field defects
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2022 ◽  
Vol 325 ◽  
pp. 107748
Author(s):  
Michal Knapp ◽  
Ezequiel González ◽  
Martin Štrobl ◽  
Miroslav Seidl ◽  
Lada Jakubíková ◽  
...  

2022 ◽  
Vol 7 (4) ◽  
pp. 717-722
Author(s):  
Poorva Shrivastava ◽  
Sheetal Morskole ◽  
Lalit Shrivastava

This study was conducted to evaluate the visual field changes in tubercular patients on anti-tubercular therapy and to assess the reversibility of these changes after the discontinuation therapy. This study was conducted as a prospective analytical study at tertiary care centres in Bhopal and Jabalpur on all newly detected tuberculosis patients. Ocular history, relevant history was recorded and detailed ocular examination was done at the time of presentation, before initiating ATT. All the patients were followed up periodically till the cessation of treatment and three months thereafter. A total of 40 cases of newly diagnosed tuberculosis were registered with mean age of 38.4±13.99 years. We documented significant deterioration in visual acuity after 3 months of initiation of therapy. Once the ATT was stopped, the improvement in visual acuity was statistically significant 3 months after the cessation of ATT as compared to visual acuity 3 months after initiation of ATT (p<0.05). But residual visual impairment even after stoppage of ATT was observed. Color vison and visual field defects were observed in higher proportions of eyes following initiation of ethambutol which improved significantly after 3 months of cessation of ATT (p<0.05). Ethambutol, even in recommended dose according to DOTS, has been associated with ocular toxicity which manifests in the form of painless progressive loss of vision, color vision defects and visual field defects. Though these changes are usually reversible, few patients have irreversible damage. Thus, patients receiving ethambutol must be explained regarding these effects and followed up periodically.


2021 ◽  
pp. 112067212110637
Author(s):  
Lurong Zhang ◽  
Ke Liu ◽  
Fen Nie ◽  
Xuanchu Duan

High myopia is of worldwide concern due to its high prevalence, and myopia is an independent risk factor for glaucoma. The purpose of this paper is to review the mechanism and clinical manifestations of optic disc tilt and rotation in high myopia and its relationship with glaucoma, to provide clues for monitoring fundus changes in high myopia and the early diagnosis of high myopia with glaucoma.


Medicine ◽  
2021 ◽  
Vol 100 (48) ◽  
pp. e27793
Author(s):  
Kang-Jung Lo ◽  
Jin-Han Yang ◽  
Hui-Chen Cheng ◽  
Hsin-Yi Chang ◽  
Tai-Chi Lin

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Maria Kruse ◽  
Thomas Bastholm Olesen ◽  
Ljubo Markovic ◽  
Dorte Glintborg ◽  
Marianne Skovsager Andersen

Abstract Background Autoimmune hypophysitis is a rare condition that often results in enlargement of the pituitary gland and hypopituitarism due to inflammatory infiltration. Management of autoimmune hypophysitis can include long-term hormonal replacement and close control of the inflammatory pituitary mass. Mass-related symptoms in patients with autoimmune hypophysitis are treated with anti-inflammatory therapy, surgery, and/or radiotherapy. Case presentation We present a 25-year-old White man with visual field defects of the right eye, headache, and weight loss. Magnetic resonance imaging showed a sellar mass, and the patient underwent transcranial surgery. Histopathology revealed autoimmune hypophysitis with predominantly CD20 positive B-cell infiltration. Progression of visual field defects necessitated postoperatively anti-inflammatory treatment with prednisolone. Azathioprine was initiated under gradual tapering of prednisolone with stable conditions at first, but relapse followed after dose reduction. Therefore, rituximab treatment was initiated, which resulted in regression of the pituitary mass. Rituximab treatment was discontinued after 25 months. The patient has continuously been in remission for 4 years after rituximab treatment was stopped. Conclusion This case illustrates that rituximab might be an effective alternative treatment in B-cell predominant autoimmune hypophysitis.


2021 ◽  
Vol 62 (11) ◽  
pp. 1527-1538
Author(s):  
Joon Hyuck Jang ◽  
Kyung Wha Lee ◽  
Sung Uk Baek

Purpose: As routine health examinations become more common, many patients first diagnosed with glaucoma have advanced glaucoma. We analyzed the routes to diagnosis and the characteristics of patients initially diagnosed with advanced glaucoma.Methods: We retrospectively retrieved the medical records of patients first diagnosed with advanced glaucoma in our tertiary care center. The inclusion criteria were a mean deviation (MD) less than -12 dB on the visual field test, accompanied by structural damage. All patients were classified in terms of unilateral/bilateral disease, the intraocular pressure before medication, and lens status. We divided patients into those with monocular or binocular advanced glaucoma, high- or normal-pressure glaucoma, and those who were pseudophakic or phakic.Results: We included 73 patients of mean age 69.3 years. The visual field test MD was -19.6 dB. In those with binocular advanced glaucoma, incidental ophthalmic examination was the most common means of diagnosis (52.2%). Central-island visual field defects were the most common defects (54.2%). In those with monocular advanced glaucoma, glaucoma-associated symptoms most commonly triggered diagnosis (46.9%). Both superior and inferiorvisual field defects were the most common defects (42.8%). Glaucoma-associated symptoms were present in 68.2 and 22.8% of patients with high- and normal-pressure glaucoma, respectively. Central-island visual field defects were present in 43.6 and 29.4% of those with high- and normal-pressure glaucoma, respectively.Conclusions: We analyzed the routes to diagnosis and the clinical characteristics of patients with advanced glaucoma. In those with binocular disease, glaucoma was most commonly diagnosed on incidental ophthalmic examination. Central-island visual field defects were the most common defects in patients with binocular and high-pressure glaucoma, and the pseudophakic group. A multi-center longitudinal study on risk factors for delayed glaucoma diagnosis is needed.


