User login
We read with interest Dr. Henry A. Nasrallah’s call to unify psychiatry and neurology into 1 specialty (Current Psychiatry, From the Editor, August 2013, p. 8-9; http://bit.ly/16wImL3). Trends in this direction already are evident. Medical schools, including New York University School of Medicine, the University of Massachusetts Medical School, and the Medical University of South Carolina, have 6-year combined psychiatry and neurology residency programs that prepare students for board exams in either specialty or both specialties. We offer considerations that we hope will energize and inform the discussion, in turn moving us toward discovery of an optimal framework for all stakeholders.
In support of unification, Dr. Nasrallah’s editorial points to research advances in pharmacology, neuroimaging, and genetics. He writes that a “neuropharmacological revolution” is occurring, and it includes the discovery of medications that control symptoms of mood and anxiety disorders. The use of psychotropic medications certainly is escalating; >1 in every 10 Americans currently takes an antidepressant,1,2 reflecting a >400% increase over the past 2 decades.2
However, increasing use does not prove efficacy or establish causal mechanisms. Controversy persists regarding antidepressant efficacy, particularly for mild-to-moderate depression. The Sequenced Treatment Alternatives to Relieve Depression trial3 was the largest study to evaluate antidepressant effectiveness.3 Summarizing the findings, Thomas Insel, MD, Director of the National Institute of Mental Health stated, “Most important, this study demonstrates that for at least 70% of patients, appropriate treatment with an SSRI [selective serotonin reuptake inhibitor] is not enough.”4 What is clear is that the benefits of antidepressants are smaller than originally thought, and may be limited to patients with particular types of (severe) depression.
We agree that developments in neuroimaging and genetics of mental illness are exciting and some day may change the relationship between neurology and psychiatry. However, advanced neuroimaging technologies such as functional magnetic resonance imaging (fMRI) and diffusion tensor imaging (or diffusion MRI) have shown abnormalities involving brain-wide networks in psychiatric disorders5—not distinct regional abnormalities. In other words, psychiatry deals with mental phenomena that are modular in nature and not always reducible to their molecular origins, whereas in neurologic disorders, research linear cause-effect relationships and regional abnormalities are more common.
Genome-wide association studies have shown that few polymorphisms can be associated with numerous mental disorders6 (ie, multifinality), and that several genes may be associated with a particular disorder (ie, equifinality). Multifinality and equfinality are characteristics of complex disorders, with nonlinear gene × gene and gene × environment interactions. In contrast, most heritable neurologic disorders follow a Mendelian pattern of inheritance and predictable cause-effect neuropathology. Furthermore, recent advances in epigenetics—in which environmental and social factors modify gene expression and affect patterns of inheritance7—have further complicated our understanding of genetic contributions to psychiatric illness, and have revealed limitations in reductionist models.
Although neurologic and psychiatric disorders ultimately reflect cerebral pathology, the former commonly result from circumscribed lesions, and the latter are more complexly determined, resulting from disruptions in brain circuitry influenced by genetic, epigenetic, environmental, and social factors.7 As much as we might like it, research in psychiatry has not progressed to the point of fully explaining the brain-based processes underlying complex psychiatric disorders, decipher complex gene × gene and gene × environment interactions, or associate certain genes and biological pathways with specific disorders. A move to formally combine neurology and psychiatry may be prescient but premature because different sets of skills and methodologies might be required of clinicians and researchers in either specialty. More research is needed to shape and refine our disease and training models, and inform evidence-based practice.
Patrick J. Lustman, PhD
St. Louis VA Medical Center
John Cochran Hospital Division
Department of Psychiatry
Washington University School of Medicine
John M. Ray, MA
St. Louis VA Medical Center
John Cochran Hospital Division
Andrea L. Taylor, PhD
St. Louis VA Medical Center
John Cochran Hospital Division
Kenneth E. Freedland, PhD
Department of Psychiatry
Washington University School of Medicine
Dragan M. Svrakic, MD
St. Louis VA Medical Center
John Cochran Hospital Division
Department of Psychiatry
Washington University School of Medicine
St. Louis, Missouri
1. Charney DS, Nemeroff CB, Lewis L, et al. National Depressive and Manic-Depressive Association consensus statement on the use of placebo in clinical trials of mood disorders. Arch Gen Psychiatry. 2002;59(3):262-270.
