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Rationale: Fibromyalgia (FM) is characterized by idiopathic persistent chronic pain in the ligaments or musculoskeletal system, and more than half of the patients with FM might have migraine headaches. Direct musculoskeletal intervention could be a non-pharmacological management to relieve symptoms. However, patients with severe FM often have intense pain from only a soft touch, thereby rendering musculoskeletal intervention challenging., Patient Concerns: A 47-year-old man had progressing intense pain, and this affected his everyday life. There were no abnormal physical findings on laboratory examination such as levels of complement, antinuclear antibodies, and C-reactive protein, which were within normal limits. Magnetic resonance imaging did not indicate abnormalities., Diagnoses, Interventions, and Outcomes: The patient satisfied the American College of Rheumatology criteria. Finally, we made a final diagnosis of fibromyalgia. The therapeutic intervention of Kanshoho, the unique muscle relaxation technique with low force, relieved his pain., Lessons: If Kanshoho is carefully applied in a state of hospitalization under surveillance by an experienced physician, it could be a promising muscle relaxation method. Relaxing the trapezius muscle and reducing its intramuscular pressure might be key in treating patients with severe FM. However, it needs elucidation of its mechanism., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2024 the Author(s). Published by Wolters Kluwer Health, Inc.)

Rationale: Anorexia nervosa is characterized by an extreme fear of weight gain. Clinicians often prescribe meal replacement shakes if patients are unable or unwilling to consume typical foods. However, these shakes sometimes lack essential micronutrients, such as selenium, which may lead to health risks. Moreover, selenium deficiency induces macrocytic anemia. Herein, we present a case of a patient with anorexia nervosa with macrocytic anemia due to selenium deficiency, which was alleviated by selenium supplementation., Patient Concerns: An 18-year-old female was admitted to our hospital. The patient was diagnosed with anorexia nervosa. Ultimately, she was unable to walk independently because of fatigue and electrolyte disturbances., Clinical Findings: On admission, the height, weight, and body mass index of the patient were 158.5 cm, 27.1 kg, and 10.8, respectively. Our treatment for anorexia nervosa showed relative effectiveness, and the patient's body weight recovered to 29.2 kg by day 60. However, the mean corpuscular volume increased from day 20, suggesting macrocytic anemia., Diagnoses, Interventions, and Outcomes: Despite our vitamin B12 and folic acid supplementation interventions, the mean corpuscular volume continued to rise. On day 60, the patient was diagnosed with selenium deficiency, and selenium administration of 100 μg/day was initiated., Outcomes: The macrocytic anemia in the patient was alleviated, and treatment for anorexia nervosa was continued in our hospital., Lessons: To the best of our knowledge, this is the first case of macrocytic anemia induced by selenium deficiency with anorexia nervosa comorbidity, underscoring the importance of selenium supplementation in patients with anorexia nervosa, especially in those with macrocytic anemia., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Stress is inevitable in humans and stress changes our physical and mental states. Stress has been studied epidemiologically, biologically, and psychologically. First defined in 1990, emotional intelligence (EI) affects psychological stress management. In contrast, the prefrontal cortex (PFC) is suggested to play a vital role in stress management. Human PFC activity can be inferred from the balance of oxygenated and deoxygenated hemoglobin in cerebral blood flow, which can be measured and calculated using functional near-infrared spectroscopy (fNIRS). An important cognitive activation task to activate the PFC is the verbal fluency task (VFT). Therefore, if the PFC is activated by the VFT and monitored by fNIRS, and the activity correlates with EI, fNIRS can be used to measure EI. In this study, Psychological tests using the self-rating depression scale, state-trait anxiety inventory (STAI), and trait emotional intelligence questionnaire-short form (TEIQue-SF) were conducted to evaluate the correlation with VFT performance. Relative oxygenated and deoxygenated hemoglobin concentrations were measured using an fNIRS device, and their correlation with VFT performance was tested. Spearman correlation coefficient was used to determine correlations. Results were as follows. Although VFT performance did not correlate with the oxygenated hemoglobin concentration ([Oxy-Hb]) changes, [Oxy-Hb] was elevated in all channels. VFT performance was significantly negatively correlated with the Zung self-rating depression scale (ρ = 0.063, P = .759), trait anxiety or anxiety level as a personal characteristic of STAI (ρ = 0.243, P = .232), and state anxiety or anxiety about an event of STAI (ρ = -0.138, P = .500), whereas no correlation was found with the TEIQue-SF (ρ = 0.303, P = .132). Healthy individuals PFC activity is not severely affected by their mental state and cognitive activation successfully activates the PFC, supporting the hypothesis that EI is correlated with frontal cortical activation during the VFT in a nonclinical population. EI may play a vital role in reducing stress associated with depression and anxiety in our social lives. Although we failed to show a statistical correlation between TEIQue-SF and [Oxy-Hb] due to a sample size shortage, our preliminary study was the first to attempt to show the PFC activity of EI through a hemodynamic response. Future research may elucidate the role of EI in reducing psychological stress in social life., Competing Interests: The authors have no conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Rationale: Refeeding syndrome (RS) is a fatal condition caused by rapid calorie intake during starvation. Self-neglected fasting in psychiatric disorders is associated with RS. However, overeating resulting from circumventing the clinician's instructions does not have a reportedly high risk of RS., Patient Concerns: A 47-year-old undernourished woman with borderline personality disorder was hospitalized for nausea, vomiting, and diarrhea., Clinical Findings: She had not eaten much for 10 days and had lost weight (56.5-51.1 kg) over 3 weeks. No abnormalities were indicated on physical examination and imaging examinations., Diagnoses, Interventions, and Outcomes: Infectious diseases and malignancies were excluded from the differential diagnosis. On the third day of admission, the patient's serum phosphorus level significantly decreased to 0.7 mg/dL, and additional sodium phosphate was administered intravenously. On the fourth day, despite our instructions, the patient was found to be eating nonhospital food from the first day of admission. In conjunction with her history, a final diagnosis of RS was made. After appropriate treatments, the patient was discharged on the 15th day of hospitalization. The patient's nausea, vomiting, and diarrhea were improved., Lessons: When undernourished patients have psychiatric disorders, including borderline personality disorder or schizophrenia, the occurrence of RS should be considered based on the patients' poor adherence to physicians' instructions., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Rationale: Idiopathic achalasia is an esophageal peristaltic dysfunction of the lower esophageal sphincter (LES). The initial symptom is progressive dysphagia. However, due to its rarity, it is often misdiagnosed as an esophageal disorder. High LES pressure on esophageal manometry is an essential finding for the diagnosis., Patient Concerns: A 55-year-old man was hospitalized with saliva-like vomitus, stuck-in-throat feeling of dysphagia, and weight loss., Clinical Findings: On initial admission, gastrointestinal endoscopy, esophageal manometry, laboratory tests, and physical examination results were within normal limits., Diagnoses, Interventions, and Outcomes: Initially, the patient was diagnosed with globus sensation and recovered with medication. However, the symptoms recurred. He requested another examination on the second admission and was diagnosed with achalasia based on repeat esophageal manometry. The patient recovered after surgical treatment., Lessons: When patients still suffer from these symptoms, there is a need to reconsider achalasia, even if it is initially excluded from the differential diagnosis. Medication is not a radical treatment; however, it sometimes ameliorates symptoms. Moreover, the psychosomatic approach can be useful in such cases., Competing Interests: The authors have no funding and conflicts of interest to disclose., (Copyright © 2023 the Author(s). Published by Wolters Kluwer Health, Inc.)

