Characteristics and risk factors of deep vein thrombosis in hemiplegic, healthy and bilateral limbs of hemiplegic patients: a 10-year retrospective study.

Deep vein thrombosis (DVT) in hemiplegic patients mainly affects hemiplegic limbs, DVT can also occur only in healthy limbs, and some hemiplegic patients have DVT in both limbs. Characteristics and risk factors of DVT in hemiplegic, healthy, and bilateral limbs are unknown. To describe the proportion, risk factors, extent, and timing of DVT in hemiplegic, healthy and bilateral limbs. A 10-year retrospective review of consecutive patients was performed. DVT affected hemiplegic limbs in 34 (62%), healthy limbs in 11 (20%), and was bilateral in 10 (18%). DVT was more likely to develop in healthy limbs of hemiplegic patients without surgery (odds ratio (OR) 0.022; 95% confidence interval (CI) 0.001-0.922), and without diabetes (OR 0.023, 95% CI 0.001-0.853). Among the veins at the level of which DVT occurred, intermuscular veins represented 20 (45%) in hemiplegic, 5 (37%) in healthy, and 6 (74%) in bilateral limbs. The median time that DVT occurred after hemiplegia onset was 18 days (interquartile range [IQR] 9-79) in hemiplegic, 17 days (IQR 10-56) in healthy, and 21 days (IQR 8-27) in bilateral limbs. Early and effective prevention of DVT after surgery and optimal management of diabetes may reduce the risk of DVT in bilateral limbs. It's important to prevent proximal extension of calf vein DVT. DVT prophylaxis should be started early and continued for at least 3 weeks after hemiplegia onset.

Spinal cord injury causes insulin resistance associated with PI3K signaling pathway in hypothalamus.

Spinal cord injury (SCI) is an independent risk factor for type 2 diabetes, and may induce insulin resistance that leads to this disease. Studies have shown that greater phosphoinositide 3-kinase (PI3K) activation in the hypothalamus leads to activation of the anti-inflammatory pathway, and the anti-inflammatory reflex may protect against insulin resistance and type 2 diabetes. However, the importance of this phenomenon in type 2 diabetes pathogenesis after SCI remains elusive. In the present study, the expression of c-Fos in the hypothalamus of rats with SCI was elevated, and the hypothalamus injury was observer following SCI. Then we showed that SCI could induce increased levels of blood glucose and glucose tolerance in rats. Also, we found that SCI could damage the liver, adipocyte and pancreas, and led to lipid position in liver. Western blots were used to detect the level of PI3K and p-Akt in the hypothalamus, and the results showed a significant downregulation of PI3K and p-Akt after SCI. Furthermore, to verify the activity of the PI3K signaling pathway, immunofluorescence was used to examine the expression of neurons positive for p-S6 (a marker of PI3K activation) after SCI. The results showed that the expression of p-S6-positive neurons decreased after SCI. In addition, the effect of SCI on peripheral inflammation was also investigated. Following SCI, the serum levels of tumor necrosis factor-α, interleukin (IL)-1ß, and IL-6 increased. Collectively, our results suggest abnormality in glucose metabolism after SCI, and demonstrate that SCI may impair activation of the PI3K signaling pathway in the hypothalamus. The reduced activity of the PI3K signaling pathway in the hypothalamus may lead to peripheral inflammation, which might be the mechanism underlying the development of insulin resistance and type 2 diabetes following SCI.

What drives progressive motor deficits in patients with acute pontine infarction?

Progressive motor deficits are relatively common in acute pontine infarction and frequently associated with increased functional disability. However, the factors that affect the progression of clinical motor weakness are largely unknown. Previous studies have suggested that pontine infarctions are caused mainly by basilar artery stenosis and penetrating artery disease. Recently, lower pons lesions in patients with acute pontine infarctions have been reported to be related to progressive motor deficits, and ensuing that damage to the corticospinal tracts may be responsible for the worsening of neurological symptoms. Here, we review studies on motor weakness progression in pontine infarction and discuss the mechanisms that may underlie the neurologic worsening.