Introduction
Psychotic disorders typically have their onset in adolescence and early adulthood, with the peak of the risk occurring between the ages of 12 and 25 years [
1]. After the onset of the disorder, it is challenging to improve its course and lead the patient to complete recovery [
2,
3]. Therefore, prevention of psychosis and early intervention are promising paths for improving outcomes [
4]. In light of the above, in the last twenty years, attention to prevention has focused on the clinical-high risk for psychosis (CHR-P) population. CHR-P population includes three subgroups: Attenuated psychotic Syndrome (APS), Brief intermittent psychotic symptoms (BLIPS), and Genetic risk and Deterioration Syndrome (GRD) [
5]. Several studies have highlighted the importance of detection, prognosis, and interventions for CHR-P individuals and the formulation of updated recommendations, mainly because detection of CHR-P individuals is based on patients’ referral, and symptoms may remain undetected for a long time [
6]. So, childhood and adolescence represent a critical developmental window where opportunities to gain social and adaptive abilities depend on the individuals' neurocognitive performance [
1]. Therefore, early intervention and particularly preventive approaches in young people with subtle signs and symptoms of the psychotic disorder (termed ‘primary indicated prevention’ [
4,
7]) have the potential to benefit the lives of many young people.
Although the CHR-P prevention paradigm is particularly promising, especially in young people, empirical challenges arise [
8]. Researchers stated that neurocognition could be a biomarker that may help professionals distinguish CHR-P from health controls (HC) and could help determine the risk of transition to psychosis. In this connection, a recent meta-analysis [
9] comparing a total of 78 independent studies with 5162 CHR-P individuals and 2865 HC described that the first group showed medium to large deficits in the studied neurocognitive domains. Moreover, CHR-P people were less impaired than individuals with a first episode of psychosis. Knowing the global functioning and performance trends of CHR-P patients on neuropsychological tests can also help clinicians intervene early to reduce the risk of transition to psychosis, which is currently relevant in the adolescent population [
10,
11].
Despite this recent work, there is not much evidence that synthesizes current knowledge about neurocognitive functioning in adolescent individuals [
12‐
17], specifically about longitudinal changes across time in this population [
13,
17]. Moreover, as shown in the metanalysis [
9], studies in adolescence show different results because of different tasks used, non-homogeneous samples, or severe comorbid disorders [
8,
17]. Indeed, it is crucial to find biological and psychological markers of transition to psychosis to help clinicians detect psychotic symptoms, prevent psychotic disorders, and formulate a prognosis to offer the most appropriate interventions. Overall, the empirical literature on the neurocognitive performance of children and adolescents is poorer in comparison with the one on young adults, so there is a gap in the literature.
In light of that, this study aimed to identify differences in neurocognitive functioning and overall functioning in three groups of adolescent patients divided according to their emerging psychopathology ascertained through the semi-structured interview Comprehensive Assessment of At-Risk Mental States (CAARMS) criteria [
18]: i) Psychosis, ii) CHR-P, and iii) non-CHR-P.
We expected to find worse performance in neurocognitive tasks and lower functioning in the psychosis group, moderate deficits in the CHR-P group, and average performances and adequate global functioning in the non-CHR-P group.
Results
Participants
The sample comprised 116 adolescents aged between 12 and 17 years old. Figure
1 shows the study population flowchart.
Considering the whole sample, 26 adolescents (22.4%) came from low socio-economic status (SES) families, 26 (22.4%) came from low-to-medium–low SES families, 36 adolescents (31.0%) from medium SES families, 18 (15.5%) from medium-to-high SES families, and 6 (5.2%) from high SES families.
At baseline, 19 out of 116 (16.4%) met the CAARMS criteria for psychosis, 47 (40.5%) met the criteria for CHR-P, and 50 (43.1%) met neither criterion. Table
1 shows sociodemographic information and family history of psychiatric disorders in the total sample and the three subgroups.
