A concise presentation on major depressive disorder, the drug treatment options available i.e. conventional and emerging therapies which are available.
Depressive Disorders: An Overview of Full Spectrum. Dr. Ashok Kumar Batham.DrAshok Batham
Medical specialists outside the area of psychiatry and those who practice family medicine generally get fragmented information about mental depression. Therefore, an endeavour has been made to provide a complete overview of various depressive disorders, such as, Major Depressive Disorder (MDD), Persistent Depressive Disorder (PDD) or Dysthymia, Disruptive Mood Dysregulation Disorder (DMDD), Premenstrual Dysphoric Disorder (PMDD), Substance/Medication Induced Depressive Disorder, Depressive Disorder Due to Another Medical Condition, and other depressive disorders. DSM-5 diagnostic criteria of each of these disorders are given along with vignettes of diagnosis and treatment of the same are presented. Hopefully, this slide share will help non-psychiatrists to understand the complete spectrum of depressive disorders.
Depressive Disorders: An Overview of Full Spectrum. Dr. Ashok Kumar Batham.DrAshok Batham
Medical specialists outside the area of psychiatry and those who practice family medicine generally get fragmented information about mental depression. Therefore, an endeavour has been made to provide a complete overview of various depressive disorders, such as, Major Depressive Disorder (MDD), Persistent Depressive Disorder (PDD) or Dysthymia, Disruptive Mood Dysregulation Disorder (DMDD), Premenstrual Dysphoric Disorder (PMDD), Substance/Medication Induced Depressive Disorder, Depressive Disorder Due to Another Medical Condition, and other depressive disorders. DSM-5 diagnostic criteria of each of these disorders are given along with vignettes of diagnosis and treatment of the same are presented. Hopefully, this slide share will help non-psychiatrists to understand the complete spectrum of depressive disorders.
TREATMENT RESISTANT DEPRESSION IS A AREA THAT IS NOT EXPLORED MUCH, BUT IT REALLY NEEDS LOT OF ATTENTION AS IT IS ONE OF THE MOST COMMON OBSTACLE IN ACHIEVING COMPLETE REMISSION IN DEPRESSION
As a Social Work student specialized in Medical and Psychiatry, I was assigned to study and present on Psychotropic Drugs in class. Hope it helps you!
This contains introduction to psychotropic drugs, definitions, a brief history of psychiatric treatment, classification, characteristics of an ideal psychotropic drug as well as the references to my sources.
TREATMENT RESISTANT DEPRESSION IS A AREA THAT IS NOT EXPLORED MUCH, BUT IT REALLY NEEDS LOT OF ATTENTION AS IT IS ONE OF THE MOST COMMON OBSTACLE IN ACHIEVING COMPLETE REMISSION IN DEPRESSION
As a Social Work student specialized in Medical and Psychiatry, I was assigned to study and present on Psychotropic Drugs in class. Hope it helps you!
This contains introduction to psychotropic drugs, definitions, a brief history of psychiatric treatment, classification, characteristics of an ideal psychotropic drug as well as the references to my sources.
An overview of atypical anti depressantsBrajesh Lahri
This powerpoint presentation deals with the pharmacology and psychiatric uses of atypical anti-depressants. TCAs and SSRIs are considered as typical anti-depressants, while other classes include SNRI, RIMAs and atypical antidepressants. In this presentation, i have briefly given an overview of atypical anti-depressants as well as of SNRIs and RIMAs.
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All about antidepressants
Types
Side effects
Uses
Efficacy
Choosing
In pregnancy and nursing
Alternatives
How they work
Taking effect
Treatment duration
Summary
Antidepressants can help relieve the symptoms of depression. They can also help to treat social anxiety disorder, other anxiety disorders, and seasonal affective disorder.
They work by correcting chemical imbalances of neurotransmitters in the brain. Experts believe these are responsible for changes in mood and behavior.
This article will cover the different types of antidepressants, how they work, their side effects, other uses, and alternative options.
Types
blackCAT/Getty Images
Doctors tend to divide antidepressants into different types. These include:
Selective serotonin reuptake inhibitors (SSRIs)
SSRIs are a first-line treatment option for depression.
