POLYTECHNIC UNIVERSITY OF THE PHILIPPINES

COLLEGE OF SOCIAL SCIENCES AND DEVELOPMENT

BACHELOR OF SCIENCE IN PSYCHOLOGY

In Partial Fulfillment of the Requirements for

PSYC 102: Physiological and Biological Psychology

Unraveling the Neurobiology of Post-Traumatic Stress

Disorder (PTSD): Insights and Strategies for Effective
Management

Prepared by:
Anastacio, Bien Tristan P.
Bonganay, Regin
Garcia, Maylyn A.
Laniog, Mary Dawn Jhoana E.
Perez, May M.
Roy, Trina B.
Simangan, Pia Flor

Presented to:
Prof. Adrian Guinto

July 10, 2023

INTRODUCTION

Exposure to traumatic experiences can lead to post-traumatic stress disorder

(PTSD), a severe mental health condition. Various post-traumatic symptoms and

functional deficits are characteristic of this condition. In recent years have seen an

uptick in research aimed at deciphering the neurological bases of PTSD to understand

better the intricate processes that contribute to the disorder including altered

learning/extinction, heightened arousal, and intermittent dissociative behavior as

examples relevant to each of the three primary domains. In the study of Jovanovic et al.

(2013), individuals with trauma-related disorders, including PTSD, exhibit enhanced fear

potentiation, impaired fear inhibition, and heightened arousal. The study findings

suggest that these alterations in fear learning, extinction, and stress response

contribute to the clinical features observed in trauma-related disorders, such as

persistent fear, difficulties in suppressing fear responses, and hypervigilance.

This article thoroughly assesses the neurobiological anomalies seen in PTSD,

illuminating the complex relationship between predisposition and protective variables in

terms of genetics, development, and life experiences. Sherin and Nemeroff (2011)

stress the need to expand beyond a fundamental perspective of trauma intensity as the

primary driver of the severity of PTSD by examining the role of psychological trauma in

developing the condition.

The review centers on the three basic categories of PTSD symptoms: recalling the

traumatic experience, becoming activated, and then becoming deactivated. It explores

the endocrine and neurotransmitter pathways and the specific brain regions engaged in
fear behavior that govern stress reactions. The authors highlight existing evidence for

neurological anomalies in people with PTSD and their potential contribution to the

clinical aspects of the condition by conducting a comprehensive review of research

data. In the study by Shin and Liberzon (2010), the authors discuss the neurocircuitry

underlying fear, stress, and anxiety disorders, including PTSD. They emphasize the

involvement of brain regions such as the amygdala, hippocampus, and prefrontal cortex

in fear processing and regulation. These brain regions are crucial for fear conditioning,

fear extinction, and the modulation of fear responses.

In addition to discussing the common symptoms, the article delves into the

remarkable similarities between post-traumatic stress disorder (PTSD) and traumatic

brain injury (TBI), finding shared neurobiological abnormalities. It discusses the impact

of confounding variables on the recovery of neurobiological systems after trauma,

including but not limited to genetic predisposition, gender, history of trauma,

developmental stage at the time of trauma, and severity of injury.

The authors concede that many elements of PTSD remain mysterious, leading to

continuous disputes within the scientific and clinical communities, despite significant

advances in understanding and treating the disorder. They highlight the significance of

ongoing research to uncover molecular markers for PTSD and to clarify the pre-existing

or trauma-induced neurobiological abnormalities associated with the disorder.

The neurological abnormalities identified in PTSD are thoroughly explored in this

review, providing vital insights into the disorder's underlying causes. The article opens
the path for future research efforts to improve our understanding, diagnosis, and

treatment of PTSD by combining existing knowledge and highlighting areas of doubt.

SUMMARY

The biology of PTSD

Endocrine Factor

The main endocrine characteristics of post-traumatic stress disorder (PTSD) are

discussed in this paragraph, focusing on the dysregulation of the thyroid and

cortisol hormones. Examined concerning PTSD is the

hypothalamic-pituitary-adrenal (HPA) axis, which is crucial to the stress

response. As part of the HPA axis, the hypothalamus releases

corticotropin-releasing hormone (CRH), which in turn promotes the pituitary

gland's synthesis of adrenocorticotropin (ACTH), which in turn causes the

adrenal glands to release glucocorticoids, including cortisol.

