Journal of ECT • Volume 31, Number 2, June 2015
Spontaneous Happiness, discusses in great detail the fact that physical health and mental health cannot be considered in isolation from each other. Steps that we take, whether medical treatments or self-help interventions, work in conjunction with each other to improve our overall well-being. A bio-psycho-spiritual approach is often considered to be holistic because it takes into account multiple ways of knowing and understanding the person who is being treated.3 This has been my experience of ECT. When nurses, physicians, and technicians in the ECT department ask me how things are going for me (not just adhering to the symptom checklist on the computer screen), when they attend to my physical and emotional comfort, and when they communicate with me in an authentic way, then the experience does take into account my emotional and social well-being, in addition to the administration of a medical treatment.4 I am fortunate because I do receive this kind of person-centered care from my ECT providers. Interestingly, in my own experience, the psychiatrists who were the most biological in their orientation to mental illness and its treatment have been the doctors who treated me with the most respect and concern. The biological psychiatrists were the ones who held out the most hope that I could recover and live a good quality of life. This is in contrast to the psychodynamic psychiatrists, who argued that I had such a severe personality disorder that recovery was completely out of reach. For me, as a patient who receives maintenance ECT, this very biological treatment actually helps me to achieve a degree of emotional stability that supports the other aspects of my recovery. As a result of the stable moods made possible by ECT, my mind is usually clear, and the psychotic symptoms that haunted me for years have largely vanished. This mental clarity enables me to engage in self-help activities as well as professional therapies that have helped me to grow in maturity and self-sufficiency. Electroconvulsive therapy works in conjunction with other treatments to keep me happy and healthy. For me, ECT promotes holistic health. The biomedical treatment I receive helps me to practice positive thinking habits, mindfulness, healthy communication skills, and other “emotional” practices that have helped me remain employed, in my own home, and well-situated in the social life of my community. Scientists still do not completely understand why ECT can alleviate severe psychiatric symptoms, but in truth, we do not really understand the way that most psychological or alternative therapies work, either. Electroconvulsive therapy does as
Letters to the Editor
much to address the mind-body connection of mental health as any other treatment, given that providers approach the patients in the ECT suite with concern, care, and most of all, hope for recovery. Melissa A. Hensley, PhD, LISW Augsburg College Minneapolis, MN [email protected]
The authors have no conflicts of interest or financial disclosures to report. REFERENCES 1. Breggin PR. Toxic Psychiatry. New York, NY: St. Martin's Press; 1994. 2. Mayo Clinic. Tests and Procedures: Electroconvulsive Therapy. [Mayo Clinic Web site]. Available at: http://www.mayoclinic.org/ tests-procedures/electroconvulsive-therapy/ basics/definition/prc-20014161. Accessed December 19, 2014. 3. Weil A. Spontaneous Happiness. New York, NY: Little, Brown, & Company; 2011. 4. Epstein RM, Street RL. The values and value of patient-centered care. Ann Fam Med. 2011;9: 100–103.
