Major Depressive Disorder (MDD): A Case Study

As a result of its occurrence, severity, and likelihood to cause premature death throughout the world, major depressive disorder has received much attention in the recent past to an extent that it has been the subject of numerous studies and analyses. One of the recent studies to be conducted on the topic examines the link between depression severity and neurocognitive function in major depressive

During the book, Steven talks about his depression because of the traumatic experiences with his father. When Steven says, “At this point, my depression really kicked in” (pg. 45). This is because his hippocampus has shrunk. It has been researched, that people that have major depression, have a shrunken hippocampus. The longer Steven has been depressed, results in his hippocampus getting smaller and loses the ability to work correctly. In addition to the hippocampus, the amygdala has a role in depressive behavior as well. The amygdala forms part of the limbic system and is a set of neurons that are shown to play a major role in the processing of emotions. The amygdala is a part of the brain that has a direct correlation to depression and oversees evaluating the emotional significance of different kinds of stimuli. For example, the amygdala is overly active in people with depression when you show them sad stimuli, and is under-active when shown positive things like rewards. This part of the brain also organizes the emotional experience in expression. What this means is that it organizes endocrine response to stress and threats. The more depressed a person is, the more their amygdala must act. The DLPFC, stands for dorsolateral prefrontal cortex, and is the latest part of the brain to form in humans and other mammals. This part of the brain also has a lot to do with major depressive disorder because

A probable reason why CBT works with depressed patients is that depression interacts with both cognitive and motivational processes. This is well evidenced in experimental analogue research with healthy and depressed individuals. Individuals with depression show deficits on a range of cognitive tests (Brown, Scott, Bench, 1994) with the pattern of dysfunction having many of the characteristics associated with fronto-subcortical impairment. Reischies and Neu (2000) found that depressed individuals displayed mild cognitive impairments in comparison with matched controls, particularly in the areas of "adverbial" memory, psychomotor speed and verbal fluency. Further in these patients there appears to be considerable variation in the recovery of cognitive function with remission of the depressive episode.

Russo SJ, Nestler EJ. The brain reward circuitry in mood disorders. Nat Rev Neurosci. 2013;14(9):609-625.

Disruption of hippocampal function, including the capacity for neuroplasticity, could contribute to a range of aspects of major depression. In addition to the role in declarative memory, the hippocampus is the primary regulator of prefrontal cortical function; hippocampus and DLPFC function together to regulate explicit memory. Disruption of hippocampal function in major depression may therefore add to observed deficits in concentration. Hippocampal afferents are important regulators of both the nucleus accumbens and the ventral tegmental area (VTA). It has been suggested that an indirect excitatory projection from hippocampus to VTA is critical for coordinating the firing of VTA cells in response to novelty; impairment of this hippocampal

Lastly, according to the Archives of General Psychology (2003) , Cognitive Behavior therapy produces a different pattern of brain activity than SSRIs. The researchers scanned seventeen patients, who had not been treated for depression, before and after a session of Cognitive Behavioral Therapy. There was an improvement in the depression; the tomography disclosed that there was increased activity in the dorsal cingulate regions and hippocampus. These results were then compared to a set of participants with nearly the same intensities of depression before and after taking SSRIs. Scans showed changes in brain activity in the opposite direction, with increases in the prefrontal cortex and decreases in the hippocampus and dorsal cingulate regions.

Major depressive disorder is one of the most common mental disorders, with a 12-month prevalence of 6.7% of adults in the United States (NIMH). There is no definite etiology of depression, but several risk factors have been identified. Functional and structural changes in the brain have also been explored. The most common treatment for depression is the use of drugs that act on monoamine transmitters, including norepinephrine, dopamine, and serotonin. Decreases in these transmitters, especially serotonin, were hypothesized to play an important role in the cause of depression (Breedlove & Watson, 2013). The serotonin hypothesis led to the development of selective-serotonin reuptake inhibitors (SSRIs), which increase the amount of serotonin in the brain. Further research suggests that the serotonin hypothesis is not entirely accurate and the neurobiology of depression is much more complex. The “chemical imbalance” explanation of depression may not reflect the full range of causes and may be given greater credibility by patients and doctors than is supported by evidence based research.

