Methanol-induced Optic Neuropathy Research Articles

Predicting the outcome in methanol-induced optic neuropathy cases: A guessing game?

Predicting the outcome in methanol-induced optic neuropathy cases: A guessing game?

Visual outcome of methanol toxic optic neuropathy after erythropoietin treatment in Riyadh, Saudi Arabia.

The purpose of this study is to evaluate the visual response of methanol-induced optic neuropathy to management with erythropoietin (EPO) along with conventional therapy. This retrospective case series examines the ophthalmological data of patients diagnosed with methanol-induced optic neuropathy between 2020 and 2021 at two centers, Riyadh, Saudi Arabia. Patients' characteristics and the results of initial and final ophthalmological examinations were documented and compared between patients who received EPO in addition to conventional management and those who received only conventional management. A total of nine cases were reviewed, of which eight (88.9%) were males and one was female (11.1%). The mean age was 37.7 years. At presentation, funduscopic examination revealed optic disc edema in four eyes (two patients), and 14 eyes had normal appearance (seven patients). Among the nine patients who received conventional management, 5 (55.6%) additionally received intravenous EPO during the treatment course. There was no clinically or statistically significant difference in terms of visual outcome between the two groups. The mean visual acuity at the final presentation was 1.32 ± 0.79 logarithm of the minimum angle of resolution (LogMAR) in the EPO group and 1.36 ± 0.85 LogMAR in the non-EPO group. Optical coherence tomography indicated that the EPO group had an average retinal nerve fiber layer thickness of 48.13μm (±6.2), at the final assessment. Managing the visual impairments in individuals with methanol-induced optic neuropathy using intravenous EPO resulted in similar final visual outcomes compared to conventional management.

Outbreak of methanol-induced optic neuropathy in early COVID-19 era; effectiveness of erythropoietin and methylprednisolone therapy.

Methanol is a highly toxic, non-potable alcohol. Outbreaks of methanol toxicity occur due to its fraudulent addition to alcoholic beverages as a cheaper substitute for ethanol. Recently, alongside the coronavirus disease 2019 (COVID-19) pandemic, rumors circulated on social media that consuming alcohol can prevent or cure the virus, leading to a COVID-19 and methanol-induced optic neuropathy (MON) syndemic. To investigate the impact of erythropoietin (EPO) on the outcomes of patients diagnosed with MON. In this prospective study, 105 patients presenting with acute bilateral visual loss secondary to methanol intoxication were enrolled from March to May 2020 at Farabi Eye Hospital. A comprehensive ocular examination was conducted for all participants. Recombinant human EPO and methylprednisolone were administered intravenously to all patients for three consecutive days. The mean age of the participants was 39.9 years (± 12.6). Ninety-four patients were male and eleven were female. The mean pre-treatment best corrected visual acuity (BCVA) improved from 2.0 ± 0.86 to 1.39 ± 0.69 logarithm of the minimum angle of resolution post-treatment (P < 0.001), with significant improvement observed in all age categories and genders (P < 0.001). Visual acuity improvement was also significant regardless of whether the patient presented before or after 72 h (P < 0.001), and the post-treatment BCVA remained significant at all monthly follow-up visits (P < 0.001). EPO and methylprednisolone therapy have been shown to be effective in improving visual outcomes in patients with MON when administrated within the first month of exposure. Public awareness efforts are necessary to prevent further outbreaks of methanol toxicity in the current COVID-19 era.

Acute Treatment of Methanol-Induced Optic Neuropathy.

Acute Treatment of Methanol-Induced Optic Neuropathy.

Clinical Characteristics of Methanol-Induced Optic Neuropathy: Correlation between Aetiology and Clinical Findings

To show the clinical characteristics, identify the magnetic resonance imaging (MRI) and optical coherence tomography (OCT) features, and observe the visual outcome of methanol-induced optic neuropathy. Clinical data were retrospectively collected from in-patients diagnosed with methanol-induced optic neuropathy in the Neuro-Ophthalmology Department of the Chinese People's Liberation Army General Hospital from January 2016 to January 2021. Eight patients were included in this study. The exposure time was 6-34 h for ingestion, 3-4 months for inhalation, and more than ten years for skin absorption. All patients demonstrated bilateral acute visual impairment. Seven of eight patients had other accompanying systemic symptoms. Seven of eight patients demonstrated optic nerve lesions in MRI, and five presented with a hyperintense T2 signal in a "central" type. OCT showed the macular ganglion cell layer and inner plexiform layer (mGCL-IPL) thinning before the peripapillary retinal nerve fiber layer (pRNFL) thinning. The visual improvement was achieved transiently for seven of eight patients after treatment. One patient with a mitochondrial DNA mutation maintained a bilateral no-light perception (NLP) from the onset to the last visit. All patients had poor visual prognoses, with either light perception or NLP. Methanol-induced optic neuropathy is a rare bilateral optic neuropathy with a poor visual outcome. A centrally hyperintense T2 signal of the optic nerve is common in methanol-induced optic neuropathy. The thinning of the mGCL-IPL is more sensitive than that of the pRNFL for early diagnosis. A mitochondrial genetic defect may be a predisposing factor for methanol-induced optic neuropathy.