Objective: To investigate the clinicopathologic features of eosinophilic granulomatosis with polyangiitis (EGPA)-associated neuropathy with a focus on the presence or absence of anti-neutrophil cytoplasmic antibodies (ANCAs)., Methods: We examined the clinical features and pathologic findings of sural nerve biopsy specimens from 82 patients with EGPA-associated neuropathy. Of these patients, 32.9% were myeloperoxidase (MPO)-ANCA positive, and 67.1% were MPO-ANCA negative. PR3-ANCA was negative in all of 78 examined patients., Results: Upper limb symptoms were more frequently reported as initial neuropathic manifestations in the MPO-ANCA-positive group than in the MPO-ANCA-negative group (44.4% vs 14.6%, p < 0.01). The serum levels of C-reactive protein were significantly higher in the MPO-ANCA-positive group than in the MPO-ANCA-negative group ( p < 0.05). Sural nerve biopsy specimens showed findings suggestive of vasculitis (i.e., destruction of vascular structures) in epineurial vessels; these results were seen more frequently in the MPO-ANCA-positive group than in the MPO-ANCA-negative group ( p < 0.0001). Conversely, the numbers of eosinophils in the lumen of the epineurial vessels ( p < 0.01) and epineurial vessels occluded by intraluminal eosinophils ( p < 0.05) were higher in the MPO-ANCA-negative group than in the MPO-ANCA-positive group. Furthermore, the incidence of eosinophil infiltration in the endoneurium was higher in the MPO-ANCA-negative group than in the MPO-ANCA-positive group ( p < 0.01)., Conclusions: This study suggests that the pathogenesis of EGPA comprises at least 2 distinct mechanisms: ANCA-associated vasculitis resulting in ischemic effects and inflammation, which is prominent in MPO-ANCA-positive patients, and eosinophil-associated vascular occlusion leading to ischemia and eosinophil-associated tissue damage, which is conspicuous in MPO-ANCA-negative patients., (© 2020 American Academy of Neurology.)