There is proof of aberrant cortisol regulation in PTSD patients. Compared to

healthy controls, several studies have found lower cortisol concentrations in

PTSD patients, albeit this conclusion is not universal. These contradictory results

have been attributed to comorbid illnesses, hereditary variables, trauma's timing

and severity, and comorbid trauma. Further evidence for the dysregulation of the

HPA axis has been found in PTSD patients, including sensitized negative
feedback inhibition, raised CRH concentrations in cerebrospinal fluid, and

enhanced glucocorticoid receptor binding and activity.

It is interesting to note that low cortisol levels during psychological trauma

exposure may predict the development of PTSD, indicating that hypocortisolism

may be a risk factor for PTSD susceptibility and maladaptive stress responses. It

has been demonstrated that administering hydrocortisone soon after being

exposed to trauma can prevent PTSD and that treating PTSD symptoms by

restoring normal cortisol rhythms with exogenous hydrocortisone injection. It is

crucial to remember that glucocorticoids can impair the recall of traumatic

memories, which could help to alleviate PTSD symptoms on its own.

The hypothalamic-pituitary-thyroid (HPT) axis and its potential role in

stress-related illnesses, such as PTSD, are also briefly discussed in the passage.

Tri-iodothyronine (T3) and thyroxine (T4) have been demonstrated in studies to

have elevated baseline levels in veterans with PTSD, with T3 levels continuing to

be elevated over time. This shows that higher T3 levels and subjective anxiety in

people with PTSD may be related.

Overall, the paragraph emphasizes how the HPA and HPT axis, particularly, are

affected by the dysregulation of thyroid and cortisol hormones in PTSD. It implies

that alterations in these endocrine systems may be responsible for the peculiar

stress reactions and symptoms seen in people with PTSD.

Neurochemical factors

The dysregulation of numerous neurotransmitters involved in stress and anxiety

reactions is the main focus of this passage's discussion of the vital

neurochemical characteristics of post-traumatic stress disorder (PTSD).

Catecholamines (dopamine and norepinephrine), serotonin, amino acids (GABA

and glutamate), and peptides (CRH, neuropeptide Y, and endogenous opioids)

are among the neurotransmitters mentioned.

Increased urine excretion of dopamine and its metabolite have been seen in

PTSD patients, and abnormal catecholamine control is seen in the illness.

Norepinephrine is involved in autonomic stress responses, and PTSD patients

have hyperactivity of the autonomic sympathetic branch. The hyperarousal,

heightened startle response, and enhanced encoding of terror memories in

PTSD are all attributed to the dysregulation of norepinephrine.

Serotonin plays a role in regulating emotional and stress reactions. PTSD

symptoms include hypervigilance, heightened startle response, impulsivity, and

intrusive memories related to dysregulation of the serotonin system, including

changes in receptor types and responsiveness. SSRIs, or selective serotonin

reuptake inhibitors, are effective in treating PTSD.

The amino acids glutamate and GABA may also cause PTSD. GABA has

calming effects and blocks the neural circuits responsible for stress and terror

reactions. People with PTSD have altered GABA/benzodiazepine receptor

complexes, which may indicate a decrease in receptor density or affinity. The

central excitatory neurotransmitter glutamate is involved in learning and memory,

including consolidating traumatic memories in post-traumatic stress disorder

(PTSD).

The stress response involves peptides like CRH and neuropeptide Y. Particularly,

CRH is linked to stress reactions and fear conditioning. CRH system

dysregulation, including elevated CRH activity and aberrant receptor functioning,

may be a factor in PTSD symptoms such as hyperarousal, conditioned fear

reactions, and startle reactivity. Contrarily, neuropeptide Y possesses anti-anxiety

and stress-relieving qualities, and its decreased activity in PTSD may be a factor

in noradrenergic hyperactivity.

The stress response is inhibited by endogenous opioid peptides such as

endorphins and enkephalins. Specific PTSD symptoms like numbness,

stress-induced analgesia, and dissociation are linked to changes in endogenous

opioids. Opioid receptor antagonists can potentially help traumatized people with

dissociation and flashbacks.

Overall, the many symptoms and characteristics of PTSD result from the

dysregulation of these neurotransmitters. Understanding these neurochemical

alterations may aid in creating PTSD treatments that work.

