Background: Rosacea is a chronic inflammatory skin disorder characterized by erythema, papules, ocular symptoms, and heightened sensitivity. Patients with neurogenic symptoms such as burning or stinging remain particularly difficult to manage. Current guidelines often underrepresent energy-based devices (EBDs), pigmentary sequelae, psychosocial burden, and ocular comorbidities. Objective: To examine Korean dermatologists’ expert perspectives on rosacea management, focusing on skin sensitivity, neurogenic symptoms, pigmentary changes, psychosocial impact, ocular involvement, and EBD use. Methods: A web-based, 29-item survey was administered to 25 board-certified Korean dermatologists (May–June 2025). Quantitative and qualitative responses were analyzed. Results: Erythematotelangiectatic and papulopustular phenotypes with sensitivity skin predominated. EBDs (pulsed dye laser, intense pulsed light) were frequently used but limited by cost and sensitivity issues. Neurogenic symptoms were recognized but rarely treated with neuromodulators. Post-inflammatory hyperpigmentation was infrequent, yet monitoring was inconsistent.Psychosocial and ocular aspects were acknowledged but seldomly systematically addressed.Respondents expressed interest in emerging adjunctive treatments such as cold plasma, skin boosters, and holistic care approaches. Conclusion Korean dermatologists adopt individualized strategies for rosacea, yet practice gaps remain regarding neurogenic symptoms, pigmentary complications, and psychosocial and ocular comorbidities. Findings support the need for updated multidisciplinary, phenotype-driven guidelines aligned with real-world practice.

The prelacrimal recess approach (PLRA) has advanced endoscopic sinonasal surgery by providing improved access to the maxillary sinus and adjacent anatomical regions while preserving critical structures such as the inferior turbinate (IT) and nasolacrimal duct (NLD). First introduced in 2013, the PLRA has become an important technique for addressing various sinonasal pathologies. This review comprehensively evaluates the advancements, applications, and outcomes associated with the PLRA. The PLRA enables superior visualization and access to regions that are traditionally difficult to reach with conventional techniques. Standardized surgical steps emphasize meticulous preservation of the NLD and IT, while technical modifications have broadened its feasibility in patients with narrow prelacrimal recesses. Applications of the PLRA span diverse pathologies, including sinonasal inverted papilloma, fungal infections, odontogenic cysts, and tumors of the lacrimal system, orbit, and skull base. Anatomical studies reveal significant variations in prelacrimal recess dimensions across populations, affecting surgical feasibility. Sex-specific differences, ethnic variations, and age-related factors are important in patient selection. Clinical outcomes from multiple investigations validate the PLRA’s efficacy in maintaining sinonasal function while achieving comprehensive lesion removal. Comparative analyses with traditional approaches underscore the PLRA’s advantages in reducing postoperative morbidity and recurrence rates. Integration of the PLRA with complementary surgical approaches further expands its therapeutic applications while maintaining favorable safety profiles. The PLRA is a safe and effective surgical method that offers favorable outcomes in disease management, symptom resolution, and anatomical preservation. With ongoing innovations and refinements, the PLRA is poised to remain a cornerstone of minimally invasive sinonasal surgery, enabling the precise and safe treatment of complex pathologies.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

The prelacrimal recess approach (PLRA) has advanced endoscopic sinonasal surgery by providing improved access to the maxillary sinus and adjacent anatomical regions while preserving critical structures such as the inferior turbinate (IT) and nasolacrimal duct (NLD). First introduced in 2013, the PLRA has become an important technique for addressing various sinonasal pathologies. This review comprehensively evaluates the advancements, applications, and outcomes associated with the PLRA. The PLRA enables superior visualization and access to regions that are traditionally difficult to reach with conventional techniques. Standardized surgical steps emphasize meticulous preservation of the NLD and IT, while technical modifications have broadened its feasibility in patients with narrow prelacrimal recesses. Applications of the PLRA span diverse pathologies, including sinonasal inverted papilloma, fungal infections, odontogenic cysts, and tumors of the lacrimal system, orbit, and skull base. Anatomical studies reveal significant variations in prelacrimal recess dimensions across populations, affecting surgical feasibility. Sex-specific differences, ethnic variations, and age-related factors are important in patient selection. Clinical outcomes from multiple investigations validate the PLRA’s efficacy in maintaining sinonasal function while achieving comprehensive lesion removal. Comparative analyses with traditional approaches underscore the PLRA’s advantages in reducing postoperative morbidity and recurrence rates. Integration of the PLRA with complementary surgical approaches further expands its therapeutic applications while maintaining favorable safety profiles. The PLRA is a safe and effective surgical method that offers favorable outcomes in disease management, symptom resolution, and anatomical preservation. With ongoing innovations and refinements, the PLRA is poised to remain a cornerstone of minimally invasive sinonasal surgery, enabling the precise and safe treatment of complex pathologies.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

The prelacrimal recess approach (PLRA) has advanced endoscopic sinonasal surgery by providing improved access to the maxillary sinus and adjacent anatomical regions while preserving critical structures such as the inferior turbinate (IT) and nasolacrimal duct (NLD). First introduced in 2013, the PLRA has become an important technique for addressing various sinonasal pathologies. This review comprehensively evaluates the advancements, applications, and outcomes associated with the PLRA. The PLRA enables superior visualization and access to regions that are traditionally difficult to reach with conventional techniques. Standardized surgical steps emphasize meticulous preservation of the NLD and IT, while technical modifications have broadened its feasibility in patients with narrow prelacrimal recesses. Applications of the PLRA span diverse pathologies, including sinonasal inverted papilloma, fungal infections, odontogenic cysts, and tumors of the lacrimal system, orbit, and skull base. Anatomical studies reveal significant variations in prelacrimal recess dimensions across populations, affecting surgical feasibility. Sex-specific differences, ethnic variations, and age-related factors are important in patient selection. Clinical outcomes from multiple investigations validate the PLRA’s efficacy in maintaining sinonasal function while achieving comprehensive lesion removal. Comparative analyses with traditional approaches underscore the PLRA’s advantages in reducing postoperative morbidity and recurrence rates. Integration of the PLRA with complementary surgical approaches further expands its therapeutic applications while maintaining favorable safety profiles. The PLRA is a safe and effective surgical method that offers favorable outcomes in disease management, symptom resolution, and anatomical preservation. With ongoing innovations and refinements, the PLRA is poised to remain a cornerstone of minimally invasive sinonasal surgery, enabling the precise and safe treatment of complex pathologies.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Hemorrhagic moyamoya disease (MMD) often manifests with pure intraventricular hemorrhage (IVH) or intracerebral hemorrhage (ICH) with IVH, causing increased intracranial pressure (ICP) and neurological decline. Although intraventricular injection of recombinant tissue plasminogen activator (rt-PA) has been proven safe, its safety in MMD is uncertain. We introduce a case of rescue intraventricular rt-PA injection for an ICP crisis caused by IVH in MMD. A patient with MMD presented with acute ICH with IVH. Bilateral external ventricular drains (EVD) were placed, but the both EVD lost patency immediately due to an intraventricular clot. The next day, due to increased ICP, we injected rt-PA into the right EVD catheter to facilitate intraventricular drainage and reduce clot burden. After injection, IVH volume and ICP decreased significantly without rebleeding, leading to gradual neurological improvement. Intraventricular rt-PA effectively reduced ICP and IVH burden without rebleeding in hemorrhagic MMD, warranting further safety studies.