Continuation and Maintenance Electroconvulsive Therapy—A Conceptual Framework? To the Editor: he important review of research in continuation and maintenance electroconvulsive therapy (CMECT) by Brown et al1 concludes that CMECT is a viable option for the prevention of relapse/recurrence of depression, is at least comparable to medication, and is likely enhanced when used in combination with pharmacotherapy and a flexible dosing schedule. Another recent review of the subject by Petrides et al2 reached similar conclusions. Nonetheless, considerable uncertainty remains about how best to use this increasingly important treatment modality. Hypotheses about fundamental characteristics of the major mood disorders, and about their putative impact by CMECT, may suggest a conceptual framework to guide treatment decisions while we await data-based recommendations.3 Kraepelin4 asserted that manic depressive disease—and he believed that what we call major depression and bipolar disorder were variants of the same condition—was a chronic and recurrent illness. He observed that episodes recurred with increasing frequency over time, and that the duration of episodes—although highly variable among individuals—tended to be approximately
T
consistent within individuals, usually showing a gradual increase over time. He reported that, although the average “attack” of depression lasted 6 to 8 months, episodes lasting 2 to 4 years were “not at all rare” and that “double attacks” twice that long were possible. Subsequent research has largely confirmed Kraepelin's observations.5–8 However, Kraepelin4 also emphasized the heterogeneity of the mood disorders, as have subsequent investigators.9,10 He observed that the periodicity of these disorders was only a tendency, not absolute. Nonetheless, the common tendency of mood disorders to demonstrate a certain rhythmicity—highly variable among individuals but fairly consistent within individuals—suggests that close attention to a patient's history may provide useful guidelines for prognosis and treatment. For example, a patient whose history demonstrates a relatively consistent pattern of long-lasting episodes, and whose treatment commences early on in the course of an episode can be expected to require more extended continuation treatment than one whose episodes are relatively brief or who initiates treatment closer to an anticipated spontaneous end point.11,12 A series of studies conducted during the 1960s and 1970s13–15 demonstrated that when antidepressant treatment was discontinued as soon as symptomatic recovery occurred, approximately 50% to 70% of the patients relapsed, most of them during the first 8 weeks after discontinuation. However, when the treatment was continued for 16 to 20 weeks after remission, rapid relapse was seen in only approximately 15% to 20%. These observations indicated that antidepressant treatment should be continued for 4 to 5 months after remission, and suggested the hypothesis that somatic treatment—both medication and electroconvulsive therapy (ECT)—does not alter the underlying pathophysiology of the disease but rather suppresses symptoms while the disease runs its natural course.15–17 It follows from the above discussion, and from subsequent research, that optimal strategy for maintaining remission after an acute course of ECT entails gradually, tapering the frequency of ECT treatments over 4 to 5 months, administering the minimum number of treatments consistent with maintaining remission, and individualizing treatment decisions.18,19 Nonetheless, the heterogeneity of the mood disorders, and the multiple factors—both known and unknown—which impact the disease course, likely render universal treatment guidelines unachievable. Although assuring that a patient is clearly well and stable at 1 interval before proceeding to a longer interval minimizes the risk for relapse, the risk cannot be
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.ectjournal.com
e27
Journal of ECT • Volume 31, Number 2, June 2015
Letters to the Editor
eliminated.20,21 Furthermore, although we have the ability to keep symptoms of a single episode suppressed until spontaneous remission occurs, we do not have the ability to prevent the occurrence of new episodes. Engaging the patient and significant others in a necessarily empirical course of treatment—that is, clarifying what we know, what we do not know, and what we are trying to achieve—enhances collaboration and compliance. Candid discussion of the inevitable uncertainties, and consistent efforts to provide a delicate balance among comfort, candor, and hope—the possible “psychosocial” components of ECT treatment1— are likely to maximize the likelihood of sustained remission. Herbert A. Fox, MD Weill Cornell College of Medicine and The Mount Sinai Beth Israel Medical Center New York, NY [email protected]
The author has no conflict of interest or financial disclosures to report. REFERENCES 1. Brown ED, Lee H, Scott D, et al. Efficacy of continuation/maintenance electroconvulsive therapy for the prevention of recurrence of a major depressive episode in adults with unipolar depression. J ECT. 2014;30:195–202. 2. Petrides G, Tobias KG, Kellner CH. Continuation and maintenance electroconvulsive therapy for mood disorders: review of the literature. Neuropsychobiology. 2011;64:129–140. 3. Kellner CH. Prolonging remission in depressed elderly (PRIDE). NCT01028508. Clinicaltrials. gov registered 2009. 4. Kraepelin E. Manic-Depressive Insanity and Paranoia. Edinburgh, United Kingdom: E. & S. Livingstone; 1921. 5. Angst J, Weis P. Periodicity of depressive psychoses. In: Brill H, Cole JO, Hippius H, Bradley PB, eds. Neuropsychopharmacology: Proceedings of the Fifth International Congress of the Collegium International Neuro-psycho-pharmacologicum. Amsterdam, the Netherlands: Exerpta Medica; 1967:703–710. 6. NIMH/NIH Consensus Development Conference. Mood disorders: pharmacologic prevention of recurrences. Am J Psychiatry. 1985;142:469–476. 7. Goodwin FK, Jamison KR. Manic-Depressive Illness. New York, NY: Oxford University Press, 1990. 8. Solomon DA, Keller MB, Leon AC, et al. Recovery from major depression: a 10-year prospective follow-up across multiple episodes. Arch Gen Psychiatry. 1997;54:1001–1006. 9. Keller MB. Diagnostic issues and clinical course of unipolar illness. In: Frances AJ, Hales RE, eds. American Psychiatric Press Review of Psychiatry, Vol 7. Washington, DC: American Psychiatric Press, 1988:188–212.