Brain Circuitry

The following subsection addresses the typical alterations in brain structure and

function identified using brain imaging techniques in people with post-traumatic

stress disorder (PTSD). The hippocampus, amygdala, and cortical regions like
the anterior cingulate cortex, insula, and orbitofrontal region are among the brain

areas that exhibit changes in PTSD patients.

The hippocampus, essential for memory, fear conditioning, and stress

management, is frequently shown to have less volume in people living with

PTSD. Long-term stress and excessive glucocorticoid levels can harm the

hippocampus, causing structural alterations and neuronal integrity problems.

Studies using functional MRI have revealed deficiencies in the hippocampus

activation of memory tasks in PTSD patients. However, selective serotonin

reuptake inhibitors (SSRIs) therapy can partially correct these deficiencies.

The amygdala, which is involved in processing emotions and triggering fear

reactions, exhibits hyperactivity in those with PTSD. According to functional

imaging studies, emotional inputs, traumatic reminders, and stressful scripts

cause the amygdala to become more active. Amygdala reactivity that is

increased may be a physiologic risk factor for PTSD.

The cortical areas, particularly the medial prefrontal cortex (PFC), mediate the

inhibitory control of stress reactions and emotional reactivity. There are

anomalies in the ACC's structure and neuronal integrity, and patients with PTSD

have lower volumes of the frontal cortex, especially the anterior cingulate cortex

(ACC). According to functional MRI studies, PTSD sufferers' medial PFCs are

less activated in response to traumatic and unfavorable emotional events. The

severity of the symptoms is correlated with reduced activation of the medial PFC,

and effective SSRI therapy can restore activation patterns in this area. PTSD has
 also been researched for the connectivity between the amygdala and medial

PFC and their relationship in activation patterns, albeit with mixed results.

Overall, the hippocampus, amygdala, and cortical regions of people with PTSD

show structural and functional changes, according to brain imaging studies. The

etiology and symptoms of the condition, such as the impairments in stress

management, fear processing, and emotional control, are thought to be

influenced by these changes.

The Origin of Neurobiological Abnormalities in PTSD

Several research projects have been done to comprehend the neurobiological

abnormalities linked to post-traumatic stress disorder (PTSD) and how they relate to the

emergence of the disorder. The investigations seek to ascertain if traumatic exposure,

pre-existing risk factors, or both cause these alterations in the brain.

Cortisol, a hormone associated with the stress reaction, was one factor that one

study looked at in predicting the onset of PTSD. It was discovered that the disease may

already have a pre-existing risk factor in the form of low cortisol levels at the time of

trauma. Low cortisol levels may disinhibit particular brain circuits, resulting in

heightened stress reactions and fear conditioning, which aid in the onset of PTSD.

The shrinkage of the hippocampus, a part of the brain involved in memory and

emotion processing, in people with PTSD has also been the subject of research. The

debate has centered on whether this decrease results from trauma exposure or if it
already existed before the traumatic occurrence. A study involving twins with different

histories of trauma exposure was carried out to address this. The hippocampus was

smaller in PTSD-affected Vietnam Veterans than in control subjects. It appears that a

smaller hippocampus may be a pre-existing vulnerability factor for developing PTSD,

presumably with a genetic and neurodevelopmental foundation, as even twins without

PTSD had a smaller hippocampus.

The study also raises the possibility that PTSD may be inherited with gray matter

reduction in the anterior cingulate cortex (ACC), another brain area involved in emotion

regulation.

In order to better understand the illness and create successful interventions,

more research is required to ascertain the timing and causes of other brain changes

connected to PTSD.

Risk and resilience for developing PTSD

Risk and resilience for developing PTSD cover the variations in how people react

to stressful experiences and the variables that affect how post-traumatic stress disorder

(PTSD) develops. After a traumatic occurrence, some people could feel brief

irregularities or distress, but fewer people will experience chronic psychopathology that

lasts for a long time.

It is crucial to comprehend why some people experience PTSD while others do

not. Finding the causes of vulnerability or resilience is crucial because the majority of
trauma survivors do not go on to develop PTSD. Three aspects are emphasized in the

passage: hereditary determinants, gender disparities, and early developmental

stressors. Gender differences may affect how people react to and recover from stress,

and genetic variables may affect a person's propensity to develop PTSD. Additionally, a

person's likelihood of having PTSD may be affected by early experiences of stress and

hardship during development.

