Post-Traumatic Stress Disorder (PTSD) was recognized as a disorder in 1980 [
1]. Approximately 6-8% of the general population is identified with PTSD at some point in their lives making the diagnosis quite common. PTSD is widespread characterized by maladaptive fear responses following a traumatic event [
2,
3,
4,
5,
6,
7,
8,
9]. PTSD experienced by refugees has been linked to poor self-reported quality of life. Refugees are typically exposed to multiple types of traumatic events in their countries of origin. These events are often repeated, prolonged and interpersonal in nature, and have been demonstrated to have deleterious effects on mental health [
9,
10,
11]. The effect of war on refugees’ lives is not temporary but persists over many years. Potentially traumatic events commonly experienced by refugees and asylum-seekers in their home countries include interpersonal violence, sexual violence, life-threatening injuries, witnessing death of loved ones, and torture. The extent of exposure to traumatic events may vary according to several factors including area/country of origin, characteristics of conflict and personal factors such as gender, age, ethnicity, and sexual orientation. The exposure to potentially traumatic events contributes considerably to psychopathology [
3,
12]. Elevated rates of psychological disorders including Major Depressive Disorder (MDD) and PTSD are frequently reported among refugees and asylum-seeker populations [
13,
14,
15,
16,
17,
18,
19,
20]. In addition, refugees face several daily challenges during displacement, as well as in the post-migration environment, including those related to lack of resources, family separation, social isolation and discrimination, socioeconomic factors, and immigration and refugee policies [
16,
21,
22,
23,
24,
25]. The growing number of displaced individuals worldwide and their disproportionately high rates of mental disorders have prompted the World Health Organization (WHO) to call upon treatment services to be responsive to the needs of asylum-seekers and refugees [
26].
Considerable evidence sustains abnormalities in affective processing. Psychophysiological research provided evidence for increased amygdala activation and decreased activation in prefrontal cortical areas as well as reduced hippocampal volumes in PTSD, leading to a hypothetically over-reactive threat detection, possibly diminished regulatory control, and disrupted adaptive memory processes. Furthermore, the hyper-active negative valence system (NVS) - with increased physiological reactivity to aversive stimuli and reduced habituation of these reactions - has been involved in PTSD symptomatology. However, the heterogeneity of symptom profiles may be coupled with distinct aspects. It was showed that hyperarousal symptoms may be associated with increased neural responsiveness to negative stimuli and difficulties down-regulating emotions, with increased attentional focus to possibly threatening stimuli constantly demonstrated. Conversely, findings suggested that re-experiencing symptoms may be related with effortful suppression of intrusive emotions and thoughts. Moreover, avoidance and numbing may manifest as an overall disengagement from emotional processing with reduced neural responsiveness. To date, popular theoretical models of PTSD and psychophysiological research have mainly focused on the inhibition system - fear learning, maintenance, and extinction - due to the nature of the disorder’s fear-related symptoms [
15,
27,
28,
29,
30]. Even though less explored, PTSD also involves depressive symptomatology, such as emotional numbing which is related to the reward system. The investigation of the relationship between PTSD and the reward system is not conclusive regarding whether reward system deficits are distinct from negative valence symptoms [
3,
31,
32]. The reward system concerns an aggregate of neural circuitry that process appetitive stimuli - including the limbic system (septal area, thalamus, hypothalamus, amygdala), basal ganglia (containing the ventral and dorsal striatum), prefrontal cortex (ventromedial prefrontal cortex, in particular), ventral tegmental area (VTA), and substantia nigra. This system depends on neurotransmitters including serotonin, dopamine, and norepinephrine. Both opioid and cannabinoid systems are involved [
3,
33]. Some evidence suggests that PTSD might imply hypo-active positive valence system (PVS) (e.g., less neural activation towards rewards), as revealed by defective reward anticipation, diminished approach (reward-seeking) behavior, and reduced hedonic responses to rewards [
27,
34,
35,
36]. Abnormal reward-seeking and risky behaviors are in the PTSD criterion E2. Notably, PTSD is also highly comorbid with substance abuse (e.g.: alcohol, nicotine, cannabis, and opioids). Elevated levels of external reward seeking may be indication of reward system dysfunction in PTSD [
37,
38,
39]. On the other hand, this maladaptive dimension in PTSD could be the consequence of an enhanced responsivity to negative stimuli [
32]. In this perspective, considerable evidence relates this condition to oversensitivity of the negative system, revealing among PTSD individuals increased response to aversive or threatening stimuli [
27,
40], potentially reflecting symptoms of hyperarousal and intrusion (i.e., re-experiencing) [
41]. The role of the neural negative valence system (NVS) in PTSD has been constantly recognized as atypically heightened salience network activation [
42,
43,
44]. PTSD appears to be linked with biased neural valence processing, as indicated by hyper-responsivity to negative aversive stimuli and hypo-responsivity to positive rewarding stimuli [
24,
45,
46]. However, depending on the involved methodologies and paradigms, the relative contribution of emotional processing to the development of PTSD remains mostly unknown [
31,
47] and there is still a need for further research to form a more definite picture [
48]. Properly characterizing PTSD symptoms associated with the reward system, could empower professionals to effectively recognize predictive factors for the disorder, appropriately diagnose it [
49,
50,
51] also developing treatments program that go beyond reversal of fear sustaining the prevention of weak outcomes, such as risk behaviors [
52,
53,
54,
55]. On the other hand, some evidence does support the existence of reward learning deficits in the neural circuits of individuals with PTSD [
27,
56,
57,
58,
59]. Accordingly, addressing these issues may guide research toward a better understanding of mental disorders and their underlying psychological, neural, and biological mechanisms, ultimately leading to improved treatments through the diagnostic specificity, which is essential to develop precise interventions.
With the aim to focus implicit processing abnormalities of affective pictures in PTSD and potential underlying dimensions, we choose as research’s participants immigrants and refugees, as these groups have been frequently exposed to severe potentially traumatic experiences. Among this population, we compared individuals with a probable PTSD with people who had experienced identical events but did not fulfill PTSD criteria. We were able to examine participants having no history of diagnosis and treatment involving psychoactive medication or drug abuse. By comparing these groups, we intended at disentangle between effects related to trauma exposure and those related to the presence of PTSD. We explored these questions: (1) What is the effect of probable PTSD on affective evaluations of positive, negative, and neutral items? (2) What is the effect of trauma-exposure on affective ratings? Firstly, with respect to the presented literature, we suggested that if the disorder involves a numbing, then participants with probable PTSD would show lower valence ratings (i.e., less pleasure affect) and/or larger ratings of arousal/activation (i.e., reduced emotional activation) in response to negative photographs compared with the trauma-exposed individuals.