Background/Objectives: Mental health problems among university students represent a growing public health concern and are shaped by both psychological and socioeconomic determinants that may act independently and interactively. This systematic review aimed to evaluate the separate and combined effects of these determinants on depression, anxiety, stress, and psychological distress in higher education students. Methods: A structured and targeted search strategy using predefined keyword groups and Boolean combinations across PubMed, Scopus, Web of Science, and Google Scholar identified 99 records, of which 19 duplicates were removed. After screening 80 titles and 52 abstracts, 34 full-text articles were assessed for eligibility, and 30 studies were ultimately included in the final review. Data were extracted on study characteristics, mental health outcomes, psychological determinants, socioeconomic factors, and their interactions. Results: The included studies consistently showed that psychological factors, including resilience, coping strategies, loneliness, self-efficacy, and perceived control, were associated with mental health outcomes, with higher resilience and self-efficacy linked to lower levels of depression and anxiety, and maladaptive coping and loneliness associated with increased psychological distress. Socioeconomic determinants, including financial stress, low socioeconomic status, parental education, housing insecurity, and food insecurity also independently contributed to elevated risks of depression, anxiety, and stress. Importantly, several studies demonstrated an interaction between these domains, where socioeconomic disadvantage amplified the adverse effects of poor coping capacity, low resilience, and social isolation, whereas social support and adaptive coping mitigated these effects. Conclusions: Student mental health is influenced by both distinct and interacting psychological and socioeconomic mechanisms, emphasizing the need for integrated institutional strategies that address structural vulnerabilities alongside individual psychological resilience.

Background and Objectives: Infantile spasms (ISs), or West syndrome (WS), represent an early-onset epileptic encephalopathy in which diverse structural, genetic, metabolic, infectious, and neurocutaneous conditions converge on a shared pattern of hypsarrhythmia, clustered spasms, and later developmental impairment. Growing use of genomic diagnostics has revealed that variants in STXBP1, KCNQ2, GRIN2A, GRIN2B, and TSC-related genes are more common than previously recognized and can be linked to partially actionable pathways. This review aimed to synthesize current evidence on the multifactorial etiology, network-based pathogenesis, and evolving targeted therapies for ISs, with particular attention to TSC-related forms. Materials and Methods: A structured narrative review was undertaken of publications from 1990 to 2025 in PubMed, Scopus, Web of Science, and Embase using terms related to ISs, WS, genetics, mTOR, ACTH, vigabatrin, ketogenic diet, and precision therapies. Authoritative guidance from ILAE and AAN was incorporated. Clinical, molecular, and therapeutic data were grouped under etiological, pathogenetic, and management domains. Results: Structural causes remained the largest group, but combined genetic, genetic–structural, and metabolic etiologies accounted for about one third of contemporary cohorts. Early network disruption involving cortex, thalamus, basal ganglia, and brainstem, together with imbalances in NGF, BDNF, and IGF-1, explained why distinct primary insults produce a uniform electroclinical phenotype. Early treatment with ACTH or high dose prednisolone, with or without vigabatrin, was consistently associated with higher electroclinical remission and better developmental outcome. Everolimus and related mTOR inhibitors showed benefit in TSC-associated ISs, while agents directed at NMDA receptors or KCNQ channels are emerging for genotype defined subgroups. Conclusions: ISs should be approached as a heterogeneous but mechanistically convergent disorder in which rapid diagnosis, parallel genetic testing, and early disease modifying therapy improve prognosis. Integration of molecular profiling with standardized outcome monitoring is likely to move management from symptomatic seizure control to pathway-specific intervention.