Published online Apr 19, 2026. doi: 10.5498/wjp.v16.i4.115373
Revised: November 14, 2025
Accepted: December 25, 2025
Published online: April 19, 2026
Processing time: 166 Days and 5 Hours
Cognitive impairment is a well-recognized complication of liver diseases, pri
To characterize cognitive performance and determine the prevalence of deficits across multiple domains in a large cohort of patients with HSS.
This cross-sectional study enrolled 200 adult patients with confirmed HSS at a Brazilian reference center. Participants underwent a comprehensive psychometric battery, including Mini-Mental State Examination for global cognition, the animal verbal fluency test for MHE and semantic fluency, the clock drawing test for visuospatial and executive functions, the digit span test (DST) for attention and working memory, and the Go/no-Go test for inhibitory control. Impairment was defined using es
The cohort had a mean age of 56.4 years and limited formal education (mean 4.9 years). Global cognitive im
Cognitive impairment in HSS is highly prevalent and encompasses a broad range of deficits, extending well beyond MHE. These findings support the implementation of routine, multidimensional cognitive screening in standard management of HSS patients.
Core Tip: Cognitive impairment in hepatosplenic schistosomiasis goes well beyond minimal hepatic encephalopathy, affecting areas such as visuospatial abilities, working memory, and inhibitory control. Our study, using a brief, culturally adapted assessment battery, found over two-thirds of patients impaired in these domains, often independent of portosystemic shunt presence. These findings call for a paradigm shift from solely minimal hepatic encephalopathy-focused screening to comprehensive, multidimensional cognitive assessment in hepatosplenic schistosomiasis, enabling earlier detection and a more holistic approach to management in endemic, low-resource settings.
- Citation: Lucas IC, Filgueira NA, Domingues AL, Lopes EP, Albuquerque IKP, Barbosa BJAP. Multidimensional cognitive impairment in hepatosplenic schistosomiasis: A cross-sectional study. World J Psychiatry 2026; 16(4): 115373
- URL: https://www.wjgnet.com/2220-3206/full/v16/i4/115373.htm
- DOI: https://dx.doi.org/10.5498/wjp.v16.i4.115373
Hepatosplenic schistosomiasis (HSS) is a prominent cause of non-cirrhotic portal hypertension (NCPH), characterized by periportal fibrosis and the frequent development of portosystemic shunts (PSS)[1,2]. Although gastrointestinal bleeding is a well-documented complication that can lead to hepatic encephalopathy (HE), the neurocognitive sequelae remain critically underexplored and warrant further investigation[3].
HE, particularly its minimal HE (MHE), is increasingly recognized in NCPH, including HSS, where PSS facilitate the systemic circulation of neurotoxins[4,5]. However, the cognitive profile in HSS likely extends beyond the traditional attentional and psychomotor deficits associated with MHE. Executive dysfunction, affecting working memory, cognitive flexibility, inhibitory control, and visuospatial planning, is a core feature of HE-related cognitive decline[6-8]. These impairments significantly affect daily functioning, medication adherence, and quality of life, yet they are rarely assessed systematically in HSS cohorts[9].
Emerging evidence indicates that the pathophysiology of cognitive impairment in schistosomiasis is multifactorial. In addition to the effects of portal hypertension, systemic inflammation and neuroinflammatory pathways triggered by chronic Schistosoma mansoni infection have been implicated in neurodegeneration and cognitive deficits, as demonstrated in experimental models[10]. This hypothesis is supported by clinical evidence. A systematic review by Ezeamama et al[11] reported that schistosome infection was associated with deficits in learning and memory among school-aged children, highlighting the broader cognitive impact of this neglected tropical disease beyond hepatic complications. This collective evidence suggests the existence of a distinct and wider cognitive phenotype in HSS that may not solely depend on the presence of overt PSS.
While portosystemic shunting of neurotoxins, such as ammonia, is central to the pathophysiology of HE and MHE[12], the cognitive profile in HSS may involve complementary mechanisms. Chronic Schistosoma mansoni infection is characterized by persistent immune activation and systemic inflammation. Experimental models indicate that this chronic inflammatory state can induce neuroinflammation, possibly mediated by circulating pro-inflammatory cytokines that disrupt the blood-brain barrier and impair neuronal function independently of ammonia levels[10]. Furthermore, longstanding portal hypertension may lead to alterations in cerebral blood flow and subtle metabolic changes, further contributing to cognitive dysfunction[13]. Consequently, cognitive deficits in HSS are likely multifactorial, resulting from a combination of shunt-dependent and shunt-independent pathways.