Major depressive disorder affects nearly 15 million of American adults in a given year. (Kessler, Chiu, Demler & Walters, 2005). With the impact it has on the society as well as the well-being of the individual, it must be in the interest of the healthcare to be able to provide patients with the most effective treatment method. Extensive research has been conducted on the efficacy of antidepressant medication and cognitive therapy, the two main treatment methods used for depression today. The discussion has, however, been characterized by conflicting claims, resulting in a debate over what should be used rather than us having definite conclusion of how patients are best helped.

Abnormal metabolite levels across major WM pathways suggested abnormal transmission of information in patients with DD. Abnormal neurotransmission, in turn, would lead to abnormal integration and processing of information in gray matter. Metabolite levels were abnormal in several GM regions that support emotional and cognitive processes. In particular, patients had abnormal levels in (a) the insula, which supports subjective emotional experience, emotional processing51, empathy, and social decision making52; and (b) the caudate and putamen, which in addition to regulating planning53 and sequencing54 of fine motor tasks55,56, regulate working memory focus57, motivation, and reward perception58,59. Thus, our findings indicate possible neuroanatomic substrata for disrupted cognitive-emotional processing in patients with DD.

Research has determined that depression is identified by an individual's failure to concentrate, biases seem to be implying that this comes from a negative set of memories and experiences that make up a persons’ beliefs. This mind set results in a deeply thoughtful style described by a lack of logical thinking which leads to depressed emotions and behaviours. The neurobiology behind depression shows that changes in the brain system are commonly linked to this theoretical way of thinking. This similarity proves the cognitive process behind the theory of depression and it also shows the noticeable features of a depressed brain described by neurobiologists

Psychology, as most know, is the study of the mind and personal or group thoughts, feelings, and emotions in humans and animals. Scientists study, analyze, and investigate many areas of psychology, but the causes and effects of mood disorders and emotion irregularities are still unrecognized. Many studies were an attempt to find more information on mental illnesses. One of the most common illnesses in the United States is depression, also; it is the most often recognized mental illness in the world. What most clinicians don’t know, however, is what happens in the brains of patients before, during, and after depressive episodes.

Through my research, I’ve learned that in terms of depression, there are three major parts of the brain that play a significant role in the illness: the amygdala, the hypothalamus, and the hippocampus. The limbic system, as a whole, and other parts of the brain are also involved when dealing with depression. However, the amygdala, hypothalamus, and hippocampus are three parts that show up most commonly when researching the effects of depression on the brain. The amygdala – like the other effected parts of the brain – is part of the limbic system, which is a set of structures in the brain that controls actions and emotions that ensure survival. The amygdala is primarily associated with emotions like anger, fear, pleasure, sorrow, and sexual arousal. Activity in the amygdala is higher when sad or depressed. The hypothalamus acts to regulate things like body temperature, appetite, sleep, sex drive, stress reaction, aggressive behavior, reactions to pain, and it helps control the pituitary gland – which regulates hormone control. When dealing with depression, the hypothalamus is prone to hyperactivity. Finally, the hippocampus’ role in the brain is to make short term memories into long term memories. It also plays an important role in spatial navigation. In depressed people, the hippocampus is generally smaller than those not suffering from depression. Brain activity, as a whole, is generally lower in people suffering from the

Biological Theories. The monoamine neurotransmitters—norepinephrine, dopamine, serotonin, histamine—are the main focus of theories regarding the cause of depression. However, the focus is not on a single neurotransmitter but on the “studying neurobehavioral systems, neural circuits, more intricate neuroregulatory mechanisms” (Kaplan Sadock 531).

Biological and neurobiological studies have become more and more closely correlated with mental disorders throughout the past decade of scientific progress. This paper aims to expound models that have contributed to our developing understanding of the origins of Major depressive disorder (MDD) and treatment guidance, from both neurobiological and biological fields. It will also explore the implications, both positive and negative, for societal and personal integration of the knowledge that these advancements provide.

Schardt et al. (2010), suggest that increased relationships between the lateral prefrontal cortex and the amygdala results in increased success at self-regulation in the form of emotion regulation. Thus, a decrease in links between the neuronal structures is often found in individuals with mood disorders such