England-2011-johanna/finalpaper

From Earlham Cluster Department

(Difference between revisions)
Jump to: navigation, search
m (Chemicals in the Brain)
m (Chemicals in the Brain)
Line 37: Line 37:
A popular hypothesis amongst drug manufacturers is that depressive disorders are caused by imbalances in serotonin or nor-epinephrine in the brain<ref name = adsinsci> Lacasse, Jeffrey R. and Jonathon Leo. "Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature." (2005)Public Library of Science. Web. 04/25/2011. <http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.0020392>.</ref>.  These are neurotransmitters, chemicals that are produced by neuron cells(9).  Neurons are form networks in the brain and nervous system via connections called synapses(22), which are specialized gaps between cells that permit the transference of information between neurons by electrical and chemical signaling (9).  What this means is that chemicals like serotonin and nor-epinephrine cross the synapse -- the gap between cells -- when the neuron cell is stimulated, and a receptor cell on the other side receives the chemicals, where they produce a biological effect (9).  The image below is a simplified diagram that shows neurotransmitters crossing the synapse to a receptor cell on the other side.   
A popular hypothesis amongst drug manufacturers is that depressive disorders are caused by imbalances in serotonin or nor-epinephrine in the brain<ref name = adsinsci> Lacasse, Jeffrey R. and Jonathon Leo. "Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature." (2005)Public Library of Science. Web. 04/25/2011. <http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.0020392>.</ref>.  These are neurotransmitters, chemicals that are produced by neuron cells(9).  Neurons are form networks in the brain and nervous system via connections called synapses(22), which are specialized gaps between cells that permit the transference of information between neurons by electrical and chemical signaling (9).  What this means is that chemicals like serotonin and nor-epinephrine cross the synapse -- the gap between cells -- when the neuron cell is stimulated, and a receptor cell on the other side receives the chemicals, where they produce a biological effect (9).  The image below is a simplified diagram that shows neurotransmitters crossing the synapse to a receptor cell on the other side.   
-
[[File:neurotransmitters.gif]]
+
[[File:neurotransmitters.gif]] <ref>"Neurotransmitter Restoration Therapy." MindBody Medicine Center. 2010.Web. <http://www.healmindbody.com/Services/Body-And-Mind/Neurotransmitter-Restoration.aspx>.</ref>
Also shown in the diagram is the phenomenon of reuptake.  When a neurotransmitter is released across the synapse, some of the molecules will be taken back in by the firing neuron rather than the receptor cell.  The serotonin hypothesis states that depression is caused by a lack of serotonin in the brain, so reuptake will be discussed again in the portion of this paper that covers antidepressant medications.
Also shown in the diagram is the phenomenon of reuptake.  When a neurotransmitter is released across the synapse, some of the molecules will be taken back in by the firing neuron rather than the receptor cell.  The serotonin hypothesis states that depression is caused by a lack of serotonin in the brain, so reuptake will be discussed again in the portion of this paper that covers antidepressant medications.

Revision as of 18:14, 25 April 2011

Click here to return to main journal page.


Contents

S,T & S Final Research Paper: Depression

The aim of this paper is to synthesize and summarize the current information and discourse about depression through the lenses of science, technology, and society. Though the paper has been structured in such a way as might suggest that these three categories could stand on their own, what should become evident is that, while it is possible to address them separately, there are beneficial insights to be gained by addressing them jointly. Science (what we know about depression), technology (the tools we use to work against the problems it causes), and the society (for our purposes, the cultural and economic forces that surround, interact with, act upon, and respond to science and technology), all influence each other. As depression becomes more and more widely diagnosed, especially in higher-income nations, what scientists understand about it and how we go about treating it is becoming more and more important.

Science: What is Depression?

What is colloquially referred to as depression is actually classified by the Diagnostic and Statistical Manual of Mental Disorders IV as several different mood disorders. A mood disorder is a mental disorder in which the root cause of symptoms is extreme, or extremely limited, mood outside the range considered healthy and normal [1]. The two main forms of mood dysfunction are mania, an abnormally elevated or irritable mood [2] and depression, an abnormally or abnormally extended low mood [3]. Some mood disorders are the result of just one or the other of these conditions, while others result from a combination of the two. Bipolar disorder (previously know as manic depression)is one of the later. Disorders that result from depressive mood include major and minor depressive disorders, dysthymia, and seasonal affective disorder.

