Objective: Bipolar disorder (BD), schizoaffective disorder (SAD), and schizophrenia (SCH) are psychiatric disorders characterized by persistent cognitive impairments, even during periods of remission. Psychotropic medications commonly used to manage these conditions have anticholinergic properties, which may contribute to cognitive impairment. Methods: This study examined the relationship between anticholinergic medication burden and cognitive function in individuals diagnosed with BD, SAD, and SCH. Anticholinergic burden was assessed using two validated scales, the Anticholinergic Cognitive Burden Scale (ACB) and the CRIDECO Anticholinergic Load Scale (CALS). Cognitive function was evaluated using the Digit Span and the Öktem Verbal Memory Process Test. Retrospective data analysis was conducted to examine the association between anticholinergic medication burden and cognitive performance. Results: The study included 132 participants including individuals with BD (n = 45), SAD (n = 29), and SCH (n = 58). Higher scores on the ACB and CALS scales were associated with impairments in working memory and immediate memory in the BD group. Similarly, increased anticholinergic burden was associated with immediate memory deficits in the SCH group. However, no significant association was found in the SAD group despite a higher anticholinergic burden. Conclusion Our findings highlight the impact of anticholinergic burden on neurocognitive function in individuals with severe psychiatric disorders. The association between anticholinergic burden and cognitive impairment extends beyond SCH spectrum disorders to include BD. These findings underscore the importance of considering anticholinergic burden in psychiatric treatment strategies and call for further research with larger samples to better understand cognitive consequences and refine prescribing practices.

Objective: Bipolar disorder (BD), schizoaffective disorder (SAD), and schizophrenia (SCH) are psychiatric disorders characterized by persistent cognitive impairments, even during periods of remission. Psychotropic medications commonly used to manage these conditions have anticholinergic properties, which may contribute to cognitive impairment. Methods: This study examined the relationship between anticholinergic medication burden and cognitive function in individuals diagnosed with BD, SAD, and SCH. Anticholinergic burden was assessed using two validated scales, the Anticholinergic Cognitive Burden Scale (ACB) and the CRIDECO Anticholinergic Load Scale (CALS). Cognitive function was evaluated using the Digit Span and the Öktem Verbal Memory Process Test. Retrospective data analysis was conducted to examine the association between anticholinergic medication burden and cognitive performance. Results: The study included 132 participants including individuals with BD (n = 45), SAD (n = 29), and SCH (n = 58). Higher scores on the ACB and CALS scales were associated with impairments in working memory and immediate memory in the BD group. Similarly, increased anticholinergic burden was associated with immediate memory deficits in the SCH group. However, no significant association was found in the SAD group despite a higher anticholinergic burden. Conclusion Our findings highlight the impact of anticholinergic burden on neurocognitive function in individuals with severe psychiatric disorders. The association between anticholinergic burden and cognitive impairment extends beyond SCH spectrum disorders to include BD. These findings underscore the importance of considering anticholinergic burden in psychiatric treatment strategies and call for further research with larger samples to better understand cognitive consequences and refine prescribing practices.

Objective: Bipolar disorder (BD), schizoaffective disorder (SAD), and schizophrenia (SCH) are psychiatric disorders characterized by persistent cognitive impairments, even during periods of remission. Psychotropic medications commonly used to manage these conditions have anticholinergic properties, which may contribute to cognitive impairment. Methods: This study examined the relationship between anticholinergic medication burden and cognitive function in individuals diagnosed with BD, SAD, and SCH. Anticholinergic burden was assessed using two validated scales, the Anticholinergic Cognitive Burden Scale (ACB) and the CRIDECO Anticholinergic Load Scale (CALS). Cognitive function was evaluated using the Digit Span and the Öktem Verbal Memory Process Test. Retrospective data analysis was conducted to examine the association between anticholinergic medication burden and cognitive performance. Results: The study included 132 participants including individuals with BD (n = 45), SAD (n = 29), and SCH (n = 58). Higher scores on the ACB and CALS scales were associated with impairments in working memory and immediate memory in the BD group. Similarly, increased anticholinergic burden was associated with immediate memory deficits in the SCH group. However, no significant association was found in the SAD group despite a higher anticholinergic burden. Conclusion Our findings highlight the impact of anticholinergic burden on neurocognitive function in individuals with severe psychiatric disorders. The association between anticholinergic burden and cognitive impairment extends beyond SCH spectrum disorders to include BD. These findings underscore the importance of considering anticholinergic burden in psychiatric treatment strategies and call for further research with larger samples to better understand cognitive consequences and refine prescribing practices.

