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

Nurieva, Olga; Kotikova, Katerina; Urban, Pavel; Pelclová, Daniela; Petrik, Vit; Navrátil, Tomáš; Zakharov, Sergey

doi:10.1007/s00706-015-1580-y

Cited by 20 publications

(12 citation statements)

References 39 publications

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“…Finally, in the group of patients with brain haemorrhages, the long‐term visual damage was present more often than in the group of patients without haemorrhagic lesions ( p < 0.001) and in the group of patients with non‐haemorrhagic CNS damage ( p = 0.015), as it was shown earlier . This fact confirms that brain haemorrhages generally occur in the most severely poisoned patients with combined damage of the optic nerve, retinal–blood barrier, retinal ganglion cells and brain structures.…”

Section: Discussionsupporting

confidence: 82%

Acute Methanol Poisoning: Prevalence and Predisposing Factors of Haemorrhagic and Non‐Haemorrhagic Brain Lesions

Zakharov

Kotikova

Vaněčková

et al. 2016

Basic Clin Pharma Tox

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Abstract:The purpose was to study the prevalence and predisposing factors of brain lesions in survivors of acute methanol poisoning. Clinical data on 106 patients with methanol poisoning were collected during the Czech mass poisoning outbreak. Of 83 survivors, in 46 (55%) patients, follow-up examinations including magnetic resonance imaging of brain (MR) were performed 3-8 and 24-28 months after discharge from the hospital. Of 46 patients with a median age of 49 (interquartile range, 35-57) years, 24 (52%) patients had a total of 40 abnormal brain findings with haemorrhagic lesions detected in 15 (33%) and non-haemorrhagic lesions found in 9 (19%) patients. The patients with haemorrhagic brain lesions were more acidemic (lower arterial blood pH, higher base deficit) and had higher glycaemia and lactacidaemia on admission than those without haemorrhages (all p < 0.05). Thirteen of 32 (41%) of patients with systemic anticoagulation and 2 of 14 (14%) of patients without it had haemorrhagic lesions (p = 0.080). Bleeding complications during the treatment occurred in 4 of 15 (27%) patients, and 5 of 15 (33%) patients had conditions predisposing to haemorrhage in the group with haemorrhagic lesions. In three cases with a series of computer tomography (CT)/MR performed during hospitalization, the necrotic lesions in the brain remained non-haemorrhagic during hospitalization and haemorrhagic lesions were detected on the follow-up MR examinations only. No association between brain haemorrhages and systemic anticoagulation during dialysis was found: brain haemorrhages might occur in severely poisoned patients treated without systemic anticoagulation, whereas treatment with high doses of heparin might not lead to brain haemorrhages.Methanol poisoning due to the consumption of illicit alcoholic beverages represents an important medical problem throughout the world [1][2][3][4][5]. This poisoning generally occurs either intentionally through abuse or attempted suicide or unintentionally through misuse or accident [6,7]. Despite the progress in diagnosis and treatment of methanol poisoning, morbidity and mortality are still high [8,9]. If therapeutic measures are inadequate or delayed, mortality may exceed 40% and serious longterm visual and central nervous system (CNS) sequelae may occur [10][11][12]. The strategy of active case finding and prehospital ethanol administration in the patients with suspected poisoning can improve outcome in a large-scale outbreak of methanol poisoning [13,14].Methanol in the human organism is metabolized to the highly toxic formic acid/formate ion, which inhibits mitochondrial respiration [15][16][17][18]. The accumulation of formic acid results in metabolic acidosis, visual impairment and damage to basal ganglia [19][20][21]. Rapid administration of antidotes and haemodialysis are crucial for successful treatment [22][23][24][25]. Importance.The role of haemodialysis in the treatment of methanol poisoning is well-established: it effectively eliminates both methanol and formate and helps to cor...

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Section: Discussionsupporting

confidence: 82%

Acute Methanol Poisoning: Prevalence and Predisposing Factors of Haemorrhagic and Non‐Haemorrhagic Brain Lesions

Zakharov

Kotikova

Vaněčková

et al. 2016

Basic Clin Pharma Tox

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“…We previously reported that the conductivity of the optic nerve had been restored in more than 80% of patients during the 2 years after acute methanol-induced optic neuropathy. 49 On the other hand, progressing chronic retinal axonal degeneration leads to the strengthening of the association between RNFL thickness and the N1P1 amplitude of VEP. 50 The interesting finding was the association between the amplitude of VEP and the rate of chronic axonal loss: the lower the initial N1P1amplitude (ie, the higher the number of acutely damaged retinal ganglion cells), the higher the rate of chronic axonal degeneration during the following years.…”

Section: Discussionmentioning

confidence: 99%

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

Nurieva

Diblik

Kuthan

et al. 2018

American Journal of Ophthalmology

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“…In acute methanol-induced neuronal damage of optic nerve and retina, the residual peripapillary edema persists for up to 2 months after discharge and the process of chronic remyelination of axons lasts for up to 2 years after acute optic neuritis [55,56]. The same process might take place in the brain neurons (optic nerve is part of CNS), what could have an impact on the biomarkers of neuroinflammation and lipid peroxidation during the first months after acute poisoning.…”

Section: Discussionmentioning

confidence: 99%

Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning

Hlusicka

Löster

Lischková

et al. 2018

Clinical Toxicology

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Our results demonstrate that lipid peroxidation plays a significant role in the mechanisms of acute methanol poisoning. The acute concentrations of three measured biomarkers were elevated in comparison with the follow-up concentrations. Neuronal membrane lipid peroxidation seems to activate leukotriene-mediated inflammation as a part of the neuroprotective mechanisms. No cases of persistent elevation were registered among the survivors 2 years after discharge.

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

Cited by 20 publications

References 39 publications

Acute Methanol Poisoning: Prevalence and Predisposing Factors of Haemorrhagic and Non‐Haemorrhagic Brain Lesions

Acute Methanol Poisoning: Prevalence and Predisposing Factors of Haemorrhagic and Non‐Haemorrhagic Brain Lesions

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

Role of activation of lipid peroxidation in the mechanisms of acute methanol poisoning

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