Noropsikiyatri Arsivi-Archives of Neuropsychiatry最新文献

Delirium tremens represents the most severe condition of alcohol withdrawal, with the associated highest mortality rate. The primary treatment for cases of delirium tremens consists of benzodiazepines. Within the literature, prolonged cases of delirium tremens have been identified that do not respond to high-dose benzodiazepine treatments or respond late. Different treatment modalities, such as propofol, dexmedetomidine, and parenteral antipsychotic administrations, are being attempted in the management of these cases. In this case, a case of prolonged delirium tremens with insufficient response to benzodiazepine treatment will be presented.

Introduction: This study aims to investigate retinal neuronal and vascular structural alterations in Parkinson's disease (PD) patients concerning disease duration and severity, levodopa dosage, and stroke risk.

Methods: This retrospective study included 40 PD patients and 40 age- and sex-matched controls. Retinal parameters, including central foveal thickness (CFT), macular thickness (MT), retinal nerve fiber layer (RNFL), and retinal vascular density, were measured using optical coherence tomography (OCT) and optical coherence tomography angiography (OCTA). Disease severity was assessed using the Hoehn & Yahr (H&Y) scale, and stroke risk was evaluated using the Stroke Risk Assessment (SRA) tool.

Results: PD patients demonstrated significantly reduced MT in the temporal quadrant and reduced vascular density in both the superficial (SCP) and deep (DCP) capillary plexuses compared to controls. Additionally, the superficial and deep foveal avascular zone (FAZ) areas showed notable enlargement. A negative correlation between disease duration and both the temporal and nasal quadrants of the SCP and a positive correlation between disease severity and deep FAZ area was observed, while disease severity exhibited negative correlations with temporal MT, average and superior quadrant RNFL. Levodopa dosage was inversely correlated with inferior and temporal MT and temporal SCP and DCP and positively correlated with the deep FAZ area. No significant correlation was found between the SRA score and retinal vascular changes.

Conclusion: This study is the first to evaluate retinal neuronal and vascular changes in PD regarding stroke risk assessment. Our findings suggest that retinal changes are associated with disease severity and duration in PD patients. Further prospective studies with larger sample sizes are needed to validate these findings and explore the potential role of OCTA in early detection and stroke prevention in PD.

Introduction: COVID-19 has been associated with various neurological complications, including cognitive impairments such as memory deficits, attention difficulties, and executive dysfunction. These symptoms raise concerns about potential long-term effects, particularly in individuals with preexisting neurodegenerative conditions. Emerging evidence suggests that systemic inflammation, blood-brain barrier (BBB) dysfunction, and neuroinflammation may contribute to cognitive decline in COVID-19 patients. However, the impact of COVID-19 on functional brain connectivity, particularly in dementia patients, remains unclear.This study aims to investigate the differences in functional connectivity across different frequency bands (delta, theta, alpha, beta, and gamma) in dementia patients with and without a history of COVID-19 (D-COVID and D-nCOVID) compared to a healthy control (HC) group. The study explores whether COVID-19 accelerates neurodegenerative processes by disrupting functional brain networks.

Methods: Functional connectivity was assessed using electroencephalography (EEG)-based network analysis in three groups: D-COVID, D-nCOVID, and HC. Connectivity metrics were compared across frequency bands, with a focus on local efficiency (LE) and global network alterations. The Kruskal-Wallis test assessed statistical significance, while the Dunn test was used for post-hoc analysis.

Results: Findings indicate a significant reduction in functional connectivity across multiple brain regions in dementia patients, with the D-COVID group exhibiting more pronounced declines. The observed decrease in connectivity suggests that COVID-19 may accelerate neurodegenerative processes. Additionally, the HC group demonstrated stronger connectivity and higher LE metrics, highlighting the widespread impact of dementia on brain networks.

Conclusion: These findings support the hypothesis that COVID-19 contributes to cognitive decline by exacerbating neurodegenerative mechanisms. The disruption of functional brain connectivity observed in D-COVID patients aligns with previous studies suggesting that SARS-CoV-2 may indirectly promote neuronal degeneration. Further longitudinal studies are needed to determine the long-term cognitive consequences of COVID-19 and potential therapeutic interventions to mitigate these effects.

Introduction: Neuromyelitis Optica (NMO) is an inflammatory disorder affecting the central nervous system, notably the optic nerve and spinal cord. Seropositive NMO is marked by serum IgG antibodies against aquaporin-4 (AQP4). The accurate identification of AQP4-IgG is crucial for distinguishing NMO from other demyelinating diseases of the central nervous system. However, traditional diagnostic assays have limitations in sensitivity and specificity. Here, we introduce our in-house flow cytometry live cell-based assay (FC-LCBA) for detecting AQP4 antibodies with enhanced sensitivity and specificity. Our objective is to report the accuracy and compare the efficacy of our newly developed in-house FC-LCBA against the commercial cell-based indirect immunofluorescence assay (IIFA) in detecting AQP4 antibodies.

