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Fluoxetine and Depersonalization Syndrome
Letters
central dopamine dysfunction? A simple study to evaluate central dopamine activity in pseudocyesis would be the measurement of plasma homovanillic acid levels during the episode and after its resolution. High plasma HVA levels have been associated with psychotic exacerbations in schizophrenic individuals. s Considering the dopamine abnormalities in schizophrenia and the side effects from neuroleptics, it is surprising that there are so few cases of pseudocyesis in schizophrenic patients reported. Are these patients not being reported because the pseudocyesis seems to be in the context of their delusional system and overlooked as true pseudocyesis, or are they in fact as rare as the literature would indicate? Alan J. Waldman, M.D. Michael J. Marchese, M.D. Richard A Greer, M.D. Department of Psychiatry University of Florida Gainesville, FL
References I. Cohen LM: A current perspective of pseudocyesis. Am } Psychiatry 119:1140-1144, 1982 2. Small GW: Pseudocyesis: an overview. Can} Psychiatry 31:452-457.1986 3. Ayers JW. Seiler JC: Neuroendocrine indices of depression in pseudocyesis.} Reprod Med 29:67-70.1984 4. Mortimer A, Banbery J. Pseudocyesis preceding psychosis. Br} Psychiatry 152:562-565, 1988 5. Pickar 0, Rodrigo L, Doran A. et al: Longitudinal measurement of plasma homovanillic acid levels in schizophrenic patients. Arch Gen Psychiatry 43:669-676. 1986
Editor's note: For further discussion of pseudocyesis, see pages 316-323 ofthis issue of Psychosomatics.
Fluoxetine and Depersonalization Syndrome SIR: Black and Wojcieszek recently reported on the precipitation of acute depersonalization during initiation of fluoxetine treatment in a patient with bipolar disorder NOS with an acute depressive episode. I The depersonalization occurred following 3 days of fluoxetine treatment VOLUME 33· NUMBER 3· SUMMER 1992
at 20 mg qd. The medication was abruptly discontinued on Day 6 and the symptoms resolved within 24 hours. This may give a clue as to the pathophysiology of depersonalization syndrome. It has been postulated that depersonalization is closely related to obsessive compulsive disorder (OCD), and that both may be mediated by dysregulation of the serotonergic system. 2 Chronic treatment with serotonin reuptake blockers, including fluoxetine, has been shown to be effective in the treatment of both depersonalization) and OCD. 4 More specifically, there is considerable evidence to support the notion that OCD may be mediated by hypersensitivity of the serotonin system. OCD symptoms have been found to increase during oral challenges of meta-chlorophenylpiperazine (m-CPP), a serotonin agonist,s Lack of behavioral hypersensitivity to m-CPP following chronic treatment with serotonin reuptake blockers suggests that down-regulation of serotonin receptors may correlate with clinical improvement,6 Induction of depersonalization symptoms after an acute dose of fluoxetine is consistent with this concept of serotonin hypersensitivity. However, improvement of depersonalization after chronic treatment with serotonin reuptake blockers would be expected, and we have shown this to be the case.) Perhaps the patient mentioned' would respond to reinstitution of fluoxetine at a lower dose to be slowly increased with the expectation of gradual improvement over time. Eric Hollander, M.D. Lisa Cohen, M.S. Concetta DeCaria, M.S. Dan 1. Stein, M.B. Sari Trungold-Apter, B.A. Mohammed Islam, M.B. New York State Psychiatric Institute New York, NY
References I. Black OW. Wojcieszek J: Depersonalization syndrome induced by fluoxetine (leiter). Psychosomatics 32:468469.1991
361
Letters
2. Hollander E: Serotonergic drugs in the treatment of disorders related to obsessive-compulsive disorder. in Current Treatments of Obsessive-Compulsi~'e Disorder. edited by Pato MT. Zohar J. Washington. DC. American Psychiatric Press, 1991, pp 217-236 3. Hollander E. Leibowitz MR, DeCaria C, et al: Treatment of depersonalization with serotonin reuptake blockers. J Clin Psychopharmacol 10:200-203. 1990 4. Zohar J. Insel TR: Obsessive-eompulsive disorder: psychobiological approaches to diagnosis. treatment and pathophysiology. Bioi Psychiatry 22:667-{)87. 1987 5. Hollander E. DeCaria CM. Nitescu A. et al: Serotonergic function in obsessive-compulsive disorder: behavioral and neuroendocrine responses to oral meta-chloro-phenylpiperazine and fenfluramine in patients and healthy volunteers. Arch Gen Psychiatry 49:21-28. 1992 6. Hollander E, DeCaria C, Gully R, et al: Effects of chronic f1uoltetine treatment on behavioral and neuroendocrine responses to meta-chloro-phenylpiperazine in obsessivecompulsive disorder. Psychiatry Res 36: 1-17. 1991
