Therapeutic effects of fenofibrate on diabetic peripheral neuropathy by improving endothelial and neural survival in db/db mice.

Neural vascular insufficiency plays an important role in diabetic peripheral neuropathy (DPN). Peroxisome proliferative-activated receptor (PPAR)α has an endothelial protective effect related to activation of PPARγ coactivator (PGC)-1α and vascular endothelial growth factor (VEGF), but its role in DPN is unknown. We investigated whether fenofibrate would improve DPN associated with endothelial survival through AMPK-PGC-1α-eNOS pathway. Fenofibrate was given to db/db mice in combination with anti-flt-1 hexamer and anti-flk-1 heptamer (VEGFR inhibition) for 12 weeks. The db/db mice displayed sensory-motor impairment, nerve fibrosis and inflammation, increased apoptotic cells, disorganized myelin with axonal shrinkage and degeneration, fewer unmyelinated fibers, and endoneural vascular rarefaction in the sciatic nerve compared to db/m mice. These findings were exacerbated with VEGFR inhibition in db/db mice. Increased apoptotic cell death and endothelial dysfunction via inactivation of the PPARα-AMPK-PGC-1α pathway and their downstream PI3K-Akt-eNOS-NO pathway were noted in db/db mice, human umbilical vein endothelial cells (HUVECs) and human Schwann cells (HSCs) in high-glucose media. The effects were more prominent in response to VEGFR inhibition. In contrast, fenofibrate treatment ameliorated neural and endothelial damage by activating the PPARα-AMPK-PGC-1α-eNOS pathway in db/db mice, HUVECs and HSCs. Fenofibrate could be a promising therapy to prevent DPN by protecting endothelial cells through VEGF-independent activation of the PPARα-AMPK-PGC-1α-eNOS-NO pathway.

Relapsed spontaneous spinal epidural hematoma associated with aspirin and clopidogrel.

An acute spontaneous spinal epidural hematoma (SSEH) is a rare spinal pathology. A 57-year-old man who had hypertension and had been on dual antiplatelet therapy with aspirin and clopidogrel for primary prevention presented with the sudden onset of mid back pain and monoplegia of the left lower extremity. Magnetic resonance imaging revealed an epidural hematoma, and the patient underwent emergency hemilaminectomy for evacuation. However, the symptoms worsened, and complete paraplegia developed. A second procedure to remove the recurrent hematoma was performed. No vascular malformation or other possible cause for SSEH was found other than the aspirin and clopidogrel medication. This case report describes relapsed SSEH caused by the combination of aspirin and clopidogrel medication and urges caution in prescribing dual antiplatelet agents.

Detectable threshold of knee effusion by ultrasonography in osteoarthritis patients.

OBJECTIVE: The aim of this study was to identify the detectable threshold of knee effusion by ultrasonography while infusing saline. DESIGN: Forty knee osteoarthritis patients were allocated randomly to either the midline or the lateral group. Intra-articular injection of 20 ml normal saline was performed under ultrasonographic guidance with the transducer fixated at the midline longitudinal or lateral longitudinal scan in the midline and lateral groups, respectively. We obtained ultrasonography images after infusing each milliliter and measured the maximum depth of effusion. RESULTS: The smallest amount of infusion detected by ultrasonography was 4.37 ± 2.11 ml in the midline group and 4.13 ± 1.71 ml in the lateral group. An effusion more than 2 mm deep was observed after infusing 7.84 ± 3.85 ml and 7.38 ± 3.01 ml in the midline and lateral groups, respectively. To obtain a 4-mm depth, infusions of 11.58 ± 5.68 ml and 13.13 ± 4.88 ml were needed in the midline and lateral groups, respectively. CONCLUSIONS: To detect knee effusion by ultrasonography, infusion of 4.26 ml (SD, 1.92 ml) of solution is needed. We think that a depth of 2 mm is more appropriate than 4 mm as the definition of knee effusion using ultrasonography.

Detection of knee effusion by ultrasonography.

OBJECTIVES: The purpose of this study was to assess which scan view was sensitive in detecting knee effusion by ultrasonography while infusing normal saline in cadaveric specimens. DESIGN: Intraarticular injection of normal saline with contrast dye was done in increments (5, 10, 15, and 20 ml) into the knee joint of eight fresh cadavers. After infusion of each amount, sonographic images were obtained with five different scans: medial, midline, and lateral on longitudinal scans, and medial and lateral on transverse scans. When 20 ml had been injected, the knee was flexed at 30 degrees and serial images were taken. RESULTS: After infusion of 10 ml, effusion of more than 2 mm depth with ultrasonography was most frequently seen in lateral transverse scans (14/14), and the next most frequent view was a lateral longitudinal scan (11/14). After knee flexion, the amount of effusion was increased on medial and middle longitudinal scans and was decreased on transverse scans. CONCLUSIONS: For detecting knee effusion by ultrasonography, lateral transverse and longitudinal scans were the most sensitive in the knee extension posture. With knee flexion at 30 degrees, effusion was more readily detected on the medial and midline longitudinal scans than with knee extension.

Intrapartum obturator neuropathy diagnosed after cesarean delivery.

Several postpartum neurologic injuries have been described in detail, while obturator nerve injuries are rarely reported. We report a woman who had weakness of the right leg and groin pain after cesarean delivery under general anesthesia. Obturator neuropathy was confirmed by electromyography and no compressive lesion of the nerve was seen on magnetic resonance imaging. The patient was treated conservatively and followed until she recovered fully.