Patterned brain stimulation is commonly employed to modulate brain circuits and treat neuropsychiatric disorders. Although widely used in clinical settings, there remains limited understanding of how stimulation alters neural oscillations and how these effects relate to baseline evoked network responses. To address this question, we applied 15 minutes of 10Hz focal electrical stimulation delivered as 5-s trains separated by 10-s rest intervals, a pattern resembling 'excitatory' transcranial magnetic stimulation, to 14 patients with epilepsy undergoing intracranial electroencephalography in premotor, parietal, and temporal cortical sites. We quantified spectral features of cortico-cortical evoked potentials (CCEPs) before and after stimulation. We hypothesized that the temporal and spectral components of the CCEP predicted the location and degree of stimulation-induced modulation. Across patients, low frequency power (alpha, beta) showed the broadest change, while the magnitude of change was stronger in high frequencies (beta, gamma). Next, we demonstrated that regions with stronger pre-stimulation evoked spectral responses were more likely to exhibit larger post-stimulation spectral changes. These findings were specific to frequency in a temporal window. Post-stimulation power changes were driven by interaction between direction of change in pre-stimulation power and temporal window. Finally, regions exhibiting early increases and late decreases in pre-stimulation power exhibited power changes after stimulation. These patterns were consistent across premotor, parietal, and temporal sites, but the magnitude and latency varied by stimulation location. Together, these findings demonstrate that time-frequency pre-stimulation features predict post-stimulation modulation of human neural oscillations and highlight temporally specific, state-dependent properties of stimulation responses in humans, thereby improving our understanding of stimulation-associated changes in human brain networks and helping inform more effective brain stimulation techniques.

Hyperkalemia is common in chronic kidney disease (CKD) and chronic heart failure (CHF), often leading to treatment dilemmas regarding renin-angiotensin-aldosterone system (RAAS) inhibitors. Although potassium binders and dietary restrictions are central to chronic management, their quality-of-life (QOL) impact remains insufficiently described. This study aimed to characterize real-world treatment patterns and evaluate treatment impact on QOL.

We analyzed baseline data from a prospective cohort in Japanese nephrology and cardiology outpatient clinics. Participants were adults with CKD (≥ stage G3) or CHF (New York Heart Association class II-IV) who initiated potassium binders within 6 months. Clinical data, serum potassium values, and patient-reported outcomes (generic QOL, disease/treatment-specific QOL, and adherence measures) were obtained at enrollment.

Among 347 patients, the median age was 75 years, and 74% were male; 93% had CKD. At enrollment, 59% were prescribed a RAAS inhibitor. Dietary therapy was implemented in 29%. Physical scores of generic QOL were lower than population norms, whereas mental scores were comparable. Treatment-specific QOL scores suggested that potassium binders may have had a relatively small impact on QOL compared with dietary therapy. Adherence to potassium binders was high.

Concurrent use of RAAS inhibitors and potassium binders was common, consistent with a role for binders in supporting RAAS inhibitor continuation. Potassium binders showed little perceived impact, indicating that pharmacologic potassium control may be acceptable to patients managing multiple lifestyle limitations.

The study was registered with ClinicalTrials.gov (NCT05297409).

The "Face of the Giant Panda" sign is a characteristic magnetic resonance imaging (MRI) appearance classically associated with Wilson disease. Although traditionally considered highly suggestive of Wilson disease, increasing evidence shows that this pattern is not pathognomonic and may occur across a wide range of neurological disorders. This review provides a comprehensive account of non-Wilsonian causes of the giant panda sign, with emphasis on pathophysiological mechanisms, characteristic imaging features, and, critically, the additional MRI findings beyond the panda configuration itself that allow these mimics to be distinguished from Wilson disease and from one another. A narrative review of the literature was conducted using PubMed/MEDLINE and Google Scholar, focusing on reports describing the giant panda sign and panda-like midbrain appearances. Reported etiologies were classified into mitochondrial, toxic-metabolic, infectious, inflammatory-demyelinating, vascular, neoplastic, prion, neurodegenerative, nutritional, and hypoxic-ischemic disorders. For each entity, we summarize diffusion-weighted imaging behavior, contrast-enhancement pattern, associated lesion distribution, and key clinical differentiators in a consolidated comparison table, and we present an expanded diagnostic algorithm incorporating these clues. Panda-related variant signs (miniature panda, double panda, and "bright eyes") are also described. Important mimics include Leigh syndrome, osmotic demyelination syndrome, methanol toxicity, isoniazid toxicity, metronidazole neurotoxicity, Japanese and West Nile encephalitis, neurocysticercosis, acute disseminated encephalomyelitis, Wernicke encephalopathy, maple syrup urine disease, primary CNS lymphoma, Creutzfeldt-Jakob disease, and select vascular and space-occupying lesions. Recognition of accompanying imaging findings-diffusion restriction, enhancement, hemorrhage, calcification, and the association of basal ganglia or white matter involvement-together with clinical and biochemical correlation, is essential for accurate diagnosis. The giant panda sign should therefore be regarded as a neuroradiological pattern of selective midbrain injury rather than a disease-specific marker.

