Xuming Hua

A clinical analysis on microvascular decompression surgery in a series of 3000 cases.

OBJECTIVE Despite the microvascular decompression (MVD) has become a definitive treatment for trigeminal neuralgia (TN) and hemifacial spasm (HFS), not all of the patients have been cured completely so far and this sort of operation is still with risk because of the critical operative area. In order to refine this surgery, we investigated thousands MVDs. METHODS Among 3000 consecutive cases of MVDs have been performed in our department, 2601 were those with typical TN or HFS, who were then enrolled in this investigation. They were retrospectively analyzed with emphasis on the correlation between surgical findings and postoperative outcomes. The differences between TN and HFS cases were compared. The strategy of each surgical process of MVD was addressed. RESULTS Postoperatively, the pain free or spasm cease occurred immediately in 88.3%. The symptoms improved at some degree in 7.2%. The symptoms unimproved at all in 4.5%. Most of those with poor outcome underwent a redo MVD in the following days. Eventually, their symptoms were then improved in 98.7% of the reoperative patients. The majority reason of the failed surgery was that the neurovascular conflict located beyond REZ or the offending veins were missed for TN, while the exact offending artery (arteriole) was missed for HFS as it located far more medially than expected. CONCLUSION A prompt recognition of the conflict site leads to a successful MVD. To facilitate the approach, the craniotomy should be lateral enough to the sigmoid sinus. The whole intracranial nerve root should be examined and veins or arterioles should not be ignored. For TN, all the vessels contacting the nerve should be detached. For HFS, the exposure should be medial enough to the pontomedullary sulcus.

Clinical features and surgical treatment of trigeminal neuralgia caused solely by venous compression

PurposeTo summarize our experience and lessons of microvascular decompression surgery for trigeminal neuralgia caused solely by venous compression.MethodsFifteen patients with idiopathic trigeminal neuralgia caused by venous compression only underwent microvascular decompression. The entire course of the trigeminal root was explored thoroughly; and coagulating and cutting techniques were preferred in decompressing the culprit veins. Their clinical features, outcomes and operative complications were analyzed.ResultsThe compressing veins included the transverse pontine vein in five cases (33.3%), the transverse pontine vein and the vein of middle cerebellar peduncle in one (6.7%), the transverse pontine vein and the vein of cerebellopontine fissure in one (6.7%), the superior petrosal vein in three (20%), the pontotrigeminal vein in one (6.7%), the vein of the cerebellopontine fissure in two (13.3%), and the plexus venosus or venule in two (13.3%). After microvascular decompression, 11 cases (73.3%) had “excellent” or “good” pain relief. Four cases (26.7%) failed the first surgery; and two of them underwent re-operation and got “excellent” pain relief. Postoperative facial numbness appeared in four cases, due to injury to trigeminal nerve when coagulation.ConclusionThe transverse pontine vein is the most common offending vein. For this type of trigeminal neuralgia, coagulating and cutting techniques are preferred in decompressing the culprit veins. The entire course of the trigeminal root should be explored and decompressed. Following these principles, excellent or good pain relief could be achieved in most cases; and recurrence is rare. However, sometimes injury to the nerve is unavoidable when coagulating the culprit vein.

Re-operation for persistent hemifacial spasm after microvascular decompression with the aid of intraoperative monitoring of abnormal muscle response.

Background and objectivesMicrovascular decompression (MVD) is the only solution that can effectively control hemifacial spasm (HFS). Regarding treatment of the patients who failed the first operation, it is still controversial. We tried to evaluate the safety and efficiency of the early re-exploration for such kinds of patients.MethodsThirteen patients failed the first MVD and received a second MVD procedure. The spasm was not resolved at all or became even more severe after the first MVD. Abnormal muscle response (AMR) persisted during the first MVD operation or disappeared once but emerged again. The patient had a strong will to do the re-operation and was aware of the high risks of operative complications.ResultsAll the 13 patients got good or excellent spasm resolution immediately after the re-operation, which involved whole-range exploration and intraoperative AMR monitoring; however, there were two cases (15.4%) of permanent facial weakness and three cases (23.0%) of transient facial weakness.ConclusionsOur experience on early repeat MVD is whole-range exploration and intraoperative AMR monitoring; in other words, re-operation cannot rely too much on experience.