Optical Coherence Tomography Angiography and Structural Analyses of the Pale Optic Discs: Is It Possible to Differentiate the Cause?

ABSTRACT Introduction: To compare the optic nerve head (ONH) structure and microvasculature in patients with optic atrophy due to non-arteritic anterior ischemic optic neuropathy (NAION), compressive optic neuropathy (CON), methanol-induced optic neuropathy (MION), and traumatic optic neuropathy (TON) using optical coherence tomography angiography. Methods: In this comparative, cross-sectional study, 32 eyes with NAION, 18 eyes with CON, 32 eyes with MION, 23 eyes with TON, and 55 normal eyes were enrolled. Radial peripapillary capillary (RPC) vessel density, peripapillary retinal nerve fiber layer (RNFL) thickness, disc area, cup volume, and cup/disc area ratio were obtained using the RTVue XR Avanti system (Optovue Inc., Fremont, CA, USA). Results: RPC vessel density and peripapillary RNFL thickness in all patients were significantly lower than normal subjects. A positive correlation was found between the RPC vessel density and peripapillary RNFL thickness in normal subjects and all study groups. The positive correlation between the inside and outside disc RPC vessel density was only found in the NAION (r = 0.36, P = .042) and MION (r = 0.42, P = .018) groups. No significant difference was found among the groups in terms of peripapillary and inside disc vascular densities (all P > .05). Disc area and cup volume in patients with MION was larger than the values in patients with NAION (P = .018) and TON (P = .044) and normal subjects (P = .015). The discriminating features among the study groups were the larger cup volume and cup/disc area ratio in patients with MION, and lower RNFL thickness in patients with TON. Conclusions: There was a positive correlation between the RNFL thickness and peripapillary RPC vessel density regardless of the cause of optic disc pallor. Structural evaluation of the ONH seems to be a better way to differentiate the cause of optic nerve head atrophy than the microangiographic changes.

Methanol-induced optic neuropathy

Methanol-induced optic neuropathy

Effects of adenosine triphosphate on methanol-induced experimental optic nerve damage in rats: biochemical and histopathological evaluation

Purpose Acute methanol exposure leads to systemic intoxication and toxic optic neuropathy. In this experimental study, we aimed to determine the protective effects of intravenous administration of ATP in methanol-induced optic neuropathy. Materials and methods A total of 18 male albino Wistar rats weighing between 267 and 282 g were used for the experiment. The animals were divided into three groups as healthy control (HC), methanol (M), and methanol + ATP (M-ATP) groups. Distilled water was given to the healthy control group (n = 6) as the solvent, while 20% methanol was administered orally to the rats in M (n = 6) and M-ATP (n = 6) groups at a dose of 3 g/kg. Four hours after the administration of 20% methanol orally to the M-ATP group, ATP was injected intraperitoneally at a dose of 4 mg/kg. Eight hours after ATP injection, the animals were sacrificed by high-dose (50 mg/kg) thiopental anaesthesia and biochemical and histopathological examinations were performed on the removed optic nerve tissues. Malondialdehyde (MDA), total glutathione (tGSH), total oxidant status (TOS) and total anti-oxidant status (TAS) were analysed with biochemical tests. Results MDA, TOS and OSI were significantly higher and tGSH and TAS levels were significantly lower in methanol administered group compared with the healthy controls or M-ATP group (p: 0.001). There was not any significant difference between healthy controls and M-ATP group regarding the oxidative stress parameters. There was a significant destruction and increase in thickness and astrocyte numbers and edema-vacuolization in methanol administered group compared with the healthy controls or M-ATP group (p: 0.001). Conclusion Intravenous ATP administration had a significant positive effect on the oxidative stress parameters and optic nerve structure in methanol-intoxicated rats. Antioxidant therapies should be considered in future studies as a possible therapy for methanol-induced toxic optic neuropathy.

Efficacy of high-dose intravenous steroid treatment in methanol-induced optic neuropathy: A systematic review

Efficacy of high-dose intravenous steroid treatment in methanol-induced optic neuropathy: A systematic review

Protective effects of Rutin against methanol induced acute toxic optic neuropathy: an experimental study.