It also discusses how physical traumas, particularly traumatic brain injuries (TBI),

increase the likelihood of developing PTSD. These concurrent physical stressors may

significantly increase the risk and severity of PTSD.

It is critical to comprehend the variables that moderate the likelihood of PTSD

after psychological stress. An individual's susceptibility to developing PTSD is

influenced by genetic variables, gender differences, early developmental stress

experiences, and co-occurring physical traumas.

Genetic risk factors for PSTD

The role of genetic factors in post-traumatic stress disorder (PTSD) is covered in

this passage. Growing data indicate that genetic variables significantly affect the chance

of getting PTSD, despite obstacles, including genetic variability and inadequate

penetrance.
 Studies on families and twins have long suggested that PTSD is partly inherited.

Evidence also connects hereditary factors to the neurobiological aspects of PTSD, such

as diminished hippocampus volume and heightened amygdala activation.

Specific genetic variants have been linked to an increased incidence of PTSD.

For instance, a variation in the dopamine transporter gene has been associated with a

higher incidence of PTSD among trauma survivors. Although the results of specific

research have been mixed, polymorphisms in the D2 receptor and serotonin transporter

have also been linked to PTSD risk.

Notably, it has been discovered that a genetic mutation in the FKBP5 gene,

which encodes a protein implicated in the glucocorticoid receptor system, moderates

the risk of developing post-traumatic stress disorder (PTSD) in connection with

childhood maltreatment. This genetic variant, which is linked to increased glucocorticoid

receptor sensitivity, combines with childhood trauma to predict adult PTSD symptoms.

Furthermore, current research suggests that the diagnosis of PTSD and elevated

levels of pituitary adenylate cyclase-activating peptide (PACAP) in females are

associated with particular genetic variants in estrogen response components and fear

physiology. These results add to our knowledge of the gender variations in PTSD risk

and shed light on the mechanistic theory of PTSD.

Research has found a number of genetic variants that increase the likelihood of

getting PTSD, despite the fact that the genetics of PTSD are complicated. These results

underline how crucial genetic factors are in determining PTSD vulnerability and may

have repercussions for how we study and treat the illness.

Gender Differences and Risk for PTSD

The gender differences in post-traumatic stress disorder (PTSD) are discussed in

this section, along with the possible causes of these variances. While the type of

exposure and the severity of the trauma may have an impact, they may not entirely

explain why women are more likely than males to experience PTSD.

There may be gender-specific changes in the neurobiological reaction to trauma,

according to research. Although results in humans are not always consistent, animal

studies show that females typically display stronger and longer-lasting stress responses

regulated by the hypothalamic-pituitary-adrenal (HPA) axis. These variations may be

attributable to the effects of sex hormones, notably estrogen, on stress-related

neurotransmitter systems such as corticotropin-releasing hormone (CRH) and

serotonin. Additionally, progesterone has been linked to the modulation of these

systems. However, regardless of the immediate effects of sex hormones, gender

disparities in stress reactions have been noted.

Genomic variations and the developmental impacts of sex hormones are two

factors that may be responsible for gender disparities in the stress response. Pregnancy

has been observed to increase the likelihood of PTSD in women, suggesting that

reproductive hormones may have an impact. The structural plasticity of the

hippocampus and amygdala, two areas of the brain implicated in the stress reaction, is

also influenced by sex hormones. There are gender disparities in the brain's response

to terror stimuli, according to functional imaging studies.

 The underlying causes of gender disparities in PTSD risk and how the effects of

trauma translate into varying susceptibilities to the condition may become more

apparent as research advances.

Early developmental factors and PSTD

Specifically, it emphasizes the importance of prior experiences, especially

childhood hardship, in reducing the likelihood of post-traumatic stress disorder (PTSD)

after trauma. It highlights how early bad events, such as prenatal and childhood stress,

can have long-lasting consequences on how the brain develops, affecting how sensitive

people are to stress and how susceptible they are to developing post-traumatic stress

disorder (PTSD).

According to research, those who endured childhood hardship are more likely to

experience PTSD in response to later stressful events like exposure to battle or natural

disasters. Early adverse experiences have the potential to "program" the

neurobiological reactions to stress and play a role in the later onset of PTSD.