Examples of SSRIs include:
citalopram (Celexa)
escitalopram (Lexapro)
fluoxetine (Prozac, Sarafem)
fluvoxamine (Luvox)
paroxetine (Paxil)
sertraline (Zoloft)
Serotonin and norepinephrine reuptake inhibitors (SNRIs)
SNRIs are a newer class of antidepressant compared with SSRIs. However, they work in a similar way.
Doctors may prescribe SNRIs for:
attention deficit hyperactivity disorder (ADHD)
obsessive-compulsive disorder (OCD)
anxiety disorders
menopausal symptoms
fibromyalgia
chronic neuropathic pain
Examples of SNRIs include:
duloxetine (Cymbalta)
venlafaxine (Effexor XR)
desvenlafaxine (Pristiq)
Tricyclic antidepressants (TCAs)
Doctors may recommend TCAs for depression, fibromyalgia, some types of anxi
Major depressive disorder(MDD) is a disorder of mood in which the individual experiences one or more major depressive episodes without a history of manic, mixed, or hypomanic episodes.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
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Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
- ARTIFICIAL INTELLIGENCE AND ETHICS
- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
3. WHAT IS MAJOR DEPRESSION ?
Major Depression is a mental disorder, characterized by
• sadness
• loss of interest or pleasure
• feelings of guilt or low self-worth
• disturbed sleep or appetite
• feelings of tiredness
• poor concentration.
7. DISADVANTAGES OF CURRENTLY AVAILABLE
ANTIDEPRESSANTS (despite their efficacy):
Several weeks taken to exert full efficacy
Inadequate response of patients
Poor tolerance problems
Co-morbid symptoms not well controlled.
8. MAJOR SIDE EFFECT OF ANTIDEPRESSANTS?
OR
OUTCOME OF UNTREATED MAJOR DEPRESSIVE
DISORDER?
10. The Serotonergic system
In these people,there are fewer presynaptic serotonin
transporter sites in the prefrontal cortex ,hypothalamus,
occipital cortex and brainstem.
Impaired serotonin input in suicide affects ventromedial
prefrontal cortex
12. 5HT 1A & 5HT
2A receptors
Upregulated
(compensatory)
Low serotonin
Levels*
VENTROMEDIAL PREFRONTAL CORTEX
*determination of serotonin and its major metabolite 5-hydroxy indole acetic acid
In the case of 5-
HT2A receptors,
this
upregulation
involves increased
gene expression.
13. No deficiency in the number of serotonin neurons, and TPH
immunoreactivity is higher in the dorsal raphe nucleus of
suicide victims with a history of major depression. The
increase in TPH immunoreactivity might be a homeostatic
feedback effect of low intrasynaptic concentrations of
serotonin.
Photomicrographs of brainstem sections stained with an antibody against tryptophan
hydroxylase at the rostral level of the dorsal raphe nucleus from a control subject
and a suicide victim. Note the higher immunoreactivity in the suicide victim.
(Images courtesy of V. Arango and M. Underwood.)
14. Low serotonin levels in
Dorsal raphe nucleus
Hence,TPH activity is
increased
(compensatory)
No deficiency in number of serotonin neurons is however noticed !
15. • Lower number of NA neurons (MDD)
– Effect of stress
• Stress induces greater release of NA
• Depletion of NA follows soon
• TH activity increases(compensatory)
• Number of alpha2 receptors increases(compensatory)
NORADRENERGIC SYSTEM
So, more TH and α2-adrenergic binding could indicate
noradrenergic depletion.
16.
17. DOPAMINERGIC SYSTEM
*D4 receptor binding not affected
*Serotonin antagonizes the effect of dopamine
*SSRIs on chronic use raise serotonin levels but indirectly reduce
dopamine activity
18. *Low HVA(homovanillic acid) seen in CSF in suicide attempters
with MDD
*HVA is a major metabolite of dopamine
*The dopamine system seems to be hypofunctional in major
depression
19. Other correlation factors
*Signal transduction and gene expression abnormalities
*In MDD,reduced PKc activity : low CREB
*Abnormalities in Mitogen activated protein(MAP) kinase
*Decreased number of cortical neurons
*Environment and stress
*Child abuse,improper upbringing of child
20. Concluding thoughts
*Antidepressants (working through serotonin pathway) :
initially raise serotonin levels and activity
*On chronic use : down-regulation of post synaptic receptors :
suicidal tendencies
MDD TREATMENT CHRONIC SUICIDE
MDD UNTREATED -----------------SUICIDE
Solution?