References 1. Mermelstein HT. Holland JC: Psychotherapy by telephone: a therapeutic tool for cancer patients. Psychosomatics 32:407-412. 1991 2. Friedman EH, Robinson RG: Speech hesitation pauses as markers for mood disorder in stroke patients? (letter and reply). J C/in Psychiatry 52: 140, 1991 3. Friedman EH: VOXAFLEX Speech Pause Time Monitor (Software Survey Section). J Child Psychol Psychiatry 31:1.1990 4. Guilford T. Dawkins MS: Receiver psychology and the evolution of animal signals. Animal Behaviour 42: 1-14. 1991 5. Friedman EH: Temporal processing (Ieller). Journal of Learninx Disabilities 24:260. 1991 6. Pindzola RH: Dysfluency characteristics of aged. normalspeaking black and white males. Journal of Fluency Disorders 15:235-243. 1990
In Reply On "Psychotherapy by Telephone: A Therapeutic Toolfor Cancer Patients" SIR: In the Fall 1991 issue. ' Hindi T. Mennelstein. M.D.• and Jimmie C. Holland. M.D.• indicate a need for visual and nonverbal cues in telephone contact with the medically ill patient. This strategy can be easily implemented by memorable graphic and tabular presentations of microcomputer analysis of speech pause time. a behavioral correlate of mood. 2-4 Additional indexes monitor participatory matching. a joint mutually responsive rhythm. and bonding. The validity of this method in assessing the medically ill whose voices are harder to evaluate and who may have dialects is supported by reproducibility across time. circumstance. diagnosis. race. and species. 5.6 Ernest H. Friedman. M.D. Departments of Medicine and Psychiatry Case Western Reserve University East Cleveland. OH
362
SIR: We thank Dr. Friedman for alerting us to a potential research tool to measure changes in speech latency and rhythym, symptoms that commonly occur in mood disorders. This may be especially useful in the longitudinal assessment of the efficacy of psychotherapy by telephone where the loss of nonverbal cues limits our ability to evaluate other fonns of psychomotor retardation. In the clinical domain we look forward to further improvements in communication technology so that distance therapy will be a better and closer approximation of face to face interventions. Hindi T. Mermelstein. M.D. Jimmie C. Holland. M.D. New York, NY
PSYCHOSOMATICS
central dopamine dysfunction? A simple study to evaluate central dopamine activity in pseudocyesis would be the measurement of plasma homovanillic acid levels during the episode and after its resolution. High plasma HVA levels have been associated with psychotic exacerbations in schizophrenic individuals. s Considering the dopamine abnormalities in schizophrenia and the side effects from neuroleptics, it is surprising that there are so few cases of pseudocyesis in schizophrenic patients reported. Are these patients not being reported because the pseudocyesis seems to be in the context of their delusional system and overlooked as true pseudocyesis, or are they in fact as rare as the literature would indicate? Alan J. Waldman, M.D. Michael J. Marchese, M.D. Richard A Greer, M.D. Department of Psychiatry University of Florida Gainesville, FL
References I. Cohen LM: A current perspective of pseudocyesis. Am } Psychiatry 119:1140-1144, 1982 2. Small GW: Pseudocyesis: an overview. Can} Psychiatry 31:452-457.1986 3. Ayers JW. Seiler JC: Neuroendocrine indices of depression in pseudocyesis.} Reprod Med 29:67-70.1984 4. Mortimer A, Banbery J. Pseudocyesis preceding psychosis. Br} Psychiatry 152:562-565, 1988 5. Pickar 0, Rodrigo L, Doran A. et al: Longitudinal measurement of plasma homovanillic acid levels in schizophrenic patients. Arch Gen Psychiatry 43:669-676. 1986
Editor's note: For further discussion of pseudocyesis, see pages 316-323 ofthis issue of Psychosomatics.