To determine the effects of Rutin on methanol induced optic neuropathy and compare the results with the effects of ethanol. Totally 30 rats were divided into 5 groups, with 6 rats in each group as follows: healthy controls (C), methotrexate (MTX), methotrexate+methanol (MTM), methotrexate+methanol+ethanol (MTME) and methotrexate+ methanol+Rutin (MTMR). In all rabbits except those of the control group, MTX, diluted in sterile serum physiologic, 0.3 mg/kg per oral was applied for 7d by the aid of a tube. After this procedure to the rats of MTM, MTME and MTMR groups, 20% methanol with a dose of 3 g/kg per oral was given by the aid of a tube. In MTME group, 4h after the application of methanol, 20% ethanol was applied by the same way with a dose of 0.5 g/kg. On the other hand, in MTMR group 4h after the application of methanol, Rutin, which was dissolved in distilled water, was applied by the same way with a dose of 50 mg/kg. There were statistically significant differences in tissue 8-hydroxy-2 deoxyguanine (8-OHdG), interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), malondialdehyde (MDA), myeloperoxidase (MPO). glutathione peroxidase (tGSH) and superoxide dismutase (SOD) levels between groups (P<0.001). In MTMR group tissue 8-OHdG, IL-1β, MDA, and MPO levels were similar with the healthy controls but significantly different than the other groups. In histopathological evaluations, in MTX group there was moderate focal destruction, hemorrhage and decrease in number of astrocytes and oligodendrocytes; in MTM group there was severe destruction and edema with decrease in number of astrocytes and oligodendrocytes; in MTME group there was mild hemorrhage, mild edema, mildly dilated blood vessels with congestion while in MTMR group, optic nerve tissue was resembling the healthy controls. Rutin may prevent methanol-induced optic neuropathy via anti-inflammatory effects and decreasing the oxidative stress. New treatment options are warranted in this disease to avoid loss of vision in patients.

Progressive Chronic Retinal Axonal Loss Following Acute Methanol-induced Optic Neuropathy: Four-Year Prospective Cohort Study

To study the dynamics and clinical determinants of chronic retinal nerve fiber layer thickness (RNFL) loss after methanol-induced optic neuropathy. Prospective cohort study. All patients underwent complete ophthalmic evaluation including spectral-domain optical coherence tomography 3 times during 4 years of observation: 4.9 (±0.6), 25.0 (±0.6), and 49.9 (±0.5) months after discharge. Eighty-four eyes of 42 survivors of methanol poisoning, mean age (standard deviation) of 45.7 (±4.4) years; and 82 eyes of 41 controls, mean age 44.0 (±4.2) years. Global and temporal RNFL loss. Abnormal RNFL thickness was registered in 13 of 42 (31%) survivors of methanol poisoning and chronic axonal loss in 10 of 42 (24%) patients. Significant decrease of global/temporal RNFL thickness during the observation period was found in the study population compared to the controls (P < .001). The risk estimate of chronic global RNFL loss for arterial blood pH < 7.3 at admission was 11.65 (95% confidence interval 1.91-71.12) after adjusting for age and sex. The patients with chronic axonal degeneration demonstrated progressive visual loss in 7 of 10 cases. The patients with abnormal RNFL thickness had magnetic resonance signs of brain damage in 10 of 13 vs 8 of 29 cases with normal RNFL thickness (P= .003). Signs of brain hemorrhages were present in 7 of 13 patients with abnormal RNFL thickness vs 5 of 29 cases with normal RNFL thickness (P= .015). Methanol-induced optic neuropathy may lead to chronic retinal axonal loss during the following years. Arterial blood pH on admission is the strongest predictor of chronic RNFL thickness decrease. Chronic retinal neurodegeneration is associated with the progressive loss of visual functions and necrotic brain lesions.

Evaluation of the effect of erythropoietin + corticosteroid versus corticosteroid alone in methanol-induced optic nerve neuropathy

Purpose: Following methanol intoxication, optic nerve neuropathy may occur, which is currently treated by different therapeutic regimens. Erythropoietin (EPO) has recently been introduced as a good therapeutic option in methanol-induced optic neuropathy. The aim of the current study was to evaluate the efficacy of EPO in improvement of the visual disturbances in methanol-intoxicated patients.Materials and methods: In a case-control study, all patients who had referred to our toxicology centre with confirmed diagnosis of methanol toxicity were considered to be included. Of them, those who had referred with visual disturbances, survived, and their visual disturbances had not improved after haemodialysis were entered. Cases received EPO and corticosteroids while controls only received corticosteroids. They were then compared regarding their visual outcome.Results: All five patients in the control group mentioned that after discharge, their visual acuity had improved while in the cases, three mentioned visual improvement, two mentioned their visual acuity had deteriorated after discharge, two mentioned no change in their visual acuity and three mentioned that their visual acuity had first improved but then deteriorated with a mean two-month interval period. In fundoscopic evaluations, two controls had normal fundospcopy while eight cases had abnormal fundoscopy (p = 0.055).Conclusions: Protective effect of EPO on methanol-induced optic nerve may be strong at the beginning of the intervention but is probably transient.

