INTRODUCTION
Post‐traumatic stress disorder (PTSD), currently included by the Diagnostic and Statistical of Mental Disorders, Fifth Edition, Text Revision (DSM‐V‐TR) in the macro category of “disorders related to traumatic and stressful events”, is a form of psychopathological distress that arises acutely as a result of direct or indirect exposure to severely stressful and traumatic events. First defined and studied in the United States primarily from the symptomatology observed in many war veterans, PTSD can occur in individuals of all ages who are victims, direct or indirect witnesses, and even rescuers of episodes of violence, deprivation, disaster conditions, and degradation. Although the literature of the 1980s mostly referred to the psychological consequences of war experiences on the person in more recent years, a much wider and more varied range of situations and events potentially led to the development of the disorder has been recognized, as well as a greater variability in the symptoms manifested, their onset and their psychological and clinical characteristics. On the psychological and behavioral manifestations of PTSD, a large and consistent literature is now available. While concerning the more purely neuroanatomical aspects of the disorder, currently still the subject of research and investigation, order and clarity are perhaps needed.
Although a traumatic event is by definition highly stressful, not everyone who experiences a life situation capable of raising their anxiety and stress levels develops a PTSD condition. Although estimates vary by sample and type of trauma, and current statistics seem to show a marked increase in the number of diagnosed cases, overall only about 20% of adults exposed to a traumatic condition develop true PTSD. The resilience displayed by the majority of the population following a highly traumatic situation could therefore suggest that, in some individuals, the neurobiological systems involved in adaptation and responses to stress evolve elements of vulnerability that correlate with the development of the disorder itself. Consistent with this hypothesis, although cause‐and‐effect relationships are still debated, it is believed that many of the psychological and behavioral manifestations of PTSD are precisely the result of structural and functional changes in the brain in response to excessive stress. Since these elements of vulnerability, together with the variability in the morpho‐volumetric evidence found among individuals with this diagnosis, undoubtedly represent a significant challenge for scientists who need to identify and characterize in greater detail the neurobiological correlates of PTSD, the goal of this paper is precisely to try to shed more light on the neuroanatomical and functional correlates in PTSD to sharply identify the differences with individuals without this disorder.
From a specifically diagnostic point of view, following the traditional DSM‐V‐TR criteria, 12 to discriminate PTSD from other trauma‐based disorders in adult patients and children above 6 years of age, it is necessary to assess and verify the presence of some parameters:
A.
Exposure to an event of a traumatic nature is characterized by the following criteria:
1)
Having personally experienced, witnessed, been made aware of, or come into close contact with an event or more events that caused shock, serious injury, death, or seriously threatened the mental and physical integrity of one's own or others.
2)
Having experienced, as a result, intense feelings of fear, helplessness, or horror (Note: these emotions may be manifested by children through the enactment of disorganized behavior or strong agitation/irritation).
B.
Presence of one or more intrusive and persistent symptoms such as recurrent memories, images, perceptions, thoughts, and/or nightmares related to the event, sudden flashbacks, severe psychological distress, and intense psychomotor activation (Note: in young children, such discomfort may be expressed through the reiteration of games, drawings, representations, or behaviors having as their object themes or elements related to the traumatic event).
C.
Constant avoidance of stimuli associated, more or less directly, with the trauma. These behaviors must have begun in the period following the traumatic experience and may be manifested through attempts to stifle or avoid memories, thoughts, and emotions or through avoidance of places or situations that evoke or symbolize to some extent the event or its aftermath.
D.
Negative alterations in functioning, thinking, or mood not present before the trauma, such as, for example, dissociative symptoms, sleep, and circadian rhythm disturbances, ease of anger or rage, difficulties in cognition and concentration, hypervigilance/hyperarousal, and marked emotional detachment from activities and/or people.
