**4.1 Diagnosis**

In the face of severe stress, information processing is impaired, and it is not possible to resolve the traumatic event. An unintegrated traumatic experience can be easily aroused and affect daily life. Painful experiences cannot be suppressed or excluded. In experiences recorded with anxiety/fear, stimuli that stimulate one of the emotion-thought elements activate all of them. This general arousal and the unorganized cognitive processing behind it are considered as the source of symptoms, such as arousal, memory disorders, and impulsivity in PTSD. The individual who encounters the trauma first experiences confusion. This unprepared/unconditioned situation changes in the next step. By using the lived experiences before the trauma, the trauma is perceived as if it had been encountered before. The same emotional and physical reactions are given in the previous cases. This is a highly learned behavior. However, since this behavior is not suitable for the new situation, it is not an appropriate response and the answers become complex. Increasing confusion also increases anxiety. To diagnose PTSD, valid, objective/empirical methods other than previous trauma have not been defined. The diagnosis depends on the clinical interview.

*New Diagnosis and Treatment Approaches to Post-Traumatic Stress Disorder DOI: http://dx.doi.org/10.5772/intechopen.104098*

The use of check-lists without recourse to clinical interviews may lead to the loss of significant clinical information that may be essential in the holistic provision of therapy and clinical care. To be diagnosed with PTSD, an adult must have all of the following for at least 1 month after a traumatic event: At least one re-experiencing symptom, one avoidance symptom, two arousals, and reactivity symptoms, and two cognition and/or mood symptoms.

The Post-traumatic Stress Disorder Checklist for DSM-5 (PCL-5) is a self-report measure to evaluate the presence and severity of PTSD symptoms (**Table 1**).

#### **4.2 Factors facilitating the occurrence and persistence of PTSD**

Inability to explain and share the effects of trauma, severity, and frequency of dissociative reactions during or immediately after trauma, childhood physical abuse, genetic predisposition, family history of psychopathology and PTSD, being a woman, excess physiological response during the traumatic event, acute stress disorder and early PTSD symptoms, previous psychiatric disease history, low socioeconomic level, and low education level, temporal intensity, and duration of trauma, memory disorders, soft neurological signs, low IQ, childhood attention deficit hyperactivity disorder symptoms are the factors related with increased risk or chronicity of PTSD [52].

PTSD is associated with many comorbidities besides causing disability on its own. Major depressive disorder, generalized anxiety disorder, alcohol and substance use disorders can be listed as the main comorbid conditions. The high-stress level accompanying PTSD increases the risk for many systemic diseases, such as hypertension, diabetes, and asthma [55].

One of the important comorbidities of PTSD is a borderline personality disorder. Borderline personality disorder causes the person to become prone to experiencing traumatic events by distorting the perception of risk. On the other hand, PTSD symptoms deepen the loss of functionality associated with a personality disorder.

#### *4.2.1 Acute and chronic PTSD*

If PTSD symptoms are present within 3 months following the trauma, it is defined as acute PTSD; and if symptoms persist for more than 3 months, it is defined as chronic PTSD [55].

#### *4.2.2 Complex PTSD*

PTSD is single-event trauma from traumatic experiences, such as rape, physical assault, or war. However, the traumatic event might be prolonged chronic victimization, such as interpersonal violence. Over time, chronic traumatization, often of an interpersonal nature, such as multiple and/or long-term developmentally negative traumatic events, came to be used to describe the term "complex trauma" [56].

#### *4.2.3 Course and prognosis*

The clinical course and outcome of PTSD vary depending on the factors before, during, and after the trauma. The nature of the symptoms observed after trauma,


*Criterion B (1–5)—at least one ≥2 Criterion C (6–7)—at least one ≥2 Criterion D (8–14)—at least one ≥2 Criterion E (15–20)—at least one ≥2.*

*Mild 0–20; Moderate 20–40; Severe 40–60; Extreme 60–80.*

#### **Table 1.**

*The PTSD Checklist for DSM-5 (PCL-5) [54].*

#### *New Diagnosis and Treatment Approaches to Post-Traumatic Stress Disorder DOI: http://dx.doi.org/10.5772/intechopen.104098*

the prognosis of the disease, or the information obtained from follow-up studies conducted at different periods makes it difficult to define a specific clinical situation for the course of the disease. PTSD starts when trauma is encountered or within the next few years, symptoms increase in the next few years and continue by drawing a plateau. Symptoms may fluctuate over time and intensify during stressful periods. Approximately 30% of patients show complete improvement, 60% have mild to moderate symptoms, and 10% have symptoms that remain unchanged or worsen. It is common for those who benefit from treatment to reappear after years of being exposed to a serious stressor.