To determine whether relative plasma hyperosmolality is independently associated with postoperative delirium (POD) and to explore the relationship between the cumulative number of concurrent perioperative variables and POD in patients aged greater than or equal to 65 years undergoing cardiac surgery.

Post hoc analysis.

This post hoc analysis of a randomized controlled trial included 195 consecutive patients enrolled between March 2019 and June 2020 at a tertiary hospital in Sweden. The incidence of POD was 36% (70/195). POD was assessed preoperatively and postoperatively on days 1 and 3, based on the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Plasma osmolality was measured on five occasions and coordinated with POD assessments. Potential perioperative variables associated with POD were analyzed using a multivariable logistic regression model.

The main findings indicate that relative hyperosmolality on the third postoperative day may represent a biochemical factor independently associated with the development of POD, and the presence of more than two concurrent perioperative factors, which may increase the likelihood of POD eightfold.

Relative plasma hyperosmolality may be associated with POD after cardiac surgery. The accumulation of concurrent perioperative variables also appears important and supports further investigation of multicomponent prevention strategies. Multicenter studies are needed to confirm these findings.

Both epilepsy and functional/dissociative seizures (FDS) can present with a wide variety of event manifestations which can appear similar in nature and contribute to misdiagnosis. Whereas many studies have addressed the misdiagnosis of FDS as epilepsy, research into the inverse, where epilepsy is mistaken for a functional disorder, remains limited. Accurate differentiation is vital, because management differs greatly, ranging from antiseizure medications and surgery to specialized mental health interventions.

A retrospective review was conducted of patients undergoing video-electroencephalographic monitoring (VEM) at a level 4 advanced epilepsy center between 2015 and 2023. VEM reports rather than video were reviewed. Patients were categorized into three primary groups: correctly diagnosed focal epilepsy, correctly diagnosed FDS, and misdiagnosed epilepsy (patients initially diagnosed with FDS but confirmed to have epileptic seizures). A fourth group of cases with FDS that were misdiagnosed as epilepsy were excluded.

Epilepsy cases that were misdiagnosed as FDS represented 6% of the total cohort. Fifty percent (n = 13) were male, and the mean age was 33.3 (range = 10-62). Compared to correctly diagnosed epilepsy, the misdiagnosed cases were significantly more likely to have semiological features, consisting of complex motor movements (p = .0009), hyperkinetic activity (p = .0095), and affective symptoms like fear (p = .0001). Notably, frontal lobe epilepsy was proportionally more common in misdiagnosed cases. In contrast, events in cases with correctly diagnosed FDS were characterized by unresponsiveness (p = .0001), hypotonia (p = .0001), and eye closure (p = .019), alongside prolonged duration (p = .0001) and fluctuating semiology (p = .0001). These features were almost entirely absent in the misdiagnosed group. FDS cases also had a significantly higher number of distinct event types but fewer semiological features per event (p = .03). Lateralizing signs were also an indicator of an epilepsy diagnosis, appearing in 58% of misdiagnosed cases compared to only 17% of FDS cases (p < .0001).

Sole reliance on individual signs of FDS can lead to diagnostic errors, particularly in frontal lobe epilepsy. To improve diagnostic certainty, clinicians should analyze the temporal evolution of semiology over isolated motor manifestations. When hyperkinetic or affective symptoms are present, a thorough clinical history and assessment of the temporal evolution of semiology should improve diagnostic certainty and reduce the chances of misdiagnosis.

