LETTERS
TO THE
EDITOR
4. Thomas CS: Dysmorphophobia: Psychiatry 1984; 144:513-516
a question
of definition.
Br J
JOHN TANQUARY, M.D. MINDA LYNCH, PH.D. PRAKASH MASAND, M.D. Syracuse, N.Y.
Dr.
Phillips
and
Dr.
McElroy
Reply
SIR: We read the letter by Dr. Tanquary and associates with great interest, as it raises important questions about the interface between obsessive-compulsive disorder and body dysmorphic disorder (a preoccupation with an imagined defect in appearance). Published cases of compulsive face picking (1) have conceptualized this behavior as a form of obsessive-cornpulsive disorder. To our knowledge, Dr. Tanquany and cobleagues are the first to note a relationship between compulsive face picking and body dysmorphic disorder. We, too, have noted a relationship between compulsive face picking and body dysmorphic disorder. In our ongoing study of body dysmorphic disorder, we have encountered nine patients (four women and five men) with repetitive, time-consuming face picking. Eight of nine patients considered this
behavior
to result
from
their
body
dysmorphic
disorder,
which in seven cases consisted of typical preoccupations with imagined on minimal acne. The eighth case was less typical; like Dr. Tanquary’s patient, the patient picked to remove imagined pus from beneath hen skin to prevent it from sunfacing on her skin and making hen ugly. In some cases, the picking caused actual mild facial scanning, which intensified the body dysmorphic disorder symptoms. The ninth patient, unlike the others, considered her face picking to be primary; i.e., not a reaction to her body dysmorphic disorder. Instead, the mild resulting disfigurement caused body dysmorphic disorder
symptoms. Is repetitive face picking best conceptualized as body morphic disorder or as obsessive-compulsive disorder? sometimes the former and sometimes the latter? Unlike
Tanquany
and his colleagues,
we consider
the face picking
dysIs it Dr.
of
eight of our nine patients to be a symptom of their body dysmorphic disorder. This behavior was a response to a preoccupation with an imagined or greatly exaggerated “defect” in their appearance. Thus, repetitive face picking appears to be one of the many ritualistic behaviors that can occur in body dysmorphic disorder, which include repetitive mirror checking, persistent questioning or requests for reassurance, and repetitive grooming behaviors, such as hair combing or makeup application. Although certain repetitive-and sometimes self-mutilatory-grooming behaviors have been conceptualized as a form of obsessive-compulsive disorder (tnichotilbomania, compulsive hand washing, and onychophagia [nail biting] in humans [2]; compulsive paw licking in dogs [canine acral lick]; and feather picking disorder in birds [3]), some compulsive grooming behaviors (e.g., hair arranging and face picking) should, in some instances, be considered a complication of body dysmorhpic disorder. But what about the relationship between obsessive-compulsive disorder and body dysmorphic disorder themselves? Might they be rebated or even the same disorder? The answer to this question is unknown, but it appears that these disorders may be related, given their similar early age of onset, often chronic course, apparent high comombidity with mood and anxiety disorders, substantial functional impairment and similar phenomenology-both consisting of persistent, intru-
1284
sive thoughts that are difficult to resist as well as compulsive, ritualistic behaviors (4). In addition, preliminary evidence suggests that body dysmorphic disorder may, like obsessive-cornpulsive disorder, respond to treatment with senotonergic antidepressants (5, 6). On the other hand, there appear to be differences between these two disorders. In our experience, patients with body dysmorphic disorder are less likely than those with obsessive-compulsive disorder to have insight into the senselessness of their preoccupations; that is, their preoccupations are more likely to consist of overvalued ideas or delusional thinking. It also appears that the ritualistic behavions of body dysmorphic disorder, such as repetitive mirror checking, are less likely to temporarily relieve anxiety. Body dysmomphic disorder also appears to often cause more social impairment and isolation. Research is needed to confirm these impressions and to further explore the interface between these two disorders. Most of our patients were extremely reluctant to discuss either their body dysmorphic preoccupations or their compubsive face picking and did so only when asked about them. Thus, it is important that clinicians specifically inquire about the presence of compulsive face picking in body dysmorphic patients and about body dysmorphic disorder in compulsive face pickers. Body dysmorphic disorder often has serious consequences, including social isolation, unemployment, hospitalization, and suicide-associated features that go beyond simple face picking and are important for clinicians to be aware of.
