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      Endoscopic Vascular Decompression for the Treatment of Trigeminal Neuralgia: Clinical Outcomes and Technical Note

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          Abstract

          Purpose

          Microvascular decompression (MVD) surgery is considered as an effective method with which to treat trigeminal neuralgia (TN). However, sometimes MVD surgery fails due to incomplete decompression of the responsible vessels caused by a poor visual field. In this study, we evaluated the benefits of endoscopic visualization and the value of full endoscopic vascular decompression (EVD) by describing the surgical results of 20 patients with TN after EVD.

          Patients and Methods

          This was a retrospective study in a single institution of 20 patients with TN who received EVD between April 2018 and October 2019. All patients underwent EVD via the suboccipital retrosigmoid approach without microscopy at any stage. Abnormal muscle response (AMR) and brainstem auditory evoked potentials (BAEPs) were routinely monitored throughout the procedure. Follow-up was conducted by outpatient and telephone interviews. The degree of facial pain was graded using the Barrow Neurological Institute (BNI) pain intensity score; a BNI of 1 was considered as the best result while a BNI of 2 or 3 was considered as a satisfactory result. Follow-up time ranged from 8 to 24 months, with a mean of 18±4.36 months.

          Results

          All 20 patients with severe preoperative pain (BNI of 5) achieved immediate relief or complete control of pain after surgery (BNI of 1 to 2). Vascular conflicts were observed during surgery in all of the patients. None of the patients experienced hearing loss, facial paralysis, intracranial infection, cerebrospinal fluid leakage, cerebral hemorrhage, or death, following the operation.

          Conclusion

          When carried out by surgeons with endoscopic experience, EVD can provide a clear surgical field of view and reduce the risk of surgical injury. Our findings indicate that EVD is a safe and effective surgical method for the treatment of TN.

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          Most cited references 19

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          Trigeminal neuralgia: pathology and pathogenesis.

           S Love,  H B Coakham (2001)
          There is now persuasive evidence that trigeminal neuralgia is usually caused by demyelination of trigeminal sensory fibres within either the nerve root or, less commonly, the brainstem. In most cases, the trigeminal nerve root demyelination involves the proximal, CNS part of the root and results from compression by an overlying artery or vein. Other causes of trigeminal neuralgia in which demyelination is involved or implicated include multiple sclerosis and, probably, compressive space-occupying masses in the posterior fossa. Examination of trigeminal nerve roots from patients with compression of the nerve root by an overlying blood vessel has revealed focal demyelination in the region of compression, with close apposition of demyelinated axons and an absence of intervening glial processes. Similar foci of nerve root demyelination and juxtaposition of axons have been demonstrated in multiple sclerosis patients with trigeminal neuralgia. Experimental studies indicate that this anatomical arrangement favours the ectopic generation of spontaneous nerve impulses and their ephaptic conduction to adjacent fibres, and that spontaneous nerve activity is likely to be increased by the deformity associated with pulsatile vascular indentation. Decompression of the nerve root produces rapid relief of symptoms in most patients with vessel-associated trigeminal neuralgia, probably because the resulting separation of demyelinated axons and their release from focal distortion reduce the spontaneous generation of impulses and prevent their ephaptic spread. The role of remyelination in initial symptomatic recovery after decompression is unclear. However, remyelination may help to ensure that relief of symptoms is sustained after decompression of the nerve root and may also be responsible for the spontaneous remission of the neuralgia in some patients. In addition to causing symptomatic relief, vascular decompression leads to rapid recovery of nerve conduction across the indented root, a phenomenon that, we suggest, is likely to reflect the reversal of compression-induced conduction block in larger myelinated fibres outside the region of demyelination. Trigeminal neuralgia can occur in association with a range of other syndromes involving vascular compression and hyperactivity of cranial nerves. Clinical observations and electrophysiological studies support the concept that demyelination and ephaptic spread of excitation underlie most, if not all, of these conditions.
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            Microvascular relations of the trigeminal nerve. An anatomical study with clinical correlation.