Children who have witnessed domestic violence or have lived through natural

catastrophes like Hurricane Katrina are more likely to develop post-traumatic stress

disorder (PTSD), according to studies. Similar symptoms to those seen in people with

PTSD include fear sensitization, hyperactivity of the corticotropin-releasing hormone

(CRH), and low cortisol levels in nonhuman monkeys exposed to inconsistent mother

care during infancy.

 Women who have experienced childhood trauma also exhibit increased

neuroendocrine and autonomic stress responses, demonstrating the long-lasting effects

of early stress on stress reactivity in adulthood.

Additional study is required to pinpoint the developmental milestones during

which the effects of early stress are most noticeable, investigate methods for

counteracting these effects, and examine the interaction between dispositional elements

(such as genes and gender) and developmental characteristics in determining the

neurobiological susceptibility to PTSD. The development of focused therapies and a

better knowledge of PTSD risk can be aided by knowing these aspects.

The influence of physical trauma (and TBI) on the development of PTSD

The increased likelihood of post-traumatic stress disorder (PTSD), when physical

harm coexists with psychological trauma, is discussed in this passage. Physical harm

can at least double the likelihood of having PTSD, according to studies on Vietnam

Veterans and more recent research on Veterans from Iraq and Afghanistan.

Traumatic brain injury (TBI) and post-traumatic stress disorder (PTSD) are

notably linked. Research on individuals with known TBI and surveys of US Marines

exposed to explosions in Iraq show that TBI increases the chance of acquiring PTSD.

Although subjective and objective symptoms of both disorders can overlap, it can be

difficult to distinguish between the dangers of PTSD and TBI. However, both conditions

share anomalies in endocrine, neurochemical, and circuitry functioning linked to PTSD.

 Diagnosis of PTSD and TBI in the same person may have an additive or even

multiplicative clinical effect. For instance, the interaction of PTSD symptoms with the

irritation and fury caused by TBI may result in a markedly increased risk profile for

violence. This is especially true when TBI accompanies frontal brain injury and

behavioral disinhibition. In addition, the helplessness that frequently comes with

physical injuries, especially TBI, can make PTSD's low self-efficacy and loss of agency

worse. For those who become progressively more reliant over time, the psychological

difficulties associated with TBI can increase their risk of being victimized long-term.

The danger and complexity of clinical outcomes are increased when physical

injury is present in addition to psychological stress, such as TBI and PTSD. Healthcare

providers can more effectively address the unique issues presented by people who

have experienced physical and psychological trauma by understanding the relationships

between these illnesses.

A basic model of PTSD Neurobiology

The changes in the body seen in people with post-traumatic stress disorder

(PTSD) are discussed in this section, along with their consequences for the

dysregulation of stress-mediating systems. In people with genetic, epigenetic, and

experiential predispositions, these biological changes are thought to happen when

subjected to harsh circumstances that cause psychological trauma.

The central corticotropin-releasing hormone (CRH) and norepinephrine (NE)

cascade can become overactive in PTSD due to a relative deficiency of baseline cortisol
during trauma, which can cause heightened and protracted stress reactions. The

heightened sensitivity to stress is also influenced by the dysregulation of GABA,

serotonin, neuropeptide Y (NPY), and other neurotransmitters. Additionally, altered

noradrenergic and stress hormone activity affects the learning and extinction processes,

which hampers PTSD. These neurochemical imbalances impact how terror memories

are stored, retrieved, and eliminated, resulting in PTSD-related re-experiencing

symptoms.

Additionally, cognitive symptoms and the generalization of fear reactions in

unrelated settings may be influenced by a damaged hippocampus in charge of

declarative memory and context training. A damaged hippocampus can make it difficult

to distinguish between threats, which can cause hypervigilance, behavioral activation,

and further acquisition of fear associations. This is often coupled with excessive

amygdala reactions. The inability of the prefrontal cortex to regulate stress responses,

fear associations, and extinction processes further exacerbates the pathology of PTSD.

The dysregulation of numerous stress-mediating systems is highlighted by these

biochemical anomalies in PTSD, which also shed light on the disorder's underlying

processes. Understanding these neurological alterations can help in the creation of

focused PTSD therapies.