Objective: Bipolar disorder (BD), schizoaffective disorder (SAD), and schizophrenia (SCH) are psychiatric disorders characterized by persistent cognitive impairments, even during periods of remission. Psychotropic medications commonly used to manage these conditions have anticholinergic properties, which may contribute to cognitive impairment. Methods: This study examined the relationship between anticholinergic medication burden and cognitive function in individuals diagnosed with BD, SAD, and SCH. Anticholinergic burden was assessed using two validated scales, the Anticholinergic Cognitive Burden Scale (ACB) and the CRIDECO Anticholinergic Load Scale (CALS). Cognitive function was evaluated using the Digit Span and the Öktem Verbal Memory Process Test. Retrospective data analysis was conducted to examine the association between anticholinergic medication burden and cognitive performance. Results: The study included 132 participants including individuals with BD (n = 45), SAD (n = 29), and SCH (n = 58). Higher scores on the ACB and CALS scales were associated with impairments in working memory and immediate memory in the BD group. Similarly, increased anticholinergic burden was associated with immediate memory deficits in the SCH group. However, no significant association was found in the SAD group despite a higher anticholinergic burden. Conclusion Our findings highlight the impact of anticholinergic burden on neurocognitive function in individuals with severe psychiatric disorders. The association between anticholinergic burden and cognitive impairment extends beyond SCH spectrum disorders to include BD. These findings underscore the importance of considering anticholinergic burden in psychiatric treatment strategies and call for further research with larger samples to better understand cognitive consequences and refine prescribing practices.

Modafinil is generally known as a drug with low addiction potential. There are few case reports in the literature demonstrating that Modafinil, stated being capable of diminishing symptoms of attention deficit/hyperactivity disorder (ADHD), causes addiction. In the present article a Modafinil addicted ADHD case, consuming usurious doses (5,000 mg/per day) of Modafinil is presented. The case presented to our psychiatry outpatient clinic due to: requirement of in taking high dose Modafinil in order to achieve the initial effects, difficulty in obtaining the drug, irritability, anxiousness, sleep irregularities, fatigue and unpleasant vivid dreams when he did not use the drug. It was realized that the patient, himself increased doses of Modafinil incrementally, in order to keep its effects on attention symptoms at the same level. It has to be kept in mind that ADHD patients can develop Modafinil addiction. It is necessary to carry out systemic studies on this subject.
Ambulatory Care Facilities ; Dreams ; Fatigue ; Humans

Objective: Psychosocial and genetic factors are considered to play roles in the etiological mechanisms of major depressive disorder (MDD). The involvement of miRNAs in the etiopathogenesis of depression and childhood traumas is still unclear. This study aims to reveal potential differences in miRNA levels between patients with depression and healthy individuals and assess their connection to childhood traumas. Methods: This study included fifty patients with MDD and 33 healthy controls. The targeting of the 3’UTR regions of the BDNF, SLC6A4/SERT/5-HTT, HTR1a, and HTR2a genes by 8 miRNAs was analyzed to explore their potential involvement in depression and childhood traumas. The Hamilton Depression Rating Scale, the Hamilton Anxiety Rating Scale, and the Childhood Trauma Questionnaire-28 were administered to the participants. Results: Patients with MDD exhibited significantly lower expression levels of miR-335 and miR-4775, as well as significantly higher expression levels of miR-15, miR-16, miR-17, miR-92, miR-182, and miR-206, when compared to healthy controls using the 2−(ΔΔCt) method. Only miR-17 and miR-92 were associated with childhood traumas in the patients with depression. Conclusion Our research reveals a possible involvement of miRNAs in the pathophysiology of depression and highlights a potential relationship between childhood traumas and specific miRNAs in depressed patients.