Assessing these multifaceted cognitive deficits in resource-limited, endemic settings poses significant challenges. While tools like the animal naming test are valuable for MHE screening[14], a comprehensive evaluation requires a battery of tests that are sensitive to various cognitive domains. Brief, culturally appropriate instruments, such as the clock drawing test (CDT), digit span test (DST), and Go/No-Go test, provide critical insights into executive functions, working memory, and inhibitory control[15]. However, their combined application in HSS populations remains limited[16]. Therefore, a critical gap remains in characterizing the full spectrum of cognitive impairment in adults with HSS. Most existing studies focus exclusively on MHE or on pediatric populations[10,11], leaving the complex neurocognitive profile in adults poorly defined. This study aimed to conduct a comprehensive cognitive assessment in a large cohort of adult patients with HSS, using a brief culturally appropriate psychometric battery to evaluate the prevalence and characteristics of cognitive deficits across multiple domains, including global cognition, executive functions, working memory, and visuospatial abilities.
This cross-sectional study enrolled 200 adult HSS patients from the reference schistosomiasis outpatient clinic at Hospital das Clínicas, Universidade Federal de Pernambuco, Brazil, between 2021 and 2023. The primary objective was to characterize the multidimensional cognitive profile of this population.
The study cohort was drawn from our previous prevalence study to ensure diagnostic consistency. Inclusion criteria comprised a confirmed diagnosis of HSS, an age between 18 years and 75 years, ultrasonographic evidence of periportal fibrosis classified as Niamey patterns D, E, or F, and signs of portal hypertension. To minimize confounding factors, we implemented strict exclusion criteria, as previously detailed. Participants were comprehensively screened for comorbid liver diseases (such as cirrhosis and viral hepatitis), recent gastrointestinal bleeding, substantial alcohol consumption, and other factors known to affect cognitive function regardless of HSS. These included pre-existing cognitive impairment [Mini-Mental State Examination (MMSE) < 17], significant psychiatric symptoms [Hospital Anxiety and Depression Scale (HADS) > 10], use of psychoactive medications, and metabolic or infectious disorders that could affect cognitive outcomes.
All participants underwent a thorough clinical interview and a comprehensive psychometric evaluation. This evaluation centered on a battery of tests specifically chosen for their sensitivity to cognitive domains most affected in HE and for their suitability for populations with diverse educational backgrounds.
Global cognitive screening: The Brazilian version of the MMSE was used as a general cognitive screen. A score below 25 was an indicator of global cognitive impairment[17,18].
Executive function and semantic fluency: The animal verbal fluency test (AVFT) assessed semantic memory and executive control. Performance was categorized using education-adjusted cut-offs: A score of ≤ 10 for individuals with ≤ 8 years of formal education and ≤ 15 for those with > 8 years of formal education to identify MHE[14].
Visuospatial and executive abilities: The CDT evaluated visuoconstructional abilities, planning, and executive functions[19]. Performance was scored according to a standardized protocol, and a score below 3 indicated clinically significant impairment in visuospatial execution and planning.
Working memory and attention: The DST from the Wechsler Adult Intelligence Scale-Third Edition was administered both forward (attention) and backward (working memory) tasks[20]. Impairment was defined by scores below normative thresholds: ≤ 6 for forward and ≤ 3 for backward sequences.
Inhibitory control and motor impulsivity: Abnormal performance on the Go/No-Go test was determined by the number of commission errors (incorrect responses on “No-Go” trials). A performance above the defined error threshold of 2 or more errors was classified as impaired, reflecting poorer inhibitory control[21]. Additional assessments included the HADS to screen for mood disorders, with significant psychiatric symptoms serving as exclusion criteria. Sociodemographic data, such as age, sex, and years of formal education, were systematically collected[22].
Data from a pilot study of 40 patients, which allowed for the estimation of MHE prevalence, served as the basis for the sample size determination. Therefore, a minimum of 196 subjects was needed to achieve 80% statistical power with a 95% confidence interval.