2. Pratt LA, Brody DJ, Gu Q. Antidepressant use in persons aged 12 and over: United States, 2005-2008. NCHS Data Brief. 2011;(76):1-8.
3. Trivedi MH, Rush AJ, Wisniewski SR, et al. Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. Am J Psychiatry. 2006;163(1):28-40.
4. Insel TR. Beyond efficacy: the STAR*D Trial. Am J Psychiatry. 2006;163(1):5-7.
5. Zhou Y, Liang M, Tian L, et al. Functional disintegration in paranoid schizophrenia using resting-state fMRI. Schizophr Res. 2007;97(1-3):194-205.
6. Sullivan PA. A framework for interpreting genome-wide association studies of psychiatric disorders. Mol Psychiatry. 2009;14(1):10-17.
7. Svrakic DM, Zorumski CF, Svrakic NM, et al. Risk architecture of schizophrenia: the role of epigenetics. Curr Opin Psychiatry. 2013;26(2):188-195.
We read with interest Dr. Henry A. Nasrallah’s call to unify psychiatry and neurology into 1 specialty (Current Psychiatry, From the Editor, August 2013, p. 8-9; http://bit.ly/16wImL3). Trends in this direction already are evident. Medical schools, including New York University School of Medicine, the University of Massachusetts Medical School, and the Medical University of South Carolina, have 6-year combined psychiatry and neurology residency programs that prepare students for board exams in either specialty or both specialties. We offer considerations that we hope will energize and inform the discussion, in turn moving us toward discovery of an optimal framework for all stakeholders.
In support of unification, Dr. Nasrallah’s editorial points to research advances in pharmacology, neuroimaging, and genetics. He writes that a “neuropharmacological revolution” is occurring, and it includes the discovery of medications that control symptoms of mood and anxiety disorders. The use of psychotropic medications certainly is escalating; >1 in every 10 Americans currently takes an antidepressant,1,2 reflecting a >400% increase over the past 2 decades.2
However, increasing use does not prove efficacy or establish causal mechanisms. Controversy persists regarding antidepressant efficacy, particularly for mild-to-moderate depression. The Sequenced Treatment Alternatives to Relieve Depression trial3 was the largest study to evaluate antidepressant effectiveness.3 Summarizing the findings, Thomas Insel, MD, Director of the National Institute of Mental Health stated, “Most important, this study demonstrates that for at least 70% of patients, appropriate treatment with an SSRI [selective serotonin reuptake inhibitor] is not enough.”4 What is clear is that the benefits of antidepressants are smaller than originally thought, and may be limited to patients with particular types of (severe) depression.
We agree that developments in neuroimaging and genetics of mental illness are exciting and some day may change the relationship between neurology and psychiatry. However, advanced neuroimaging technologies such as functional magnetic resonance imaging (fMRI) and diffusion tensor imaging (or diffusion MRI) have shown abnormalities involving brain-wide networks in psychiatric disorders5—not distinct regional abnormalities. In other words, psychiatry deals with mental phenomena that are modular in nature and not always reducible to their molecular origins, whereas in neurologic disorders, research linear cause-effect relationships and regional abnormalities are more common.
Genome-wide association studies have shown that few polymorphisms can be associated with numerous mental disorders6 (ie, multifinality), and that several genes may be associated with a particular disorder (ie, equifinality). Multifinality and equfinality are characteristics of complex disorders, with nonlinear gene × gene and gene × environment interactions. In contrast, most heritable neurologic disorders follow a Mendelian pattern of inheritance and predictable cause-effect neuropathology. Furthermore, recent advances in epigenetics—in which environmental and social factors modify gene expression and affect patterns of inheritance7—have further complicated our understanding of genetic contributions to psychiatric illness, and have revealed limitations in reductionist models.