Table 1
Sociodemographic data and family history of psychiatric disorders in the total sample and the three subgroups
Sociodemographic |
Age, mean (SD), y | 15.27 (1.56) | 15.4 (1.60) | 15.3 (1.46) | 14.85 (1.72) | 0.497 |
Sex, female, n (%) | 76 (65.0) | 34 (68) | 32 (68.1) | 10 (52.6) | 0.492 |
Ethnicity, n (%) | 0.292 |
Italian | 93 (80.2) | 38 (76) | 37 (78.7) | 18 (94.7) | |
Hispanic | 1 (0.9) | 1 (2.0) | 0 (0) | 0 (0.0) | |
Eastern European | 7 (6.0) | 4 (80) | 3 (6.4) | 1(5.3) | |
African | 3(2.6) | 0 (0.0) | 2 (4.3) | 1 (5.3) | |
Other | 9 (7.8) | 6 (12) | 3 (6.4) | 0 (0.0) | |
Socio Economic Status, median (IQR25, 75) | 30.75 (19.6, 38.9) | 30.25 (20.2, 39.0) | 30.0 (17.5, 38.7) | 32 (22.0, 37.0) | 0.789 |
Adopted, n (%) | 5 (4.3) | 3 (6.0) | 2 (4.3) | 0 (0.0) | 0.842 |
Separated-divorced parents, n (%) | 41 (35.3) | 21 (42.0) | 16 (34.0) | 4 (21.1) | 0.242 |
Family history of any DSM-5 psychiatric disorders, n (%) |
None | 39 (33.6) | 15 (30.0) | 19 (40.4) | 5 (26.3) | 0.394 |
Psychosis | 11 (9.5) | 3 (6) | 3 (8.5) | 4 (21.1) | 0.248 |
first degree | 2 (1.7) | 0 (0) | 1 (2.1) | 1 (5.3) | |
second degree | 9 (7.8) | 3 (6) | 3 (6.4) | 3 (15.8) | |
Depression | 39 (23.6) | 16 (32.0) | 14 (29.8) | 9 (47.4) | 0.747 |
first degree | 21 (18.1) | 9 (18.0) | 7 (14.9) | 5 (26.3) | |
second degree | 18 (15.5) | 7 (14.0) | 7 (14.9) | 4 (21.1) | |
Anxiety | 24 (20.7) | 11 (22.0) | 10 (21.2) | 3 (15.8) | 0.364 |
first degree | 17 (14.7) | 7 (14.0) | 9 (19.1) | 1 (5.3) | |
second degree | 7 (6.0) | 4 (8.0) | 1 (2.1) | 2 (10.5) | |
Substance abuse | 10 (9.0) | 3 (6.0) | 5 (10.6) | 2 (10.6) | 0.619 |
first degree | 19 (8.0) | 3 (6.0) | 4 (8.5) | 1 (5.3) | |
second degree | 8 (6.9) | 0 (0.0) | 1 (2.1) | 1 (5.3) | |
Disruptive disorder | 3 (2.6) | 1 (2.0) | 1 (2.1) | 1 (5.3) | 0.368 |
first degree | 1 (0.9) | 0 (0.0) | 1 (2.1) | 0 (0.0) | |
second degree | 2 (1.7) | 1 (2.0) | 0 (0.0) | 1 (5.3) | |
Eating disorder | 3 (2.6) | 2 (4.0) | 1 (2.1) | 0 (0.0) | 1.00 |
first degree | 2 (1.7) | 1 (2.0) | 1 (2.1) | 0 (0.0) | |
second degree | 1 (0.9) | 1 (2.0) | 0 (0.0) | 0 (0.0) | |
Other | 20 (25.9) | 12 (24.0) | 12 (25.5) | 6 (29.6) | 0.617 |
first degree | 8 (6.9) | 3 (6.0) | 4 (8.5) | 1 (5.3) | |
second degree | 22 (19.0) | 9 (18.0) | 8 (17.0) | 5 (26.3) | |
Table
2 shows patients’ history of psychiatric disorders, psychopathology, global functioning, and baseline exposure to psychiatric treatments in the sample and the subgroups. Additional file
2: Table S1 shows post-hoc analyses.