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a form of chronic neuropathy that is presumably caused by heterogeneous immune-mediated processes. Recent advances in the search for autoantibodies against components expressed at nodal regions, such as the nodes of Ranvier and paranodes, have substantially contributed to clarifying the pathogenesis of CIDP in a subpopulation of patients. In particular, immunoglobulin G4 (IgG4) antibodies to paranodal junction proteins, including neurofascin-155 and contactin-1, have attracted the attention of researchers. Paranodal dissection resulting from the attachment of IgG4 at paranodal junctions and the absence of macrophage-induced demyelination are characteristic pathologic features in patients who have these antibodies. By contrast, the mechanisms of neuropathy in cases with classical macrophage-induced demyelination remain unclear despite the long-standing recognition of this process in CIDP. In addition to complement-dependent damage provoked by autoantibodies, recent studies have shed light on antibody-dependent phagocytosis by macrophages without participation of complements. However, a direct association between specific autoantibodies and macrophage-induced demyelination has not been reported. Electron microscopic examination of longitudinal sections of sural nerve biopsy specimens suggested that macrophages recognize specific sites of myelinated fibers as the initial target of demyelination. The site that macrophages select to initiate myelin breakdown is located around the nodal regions in some patients and internode in others. Hence, it seems that the components that distinguish between the nodal regions and internode play a pivotal role in the behavior of macrophages that initiate phagocytosis of myelin. Further studies are needed to elucidate the mechanisms underlying macrophage-induced demyelination from this perspective., (© 2018 American Academy of Neurology.)

Neuroblastoma is the most common extracranial solid tumor in children and, when disseminated, carries a poor prognosis. Even with aggressive combinations of chemotherapy, surgery, autologous bone marrow transplant, and radiation, long-term survival remains at 30% and new therapies are needed. Recently, a patient with neuroblastoma who acquired Chagas disease was treated with nifurtimox with subsequent reduction in tumor size. The effect of nifurtimox on the neuroblastoma cell lines CHLA-90, LA1-55n, LA-N2, SMS-KCNR, and SY5Y was examined. Nifurtimox decreased cell viability in a concentration-dependent manner. Cell morphology, terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling assay, and caspase-3 activation indicate that cell death was primarily due to apoptosis. Nifurtimox also suppressed basal and TrkB-mediated Akt phosphorylation, and the cytotoxicity of nifurtimox was attenuated by a tyrosine hydroxylase inhibitor (alpha-methyl-tyrosine). Nifurtimox killed catecholaminergic, but not cholinergic, autonomic neurons in culture. In vivo xenograft models showed inhibition of tumor growth with a histologic decrease in proliferation and increase in apoptosis. These results suggest that nifurtimox induces cell death in neuroblastoma. Therefore, further studies are warranted to develop nifurtimox as a promising new treatment for neuroblastoma.

Adrenomedullin (AM) is an important vasodilator in cerebral circulation, and cerebral endothelial cells are a major source of AM. This in vitro study aimed to determine the AM-induced changes in blood-brain barrier (BBB) functions. AM administration increased, whereas AM antisense oligonucleotide treatment decreased transendothelial electrical resistance. AM incubation decreased BBB permeability for sodium fluorescein (mol. wt 376 Da) but not for Evan's blue albumin (mol. wt 67 kDa), and it also attenuated fluid-phase endocytosis. AM treatment resulted in functional activation of P-glycoprotein efflux pump in vitro. Our results indicate that AM as an autocrine mediator plays an important role in the regulation of BBB properties of the cerebral endothelial cells.

The effects of growth promoting activity (GPA) on sympathetic neurone development were investigated in vitro and compared with the effects of ciliary neurotrophic factor (CNTF). GPA interfered with sympathetic neurone proliferation and induced the expression of vasoactive intestinal peptide (VIP) in neurones from 7-day-old (E7) chick embryos. The biological effects observed with saturating levels of GPA are indistinguishable from the effects of CNTF. The effects on VIP expression suggest that GPA may be involved in the specification of sympathetic neurone phenotypes. Whereas half maximal effects are achieved at lower concentrations of GPA than CNTF, GPA competes less efficiently than CNTF for the binding of 125I-labelled CNTF. This suggests similar, but not identical interactions of CNTF and GPA with receptors on chick sympathetic neurones.