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Is There Any Relationship between Arachnoid Adhesions around Trigeminal Nerve Root Zone with HSV-1 Infection?:An Experimental Study

Author: HuQingLei
Tutor: ZhongYanJun
School: Jinan University
Course: Surgery
Keywords: Primary trigeminal neuralgia Arachnoid Herpes simplex virus type Ⅰ Latent infection
CLC: R745.11
Type: Master's thesis
Year: 2011
Downloads: 14
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Abstract


Purpose complex etiology of idiopathic trigeminal neuralgia, its pathogenesis internationally there are many theories, but without a theory to fully explain its etiology. Many theories, the theory of vascular compression has been recognized by the majority of clinicians and microvascular decompression (Microvascular decompression, MVD) treatment of trigeminal neuralgia is effective, but there is still a small number of patients treated by MVD after effect due to good. Such patients during surgery and more find the arachnoid adhesions of the trigeminal nerve root more serious, the arachnoid adhesions surrounding the trigeminal nerve root and surrounding arteries, exacerbating the artery on the trigeminal nerve root compression. By the clinical observation that most such patients will ipsilateral third nerve distribution Area facial herpes. According to the herpes simplex virus type 1 (Herpes simplex virus-1, HSV-1) the biological characteristics, consider the root zone of the trigeminal nerve arachnoid adhesions and postoperative facial herpes may occur with HSV-1 infection. The purpose of this experiment is to study the relationship between patients with trigeminal neuralgia trigeminal nerve root zone around the arachnoid adhesions with HSV-1 infection, viral infection is analyzed from the perspective of viral infection caused by the arachnoid adhesions cause of cause of trigeminal neuralgia and for the future research and clinical treatment of trigeminal neuralgia viral etiology for reference. The method experimental group of 40 patients with subarachnoid specimens taken from the root zone of the trigeminal nerve was significantly arachnoid adhesions Jining City, Shandong Province, the First People's Hospital neurosurgery patients with trigeminal neuralgia MVD from January 2008 to July 2010. 40 patients were ipsilateral trigeminal nerve distribution area facial herpes in 17 cases, specimens from facial herpes fluid. Control group of 20 patients with subarachnoid specimens, arachnoid specimens taken from patients with traumatic brain injury (bridge cerebellar area). Each case arachnoid divided into three parts, respectively: (1) paraffin biopsy: arachnoid tissue in 10% neutral formalin-fixed 12 hours, automatic tissue processor gradient alcohol dehydration, xylene, dip wax; paraffin sections on serial sections thickness 3um, choose full, no scratch, uniform thickness of wax 2, attached to the glass slide and baked 20 minutes; then the sections were dewaxed in xylene and gradient hydration, followed by hematoxylin , the ammonia back blue, eosin, gradient alcohol dehydration, xylene neutral glue cementing. (2) PCR detection the arachnoid and facial herpes fluid within the HSV-1-specific gene fragment: Organization crushing, extraction of total DNA, primers select a GC content of about 50% of the hairpin structure, inter-homologous sequences for both specific conservative The sequence amplified fragment of 452 bp. The amplification product was purified on a 1.5% agarose gel electrophoresis and ethidium bromide chromogenic agent. (3) HSV-1 monoclonal antibody detection the arachnoid and facial herpes fluid antigen specificity: arachnoid tissue extract the total protein in boiling water for 5 minutes to denature the proteins, protein to prepared SDS-PAGE gel electrophoresis, electrophoresis after the end of Proteins transferred to nitrocellulose membrane closure of non-protein-binding sites, skim milk, plus rat anti-HSV-1 monoclonal antibody overnight; plus horseradish peroxidase-labeled goat anti-mouse antibody fully binding, add chromogenic agent chromogenic. Arachnoid biopsy results of the experimental group, the light microscope, the arachnoid adhesions 6 kinds of pathological changes: 23 cases of inflammatory cell infiltration, tissue edema six cases, three cases of hyaline degeneration, pathologic calcification in 1 and myxoid degeneration in 7 cases. Arachnoid biopsy of the control group of patients with mild inflammatory cell infiltration with myxoid degeneration, three cases of cell edema light microscope, more than are normal arachnoid structure. Between the two groups of pathological changes Fisher's exact p lt; 0.00. Arachnoid specimens in the experimental group of 40 patients detected HSV-1-specific gene fragment in 29 cases, the positive rate was 72.5%; seven cases detected HSV-1-specific antigen expression, the positive rate of 17.5%. To latent infection, was a small part of the value-added infection. In 15 cases out of 17 cases of the experimental group patients face blister fluid detected HSV-1-specific DNA fragment, 12 cases detected HSV-1-specific antigen expression, that the virus in the proliferative phase. Control group, four cases was detected in HSV-1-specific gene fragment, antigen expression was not detected. Positive rate of infection in the chi-square test was used to compare between the two groups was statistically significant (P lt; 0.05), and the arachnoid tissue HSV-1 infections and no cases of infection in the pathological changes statistically significant difference (P lt; 0.05). Conclusion 1. Herpes simplex virus type Ⅰ can be formed within the arachnoid latent. Arachnoid adhesions of the trigeminal nerve root zone is closely related to herpes simplex virus type I infection. Arachnoid adhesions exacerbated the root zone artery trigeminal nerve root compression, is one of the causes of the cause of trigeminal neuralgia. Microvascular decompression in the treatment of primary trigeminal neuralgia can cause latent infection with HSV-1 reactivation.

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CLC: > Medicine, health > Neurology and psychiatry > Neurology > Peripheral nerves and ganglia disease > Brain disease > Trigeminal nerve disease
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