Visual impairment due to ophthalmological diseases significantly affects functional activity in everyday life, since good eyesight is crucial in daily activities. Data from 837 respondents were studied, allowing for analysis of such medical and demographic indicators as age, gender, level of education, visual acuity arterial hypertension and diabetes mellitus. To measure functional status, the main activities in daily life (ADL) and instrumental activities in daily life (IADL) were evaluated using a modified version of the Katz scale and the IADL OARS scale. Statistical methods of Mantel-Hansel Chi-squared analysis were used to assess differences in the prevalence of functional blindness and visual deficit. The study showed that medical and demographic factors have a relatively smaller impact on vision deficiency compared to functional blindness, with age being a significant factor in both cases. Among the medical and demographic factors, the age of patients, as well as diabetes mellitus, significantly increase the development of visual deficiency and functional blindness. Functional blindness, in comparison with visual deficiency, causes more significant restrictions on activities in everyday life and instrumental activities in everyday life, and also causes dependence on help from others.
Нарушение зрения вследствие офтальмологических заболеваний существенно влияет на функциональную активность в повседневной жизни, поскольку хорошее зрение имеет в этом решающее значение. Изучали данные 837 респондентов, позволяющие сделать анализ таких медико-демографических показателей, как возраст, пол, уровень образования, острота зрения, артериальная гипертензия и сахарный диабет. Для измерения функционального статуса оценивали основные виды деятельности в повседневной жизни (ADL) и инструментальные виды деятельности в повседневной жизни (IADL) с использованием модифицированной версии шкалы Каца и шкалы IADL OARS. Для оценки различий в распространенности функциональной слепоты и зрительного дефицита использовали статистические методы анализа χ2 Мантеля–Ханселя. Исследование показало, что медицинские и демографические факторы оказывают относительно меньшее влияние на зрительный дефицит по сравнению с функциональной слепотой, при этом возраст является существенным фактором в обоих случаях. Сахарный диабет и гипертензия способствуют развитию функциональной слепоты и дефицита зрения, в то время как уровень образования не влияет на нарушение зрения. Среди медико-демографических факторов статистически достоверно повышает развитие зрительного дефицита и функциональной слепоты возраст пациентов, а также сахарный диабет. Функциональная слепота по сравнению со зрительным дефицитом вызывает более существенные ограничения по видам деятельности в повседневной жизни и инструментальной деятельности в повседневной жизни, а также вызывает зависимость в помощи от окружающих.

UNASSIGNED: MELAS is a disorder with clinical variability that also responsible for a significant portion of unexplained hereditary or childhood-onset hearing loss. Although patients typically present in childhood, the first stroke-like episode can occur later in life in some patients, potentially related to a lower heteroplasmy level. It is crucial to consider MELAS as a potential cause of stroke-like events if age at presentation and symptoms are atypical, especially among middle-aged patients without vascular risk factors.
UNASSIGNED: MELAS syndrome (mitochondrial encephalopathy with lactic acidosis and stroke-like episodes) is a rare genetic condition that most patients develop stroke-like episodes before the age of 40. We report a 52-year-old female with a documented 40-year history of progressive sensorineural hearing loss, developed a visual field deficit and stroke-like events in her middle age who finally diagnosed was MELAS. The patient was started on vitamin E, l-carnitine, l-arginine, and coenzyme Q10 that gradually improved before dismissal from the hospital. This case highlights the importance of considering MELAS as a potential cause of stroke-like events if imaging findings are atypical for cerebral infarction, especially among middle-aged patients without vascular risk factors and an unusual cause of progressive sensorineural hearing loss.

