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  • JAMA Psychiatry October 1, 2017

    Figure 1: Between-Group Analyses Stratified by Disorder

    Because there was only 1 study, posttraumatic stress disorder was not included in the overall analysis. POTS indicates Pediatric OCD Treatment Study; RUPP, Research Unit on Pediatric Psychopharmacology Anxiety Study Group; SNRI, serotonin-norepinephrine reuptake inhibitor; SSRI, selective serotonin reuptake inhibitor.aOne study reported 2 different dosages of duloxetine.bOne study reported 2 trials that were treated independently for analyses.cOne study examined 2 forms of dosing. One treatment arm was sertraline at standard dosing and the second treatment arm was sertraline titrated slowly.
  • JAMA Psychiatry October 1, 2017

    Figure 2: Drug and Placebo Effect Size by Disorder Category

    Because there was only 1 study, posttraumatic stress disorder (PTSD) was not included in subgroup analyses. Responses to selective serotonin reuptake inhibitors (SSRIs) were significantly larger in depressive disorders (DDs) and anxiety disorders (ADs) compared with obsessive-compulsive disorder (OCD) (both P < .001). The placebo response was significantly larger in DDs compared with ADs (P < .001) and OCD (P < .001) and significantly larger in ADs compared with OCD (P < .002). SNRI indicates serotonin-norepinephrine reuptake inhibitor.
  • JAMA Psychiatry July 1, 2017

    Figure 1: Meta-analysis–Based Effect Sizes of Psychopharmacologic Augmentation of Any Antipsychotic Drug for Total Psychopathology

    Ach indicates acetylcholine; AchEsterase inhib, acetylcholinesterase inhibitors; AMSTAR, A Measurement Tool to Assess Systematic Reviews; AP, antipsychotic; DHEA, dehydroepiandrosterone; MAO, monoamine oxidase; N, number of studies; n, number of patients; NaSSA, noradrenergic and specific serotonergic antidepressant; NMDA, n-methyl-d-aspartate; NSAID, nonsteroidal anti-inflammatory drugs; NRI, norepinephrine reuptake inhibitor; PUFA, polyunsaturated fatty acids; Rec Ant, receptor antagonist; SARI, serotonin antagonist and reuptake inhibitor; SNRI, serotonin-norepinephrine reuptake inhibitor; SSRI, selective serotonin reuptake inhibitor; TCA, tricarboxylic acid.
  • JAMA Psychiatry July 1, 2017

    Figure 3: Meta-analysis–Based Effect Sizes of Psychopharmacologic Augmentation of Any Antipsychotic Drug For Positive Symptoms

    Ach indicates acetylcholine; AchEsterase inhib, acetylcholinesterase inhibitors; AMSTAR, A Measurement Tool to Assess Systematic Reviews; AP, antipsychotic; DHEA, dehydroepiandrosterone; MAO, monoamine oxidase; N, number of studies; n, number of patients; NaSSA, noradrenergic and specific serotonergic antidepressant; NMDA, n-methyl-d-aspartate; NSAID, nonsteroidal anti-inflammatory drugs; NRI, norepinephrine reuptake inhibitor; PUFA, polyunsaturated fatty acids; Rec Ant, receptor antagonist; SARI, serotonin antagonist and reuptake inhibitor; SNRI, serotonin-norepinephrine reuptake inhibitor; SSRI, selective serotonin reuptake inhibitor.
  • JAMA Psychiatry July 1, 2017

    Figure 4: Meta-analysis–Based Effect Sizes of Psychopharmacologic Augmentation of Any Antipsychotic Drug for Negative Symptoms

    Ach indicates acetylcholine; AchEsterase inhib, acetylcholinesterase inhibitors; AMSTAR, A Measurement Tool to Assess Systematic Reviews; AP, antipsychotic; DHEA, dehydroepiandrosterone; MAO, monoamine oxidase; N, number of studies; n, number of patients; NaSSA, noradrenergic and specific serotonergic antidepressant; NMDA, n-methyl-d-aspartate; NSAID, nonsteroidal anti-inflammatory drugs; NRI, norepinephrine reuptake inhibitor; PUFA, polyunsaturated fatty acids; Rec Ant, receptor antagonist; SARI, serotonin antagonist and reuptake inhibitor; SNRI, serotonin-norepinephrine reuptake inhibitor; SSRI, selective serotonin reuptake inhibitor.
  • JAMA Psychiatry November 1, 2013