The primary analytical approach of this study involved internal comparisons within the HSS cohort to evaluate specific pathophysiological hypotheses. While the diagnosis of cognitive impairment in each domain was defined using established, education-adjusted cut-off scores outlined above, our key analysis compared cognitive performance between patients with and without PSS. This design enabled us to investigate the role of shunt-dependent mechanisms in driving the cognitive deficits in HSS, by comparing patients with PSS to those without PSS within the cohort, effectively using the latter as an internal control group for this analysis.
Data analysis was performed using R software (version 3.3.1). Descriptive statistics summarized the demographic and clinical characteristics of the sample. The prevalence of impairment in each cognitive test was expressed as a proportion. Comparisons between patients with and without PSS across various cognitive domains were conducted using student’s t-test, the Mann-Whitney U test, or the χ2 test, as appropriate. All P value tests were two-sided, with a threshold of < 0.05 denoting statistical significance.
The study protocol was approved by the Institutional Ethics Committee (CAAE: 49847321.1.0000.8807; approval No. 4.958.385). All participants provided written informed consent prior to enrollment, in accordance with the principles outlined in the Declaration of Helsinki.
A total of 200 patients with HSS were enrolled in this cognitive profiling study. The cohort’s demographic and clinical characteristics are summarized in Table 1. The population was predominantly middle-aged, with a mean age of 56.44 (± 13.31) years, slightly more than half were female (53.0%), and the majority were self-identified as black (74.0%). Educational levels were notably low, with an average of 4.88 (± 3.47) years of schooling; half of the participants had between 1 year and 4 years of education. Clinically, 63.5% reported a history of upper gastrointestinal bleeding, and 47.0% had undergone splenectomy. The mean HADS was 7.88 (± 6.16).
| Variables | n (%)/mean ± SD |
| Average age (years) | 56.44 ± 13.31 |
| Gender | |
| Female | 106 (53.00) |
| Male | 94 (47.00) |
| Self-reported ethnicity | |
| Black | 148 (74.00) |
| White | 52 (26.00) |
| Average education (years) | 4.88 ± 3.47 |
| Education level | |
| 1 year to 4 years | 100 (50.00) |
| 5 years to 8 years | 48 (24.00) |
| 9 years to 12 years | 35 (17.50) |
| History of UGIB | 127 (63.50) |
| Previous splenectomy | 94 (47.00) |
| Average score on the HADS questionnaire | 7.88 ± 6.16 |
| Frequency of MMSE below 25 | 73 (36.50) |
Cognitive assessment revealed a high prevalence of deficits across multiple domains. Global cognitive impairment, defined by an MMSE score < 25, was observed in 36.5% (n = 73) of patients. The application of domain-specific tests uncovered more nuanced deficits: (1) Executive/semantic fluency: The AVFT identified 24.5% (n = 49) of participants with results consistent with MHE; (2) Visuospatial/executive function: The CDT revealed deficits in 67% (n = 134) of the cohort, making it the most common impairment; (3) Working memory: The DST revealed impairments in 53.5% (n = 107) of patients on the forward task (attention) and in 83% (n = 166) on the backward task (working memory); and (4) Inhibitory control: Abnormal performance on the Go/No-Go test indicated deficits in motor impulsivity and selective attention in 66.5% (n = 133) of the participants.
We investigated whether the presence of PSS was associated with performance across the different cognitive tests (Table 2). A significant association was found with the AVFT; 35.1% of patients with PSS tested positive for MHE, compared to 15.1% of those without PSS (P = 0.0018). In contrast, no significant associations were observed between PSS status and performance on the MMSE, CDT, DST (forward and backward), or Go/No-Go test. The prevalence of deficits in these domains remained high and consistent between groups with and without PSS.
| Variable | With PSS (n = 94) | Without PSS (n = 106) | Total | P value |
| MMSE1 | 34 (36.17) | 39 (36.79) | 73 (36.5) | 1.00 |
| Abnormal clock drawing test2 | 62 (65.95) | 72 (67.92) | 134 (67) | 0.88 |
| Go-No Go test | ||||
| 0 | 23 (24.46) | 27 (25.47) | 50 (25) | |
| 1 | 7 (7.44) | 10 (9.43) | 17 (8.5) | 0.16 |
| 2 | 9 (9.57) | 26 (24.52) | 39 (19.5) | |
| 3 | 17 (18.08) | 43 (40.56) | 94 (47) | |
| Go-No Go test | 1.97 ± 1.26 | 1.80 ± 1.22 | 1.88 ± 1.24 | 0.317 |
| Abnormal forward digit span test3 | 54 (57.44) | 63 (59.43) | 107 (53.5) | 0.888 |
| Abnormal backward digit span test4 | 78 (82.97) | 88 (83.01) | 166 (83) | 1.00 |
| Abnormal animal verbal fluency test | 33 (35.1) | 16 (15.1) | 49 (24.5) | 0.0018 |
The most striking finding of this study was the widespread nature of cognitive deficits. While the AVFT identified MHE in a quarter of the cohort, consistent with other forms of NCPH[23,24], the CDT and DST revealed impairments in over two-thirds of patients. This suggests that the cognitive burden of HSS is substantially underestimated when evaluations are limited to tools such as clinical evaluation. The high prevalence of visuospatial/planning deficits (CDT) and working memory impairments (DST) indicates significant disruption of fronto-parietal networks, which are critical for complex daily activities and are known to be vulnerable in HE[25,26].
