Evaluation of VEP Parameters in Patients Before and After Cardiopulmonary By-Pass Surgery

Introduction: Coronary bypass surgery is emphasized in aetiology of ischemic optic neuropathy. Our aim in this study was to investigate the pattern visual evoked potentials (PVEP) in patients before and after coronary bypass surgery.Methods: Thirty-one patients were included in the study. After a full ophthalmological evaluation, PVEP was assesed in the pre and postoperative periods. Operative times, hematological parameters, blood pressures, number of transfusions, body temperatures, anaesthetic drugs and systemic illnesses were recorded for each patient. Results: The mean age of the patients were 59±10.4 years. There was 22 men and 9 women in the study. Only 3 of them needed transfusion during the surgery. The mean duration of the surgery was 3.2±0.7 hours. None of the patients had a history of visual disturbance or postoperative ischemic optic neuropathy. The mean VEP P100 amplitude was not statistically significantly different but the mean VEP P100 latency showed statistically significant difference between the preoperative and postoperative periods. (p=0.014) This significance was more appereant in patients with systemic illnesses. (p= 0.023) There was a positive correlation between the age and VEP P100 latency. (r = 0.402, p< 0.05) Conclusions: Although surgical techniques and equipments are developing each day in the field of cardiopulmonary bypass surgery, the contributing factors such as hypothermia, anemia and diabetes still seem to affect neurophysiological functions even after a noncomplicated surgery.

Anterior ischemic optic neuropathy as a rare manifestation of COVID-19: a case report

Aim: A variety of manifestations in different organs could be associated with severe COVID-19; for example, ocular manifestations. Case report: A 52-year-old male complaining of sudden onset unilateral painless vision loss in the right eye for 1 month (started just 1 week after COVID-19 remission) came to the ophthalmology clinic. On further evaluations, he was diagnosed with anterior ischemic optic neuropathy (AION). Considering his past history and the result of evaluations, the hypothesis of association between AION and COVID-19 was proposed. Results & discussion: Ocular and neurologic manifestations of COVID-19 are more likely to happen in patients with more severe conditions. Complications occur secondary to two basic mechanisms including severe inflammatory response and hypercoagulable state. Conclusion: Our findings indicated that non-arteritic AION is another manifestation of microangiopathic/thrombotic events which may occur in the course of COVID-19.

Leber’s Hereditary Optic Neuropathy Plus Causing Recurrent Myelopathy due to an MT-DN1 Mutation at G3635A

A 51-year-old man with known Leber’s hereditary optic neuropathy (LHON) presented with worsening lower extremity weakness and numbness. Following an episode of myelopathy two years before, he had been ambulating with a walker but over two weeks became wheelchair bound. He also developed a sensory level below the T4 dermatome to light touch, pinprick, and vibration. MRI of his cervical and thoracic spine showed a nonenhancing T2 hyperintense lesion extending from C2 to T12. At his presentation two years earlier, he was found to have a longitudinally extensive myelopathy attributed to his LHON. Genetic testing revealed a 3635 guanine to adenine mutation. MRI at that presentation demonstrated a C1-T10 lesion involving the central and posterior cord but, unlike the new lesion, did not involve the ventral and lateral horns. Given the similarity to his prior presentation and a negative evaluation for alternative etiologies, he was thought to have recurrent myelopathy secondary to Leber’s Plus. To our knowledge, recurrent myelopathy due specifically to the G3635A mutation in Leber’s Plus has not been reported previously.

Is the Clinical Course of Non-Arteritic Ischemic Optic Neuropathy Associated with Oxidative Damage and the Dynamics of the Antioxidant Response?

Purpose: Oxidative stress is known to be a decisive factor in the wide etiopathogenesis of optic neuropathy. This study aimed to comprehensively evaluate the interaction of optic neuropathy’s clinical course with systemic oxidative damage and antioxidant response dynamics in a large series.Methods: This case-controlled clinical study included 33 non-arteritic anterior ischemic optic neuropathy patients and 32 healthy individuals. Extensive systemic oxidation profiles were statistically compared between the two groups, and correlations between the clinical and biochemical data in the patient group were analyzed.Results: Vitamin E and MDA levels were significantly higher in the patient group. Significant correlations were observed in the analyses between clinical findings and oxidative stress parameters. Correlations between vitamin E and intraocular pressure, between B12 and cup-to-disc ratio, between antioxidant glutathione and SOD enzyme systems, and between uric acid and age were found to be very significant. As significant correlations were found in either clinical and biochemical data or in oxidative stress parameters, correlations between vitamin E and cholesterol, MDA was found to be very significant. Conclusions: This study not only supplies significant information regarding oxidative damage and antioxidant response in NAION, but also points out the specific interactions of neuromodulators, like vitamin E, in intracellular signaling pathways and regulation mechanisms. A better reading of these connections may help improve diagnosis, follow-ups and treatment criteria and strategies.

Methanol-induced optic neuropathy: a still-present problem

Methanol-induced optic neuropathy (Me-ION) is a serious condition that may result in long-term or irreversible visual impairment or even blindness secondary to damage and loss of function of the optic nerve and retina. Me-ION shows a tendency to occur as mass poisonings around the world with a clear predilection for poor societies in developing countries. The main mechanism underlying the molecular basis of Me-ION is the inhibition of the mitochondrial oxidative phosphorylation process through the binding of the toxic metabolite of methanol—formic acid—with the key enzyme of this process—cytochrome c oxidase. However, other mechanisms, including damage to the eye tissues by oxidative stress causing the intensification of the oxidative peroxidation process with the formation of cytotoxic compounds, as well as an increase in the synthesis of pro-inflammatory cytokines and influence on the expression of key proteins responsible for maintaining cell homeostasis, also play an important role in the pathogenesis of Me-ION. Histopathological changes in the eye tissues are mainly manifested as the degeneration of axons and glial cells of the optic nerve, often with accompanying damage of the retina that may involve all its layers. Despite the development of therapeutic approaches, persistent visual sequelae are seen in 30–40% of survivors. Thus, Me-ION continues to be an important problem for healthcare systems worldwide.