Is There Any Relationship Between Arachnoid Adhesions Around Trigeminal Nerve Root Zone With HSV-1 Infection?:An Experimental Study

Objective Trigeminal neuralgia is a chronic pain syndrome. There are many hypotheses about the trigeminal neuralgia etiology in current, but no hypothesis can fully explain it. Currently the vascular compression theory was recognized by majority of clinicians. Microvascular decompression for trigeminal neuralgia is effective, but there is still a small part of the patients with MVD therapy was poor and, many such patients was found arachnoid adhesions serious in the surgery area of the trigeminal nerve root. Adhesion of the arachnoid surrounding the trigeminal nerve root and the artery which near the Trigeminal nerve root, exacerbated the artery pressure on the trigeminal nerve root, which is one of the reasons leading to trigeminal neuralgia. After a long-term clinical observation to such patients we found that much of those patients would occurs facial herpes in the ipsilateral trigeminal nerve distribution zone. According to the biological characteristics of herpes simplex virus type 1(HSV-1), which easy to neurotropic and potential in the nerve, we consider the arachnoid adhesions in trigeminal nerve root zone and facial herpes incidence after MVD operation is may be related to HSV-1 infection.The experimental project is to study the relationship between arachnoid adhesions around trigeminal nerve root zone with HSV-1 infection. Methods Experimental group: A toatl of 40 cases of arachnoid adhesions from Jining City, Neurosurgery, First People's Hospital from January 2008 to July 2010 and,those patients with trigeminal neuralgia was found significant arachnoid adhesions in the trigeminal nerve root zone during MVD operation, specimens some of the arachnoid adhesions. 17 cases of those 40 patients occursed facial herpes on the ipsilateral trigeminal nerve distribution area after operation. Specimens blister fluid from facial herpes. Control group: 20 cases of arachnoid from those patients with brain injury. Each arachnoid was divided into three parts, Doing the following three experiments.(1) HE stained biospy. Basic Steps: Put the arachnoid tissue in 10% neutral formalin fixed for 12 hours, then dehydration the fixed arachnoid tissue with gradient concentration alcohol, xylene and dipped wax. Liquid paraffin embedded arachnoid tissue, serial sections 3μm thick. Choose 2 complete paraffin attached to slides and baking for 20 minutes; Then hydration and HE staining, neutral gum fengpian.(2) PCR detected the HSV-1 specific gene fragment from arachnoid and blister fluid. (2) PCR detected the HSV-1 specific gene fragment from arachnoid and blister fluid. Cutting the arachnoid tissue into pieces and, extracted DNA. Selected no homologous sequences primer among the two conserved sequence-specific where G + C content of about 50% . And the amplified fragment was 452bp. Then put the PCR products with ethidium bromide on agarose gel to electrophoresis. and 110V electrophoresis for 20 minutes. Finally, use UV projection reflex analyzer to observe and analyze the results of electrophoresis.(3) Use HSV-1 monoclonal antibody to detected the specific antigen in arachnoid and blister fluid from facial herpes. Extracted total protein from arachnoid tissue,then put the protein into boiling water for 5 minutes make the protein denaturation. Moved the protein on prepared SDS-PAGE gel electrophoresis for 20 minutes and voltage is 110V.then transferred the protein on a piece of nitrocellulose membrane after the end of electrophoresis. Use skim milk closed the non-protein binding sites Plus mouse anti-human HSV-1 monoclonal antibody for overnight.then add horseradish peroxidase labeled goat anti-mouse antibody , fully integrated. Finally ues PBS-T to wash membrane for 3 times, and plus the color reagent to analyze the results.Results Arachnoid biopsy in experimental group was found with inflammatory cell infiltration, edema, calcification, and myxoid degeneration as the main pathological changes.In control group was found 1 case with mild inflammatory cell infiltration and myxoid degeneration, 3 cases with mild edema, and the other specimens are normal. Use Fisher's exact probabilities shows there is significant difference between the two groups in pathological changes. 29 cases was detected HSV-1-specific gene fragments in the experimental group.and the positive rate is 72.5%.At the same time,7 cases was detected HSV-1 antigen in the same arachnoid specimens,and the positive rate is 17.5%. The results show mostly virus were in latency. In experimental group, 17 patients arose facial herpes after MVD and, was detected 15 cases with HSV-1 specific DNA fragments and 12 cases with HSV-1 antigen in the facial blister fluid. Its shows mostly virus were in proliferative. In the control group only 4 specimens was detected HSV-1 specific gene fragment, none HSV-1 antigen was detected. Chi-square test shows there is a signifiicent difference in HSV-1 infection rate between the two groups(P<0.05). It shows great connection in the two events.Conclusions (1)Latent infection of herpes simplex virus type 1 can established in arachnoid. (2)There is a closely related between arachnoid adhesions around trigeminal nerve root zone with HSV-1 infection.(3)Arachnoid adhesions wrapping arterial and trigeminal nerve which increased pressure on the trigeminal nerve, aggravate trigeminal neuralgia.(4) Microvascular decompression in the treatment of trigeminal neuralgia may lead to latent virus to reactivation.