One of the adaptive values of long adolescence is a prolonged period of synaptogenesis, neuroplasticity, and neuronal connectivity, all processes that sustain behavioral changes, mainly in the social domain, needed for the passage to adulthood [19,20]. The adolescent brain is vulnerable to environmental perturbations and traumatic experiences occurring before or during this period have an increased saliency in affecting cognitive, emotional, and social levels. Given these bio-psycho-social changes occurring in this part of life, diagnosing trauma-related disorders in adolescence is quite complex. In this life period, besides a categorical approach, a dimensional approach should be used in the diagnostic process as a tool to capture the elements of continuity in physiological and psychopathological trajectories of development [21]. According to the fifth edition of the Diagnostic and Statistical Manual (DSM-5) of mental disorders, trauma-related disorders during adolescence imply exposure to overwhelming, aversive, threatening, or fearful experiences [22]. Affective, cognitive, and behavioral symptoms related to trauma causing significant impairment or suffering can be accompanied by dissociative symptomatology (depersonalization and derealization on the positive pole, as well as dissociative amnesia on the negative pole). As mentioned above, trauma-related symptoms in adolescence can be classified within the externalizing and internalizing domains, along with a dimension ranging from hyper- to hypoarousal, and may also lead to a Reactive Attachment Disorder or an Uninhibited Social Engagement Disorder [12,13,14]. As regards externalizing behaviors, extroverted symptoms mainly occur such as: hypervigilance, impulsivity, hyperactivity, disinhibition, aggression, mood enhancement, intrusive thoughts, disorganized cognitive processing on the paranoid side, substance abuse, difficulty in attention and concentration, hyperactivity, and hyperexcitability, accompanied by depersonalization and derealization. Conversely, introverted symptoms mainly occur in the presence of internalizing behaviors, such as: freezing, social withdrawal, mood deflection, cognitive inhibition, depressive ideation, numbing, reduced psychomotor skills, avoidance behaviors, and feelings of impotence, accompanied by dissociative amnesia.

The externalizing/internalizing conducts are grounded in a neurobiological basis, which undergo crucial changes during adolescence, especially in the presence of trauma. In fact, brain structure, function and connectivity, neurotransmitter levels, stress response, homeostasis maintenance, immune system, genetics/epigenetics, and gut microbiome undergo marked changes due to trauma exposure [23,24,25]. To improve understanding of how the effects of traumatic experiences on the brain involve changes at nearly every level of analysis, there is a need to comprehend the adolescent physiological conditions. During adolescence, brain remodeling is characterized by changes in associative and limbic circuits (such as the medial prefrontal cortex, amygdala, and hippocampus) subserving high-order processes (e.g., executive function, mentalizing, emotion regulation, and social cognition), along with dramatic changes in endocrine, immune, and biochemical systems [20,26]. The initiation of puberty represents a period of dynamic synaptogenesis and dendritic/synaptic pruning, with experience-dependent remodeling of brain circuits underlying complex behaviors [27,28]. Specifically, during this time there is substantial pruning of excitatory synapses in the cortex and in particular in the prefrontal cortex, supporting the hypothesis that overproduction and subsequent pruning of synapses is a computationally advantageous approach to building a competent brain [29]. A correct balance of activity of the GABA and glutamate systems is vital for optimal neurodevelopment and general central nervous system function, and the dysregulation of this balance has been implicated in a number of neurological conditions that range from mild to severe, including schizophrenia and epilepsy, and has been shown to increase the incidence of anxiety disorders [30,31].

In the context of trauma, the amygdala, the medial prefrontal cortex, and the hippocampus have been extensively investigated with respect to fear learning and extinction, threat reactivity, and emotion regulation [32,33,34], and they have been identified as critical loci of dysfunction following trauma [35,36]. Notably, acute exposure to threatening adversity promotes the secretion of hormones (e.g., cortisol) and pro-inflammatory cytokines, which drive changes in the structural plasticity of the amygdala and hippocampus to enhance fear learning in the occurrence of similar events [37]. Chronic exposure to traumatic events acts through these same hormonal and immune mediators to create glutamatergic excitotoxicity and atrophy in the amygdala and hippocampus linked to impaired memory and other behavioral and cognitive symptoms, commonly found in internalizing behaviors, such as depression [38]. Furthermore, deficits in the synthesis of GABAergic neurosteroids—produced from progesterone in the brain, adrenal gland, ovaries, and testes [39], clearly more active during puberty—have been implicated in the pathophysiology and recovery from trauma-related disorders [40]. For individuals raised in environments where multiple sources of threat are present and/or long-term survival is uncertain, the “developmental reprioritization” is often marked by an accelerated maturation, characterized by the early emergence of adult-like phenotypes [41,42]. Specifically, traumatized children showed adult-like neural phenotype in the functional connectivity between the amygdala and medial prefrontal cortex during threat processing [43,44,45,46], in parallel with experimental reports indicating that early adversity leads to accelerated myelination of axons in the amygdala [47].

Overall, across various types of traumatic experiences, an altered structure, function, and connectivity of the amygdala, medial prefrontal cortex, and hippocampus correspond to an increased fear reactivity, attentional biases towards threat, and difficulty with affective regulation [48,49,50], contributing to a risk of externalizing/internalizing behaviors.