A pivotal insight is the domain-specific association with PSS. The strong link between PSS and positive AVFT aligns with the well-documented role of shunts in MHE pathogenesis, as they allow neurotoxins like ammonia to bypass the liver[27]. However, the absence of significant links between PSS and deficits in the CDT, DST, or the Go/No-Go test suggests that additional pathophysiological mechanisms contribute to cognitive dysfunction. This dissociation supports a dual-hit model of cognitive impairment in HSS: One component is strongly shunt-dependent (reflected by MHE on AVFT), while alternative mechanisms may underlie the broader spectrum of executive and memory deficits.
The dissociation between PSS status and performance on tests of visuospatial abilities, working memory, and inhibitory control suggests that the cognitive burden in HSS extends beyond the classical ammonia-mediated pathway. This finding implies the contribution of alternative pathophysiological mechanisms. One plausible explanation is chronic, low-grade systemic inflammation driven by persistent Schistosoma mansoni infection. Elevated levels of pro-inflammatory cytokines, which have been documented in schistosomiasis[28], may promote neuroinflammation by compromising the blood-brain barrier and directly affecting synaptic plasticity in brain regions critical for executive functions and memory[29,30]. This cytokine-mediated neuroinflammation could underpin the widespread cognitive deficits observed, regardless of shunt presence.
Additionally, long-standing portal hypertension may contribute to cognitive impairment through mechanisms independent of shunting. Chronic reductions in cerebral perfusion due to structural vascular damage and loss of vascular autoregulation in HE pathophysiology[31] could lead to cerebral hypoxia and diffuse subcortical injury, manifested as deficits in processing speed, attention, and executive control[32]. This is consistent with our findings of significant impairment in the CDT and DST, which rely on intact fronto-parietal networks that are vulnerable to vascular and metabolic insults.
The pattern of cognitive impairment observed in HSS shows notable similarities with other chronic conditions, providing a broader context for our findings. Like patients with cirrhosis of various etiologies, individuals with HSS exhibit significant executive dysfunction and working memory deficits. However, the distinct physiology of NCPH in HSS likely influences the specific expression of this cognitive profile. Furthermore, the inflammatory dimension of cognitive impairment in HSS bears resemblance to the “brain fog” described in other chronic inflammatory states, such as hepatitis C infection[33], and shares features with human immunodeficiency virus-associated neurocognitive disorders, which are characterized by executive dysfunction and memory impairment[34]. In all these conditions, systemic inflammation is recognized as a key driver of neurocognitive sequelae. This comparative analysis places HSS within an expanding framework of neuro-systemic diseases and suggests that therapeutic knowledge arising from managing cognitive impairment in analogous conditions may offer valuable insights for future intervention strategies in HSS.
Therefore, we propose a dual-hit model for cognitive impairment in HSS. The first component is primarily shunt-dependent, reflected by tests such as the AVFT for MHE. In contrast, a broader and more pervasive component involves executive and visuospatial deficits, potentially driven by chronic neuroinflammation and other consequences of portal hypertension.
The choice of cognitive tests is critical when assessing populations with low educational attainment. While the AVFT has proven robustness and resistance to educational bias for MHE screening[14], our study demonstrates that other brief instruments, such as the CDT and Go/No-Go test, are equally feasible and valuable. These tools, which minimize reliance on literacy and formal education, uncovered a high prevalence of deficits that would likely be overlooked by more complex batteries. Their adoption is well-supported for implementation in resource-limited settings[35,36].