REFERENCES I . Stout RJ: Fluoxetine for the treatment of compulsive facial picking (letter). Am J Psychiatry 1990; 147:370 2. Leonard HL, Lenane MC, Swedo SE, Rettew DC, Rapoport JL: A double-blind comparison of clomipramine and desipramine treatment of severe onychophagia (nail biting). Arch Gen Psychiatry 1991; 48:821-827 3. Grindlinger HM, Ramsay E: Compulsive feather picking in birds (letter). Arch Gen Psychiatry 1991; 48:857 4. Phillips KA, Hollander E: Body dysmorphic disorder: DSM-IV Source Book review, in DSM-IV Source Book. Washington DC, American Psychiatric Press, in press S. Phillips KA, McElroy SL, Keck PE, Pope HG, Hudson JI: Body dysmorphic disorder: a report of 20 cases, in New Research Program and Abstracts, 144th Annual Meeting of the American Psychiatric Association. Washington, DC, APA, 1991 6. Hollander E, Liebowitz MR, Winchel R, Klumker R, Klein DF: Treatment of body-dysmorphic disorder with serotonin reuptake blockers. Am J Psychiatry 1989; 146:768-770 KATHARINE SUSAN
A. PHILLIPS, L. MCELROY, Belmont,
Simple
Schizophrenia,
Negative
Symptoms,
and
M.D. M.D. Mass.
Prefrontal
Hypodopaminemgia SIR: Kenneth viewed evidence
tenized
L. Davis, M.D., and associates suggesting that schizophrenia
by subcontical
podopaminergia.
hyperdopaminergia
It is likely
that
this
and conception
( 1 ) have reis charac-
prefrontal of the
hyrole
of
dopamine in schizophrenia will generate a great deal of research and stimulate new treatment approaches. An especially provocative component of this hypothesis is that prefrontal hypodopaminergia is associated with the development research
of negative symptoms. There are on the treatment of schizophrenia
AmJ
Psychiatry
149:9,
two that
approaches to have provided
September
1992
LETTERS
data consistent with this hypothesis and that have the potential to refine our understanding of hypodopaminengia in schizophrenia. One of these involves the use of dopamine precursors and agonists in the treatment of schizophrenia spectrum disorders such as schizoid on schizotypal personality, in which negative symptoms can be especially prominent (1). As yet, neither schizoid nor schizotypal personality disorder has been studied in this way. However, a beneficial effect of L-dOpa has been reported in a double-blind crossover trial examining patients with simple schizophrenia (2). Simple schizophrenia is a subtype of schizophrenia defined by the absence of delusions and hallucinations and a corresponding predominance of negative symptoms. The results of this study are therefore consistent with the hypothesis that hypodopaminengia underlies negative symptoms. Although this study does not appear to have stimulated additional trials of dopaminergic agents in simple schizophrenia, diagnostic criteria for this subtype that could facilitate such research have been proposed (3, 4). A second approach to investigating prefrontal hypodopaminergia examines dimensions of positive and negative symptoms rather than subtypes. In such research, patients are assessed on both of these symptom dimensions and their response to trials of dopamine precursors or agonists are evaluated. Based on the hypothesis that hypodopaminenagia underlies negative symptoms, it can be predicted that negative symptoms will demonstrate a greater beneficial response to dopamine agonists than positive symptoms. Such an effect has been reported in trials of L-dopa (5) and amphetamine (6) in patients with schizophrenia. Research on the effects of dopamine agonists in schizophrenia would be more informative if selective mesocontical dopamine receptor agonists were studied, for example, selective D1 agonists (1). In such studies, it will also be important to examine separately negative symptoms and interpersonal deficits, a distinction with important theoretical and empirical implications that has often been neglected in research on negative symptoms.