The Disorders

Because of the wide variety of causes and symptoms underlying various depressive disorders, their classifications can be difficult to pin down. It is important to keep in mind that these are the most common presentations and that there are other disorders that may be considered to fall into the category of depression. A patient may have a disorder that does not neatly fall into one of the categories below.

Major and Minor Depressive Disorders

Major depression, also referred to as clinical depression, is a case of chronic, long-term depression that can heavily interfere with a person's ability to function in day-to-day life [4]. Minor depression is sometimes used to describe a less severe case of depression.

Dysthymia and Atypical Depression

Dysthymia is a milder depressive episode that usually last for two years. While the symptoms of dysthymia are less severe than the symptoms of major depressive disorder, dysthymia can be just as, if not more, disruptive and harmful to a person's life because of its chronic nature. People displaying symptoms of dysthymia may seem to complain constantly, be overcritical, and have difficulty having fun or enjoying themselves. [5]

Atypical depression in also a chronic condition, with symptoms that are usually milder than those of major depressive disorder but much more prolonged. Atypical depression often begins during teen years and continues into a person's adult life [6].

Seasonal Affective Disorder

Those Seasonal Affective Disorder, SAD, experience symptoms of depression only during certain times of the year. Usually, depressive episodes begin in the fall and end as spring begins, however there have been cases of SAD in which the symptoms of depression present in the spring and summer months. In addition to the treatments applied to other forms of depression, SAD is also treated with light therapy, to be discussed in the technology section of this paper.

Symptoms

It is important to realize that the reason depression is classified as a mood disorder is because mood itself is the underlying cause of the symptoms displayed. Depression can be a symptom of other mental or non-mental diseases, such as mononucleosis or the early onset of Alzheimer's [3], and this can lead to complications in diagnosis. However, it is important to recognize depression as a real and serious mental illness that can deeply impact a person's ability to cope with day-to-day living.

The most typical symptoms of depression include loss of interest in formerly enjoyable activities, apathy, inexplicable sadness, low energy, loss of appetite (or, conversely, weight gain), interrupted sleep, guilty feelings, low self-esteem, and poor concentration [7]. Atypical depression often causes a sense of heaviness in the limbs and oversleeping. People with severe cases of major depressive disorder can have difficulty finding the motivation to get out of bed for days at a time, and the most serious cases of depression can lead to suicidal thoughts and suicide.

Depression can have other, perhaps more subtle, effects on interpersonal and social skills. As previously mentioned, people with dysthymia tend to be overcritical of peers and co-workers and have difficulty having fun, which heavily impacts their ability to socialize with others and can damage existing relationships. Those suffering from atypical depression often fear rejections by others and have trouble forming or maintaining relationships as a result [6].

Causes

The illnesses referred to as depressive disorders are known as such because the cause of their symptoms is depression. Because of the complex nature of mental illness, it is often hard or even impossible to name a single and specific cause of that illness within a patient, and depressive disorders are no exception. Genetic, life event, and chemical factors can all play a part, and may all be contributors to illness in a single person. The risk factors for depression include a family history of depression, grief due to a death or major loss, personal conflicts, major life events -- even positive ones, serious or long term pain or illness, certain medications and substance abuse (21).

Chemicals in the Brain

A popular hypothesis amongst drug manufacturers is that depressive disorders are caused by imbalances in serotonin or nor-epinephrine in the brain[8]. These are neurotransmitters, chemicals that are produced by neuron cells(9). Neurons are form networks in the brain and nervous system via connections called synapses(22), which are specialized gaps between cells that permit the transference of information between neurons by electrical and chemical signaling (9). What this means is that chemicals like serotonin and nor-epinephrine cross the synapse -- the gap between cells -- when the neuron cell is stimulated, and a receptor cell on the other side receives the chemicals, where they produce a biological effect (9). The image below is a simplified diagram that shows neurotransmitters crossing the synapse to a receptor cell on the other side.

Neurotransmitters.gif [9]

Also shown in the diagram is the phenomenon of reuptake. When a neurotransmitter is released across the synapse, some of the molecules will be taken back in by the firing neuron rather than the receptor cell. The serotonin hypothesis states that depression is caused by a lack of serotonin in the brain, so reuptake will be discussed again in the portion of this paper that covers antidepressant medications.