Intravitreal erythropoietin injection in late-stage optic neuropathy: a safety study on human.

To evaluate the whether intravitreal erythropoietin (EPO) administration has any beneficial or adverse effect in patients with late-stage optic neuropathy (ON) or not. The study examined 16 eyes of 16 patients who had late-stage ON and ≥1/20 best-corrected visual acuity (BCVA) in their affected eye. There were nonarteritic ischemic ON in 10 (62.5%) eyes, traumatic ON in 4 (25.0%) eyes and methanol-induced ON in 2 (12.5%) eyes. Using pars plana approach, 2000IU/0.2ml EPO was administered intravitreally with a 30-gauge needle. Injections were administered three times with 6-week intervals. We compared the differences in the BCVA, intraocular pressure (IOP), retinal nerve fiber layer (RNFL) thickness, pattern visual evoked potentials (p-VEP) and pattern electroretinography (p-ERG) parameters performed at initial examination and final visits. The mean age of the patients was 52.38±12.00years; 2 (12.50%) of them were female, and 14 (87.50%) of them were male. The mean BCVA levels of 16 patients with optic atrophy were 1.12±0.25 logMAR at the initial examination and 1.08±0.26 logMAR at the final visit (p=0.102). There was no statistically significant difference between the initial and final RNFL thicknesses, IOP values, p-ERG or p-VEP responses. Intravitreal EPO injections have no beneficial or detrimental effect on the late stage of ON. Further studies are necessary to compare our results in patients with ON in earlier stages.

Erythropoietin as an adjunctive treatment for methanol-induced toxic optic neuropathy

ABSTRACTBackground: Methanol-induced optic neuropathy (MTON) is frequently seen in countries where alcohol consumption is banned or poorly regulated. MTON frequently results in blindness and there is no empirically validated treatment. Objective: To evaluate the effect of erythropoietin (EPO) as an adjunctive treatment for MTON. Methods: In this nonrandomized interventional comparative study, all participants were diagnosed with MTON and received the steroid methylprednisolone. Eleven participants received intravenous EPO (10000 IU twice a day) for three days as an adjuvant to methylprednisolone (EPO group); 11 participants in a historical control group received methylprednisolone only (control group). Main outcomes were best-corrected visual acuity (BCVA), peripapillary retinal nerve fiber layer thickness (PRNFLT), and visual field mean deviation (MD). Results: Mean BCVA improved significantly in both groups: from 2.93 ± 0.55 to 1.75 ± 1.16 LogMAR at month 3 (p < 0.001) in the EPO group, and from 2.65 ± 0.68 to 2.19 ± 0.75 at final visit in the control group (p = 0.001). The final BCVA was significantly better in the EPO group (p = 0.012). The mean PRNFLT decreased in both groups. However, at the final follow-up, PRNFLT was significantly thinner in the control group (53 ± 6 vs. 77 ± 26 microns, respectively; p < 0.001). Conclusion: Intravenous EPO plus high-dose intravenous steroid may be an effective combination therapy for the patients with MTON.

Prevalence, dynamics, and biochemical predictors of optic nerve remyelination after methanol-induced acute optic neuropathy: a 2-year prospective study in 54 patients

We conducted a prospective study in 54 patients with a median age of 48 years (range 23–73) to determine the prevalence and dynamics of optic nerve remyelination after methanol-induced optic neuropathy. Methanol was measured by a gas chromatographic method with flame ionization detection. Formate was measured enzymatically. Measurement of full-field visual evoked potential with monocular checkerboard pattern-reversal stimulation was performed 3–8 and 24–28 months after discharge. The latency of the positive peak (P1) was used for the analysis of remyelination dynamics. Twenty-seven patients had abnormal P1 latencies. Mean P1 latency for right eyes (REs) was 115.3 ± 2.1 ms and for left eyes (LEs) was 117.4 ± 3.2 ms. The group with abnormal latency had lower arterial pH (p = 0.017), higher anion gap (p = 0.013), methanol (p = 0.027), base deficit (p = 0.033), and lactate (p = 0.048). At the second examination, shortening of P1 latencies was registered (REs/LEs 98.3 ± 2.4/102.7 ± 4.5 ms; p < 0.001). The dynamics of latency shortening for REs/LEs were 17 ± 1.3/15.1 ± 3.1 ms, with insignificant inter-eye difference (p = 0.271). The dynamics of remyelination correlated with serum methanol (r = −0.588; p < 0.001), arterial pH (r = 0.339; p = 0.040), and concentration of carbohydrate-deficient transferrin (r = −0.411; p = 0.011). Remyelination occurred in cases of mild or moderate damage of myelin sheaths; no improvement of conduction was found in severe cases. The dynamics of remyelination correlated with the degree of acidosis and severity of poisoning. Chronic alcohol abuse had a negative effect on remyelination dynamics.