Patients with Anorexia Nervosa experience difficulties in processing emotional stimuli within social contexts, which may contribute to some clinical manifestations of the disorder. However, it remains unclear whether emotional processing differs between the restrictive and binge-eating/purging types of AN. The study aimed to examine attentional biases towards emotional stimuli in restrictive, binge-eating/purging Anorexia Nervosa patients, and healthy controls. The sample included 28 restrictive (mean age = 16.5 years) and 20 binge-eating/purging patients (mean age = 25.5), and 29 healthy controls (mean age = 25.0). Attentional orienting and inhibitory control to neutral, happy, sad, and angry faces were assessed using prosaccade and antisaccade tasks with eye-tracking technology. Error rates and saccade latencies were analyzed for the prosaccade and antisaccade tasks using 4 (Valence) × 3 (Group) mixed ANCOVAs, with age and educational level as covariates. No significant differences or significant interactions were found in the prosaccade task. In the antisaccade task, the restrictive group showed a higher percentage of antisaccade errors when presented with sad and angry faces than with neutral faces. In contrast, unlike the AN-R and HC groups, Binge-eating/purging patients showed shorter antisaccade latencies to happy than to neutral faces. Overall, attentional processing of emotional facial expressions appears to differ depending on Anorexia Nervosa type, with restrictive patients showing greater difficulty inhibiting attention in response to distressing socio-emotional information, while binge-eating/purging patients showed a different pattern of attentional disengagement from positive information. These findings highlight the importance of considering differences in socio-emotional processing when tailoring interventions to Anorexia Nervosa type.

While disrupted sleep has long been linked to mental disorders there has been a notable decrease in interest and sleep-wake disorders have received low priority in psychiatric care. The aim of the paper was to present a concise guide for evaluating common sleep-wake disturbances within a psychiatric framework to revitalise the importance of sleep in psychiatry.

A systematic search strategy was conducted on the importance of sleep-wake assessment in psychiatry (search #1), the typology of sleep-wake disturbances in psychiatric practice (search #2), the guidelines on assessment of sleep-wake disturbances (search#3). Results were summarised and discussed in a narrative way.

Evidence suggests that assessing sleep-wake disturbances improves prevention and treatment outcomes in psychiatric patients. Insomnia remains the most common disorder, though other sleep disturbances are highly prevalent. A structured two-step evaluation-combining initial patient clinical interviews with standardised self-report questionnaires-may assist in diagnosis and monitor outcomes.

A concise guide on how to assess sleep-wake disturbances in psychiatry was summarised for psychiatric clinical practice.

Alexander disease (AxD) is a rare neurodegenerative disorder characterized by the pathological accumulation of Rosenthal fibers (RFs) and astrocytic inflammation. Despite advances in elucidating its genetic basis, effective therapeutic strategies remain limited. Recent studies indicate that astrocytes in AxD exhibit excessive mitochondrial fragmentation, which may cause mitochondrial dysfunction and inflammatory response. Photobiomodulation (PBM) has been shown to improve mitochondrial function and exert anti-inflammatory effects, suggesting it may be a promising candidate for the treatment of AxD. Here, we report that exposure to 1070-nm infrared light exerts therapeutic efficacy in AxD. Specifically, using the astrocytes derived from AxD patients and a mouse model of AxD, we demonstrate that PBM regulates AMPK/mTOR signaling and promotes mitophagy, thereby attenuating reactive oxygen species production from fragmented mitochondria and subsequent inflammatory status. This study suggests PBM may serve as a novel, non-invasive therapeutic approach for the treatment of AxD.

Posttraumatic stress disorder (PTSD) and related internalizing symptoms, including anxiety and depression, are associated with emotional-cognitive alterations. These alterations, such as biased attentional processing and reduced emotional inhibition, are thought to contribute to persistent distress. However, these associations may vary across individuals. Developmental neuroscience suggests that the timing of trauma exposure (childhood, adolescence, adulthood) can differentially influence brain development and emotional processing. This study examined whether the developmental period of first trauma moderated the link between internalizing symptoms and emotional-cognitive alterations. Participants were 109 women exposed to interpersonal trauma (age range: 28-53 years) who completed a visual search task assessing attentional biases and an emotional go/no-go task measuring emotional inhibition. Questionnaires evaluated trauma exposure and PTSD, anxiety, and depressive symptoms. Groups were based on the developmental period of participants' first trauma exposure: childhood (0-11 years; n = 38), adolescence (12-17 years; n = 32), or adulthood (≥ 18 years; n = 39). Among women first exposed in adulthood, higher anxiety symptoms were associated with slower reaction times to fearful faces, B = 140.66, p = .037. Depressive symptoms were negatively linked to emotional inhibition to angry faces among women first exposed during adolescence, B = -1.47, p = .010, and adulthood, B = -1.56, p < .001. These results highlight the importance of considering trauma timing when examining emotional-cognitive functions. By showing that these associations vary by trauma onset, this study underscores the need for developmentally informed clinical approaches to emotional dysregulation.