antonio, Tex.
in Parkinson’s
SIR: We present the case of a patient treated monoamine oxidase inhibitor (MAOI) phenclzine dopa-carbidopa combination who showed marked ment in both the Parkinson’s disease and depression.
Disease with the and Limprove-
I 71