            The vascular relationships of the trigeminal nerve root entry zone were examined bilaterally in 20 cadavers of individuals known to be free of facial pain. Fourteen of 40 nerves made contact with an artery, but only four of these showed evidence of compression or distortion of the nerve. In addition, the vascular relationships of 40 trigeminal nerves exposed surgically for treatment of trigeminal neuralgia were studied, and 31 nerves showed compression by adjacent arteries. Venous compression was seen in four of the cadaver nerves and in eight nerves from patients with trigeminal neuralgia. These data support the hypothesis that arterial compression of the trigeminal nerve is associated with trigeminal neuralgia.
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              A nationwide study of three invasive treatments for trigeminal neuralgia.

              Invasive procedures for treatment of trigeminal neuralgia (TGN) include percutaneous radiofrequency thermocoagulation (PRT), partial sensory rhizotomy (PSR), and microvascular decompression (MVD). Using a nationwide discharge registry from The Netherlands, we assessed the frequency of use and patient characteristics, and evaluated treatment failure for each patient undergoing PRT, PSR, or MVD from January 2002 through December 2004. Only patients without a procedure in the year prior were included. Primary outcome was readmission for repeat procedures for TGN or known complications within 1year. Comparability of patient populations was assessed through propensity scores based on hospital, age, sex, and comorbidity. Conditional logistic regression matched on propensity score was used to calculate relative risks (RR) with 95% confidence intervals (CIs) for repeat procedures or complications. During the study period, 672 patients with TGN underwent PRT, 39 underwent PSR, and 87 underwent MVD. Hospital type was the predominant determinant of procedure type; age, sex, and comorbidity were weak predictors. The RR for repeat procedures for PSR was 0.21 (95% CI: 0.07 to 0.65) and for MVD was 0.13 (95% CI: 0.05 to 0.35) compared with PRT (RR 1). For complications, the RR of PSR was 5.36 (95% CI: 1.46 to 19.64) and of MVD was 4.40 (95% CI: 1.44 to 13.42). Sex, urbanization, and comorbidity did not influence prognosis, but hospital and surgical volume did. In conclusion, although PSR and MVD are associated with a lower risk of repeat procedure than PRT, they seem to be more prone to complications requiring hospital readmission. Microvascular decompression and partial sensory rhizotomy are associated with a lower risk of undergoing a repeat procedure compared with percutaneous radiofrequency thermocoagulation but are more prone to complications requiring readmission to hospital. Copyright © 2010 International Association for the Study of Pain. Published by Elsevier B.V. All rights reserved.
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                Author and article information

                Journal
                J Pain Res
                J Pain Res
                jpr
                jpainres
                Journal of Pain Research
                Dove
                1178-7090
                03 September 2020
                2020
                : 13
                : 2205-2211
                Affiliations
                [1 ]Department of Neurosurgery, The First Affiliated Hospital of Bengbu Medical College , Bengbu 233000, People’s Republic of China
                Author notes
                Correspondence: Zhiquan Jiang Department of Neurosurgery, First Affiliated Hospital of Bengbu Medical College , 287 Changhuai Road, Bengbu, Anhui233004, People’s Republic of ChinaTel +86-13966075971 Email bbjiangzhq@163.com
                Article
                268441
                10.2147/JPR.S268441
                7478366
                © 2020 Sun et al.

                This work is published and licensed by Dove Medical Press Limited. The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed. For permission for commercial use of this work, please see paragraphs 4.2 and 5 of our Terms ( https://www.dovepress.com/terms.php).

                Page count
                Figures: 5, Tables: 2, References: 20, Pages: 7
                Funding
                Funded by: Natural Science Foundation of Anhui Province, open-funder-registry 10.13039/501100003995;
                This study is supported by the Natural Science Foundation of Anhui Province (KJ2018A0995).
                Categories
                Original Research

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