Again according to the DSM‐V‐TR diagnostic criteria, 12 the duration of symptoms (criteria B, C, and D) must be longer than 1 month and the condition must cause clinically significant distress or impairment in personal, social, occupational, affective, or other areas important to the patient's quality of life functioning but not attributable to the effects of drugs, medications, or other clinical conditions. It is also possible to distinguish three different forms of PTSD classically discriminable based on onset and duration of symptoms: “Acute,” relating to a period of symptom manifestation of fewer than 3 months; “Chronic,” if longer than 3 months; and “Late” if the symptomatology arises 6 months after the traumatic experience.
PTSD is a complex and disabling disorder that leads to a variegated symptom manifestation, mostly related to dysfunction in emotional and behavioral management, that is reflected in an equal variability of structural and functional brain abnormalities, found mainly in cortical and subcortical regions such as the hippocampus, amygdala, hypothalamus, and cingulate cortex, as well as their underlying neurocircuits. These abnormalities may correlate either with possible individual vulnerabilities, which may thus predispose the person to the risk of developing PTSD, or as consequences of exposure to trauma and/or sequelae resulting from the disorder itself. Indeed, as it turns out, morpho‐volumetric analyses conducted on these regions have led to sometimes conflicting results, generating no small amount of confusion in the scientific community. However, it is believed that these differences may depend largely on the characteristics of the specific case, such as the type, severity, and impact of the traumatic experience on the person, the existence or not of pre‐existing abnormalities, previous, and/or repeated exposures to traumatic and stressful events, specific personal and psychological characteristics, and so forth, which may result in differential potentiation or depotentiation of synaptic transmission in the different neural nuclei involved, thus explaining the volumetric variations found, between individual and individual, even at the expense of the same structure. It is known, for example, that at the striatal level, chronic stress is capable of both selectively inhibiting the function of CB1 endocannabinoid receptors and preventing the physiological reduction of GABAergic currents 66 and, at the same time, influencing the production of 2‐arachidyl‐glycerol (2‐AG) on which the modulation of glutamatergic transmission in particular depends. There is evidence that, while an acute stress experience can increase 2‐AG synthesis, especially in the hippocampus and basolateral amygdala, leading to glutamatergic hypofunctionality, chronic stress, on the other hand, can result in the diametrically opposite effect, and this clearly can have different effects on both the symptomatic manifestations of the patient and the volume of these structures. The same argument applies to the action of brain inflammatory cytokines (IL‐1β, IFN‐ϒ) produced by microglial cells as a result of stress, which can also interfere with the dopaminergic system, inhibiting striatal dopamine release and further contributing to emotional and behavioral dysregulation. In conclusion, although in recent years knowledge and awareness about PTSD and its symptomatological, psychological, and neurobiological features have greatly increased, leading to the refinement of the available treatment strategies and devising of new ones, to date, an optimal level of their effectiveness has not yet been achieved. One of the reasons for this lies in the confusion generated by the results obtained from brain investigations, which are sometimes conflicting and not always unambiguous. Nonetheless, these divergences can be an advantage because, through better knowledge and characterization, it is possible to further investigate the neurobiological processes both predisposing and underlying the development of PTSD and build increasingly effective predictive models and more specific diagnostic markers, refining and improving intervention methodologies and therapeutic approaches. Thus, the hope for future research is to dare to push itself beyond the classic purely diagnostic‐clinical boundaries to take greater account of the complex, dynamic, and often case‐specific interplay between biological, psychological, and personological variables in PTSD.
Fuente:
Ibrain. 2024 Spring; 10(1): 46–58. Published online 2024 Jan 19. doi: 10.1002/ibra.12147
PMCID: PM
C11045199PMID: 38682011
Normal versus post‐traumatic stress disorder amygdala. Image edited from original. Propriety of James Douglas Bremner. Traumatic stress from a multiple‐levels‐of‐analysis perspective. Developmental Psychopathology, 2015; pp. 656–676. doi:10.1002/9780470939390.ch16.