CRITIQUE

Qualification of the Authors

Jonathan E. Sherin, M.D., Ph.D is a psychiatrist and experimenter who has made

significant benefactions in the areas of mental health, trauma, and homelessness. He

has held leadership positions, including Chief Medical Officer for the Los Angeles

County Department of Mental Health, where he has concentrated on enhancing access

to internal health care for marginalized populations. Dr. Sherin has a substantial

publication record, with multitudinous papers and papers that punctuate motifs similar

as trauma, homelessness, and internal health interventions.

Charles B. Nemeroff, M.D., Ph.D is a distinguished psychiatrist and experimenter

known for his experience in psychopharmacology and mood diseases, with a particular

emphasis on depression. He has conducted extensive exploration on the neurobiology

of psychiatric diseases and has a productive publication history. Dr. Nemeroff's work

also encompasses clinical trials investigating the effectiveness of various medications

and treatments for mood diseases. Throughout his career, he has held academic

positions at several universities and has entered recognition and awards for his

significant contributions to the field of psychiatry. Their proficiency and knowledge in the

field of research and psychiatry proves their credibility to provide verifiable facts,

evaluation and treatment.

Purpose of the Study

The author provided a clear and informative discussion of PTSD by presenting a

concise overview of the main points covered in each section. The topics related to the

biology of PTSD, such as endocrine factors, neurochemical factors, brain circuitry,

genetic risk factors, gender differences, early developmental factors, and the influence

of physical trauma, were comprehensively addressed. The author effectively highlighted

the key findings and implications of each topic, leading to a thorough understanding of

the neurobiological aspects of PTSD. The study aimed to investigate and understand

the neurobiological factors and mechanisms involved in PTSD, with the intention of

gaining insights into the origins of neurobiological abnormalities, identifying risk and

resilience factors, and elucidating the underlying processes and dysregulation of

stress-mediating systems. The ultimate goal was to contribute to the development of

more effective interventions and treatments for individuals with PTSD.

Critique

One area where the article could be improved is in providing more robust

citations for the statistics it presents regarding the prevalence of PTSD and gender

differences in exposure to traumatic events. Strengthening the evidentiary basis of

these claims would enhance the reliability and credibility of the information presented.

By including citations from reputable sources, such as peer-reviewed journals or official

reports, the article can provide a solid foundation for its claims and contribute to the

validity of its arguments. Additionally, discussing the limitations and challenges in

estimating PTSD prevalence rates and the potential impact of cultural and societal
factors on reporting and diagnosis would provide a more comprehensive understanding

of the topic (Gilbertson MW, et, al. 2020).

In the study of Agaibi, C. E., & Wilson, J. A. (2019), utilizing recent articles allows

for a broader exploration of the latest risk and resilience factors associated with PTSD.

The field of trauma research is evolving rapidly, and new insights are continuously being

uncovered. Recent articles may delve deeper into topics such as the impact of specific

types of trauma, the role of genetic and epigenetic factors, and the influence of social

and environmental variables on the development and course of PTSD. These recent

studies can provide a more comprehensive and nuanced understanding of the complex

factors involved in PTSD. The diverse psychological and physiological effects of

different traumatic experiences, a deeper examination would provide a more

comprehensive understanding of PTSD development. Traumatic events can vary widely

in their nature, intensity, duration, and context, and these variations can have significant

implications for the development of PTSD symptoms. By exploring the nuances of

trauma exposure, such as interpersonal violence, combat experiences, or natural

disasters, the article can shed light on the different pathways that can lead to the

manifestation of PTSD symptoms and the potential factors that contribute to its

development. Furthermore, addressing the concept of complex trauma, which involves

exposure to multiple and chronic traumatic events, would provide additional insights into

the complexities of PTSD development and its impact on individuals. (Sherin and

Nemeroff, 2011).

The article's discussion of the neurobiological processes involved in PTSD

appears somewhat oversimplified. PTSD is associated with alterations in brain

structures and neurochemical systems that play a crucial role in stress regulation and

emotional processing. A more nuanced exploration of the intricate mechanisms

underlying the activation of the amygdala, hippocampus, prefrontal cortex,

hypothalamic-pituitary-adrenal (HPA) axis, and sympathetic nervous system (SNS)

would contribute to a more thorough analysis. The article could examine the intricate

interplay between these systems, including the role of neurotransmitters, stress

hormones, and brain circuitry, in modulating stress responses and emotional reactivity in

individuals with PTSD. Furthermore, the article could explore the impact of chronic

stress on neuroplasticity and neuronal connectivity, as well as the potential role of

epigenetic mechanisms in the development and persistence of PTSD symptoms

(Malejko et., 2017).

