Brain Functions In Depression Essay Example
Brain Functions In Depression Essay Example

Brain Functions In Depression Essay Example

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  • Pages: 9 (2303 words)
  • Published: August 21, 2021
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Adolescence is a critical time for children as they undergo important growth and development. This stage is marked by increased emotional reactivity and significant brain maturation, which have a substantial impact on the emergence of previously hidden depressive symptoms.

According to studies, abnormal brain structures in both the cortex and subcortex are associated with adolescent depression. In a five-year study, 205 adolescents aged eight to twenty-five underwent Magnetic Resonance Imaging (MRI) and were asked to self-report any depressive symptoms they had during this time. The findings revealed that individuals who reported experiencing depressive symptoms showed a quicker thinning of the frontal lobe.

The MRI revealed that there were volume changes in either the hippocampus or amygdala, or possibly both. However, it was concluded that the emerging depressive symptoms were more strongly linked to cortical thinning in the frontal regions (Bos

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, Peters, Van de Kamp, Crone, & Tamnes, 2018). Another study found that as the severity of depression in an adolescent individual increased, the cortical region became thinner. A thin cortical region is associated with a reduced level of parasympathetic control.

The child's lack of precise neurological control over their body to rest when overwhelmed has a significant impact. Their cardiac and respiratory function may be abnormal for the activity they are doing, leading to exhaustion in an energized adolescent and constant malaise. Nevertheless, research shows that the connection between overall cortical thickness and autonomic function, particularly parasympathetic and sympathetic control, differs based on the severity of depression.

Additional studies have been conducted to compare the thickness of the left frontal lobe and parasympathetic control in moderate and severe depression. The findings revealed that depression severity is correlated with a

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loss of autonomic function control. Patients with more severe depression displayed deviated MRI patterns and increased heart rate, respiratory rate, and general affect. These physiological indicators directly reflect the severity of depression in children (Koenig, et al., 2018). Many adolescents face a risk of Major Depressive Disorder (MDD) due to thinning of the cortex in frontal regions. The delayed maturation of the frontal limbic area significantly contributes to heightened autonomic arousal in such individuals.

Insomnia and anxiety during adolescence can harm neurological growth and development. These symptoms, along with common signs of major depressive episodes like chronic sadness, loss of interest in once enjoyable activities, consistent guilt, low energy, and diminished self-worth, directly affect interpersonal relationships, academic achievements, and overall quality of life. It is important to diagnose patients promptly to prevent further deterioration in frontal limbic growth and development (Bhowmik et al., 2012).

Additionally, a study compared cortical thickening in the frontal brain region between depressed and non-depressed individuals to evaluate the effects of cortical thickness. Thirteen young adults with mild to moderate Major Depressive Disorder who were not taking medication participated in a facial expression exam.

The Go/No-Go Task was used to assess a patient's inhibitory response with emotional stimuli. In addition, patients underwent an MRI scan to measure cortical thickness. The study found that depressed patients had thinner frontal cortical regions, which correlated with their performance on the Go/No-Go Task. The severity of depression and cortical thinning were directly related to inhibition of emotional disturbances. This research provides evidence supporting thicker left frontal brain areas in non-severely depressed young adults compared to a healthy group (Fonseka, Jaworska, Courtright, MacMaster, & MacQueen, 2016).

Depression has an impact

on brain development, specifically in terms of hindering the formation of appropriate emotional facial expressions and cues for individuals their age. During adolescence, the cortices in the frontal poles near the brain's surface initially thicken, but then gradually decline and stabilize throughout adulthood. If depression occurs during early adolescence, these brain regions do not have a chance to thicken. However, if depression happens later in life when these areas have already thickened, the structural changes in the brain will be different. Therefore, both brain anatomy and emotional well-being are directly influenced by when depression starts. It is worth noting that there is no direct correlation between cognitive performance and brain structure according to research findings.

The impact of brain structure on a person's emotional and behavioral characteristics is an important finding that can have negative implications for their social behavior and quality of life (Fonseka, Jaworska, Courtright, MacMaster, & MacQueen, 2016). There are clinical differences in how depression presents in adults and adolescents. The severity of depressive symptoms determines the appropriate psychiatric intervention. A longitudinal study found that older adolescents with more severe symptoms experienced an increase in depression over twelve months, while those with less severe symptoms remained more stable. This emphasizes the need for further research to identify specific symptoms of depression in older adolescents (Jinnin et al., 2016). Data was collected from 42 adolescents aged 7 to 12 diagnosed with Major Depressive Disorder (MDD) between March 2013 and 2014.

