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The Twentieth Century
Published in Arturo Castiglioni, A History of Medicine, 2019
Study of toxic amblyopia was developed especially in the United States by Casey wood and T. H. buller (1904). Ethyl alcohol and tobacco amblyopia have been demonstrated to be due to vitamin B1 deficiency and respond favourably to its supply.
The retina, optic nerve and vitreous humour
Published in Mary E. Shaw, Agnes Lee, Ophthalmic Nursing, 2018
The underlying cause must be treated if possible. Toxic amblyopia is treated by total abstinence of the offending toxin. Patients receiving chloroquine as treatment for rheumatoid arthritis or systemic lupus erythematosus must have regular ophthalmic examinations.
Common systemic medications that every optometrist should know
Published in Clinical and Experimental Optometry, 2022
Analgesics are generally well tolerated and may be used for chronic pain relief without adverse effects to the eyes. On rare occasion, use of ibuprofen has shown ocular toxicity with blurred vision,81,82 visual field defects,82–84 diplopia,85 and toxic amblyopia.86 Most cases reported improvement in visual symptoms after discontinuation of ibuprofen. Among the rare reported side effects of ibuprofen use is glaucoma progression, although the evidence has not shown a definitive causal link. In fact, ibuprofen may have beneficial IOP lowering effects. A pilot clinical study compared the IOP lowering effects of oral paracetamol with topical levobunolol over two weeks, concluding that the oral analgesic taken every six hours has a similar IOP reduction to that of the topical beta blocker.87 Additional studies are needed to determine the effects analgesics have on glaucoma progression. Furthermore, IOP should be monitored regularly in patients with glaucoma, and optometrists should be made aware of any changes to the patient’s medical and medication history.
The pioneer ophthalmologist Johann Friedrich Horner (1831–1886) and the clinical anatomy of the homonymous syndrome
Published in Acta Chirurgica Belgica, 2020
Markos Dafereras, Hariton Sapouridis, Konstantinos Laios, Dimosthenis Chrysikos, Evangellos Mavrommatis, Theodore Troupis
Horner published an extraordinary monograph on pediatric ophthalmology, describing various topics like toxic amblyopia, myopia, congenital colour vision defects, monocular diplopia, corneal diseases, ocular and orbital tumors, the relationship between rachitic teeth and zonular cataracts, the history of spectacles, and the eye in systemic disease. His skills in diagnosis were unparallelled, giving him the advantage of dazzling speed to sort out patients’ signs and symptoms. On the other hand, as an experienced teacher, he emphasized that all students should examine the patient in the clinic and the disease in the pathology laboratory. During his direction in the University Clinic, he had bequeathed to the university an outstanding collection of ocular pathology specimens. He continued his active practice, teaching, and research, both in private and University until his death in December 1886. Being a fragile person since his youth, he had spells of dyspnea and lost weight, probably due to arteriosclerosis of the kidneys, presenting hemiplegia and loss of speech due to a left hemisphere stroke.
Central scotoma in tobacco-alcohol toxic optic neuropathy measured with semi-automated kinetic perimetry
Published in Cutaneous and Ocular Toxicology, 2018
Katarzyna Nowomiejska, Agnieszka Kiszka, Ryszard Maciejewski, Anselm Jünemann, Robert Rejdak
Bilateral central or centrocecal scotoma in VF is the keystone for making diagnosis in TATN. The anatomical basis of centrocecal scotoma has to be established21. The “papillomacular bundle” of optic nerve fibers was originally described in autopsy studies of toxic amblyopia, not normal anatomy. Centrocecal scotoma extends from the fixation point towards the blind spot and is due to involvement of the papillomacular bundle arising from the fovea towards the optic disc20. The papillomacular bundle is affected first and its damage is responsible for the central VF loss, as well as dyschromatopsia. It is due to small diameter of nerve fibers (parvocellular population) and dependence on mitochondria18. Small diameter fibers are very energy dependent for maintaining efficient axoplasmic transport. The concentration of mitochondria is higher in unmyelinated RGC than myelinated fibers behind the lamina cribrosa. The unique anatomical features of the pre-laminar area make the papillomacular bundle vulnerable to mitochondrial dysfunction in different ways22. The susceptibility of the papillomacular bundle is due to the combination of the high-energy requirements with the low-energy production and slow axoplasmic transport.