REFERENCES 1. Davis KL, Kahn RS, Ko G, Davidson M: Dopamine in schizophrenia: a reviewand reconceptualization. AmJPsychiatry 1991; 148:1474-1486 2. Gerlach J, Luhdorf K: The effect ofL-dopa on young patients with simple schizophrenia, treated with neuroleptic drugs: a doubleblind crossover trial with madopar and placebo. Psychopharmacologia 1975; 44:105-110 3. Black DW, Boffeli TJ: Simple schizophrenia: past, present, and future. AmJ Psychiatry 1989; 146:1267-1273 4. Dworkin RH: Simple schizophrenia: an investigation of Bleuler’s criteria based on the major twin studies of schizophrenia. Acta Psychiatr Scand, in press. S. Kay SR, Opler LA: L-dopa in the treatment of negative schizophrenic symptoms: a single-subject experimental study. Int J Psychiatry Med 1985-86; 15:293-298 6. Angrist B, Peselow E, Rubinstein M, CorwinJ, RotrosenJ: Partial improvement in negative schizophrenic symptoms after amphetamine. Psychopharmacology 1982; 78:128-1 30 ROBERT H. DWORKIN, PH.D. LEWIS A. OPLER, M.D., PH.D. New York, N.Y.
Dr.
Davis
and
Associates
SIR: Dr. Dworkin the possibility that
Am
J
Psychiatry
Reply
and Dr. Opler prefrontal
I 49:9,
call particular
hypodoparninergia
September
1992
attention is associated
to
with
the development
of negative
TO THE
symptoms,
and
EDITOR
that
these
can be treated with L-dopa. We heartily agree that patients within the schizophrenia spectrum who are relatively devoid of positive symptoms might benefit from trials that enhance dopaminergic activity. Obviously a major question that ultimately must be addressed is the most effective agent to use for selective augmentation of dopaminengic activity in cortical regions. Although L-dopa remains an interesting possibility, it surely will be increasing noradrenergic activity as well. This may, or may not, be beneficial. Dopamine agonists offer an-
other
approach,
but the ideal
dopamine
receptor
to activate,
as well as how to maximize regional selectivity, remains a pharmacological dilemma. One interesting approach to this problem has been the administration of the dopamine neuptake blocker mazindol. As recently reported ( 1 ), mazindol in combination with neuroleptics in a naturalistic outpatient setting was able to substantially reduce negative symptoms. This is an interesting approach that deserves further attention, particularly if, in combination with neuroleptics, mazindol may have a unique affect on cortical dopaminengic neurons. A critical element in our reconceptualization of the role of dopamine in schizophrenia is the bidinectionality of dopamine. Hypodoparninergia in the cortex may be associated with hyperdopaminengia in subcorticol regions. Recently this possibility received some support from a study in which cenebral blood flow was measured by single photon emission cornputed tomography. Schizophrenics following the Wisconsin
Card
Sorting
Test were
found
to have diminished
frontal
con-
tical blood flow and increased stniatal blood flow compared to control subjects completing the same task (2). The mechanism that may lead to such bidirectionality has received considerable attention at the preclinical level (unpublished paper by A.Y. Deutsch). An excitatory glutarnatergic tract whose activity is diminished following cortical hypofunction may serve to mediate subcortical hypodopaminengia. Thus, isolation of the glutamatengic receptor subtype that modulates this subcontical dopaminergic response is cleanly of interest and may offer an approach to the treatment of schizophrenia.
REFERENCES I . Seibyl J, Krystal J, Johnson R, Brenner L, Heninger G, Chamney D: Mazindol augmentation of typical antipsychotics in negative symptom schizophrenics. Abs Soc Neuroscience 1991; 148:6 2. Rubin P, HoIm 5, Friberg L, Videbech P, Andersen HS, Bendsen BB, Stromso N, Larsen JK, Lassen NA, Hemmingsen R: Altered modulation of prefrontal and subcortical brain activity in newly diagnosed schizophrenia and schizophreniform disorder. Arch Gen Psychiatry 1991; 48:987-995 KENNETH L. DAVIS, M.D. MICHAEL DAVIDSON, M.D. RENE S. KAHN, M.D. GRANT KO,M.D. New York, N.Y.
Prevalence an Inpatient
of Substance Inner
City
Abuse Psychiatric
or Dependence
Diagnoses
on
Unit
SIR: The 40% prevalence of substance abuse in psychiatric patients cited in a letter by Edward B. Gogek, M.D. (1), and in studies done by Crowbey et al. (2) is relatively high; however, it is much lower than in the population I serve. Dr. Gogek’s letter prompted me to review SO consecutive discharges in the first halfof 1991 from my acute inpatient general psychiatry service.
