Cervical foraminal lipoma is a rare cause of cervical radiculopathy. We report the case of a 47-year-old woman who presented with a 1-year history of right arm pain and paresthesia that was refractory to conservative treatment. Magnetic resonance imaging demonstrated a well-defined mass within the right C5-6 neural foramen, causing compression of the exiting C6 nerve root. The patient underwent microsurgical excision via posterior cervical laminoforaminotomy. Intraoperatively, a lipomatous mass compressing the nerve root was identified and completely removed. Histopathological examination confirmed a benign lipoma. Postoperatively, the patient experienced marked symptomatic improvement, with no recurrence of symptoms at a 6-month follow-up. Although it is uncommon, cervical foraminal lipoma should be considered in patients with persistent radiculopathy and atypical imaging findings, and surgical excision can provide favorable clinical outcomes.

Spinal tuberculosis (TB) can be difficult to confirm microbiologically, and delayed treatment may result in irreversible neurological injury. We report the case of a 57-year-old Cambodian man who presented with a 2-month history of upper back pain and right-leg radiculopathy. Thoracic magnetic resonance imaging (MRI) demonstrated destructive spondylitis at T8–9 with epidural and paravertebral abscesses. Despite treatment with broad-spectrum antibiotics and decompression with biopsy at another hospital, serial MRI showed progression of the abscesses and worsening spinal cord compression, followed by bilateral lower-extremity weakness. Repeated acid-fast bacillus staining, mycobacterial culture, TB polymerase chain reaction, and histopathological examination all yielded negative results. A positive QuantiFERON-TB Gold result was considered supportive but not diagnostic evidence because interferon-γ release assays cannot distinguish latent from active TB. Nevertheless, the epidemiological background, MRI findings, chronic inflammatory pathology, and lack of response to non-specific antibiotics supported a clinicoradiological diagnosis of tuberculous spondylitis. Given the patient’s progressive neurological decline, marked destruction of T8 and T9, and overt instability, vertebral column resection was performed at T8–9, followed by anterior reconstruction with a titanium mesh cage and posterior fusion from T5 to T12. Empirical antituberculous chemotherapy was initiated on postoperative day 10. Motor strength improved, inflammatory marker levels decreased, and computed tomography and MRI obtained approximately 3 weeks postoperatively demonstrated stable reconstruction without a drainable fluid collection. This case illustrates that culture-negative spinal TB may require a clinicoradiological diagnosis, early empirical antituberculous therapy, and definitive anterior column reconstruction when progressive instability and neurological compromise are present.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Schwann cells are the most abundant cells in the peripheral nervous system, maintaining the development, function and regeneration of peripheral nerves. Defects in these Schwann cells injury response potentially contribute to the pathogenesis of diabetic peripheral neuropathy (DPN), a common complication of diabetes mellitus. The protein p66shc is essential in regulating oxidative stress responses, autophagy induction and cell survival, and is also vital in the development of DPN. In this study, we hypothesized that p66shc mediates high glucose-induced oxidative stress and autophagic dysfunction. In Schwann cells treated with high glucose; p66shc expression, levels of reactive oxygen species, autophagy impairment, and early apoptosis were elevated. Inhibition of p66shc gene expression by siRNA reversed high glucose-induced oxidative stress, autophagy impairment, and early apoptosis. We also demonstrated that the levels of p66shc was increased, while autophagy-related proteins p62 and LC3 (LC3-II/I) were suppressed in the sciatic nerve of streptozotocin-induced diabetes mice. P66shc-deficient mice exhibited the improvement in autophagy impairment after diabetes onset. Our findings suggest that the p66 plays a crucial role in Schwann cell dysfunction, identifying its potential as a therapeutic target.

Meningioma is one of the most common types of benign primary brain tumors in older adults, and multiple meningiomas are reported in fewer than 1% to 10% of cases. However, there is no definitive treatment guideline for patients with multiple meningiomas. An 80-year-old man presented with abruptly impaired cognition and was found to have two distinct meningiomas located in the temporal and frontal lobes. A single frontotemporal craniotomy was performed to remove both tumors. Pathological analysis revealed different subtypes and World Health Organization grades for each mass. The patient showed symptomatic improvement, experienced no postoperative complications, and exhibited no signs of recurrence during a 1-year follow-up period with evaluations at 3-month intervals. Despite the absence of a standard treatment for multiple meningiomas, surgical resection in a single procedure is feasible in selected patients.

Objective: Decompression with instrumented fusion is a common approach for treating spinal metastatic disease. However, in many cases, poor bone quality and compromised general condition increase the likelihood of mechanical failure and other complications. This study investigated complications, including those related to surgery, following decompression and fusion in patients with spinal metastatic disease. Methods: A study at a single tertiary medical center focusing on surgical details and perioperative complications was performed on 35 patients who underwent spinal surgery due to metastatic spinal disease based on a review of a prospective database. Data on patients' underlying conditions and the status of the primary tumors were collected, and various complications that occurred within the first month after surgery were analyzed. Results: During the study, 35 patients (mean age, 66.5 years; 26 men) were enrolled. The most frequent primary cancers were lung (34%) and prostate cancer (17%), followed by liver and breast cancer and others. The overall complication rate was 37% (14% surgery-related complications, 23% general complications). In all cases, surgery was performed due to lower extremity weakness, and 59% of patients showed improvements in motor function after surgery. Furthermore, 23% of patients regained the ability to walk. Conclusion Surgery for spinal metastasis is frequently performed as an emergency due to the severity of symptoms such as lower extremity weakness. Despite a high risk of acute complications, the procedure has significant benefits, including improvement in weakness and recovery of walking ability. Therefore, proactive treatment using appropriate surgical techniques is recommended.

Background/Aims: Achieving rapid reduction of low-density lipoprotein cholesterol (LDL-C) levels below 55 mg/dL in patients with acute myocardial infarction (AMI) can be challenging with statins alone. This single-center, retrospective study aimed to assess the impact of single-dose injection of evolocumab 140 mg on LDL-C levels during the peri-percutaneous coronary intervention (PCI) period in patients with AMI. Methods: A total of 95 patients with AMI who underwent PCI were divided into the evolocumab (n = 50) and non-evolocumab (n = 45) groups. Results: The percentage change of LDL-C level at 1–3 weeks from baseline was 78.4 ± 13.4% reduction in the evolocumab group versus 45.6 ± 22.6% in the non-evolocumab group, with a mean difference of -33.5% between the groups (95% CI: -42.6 to -24.5%; p < 0.001). The achievement rate of LDL-C levels below 55 mg/dL at 1–3 weeks was significantly higher in the evolocumab group than in the non-evolocumab group (97.7% vs. 60.0%, p < 0.001). Conclusions Patients with AMI who received single-dose injection of evolocumab 140 mg during the peri-PCI period had a significantly greater LDL-C reduction and higher proportion of patients achieved the target LDL-C level in the early phase AMI than those who did not receive evolocumab.