2021 ◽  
pp. 899-908
Author(s):  
Yui Yamashita ◽  
Yuki Hashimoto ◽  
Kenichi Namba ◽  
Kazuomi Mizuuchi ◽  
Susumu Ishida

Anterior ischemic optic neuropathy (AION) is infrequently complicated with Vogt-Koyanagi-Harada (VKH) disease. We quantitatively examined sequential changes in the morphology and circulation hemodynamics, using a C-scan of optical coherence tomography (OCT) and laser speckle flowgraphy (LSFG) in a patient with VKH disease accompanied by AION. A 65-year-old female complained of blurred vision in both of her eyes. The patient presented with optic disc swelling and remarkable choroidal thickening detected by OCT bilaterally. The diagnosis of VKH disease was established based on the presence of pleocytosis detected in the cerebrospinal fluid and hypofluorescent dark dots scattered all around the fundus, detected by indocyanine green angiography. Goldmann perimetry detected visual field defects, similar to superior altitudinal hemianopsia in the right eye and similar to inferior altitudinal hemianopsia in the left eye. The patient was suspected to have developed AION in both eyes. The patient received methylprednisolone pulse therapy, followed by oral prednisolone. With these treatments, the optic disc swelling disappeared. However, optic disc atrophy with visual field defects remained in both eyes. An OCT C-scan showed the ganglion cell complex (GCC) and circumpapillary retinal nerve fiber layer (cpRNFL) thickness getting thinner below the normal range, and LSFG showed the decrease in optic nerve head (ONH) tissue microcirculation. These results supported the occurrence of AION in this patient with VKH disease. The analysis of GCC and cpRNFL thickness and ONH microcirculation would be useful for supporting the occurrence of AION in a case of VKH disease.


2021 ◽  
Vol 11 (11) ◽  
pp. 1469
Author(s):  
Juan Fernando Ortiz ◽  
Ahmed Eissa-Garces ◽  
Samir Ruxmohan ◽  
Victor Cuenca ◽  
Mandeep Kaur ◽  
...  

Parinaud’s syndrome involves dysfunction of the structures of the dorsal midbrain. We investigated the pathophysiology related to the signs and symptoms to better understand the symptoms of Parinaud’s syndrome: diplopia, blurred vision, visual field defects, ptosis, squint, and ataxia, and Parinaud’s main signs of upward gaze paralysis, upper eyelid retraction, convergence retraction nystagmus (CRN), and pseudo-Argyll Robertson pupils. In upward gaze palsy, three structures are disrupted: the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), interstitial nucleus of Cajal (iNC), and the posterior commissure. In CRN, there is a continuous discharge of the medial rectus muscle because of the lack of inhibition of supranuclear fibers. In Collier’s sign, the posterior commissure and the iNC are mainly involved. In the vicinity of the iNC, there are two essential groups of cells, the M-group cells and central caudal nuclear (CCN) group cells, which are important for vertical gaze, and eyelid control. Overstimulation of the M group of cells and increased firing rate of the CCN group causing eyelid retraction. External compression of the posterior commissure, and pretectal area causes pseudo-Argyll Robertson pupils. Pseudo-Argyll Robertson pupils constrict to accommodation and have a slight response to light (miosis) as opposed to Argyll Robertson pupils were there is no response to a light stimulus. In Parinaud’s syndrome patients conserve a slight response to light because an additional pathway to a pupillary light response that involves attention to a conscious bright/dark stimulus. Diplopia is mainly due to involvement of the trochlear nerve (IVth cranial nerve. Blurry vision is related to accommodation problems, while the visual field defects are a consequence of chronic papilledema that causes optic neuropathy. Ptosis in Parinaud’s syndrome is caused by damage to the oculomotor nerve, mainly the levator palpebrae portion. We did not find a reasonable explanation for squint. Finally, ataxia is caused by compression of the superior cerebellar peduncle.


2021 ◽  
pp. 821-833
Author(s):  
Shivram Kumar ◽  
Kelly D. Flemming

Visual loss may develop acutely, subacutely, or insidiously. The course may be transient, static, or progressive. This chapter reviews the causes, diagnosis, and treatment of various disorders resulting in visual loss or abnormal visual perception. In addition, it reviews clinical disorders of the eyelids and pupils. Disorders of visual perception involve visual acuity, color perception, visual field defects, and other visual changes. Historical information and physical findings on examination can help to localize the problem and define the cause.


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