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10. Merikangas KR, Wicki W, Angst J. Heterogeneity of depression: classification of depressive subtypes by longitudinal course. Br J Psychiatry. 1994;164:342–348. 11. Fox HA. Continuation and maintenance ECT. J Psychiatr Pract. 1996;2:357–363. 12. Fox HA. The natural course of depression: Kraepelin and beyond. Harv Rev Psychiatry. 2002;10:249–253. 13. Seager CP, Bird RL. Imipramine with electrical treatment in depression—a controlled trial. J Ment Sci. 1962;108:704–707. 14. Imlah NW, Ryan E, Harrington JA. The influence of antidepressant drugs on the response to electroconvulsive therapy and on subsequent relapse rates. Neuropsychopharmacol. 1965;4:438–442. 15. Mindham RH, Howland C, Shepard M. An evaluation of continuation therapy with tricyclic antidepressants in depressive illness. Psychol Med. 1973;3:5–17. 16. Prien RF, Klett CJ, Caffey EM Jr. Lithium carbonate and imipramine in prevention of affective episodes: a comparison in recurrent depressive illness. Arch Gen Psychiatry. 1973; 29:420–425. 17. Fox H. Switches, dimmer switches and ECT. J ECT. 2013;29:e70. 18. Odeberg H, Rodriguez-Silva B, Salander P, et al. Individualized continuation electroconvulsive therapy and medication as a bridge to relapse prevention after an index course of electroconvulsive therapy in severe mood disorders: a naturalistic 3-year cohort study. J ECT. 2008;24:183–190. 19. Huuhka K, Vikki M, Tammentie T, et al. One-year follow-up after discontinuing maintenance electroconvulsive therapy. J ECT. 2012;28:225–228. 20. Prien RF, Kupfer DJ. Continuation drug therapy for major depressive episodes: how long should it be maintained? Am J Psychiatry. 1986; 143:18–23. 21. Fox H. Extended continuation and maintenance ECT for long-lasting episodes of major depression. J ECT. 2001;17:60–64.