Look for alternative pathways.
REFERENCE: Nature reviews/neuroscience Vol 4 Oct 2003
22. SAFETY & EFFICACY OF REPEATED-DOSE INTRAVENOUS KETAMINE
FOR TREATMENT OF RESISTANT DEPRESSION
•Dose : 40 minutes IV infusion of Ketamine (0.5mg/kg) & 4 hrs
monitoring period.
• Repeated dose of IV ketamine is feasible for acute treatment
of resistant depression.
•Studies clearly demonstrated that IV ketamine is safe & has a
rapid & profound short term effect on depressive symptoms,
including suicidality, even among patients considered treatment
resistant to standard medication or ECT.
REFERENCE: www.sobp.org (Journal:BIOLPSYCHIATRY,2010)
23. SERTRALINE TREATMENT OF MAJOR DEPRESSION IN
PATIENT’S WITH ACUTE MI OR UNSTABLE ANGINA
•Dose : 50 to 200 mg/d ay or placebo.
•MDD occurs in 15-23% of patients with acute coronary syndromes.
•Intervention with sertraline has the potential to provide depressed patients
with cardiac disease relief from their depressive symptoms , improvement in
quality of life & a potential benefit in their cardiovascular risk profile.
REFERENCE: www.jama.com August 2002 Vol.288
24. COMPARATIVE EFFICACY OF ESCITALOPRAM IN TREATMENT OF
MAJOR DEPRESSIVE DISORDER
• Meta analysis studies using escitalopram showed superior effficacy
compared with citalopram and with SSRIS combined.
• Escitalopram shows similar efficacy to SNRIS but the number of trials
for these comparisons are limited; but these trials have shown clinically
relevant efficacy differences especially in more severely depressed
patients.
• Escitalopram shows increased efficacy because of dual mechanism
where it acts both on the primary and allosteric binding sites of serotonin
transporter.
• Apart from efficacy of the drug the side effect profile,drug
interactions,simplicity of use and cost effectiveness must be considered.
• while making clinical decision for a first choice antidepressant .
REFERENCE: www.dovepress.com (Neuropsychiatric disease and
treatment 2011)
26. • Use of me-too drugs: example-Desvenlafaxine (Pristiq)
which is Venlafaxine’s (Effexor) main metabolite.
Advantage: The side effect and efficacy profile for such drugs
show slight differences which can be helpful to patients.
• Augmentation of antidepressants: Addition of an atypical
antipsychotic to an antidepressant can boost its
effectiveness.
• Glutamate system and depression: example-NMDA receptor
antagonists like Ketamine and Riluzole which are under
study for treatment of resistant depression
• Triple Reuptake Inhibitors
• Melatonin
28. TRIPLE REUPTAKE INHIBITORS:A PREMISE
AND PROMISE
• This is a new class of psychoactive medications which inhibit neuronal
reuptake of 5-HT,NE and Dopamine
• These TRI’S may also have efficacy in obesity, addiction and pain
syndromes
• TRI’s exert their activity by treating more symptoms of MD and/or
attenuate some side effects observed for the traditional antidepressants
Example: Dopamine component of TRI may prevent sexual dysfunction
induced by increase in brain 5-HT
29. SOME TRIPLE REUPTAKE INHIBITORS (TRI’S):
• BICIFADINE (approved TRI)
TRI’S which are in Phase II clinical trials:
• NS2330
• SEP225289
• DOV216303
• DOV21947
• 21947
30. PRE-CLINICAL IN VITRO PROPERTIES OF TRI’S
The analysis of the binding properties indicate that the more important
property of TRI’S is their relative balanced binding profile rather than their
potency at blocking monoamine transporters.
31. CLINICAL PROPERTIES OF TRI’S
• Drugs that block dopamine transporter have a potential reinforcing property
and abuse liability.
• But it is found that to induce such reinforcing effects the dopamine
transporter blocking drugs must induce more than 50% blockade
• Dopamine reuptake inhibitors are of two types:
• Type I : produce addiction, euphoria
• Type II : do not produce above effects
• This should be considered carefully with agents like TRI’s.