Although the neurotransmitter imbalance hypothesis is widely known to the American public because of advertisements for antidepressant drugs, it has recently been called into question. Scientists and researchers are pointing out that it has never actually been confirmed, and more and more evidence is beginning to say that the hypothesis is not valid[8]. Scientists have not actually been able to identify a specific level of serotonin or nor-epinephrine that is "correct" for most people, and tests that deprive the brain of serotonin or introduce more into it have been largely inconclusive[8].

Genetics and Heredity

Scientific studies have determined that symptoms of depression are heritable, meaning that a person is more likely to display symptoms of depression if their family members do (37). If depressive disorders can be inherited, then genetics must play a part in the likelihood that a person will experience a depressive episode. Many different research approaches have been taken to try to account for the genetic influence on mood disorders. Recently, a research article was published that identifies 169 genes that have a high correlation with depression (38). Modern technology has allowed scientists to identify the genetic code in thousands of DNA samples. By the comparing of such samples with the characteristics of the people they come from, researchers were able to identify from a list of thousands those genes that were most likely to be related to depression. They found that most of these genes are expressed in human brain and nerve tissue, a fact that supports the hypothesis that neurotransmitters play a role in the cause of depression. However, the large number of genes that could possibly be influencing a person's tendency towards developing a depressive disorder suggests that the issues is far more complex than simply the amount of serotonin or dopamine in the brain (38).

This is a prime example of the way technology is able to inform science. Rather than using technology to look at genes already suspected to contribute to depression, this research involves using technology to collect new data that can be transformed into new scientific information.

Other Causes to Consider

While genetics and brain chemistry are certainly factors which can cause depression, it is important to note that social and cultural conditions can also play an important role. Below is a map showing the prevalence of variants of the serotonin transport gene (SERT) that are associated with depression. The scale on the left denotes the percentage of the population who posses these variants represented by the colors on the map.

ChiaoGlobalMapSalleles1.jpg(20)

Now, see the distribution of people who have been diagnosed with a mood disorder. The scale on the left denotes how the colors on the map represent the percentage of people in each country who have been diagnosed.

ChiaoMapMoodDisorders1.jpg(20)

While the potential for a mood disorder can be seen in the genetic code, how that code presents phenotypically seems to be influenced by other factors. The above images come from a paper by Chiao and Blizinsky, a Northwestern University psychologist and her graduate student, published by the Royal Society in 2009. They concluded that while misdiagnoses might account for some of the discrepancy that can be seen in these two maps, it cannot account for all, and that cultural factors are clearly at play in this comparison.

Technology: What tools do we have to fight depression?

Science has determined the existence of depressive mood disorders, has cataloged their causes and symptoms, and continues to develop a body of knowledge surrounding the physical, emotional, chemical, and genetic aspects of depression. Scientists and medical practitioners have developed technologies to deal with depression on a practical level. Diagnostic and treatment methods have been developed that can significantly improve the quality of life of a depressed patient and even save patients' lives, and all but the most severe cases of depressive disorders can be fully recovered from when given appropraite attention.

It is important to keep the distinction between science and technology in mind during the discussion of treatment for depressive disorders. It will become clear as a description of treatment methods unfolds that, while the technology of treatment uses the knowledge that science provides for it, it also effectively uses tools and methods for which science cannot provide a solid explanation. The benefits of exchange between science and technology, as well as the misunderstandings it might produce, are made clear in the example of depressive disorders and their treatment.

Diagnostic Tools

A standard process for the diagnosis of mood disorders, including depressive disorders, is laid out in the Diagnostic and Statistical Manual of Mental Disorders IV. It has been refined through previous editions and that process will continue as new editions are produced [1]. There are also a variety of tests and questionnaires that have been developed that try to determine the severity or type of depression that a patient is experiencing. Since depression is not only a mental disorder, but can also be the symptom of other illnesses, the first steps of the diagnostic process involve ruling out other causes of depressive symptoms(12). The complexity and variety of causes and symptoms of depressive disorders mean that the process of diagnosis must often be coupled with careful experimentation in the area of treatment. This means that after a diagnosis is given, it is still important that a patient continues to have a dialog with his or her healthcare professional in order to adjust treatment appropriately.