Endothelial Nitric Oxide Synthase Protects Neurons against Ischemic Injury through Regulation of Brain-Derived Neurotrophic Factor Expression

Several lines of evidence demonstrated that endothelial nitric oxide synthase (eNOS) confers protective effects during cerebral ischemia. In this study, we explored the underlying cellular and molecular mechanisms of neuroprotection by eNOS.

Surgical treatment of hemifacial spasm with zone-4 offending vessel

BackgroundIncreasing evidence shows that vascular compression on any of the four zones of facial nerve may cause hemifacial spasms. Vascular compression on zone 4 (the cisternal portion) of the nerve is quite common, but only a very small percentage of such compression will elicit hemifacial spasm, because zone 4 is less susceptible than zone 3 (the root exit zone). Therefore, it seems difficult for the neurosurgeons to distinguish the real culprit vessels in zone 4. Here, our experience in treating vascular compression located in zone 4 of the facial nerve is reported.MethodsTwelve patients of HFS due to compression of zone 4 were treated with microvascular decompression (MVD) surgery with the aid of combined monitoring of abnormal muscle response (AMR) and Z-L response (ZLR).ResultsAll of the 12 patients had a zone 4 compression. In addition, there were vascular compressions on zone 3 (the root exit zone) and/or zone 2 (the attached segment) in six cases. AMR was absent in two cases, unstable in one case, and persisted after vascular decompression in another one case. ZLR was stable before decompression of zone 4 and disappeared after decompression in all cases. After MVD surgery, 11 patients were cured and one patient achieved good resolution of spasm. One patient had postoperative transient tinnitus.ConclusionsThe neurosurgeon should not ignore vascular compression at zone 4, especially when compressions at zones 2 and 3 co-exist. With the aid of AMR and ZLR, we are able to judge whether offending vessels exist at zone 4.

The strategy of microvascular decompression for hemifacial spasm: how to decide the endpoint of an MVD surgery.

ObjectiveMicrovascular decompression (MVD) has become the standard treatment for hemifacial spasm. As not all patients get complete relief, this strategy is still controversial. The study aimed to figure out how to tell the proper endpoint to the surgery.MethodsA series of 356 consecutive patients with hemifacial spasm were enrolled in this study. All patients fell into two groups according to the period they presented. Two different criteria (simple criterion vs. complex criterion) to end an operation were applied respectively. The intra-operative finding, results and complications of these two groups were compared. The advantage of the complex criterion was analyzed.ResultsThe group which used complex criterion got better results than the group which used simple criterion. The complex criterion which combines full-length evidence, vascular evidence and electrophysiological evidence proved to be reliable to tell the proper endpoint to the surgery.ConclusionMVD operations can be ended only after the full-length evidence, vascular evidence and electrophysiological evidence are all present.

Overexpression of TREM2 enhances glioma cell proliferation and invasion: a therapeutic target in human glioma

Gliomas are the most common and aggressive type of primary adult brain tumors. Although TREM2 mutation is reported to be related to Nasu-Hakola disease and Alzheimers disease, little is known about the association between TREM2 and gliomas. Here, we reported that TREM2 was significantly overexpressed in glioma tissues compared with non-tumorous brain tissues. Furthermore, TREM2 expression was closely related to pathological grade and overall survival of patients with gliomas. Down-regulation of TREM2 in two glioma cell lines, U87 and U373, resulted in a significant reduction in cell proliferation, migration and invasion and a dramatic increase in S phase arrest and apoptosis. In vivo tumorigenesis experiment also revealed that depletion of TREM2 expression inhibited U87 cell proliferation. Moreover, based on gene set enrichment analysis (GSEA) with The Cancer Genome Atlas (TCGA) dataset, we found that TREM2 was positive related to Kyoto Encyclopedia of Genes and Genomes (KEGG) apoptosis, Cromer metastasis and KEGG chemokine pathways, which was further validated by western blot in TREM2 knockdown glioma cells and indicated a possible mechanism underlying its effects on glioma. In summary, our study suggests that TREM2 may work as an oncogene and a new effective therapeutic target for glioma treatment.