Table 2
Personal history of psychiatric disorders, psychopathology, functioning, baseline exposure to psychiatric treatments in the whole sample and subgroups
Personal history of any DSM-5 psychiatric disorder |
Number of DSM-5 diagnoses, mean ± SD | 1.62 ± 1.4 | 1.5 ± 0.6 | 1.8 ± 0.7 | 1.4 ± 0.7 | .039* |
Number of diagnoses ≥ 3, n(%) | 9(7.8) | 2(4.0) | 6(12.8) | 1(5.3) | 0.247 |
Onset of psychiatric symptoms, months, median (IQR25,75) | 18.0(8.0,48.0) | 21.0(8.0, 60.0) | 18.0(8.0, 48.0) | 18.0(9.0, 48.0) | 0.94 |
Type of DSM-5 diagnoses, n(%) |
Depressive disorders | 43(37.1) | 18(36.0) | 21(44.7) | 4(21.1) | 0.155 |
Anxiety disorders | 28(24.1) | 13(26.0) | 13(27.7) | 2(10.5) | 0.273 |
Personality disorders | 25(21.6) | 9(18.0) | 15(31.9) | 1(5.3) | .035* |
Disruptive, impulse-control, and conduct disorders | 7(6.0) | 3(6.0) | 2(4.3) | 2(10.5) | 0.656 |
Eating disorders | 15(12.9) | 6(12.0) | 8(17.0) | 1(5.3) | 0.394 |
Bipolar symptoms | 6(5.2) | 0.0(0.0) | 6(12.8) | 0(0.0) | .009* |
Conversion disorder | 5(4.3) | 2(4.0) | 3(6.4) | 0 (0) | 0.494 |
Obsessive–compulsive and related disorders | 4(3.4) | 1(2.0) | 2(4.3) | 1(5.3) | 0.753 |
Othersa | 26(22.4) | 12(24.0) | 6(12.8) | 8(42.1) | .042* |
Specific psychiatric disorders |
Depressive disorders | | | | | 0.330 |
Major depressive disorder | 15(12.9) | 5(10) | 8(17.0) | 2.0(10.5) | |
Other specified depressive disorder | 25(21.6) | 13(26.0) | 10(21.3) | 2(10.5) | |
Persistent depressive disorder | 2(1.7) | 0(0.0) | 2(4.3) | 0(0.0) | |
Anxiety disorders | | | | | 0.499 |
Generalized anxiety disorder | 5(4.3) | 1(2.0) | 3(6.4) | 1(5.3) | |
Social anxiety disorder | 3(2.6) | 1(2.0) | 1(2.1) | 1(5.3) | |
Other specified anxiety disorder | 11(9.5) | 7(14.0) | 4(8.5) | 0(0) | |
Separation anxiety disorder | 0(0.0) | 0(0.0) | 0(0.0) | 0(0) | |
Panic disorder | 6(5.2) | 2(4.0) | 4(8.5) | 0(0) | |
Personality disorders (PD) | | | | | 0.116 |
Borderline | 11(9.5) | 3(6.0) | 7(14.9) | 1(5.3) | |
Others PDb | 14(12.1) | 6(12.0) | 8(17.0) | 0(0) | |
Eating disorders | | | | | 0.140 |
Anorexia nervosa | 10(8.6) | 2(4.0) | 7(14.9) | 1(5.3) | |
Others (bulimia/binge eating) | 5(4.3) | 4(8.0) | 1(2.1) | 0 (0) | |
Bipolar symptoms | | | | | 0.099 |
Bipolar I or II symptoms | 4(3.4) | 0(0.0) | 4(8.5) | 0(0) | |
Other specified bipolar symptoms | 1(0.9) | 0(0.0) | 1(2.1) | 0(0) | |
Psychosis | | | | | |
Psychosis | 5 (4.31) | 1 (2.0) c | 0 (0) | 4 (21.05) | |
APS | 47 (40.52) | 0 (0) | 47 (100) | 0 (0) | |
Other psychotic disorder | 14 (12.07) | 5 (10.0) | 0 (0) | 9 (47.37) | |
Presence of negative symptoms, n (%) | 90(77.6) | 33(66.0) | 39(83.0) | 18(94.7) | .020* |
CAARMS median (IRQ 25,75) |
P1. Unusual thought content |
Severity | 1.0(0.0,4.0) | 0.0(0.0,0.75) | 2.0(1.0, 4.0) | 5.0(2.0,5.0) | < .001** |
Frequency | 2.0(0.0,4.0) | 0.0 (0.0,0.75) | 3.0(1.5, 4.5) | 5.0(3.0,5.0) | < .001** |