    Figure: Neural Circuitry Associated With Obsessive-Compulsive Disorder (OCD)

    For more than 20 years, cortical-striatal-thalamic-cortical (yellow arrows) dysfunction has been associated with OCD symptoms, with the orbitofrontal cortex (OFC) being most directly implicated. Multiple regions within this behavioral circuit, in particular the striatum and OFC, are heavily innervated and modulated by the amygdala in response to emotional stimuli (red arrows). Functional imaging studies have suggested dysfunction within these pathways and abnormal circuit regulation correlating with OCD symptoms. These cortical and subcortical regions are regulated by the 3 monoamine systems that are targeted by current psychiatric medications, serotonin from the raphe nuclei, dopamine from the ventral tegmental area (VTA) and substantia nigra, and norepinephrine from the locus coeruleus (LC). Selective serotonin reuptake inhibitors and antipsychotics are thought to act primarily by altering serotonin and dopamine synapse functioning, respectively, thus altering monoaminergic regulation as their mechanism of symptom reduction. In contrast, exposure and ritual prevention is thought to directly alter the connectivity in the cortical-striatal-thalamic-cortical–amygdala circuits via emotional learning processes.
  • JAMA Psychiatry February 1, 2013

    Figure: Elevated C-Reactive Protein Levels, Psychological Distress, and Depression in 73 131 Individuals

    Figure 4. Cross-sectional analyses of the association between end points of psychological distress, hospitalization with depression, self-reported and prescription antidepressant use, and different types of antidepressants and doubled levels of C-reactive protein (CRP). Findings are based on 73 131 participants from the Copenhagen General Population and the Copenhagen City Heart studies combined. Multiple factors include age, sex, smoking, alcohol consumption, physical activity, educational level, income, body mass index (BMI), and register-based chronic disease. NARIs indicates noradrenaline reuptake inhibitors; NaSSAs, noradrenergic and specific serotonergic antidepressants; OR, odds ratio; SNRIs, serotonin and noradrenaline reuptake inhibitors; SSRIs, selective serotonin reuptake inhibitors; and TCAs, tricyclic antidepressants.
  • JAMA Psychiatry December 1, 2010

    Figure 1: Inflammation, Sanitation, and Consternation: Loss of Contact With Coevolved, Tolerogenic Microorganisms and the Pathophysiology and Treatment of Major Depression

    Psychosocial stress, inflammation, and immunoregulation in major depressive disorder (MDD). A, Psychosocial stress and factors that contribute to stress, such as social isolation and maladaptive personality, activate brain areas evolved to evaluate and respond to environmental danger. B, These brain areas contribute to activation of stress outflow pathways, including the sympathetic nervous system, with resultant norepinephrine (NE) production, and the hypothalamic-pituitary-adrenal axis, with resultant glucocorticoid (GC) release. In response to psychosocial stress, parasympathetic signaling is also withdrawn, leading to attenuated acetylcholine (ACh) release. C, In general, sympathetic activation promotes innate immune inflammatory processes, whereas parasympathetic signaling and glucocorticoids attenuate inflammation. D, Environmental adversity (whether via α- or β-adrenoreceptor [α/β-AR] stimulation in response to stress or via toll-like receptor [TLR] stimulation in response to infection, tissue trauma, or neoplasm) activates intracellular inflammatory signaling cascades (eg, nuclear factor-κβ [NF-κβ]) within innate immune cells (eg, macrophages and dendritic cells) leading to the production and release of inflammatory cytokines, including interleukin 1β (IL-1β), tumor necrosis factor α (TNF-α), and IL-6. α7 nAChR indicates α7 nicotinic acetylcholine receptor. E, These cytokines access the brain via leaky regions of the blood-brain barrier or active transport across the blood-brain barrier and can influence brain function via activation of afferent nerve fibers (ie, sensory vagus). Once in the brain, cytokine signals participate in processes known to be involved in the development of MDD, including alterations in monoaminergic neurotransmission, reduction in neurotrophic support, and increased production of excitotoxic/oxidative species that damage neurons and glial cells. F, Environmental adversities that activate inflammation (A and D) also stimulate immunoregulatory mechanisms that constrain inflammatory responses (F), in part via production of anti-inflammatory cytokines, including IL-10 and transforming growth factor β (TGF-β). G, Whereas inflammatory responses to psychosocial adversity are associated with MDD (E), immunoregulatory pathways antagonize these responses and by doing so promote psychosocial resilience, which enhances interpersonal functioning, contributing to euthymia (G). Immunoregulatory processes also likely contribute to euthymia by attenuating background levels of inflammatory activity that have been shown to be elevated in MDD.
  • JAMA Psychiatry May 1, 2010