Treatment

The two most effective and well-tolerated tools with which we can treat depressive disorders are psychotherapy and medication (8). According to the World Health Organization, a combination of anti-depressants and "brief, structured forms of psychotherapy" is successful in 60-80% of cases (9). As previously mentioned, light therapy is helpful for those afflicted with SAD. In severe cases of depression for which faster improvement is deemed necessary for the health and safety of a patient, electroshock therapy is sometimes employed.

Psychotherapy

Talk therapy or counseling can be a highly useful tool in the treatment of depression, and most doctors recommend that it should accompany any other treatments a patient might undergo. There are a variety of strategies that a therapist might employ, most involving encouraging a patient to examine patterns of thought and behavior, and providing them with techniques to reframe or alter these patterns. The National Institute for Clinical Excellence has advised that non-pharmacological treatment methods are the best approach in treating cases of mild depression (8). A study released in the Archives of General Psychiatry has found that for moderate to severe depression, 16 weeks of cognitive therapy was equally effective across a test group as 16 weeks of treatment via medication, although the experience and expertise of individual therapists is admitted to be an important factor in the efficacy of such therapy (31). The rate of relapse was slightly lower for patients undegoing therapy than for patients undergoing pharmaceutical treatment -- 40% versus 46% respectively (31).

Antidepressant Medication

The most well-known and commonly prescribed antidepressant medications currently available are SSRIs -- selective serotonin re-uptake inhibitors. As mentioned previously, some scientists have hypothesized that imbalances of the neurotransmitter serotonin contributes to depression. SSRIs do exactly what their name says; they prevent the reuptake of serotonin by neurons that release it, increasing the amount of serotonin being transmitted in the brain (8). Some well known SSRIs include fluoxetine (Prozac), sertraline (Zoloft), escitalopran (Lexapro), and citalopram (Celexa), and there are a few others. These medications are FDA approved to treat a variety of disorders from depressive disorders to obsessive-compulsive disorder, social anxiety disorder, and premenstral dysphoric disorder (8).

Although their name seems to imply that the inhibition of serotonin reuptake is what eases depression in the patients taking these medications, the scientific community is actually uncertain as to whether or not this is the case. It takes only hours for SSRI medications to affect an increase in serotonin levels in the brain, but a patient must take a medication for several weeks before they begin to feel an ease to their depression (12). The serotonin hypothesis is thrown into further doubt by the fact the SSRIs seem to be equally effective in the treatment of such a wide variety of disorders (8). As previously mentioned, researchers have never actually been able fully confirm the link between serotonin levels in the brain and depressive disorders.

Journal.pmed.0020392.g001.png (8)

Antidepressant medications are helpful for some patients and not for others, and a patient may need to try more than one medication before they find a successful treatment (8). Because the exact mechanism by which SSRIs treat depressive disorders is uncertain, and there is no way to measure serotonin levels in a living brain anyway, it is difficult for doctors to predict which medications will be most useful to individual patients. In addition to this, there are a whole host of side-effects that may come along with the benefits of an SSRI, including decreased libido, drowsiness, restlessness, insomnia, nausea, and weight loss or gain (12). In some cases, SSRIs can actually increase symptoms of anxiety or depression and introduce new ones, and in the most severe instances can bring abut suicidal thoughts. These problems are more likely to be seen in teenagers and children, and in patients over the age of 65 (12).

Pharmaceutical companies have recently begun producing new drugs refferred to collectively as atypical antidepressants. They function much in the same way that SSRIs do, except that they work with other neurotransmitters -- usually dopamine or nor-epinephrine -- instead of or in addition to serotonin (12). Some familiar medications in this class may include bupropion (Wellbutrin) and duloxtine (Cymbalta), and their side-effects are much the same as those of the SSRIs (12).

The medications known as tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs) are older technologies that are still prescribed to some patients, although usually only after other treatments have failed. This is because their side-effects can be far more severe than those of the SSRIs and atypical antidepressants (12). They also work to manage the levels of serotonin and nor-epinephrine in the brain (33).

Light Therapy

Light therapy is used to treat several skin, sleeping, and psychological disorders. The United States Food and Drug Administration has not approved light therapy as a treatment method for Seasonal Affective Disorder, but it is still commonly used as such. Clinical trials in this area have not produced clear results, and full sunlight is preferable as a method of treatment, but exposure to light from lamps that emit specific wavelengths of light may be helpful in its absence. Experimentation to determine the most effective wavelengths for the purposes of treating SAD is ongoing (32).