Objective: Psychosocial and genetic factors are considered to play roles in the etiological mechanisms of major depressive disorder (MDD). The involvement of miRNAs in the etiopathogenesis of depression and childhood traumas is still unclear. This study aims to reveal potential differences in miRNA levels between patients with depression and healthy individuals and assess their connection to childhood traumas. Methods: This study included fifty patients with MDD and 33 healthy controls. The targeting of the 3’UTR regions of the BDNF, SLC6A4/SERT/5-HTT, HTR1a, and HTR2a genes by 8 miRNAs was analyzed to explore their potential involvement in depression and childhood traumas. The Hamilton Depression Rating Scale, the Hamilton Anxiety Rating Scale, and the Childhood Trauma Questionnaire-28 were administered to the participants. Results: Patients with MDD exhibited significantly lower expression levels of miR-335 and miR-4775, as well as significantly higher expression levels of miR-15, miR-16, miR-17, miR-92, miR-182, and miR-206, when compared to healthy controls using the 2−(ΔΔCt) method. Only miR-17 and miR-92 were associated with childhood traumas in the patients with depression. Conclusion Our research reveals a possible involvement of miRNAs in the pathophysiology of depression and highlights a potential relationship between childhood traumas and specific miRNAs in depressed patients.

Objective: Psychosocial and genetic factors are considered to play roles in the etiological mechanisms of major depressive disorder (MDD). The involvement of miRNAs in the etiopathogenesis of depression and childhood traumas is still unclear. This study aims to reveal potential differences in miRNA levels between patients with depression and healthy individuals and assess their connection to childhood traumas. Methods: This study included fifty patients with MDD and 33 healthy controls. The targeting of the 3’UTR regions of the BDNF, SLC6A4/SERT/5-HTT, HTR1a, and HTR2a genes by 8 miRNAs was analyzed to explore their potential involvement in depression and childhood traumas. The Hamilton Depression Rating Scale, the Hamilton Anxiety Rating Scale, and the Childhood Trauma Questionnaire-28 were administered to the participants. Results: Patients with MDD exhibited significantly lower expression levels of miR-335 and miR-4775, as well as significantly higher expression levels of miR-15, miR-16, miR-17, miR-92, miR-182, and miR-206, when compared to healthy controls using the 2−(ΔΔCt) method. Only miR-17 and miR-92 were associated with childhood traumas in the patients with depression. Conclusion Our research reveals a possible involvement of miRNAs in the pathophysiology of depression and highlights a potential relationship between childhood traumas and specific miRNAs in depressed patients.

Objective: Psychosocial and genetic factors are considered to play roles in the etiological mechanisms of major depressive disorder (MDD). The involvement of miRNAs in the etiopathogenesis of depression and childhood traumas is still unclear. This study aims to reveal potential differences in miRNA levels between patients with depression and healthy individuals and assess their connection to childhood traumas. Methods: This study included fifty patients with MDD and 33 healthy controls. The targeting of the 3’UTR regions of the BDNF, SLC6A4/SERT/5-HTT, HTR1a, and HTR2a genes by 8 miRNAs was analyzed to explore their potential involvement in depression and childhood traumas. The Hamilton Depression Rating Scale, the Hamilton Anxiety Rating Scale, and the Childhood Trauma Questionnaire-28 were administered to the participants. Results: Patients with MDD exhibited significantly lower expression levels of miR-335 and miR-4775, as well as significantly higher expression levels of miR-15, miR-16, miR-17, miR-92, miR-182, and miR-206, when compared to healthy controls using the 2−(ΔΔCt) method. Only miR-17 and miR-92 were associated with childhood traumas in the patients with depression. Conclusion Our research reveals a possible involvement of miRNAs in the pathophysiology of depression and highlights a potential relationship between childhood traumas and specific miRNAs in depressed patients.