This study has some limitations. The absence of comprehensive neuroimaging prevents the exclusion of other intracranial pathologies and limits detailed characterization of PSS. Additionally, while our cognitive battery was designed for practicality, it does not provide the depth of a comprehensive neuropsychological assessment. The cross-sectional nature of the study also restricts conclusions regarding the temporal progression of these cognitive deficits. Nonetheless, the study’s strengths include a substantial and well-characterized cohort of patients with a neglected disease. It also applied a pragmatic, multi-domain cognitive battery specifically tailored for a low-education population, which provides a novel and clinically relevant overview of the cognitive profile in HSS.
Our results support a paradigm shift in HSS management, from focusing on screening solely for MHE to adopting a more comprehensive cognitive assessment. We suggest that a brief battery, including AVFT, CDT, and a working memory test, could markedly improve the detection of clinically significant cognitive impairment. Future research should employ longitudinal designs to track cognitive decline, incorporate advanced imaging techniques to identify the structural and functional brain changes underlying these deficits, and explore tailored interventions focusing on this unique patient population, from ammonia-lowering strategies to cognitive rehabilitation.
In conclusion, cognitive impairment in HSS is highly prevalent and encompasses multiple domains. The cognitive profile extends beyond MHE to include widespread deficits in visuospatial abilities, working memory, and inhibitory control, which seem to be partially independent of PSS presence. The use of a brief culturally adapted cognitive battery is both feasible and essential for accurately assessing and addressing the significant neurocognitive burden borne by patients with this neglected tropical disease.
The authors extend their deepest gratitude to all the patients who generously participated in this study. Their willingness to contribute their time and experiences was fundamental to the success of this research. We hope that our findings may contribute to the improved care and quality of life for individuals living with HSS.
| 1. | Veiga ZST, Fernandes FF, Guimarães L, Piedade J, Pereira GHS. Natural History of Hepatosplenic Schistosomiasis (HSS) Non-Cirrhotic Portal Hypertension (NCPH): Influence of Gastrointestinal Bleeding and Decompensation in Prognosis. Trop Med Infect Dis. 2023;8:145. [PubMed] [DOI] [Full Text] |
| 2. | Hudson D, Cançado GGL, Afzaal T, Malhi G, Theiventhiran S, Arab JP. Schistosomiasis: Hepatosplenic Disease and Portal Hypertensive Complications. Curr Hepatology Rep. 2023;22:170-181. [DOI] [Full Text] |
| 3. | Ross AG, Bartley PB, Sleigh AC, Olds GR, Li Y, Williams GM, McManus DP. Schistosomiasis. N Engl J Med. 2002;346:1212-1220. [PubMed] [DOI] [Full Text] |
| 4. | Gioia S, Nardelli S, Ridola L, Riggio O. Causes and Management of Non-cirrhotic Portal Hypertension. Curr Gastroenterol Rep. 2020;22:56. [PubMed] [DOI] [Full Text] |
| 5. | Watanabe A. Portal-systemic encephalopathy in non-cirrhotic patients: classification of clinical types, diagnosis and treatment. J Gastroenterol Hepatol. 2000;15:969-979. [PubMed] [DOI] [Full Text] |
| 6. | Tsai CF, Tu PC, Wang YP, Chu CJ, Huang YH, Lin HC, Hou MC, Lee FY, Liu PY, Lu CL. Altered cognitive control network is related to psychometric and biochemical profiles in covert hepatic encephalopathy. Sci Rep. 2019;9:6580. [PubMed] [DOI] [Full Text] |
