Neurodevelopmental psychiatric disorders such as autism spectrum disorders, schizophrenia and anxiety disorders, which typically emerge in children and adolescents, have been extensively investigated worldwide for decades. The pathogenesis and mechanism remained unclear, and no effective treatment has been identified so far. Recently, a variety of studies identified prenatal stress (PS) as a risk factor for neurodevelopmental socioemotional disorders (Khashan et al., 2008, Kinney et al., 2008, Ronald et al., 2010, Monk et al., 2012). A popular thesis proposed that socioemotional disorders arise from PS-induced perturbations to early brain development, especially the neurophysiology of amygdala. Various studies have shown that the amygdala is implicated in the pathophysiology of neurodevelopmental psychiatric disorders (Quirk and Gehlert, 2003), also several studies have identified that PS affects amygdala development (Kraszpulski et al., 2006, Laloux et al., 2012). However, little is known about how PS influences the amygdala developmental trajectory. Ehrlich et al. conducted this study to first investigate whether PS has an effect on socioemotional behavior of adolescents and adults, and secondly whether and how PS alters amygdala neuron excitability. They were motivated to explain the relationship among PS, amygdala neuronal activity and socioemotional behaviors because understanding the trajectory of brain development can provide potential targets for intervention of the
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A critique of “Ehrlich, David E, and Donald G Rainnie. 'Prenatal Stress Alters The Development Of Socioemotional Behavior And Amygdala Neuron Excitability In Rats '.
Childhood maltreatment is a prevalent problem through out the world. As a child grows and matures the brain continues to develop according its experiences. During this time sensitive periods of development for different areas of the brain. A few areas that are of interest are the stress-influenced areas, which are at an increased risk for developmental problems when exposed to maltreatment. The extra stress from such exposures can influence abnormalities throughout the brain, which have been linked to structure changes with in the corpus callosum, anterior cingulate, dorsolateral prefrontal, orbitofrontal cortex, and hippocampus, amygdala, and cerebellum, as well as changes to stress related hormone systems. These structural changes are associated with an increased risk of psychopathology and other life long educational and physiological risk.
Throughout life, both children and adults experience varying amounts of stress in their everyday lives. For the most part, this has been proven to be healthy and crucial in strengthening their response to such stimuli later in life. This paper will focus on the findings of various studies in which researchers have found links between stress exposure and childhood development. Specifically, this paper will focus on the effects of what is known as toxic stress and its effects on the development of a child and its role in the development of mental disorders as the child transitions into adulthood.
However, to understand the impact of adversity on young children’s development and learning, our genes supply the basic blueprint for brain development. “Thus, toxic stress in early childhood not only is a risk factor for later risky behavior but also can be a direct source of biological injury or disruption that may have lifelong consequences independent of whatever circumstances might follow later in life (Shonoff and Garner, 2012, page 238). Poverty, neglect, or family stress can make it especially difficult for young children to develop the self-discipline and habits of mind they will need to succeed in the classroom and beyond. Researchers have found that chronic, sustained stress, such as that caused by neglect, abuse, or deprivation,
The brain develops in such a way that it leaves itself vulnerable to these negative influences. The prenatal brain develops an overabundance of neurons, some of which are then carefully eliminated before age 4 (5). In a process similar to this, the amount of synapses between neurons is built up during early childhood and then pruned back for the next 30 years of life (5). These two processes are both disturbed by elevated levels of stress hormones (5). The two centers of the brain with the most postnatal changes, including the growth of new neurons after birth, are the hippocampus, which is part of the limbic system, and the cerebellar vermis (6). The hippocampus is in charge of creating and retrieving memories, working together with the other parts of the limbic system, such as the amygdala, which records the emotions for each memory. The vermis controls the production and release of two of the catecholamine neurotransmitters, dopamine and norepinephrine (6). Both the vermis and the limbic system have higher concentrations of receptors for the stress hormone cortisol than anywhere else in the brain (6). Due to this fact, these still-developing areas are the most vulnerable to the damage done by elevated levels of stress hormones.
The ACE Study was designed to answer the question: “If risk factors for disease, disability, and early mortality are not randomly distributed, what early life influences precede the adoption or development of them (preventchildabuse.org)?” Adverse Childhood Experience does not evoke preconceived notions or biases about the perpetrators or victims of child abuse, domestic violence, or persons with mental health or substance abuse issues. The term “adverse” implies stress. However, the biologic stress response is largely responsible for the negative impact of ACEs on brain development. “Experiences” was the term chosen rather than “Environment” because the latter term can imply exposure to environmental toxins. As framed by the study, “Childhood” refers to the first 18 years of life (preventchildabuse.org).