Clear cell meningioma: clinical features, CT, and MR imaging findings in 23 patients.

Background Clear cell meningioma (CCM) is a rare meningioma, with radiologic features not well characterized in literature. The purpose of this study was to describe and characterize the clinical features and imaging findings of CCM. Materials and Methods The computed tomography (n = 16) and magnetic resonance (n = 23) images of 23 patients (12 men and 11 women; mean age, 34.6 years) were retrospectively reviewed. All of the patients underwent surgical resection. Follow-up was performed through clinical observations. Results Cerebellopontine angle was the most frequently presenting location (n = 10). The tumors were isointense (n = 12) or hypointense but associated with isointense (n = 7) appearance to gray matter on T1-weighted images. However, the tumors seemed to be isointense (n = 6) or isointense and hyperintense (n = 13) on T2-weighted images. On gadolinium-enhanced T1-weighted images, heterogeneous enhancement was seen in 14 lesions. Four lesions had amorphous calcifications, 18 showed peritumoral edema, 14 had cystic areas, 2 had bone hyperostosis, and 8 manifested bone destruction. On initial surgery, 17 patients underwent complete resection, whereas 5 patients underwent subtotal resection of their tumors. The operative result for the remaining patient was unknown. Follow-up was possible in 22 patients. Eleven patients had recurrence and 2 had died. Conclusions Clear cell meningioma is a rare subtype of meningioma that occurs in younger patients and often recurs. Cerebellopontine angle is the most affected area in this series. The extent of initial surgical resection is the most important prognostic factor. In radiological studies, CCM tends to have marked heterogeneous enhancement, prominent peritumoral edema, intratumoral cystic components, and involvement of the adjacent bone.

A Successful Treatment of Coexistent Hemifacial Spasm and Trigeminal Neuralgia Caused by a Huge Cerebral Arteriovenous Malformation: A Case Report

AbstractRegardless hemifacial spasm (HFS) or trigeminal neuralgia (TN) is commonly caused by an offending artery, 36 cases caused by an arteriovenous malformation (AVM) have been reported in the literature. However, the concurrent HFS and TN caused by AVM have never been reported so far. We reported a case of coexistent HFS-TN associated with a huge AVM, and the symptoms of both spasm and pain relieved gradually after endovascular embolization of the nidus. The etiology and pathogenesis as well as the treatment of this disorder are discussed and reviewed in the article.

Beclin 1, an autophagy-related gene, augments apoptosis in U87 glioblastoma cells

Beclin 1 acts as a tumor suppressor and is an essential mediator of autophagy. Beclin 1 also interacts with Bcl-2 and can induce apoptosis by activating the mitochondrion permeabilizing function of proapoptotic multidomain proteins from the Bcl-2 family. Moreover, these Bcl-2 family members can activate autophagy by liberating Beclin 1 from its inhibition by Bcl-2/Bcl-XL at the level of the endoplasmic reticulum. We found that overexpression of Beclin 1 in U87 glioblastoma cells enhanced the capacity for cellular autophagy and induced apoptosis. Silencing of Beclin 1 decreased autophagic capacity but had little effect on apoptosis and cell proliferation. Beclin 1-Bcl-2 and Beclin 1-Bcl-xL complexes were detected by immunoprecipitation in cells that overexpressed Beclin 1. Furthermore, the levels of cytochrome c in the cytosol and the activity of caspases-3/-9 in the cytosol increased after overexpression of Beclin 1. Our results suggest that Beclin 1 induces apoptosis via binding to Bcl-2 and Bcl-xL, followed by the release of cytochrome c into the cytosol and activation of caspases-3/-9.