    Figure 2Variation in the Risk of Suicide Attempts and Completed Suicides by Antidepressant Agent in Adults: A Propensity Score–Adjusted Analysis of 9 Years' Data

    Probability of remaining free of suicide or suicide attempt by antidepressant class and time since treatment initiation. MAOIs indicates monoamine oxidase inhibitors; SNRI, serotonin-norepinephrine reuptake inhibitor; SSRIs, selective serotonin reuptake inhibitors; and TCAs, tricyclic agents.
  • JAMA Psychiatry March 1, 2007

    Figure 3: The Role of Dopamine in the Pathophysiology of Depression

    Differing structures of dopamine terminals in the striatum and prefrontal cortex. Reprinted with permission from Sesack et al (1998). COMT indicates catechol-O-methyltransferase; DA, dopamine; and NE, norepinephrine.
  • Elevated Monoamine Oxidase A Levels in the Brain: An Explanation for the Monoamine Imbalance of Major Depression

    Abstract Full Text
    free access
    Arch Gen Psychiatry. 2006; 63(11):1209-1216. doi: 10.1001/archpsyc.63.11.1209
  • JAMA Psychiatry November 1, 2006

    Figure: Elevated Monoamine Oxidase A Levels in the Brain: An Explanation for the Monoamine Imbalance of Major Depression

    Figure 3. Modernization of monoamine theory of depression. A, Description of monoamine release in a synapse in a healthy person. B, During a major depressive episode, monoamine oxidase A (MAO-A) density is elevated, resulting in greater metabolism of monoamines, such as serotonin, norepinephrine, and dopamine, in the brain. C and D, Range of outcomes. If the monoamine transporter density for a particular monoamine is low during a major depressive episode (C), the effect of an elevated MAO-A level on reducing that particular monoamine in the extracellular space is somewhat attenuated, resulting in a moderate loss of monoamine. This eventually results in a moderate severity of symptoms associated with long-term loss of that particular monoamine. If the monoamine transporter density for a particular monoamine is not low during a major depressive episode (D), then there is no protection against the effect of elevated MAO-A levels. The extracellular concentration of the monoamine is severely reduced, and symptoms associated with long-term loss of that particular monoamine eventually become severe. Some postsynaptic receptors increase in density when their endogenous monoamine level is low in the long term. Mostly, MAO-A is found in norepinephrine-releasing neurons but is reported to be detectable in other cells, such as serotonin-releasing neurons and glia. Even so, MAO-A metabolizes serotonin, norepinephrine, and dopamine in vivo.
  • JAMA Psychiatry April 1, 2004

    Figure 3: Cortisol and Catecholamines in Posttraumatic Stress Disorder: An Epidemiologic Community Study

    Urine norepinephrine excretionlevels in night, morning (AM), and evening (PM) (men and women) by psychiatricdiagnoses. The groups with posttraumatic stress disorder (PTSD) only and PTSDcomorbid with major depressive disorder (MDD) had significantly higher levelsthan the other 2 groups.
  • The Neurobiology of Sexual Function

    Abstract Full Text
    Arch Gen Psychiatry. 2000; 57(11):1012-1030. doi: 10.1001/archpsyc.57.11.1012
  • JAMA Psychiatry August 1, 2000