Although neurologic and psychiatric disorders ultimately reflect cerebral pathology, the former commonly result from circumscribed lesions, and the latter are more complexly determined, resulting from disruptions in brain circuitry influenced by genetic, epigenetic, environmental, and social factors.7 As much as we might like it, research in psychiatry has not progressed to the point of fully explaining the brain-based processes underlying complex psychiatric disorders, decipher complex gene × gene and gene × environment interactions, or associate certain genes and biological pathways with specific disorders. A move to formally combine neurology and psychiatry may be prescient but premature because different sets of skills and methodologies might be required of clinicians and researchers in either specialty. More research is needed to shape and refine our disease and training models, and inform evidence-based practice.
Patrick J. Lustman, PhD
St. Louis VA Medical Center
John Cochran Hospital Division
Department of Psychiatry
Washington University School of Medicine
John M. Ray, MA
St. Louis VA Medical Center
John Cochran Hospital Division
Andrea L. Taylor, PhD
St. Louis VA Medical Center
John Cochran Hospital Division
Kenneth E. Freedland, PhD
Department of Psychiatry
Washington University School of Medicine
Dragan M. Svrakic, MD
St. Louis VA Medical Center
John Cochran Hospital Division
Department of Psychiatry
Washington University School of Medicine
St. Louis, Missouri
We read with interest Dr. Henry A. Nasrallah’s call to unify psychiatry and neurology into 1 specialty (Current Psychiatry, From the Editor, August 2013, p. 8-9; http://bit.ly/16wImL3). Trends in this direction already are evident. Medical schools, including New York University School of Medicine, the University of Massachusetts Medical School, and the Medical University of South Carolina, have 6-year combined psychiatry and neurology residency programs that prepare students for board exams in either specialty or both specialties. We offer considerations that we hope will energize and inform the discussion, in turn moving us toward discovery of an optimal framework for all stakeholders.
In support of unification, Dr. Nasrallah’s editorial points to research advances in pharmacology, neuroimaging, and genetics. He writes that a “neuropharmacological revolution” is occurring, and it includes the discovery of medications that control symptoms of mood and anxiety disorders. The use of psychotropic medications certainly is escalating; >1 in every 10 Americans currently takes an antidepressant,1,2 reflecting a >400% increase over the past 2 decades.2
However, increasing use does not prove efficacy or establish causal mechanisms. Controversy persists regarding antidepressant efficacy, particularly for mild-to-moderate depression. The Sequenced Treatment Alternatives to Relieve Depression trial3 was the largest study to evaluate antidepressant effectiveness.3 Summarizing the findings, Thomas Insel, MD, Director of the National Institute of Mental Health stated, “Most important, this study demonstrates that for at least 70% of patients, appropriate treatment with an SSRI [selective serotonin reuptake inhibitor] is not enough.”4 What is clear is that the benefits of antidepressants are smaller than originally thought, and may be limited to patients with particular types of (severe) depression.
We agree that developments in neuroimaging and genetics of mental illness are exciting and some day may change the relationship between neurology and psychiatry. However, advanced neuroimaging technologies such as functional magnetic resonance imaging (fMRI) and diffusion tensor imaging (or diffusion MRI) have shown abnormalities involving brain-wide networks in psychiatric disorders5—not distinct regional abnormalities. In other words, psychiatry deals with mental phenomena that are modular in nature and not always reducible to their molecular origins, whereas in neurologic disorders, research linear cause-effect relationships and regional abnormalities are more common.
Genome-wide association studies have shown that few polymorphisms can be associated with numerous mental disorders6 (ie, multifinality), and that several genes may be associated with a particular disorder (ie, equifinality). Multifinality and equfinality are characteristics of complex disorders, with nonlinear gene × gene and gene × environment interactions. In contrast, most heritable neurologic disorders follow a Mendelian pattern of inheritance and predictable cause-effect neuropathology. Furthermore, recent advances in epigenetics—in which environmental and social factors modify gene expression and affect patterns of inheritance7—have further complicated our understanding of genetic contributions to psychiatric illness, and have revealed limitations in reductionist models.