Prolactin Serum Concentrations After Electroconvulsive Therapy in a Depressed Patient With Cabergoline-Treated Prolactinoma Implications for Treatment To the Editor: e report on the case of a 62-year-old woman who was admitted to our psychiatric hospital due to a second depressive episode in which a hormone-producing tumor of the pituitary gland was diagnosed. Six months before admission to our clinic,
W
the woman had experienced sudden onset of depressive symptoms in the absence of a known stressor, leading to an initial period of inpatient psychiatric treatment. Her personal history was unremarkable, except for a recent period of hypertension. There was no previous psychiatric history. A diagnosis of major depressive disorder, which was single episode and severe with psychotic features (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, 296.24), was rendered; she was treated with 150 mg of sertraline OD, 30 mg of mirtazapine OD, 1 mg of lorazepam qid, and antipsychotics (3 mg of risperidone OD first; 800 mg of quetiapine OD second) because of nihilistic thinking. After 4 months of hospital treatment, the patient was discharged in remission. However, 1 month before admission to our hospital, Ms A had developed deep venous thrombosis with pulmonary artery embolism (requiring transitory anticoagulation). On admission, Ms A was severely depressed with lack of interest and presented with apathy, anhedonia, sleep disturbance, and reduced appetite. Recurrent suicidal thinking, diffuse anxiety, and nihilistic delusions were also present. The Hamilton Depression Rating Scale (observer rating scale) scored 32 (severe depression). At this time, the Beck Depression Inventory (self-report inventory) could not be administered because of extreme apathy and loss of drive. Familial history for psychiatric and neurological diseases was negative and substance abuse was negated. Apart from hypertension, neither somatic nor neurological examinations demonstrated any pathological findings. Routine laboratory testing was normal besides hypercholesterolemia. Although tests for ruling out a clinically relevant dementia were almost within reference ranges (Mini-Mental State Examination [score 28] and DemTect [score 13 = age appropriate]), the ClockDrawing Test showed slight deficits, which were possibly related to psychomotor restraint and anhedonia (score, 2–3; 1 = no error/6 = no clock identifiable). Magnetic resonance imaging (MRI) of the brain showed mild parietal and frontal cortical atrophy as well as few nonspecific white matter T2 hyperintensities. 18F-fluoro-deoxy-glucose positron emission tomography of the brain did not exhibit typical patterns of neurodegenerative disorders. Cerebrospinal fluid examination including τ and amyloid-β (1–42) was normal. Borrelia burgdorferi and Treponema pallidum antibodies were absent. Absence of paraneoplastic antibodies in serum and cerebrospinal fluid (amphiphysin, CV2, Ri, Hu, Yo, recoverin, SOX1, connectin, PNMA2/Ma 2Ta, GAD; NMDA-, AMPA-1-und−2-, GABAB1 receptor antibodies; CASPR2, LGI1 antibodies)
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
Spontaneous Happiness, discusses in great detail the fact that physical health and mental health cannot be considered in isolation from each other. Steps that we take, whether medical treatments or self-help interventions, work in conjunction with each other to improve our overall well-being. A bio-psycho-spiritual approach is often considered to be holistic because it takes into account multiple ways of knowing and understanding the person who is being treated.3 This has been my experience of ECT. When nurses, physicians, and technicians in the ECT department ask me how things are going for me (not just adhering to the symptom checklist on the computer screen), when they attend to my physical and emotional comfort, and when they communicate with me in an authentic way, then the experience does take into account my emotional and social well-being, in addition to the administration of a medical treatment.4 I am fortunate because I do receive this kind of person-centered care from my ECT providers. Interestingly, in my own experience, the psychiatrists who were the most biological in their orientation to mental illness and its treatment have been the doctors who treated me with the most respect and concern. The biological psychiatrists were the ones who held out the most hope that I could recover and live a good quality of life. This is in contrast to the psychodynamic psychiatrists, who argued that I had such a severe personality disorder that recovery was completely out of reach. For me, as a patient who receives maintenance ECT, this very biological treatment actually helps me to achieve a degree of emotional stability that supports the other aspects of my recovery. As a result of the stable moods made possible by ECT, my mind is usually clear, and the psychotic symptoms that haunted me for years have largely vanished. This mental clarity enables me to engage in self-help activities as well as professional therapies that have helped me to grow in maturity and self-sufficiency. Electroconvulsive therapy works in conjunction with other treatments to keep me happy and healthy. For me, ECT promotes holistic health. The biomedical treatment I receive helps me to practice positive thinking habits, mindfulness, healthy communication skills, and other “emotional” practices that have helped me remain employed, in my own home, and well-situated in the social life of my community. Scientists still do not completely understand why ECT can alleviate severe psychiatric symptoms, but in truth, we do not really understand the way that most psychological or alternative therapies work, either. Electroconvulsive therapy does as
Letters to the Editor
much to address the mind-body connection of mental health as any other treatment, given that providers approach the patients in the ECT suite with concern, care, and most of all, hope for recovery. Melissa A. Hensley, PhD, LISW Augsburg College Minneapolis, MN [email protected]
The authors have no conflicts of interest or financial disclosures to report. REFERENCES 1. Breggin PR. Toxic Psychiatry. New York, NY: St. Martin's Press; 1994. 2. Mayo Clinic. Tests and Procedures: Electroconvulsive Therapy. [Mayo Clinic Web site]. Available at: http://www.mayoclinic.org/ tests-procedures/electroconvulsive-therapy/ basics/definition/prc-20014161. Accessed December 19, 2014. 3. Weil A. Spontaneous Happiness. New York, NY: Little, Brown, & Company; 2011. 4. Epstein RM, Street RL. The values and value of patient-centered care. Ann Fam Med. 2011;9: 100–103.