1285
TO THE
EDITOR
4. Thomas CS: Dysmorphophobia: Psychiatry 1984; 144:513-516
a question
of definition.
Br J
JOHN TANQUARY, M.D. MINDA LYNCH, PH.D. PRAKASH MASAND, M.D. Syracuse, N.Y.
Dr.
Phillips
and
Dr.
McElroy
Reply
SIR: We read the letter by Dr. Tanquary and associates with great interest, as it raises important questions about the interface between obsessive-compulsive disorder and body dysmorphic disorder (a preoccupation with an imagined defect in appearance). Published cases of compulsive face picking (1) have conceptualized this behavior as a form of obsessive-cornpulsive disorder. To our knowledge, Dr. Tanquany and cobleagues are the first to note a relationship between compulsive face picking and body dysmorphic disorder. We, too, have noted a relationship between compulsive face picking and body dysmorphic disorder. In our ongoing study of body dysmorphic disorder, we have encountered nine patients (four women and five men) with repetitive, time-consuming face picking. Eight of nine patients considered this
behavior
to result
from
their
body
dysmorphic
disorder,
which in seven cases consisted of typical preoccupations with imagined on minimal acne. The eighth case was less typical; like Dr. Tanquary’s patient, the patient picked to remove imagined pus from beneath hen skin to prevent it from sunfacing on her skin and making hen ugly. In some cases, the picking caused actual mild facial scanning, which intensified the body dysmorphic disorder symptoms. The ninth patient, unlike the others, considered her face picking to be primary; i.e., not a reaction to her body dysmorphic disorder. Instead, the mild resulting disfigurement caused body dysmorphic disorder
symptoms. Is repetitive face picking best conceptualized as body morphic disorder or as obsessive-compulsive disorder? sometimes the former and sometimes the latter? Unlike
Tanquany
and his colleagues,
we consider
the face picking
dysIs it Dr.
of
eight of our nine patients to be a symptom of their body dysmorphic disorder. This behavior was a response to a preoccupation with an imagined or greatly exaggerated “defect” in their appearance. Thus, repetitive face picking appears to be one of the many ritualistic behaviors that can occur in body dysmorphic disorder, which include repetitive mirror checking, persistent questioning or requests for reassurance, and repetitive grooming behaviors, such as hair combing or makeup application. Although certain repetitive-and sometimes self-mutilatory-grooming behaviors have been conceptualized as a form of obsessive-compulsive disorder (tnichotilbomania, compulsive hand washing, and onychophagia [nail biting] in humans [2]; compulsive paw licking in dogs [canine acral lick]; and feather picking disorder in birds [3]), some compulsive grooming behaviors (e.g., hair arranging and face picking) should, in some instances, be considered a complication of body dysmorhpic disorder. But what about the relationship between obsessive-compulsive disorder and body dysmorphic disorder themselves? Might they be rebated or even the same disorder? The answer to this question is unknown, but it appears that these disorders may be related, given their similar early age of onset, often chronic course, apparent high comombidity with mood and anxiety disorders, substantial functional impairment and similar phenomenology-both consisting of persistent, intru-
1284
sive thoughts that are difficult to resist as well as compulsive, ritualistic behaviors (4). In addition, preliminary evidence suggests that body dysmorphic disorder may, like obsessive-cornpulsive disorder, respond to treatment with senotonergic antidepressants (5, 6). On the other hand, there appear to be differences between these two disorders. In our experience, patients with body dysmorphic disorder are less likely than those with obsessive-compulsive disorder to have insight into the senselessness of their preoccupations; that is, their preoccupations are more likely to consist of overvalued ideas or delusional thinking. It also appears that the ritualistic behavions of body dysmorphic disorder, such as repetitive mirror checking, are less likely to temporarily relieve anxiety. Body dysmomphic disorder also appears to often cause more social impairment and isolation. Research is needed to confirm these impressions and to further explore the interface between these two disorders. Most of our patients were extremely reluctant to discuss either their body dysmorphic preoccupations or their compubsive face picking and did so only when asked about them. Thus, it is important that clinicians specifically inquire about the presence of compulsive face picking in body dysmorphic patients and about body dysmorphic disorder in compulsive face pickers. Body dysmorphic disorder often has serious consequences, including social isolation, unemployment, hospitalization, and suicide-associated features that go beyond simple face picking and are important for clinicians to be aware of.