| 7. | Amodio P, Schiff S, Del Piccolo F, Mapelli D, Gatta A, Umiltà C. Attention dysfunction in cirrhotic patients: an inquiry on the role of executive control, attention orienting and focusing. Metab Brain Dis. 2005;20:115-127. [PubMed] [DOI] [Full Text] |
| 8. | Yang ZT, Chen HJ, Chen QF, Lin H. Disrupted Brain Intrinsic Networks and Executive Dysfunction in Cirrhotic Patients without Overt Hepatic Encephalopathy. Front Neurol. 2018;9:14. [PubMed] [DOI] [Full Text] |
| 9. | Mina A, Moran S, Ortiz-Olvera N, Mera R, Uribe M. Prevalence of minimal hepatic encephalopathy and quality of life in patients with decompensated cirrhosis. Hepatol Res. 2014;44:E92-E99. [PubMed] [DOI] [Full Text] |
| 10. | Gasparotto J, Senger MR, Telles de Sá Moreira E, Brum PO, Carazza Kessler FG, Peixoto DO, Panzenhagen AC, Ong LK, Campos Soares M, Reis PA, Schirato GV, Góes Valente WC, Araújo Montoya BO, Silva FP, Fonseca Moreira JC, Dal-Pizzol F, Castro-Faria-Neto HC, Gelain DP. Neurological impairment caused by Schistosoma mansoni systemic infection exhibits early features of idiopathic neurodegenerative disease. J Biol Chem. 2021;297:100979. [PubMed] [DOI] [Full Text] |
| 11. | Ezeamama AE, Bustinduy AL, Nkwata AK, Martinez L, Pabalan N, Boivin MJ, King CH. Cognitive deficits and educational loss in children with schistosome infection-A systematic review and meta-analysis. PLoS Negl Trop Dis. 2018;12:e0005524. [PubMed] [DOI] [Full Text] |
| 12. | Chen A, Tait C, Minacapelli C, Rustgi V. Pathophysiology of Hepatic Encephalopathy: A Framework for Clinicians. Clin Liver Dis. 2024;28:209-224. [PubMed] [DOI] [Full Text] |
| 13. | Guevara M, Bru C, Ginès P, Fernández-Esparrach G, Sort P, Bataller R, Jiménez W, Arroyo V, Rodés. Increased cerebrovascular resistance in cirrhotic patients with ascites. Hepatology. 1998;28:39-44. [PubMed] [DOI] [Full Text] |
| 14. | Campagna F, Montagnese S, Ridola L, Senzolo M, Schiff S, De Rui M, Pasquale C, Nardelli S, Pentassuglio I, Merkel C, Angeli P, Riggio O, Amodio P. The animal naming test: An easy tool for the assessment of hepatic encephalopathy. Hepatology. 2017;66:198-208. [PubMed] [DOI] [Full Text] |
| 15. | Ryu HJ, Yang DW. The Seoul Neuropsychological Screening Battery (SNSB) for Comprehensive Neuropsychological Assessment. Dement Neurocogn Disord. 2023;22:1-15. [PubMed] [DOI] [Full Text] |
| 16. | Kasambala M, Mukaratirwa S, Vengesai A, Mduluza-Jokonya T, Jokonya L, Midzi H, Makota RB, Mutemeri A, Maziti E, Dube-Marimbe B, Chibanda D, Mutapi F, Mduluza T. The association of systemic inflammation and cognitive functions of pre-school aged children residing in a Schistosoma haematobium endemic area in Zimbabwe. Front Immunol. 2023;14:1139912. [PubMed] [DOI] [Full Text] |
| 17. | Bertolucci PH, Brucki SM, Campacci SR, Juliano Y. O Mini-Exame do Estado Mental em uma população geral: impacto da escolaridade. Arq Neuropsiquiatr. 1994;52:1-7. [DOI] [Full Text] |
| 18. | Brucki SM, Nitrini R, Caramelli P, Bertolucci PH, Okamoto IH. [Suggestions for utilization of the mini-mental state examination in Brazil]. Arq Neuropsiquiatr. 2003;61:777-781. [PubMed] [DOI] [Full Text] |
| 19. | Atalaia-Silva KC, Lourenço RA. Translation, adaptation and construct validation of the Clock Test among elderly in Brazil. Rev Saude Publica. 2008;42:930-937. [PubMed] [DOI] [Full Text] |
| 20. | Figueiredo VLMD, Nascimento ED. Desempenhos nas duas tarefas do subteste dígitos do WISC-III e do WAIS-III. Psic: Teor e Pesq. 2007;23:313-318. [DOI] [Full Text] |
| 21. | Bari A, Robbins TW. Inhibition and impulsivity: behavioral and neural basis of response control. Prog Neurobiol. 2013;108:44-79. [PubMed] [DOI] [Full Text] |
