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The Experimental Research of Trigeminal Neuralgia Combined Trigeminal Nerve Root Zone Arachnoids’ Adhesions with HSV-1 Virus Infection

Author: SunYanChun
Tutor: ChenJian
School: Jinan University
Course: Surgery
Keywords: Trigeminal neuralgia Arachnoid Herpes simplex virus type Ⅰ Proliferative infection Interleukin- 6
CLC: R745.11
Type: Master's thesis
Year: 2011
Downloads: 12
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Abstract

Purpose has been the cause of trigeminal neuralgia is unclear, the trigeminal nerve root compression by vascular anomalies only at least a factor of two. Viral infections, especially herpes simplex virus type I, because of its latent and neurotropic in the body after the initial infection with the virus, along the trigeminal nerve retrograde into the trigeminal ganglion, and the formation of latent infection here, when the body suffer from stress, trauma, radiation, and other immunosuppressant drugs, poor immune function or immune disorders, the virus can be activated again, thus the formation of proliferative infection. Therefore, TN occurrence and development process plays a decisive role. And IL-6 is a molecular weight of 21 ~ 26 KD, the 184 amino acid residues of a glycoprotein, which not only can mediate and regulate the immune response is also involved in a number of latent viral infections and recurrent diseases regulation. In HSV-1 infection and reactivation of latent infection during the formation of proliferation, IL-6 have played an important role, and can induce recurrence of HSV-1. To this end, we want to start from the arachnoid adhesions organizations to explore the trigeminal nerve in patients with trigeminal neuralgia root zone arachnoid adhesions tissue of HSV-1 infection, in combination with IL-6 对 effect of HSV-1, HSV-1 and thus to further explore the relationship between infection and trigeminal neuralgia. Methods 79 cases for patients with trigeminal neuralgia microvascular decompression. Among 57 patients in the intraoperative see the trigeminal nerve root zone exists arachnoid adhesions, whichever arachnoid as the experimental group; (which merged with thickened arachnoid adhesions and no vascular compression or venous vascular oppressors only see 7 cases, there arachnoid adhesions and associated with arterial vascular oppressors 50 cases). Another 22 patients in the microvascular decompression in the see the trigeminal nerve root zone and no significant presence of vascular compression arachnoid adhesions were arachnoid whichever root zone as a control group. And specimens from all patients in the preoperative fasting blood after centrifugation serum specimens. First detected by PCR arachnoid tissue adhesions, no adhesion of arachnoid tissue specificity of HSV-1 DNA fragments were detected by Western Blot and then HSV-1 antigen expression; based on PCR and Western Blot results to determine the viral infection status (latent infection: positive for viral DNA fragments of the virus antigen negative; proliferation infection: positive for viral DNA fragment, and the viral antigen-positive), the re-divided latent HSV-1 infection, proliferation and infection, uninfected group, then ELISA quantitative detection method were three groups of arachnoid specimens and serum IL-6 levels. Results The 57 cases of specimens with 40 cases HSV-1 DNA, the positive rate was 70.18%; specimens of the control group 22 cases, 13 cases, the positive rate was 59.09%; After statistical analysis, found that the positive rate of the two groups showed no statistically significant difference (p gt; 0.05). While the experimental group 57 cases, 28 cases specimens viral antigen, the positive rate was 49.12%; specimens in the control group 22 cases, 5 cases, the positive rate was 22.73%. The statistical analysis showed that the experimental group HSV-1 virus antigen positive rate was higher, and there is statistically significant difference (p lt; 0.05). According to results of PCR and Western Blot, and then 79 cases of trigeminal neuralgia patients were divided into latent infection arachnoid 20 patients, 33 patients infected with the proliferation of uninfected group, 26 cases; proliferation of arachnoid tissue infection of IL-6 higher than latent infection, also higher than the uninfected group; latent infection group and also higher than the non-infected group were statistically significant (p lt; 0.01); while serum IL-6 levels in the three groups were no significant difference (p gt; 0.05). Conclusion 1, HSV-1 infection may induce proliferation or aggravate the trigeminal nerve root zone arachnoid adhesions. 2, IL-6 may be infected with HSV-1 proliferation important in the process medium. 3, arachnoid tissue may also be latent HSV-1 base. 4, HSV-1 infection may be caused by following the vascular compression of the trigeminal nerve root zone outside the arachnoid adhesions another reason. 5, HSV-1 infection may be associated with trigeminal neuralgia, the development of a certain relationship.

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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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