REFERENCES I . Stout RJ: Fluoxetine for the treatment of compulsive facial picking (letter). Am J Psychiatry 1990; 147:370 2. Leonard HL, Lenane MC, Swedo SE, Rettew DC, Rapoport JL: A double-blind comparison of clomipramine and desipramine treatment of severe onychophagia (nail biting). Arch Gen Psychiatry 1991; 48:821-827 3. Grindlinger HM, Ramsay E: Compulsive feather picking in birds (letter). Arch Gen Psychiatry 1991; 48:857 4. Phillips KA, Hollander E: Body dysmorphic disorder: DSM-IV Source Book review, in DSM-IV Source Book. Washington DC, American Psychiatric Press, in press S. Phillips KA, McElroy SL, Keck PE, Pope HG, Hudson JI: Body dysmorphic disorder: a report of 20 cases, in New Research Program and Abstracts, 144th Annual Meeting of the American Psychiatric Association. Washington, DC, APA, 1991 6. Hollander E, Liebowitz MR, Winchel R, Klumker R, Klein DF: Treatment of body-dysmorphic disorder with serotonin reuptake blockers. Am J Psychiatry 1989; 146:768-770 KATHARINE SUSAN
A. PHILLIPS, L. MCELROY, Belmont,
Simple
Schizophrenia,
Negative
Symptoms,
and
M.D. M.D. Mass.
Prefrontal
Hypodopaminemgia SIR: Kenneth viewed evidence
tenized
L. Davis, M.D., and associates suggesting that schizophrenia
by subcontical
podopaminergia.
hyperdopaminergia
It is likely
that
this
and conception
( 1 ) have reis charac-
prefrontal of the
hyrole
of
dopamine in schizophrenia will generate a great deal of research and stimulate new treatment approaches. An especially provocative component of this hypothesis is that prefrontal hypodopaminergia is associated with the development research
of negative symptoms. There are on the treatment of schizophrenia
AmJ
Psychiatry
149:9,
two that
approaches to have provided
September
1992
LETTERS
data consistent with this hypothesis and that have the potential to refine our understanding of hypodopaminengia in schizophrenia. One of these involves the use of dopamine precursors and agonists in the treatment of schizophrenia spectrum disorders such as schizoid on schizotypal personality, in which negative symptoms can be especially prominent (1). As yet, neither schizoid nor schizotypal personality disorder has been studied in this way. However, a beneficial effect of L-dOpa has been reported in a double-blind crossover trial examining patients with simple schizophrenia (2). Simple schizophrenia is a subtype of schizophrenia defined by the absence of delusions and hallucinations and a corresponding predominance of negative symptoms. The results of this study are therefore consistent with the hypothesis that hypodopaminengia underlies negative symptoms. Although this study does not appear to have stimulated additional trials of dopaminergic agents in simple schizophrenia, diagnostic criteria for this subtype that could facilitate such research have been proposed (3, 4). A second approach to investigating prefrontal hypodopaminergia examines dimensions of positive and negative symptoms rather than subtypes. In such research, patients are assessed on both of these symptom dimensions and their response to trials of dopamine precursors or agonists are evaluated. Based on the hypothesis that hypodopaminenagia underlies negative symptoms, it can be predicted that negative symptoms will demonstrate a greater beneficial response to dopamine agonists than positive symptoms. Such an effect has been reported in trials of L-dopa (5) and amphetamine (6) in patients with schizophrenia. Research on the effects of dopamine agonists in schizophrenia would be more informative if selective mesocontical dopamine receptor agonists were studied, for example, selective D1 agonists (1). In such studies, it will also be important to examine separately negative symptoms and interpersonal deficits, a distinction with important theoretical and empirical implications that has often been neglected in research on negative symptoms.
