Surgical Treatment for Traumatic Optic Neuropathy

Oh, Hyung Geun; Yeo, Dong-Gyu; Hwang, Sun Chul

doi:10.13004/kjnt.2018.14.2.55

Cited by 24 publications

(23 citation statements)

References 34 publications

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“…Although numerous clinical trials and fundamental research has been conducted, therapeutic strategies for TON are still limited, which may be owing to the insufficient perception of the pathophysiological mechanisms in the progression of TON ( Chaon and Lee, 2015 ; Sosin et al, 2016 ). Nowadays, corticosteroids and optic nerve decompressive surgery are major treatments for TON, though neither of them could reach definitive curative effects ( Emanuelli et al, 2015 ; Oh et al, 2018 ). Therefore, it is urgent to explore more effective ways to improve the vision of TON patients.…”

Section: Introductionmentioning

confidence: 99%

The Alteration of M6A-Tagged Transcript Profiles in the Retina of Rats After Traumatic Optic Neuropathy

Zhu

et al. 2021

Front. Genet.

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Messager RNA (mRNA) can be modified in a variety of ways, among which the modification of N6-methyladenosine (m6A) is one of the most common ones. Recent studies have found that the m6A modification in mRNA could functionally regulate the splicing, localization, translation, and stability of mRNA, which might be closely related to multiple diseases. However, the roles of m6A modification in traumatic optic neuropathy (TON) are unknown. Herein, we detected the expression of m6A-related genes via quantitative real-time PCR (qRT-PCR) and performed methylated RNA immunoprecipitation sequencing (MeRIP-seq) as well as RNA-sequencing to analyze the alteration profiles of m6A modification after TON. The results showed that the expression of m6A-related genes (METTL3, WTAP, FTO, and ALKBH5) were all upregulated after TON. In all, 2,810 m6A peaks were differentially upregulated and 689 m6A peaks were downregulated. In addition, the hypermethylated and hypomethylated profiles of mRNA transcripts were also identified. To sum up, our study revealed the differentially expressed m6A modification in the early stage of TON, which may provide novel insights into the mechanism and treatment of TON.

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Section: Introductionmentioning

confidence: 99%

The Alteration of M6A-Tagged Transcript Profiles in the Retina of Rats After Traumatic Optic Neuropathy

Zhu

et al. 2021

Front. Genet.

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“…Releasing the compression exerted by edema, hematoma, or fractured bone segments on the optic nerve is the rationale for surgery in TON. It can be indicated in the following situations: presence of bone segments or hematoma compressing the nerve in initial posttrauma images, poor response to initial medical treatment, evidence of optic nerve damage in preoperative VEP scan, or lack of evident damage to ocular tissues and intracranial optic nerve [ 70 ].…”

Section: Resultsmentioning

confidence: 99%

“…Accordingly, it may be recommended that in selected patients with appropriate indications, late surgical intervention is better than not intervening. Apparently, complete atrophy of the nerve, disruption of the intracranial portion of the ON, presence of carotid-cavernous fistula, and unstable systemic condition for general anesthesia should be considered as contraindications for any kind of surgical intervention [70]. e three main approaches performed for decompression of the optic nerve include medial transorbital and external ethmoidectomy, transcranial surgery, and endoscopic transnasal approach.…”

Section: Surgical Treatment Of Tonmentioning

confidence: 99%

A Systematic Literature Review on Traumatic Optic Neuropathy

Karimi

Arabi

Ansari

et al. 2021

Journal of Ophthalmology

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Traumatic optic neuropathy (TON) is an uncommon vision-threatening disorder that can be caused by ocular or head trauma and is categorized into direct and indirect TON. The overall incidence of TON is 0.7–2.5%, and indirect TON has a higher prevalence than direct TON. Detection of an afferent pupillary defect in the presence of an intact globe in a patient with ocular or head trauma with decreased visual acuity strongly suggests TON. However, afferent pupillary defects may be difficult to detect in patients who have received narcotics that cause pupillary constriction and in those with bilateral TON. Mechanical shearing of the optic nerve axons and contusion necrosis due to immediate ischemia from damage to the optic nerve microcirculation and apoptosis of neurons is a probable mechanism. The proper management of TON is controversial. High-dose corticosteroid therapy and decompression of the optic nerve provide no additional benefit over observation alone. Intravenous erythropoietin may be a safe and efficient treatment for patients with TON.

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“…Little evidence exists on the positive impact of ON decompression surgery in TON, both in animal models and in clinical trials (Ohlsson & Svensson, 2007;Wohlrab, Maas, & Carpentier, 2002). Most of the publications on the subject mainly involve retrospective case series (Oh, Yeo, & Hwang, 2018) and fail to demonstrate strong evidence that surgical decompression is significantly better that other treatment options. Moreover, in these studies, different surgical techniques were applied making the decision for the optimal approach even more difficult.…”

Section: Current Treatmentmentioning

confidence: 99%

Models and treatments for traumatic optic neuropathy and demyelinating optic neuritis

Bastakis

Ktena

Καραγωγεωσ

et al. 2019

Developmental Neurobiology

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Pathologies of the optic nerve could result as primary insults in the visual tract or as secondary deficits due to inflammation, demyelination, or compressing effects of the surrounding tissue. The extent of damage may vary from mild to severe, differently affecting patient vision, with the most severe forms leading to complete uni‐ or bilateral visual loss. The aim of researchers and clinicians in the field is to alleviate the symptoms of these, yet uncurable pathologies, taking advantage of known and novel potential therapeutic approaches, alone or in combinations, and applying them in a limited time window after the insult. In this review, we discuss the epidemiological and clinical profile as well as the pathophysiological mechanisms of two main categories of optic nerve pathologies, namely traumatic optic neuropathy and optic neuritis, focusing on the demyelinating form of the latter. Moreover, we report on the main rodent models mimicking these pathologies or some of their clinical aspects. The current treatment options will also be reviewed and novel approaches will be discussed.

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Surgical Treatment for Traumatic Optic Neuropathy

Cited by 24 publications

References 34 publications

The Alteration of M6A-Tagged Transcript Profiles in the Retina of Rats After Traumatic Optic Neuropathy

The Alteration of M6A-Tagged Transcript Profiles in the Retina of Rats After Traumatic Optic Neuropathy

A Systematic Literature Review on Traumatic Optic Neuropathy

Models and treatments for traumatic optic neuropathy and demyelinating optic neuritis

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