While the article briefly mentions developmental trauma as a risk factor for

PTSD, it lacks a detailed analysis of this aspect. Developmental trauma refers to

adverse experiences that occur during critical periods of brain development, such as

childhood abuse, neglect, or prolonged exposure to stress. These experiences can

have profound and long-lasting effects on neurodevelopment and increase the

vulnerability to psychiatric disorders, including PTSD. Further examination of

developmental trauma, including its effects on brain development, attachment

processes, emotion regulation, and the long-term consequences on mental health,

would enhance the article's comprehensiveness. By exploring the unique challenges

and vulnerabilities associated with early life trauma, the article can provide insights into

the specific risk factors that contribute to the development of PTSD in this population.

Additionally, discussing the potential mechanisms underlying the transgenerational

transmission of trauma and its implications for the intergenerational impact of PTSD

would broaden the scope of the analysis (Sakellariou & Stefanatou, 2017b).

In addition to exploring risk factors, the article could provide a more

comprehensive exploration of resilience factors. While resilience is mentioned, its

significance in mitigating the development of PTSD could be further discussed.

Resilience refers to the ability to adapt and bounce back from adversity, and it plays a

crucial role in individuals' ability to cope with traumatic experiences. Considering a

broader array of individual, interpersonal, and environmental factors influencing

resilience would enrich the analysis. The article could delve into protective factors such

as social support, positive coping strategies, self-efficacy, cultural factors, and cognitive

flexibility, which have been shown to promote resilience in the face of trauma. By

examining the protective factors that contribute to resilience, the article can highlight the

importance of resilience in mitigating the impact of traumatic experiences and reducing

the risk of developing PTSD. Moreover, exploring the potential role of resilience-focused

interventions and the mechanisms through which resilience can be enhanced would

provide practical insights for clinical practice and public health initiatives (Christiansen

and Berke, 2020)

Moreover, the article would benefit from a more critical analysis. Engaging with

alternative theories, conflicting evidence, and gaps in knowledge within the field of

PTSD research would provide a more balanced and objective perspective. PTSD is a

complex disorder with multifaceted etiology and diverse clinical presentations, and there

are still many unanswered questions and ongoing debates in the field. By

acknowledging the limitations of current research and exploring areas of uncertainty, the
article can contribute to a more nuanced understanding of PTSD. Additionally,

considering alternative perspectives and theories, such as the diathesis-stress model,

the allostatic load framework, or the interaction between genetic and environmental

factors, can stimulate further discussion and research in the field, leading to new

insights and advancements in our understanding of PTSD (Kelmendi et al., 2017)

Lastly, although the article raises questions about the potential application of

neurobiological findings in the treatment of PTSD, it lacks concrete suggestions or

examples. Expanding on effective psychotherapeutic interventions, pharmacotherapy

approaches, and their integration with neurobiological research would increase the

practical relevance of the discussion. PTSD treatments encompass a range of

modalities, including cognitive-behavioral therapies (CBT), eye movement

desensitization and reprocessing (EMDR), pharmacotherapy, neurofeedback, and

complementary approaches. By highlighting evidence-based treatment approaches and

discussing how neurobiological knowledge can inform treatment decisions and

strategies, the article can provide valuable insights into the translation of research

findings into clinical practice. This would not only enhance the practical relevance of the

discussion but also facilitate the dissemination of knowledge to clinicians and promote

the use of effective interventions for individuals with PTSD Toloza et al. (2020).

Overall, this critique outlined several areas where the article on PTSD could be

further improved. Strengthening citations, exploring variations in the impact of traumatic

events, delving into neurobiological processes, analyzing developmental trauma,

discussing resilience factors, engaging in critical analysis, and exploring practical

applications for treatment would enhance the overall quality and depth of the article. By
addressing these areas, the article can provide a more comprehensive and

well-rounded understanding of the complex interplay between biology and the

development of PTSD. Furthermore, it would contribute to the ongoing efforts to

advance our knowledge of PTSD and improve clinical interventions for individuals

affected by this debilitating disorder.