REFERENCES 1. Davis KL, Kahn RS, Ko G, Davidson M: Dopamine in schizophrenia: a reviewand reconceptualization. AmJPsychiatry 1991; 148:1474-1486 2. Gerlach J, Luhdorf K: The effect ofL-dopa on young patients with simple schizophrenia, treated with neuroleptic drugs: a doubleblind crossover trial with madopar and placebo. Psychopharmacologia 1975; 44:105-110 3. Black DW, Boffeli TJ: Simple schizophrenia: past, present, and future. AmJ Psychiatry 1989; 146:1267-1273 4. Dworkin RH: Simple schizophrenia: an investigation of Bleuler’s criteria based on the major twin studies of schizophrenia. Acta Psychiatr Scand, in press. S. Kay SR, Opler LA: L-dopa in the treatment of negative schizophrenic symptoms: a single-subject experimental study. Int J Psychiatry Med 1985-86; 15:293-298 6. Angrist B, Peselow E, Rubinstein M, CorwinJ, RotrosenJ: Partial improvement in negative schizophrenic symptoms after amphetamine. Psychopharmacology 1982; 78:128-1 30 ROBERT H. DWORKIN, PH.D. LEWIS A. OPLER, M.D., PH.D. New York, N.Y.
Dr.
Davis
and
Associates
SIR: Dr. Dworkin the possibility that
Am
J
Psychiatry
Reply
and Dr. Opler prefrontal
I 49:9,
call particular
hypodoparninergia
September
1992
attention is associated
to
with
the development
of negative
TO THE
symptoms,
and
EDITOR
that
these
can be treated with L-dopa. We heartily agree that patients within the schizophrenia spectrum who are relatively devoid of positive symptoms might benefit from trials that enhance dopaminergic activity. Obviously a major question that ultimately must be addressed is the most effective agent to use for selective augmentation of dopaminengic activity in cortical regions. Although L-dopa remains an interesting possibility, it surely will be increasing noradrenergic activity as well. This may, or may not, be beneficial. Dopamine agonists offer an-
other
approach,
but the ideal
dopamine
receptor
to activate,
as well as how to maximize regional selectivity, remains a pharmacological dilemma. One interesting approach to this problem has been the administration of the dopamine neuptake blocker mazindol. As recently reported ( 1 ), mazindol in combination with neuroleptics in a naturalistic outpatient setting was able to substantially reduce negative symptoms. This is an interesting approach that deserves further attention, particularly if, in combination with neuroleptics, mazindol may have a unique affect on cortical dopaminengic neurons. A critical element in our reconceptualization of the role of dopamine in schizophrenia is the bidinectionality of dopamine. Hypodoparninergia in the cortex may be associated with hyperdopaminengia in subcorticol regions. Recently this possibility received some support from a study in which cenebral blood flow was measured by single photon emission cornputed tomography. Schizophrenics following the Wisconsin
Card
Sorting
Test were
found
to have diminished
frontal
con-
tical blood flow and increased stniatal blood flow compared to control subjects completing the same task (2). The mechanism that may lead to such bidirectionality has received considerable attention at the preclinical level (unpublished paper by A.Y. Deutsch). An excitatory glutarnatergic tract whose activity is diminished following cortical hypofunction may serve to mediate subcortical hypodopaminengia. Thus, isolation of the glutamatengic receptor subtype that modulates this subcontical dopaminergic response is cleanly of interest and may offer an approach to the treatment of schizophrenia.
REFERENCES I . Seibyl J, Krystal J, Johnson R, Brenner L, Heninger G, Chamney D: Mazindol augmentation of typical antipsychotics in negative symptom schizophrenics. Abs Soc Neuroscience 1991; 148:6 2. Rubin P, HoIm 5, Friberg L, Videbech P, Andersen HS, Bendsen BB, Stromso N, Larsen JK, Lassen NA, Hemmingsen R: Altered modulation of prefrontal and subcortical brain activity in newly diagnosed schizophrenia and schizophreniform disorder. Arch Gen Psychiatry 1991; 48:987-995 KENNETH L. DAVIS, M.D. MICHAEL DAVIDSON, M.D. RENE S. KAHN, M.D. GRANT KO,M.D. New York, N.Y.
Prevalence an Inpatient
of Substance Inner
City
Abuse Psychiatric
or Dependence
Diagnoses
on
Unit
SIR: The 40% prevalence of substance abuse in psychiatric patients cited in a letter by Edward B. Gogek, M.D. (1), and in studies done by Crowbey et al. (2) is relatively high; however, it is much lower than in the population I serve. Dr. Gogek’s letter prompted me to review SO consecutive discharges in the first halfof 1991 from my acute inpatient general psychiatry service.
1285