Methods: This single-blind study was approved by the ethical committee and involved 101 serum samples. Twenty-five samples (including retests) from 17 patients evaluated in the NMO spectrum who had at least one positive cell-based IIFA test during the diagnosis or follow-up are tested in parallel with our in-house FC-LCBA and cell-based IIFA. In addition, 36 serum samples from myelin oligodendrocyte glycoprotein-associated disease (MOGAD) patients and 40 serum samples from healthy subjects are also referred for specificity analysis.

Results: Our in-house FC-LCBA displayed superior sensitivity, detecting positive results even when the cell-based IIFA yielded negative results in patients under immunosuppressive treatments. Additionally, FC-LCBA exhibited high specificity for NMO, showing negligible antibody levels in patients with MOGAD diagnosis and healthy individuals. The assay's stability was confirmed through consistent results in retests.

Conclusion: Our in-house FC-LCBA emerges as a promising diagnostic tool for detecting AQP4 antibodies, offering improved sensitivity, specificity, and reliability, instilling confidence in its potential.

Introduction: The purpose of the present study is to examine the psychometric properties of the Turkish form of the Sensory Experience Questionnaire Short Version (SEQv2.1), which is based on parent or primary caregiver reports, consisting of three sensory response patterns (hyporeactivity, hyperreactivity, and sensory seeking) previously validated in different clinical groups and the general population, on young children with autism spectrum disorder (ASD).

Method: The study participants consisted of 180 children with ASD and 65 typically developing children aged between 24 and 80 months. The children's sensory characteristics were measured using the SEQv2.1, which was filled out by their mothers. The study used the Childhood Autism Rating Scale (CARS) to examine concurrent criterion validity and confirm the children's ASD diagnosis. After the SEQv2.1 was translated, the questionnaire's validity was examined with construct and criterion validity, while its reliability was examined with Cronbach's alpha and McDonald's omega internal consistency coefficient.

Results: The analyses conducted to examine construct validity showed that the model fit indices for the questionnaire's three-factor structure were acceptable, but not all items had acceptable loading values. Furthermore, the sub-factors of the SEQv2.1 were moderately positively correlated with each other and highly positively correlated with the overall scale, and the mean scores of children with ASD and typically developing children from the sub-factors of the SEQv2.1 and the overall scale significantly differed from each other. The analyses performed for criterion validity demonstrated that the sub-factors of the SEQv2.1 and the overall scale were moderately positively correlated with the CARS. Finally, reliability analyses determined that the sub-factors of the SEQv2.1 were acceptable and the overall scale had a good level of internal consistency reliability.

Conclusion: The Turkish form of the SEQv2.1, which includes three sensory response patterns (hyporeactivity, hyperreactivity, and sensory seeking), is generally valid and reliable in determining the sensory characteristics of young children with ASD. However, since not all items have satisfactory loading values, it is thought that inferences regarding the Turkish version of the SEQv2.1 should be made more carefully. Furthermore, since this may be related to the participants' ages, it is recommended that future research be conducted with an older age group.

Introduction: Novelty processing is one of the basic survival mechanisms for living organisms. Among the various types of novelty, stimulus novelty is the effect created by stimuli that are unlikely to be encountered throughout one's lifetime. However, the oddball design mostly used in studying stimulus novelty also includes an obligatory contextual novelty effect, which actually requires the presence of schemas about sensory input in the memory. In this study, we aimed to investigate the neural circuits related purely to the detection of stimulus novelty using functional magnetic resonance imaging (fMRI) by applying an experimental design that excludes any contextual novelty effect.

Methods: Fifteen right-handed healthy participants were included in the study. The stimulus novelty effect was generated by the images of object-like structures that could not be named and did not correspond to a real object. These stimuli were shuffled with images of familiar objects frequently encountered in daily life. SPM12 and CONN were used for the preprocessing stages and activation analysis of fMRI data. In the analyses, the cluster formation threshold was determined as p <0.001 and the cluster level significance threshold with family-wise error (FWE) correction was set at pFWE <0.05.

Results: The activity of the fusiform, middle occipital, inferior occipital and superior occipital gyri increased during the processing of the stimulus novelty, while the activity of the inferior parietal cortex and supramarginal gyrus decreased.

Conclusion: With the experimental paradigm that excluded the confounding effects of contextual novelty, anatomical regions that respond specifically to stimulus novelty could be identified. Our results suggest that, while stimulus novelty intensively activates brain areas related with higher-order visual processing, the brain regions that associate sensory inputs with the schemas in the memory are less active.