P2. Non-bizarre ideas |
Severity | 2.0(0.0, 4.0) | 0.0(0.0,2.0) | 3.0(2.0, 4.0) | 5.0(5.0,6.0) | < .001** |
Frequency | 3.0(0.0, 5.0) | 0.0(0.0,2.0) | 4.0(1.5, 5.0) | 5.0 (5.0, 6.0) | < .001** |
P3. Perceptual abnormalities |
Severity | 3.0(0.0,4.0) | 0.0(0.0,2.0) | 3.0(2.0,4.0) | 5.0(4.0,5.0) | < .001** |
Frequency | 2.0(0.0,4.0) | 0.0(0.0,1.7) | 3.0(1.0,4.0) | 4.0(3.0,5.0) | < .001** |
P4. Disorganized speech |
Severity | 1.5(0,3.0) | 0.0(0.0,0.7) | 2.0(0.0,3.0) | 3.0 (2.0,5.0) | < .001** |
Frequency | 1.0(0.0,4.0) | 0.0(0.0,1.0) | 3.0(0.0,4.0) | 5.0(3.0,6.0) | < .001** |
Clinical Global Impression-Severity (CGI-S) median (IRQ 25, 75) | 4.0 (3.0, 6.0) | 3.0 (3.0, 4.0) | 5.0 (4.0, 6.0) | 6.0 (6.0, 6.0) | < .001** |
Functioning |
Current SOFAS median (IRQ 25,75) | 51.0 (40.0,60.0) | 60.0 (55.0,70.0) | 50.0 (40.0,53.0) | 32.0 (30.0,41.0) | <.001** |
Current role functioning (GF:R) median (IRQ 25,75) | 5.0 (3.0, 6.0) | 6.0 (5.0,7.0) | 4.0 (3.0,6.0) | 3.0 (2.0,3.0) | < .001** |
Current social functioning (GF:S) median (IRQ 25,75) | 5.0 (3.0,7.0) | 6.0 (5.0,7.75) | 5.0 (3.0,6.0) | 3.0 (2.0,4.0) | < .001** |
Global assessment functioning (CGAS) | 50.0 (40.0,60.0) | 60.0 (51.0,70.0) | 50.0 (41.0,50.0) | 35.0 (30.0,40.0) | < .001** |
Before baseline exposure to psychiatric treatments |
Psychotropic drugs, yes, n (%) | 46 (39.7) | 11 (22.0) | 22 (46.0) | 13 (86.0) | < .001** |
Number of psychotropic drugs, median (min, max) | 0.0 (0.0,4.0) | 0.0 (0.0,3.0) | 0.0 (0.0,4.0) | 1.0 (0.0,3.0) | 0.11 |
Type of psychotropic drugs, n (%) | | | | | |
Antipsychotics | 23 (19.8) | 4 (8.0) | 10 (21.3) | 9 (47.4) | .002* |
Antidepressants | 22 (19.0) | 7 (14.0) | 11 (23.4) | 4 (21.1) | 0.511 |
Benzodiazepines | 23 (19.8) | 3 (6.0) | 13 (27.7) | 7 (36.8) | .005* |
Mood stabilizers | 4.0 (3.4) | 1 (2.0) | 2 (4.3) | 1 (5.3) | 0.765 |
Duration of psychotropic treatment, days, median (IQR 25, 75) | 0.0 (0.0,30.0) | 0.0 (0.0,0.0) | 0.0 (0.0,6.0) | 2.0 (0.0,24.0) | .009* |
Before baseline exposure to psychiatric treatments |
Drugs prescription during baseline, yes, n (%) | 72 (62.1) | 19 (38.0) | 36 (76.6) | 17 (89.5) | < .001** |
Antipsychotics | 41 (35.3) | 7 (14.0) | 18 (38.3) | 16 (84.2) | < .001** |
Antidepressants | 44 (37.9) | 14 (28.0) | 22 (46.8) | 8 (42.1) | 0.168 |
Benzodiazepines | 26 (22.4) | 6 (12.0) | 12 (25.5) | 8 (42.1) | .031* |
Mood stabilizers | 7 (6.0) | 1 (2.0) | 4 (8.5) | 1 (10.5) | 0.291 |
Psychotherapy, yes, n (%) | 51 (44.0) | 20 (40.0) | 23 (48.9) | 8 (42.1) | 0.666 |
Psychotherapy duration, days, median (IQR 25, 75) | 0.0 (0.0,12.0) | 0.0 (0.0,10.0) | 1.0 (0.0, 10.5) | 0.0 (0.0,12.0) | 0.960 |
The three groups (i.e., psychosis, CHR-P, non-CHR-P) did not differ in terms of age H (2) = 1.398, p = 0.49; gender, H (2) = 1.670, p = 0.43; SES, H (2) = 4.796, p = 0.78; or ethnicity, H (2) = 2.822, p = 0.24.