#### **4.3 Neuroimagination studies**

Several neuroimaging studies have been implemented to investigate the pathophysiology of PTSD. Some symptoms associated with PTSD are related to changes in brain structure and function [57]. Brain regions implicated in the development of PTSD include the hippocampus, amygdala, and medial prefrontal cortex [58].

Advanced neuroimaging techniques contributed to our understanding of the possible pathophysiology of PTSD. The results of neuroimaging studies point to the importance of the hippocampus in PTSD. Exposure to chronic stress results in disturbances in memory function and neural damage to the hippocampus. The HPA axis controls stress response in the body by producing cortisol. The neural damage might be related to high levels of glucocorticoids, changes in serotonergic function, inhibition of neurogenesis in the hippocampus, or inhibition of brain-derived neurotrophic factors [59].

The magnetic resonance imaging (MRI) studies in PTSD consistently revealed reduced hippocampal and inferior temporal cortex volumes. The decreased volume of the inferior temporal cortex was inversely correlated with anxiety levels in PTSD [60]. Other neural structures often implicated in the pathophysiology of PTSD include the amygdala and prefrontal cortex. Amygdala is the integrative center for emotions, emotional behavior, and motivation. Functional magnetic resonance imaging (fMRI) studies with PTSD patients present increased activity in the amygdala in response to threat stimuli compared [57]. However, investigation of a large sample of nearly a hundred PTSD patients was characterized by reduced amygdala volumes [61].

Several methods have been used to study the pathophysiology of PTSD. Many neural networks and pathways that play a role in PTSD have been revealed, and these pathways can be studied in-depth due to the advances in techniques for neuroimaging.

#### **4.4 PTSD treatment strategies**

PTSD is associated with functional impairment and comorbidity. Therefore, early diagnosis and appropriate treatment are essential in PTSD. Existing treatment guidelines for the treatment of PTSD disorder generally aim to—reduce PTSD symptoms or achieve remission, loss of diagnosis, treatment of comorbid medical and psychiatric diseases, improvement of quality of life, correction of impairment in functional areas, return to work or duties. Treatment guidelines include psychological, pharmacological, and neuro-modulatory treatments [55]. However, a major limitation must be recognized: the current therapies described for PTSD are based on western cultures and modern technologies, and many of these approaches do not easily apply to rural communities in low- and middle-income countries. Clinicians

or psychotherapists should, therefore, adopt psychotherapeutic strategies that are appropriate to the cultures in which they work.

### **4.5 Pharmacological interventions**

It includes the use of various psychotropic drugs to target the core symptoms of PTSD. Medications that target key symptoms of PTSD, including intrusions, avoidance, negative changes in cognition and mood, and changes in arousal and responsiveness, include selective serotonin reuptake inhibitors, serotonin and norepinephrine reuptake inhibitors, atypical antipsychotics, β-blockers, and sleep medications (e.g., α-blockers, nabilone, hypnotics). Pharmacological treatments include antidepressants (e.g., sertraline), antipsychotics (e.g., risperidone), anticonvulsants (e.g., topiramate), hypnotics (e.g., zopiclone), and mood stabilizers (e.g., lithium), mood stabilizers; adrenergic agents; benzodiazepines; and other pharmacological agents [55].

Selective serotonin reuptake inhibitor (SSRI) stands out among pharmacological treatments because it is effective in most PTSD symptoms, easy to use, and has low side-effect profiles. They are the most valid and widely used drugs for the treatment of re-experiencing, avoidance, emotional blunting, and hyperarousal symptoms. SSRIs have been found to be effective in PTSD in double-blind, placebo-controlled randomized trials.

Mood stabilizers have the effect of reducing the sensitization of the limbic system, which develops in the first weeks and months after the traumatic event. Lamotrigine was found to be effective in re-experiencing and avoiding symptoms of PTSD. Studies are reporting that lithium, valproic acid, carbamazepine, oxcarbazepine, and gabapentin are effective. It has been found that propranolol, a beta-blocker, has positive effects on nighttime nightmares, remembering repetitive anxiety-provoking situations, jumping, sleep disturbances, and self-esteem.