Conclusion

Jonathan E. Sherin and Charles B. Nemeroff's journal focusing on the

neurobiological impact of psychological trauma in PTSD provided valuable insights with

the intentions of gaining insights into the origins of neurobiological abnormalities,

identifying risk and resilience factors, elucidating the underlying processes and

dysregulation of stress-mediating systems, and educate readers is effectively achieved

through the comprehensive analysis. Moreover, the cross-analysis of data further

supports the report's findings.

The critique serves as a valuable resource for researchers, psychologists and

can serve as a guide for future studies on post-traumatic stress disorder (PTSD). It

highlights areas of improvement and provides suggestions for enhancing the

understanding and treatment of PTSD. However, researchers and psychologists should

critically evaluate and customize the recommendations to align with their research

objectives and methodologies. It is also crucial to consult and reference original,

peer-reviewed sources that directly support their arguments and findings.

 In summary, the critique offers constructive feedback on how the original article

on PTSD can be enhanced, providing valuable suggestions to improve the quality,

depth, and practical relevance of the discussion. By incorporating these suggestions, a

more comprehensive understanding of PTSD can be achieved, leading to improved

clinical interventions for individuals living with the disorder.

Recommendation:

Based on the findings presented in the reviewed article on post-traumatic stress

disorder (PTSD), the following recommendations can be made to various stakeholders

to enhance understanding, prevention, and treatment of PTSD:

· Mental Health Professionals:

Incorporate trauma-focused therapies: Mental health professionals should integrate

evidence-based trauma-focused therapies, such as cognitive-behavioral therapy (CBT)

and eye movement desensitization and reprocessing (EMDR), into their practice. These

therapies have shown effectiveness in treating PTSD symptoms by targeting the

underlying mechanisms of trauma-related distress.

Implement early screening and intervention: Mental health professionals should

advocate for the implementation of routine screening for trauma exposure and PTSD

symptoms in healthcare settings. Early identification and intervention can prevent the

escalation of symptoms and improve outcomes for individuals with PTSD.

· Researchers and Academics:

Investigate personalized treatment approaches: Researchers should further explore

personalized treatment approaches for PTSD based on individual characteristics,

including genetic factors, developmental history, and symptom profiles. Understanding

the heterogeneity of PTSD and identifying predictors of treatment response can lead to

more tailored and effective interventions.

Conduct longitudinal studies: Longitudinal studies are needed to investigate the

long-term outcomes of individuals with PTSD, including factors associated with

resilience and recovery. Research should examine the interplay between biological,

psychological, and social factors over time to gain a comprehensive understanding of

the disorder.

· Parents and Caregivers:

Foster a supportive and safe environment: Parents and caregivers should create a

supportive and safe environment for individuals, especially children and adolescents,

who have experienced trauma. This involves promoting open communication, providing

reassurance, and actively listening to their concerns. Creating a nurturing environment

can facilitate healing and resilience.

Educate themselves about trauma and its effects: Parents and caregivers should

educate themselves about the effects of trauma and PTSD symptoms. Understanding

the behavioral and emotional manifestations of PTSD can help them provide

appropriate support and seek professional help when needed.

· Individuals with Lived Experiences:

Seek professional help: Individuals who have experienced trauma and suspect they

may have PTSD should seek professional help from mental health practitioners.

Seeking therapy and engaging in evidence-based treatments can assist in symptom

management and facilitate recovery.

Practice self-care and stress management: Individuals with PTSD should prioritize

self-care activities, such as exercise, relaxation techniques, and engaging in hobbies, to

reduce stress and promote well-being. It is important to develop healthy coping

strategies and engage in activities that bring joy and a sense of fulfillment.

Connect with support networks: Joining support groups or engaging in peer support can

be beneficial for individuals with PTSD. Interacting with others who have similar

experiences provides a sense of validation, understanding, and shared coping

strategies.

By implementing these recommendations, mental health professionals can

enhance their treatment approaches, researchers can expand our knowledge of PTSD,

parents, and caregivers can create a supportive environment, and individuals with lived

experiences can take steps towards healing and recovery. It is through collaborative

efforts across these different stakeholder groups that we can improve the lives of

individuals affected by PTSD and work towards reducing the burden of this complex

disorder.
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