Fluoxetine and Depersonalization Syndrome SIR: Black and Wojcieszek recently reported on the precipitation of acute depersonalization during initiation of fluoxetine treatment in a patient with bipolar disorder NOS with an acute depressive episode. I The depersonalization occurred following 3 days of fluoxetine treatment VOLUME 33· NUMBER 3· SUMMER 1992
at 20 mg qd. The medication was abruptly discontinued on Day 6 and the symptoms resolved within 24 hours. This may give a clue as to the pathophysiology of depersonalization syndrome. It has been postulated that depersonalization is closely related to obsessive compulsive disorder (OCD), and that both may be mediated by dysregulation of the serotonergic system. 2 Chronic treatment with serotonin reuptake blockers, including fluoxetine, has been shown to be effective in the treatment of both depersonalization) and OCD. 4 More specifically, there is considerable evidence to support the notion that OCD may be mediated by hypersensitivity of the serotonin system. OCD symptoms have been found to increase during oral challenges of meta-chlorophenylpiperazine (m-CPP), a serotonin agonist,s Lack of behavioral hypersensitivity to m-CPP following chronic treatment with serotonin reuptake blockers suggests that down-regulation of serotonin receptors may correlate with clinical improvement,6 Induction of depersonalization symptoms after an acute dose of fluoxetine is consistent with this concept of serotonin hypersensitivity. However, improvement of depersonalization after chronic treatment with serotonin reuptake blockers would be expected, and we have shown this to be the case.) Perhaps the patient mentioned' would respond to reinstitution of fluoxetine at a lower dose to be slowly increased with the expectation of gradual improvement over time. Eric Hollander, M.D. Lisa Cohen, M.S. Concetta DeCaria, M.S. Dan 1. Stein, M.B. Sari Trungold-Apter, B.A. Mohammed Islam, M.B. New York State Psychiatric Institute New York, NY
References I. Black OW. Wojcieszek J: Depersonalization syndrome induced by fluoxetine (leiter). Psychosomatics 32:468469.1991
361
Letters
2. Hollander E: Serotonergic drugs in the treatment of disorders related to obsessive-compulsive disorder. in Current Treatments of Obsessive-Compulsi~'e Disorder. edited by Pato MT. Zohar J. Washington. DC. American Psychiatric Press, 1991, pp 217-236 3. Hollander E. Leibowitz MR, DeCaria C, et al: Treatment of depersonalization with serotonin reuptake blockers. J Clin Psychopharmacol 10:200-203. 1990 4. Zohar J. Insel TR: Obsessive-eompulsive disorder: psychobiological approaches to diagnosis. treatment and pathophysiology. Bioi Psychiatry 22:667-{)87. 1987 5. Hollander E. DeCaria CM. Nitescu A. et al: Serotonergic function in obsessive-compulsive disorder: behavioral and neuroendocrine responses to oral meta-chloro-phenylpiperazine and fenfluramine in patients and healthy volunteers. Arch Gen Psychiatry 49:21-28. 1992 6. Hollander E, DeCaria C, Gully R, et al: Effects of chronic f1uoltetine treatment on behavioral and neuroendocrine responses to meta-chloro-phenylpiperazine in obsessivecompulsive disorder. Psychiatry Res 36: 1-17. 1991
References 1. Mermelstein HT. Holland JC: Psychotherapy by telephone: a therapeutic tool for cancer patients. Psychosomatics 32:407-412. 1991 2. Friedman EH, Robinson RG: Speech hesitation pauses as markers for mood disorder in stroke patients? (letter and reply). J C/in Psychiatry 52: 140, 1991 3. Friedman EH: VOXAFLEX Speech Pause Time Monitor (Software Survey Section). J Child Psychol Psychiatry 31:1.1990 4. Guilford T. Dawkins MS: Receiver psychology and the evolution of animal signals. Animal Behaviour 42: 1-14. 1991 5. Friedman EH: Temporal processing (Ieller). Journal of Learninx Disabilities 24:260. 1991 6. Pindzola RH: Dysfluency characteristics of aged. normalspeaking black and white males. Journal of Fluency Disorders 15:235-243. 1990
In Reply On "Psychotherapy by Telephone: A Therapeutic Toolfor Cancer Patients" SIR: In the Fall 1991 issue. ' Hindi T. Mennelstein. M.D.• and Jimmie C. Holland. M.D.• indicate a need for visual and nonverbal cues in telephone contact with the medically ill patient. This strategy can be easily implemented by memorable graphic and tabular presentations of microcomputer analysis of speech pause time. a behavioral correlate of mood. 2-4 Additional indexes monitor participatory matching. a joint mutually responsive rhythm. and bonding. The validity of this method in assessing the medically ill whose voices are harder to evaluate and who may have dialects is supported by reproducibility across time. circumstance. diagnosis. race. and species. 5.6 Ernest H. Friedman. M.D. Departments of Medicine and Psychiatry Case Western Reserve University East Cleveland. OH
362
SIR: We thank Dr. Friedman for alerting us to a potential research tool to measure changes in speech latency and rhythym, symptoms that commonly occur in mood disorders. This may be especially useful in the longitudinal assessment of the efficacy of psychotherapy by telephone where the loss of nonverbal cues limits our ability to evaluate other fonns of psychomotor retardation. In the clinical domain we look forward to further improvements in communication technology so that distance therapy will be a better and closer approximation of face to face interventions. Hindi T. Mermelstein. M.D. Jimmie C. Holland. M.D. New York, NY
PSYCHOSOMATICS