| 22. | Botega NJ, Bio MR, Zomignani MA, Garcia C Jr, Pereira WA. [Mood disorders among inpatients in ambulatory and validation of the anxiety and depression scale HAD]. Rev Saude Publica. 1995;29:355-363. [PubMed] [DOI] [Full Text] |
| 23. | Nicoletti V, Gioia S, Lucatelli P, Nardelli S, Pasquale C, Nogas Sobrinho S, Pentassuglio I, Greco F, De Santis A, Merli M, Riggio O. Hepatic encephalopathy in patients with non-cirrhotic portal hypertension: Description, prevalence and risk factors. Dig Liver Dis. 2016;48:1072-1077. [PubMed] [DOI] [Full Text] |
| 24. | Mohan P, Venkataraman J. Minimal hepatic encephalopathy in noncirrhotic portal hypertension. Eur J Gastroenterol Hepatol. 2011;23:194-195. [PubMed] [DOI] [Full Text] |
| 25. | D'Antiga L, Dacchille P, Boniver C, Poledri S, Schiff S, Zancan L, Amodio P. Clues for minimal hepatic encephalopathy in children with noncirrhotic portal hypertension. J Pediatr Gastroenterol Nutr. 2014;59:689-694. [PubMed] [DOI] [Full Text] |
| 26. | Lövdén M, Fratiglioni L, Glymour MM, Lindenberger U, Tucker-Drob EM. Education and Cognitive Functioning Across the Life Span. Psychol Sci Public Interest. 2020;21:6-41. [PubMed] [DOI] [Full Text] |
| 27. | Aneja P, Kinna T, Newman J, Sami S, Cassidy J, McCarthy J, Tiwari M, Kumar A, Spencer JP. Leveraging technological advances to assess dyadic visual cognition during infancy in high- and low-resource settings. Front Psychol. 2024;15:1376552. [PubMed] [DOI] [Full Text] |
| 28. | Masamba P, Kappo AP. Immunological and Biochemical Interplay between Cytokines, Oxidative Stress and Schistosomiasis. Int J Mol Sci. 2021;22:7216. [PubMed] [DOI] [Full Text] |
| 29. | Bourgognon JM, Cavanagh J. The role of cytokines in modulating learning and memory and brain plasticity. Brain Neurosci Adv. 2020;4:2398212820979802. [PubMed] [DOI] [Full Text] |
| 30. | Blossom V, Ullal SD, D'Souza MM, Ranade AV, Kumar NA, Rai R. Implicating neuroinflammation in hippocampus, prefrontal cortex and amygdala with cognitive deficit: a narrative review. 3 Biotech. 2025;15:320. [PubMed] [DOI] [Full Text] |
| 31. | Macías-Rodríguez RU, Duarte-Rojo A, Cantú-Brito C, Sauerbruch T, Ruiz-Margáin A, Trebicka J, Green-Gómez M, Díaz Ramírez JB, Sierra Beltrán M, Uribe-Esquivel M, Torre A. Cerebral haemodynamics in cirrhotic patients with hepatic encephalopathy. Liver Int. 2015;35:344-352. [PubMed] [DOI] [Full Text] |
| 32. | Wang X, Cui L, Ji X. Cognitive impairment caused by hypoxia: from clinical evidences to molecular mechanisms. Metab Brain Dis. 2022;37:51-66. [PubMed] [DOI] [Full Text] |
| 33. | Senzolo M, Schiff S, D'Aloiso CM, Crivellin C, Cholongitas E, Burra P, Montagnese S. Neuropsychological alterations in hepatitis C infection: the role of inflammation. World J Gastroenterol. 2011;17:3369-3374. [PubMed] [DOI] [Full Text] |
| 34. | Saylor D, Dickens AM, Sacktor N, Haughey N, Slusher B, Pletnikov M, Mankowski JL, Brown A, Volsky DJ, McArthur JC. HIV-associated neurocognitive disorder--pathogenesis and prospects for treatment. Nat Rev Neurol. 2016;12:234-248. [PubMed] [DOI] [Full Text] |
| 35. | Paddick SM, Yoseph M, Gray WK, Andrea D, Barber R, Colgan A, Dotchin C, Urasa S, Kissima J, Haule I, Kisoli A, Rogathi J, Safic S, Mushi D, Robinson L, Walker RW. Effectiveness of App-Based Cognitive Screening for Dementia by Lay Health Workers in Low Resource Settings. A Validation and Feasibility Study in Rural Tanzania. J Geriatr Psychiatry Neurol. 2021;34:613-621. [PubMed] [DOI] [Full Text] |
| 36. | Williams ME, Corn EA, Martinez Ransanz S, Berl MM, Andringa-Seed R, Mulkey SB. Neurodevelopmental assessments used to measure preschoolers' cognitive development in Latin America: a systematic review. J Pediatr Psychol. 2024;49:321-339. [PubMed] [DOI] [Full Text] |