Continuation and Maintenance Electroconvulsive Therapy—A Conceptual Framework? To the Editor: he important review of research in continuation and maintenance electroconvulsive therapy (CMECT) by Brown et al1 concludes that CMECT is a viable option for the prevention of relapse/recurrence of depression, is at least comparable to medication, and is likely enhanced when used in combination with pharmacotherapy and a flexible dosing schedule. Another recent review of the subject by Petrides et al2 reached similar conclusions. Nonetheless, considerable uncertainty remains about how best to use this increasingly important treatment modality. Hypotheses about fundamental characteristics of the major mood disorders, and about their putative impact by CMECT, may suggest a conceptual framework to guide treatment decisions while we await data-based recommendations.3 Kraepelin4 asserted that manic depressive disease—and he believed that what we call major depression and bipolar disorder were variants of the same condition—was a chronic and recurrent illness. He observed that episodes recurred with increasing frequency over time, and that the duration of episodes—although highly variable among individuals—tended to be approximately
T
consistent within individuals, usually showing a gradual increase over time. He reported that, although the average “attack” of depression lasted 6 to 8 months, episodes lasting 2 to 4 years were “not at all rare” and that “double attacks” twice that long were possible. Subsequent research has largely confirmed Kraepelin's observations.5–8 However, Kraepelin4 also emphasized the heterogeneity of the mood disorders, as have subsequent investigators.9,10 He observed that the periodicity of these disorders was only a tendency, not absolute. Nonetheless, the common tendency of mood disorders to demonstrate a certain rhythmicity—highly variable among individuals but fairly consistent within individuals—suggests that close attention to a patient's history may provide useful guidelines for prognosis and treatment. For example, a patient whose history demonstrates a relatively consistent pattern of long-lasting episodes, and whose treatment commences early on in the course of an episode can be expected to require more extended continuation treatment than one whose episodes are relatively brief or who initiates treatment closer to an anticipated spontaneous end point.11,12 A series of studies conducted during the 1960s and 1970s13–15 demonstrated that when antidepressant treatment was discontinued as soon as symptomatic recovery occurred, approximately 50% to 70% of the patients relapsed, most of them during the first 8 weeks after discontinuation. However, when the treatment was continued for 16 to 20 weeks after remission, rapid relapse was seen in only approximately 15% to 20%. These observations indicated that antidepressant treatment should be continued for 4 to 5 months after remission, and suggested the hypothesis that somatic treatment—both medication and electroconvulsive therapy (ECT)—does not alter the underlying pathophysiology of the disease but rather suppresses symptoms while the disease runs its natural course.15–17 It follows from the above discussion, and from subsequent research, that optimal strategy for maintaining remission after an acute course of ECT entails gradually, tapering the frequency of ECT treatments over 4 to 5 months, administering the minimum number of treatments consistent with maintaining remission, and individualizing treatment decisions.18,19 Nonetheless, the heterogeneity of the mood disorders, and the multiple factors—both known and unknown—which impact the disease course, likely render universal treatment guidelines unachievable. Although assuring that a patient is clearly well and stable at 1 interval before proceeding to a longer interval minimizes the risk for relapse, the risk cannot be
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
www.ectjournal.com
e27
Journal of ECT • Volume 31, Number 2, June 2015
Letters to the Editor