In a study, adolescents with Major Depressive Disorder were compared to those without chronic mental or physical illnesses. The researchers used various tools to gather reliable and comprehensive data on the participants' physical and mental

health. The findings revealed that 81% of the adolescents diagnosed with Major Depressive Disorder had one or more additional psychiatric comorbidities. Among the commonly reported comorbidities were anxiety disorders, including separation anxiety, disruptive behavior disorder, and ADHD (Bilginer ; Kandil, 2015).

The study discovered that teenagers with chronic depression have lower scores on tests gauging their social relationships and school performance due to anxiety and behavioral disorders. These teenagers also encounter more frequent emotional and behavioral issues both at school and home. As a result, it was concluded that adolescents who have few friends and struggle academically are more prone to exhibiting symptoms of depression. Adolescent depression is distinct because the social skills learned during this stage are pivotal. The lack of social interaction may be the cause or consequence of pre-existing behavioral problems before being diagnosed with depression. Therefore, it is evident that academic challenges and antisocial behavior act as clinical indicators of adolescent depression that should be assessed when identified (Bilginer ; Kandil, 2015).

Research has found that adolescents diagnosed with Major Depressive Disorder (MDD) exhibit higher levels of externalized behaviors compared to non-MDD children. These behaviors, which are typically seen during adolescence, include increased aggression, severe rule-breaking at home and school, and self-injury. Surprisingly, approximately 57% of MDD children have a history or currently experience suicidal thoughts. Consequently, these adolescents face an elevated risk of engaging in self-harm. Adolescents often turn to self-harm as a way to express their emotional distress and substitute intangible mental suffering with physical pain. Therefore, it is crucial to examine the internal factors contributing to an adolescent's self-injurious behaviors.

Despite the availability of various anxiety and depression medications, it is

important to note that identifying clinical symptoms associated with these conditions in a timely manner may not always happen. In Poland, suicide stands as the third leading cause of death among adolescents aged fourteen and older, as well as children between five and fourteen years old. It is crucial to acknowledge that depression presents differently in children compared to adults. Therefore, instead of solely relying on typical manifestations observed in adult depression, studying a child's behavior and subconscious signals becomes vital (S?opie?, 2019). The older medications, referred to as first-generation drugs, are less frequently utilized. An example of such medication is Mono Amine Oxidase Inhibitors (MAOIs), which represent one of the earliest developed antidepressants.

Nardil and Parnate are types of MAOI medications that block the main enzyme responsible for breaking down neurochemicals, such as norepinephrine, in brain synapses. By inhibiting this enzyme, these medications elevate the level of norepinephrine in the brain by preventing its breakdown. Nonetheless, since this enzyme also metabolizes tyramine, an amino acid, MAOIs hinder the body's capacity to process tyramine. Tyramine is commonly present in various foods like nuts, chocolate, cheese, wine, and others.

Educating individuals who are prescribed MAOIs about necessary dietary adjustments is crucial. The consumption of tyramine while MAOIs are in the body can be risky, as it may lead to a dangerous increase in blood pressure. Furthermore, it is important to avoid over-the-counter cough and cold medications, as they have the potential to cause excessively high blood pressure levels. Unfortunately, the lack of compliance or knowledge regarding potential interactions between drugs and food has resulted in MAOIs no longer being used as the primary treatment for depression (Bhowmik et

al., 2012).

Tricyclic antidepressants (TCAs), which were developed in the 1950’s and 1960’s, are first-generation depression medications. Their name "tricyclic" comes from their chemical structure consisting of three rings. Examples of TCAs include Elavil, Norpramin, and Triavil. The primary mechanism of action for these medications is to increase the levels of norepinephrine and serotonin in the brain, thereby alleviating depression (Bhowmik et al., 2012).

There is ongoing debate regarding the use of Tricyclic Antidepressants (TCAs) in children and teenagers due to their potential for causing fatality and heart harm, even when used within the appropriate therapeutic range (Hazell, O'Connell, Heathcote, Robertson,& Henry ,1995). In young children and adolescents, the neurotransmitter system responsible for regulating the effects of Tricyclic Drugs is not fully developed. This incomplete development can result in uncontrollable manic behavior as a side effect. Additionally, at this stage, the noradrenergic nervous system does not reach full maturity, leading to rapid metabolism of TCAs by the liver. Consequently, an imbalance in serotonin and noradrenergic levels occurs which explains the heightened hyperactivity observed in these age groups when taking TCAs (Hazell, O'Connell, Heathcote, Robertson,& Henry ,1995).