The amygdala is responsible for emotions, survival instincts, and memory. (http://study.com). Also, even though it is unimportant for the development of infant and child, but the amygdala is also responsible for sex drive, when males do not produce enough testosterone, this causes a low sex drive and for the amygdala to be smaller than the average amygdala. Although children do not have any reason to need a sex drive, they still have hormones coursing through their bodies; the low testosterone in males, could unknowingly affect their emotions, survival instincts, and memory as well. Logically, this could also be a reasonable explanation for the depression, low test scores, and antisocial behaviors in children. Add to the fact that children, who live in poverty, are already affected by depression, low test scores, and antisocial behaviors, children with low testosterone might have even worse depression, worse scores, and antisocial
A psychological disorder is a condition characterized by abnormal thoughts, feelings, and behaviors, and both depression and bipolar fall under psychological disorders. (Module 13.1). A person who suffers from bipolar disorder previously known as Maniac depression. Additionally, people how suffer from bipolar also likely suffer from some type of depression. A person with bipolar disorder experiences a state of mood swings from depression to mania. In order words they can be happy one minute, and extremely mad the next. So, to be diagnosed with Bipolar, one needs to experience one maniac episode once in there life. Characteristics of bipolar include extremely talkative, reckless behavior, or attempt to do too many activities simultaneously.
As scientists continue their research on mental illness, it is becoming clear that many of these disorders are caused by a combination of factors, including changes in the brain and environmental stress. (Goldberg)
The authors explored the traditional view, focusing on structural and functional studies of grey matter and developmental differences in frontal lobe and emotion-related brain areas. They provided two explanations that weakened this view. First, biological factors were primarily responsible for predisposing risk tendencies. This made it difficult to account for cross-cultural differences. Second, because the brain was responsive to environmental stressors and was able to change accordingly, it was not known whether structural changes reflected those stressors.
In order to understand how severe bullying can result in the development of PTSD in adolescents, it is important to understand how the adolescent brain processes peer hostility and rejection, especially in relation to how an adult brain would process similar situations. There is a large amount of literature on the many unique factors of the adolescent brain. “The Adolescent Brain”, an article by BJ Casey, addresses limbic system development and prefrontal cortex development in adolescents, both of which are extremely relevant to perceptions and reactions to peer aggression. The limbic system is comprised of brain structures that are involved with emotional regulation, reward sensitivity, and impulsivity. The prefrontal cortex is the portion of the brain that is responsible for planning and decision making. In the article, Casey discusses how the limbic system matures at the onset of puberty in adolescents, while the prefrontal cortex isn’t mature until a few years later, at the beginning of early adulthood. This means that adolescents are unique in their combination of high levels of risk taking, impulsivity, emotional sensitivity, and reactivity to stress without the influence of the prefrontal cortex’s tendency for planning and reasoning (Casey 112).
It also interacts with bad early breeding experience to influence attention and emotional resources, stress, nervousness, and alcohol choice and addiction. Then again, the [few] mechanisms by which the stress increases disorder risk in adulthood is not known but may include epigenetics (deals with changes in gene expression patterns that are independent of the underlying DNA sequence) programming of gene expression.
The importance of the amygdala in social cognitions has been examined in both primate and human studies. Use of primates to study the social brain suggests that the amygdala contributes to social cognition. Kluver and Bucy made large bilateral lesions in monkey brains made across the amygdala, temporal neocortex, and surrounding structure. After the lesion, the animals engaged in hypersexual behaviors, unusual tameness, and a lack of knowledge about emotional stimuli. Lesions exclusively targeting the monkey’s amygdala resulted in similar, but more subtle impairments. This suggest that the amygdala may play a role in emotions elicited by social cues. Studies of the amygdala’s role in human social cognition suggest that the temporal lobes process socially relevant facial information from humans. Emotions from facial expressions, in particular fear are projected to the amygdala. Studies using FMRI to examine typical subjects and subjects with amygdala damage support this theory. Individuals with amygdala damage have difficulty recognizing facial expressions, specifically negative emotions such as fear.
Schizophrenic patients often have difficulties performing mundane tasks due to deficits in processing relevant stimuli. This leads to fragmented thoughts and distractibility as the brain becomes hypersensitive to sensory cues. Animal models emulate the symptomology of schizophrenia and are thereby extremely important in comprehending the unknown aetiology of this neuropsychiatric illness. A growing body of research believes in the relation between genes and the environment. This theory is known as the neurodevelopmental hypothesis of schizophrenia.
The neurodevelopmental disorders, according to the DSM 5, are a group of conditions with onset in the developmental period. The disorders typically manifest early in development, often before the child enters grade school, and are characterized by developmental deficits that produce impairments of personal, social, academic, or occupational functioning. Autism spectrum disorder (ASD) is newly classified as such; it was once classified as “Asperger’s Syndrome.” ASD is a severe neurodevelopmental impairment. The disorder limits the functioning capabilities of children and their capacity to communicate as well as interact with others. ASD effects how children perceive the world around them; socializing with others happens to be the most vital piece of development. Onset for ASD can occur as early as infancy, some children, however, may develop normal and then begin to suddenly withdraw and become unusually aggressive with those around them, they also begin to lose vocabulary and language skills they’ve once had. Other medical conditions may be comorbid with ASD; for example, epilepsy, intellectual and structural language disorders, mental disorders, sleep disorders, and avoidant-restrictive food intake disorders, (DSM 5, pg. 59).