REFERENCE: www.intechopen.com (A new class of antidepressants in the
treatment of psychiatric disorders:The Triple Reuptake Inhibitors)
Journal:Psychiatric disorders: Trends and development.
32. A DRUG WHICH ACTS THROUGH NON-MONOAMINERGIC
SYSTEM: AGOMELATINE
In depression, sleep is greatly disturbed.
Melatonin produced by the pineal gland is an important
regulator of circadian rhythms/sleep cycle
Chemically melatonin is N-acetyl-5-methoxytryptamine.
Agomelatine(naphthalene derivative of melatonin) acts on
both the melatonergic(MT1 and MT2)and 5HT2C receptors
co-localized in the SCN of the brain.
36. ST. JOHN’S WORT FOR TREATMENT OF MAJOR
DEPRESSION
• St. John’s Wort or Hypericum perforatum is a plant which
grows in the wild and is widely prescribed for depression in
Europe
• Mechanism of action : Partially understood but is similar to
that of SSRI’s
• Clinical trials carried out have found it as effective as a
commonly prescribed antidepressant
• But the FDA has not approved it as a OTC prescription drug
• This herb shows many side effects and drug interactions:
• Combining antidepressants and SSRI’s leads to
serotonin syndrome
• Psychosis is also possible
• It can induce metabolism of drugs like:
• Cyclosporine, Digoxin, Warfarin, Birth control pills
,Indinavir etc.
37. AUGMENTATION THERAPY
In case of inadequate response to conventional antidepressant
therapy augmentation therapy is followed which includes combining of
an augmenting agents along with the conventional antidepressant
Augmentation therapy, can avoid patients from unnecessary switching
between antidepressants which may jeopardize the remission rates
and even aggravate existing side effects
Augmentation:
the action or
process of making
or becoming
greater in size or
amount
39. The possible augmenting agents:
A. Lithium Augmentation
B. Triiodothyronine (T3) Augmentation
C. Benzodiazepine Augmentation
D. S-Adenosyl-L-Methionine (SAMe) Augmentation
E. Atypical Antipsychotic Augmentation Treatments
40. A.Lithium Augmentation
Lithium augmentation, synergistically increase serotonergic action
of antidepressants on brain 5-HT pathways
There is positive association between lithium levels and
presynaptic formation, storage, and release of serotonin
It can be combined with TCA & MAOI without any adverse effects
It can also be combined with SSRI as well but it may potentiate
serotonin syndrome
Combination of lithium and fluoxetine resulted in mania and
hypomania
41. Optimum level of lithium in blood = 0.6 - 1.2 mEq/L
Dose = 900 – 2400 mg/day (2 – 4 divided doses)
Lithium carbonate is given in form of lithium carbonate (Lithobid,
Eskalith tablets)
43. B. Triiodothyronine (T3) Augmentation
A viable, safe, inexpensive and effective augmentation treatment
T3 hold a slight advantage over lithium in efficacy and tolerability and
also is easier to use and there is no need for blood monitoring
T3 augmentation of patients with MAOIs and TCAs showed clinical
improvement with no significant adverse effects
T3 dose = 25-50 µg/day
Cytomel and thyrovin tablets are available in the market
44. C. Benzodiazepine Augmentation
Benzodiazepine augmentation is shown to be beneficial in
depression
It was found that compared to antidepressant treatment alone,
adjunctive benzodiazepines decrease drop outs from treatment
But potential benefits should be weighed against possible
complications related to benzodiazepine augmentation, such as
* the development of dependence
* decline in the drug’s effect over time
* accident proneness
Clonazepam 0.5 to 1 mg/day with fluoxetine
49. Major Depression is accompanied with an increased production of
pro-inflammatory cytokines like Interlukin-6 (IL-6), Interlukin-1 (IL-1),
Tissue Necrosis factor α.
Tissue Necrosis Factor (TNF) antagonist INFLIXIMAB is used in the
trial for treatment of Treatment resistant Depression
INFLIXIMAB: monoclonal antibody against tumor necrosis factor α
Three infusions of infliximab (5 mg/kg) or placebo at baseline and
week 2 and week 6 of a 12-week trial.
