Percutaneous microballoon compression of the trigeminal ganglion is a brand new operative technique for the treatment of trigeminal neuralgia. However, it is unclear how the procedure mediates pain relief, and there are no standardized criteria, such as compression pressure, com-pression time or balloon shape, for the procedure. In this study, percutaneous microballoon compression was performed on the rabbit trigeminal ganglion at a mean inlfation pressure of 1,005 ± 150 mmHg for 2 or 5 minutes. At 1, 7 and 14 days after percutaneous microballoon compression, the large-diameter myelinated nerves displayed axonal swelling, rupture and demy-elination under the electron microscope. Fragmentation of myelin and formation of digestion chambers were more evident after 5 minutes of compression. Image analyzer results showed that the diameter of trigeminal ganglion cells remained unaltered after compression. These experi-mental ifndings indicate that a 2-minute period of compression can suppress pain transduction. Immunohistochemical staining revealed that vascular endothelial growth factor expression in the ganglion cells and axons was signiifcantly increased 7 days after trigeminal ganglion compression, however, the changes were similar after 2-minute compression and 5-minute compression. The upregulated expression of vascular endothelial growth factor in the ganglion cells after percu-taneous microballoon compression can promote the repair of the injured nerve. These ifndings suggest that long-term compression is ideal for patients with recurrent trigeminal neuralgia.

Objective: To determine the efficacy and safety of early intervention with nimodipine treatment in diffuse axonal injury.Methods: Based on the characteristic radiological signs and criteria for diffuse axonal injury (DAI), 89patients with the diagnosis of DAI were enrolled in this randomized, double-blind, placebo-controlled trial. Results: Nimodipine proved to be safe and well tolerated. With TCD sonography we found that there was a higher incidence of cerebral vasospasm in this series (38.2%). Overall, Nimodipine produced a better clinical result than placebo, but there was no statistically significant difference in favorable outcome at 3 months after injury (P ＝ 0.11 ) between the two groups. A trend toward a favorable effect was suggested by the analyses in two small subgroups, either in the patients suffering from clinical Grade Ⅲ DAI (P ＝ 0.04), or in those with the TCDevidence of cerebral vasospasm during clinical observation (P ＝ 0.049).Conclusions: We postulate that a clinically valuable benefit is possible with nimodipine treatment in DAI patients. However, the effects on outcome should be verified by further controlled study.

Objective: To explore the content change of neurofilament (NF) protein subunits in the experimental brain diffuse axonal injury (DAI) by lateral head rotation.Methods: Twenty-four Sprague Dawley (SD) rats were equally divided into three injury groups (2 h, 12 h,and 24 h post injury) and one control group. The models of DAI were made in the injury groups by lateral head rotation. Western blotting technique was used to measure the content of NF68 (a kind of NF protein subunit) in the brainstem tissues among all the injured and control rats.The NF68 immunohistochemical staining was used in another six SD rats in order to observe the morphological changes in DAI.Results: The NF68 content in the brainstem tended to decrease at 2 h post injury, decreased significantly at 12 h and continued its decrease at 24 h. NF56 and NF52, as the breakdown products of NF68, had a tendency to increase at 2-12 h after the injury, and amounted to a significantly higher level at 24 h. Microscopically, there were a lot of swelling neuronal axons in the ventral part of the medullar oblongata at 2 h after the injury. Some axons were disconnected, and axonal retraction balls formed on their proximal end.Conclusions: There is an occurrence of phosphorolysis within the brainstem in DAI by lateral head rotation. These reactions cause the breakdown of NF68,which results in the decrease of NF68 in content. It suggests that the breakdown of neurofilament protein subunits is an important reason for structural destroy of neurofilaments in DAI.