Although neurologic and psychiatric disorders ultimately reflect cerebral pathology, the former commonly result from circumscribed lesions, and the latter are more complexly determined, resulting from disruptions in brain circuitry influenced by genetic, epigenetic, environmental, and social factors.7 As much as we might like it, research in psychiatry has not progressed to the point of fully explaining the brain-based processes underlying complex psychiatric disorders, decipher complex gene × gene and gene × environment interactions, or associate certain genes and biological pathways with specific disorders. A move to formally combine neurology and psychiatry may be prescient but premature because different sets of skills and methodologies might be required of clinicians and researchers in either specialty. More research is needed to shape and refine our disease and training models, and inform evidence-based practice.
Patrick J. Lustman, PhD
St. Louis VA Medical Center
John Cochran Hospital Division
Department of Psychiatry
Washington University School of Medicine
John M. Ray, MA
St. Louis VA Medical Center
John Cochran Hospital Division
Andrea L. Taylor, PhD
St. Louis VA Medical Center
John Cochran Hospital Division
Kenneth E. Freedland, PhD
Department of Psychiatry
Washington University School of Medicine
Dragan M. Svrakic, MD
St. Louis VA Medical Center
John Cochran Hospital Division
Department of Psychiatry
Washington University School of Medicine
St. Louis, Missouri
1. Charney DS, Nemeroff CB, Lewis L, et al. National Depressive and Manic-Depressive Association consensus statement on the use of placebo in clinical trials of mood disorders. Arch Gen Psychiatry. 2002;59(3):262-270.
2. Pratt LA, Brody DJ, Gu Q. Antidepressant use in persons aged 12 and over: United States, 2005-2008. NCHS Data Brief. 2011;(76):1-8.
3. Trivedi MH, Rush AJ, Wisniewski SR, et al. Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. Am J Psychiatry. 2006;163(1):28-40.
4. Insel TR. Beyond efficacy: the STAR*D Trial. Am J Psychiatry. 2006;163(1):5-7.
5. Zhou Y, Liang M, Tian L, et al. Functional disintegration in paranoid schizophrenia using resting-state fMRI. Schizophr Res. 2007;97(1-3):194-205.
6. Sullivan PA. A framework for interpreting genome-wide association studies of psychiatric disorders. Mol Psychiatry. 2009;14(1):10-17.
7. Svrakic DM, Zorumski CF, Svrakic NM, et al. Risk architecture of schizophrenia: the role of epigenetics. Curr Opin Psychiatry. 2013;26(2):188-195.
1. Charney DS, Nemeroff CB, Lewis L, et al. National Depressive and Manic-Depressive Association consensus statement on the use of placebo in clinical trials of mood disorders. Arch Gen Psychiatry. 2002;59(3):262-270.
2. Pratt LA, Brody DJ, Gu Q. Antidepressant use in persons aged 12 and over: United States, 2005-2008. NCHS Data Brief. 2011;(76):1-8.
3. Trivedi MH, Rush AJ, Wisniewski SR, et al. Evaluation of outcomes with citalopram for depression using measurement-based care in STAR*D: implications for clinical practice. Am J Psychiatry. 2006;163(1):28-40.
4. Insel TR. Beyond efficacy: the STAR*D Trial. Am J Psychiatry. 2006;163(1):5-7.
5. Zhou Y, Liang M, Tian L, et al. Functional disintegration in paranoid schizophrenia using resting-state fMRI. Schizophr Res. 2007;97(1-3):194-205.
6. Sullivan PA. A framework for interpreting genome-wide association studies of psychiatric disorders. Mol Psychiatry. 2009;14(1):10-17.
7. Svrakic DM, Zorumski CF, Svrakic NM, et al. Risk architecture of schizophrenia: the role of epigenetics. Curr Opin Psychiatry. 2013;26(2):188-195.