Tricyclic Antidepressants (TCA’s) have anticholinergic side effects that also impact the parasympathetic nervous system. These effects include dry mouth, blurred vision, constipation, dizziness, and low blood pressure. First generation Tricyclic drugs are generally not prescribed for depression in adolescence due to their controversial negative side effects and potential toxicity even at therapeutic levels (Bhowmik et al., 2012).

On the other hand, second generation antidepressants such as Selective Serotonin Reuptake Inhibitors (SSRIs) are commonly used for depressive symptoms and are considered safer, especially in adolescence. SSRIs work by blocking the reuptake of serotonin at

the synapses, which increases its level in the brain.

SSRIs have the advantage of increasing serotonin levels and concentration, which helps alleviate depressive symptoms by making more serotonin available in the body. Unlike TCA and MAOI medications, SSRIs have minimal or no side effects and require fewer lifestyle adjustments. As a result, they are often prescribed as the first-line treatment for adolescent depression.

SSRI medications like Prozac, Zoloft, and Celexa are generally well tolerated with minimal side effects. Typical side effects include nausea, headaches, and insomnia; however, these usually diminish within the first month. Nevertheless, there is a small risk of developing Serotonin Syndrome if high doses of SSRI medication are taken for an extended period. Serotonin Syndrome is a neurological condition that initially manifests as fever, nausea, and vomiting but can advance to include elevated body temperature, tremors, seizures, and irregular heartbeats.

It is essential to monitor patients in order to prevent the development of a rare syndrome (Bhowmik, Sampath Kumar, Srivastava, Paswan, & Dutta, 2012). Another type of second-generation antidepressant commonly prescribed is known as SNRIs or Serotonin and Norepinephrine Reuptake Inhibitors. These medications are more recent and affect the reuptake of serotonin and norepinephrine in the synapses of the brain. Examples of SNRI drugs include Cymbalta, Pristiq, and Effexor.

Patients who experience one episode of depression will be given medication for that specific episode. However, individuals who have multiple episodes of depression (usually two or three) will typically be prescribed a maintenance dose of medication as a preventive measure for future episodes. It is important to note that medications, even those with minimal side effects like SNRIs or SSRIs, are not the first treatment option. This

is because adolescents go through brain maturation and often explore alternative therapies before considering medication for managing symptoms (Bhowmik et al., 2012). One alternative approach to traditional antidepressant medication is electroconvulsive therapy (ECT), also known as ECT.

The therapy consists of approximately six to ten treatments at an outpatient facility, typically demonstrating results within one to two weeks. It involves giving an electrical shock that induces convulsions in the brain, resulting in the release of neurochemicals that alleviate depressive symptoms. Despite being initially stigmatized and feared, the mini seizures caused by this treatment are brief and last no longer than 20-90 seconds. Patients regain complete consciousness within 5-10 minutes after finishing the therapy. ECT has been proven effective when other methods have failed.

Despite any potential hesitancy towards electroconvulsive therapy (ECT), it is important to note that this therapy has minimal negative side effects. The only observed side effect is short term memory loss, which typically resolves after the completion of the three to four month treatment course. It is worth mentioning that this memory loss does not cause any long term harm for the patient (Bhowmik, Sampath Kumar, Srivastava, Paswan, & Dutta, 2012). Another non-pharmacologic option for treating depression is transcranial magnetic stimulation (TMS), which involves sending vibrations to activate neurologic cells in the brain by containing and releasing energy. Additionally, light therapy serves as a third available treatment option.

This article discusses the use of seasonal affective disorder (SAD) therapy and its effectiveness in relieving symptoms of depression. It also highlights a study that connects low Vitamin D levels in children aged 9-13 to signs of depression. Increasing Vitamin D levels through supplements and alternative therapies

may improve symptoms, but more research is needed to confirm the efficacy of this treatment. Additionally, psychotherapy options can be tailored to individual patients based on their internal conflicts.

Some children experience a single episode of depression that can be treated with medication or alternative therapies. However, for those who have recurring episodes or chronic depression, it is essential to undergo long-term therapy. During adolescence, individuals may develop negative coping strategies or engage in harmful behaviors that can exacerbate their depressive symptoms and self-esteem issues (Bhowmik, Sampath Kumar, Srivastava, Paswan, & Dutta, 2012) (S?opie?, 2019).

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