eliminated.20,21 Furthermore, although we have the ability to keep symptoms of a single episode suppressed until spontaneous remission occurs, we do not have the ability to prevent the occurrence of new episodes. Engaging the patient and significant others in a necessarily empirical course of treatment—that is, clarifying what we know, what we do not know, and what we are trying to achieve—enhances collaboration and compliance. Candid discussion of the inevitable uncertainties, and consistent efforts to provide a delicate balance among comfort, candor, and hope—the possible “psychosocial” components of ECT treatment1— are likely to maximize the likelihood of sustained remission. Herbert A. Fox, MD Weill Cornell College of Medicine and The Mount Sinai Beth Israel Medical Center New York, NY [email protected]
The author has no conflict of interest or financial disclosures to report. REFERENCES 1. Brown ED, Lee H, Scott D, et al. Efficacy of continuation/maintenance electroconvulsive therapy for the prevention of recurrence of a major depressive episode in adults with unipolar depression. J ECT. 2014;30:195–202. 2. Petrides G, Tobias KG, Kellner CH. Continuation and maintenance electroconvulsive therapy for mood disorders: review of the literature. Neuropsychobiology. 2011;64:129–140. 3. Kellner CH. Prolonging remission in depressed elderly (PRIDE). NCT01028508. Clinicaltrials. gov registered 2009. 4. Kraepelin E. Manic-Depressive Insanity and Paranoia. Edinburgh, United Kingdom: E. & S. Livingstone; 1921. 5. Angst J, Weis P. Periodicity of depressive psychoses. In: Brill H, Cole JO, Hippius H, Bradley PB, eds. Neuropsychopharmacology: Proceedings of the Fifth International Congress of the Collegium International Neuro-psycho-pharmacologicum. Amsterdam, the Netherlands: Exerpta Medica; 1967:703–710. 6. NIMH/NIH Consensus Development Conference. Mood disorders: pharmacologic prevention of recurrences. Am J Psychiatry. 1985;142:469–476. 7. Goodwin FK, Jamison KR. Manic-Depressive Illness. New York, NY: Oxford University Press, 1990. 8. Solomon DA, Keller MB, Leon AC, et al. Recovery from major depression: a 10-year prospective follow-up across multiple episodes. Arch Gen Psychiatry. 1997;54:1001–1006. 9. Keller MB. Diagnostic issues and clinical course of unipolar illness. In: Frances AJ, Hales RE, eds. American Psychiatric Press Review of Psychiatry, Vol 7. Washington, DC: American Psychiatric Press, 1988:188–212.
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10. Merikangas KR, Wicki W, Angst J. Heterogeneity of depression: classification of depressive subtypes by longitudinal course. Br J Psychiatry. 1994;164:342–348. 11. Fox HA. Continuation and maintenance ECT. J Psychiatr Pract. 1996;2:357–363. 12. Fox HA. The natural course of depression: Kraepelin and beyond. Harv Rev Psychiatry. 2002;10:249–253. 13. Seager CP, Bird RL. Imipramine with electrical treatment in depression—a controlled trial. J Ment Sci. 1962;108:704–707. 14. Imlah NW, Ryan E, Harrington JA. The influence of antidepressant drugs on the response to electroconvulsive therapy and on subsequent relapse rates. Neuropsychopharmacol. 1965;4:438–442. 15. Mindham RH, Howland C, Shepard M. An evaluation of continuation therapy with tricyclic antidepressants in depressive illness. Psychol Med. 1973;3:5–17. 16. Prien RF, Klett CJ, Caffey EM Jr. Lithium carbonate and imipramine in prevention of affective episodes: a comparison in recurrent depressive illness. Arch Gen Psychiatry. 1973; 29:420–425. 17. Fox H. Switches, dimmer switches and ECT. J ECT. 2013;29:e70. 18. Odeberg H, Rodriguez-Silva B, Salander P, et al. Individualized continuation electroconvulsive therapy and medication as a bridge to relapse prevention after an index course of electroconvulsive therapy in severe mood disorders: a naturalistic 3-year cohort study. J ECT. 2008;24:183–190. 19. Huuhka K, Vikki M, Tammentie T, et al. One-year follow-up after discontinuing maintenance electroconvulsive therapy. J ECT. 2012;28:225–228. 20. Prien RF, Kupfer DJ. Continuation drug therapy for major depressive episodes: how long should it be maintained? Am J Psychiatry. 1986; 143:18–23. 21. Fox H. Extended continuation and maintenance ECT for long-lasting episodes of major depression. J ECT. 2001;17:60–64.