Electroconvulsive Therapy

Electroconvulsive Therapy, ECT, is sometimes prescribed for patients with severe depressive disorders for whom medication and psychotherapy are not productive means of treatment, and is called by Mayo Clinic, "a safe and effective treatment for severe and prolonged depression"(34). A patient receiving ECT is put under anesthesia and subject to a carefully measured electrical shock to the brain that induces seizure. Usually six to ten treatments are employed (34).

A review of several studies was released in 2003 that concluded that actual ECT was, in fact, significantly more effective than simulated ECT in clinical trials, and that it may even be more effective than medication (35). High-dose ECT is far more effective than low-dose ECT (35). It should be kept in mind, however, that this review was only able to make confident conclusions about the effectiveness of ECT in the short-term.

The side effects of ECT are heavily dependent on the amount of electricity introduced to the brain and its location. The most common problem is memory loss and confusion for a few hours following a treatment session, but depending on the treatment, amnesia can be permanent (36).

Society

Although the World Health Organization cites depression as a leading cause of disability worldwide, and the leading cause of disability in those ages 15-44. However, less than 25% of those afflicted have access to treatment, and in some countries the figure is as low as 10%. The WHO attributes this phenomenon to a lack of resources and trained providers, and the social stigma surrounding depression [7].

Even in Westernized countries, where mental healthcare is widely available, many do not receive the appropriate attention. Advertising by drug manufacturers in magazines and on television usually implies that the previously discussed serotonin hypothesis has been confirmed by the scientific community and is commonly held as fact (8). This sort of advertising leads many people to self-diagnose not only a depressive disorder, but also feel they are certain as to its cause (8). There are no large, successful companies advertising the benefits of exercise, healthy diet, balanced lifestyle, or even comparably prominent advertising for the various methods of psychotherapy available, because there is less money to be made in these areas. Perhaps the distinction between a technology and a science is lost on some.

It is also important to consider that depression, for all the science that tries to explain it and the technology that tries to heal it, may be partly a condition of the society in which a person lives. The two maps displayed above, that compare the prevalence of SERT gene variants with the prevalence of mood disorder diagnoses, should be compared with a third map , below. This map shows the ranking of certain countries on a spectrum of individualism to collectivism as proposed by sociologist Geert Hofstede (30).

ChiaoMapIndividualsmVcollectivitism2.jpg (20)

What Chiao and Blizinksy ultimately were able to confirm their hypothesis that prevalence of the SERT gene variants associated with depression is a predictor of individualism vs. collectivism across 29 countries (30). Their findings further the cause of "culture-gene coevolutionary theory," the idea that cultures are produced and changed partly in response to the genetic construction and needs of its populace (30).

This example demonstrates most acutely the way in which science, technology, and society must be in constant communication in order to discover the ways that all three influence and can improve the human condition. Since it is a leading disability around the world, it is becoming more and more crucial that we understand depression. From understanding how it works, to treating the individual, to improving the mental health of a society, there is still much work to be done.

Works Cited

  1. 1.0 1.1 "Psychiatric Disorders." AllPsych Online: The Virtual Psychology Classroom.Web. <http://allpsych.com/disorders/mood/index.html>.
  2. "Mania." Wikipedia. April 20, 2011 2011.Web. <http://en.wikipedia.org/wiki/Mania>.
  3. 3.0 3.1 "Depression (mood)." Wikipedia. April 24, 2011 2011.Web. <http://en.wikipedia.org/wiki/Depression_(mood)>.
  4. "Depression (major depression)." Mayo Clinic. Febraury 11, 2010 2010.Web. <http://www.mayoclinic.com/health/depression/DS00175>.
  5. "Dysthymia." Mayo Clinic. August 26, 2010 2010.Web. <http://www.mayoclinic.com/health/dysthymia/DS01111>.
  6. 6.0 6.1 Mayo Clinic staff. "Atypical Depression." Mayo Clinic. May 20, 2010 2010.Web. <http://www.mayoclinic.com/health/atypical-depression/DS01181>.
  7. 7.0 7.1 "Mental Health: Depression." World Health Organization. 2011.Web. <http://www.who.int/mental_health/management/depression/definition/en/>.
  8. 8.0 8.1 8.2 Lacasse, Jeffrey R. and Jonathon Leo. "Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature." (2005)Public Library of Science. Web. 04/25/2011. <http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.0020392>.
  9. "Neurotransmitter Restoration Therapy." MindBody Medicine Center. 2010.Web. <http://www.healmindbody.com/Services/Body-And-Mind/Neurotransmitter-Restoration.aspx>.