50.
51. C-reactive protein :
Protein found in blood whose level rise in response to
inflammation
It is used as marker of inflammation in this trial
A high-sensitivity CRP (hs-CRP) test measures low levels of CRP
using laser nephelometry. The test gives results in 25 minutes with
a sensitivity down to 0.04 mg/L
Normal concentration = 10 mg/L
Mild Inflammation = 10-40 mg/L
Acive Inflammation = 40-200 mg/L
52. Result
Response is considered if 50% reduction in HAM-D score at any
point of 12 week trial
% of patient Therapy
62 % Infliximab treated
33 % Placebo
TNF antagonist does not have generalized efficacy but may improve
symptom in patient with high baseline inflammatory biomarkers
53. 1. Oxidative stress: causes & consequence of disease
2. Neurotropic support and oxidative stress: converging effects in the normal &
diseased nervous system
3. CORRELATION BETWEEN MDD,SSRIs AND SUICIDE
Nature reviews/neuroscience Vol 4 Oct 2003
4. COMPARATIVE EFFICACY OF ESCITALOPRAM IN TREATMENT OF MAJOR
DEPRESSIVE DISORDER
www.dovepress.com (Neuropsychiatric disease and treatment 2011)
5. SAFETY & EFFICACY OF REPEATED-DOSE INTRAVENOUS KETAMINE FOR
TREATMENT OF RESISTANT DEPRESSION
www.sobp.org (Journal:BIOLPSYCHIATRY,2010)
6. SERTRALINE TREATMENT OF MAJOR DEPRESSION IN PATIENT’S WITH
ACUTE MI OR UNSTABLE ANGINA
www.jama.com August 2002 Vol.288
7. www.intechopen.com A new class of antidepressants in the treatment of
psychiatric disorders:The Triple Reuptake Inhibitors
Journal:Psychiatric disorders: Trends and development.
REFERENCES:
54. 8. www.nature.com/reviews/drugdisc (Agomelatine:The first melatonergic
antidepressant:discovery,characterization and development) August 2010,
Vol 9
9. www.nccam.nih.gov/health/stjohnswort fordepression
www.psychcentral.com/stjohnswortfordepression
10. Atypical Antipsychotics and Other Therapeutic Options for
Treatment of Resistant Major Depressive Disorder
Rubo J. Seo, Holly MacPherson and Allan H. Young *
www.mdpi.com/journal/pharmaceuticals
11. An Evidence-Based Approach to Augmentation and Combination
Strategies for
Treatment-Resistant Depression
Jeremy Barowsky, MD and Thomas L. Schwartz, MD
13. Role of S-adenosyl-L-methionine in the treatment of depression:a
review of the evidence
David Mischoulon and Maurizio Fava
The American journal of clinical nutrition
55. 14. The inflammatory & neurodegenerative (I&ND) hypothesis of depression:
leads for future researchand new drug developments in depression
Michael Maes & Raz Yirmyia & Jens Noraberg & Stefan Brene & Joe Hibbeln
& Giulia Perini & Marta Kubera & Petr Bob & Bernard Lerer & Mario Maj 2008
15. Cytokines and major depression
Olga J.G. Schiepers,
Marieke C. Wichers Michael Maes
Department of Psychiatry and Neuropsychology, Maastricht University, P.O.
BOX 616, 6200 MD Maastricht, The Netherlands
16. Inflammation and Its Discontents: The Role of Cytokines in the
Pathophysiology of Major Depression, Andrew H. Millera, Vladimir Maleticb,
Charles L. Raison
17. A Randomized Controlled Trial of the Tumor Necrosis Factor Antagonist
Infliximab for Treatment-Resistant DepressionThe Role of Baseline
Inflammatory Biomarkers
Charles L. Raison, MD; Robin E. Rutherford, MD; Bobbi J. Woolwine, MSW;
Chen Shuo, MS; Pamela Schettler, PhD; Daniel F. Drake, PhD; Ebrahim
Haroon, MD; Andrew H. Miller, MD
JAMA Psychiatry. 2013;70(1):31-41. doi:10.1001/2013.jamapsychiatry.4.
Editor's Notes
Lithium can be used in the form of lithiun carbonate