Publication:
Visual Evoked Potentials in Patients with Vitamin B12 Deficiency

dc.authorscopusid56060156200
dc.authorscopusid22937689800
dc.authorwosidYildiz, Mustafa Onur/Gry-0328-2022
dc.contributor.authorYildiz, Onur
dc.contributor.authorTilki, Hacer Erdem
dc.date.accessioned2025-12-11T00:42:02Z
dc.date.issued2023
dc.departmentOndokuz Mayıs Üniversitesien_US
dc.department-temp[Yildiz, Onur] Ondokuz Mayis Univ, Fac Med, Dept Neurol, Samsun, Turkiye; [Yildiz, Onur] Ondokuz Mayis Univ, Fac Med, Dept Clin Neurophysiol, Samsun, Turkiyeen_US
dc.description.abstractPurpose: The aim of this study was to investigate the subclinical involvement of the optic nerve in asymptomatic patients with vitamin B12 deficiency using visual evoked potentials.Methods: This study included 40 asymptomatic patients diagnosed with vitamin B12 deficiency (considered as serum levels below 150 pg/mL) and a control group of 40 healthy individuals. All participants underwent a visual evoked potential examination. Routine screening for homocysteine was performed for patients with vitamin B12 deficiency. The levels of vitamin B12 and homocysteine and the presence of megaloblastic anemia were analyzed statistically compared with P100, N75, and N135 latencies and amplitudes.Results: The mean vitamin B12 level was 96 pg/mL in the patient group and 374 pg/mL in the control group. In the patient group, 24 (60%) patients had hyperhomocysteinemia and 8 (20%) patients had megaloblastic anemia. The P100 wave latency of patients with vitamin B12 deficiency was significantly prolonged compared with the control group (P , 0.01). There was no significant difference in the P100 amplitude between the patient group and the control group. P100 latencies were significantly longer in patients with hyperhomocysteinemia (P 1/4 0.002).Conclusions: Our study showed that patients with vitamin B12 deficiency may have visual evoked potential abnormalities without visual symptoms or examination findings. In addition, high homocysteine levels led to a prolonged P100 latency in the patient group independent of vitamin B12 levels.en_US
dc.description.woscitationindexScience Citation Index Expanded - Conference Proceedings Citation Index - Science
dc.identifier.doi10.1097/WNP.0000000000000920
dc.identifier.endpage540en_US
dc.identifier.issn0736-0258
dc.identifier.issn1537-1603
dc.identifier.issue6en_US
dc.identifier.pmid35349545
dc.identifier.scopus2-s2.0-85169503038
dc.identifier.scopusqualityQ3
dc.identifier.startpage535en_US
dc.identifier.urihttps://doi.org/10.1097/WNP.0000000000000920
dc.identifier.urihttps://hdl.handle.net/20.500.12712/38546
dc.identifier.volume40en_US
dc.identifier.wosWOS:001060044100010
dc.identifier.wosqualityQ3
dc.language.isoenen_US
dc.publisherLippincott Williams & Wilkinsen_US
dc.relation.ispartofJournal of Clinical Neurophysiologyen_US
dc.relation.publicationcategoryKonferans Öğesi - Uluslararası - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectVisual Evoked Potentialen_US
dc.subjectVitamin B12 Deficiencyen_US
dc.subjectVisual Pathwaysen_US
dc.titleVisual Evoked Potentials in Patients with Vitamin B12 Deficiencyen_US
dc.typeConference Objecten_US
dspace.entity.typePublication

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