(12) "Antidepressants." Helpguide.org.Web. <http://helpguide.org/mental/medications_depression.htm>.

(21) "Are you at risk for depression??" WebMD. March 01, 2010 2010.Web. <http://www.webmd.com/depression/guide/depression-are-you-at-risk>.

(30) Chiao, Joann Y. and Katherine D. Blizinsky. "Culture?gene Coevolution of individualism?collectivism and the Serotonin Transporter Gene." The Proceedings of The Royal Society (2009): April 25, 2011. Web. <http://www.subjectpool.com/ed_teach/y5_ID/jc/politics/Chiao_&_Blizinsky_2009_-_Culture-gebe_coevolution_of_5HTTLPR_and_collectivism.pdf>.

(9) Chuddler, Eric H. "Neurotransmitters and Neuroactive Peptides." Neuroscience for Kids.Web. <http://faculty.washington.edu/chudler/chnt1.html>.

(3) "Depression (mood)." Wikipedia. April 24, 2011 2011.Web. <http://en.wikipedia.org/wiki/Depression_(mood)>.

(33)(34) "Depression: Treatment." Mayo Clinic.Web. <http://www.mayoclinic.org/depression/treatment.html?mc_id=comlinkpilot&placement=bottom>.

(20) Dobbs, David. "The depression map: genes, culture, serotonin, and a side of pathogens." Wired.com. September 14, 2010 2010.Web. <http://www.wired.com/wiredscience/2010/09/the-depression-map-genes-culture-serotonin-and-a-side-of-pathogens/>.

(13)(36) "Electroconvulsive Therapy." Wikipedia. April 20, 2011 2011.Web. <http://en.wikipedia.org/wiki/Electroconvulsive_therapy#Duration_of_Effect>.

(8) Lacasse, Jeffrey R. and Jonathon Leo. "Serotonin and Depression: A Disconnect between the Advertisements and the Scientific Literature." (2005)Public Library of Science. Web. 04/25/2011. <http://www.plosmedicine.org/article/info%3Adoi%2F10.1371%2Fjournal.pmed.0020392>.

(2) "Mania." Wikipedia. April 20, 2011 2011.Web. <http://en.wikipedia.org/wiki/Mania>.

(6) Mayo Clinic staff. "Atypical Depression." Mayo Clinic. May 20, 2010 2010.Web. <http://www.mayoclinic.com/health/atypical-depression/DS01181>.

(4) "Depression (major depression)." Mayo Clinic. Febraury 11, 2010 2010.Web. <http://www.mayoclinic.com/health/depression/DS00175>.

(5) "Dysthymia." Mayo Clinic. August 26, 2010 2010.Web. <http://www.mayoclinic.com/health/dysthymia/DS01111>.

(7)(10) "Mental Health: Depression." World Health Organization. 2011.Web. <http://www.who.int/mental_health/management/depression/definition/en/>.

(11) "Neurotransmitter Restoration Therapy." MindBody Medicine Center. 2010.Web. <http://www.healmindbody.com/Services/Body-And-Mind/Neurotransmitter-Restoration.aspx>.

(1) "Psychiatric Disorders." AllPsych Online: The Virtual Psychology Classroom.Web. <http://allpsych.com/disorders/mood/index.html>.

(31)(32) Robert J. DeRubeis, PhD, et al. "Cognitive Therapy Vs Medications in the Treatment of Moderate to Severe Depression." Archives of General Psychiatry 62.4 (2005): April 25, 2011. Web.

(35) UK ECT Review Group. "Efficacy and Safety of Electroconvulsive Therapy in Depressive Disorders: A Systematic Review and Meta-Analysis.." The Lancet (2003): April 25, 2011. PubMed.gov. Web.

Personal tools
Namespaces
Variants
Actions
websites
wiki
this semester
Toolbox