Neurocognition
Table
3 show between-groups comparisons of IQ dimensions, neurocognitive tasks, and post-hoc analyses. Results revealed significant differences in the working memory performance and processing speed subtests of the Wechsler scale between adolescents from psychosis and non-CHR-P groups, showing psychotic adolescents perform worse than the non-CHR-P ones. Focusing on neuropsychological domains, adolescents from the psychosis group significantly differed from the CHR-P and non-CHR-P group in TMT-A, indicating a lower performance, BVN categorical fluency, revealing more inadequate flexibility skills. Psychotic adolescents also had a lower performance in BVN forward and backward verbal digit span and visual attention than Non-CHR-P adolescents and worse performance in Rey–Osterrieth complex figure test than CHR-P adolescents.
Table 3
Comparisons of IQ dimensions and neurocognitive tasks, and post-hoc analyses
Wechsler scale | Full scale IQ | 101.33 | 17.895 | 98.47 | 16.367 | 91.58 | 14.535 | 4.089 | 0.129 | | | |
VCI | 104.02 | 18.503 | 103.62 | 18.184 | 102.26 | 16.931 | 0.425 | 0.809 | | | |
PRI | 103.38 | 17.308 | 104.20 | 16.280 | 98.89 | 15.376 | 1.132 | 0.568 | | | |
WMI | 94.58 | 14.094 | 91.38 | 13.202 | 84.89 | 11.818 | 6.430 | .040* | 0.470 | 0.051 | .012* |
PSI | 98.58 | 16.354 | 93.82 | 15.686 | 82.68 | 15.567 | 10.686 | .005* | 0.177 | .027* | .001** |
TMT | TMT A | 34.87 | 14.385 | 34.71 | 10.509 | 47.89 | 14.476 | 12.679 | .002* | 0.601 | .002* | < .001** |
TMT B | 74.79 | 26.899 | 77.67 | 36.662 | 96.53 | 62.180 | 3.975 | 0.137 | | | |
TMT B-A | 39.88 | 21.825 | 44.78 | 29.460 | 58.32 | 46.386 | 3.216 | 0.200 | | | |
BVN 12–18 | Lexical Denomination | 89.575 | 32.721 | 90.718 | 14.796 | 84.379 | 19.907 | 3.590 | 0.166 | | | |
Forward verbal digit span | 93.929 | 14.038 | 90.673 | 18.895 | 84.311 | 8.365 | 8.394 | .15* | 0.469 | .022* | .004* |
Backward verbal digit span | 99.502 | 17.606 | 93.407 | 12.401 | 89.432 | 13.575 | 6.650 | .036* | 0.164 | 0.146 | .011* |
Corsi Block-tapping test | 99.079 | 17.519 | 92.021 | 21.672 | 90.197 | 19.117 | 3.035 | 0.219 | | | |
Selective auditory | 85.217 | 26.391 | 74.838 | 41.761 | 75.974 | 31.133 | 2.760 | 0.252 | | | |
Visual attention | 109.187 | 14.590 | 107.896 | 14.331 | 93.874 | 28.510 | 7.984 | .018* | 0.469 | .026* | .005* |
Phonemic fluency | 100.604 | 19.661 | 102.031 | 18.224 | 94.689 | 26.958 | 2.937 | 0.230 | | | |
Categorial fluency | 95.542 | 19.110 | 95.584 | 15.670 | 81.768 | 16.946 | 8.714 | .013* | 0.914 | .006* | .007* |
Elithorn perceptual maze | 97.985 | 20.333 | 93.673 | 25.238 | 80.605 | 31.616 | 2.862 | 0.239 | | | |
ROCF | Copy | 32.630 | 4.170 | 32.468 | 3.580 | 30.579 | 4.605 | 4.72 | 0.94 | | | |
Drawing from memory | 22.100 | 6.434 | 22.521 | 6.994 | 17.289 | 6.449 | 8.57 | .014* | 0.753 | .005* | .009* |
Functioning
Results showed the CHR-P group to have a more adaptive functioning (e.g., SOFAS, GF:R, GF:S, and CGAS) than the psychosis group but worse functioning than the non-CHR-P group on all the scales. We also found that the CHR-P group presented a lower CGI-S level than the psychosis group but higher than the non-CHR-P one, as shown in Table
2.