Glaucoma and cataract continue to be the leading causes of visual deficits, especially in older age groups, but the association of visual deficits with cognitive impairments has not been sufficiently studied. The aim of this study is to study visual impairment as a marker of cognitive impairment in patients with cataracts and glaucoma. The study included 326 elderly patients with cataracts and 318 elderly patients with primary open-angle glaucoma. The degree of cognitive impairment was determined using the Mini-Mental State Examination (MMSE) scale. Visual deficit was assessed by visual acuity without correction and maximum corrected visual acuity, and the severity of visual deficit was assessed by the scale we proposed. It was found that with low visual deficit (visual acuity without correction 0,51-0,60 and over 0,61) in the examined patients, the average score on the MMSE scale varied from 28,4±0,6 to 28,7±0,8 points (p>0,05), corresponding to subjective cognitive disorders. However, with a pronounced visual deficit (visual acuity without correction to 0,20 and 0,21-0,30), the average score is 13,9±0,3 and 16,5±0,4 (p<0,001), which indicates moderate dementia. Practically similar patterns about the association of cognitive impairments with the magnitude of visual deficit were also obtained when assessing visual deficit by maximum corrected visual acuity. The associativity of cognitive impairment with visual defect in patients with cataract and glaucoma was confirmed by the correlation method, according to which the correlation coefficient with visual acuity without correction is r=+0,428 (p<0,05), and with maximum corrected visual acuity - r=+0,385 (p<0,05). The results of the study allow us to consider visual deficit as a marker of cognitive impairment.
Глаукома и катаракта продолжают оставаться ведущими причинами зрительного дефицита, особенно в старших возрастных группах, но ассоциация зрительного дефицита с когнитивными нарушениями изучена недостаточно. Цель исследования — изучение зрительного дефицита в качестве маркера когнитивных нарушений у пациентов с катарактой и глаукомой. В исследование были включены 326 пациентов пожилого возраста с катарактой и 318 пациентов пожилого возраста с первичной открытоугольной глаукомой. Определение степени когнитивных нарушений выполнено посредством шкалы Mini-Mental-State Examination (MMSE). Зрительный дефицит оценивали по остроте зрения без коррекции и максимальной корригированной остроте зрения, а выраженность зрительного дефицита — по предложенной нами шкале. Установлено, что при низком зрительном дефиците (острота зрения без коррекции 0,51–0,60 и свыше 0,61) у обследованных пациентов средний балл по шкале MMSE варьировал от 28,4±0,6 до 28,7±0,8 балла (p>0,05), соответствуя субъективным когнитивным расстройствам. Однако при выраженном зрительном дефиците (острота зрения без коррекции до 0,20 и 0,21–0,30) средний балл был равен 13,9±0,3 и 16,5±0,4 (p<0,001), что указывает на деменцию средней степени тяжести. Практически аналогичные закономерности в ассоциации когнитивных нарушений с величиной зрительного дефицита получены и при оценке зрительного дефицита по максимальной корригированной остроте зрения. Ассоциативность когнитивных нарушений со зрительным дефицитом у пациентов с катарактой и глаукомой подтверждена корреляционным методом, согласно которому коэффициент корреляции с остротой зрения без коррекции составляет r=+0,428 (p<0,05), с максимальной корригированной остротой зрения — r=+0,385 (p<0,05). Результаты исследования позволяют считать зрительный дефицит маркером когнитивных нарушений.

BACKGROUND: Repetitive mild traumatic brain injury (mTBI) can result in chronic visual dysfunction. G-protein receptor 110 (GPR110, ADGRF1) is the target receptor of N-docosahexaenoylethanolamine (synaptamide) mediating the anti-neuroinflammatory function of synaptamide. In this study, we evaluated the effect of an endogenous and a synthetic ligand of GPR110, synaptamide and (4Z,7Z,10Z,13Z,16Z,19Z)-N-(2-hydroxy-2-methylpropyl) docosa-4,7,10,13,16,19-hexaenamide (dimethylsynaptamide, A8), on the mTBI-induced long-term optic tract histopathology and visual dysfunction using Closed-Head Impact Model of Engineered Rotational Acceleration (CHIMERA), a clinically relevant model of mTBI.
METHODS: The brain injury in wild-type (WT) and GPR110 knockout (KO) mice was induced by CHIMERA applied daily for 3 days, and GPR110 ligands were intraperitoneally injected immediately following each impact. The expression of GPR110 and proinflammatory mediator tumor necrosis factor (TNF) in the brain was measured by using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) in an acute phase. Chronic inflammatory responses in the optic tract and visual dysfunction were assessed by immunostaining for Iba-1 and GFAP and visual evoked potential (VEP), respectively. The effect of GPR110 ligands in vitro was evaluated by the cyclic adenosine monophosphate (cAMP) production in primary microglia isolated from adult WT or KO mouse brains.
RESULTS: CHIMERA injury acutely upregulated the GPR110 and TNF gene level in mouse brain. Repetitive CHIMERA (rCHIMERA) increased the GFAP and Iba-1 immunostaining of glia cells and silver staining of degenerating axons in the optic tract with significant reduction of N1 amplitude of visual evoked potential at up to 3.5 months after injury. Both GPR110 ligands dose- and GPR110-dependently increased cAMP in cultured primary microglia with A8, a ligand with improved stability, being more effective than synaptamide. Intraperitoneal injection of A8 at 1 mg/kg or synaptamide at 5 mg/kg significantly reduced the acute expression of TNF mRNA in the brain and ameliorated chronic optic tract microgliosis, astrogliosis, and axonal degeneration as well as visual deficit caused by injury in WT but not in GPR110 KO mice.
CONCLUSIONS: Our data demonstrate that ligand-induced activation of the GPR110/cAMP system upregulated after injury ameliorates the long-term optic tract histopathology and visual impairment caused by rCHIMERA. Based on the anti-inflammatory nature of GPR110 activation, we suggest that GPR110 ligands may have therapeutic potential for chronic visual dysfunction associated with mTBI.