    Figure 2: Reduced Brain Norepinephrine and Dopamine Release in Treatment-Refractory Depressive Illness: Evidence in Support of the Catecholamine Hypothesis of Mood Disorders

    Internal jugular venous plasma concentration gradients of norepinephrine (NE) and its principal central nervous system–occurring metabolites, dihydroxyphenylglycol (DHPG) and 3-methoxy-4-hydroxyphenylglycol (MHPG), the dopamine metabolite homovanillic acid (HVA), and the serotonin metabolite 5-hydroxyindoleacetic acid (5-HIAA) in healthy subjects (n = 19) and in patients with unipolar depressive illness (n = 9). In 1 patient, internal jugular venous HVA overflow was not measured. Values shown are mean ±SE. Asterisk indicates P<.05; dagger, P<.01; values are significantly different from the corresponding values in healthy subjects.
  • Reduced Brain Norepinephrine and Dopamine Release in Treatment-Refractory Depressive Illness: Evidence in Support of the Catecholamine Hypothesis of Mood Disorders

    Abstract Full Text
    free access
    Arch Gen Psychiatry. 2000; 57(8):787-793. doi: 10.1001/archpsyc.57.8.787
  • JAMA Psychiatry May 1, 2000

    Figure 1: Evidence of the Dual Mechanisms of Action of Venlafaxine

    Neurotransmitter uptake and models of serotonergic (top) and noradrenergic neurons (bottom). Top, Serotonin (5-HT) is released by the neuron. Its action is terminated by active reuptake into the neuron, where it is further sequestered in storage vesicles. Drugs that inhibit the 5-HT uptake pump reduce the accumulation of intracellular 5-HT and prolong extracellular action. Bottom, Tyramine (TYR) is taken into the norepinephrine (NE) neuron via the NE uptake pump. Inside the neuron, TYR displaces NE from storage vesicles. Norepinephrine is released from the cell and acts at the receptor sites of effector cells to elevate blood pressure. Drugs that inhibit the NE uptake pump prevent accumulation of TYR, subsequent displacement of NE, and blunt the pressor response.
  • JAMA Psychiatry May 1, 1999

    Figure 1: Transient Depressive Relapse Induced by Catecholamine Depletion: Potential Phenotypic Vulnerability Marker?

    The synthesis of catecholamines is depicted schematically, with the shaded area denoting norepinephrine (NE) neurons and the unshaded area denoting dopamine (DA) neurons. The synthetic pathway shared by both neurons is shown overlapping both areas. The amino acid tyrosine is actively transported into the cytoplasm and is converted to dihydroxyphenylalanine (DOPA) via enzymatic reaction with tyrosine hydroxylase (TH). This rate-limiting step in catecholamine synthesis may be blocked by α-methylparatyrosine, a TH inhibitor. The α-methylparatyrosine presumably diminishes production of DOPA and ultimately may result in diminished synaptic release of catecholamine neurotransmitters in human subjects. The DOPA is converted to DA via L-aromatic amino acid decarboxylase. In noradrenergic neurons, DA subsequently is stored in granules and is converted by DA-α-hydroxylase to NE. This storage process in catecholamine neurons is disrupted by reserpine. Synaptic enzymes metabolize NE and DA to 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) or homovanillic acid (HVA), respectively.
  • JAMA Psychiatry December 1, 1998

    Figure 1: Family History of Alcoholism and Hypothalamic Opioidergic Activity

    Administration of naloxone hydrochloride stimulates plasma cortisol by blocking opioidergic input on the corticotropin-releasing factor (CRF) neuron, thereby providing a noninvasive method for measuring hypothalamic opioid tone. GABA indicates γ-aminobutyric acid; NE, norepinephrine.
  • Sympathetic Activity in Patients With Panic Disorder at Rest, Under Laboratory Mental Stress, and During Panic Attacks

    Abstract Full Text
    free access
    Arch Gen Psychiatry. 1998; 55(6):511-520. doi: 10.1001/archpsyc.55.6.511