Background: Insomnia is markedly more prevalent in rheumatoid arthritis (RA) patients than in the general population and is closely linked to pain, fatigue, psychological comorbidities, and systemic inflammation. Evidence suggests a bidirectional relationship, where active disease worsens sleep quality, while poor sleep amplifies inflammatory activity and symptom severity. Methods: A narrative review was conducted using PubMed, Scopus, Web of Science, and Embase to identify studies from the last 15 years involving adult RA patients. Inclusion criteria required assessment of insomnia or sleep quality in relation to disease activity, treatment outcomes, or inflammatory markers. Data from clinical trials, cohort studies, and reviews were synthesized to examine prevalence, mechanisms, and therapeutic implications. Results: Insomnia affects up to 45% of RA patients and correlates with higher DAS28 scores, elevated CRP/ESR, increased pain sensitivity, and reduced quality of life. Contributing factors include chronic pain, stiffness, elevated IL-6 and TNF-α, depression, anxiety, and medication side effects. Conventional DMARDs, corticosteroids, and biologics indirectly improve sleep via inflammation control, with IL-6 inhibition showing potential sleep-specific benefits. Psychotropic agents may help in comorbid depression/anxiety but are best combined with cognitive behavioral therapy for insomnia (CBT-I). Conclusions: Insomnia is a prevalent, multifactorial problem in RA that adversely affects disease activity, symptom burden, and functional outcomes. Integrating sleep evaluation into routine RA management and adopting interdisciplinary strategies that address both inflammation and sleep disturbance may enhance patient outcomes. High-quality longitudinal studies using objective sleep measures are needed to clarify causal relationships and optimize therapy.

Several studies indicate the impact of antipsychotics like risperidone and paliperidone on oxidative stress parameters, yet data remain inconsistent. We investigated the link between these medications, hyperprolactinemia (HPRL), and oxidative stress. This study was conducted at the Psychiatry Clinic, University Clinical Center, Kragujevac, between November 2022 and August 2023. Inclusion criteria comprised diagnosed psychotic disorders from the ICD-10-based F20-F29 spectrum and clinical stability on risperidone/paliperidone for ≥12 weeks with no recent dose adjustments. Exclusion criteria included pregnancy, breastfeeding, relevant medical conditions, or co-therapy with prolactin-secreting drugs. Data encompassed drug choice, administration method, therapy duration, and daily dose. Prolactin (PRL) levels, oxidative stress parameters (TBARS, H₂O₂, O₂⁻, NO₂⁻), and antioxidant system (CAT, GSH, SOD) were assessed. Of 155 subjects, women exhibited significantly higher PRL levels (p < 0.001) and symptomatic HPRL (p < 0.001). Drug choice and regimen significantly influenced TBARS (p < 0.001), NO₂⁻ (p < 0.001), O₂⁻ (p = 0.002), CAT (p = 0.04), and GSH (p < 0.001) levels. NO₂⁻ levels were affected by drug dose (p = 0.038). TBARS (p < 0.001), O₂⁻ (p < 0.001), and SOD (p = 0.022) inversely correlated with PRL levels, suggesting PRL’s protective role against oxidative stress. The female sex association with higher PRL levels implies additional factors influencing PRL’s antioxidant role. Antipsychotic choice and dosage impact PRL and oxidative stress markers, necessitating further exploration.

Evidence suggests that treatment-resistant depression (TRD), defined as the occurrence of an insufficient clinical response after adequate antidepressant therapy among patients diagnosed with major depression, is one of the most important public health problems and is associated with significant disability and psychosocial impairment. Here we present a case of depression resistance to the treatment of a 22-year-old man and the effects of Memantine augmentation. The first symptoms of depression appeared in January 2019, and pharmacotherapeutic treatment began in March of the same year. He was in a bad mood, sad, hopeless, tense, lacked energy, lost interest, and decreased libido. During his two-year pharmacotherapeutic therapy, he took SSRIs, SNRIs, TeCAs, SARIs, atypical antipsychotics with antidepressant effects, such as aripiprazole and cariprazine. Since the patient still did not have adequate therapeutic response and new drugs were available, the choice fell on Memantine after researching several databases and collecting the data listed at the beginning of the article. The initial dose was 5 mg daily and was gradually increased by 5 mg each week to a maximum of 20 mg. After 2 weeks at a stable dose, the patient reported feeling a little better. Significant improvement in symptoms was observed in the MADRS score, which was then applied to assess the effects of augmentation. After four weeks of therapy, he entered remission which is still ongoing.