Discussion
This work highlighted significant differences between the three groups of patients in neurocognition and functioning. However, they did not differ in age, gender, socio-economic status, ethnicity, adoption, separated/divorced parents, or history of family psychiatric disorders. Regarding neurocognitive functioning, the CHR-P group performed better than the psychosis group on the working memory and backward verbal digit span tasks, as previous research suggested [
14,
16]. Results in the adult population showed that the CHR-P group could be distinguished from the psychosis group using verbal learning tasks, since the latter group seem to perform worse [
9]. This could be explained because language development is still evolving in adolescents; at this stage of life, they learn to think abstractly and develop the use of pragmatics and semantics. Therefore, language-related difficulties may be more evident in an adult population sample. Moreover, the difference between our data and adults and adolescent-adult samples may be explained by possible biases due to the greater presence of females in our sample that may have created a bias given the higher prevalence of psychotic onset in the male population. Literature states that psychosis typically onsets in adolescence and early adulthood [
1] and much research has highlighted the importance of detection, prognosis, and interventions for improving the outcomes of CHR-P people because it is challenging to lead the patient to complete recovery from psychosis [
2,
3]. Despite childhood and adolescence representing a complex developmental phase studies in this population are few [
12‐
17,
48] as it is challenging to investigate neurocognition in young patients. This is one of the few works that explored this domain.
Furthermore, our data did not show substantial differences in neurocognition between CHR-P and non-CHR-P patients’ performances, maybe because our non-CHR-P sample was composed of patients who presented other psychiatric symptoms without psychotic symptoms and were not healthy controls. Likewise, our results did not match those found among adults between CHR-P patients and healthy controls, which see the CHR-P group performing worse in every neurocognitive task, maybe because the adolescent brain goes through a critical developmental period of increased neural plasticity, unlike adults, and this may also reflect the greater number of comorbidities in our patient sample [
9,
49]. Moreover, as previous literature stated [
50], we should consider adolescents as a more heterogeneous group than adults, and we have to think in terms of a developmental psychopathology perspective, not only to deepen the knowledge of adolescent psychopathology but also to understand developmental processes more generally [
1].
In line with previous literature [
14‐
16], patients in the psychosis group compared to the non-CHR-P group, exhibited significant deficits in working memory, processing speed, forward verbal digit span, backward verbal digit span, visual attention, categorical fluency, executive functions, psychomotor speed, and visuospatial attention and planning tasks.
As for the overall functioning, the CHR-P group exhibited better global functioning, better role and social functioning than the psychosis group, but still worse functioning than the non-CHR-P group [
51]. Moreover, the CHR-P group showed a more significant presence of diagnoses of structuring personality disorder and bipolar symptoms. This group has many diagnoses of eating disorders [
52,
53]. In line with the literature [
16], we found that the psychosis group had a massive presence of severe positive and negative symptoms compared to the other groups and was also the group with the lowest global functioning, the most compromised role and social functioning, and the most severe level of disorder severity based on clinical evaluation.
The study has some limitations. Future studies could consider a larger sample of adolescent patients or even younger participants to study the possibility of increasingly early prevention of developing psychotic symptoms. Furthermore, researchers could select different neuropsychological tests to identify better areas that do not show a significant difference in our population sample (e.g., problem-solving, comprehension tasks, Theory of Mind). Finally, our results could be implemented by including a longitudinal study phase that could document transition rates.
These results examining a population understudied contribute to making the assessment more rigorous, and specific functional and neurocognitive impairments can be a prognostic biomarker in identifying particular groups of patients, even in a developmentally complex period such as adolescence, and recommending the most appropriate course of treatment and preparing, where necessary, prevention pathways, as many studies over the years have pointed out [
9,
17,
54‐
58]. Moreover, given the not consistently overlapping results [
9], this research opens up new studies to standardize the assessment and to better detect the risk of transition to psychosis.
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