Prolactin Serum Concentrations After Electroconvulsive Therapy in a Depressed Patient With Cabergoline-Treated Prolactinoma Implications for Treatment To the Editor: e report on the case of a 62-year-old woman who was admitted to our psychiatric hospital due to a second depressive episode in which a hormone-producing tumor of the pituitary gland was diagnosed. Six months before admission to our clinic,
W
the woman had experienced sudden onset of depressive symptoms in the absence of a known stressor, leading to an initial period of inpatient psychiatric treatment. Her personal history was unremarkable, except for a recent period of hypertension. There was no previous psychiatric history. A diagnosis of major depressive disorder, which was single episode and severe with psychotic features (Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, 296.24), was rendered; she was treated with 150 mg of sertraline OD, 30 mg of mirtazapine OD, 1 mg of lorazepam qid, and antipsychotics (3 mg of risperidone OD first; 800 mg of quetiapine OD second) because of nihilistic thinking. After 4 months of hospital treatment, the patient was discharged in remission. However, 1 month before admission to our hospital, Ms A had developed deep venous thrombosis with pulmonary artery embolism (requiring transitory anticoagulation). On admission, Ms A was severely depressed with lack of interest and presented with apathy, anhedonia, sleep disturbance, and reduced appetite. Recurrent suicidal thinking, diffuse anxiety, and nihilistic delusions were also present. The Hamilton Depression Rating Scale (observer rating scale) scored 32 (severe depression). At this time, the Beck Depression Inventory (self-report inventory) could not be administered because of extreme apathy and loss of drive. Familial history for psychiatric and neurological diseases was negative and substance abuse was negated. Apart from hypertension, neither somatic nor neurological examinations demonstrated any pathological findings. Routine laboratory testing was normal besides hypercholesterolemia. Although tests for ruling out a clinically relevant dementia were almost within reference ranges (Mini-Mental State Examination [score 28] and DemTect [score 13 = age appropriate]), the ClockDrawing Test showed slight deficits, which were possibly related to psychomotor restraint and anhedonia (score, 2–3; 1 = no error/6 = no clock identifiable). Magnetic resonance imaging (MRI) of the brain showed mild parietal and frontal cortical atrophy as well as few nonspecific white matter T2 hyperintensities. 18F-fluoro-deoxy-glucose positron emission tomography of the brain did not exhibit typical patterns of neurodegenerative disorders. Cerebrospinal fluid examination including τ and amyloid-β (1–42) was normal. Borrelia burgdorferi and Treponema pallidum antibodies were absent. Absence of paraneoplastic antibodies in serum and cerebrospinal fluid (amphiphysin, CV2, Ri, Hu, Yo, recoverin, SOX1, connectin, PNMA2/Ma 2Ta, GAD; NMDA-, AMPA-1-und−2-, GABAB1 receptor antibodies; CASPR2, LGI1 antibodies)
© 2015 Wolters Kluwer Health, Inc. All rights reserved.
Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved.