Introduction: Childhood Absence Epilepsy, a subtype of genetic generealised epilepsy, is characterised by sudden and brief episodes of impaired consciousness. The Leucine-rich glioma-inactivated protein 1 (LGI1) and N-methyl-D-aspartate receptor (NMDAR) are key proteins involved in regulating neuronal excitability. In conditions like anti-LGI1 encephalitis and anti-NMDAR encephalitis, autoantibodies target and disrupt these proteins, causing memory deficits, behavioural changes, sleep disturbances, and epileptic seizures. However, the roles of LGI1 and NMDAR dysfunction in the pathophysiology of absence of seizures remain unclear. This study aims to investigate the effects of LGI1 and NMDAR antibodies on absence seizures using two experimental models: Genetic Absence Epilepsy Rats from Strasbourg (GAERS) and a low-dose pentylenetetrazol (PTZ) model of absence seizures.

Methods: IgG purified from the peripheral blood of healthy controls (HC IgG), and patients with anti-NMDAR, and anti-LGI1 encephalitis, was administered intracerebroventricularly into GAERS and Wistar rats every other day for 11 days. Before and after antibody administration, electroencephalography (EEG) recordings were performed to analyse spontaneous spike-and-wave discharges (SWDs) in GAERS. In Wistar rats, after the completion of antibody infusions, PTZ was administered (35 mg/kg) on the 12 th day to induce absence seizures. The occurrence of PTZ-induced SWDs was quantified.

Results: NMDAR IgG significantly increased the duration and number of SWDs in GAERS compared to HC IgG. LGI1 IgG had no significant effect, suggesting a differential role of NMDAR and LGI1 antibodies in modulating SWD activity. Similarly, NMDAR IgG-treated Wistar rats showed increased susceptibility to PTZ-induced absence seizures, while LGI1 IgG did not cause significant changes in PTZ-induced SWDs.

Conclusion: These results reveal a distinct pro-epileptogenic effect of NMDAR antibodies in both genetic and pharmacological models of absence epilepsy, while LGI1 antibodies appear to have a negligible effect. These findings suggest a specific role for NMDAR dysfunction in absence seizure pathophysiology and support further investigation into antibody-mediated seizure mechanisms.

Introduction: This study aims to investigate obstructive sleep apnoea syndrome (OSAS), quality of sleep, excessive daytime sleepiness (EDS) and quality of life in patients with epilepsy.

Methods: One hundred and eleven epilepsy patients, diagnosed with ILAE (international league against epilepsy) criteria, were included in this study. The mean age of the patients was 37.6 ±13.1 (19-77) years. Fifty-four of the patients were (48.6%) men and 57 were (51.5%) women. Age, gender, education level, body mass index, seizure frequency, types of seizures, electroencephalography (EEG) findings, seizures during sleep, and number of anti-seizure drugs were recorded. Berlin Questionnaire (BQ) was used to screen OSAS. Sleep and quality of life were assessed with Pittsburgh Sleep Quality Index (PSQI), Epworth Sleepiness Scale (ESS) and Quality of Life in Epilepsy-31(QOLIE-31) scales.

Results: Thirty-six percent of the patients' quality of sleep was poor and 20.7% had mild EDS. Low risk of OUAS was found in 89.2% of the patients. Quality of life was poor according to QOLIE-31. QOLIE 31 and PSQI total score had a statistically significant low negative correlation with BQ. PSQI total score had a statistically significant, low negative correlation with QOLIE-31. Poor sleep quality, EDS, OUAS and quality of life showed no correlation with demographic features, duration of disease, types of seizures, seizure frequency, number of anti-seizure drugs.

Conclusion: The poor quality of sleep was 36% in our study. Poor quality of sleep, excessive daytime sleepiness and obstructive sleep apnoea syndrome had no correlation with the demographic and clinical features of the patients with epilepsy but showed low correlation with quality of life.

Introduction: Mapping the functional connectivity of brain regions became appealing in recent research in neurology. Accordingly, a growing body of evidence shows resting-state functional connectivity (rsFC) changes in neurodegenerative disorders including Parkinson's Disease (PD). As characterised by extensive and progressive dopaminergic loss in the substantia nigra, PD emerges with serious motor and non-motor dysfunctions. In the literature, the minority of PD cases have been associated with certain genetic mutations. The aim of this study was to investigate the rsFC in a group of PD patients having Parkin gene mutation.

Method: Twelve PD patients with Parkin mutation (PP-PD), 12 PD patients without Parkin mutation (PN-PD) and 12 healthy controls (HC) were included in the study. All participants underwent a resting-state functional magnetic resonance imaging as well as a neuropsychological assessment and clinical examination.

Results: Results indicated that PP-PD had longer disease duration, a higher rate of dyskinesia and lower scores on complex visual perception tests. The resting state networks showed that all PD (consisting of PP-PD and PN-PD) and PP-PD groups had increased functional connectivity in the frontoparietal network as compared to the HC. In addition, the PP-PD group displayed decreased functional connectivity in the dorsal attention network compared to the PN-PD.

Conclusion: In conclusion, our data suggests that PD with Parkin gene mutation might be emerging with distinct resting state functional connectivity changes in the brain.