Early surgical intervention for patients with pituitary apoplexy (PA) is thought to improve visual outcomes and decrease mortality. However, some patients may have good clinical outcomes without surgery. The authors sought to compare the radiological and clinical outcomes of patients with PA who were managed conservatively versus those who underwent early surgery.
Patients with symptomatic PA were identified. Radiological, endocrinological, and ophthalmological data were reviewed. Patients with progressive visual deterioration or ophthalmoplegia were candidates for early surgery (within 7 days). Patients without visual symptoms or whose symptoms improved on high-dose steroids were treated conservatively. Log-rank and univariate analysis compared clinical and radiological outcomes between those receiving early surgery and those who underwent intended conservative management.
Sixty-four patients with PA were identified: 47 (73.4%) underwent intended conservative management, while 17 (26.6%) had early surgery. Patients receiving early surgery had increased rates of impaired visual acuity (VA; 64.7% vs 27.7%, p = 0.009); visual field (VF) deficits (64.7% vs 19.2%, p = 0.002); and cranial neuropathies (58.8% vs 29.8%, p < 0.05) at presentation. Tumor volumes were greater in the early surgical cohort (15.1 ± 14.8 cm3 vs 4.5 ± 10.3 cm3, p < 0.001). The median clinical and radiological follow-up visits were longer in the early surgical cohort (70.0 and 64.4 months vs 26.0 and 24.7 months, respectively; p < 0.001). Among those with VA/VF deficits, visual outcomes were similar between both groups (p > 0.9). The median time to VA improvement (2.0 vs 3.0 months, p = 0.9; HR 0.9, 95% CI 0.3-3.5) and the median time to VF improvement (2.0 vs 1.5 months; HR 0.8, 95% CI 0.3-2.6, p = 0.8) were similar across both cohorts. Cranial neuropathy improvement was more common in conservatively managed patients (HR 4.8, 95% CI 1.5-15.4, p < 0.01). Conservative management failed in 7 patients (14.9%) and required surgery. PA volumes spontaneously regressed in 95.0% of patients (38/40) with successful conservative management, with a 6-month regression rate of 66.2%. Twenty-seven patients (19 in the conservative and 8 in the early surgical cohorts) responded to a prospectively administered Visual Function Questionnaire-25 (VFQ-25). VFQ-25 scores were similar across both cohorts (conservative 95.5 ± 3.8, surgery 93.2 ± 5.1, p = 0.3). Younger age, female sex, and patients with VF deficits or chiasmal compression were more likely to experience unsuccessful conservative management. Surgical outcomes were similar for patients receiving early versus delayed surgery.
These data suggest that a majority of patients with PA can be successfully managed without surgical intervention assuming close neurosurgical, radiological, and ophthalmological follow-up is available.

We present the results of 51 stroke patients with free central visual fields of which about half suffer from clear deficits of midlevel vision undetected by standard clinical tests. These patients yield significantly elevated thresholds for detection and/or discrimination between forms defined by motion, colour, or line orientation (\'texture\'). As demonstrated by voxel-based lesion-symptom mapping (VLSM) the underlying lesions involve mainly area human V4 (hV4) located in the posterior third of the fusiform gyrus and extending into the lingual gyrus. Patient\'s detection thresholds correlate only very weakly between the submodalities tested, indicating partly separate neural networks on mid-level vision for colour, motion, and texture detection. Correlations are far stronger for form discrimination tasks, indicating partly shared mechanisms for even simple form discrimination of distinct visual submodalities. We conclude that deficits of visual perception are far more common after strokes in visual brain areas than is apparent in clinical practice. Our results further clarify the functional organization of midlevel visual cortical areas.

Multiple hypotheses have been proposed to explain the reading difficulty caused by developmental dyslexia (DD). The current study examined visuo-orthographic processing in children with dyslexia to determine whether orthographic deficits are explainable based solely on visual deficits. To identify orthographic-specific, visual perception-specific, and overlapping deficits, we included two tasks (lexical and perceptual) in three Chinese subject groups: children with DD, age-matched controls (AC), and reading matched controls (RC) using functional magnetic resonance imaging (fMRI). We found that the left precuneus showed decreased activation across both tasks for the DD group compared to the two control groups, thus reflecting visual processing deficits in children with DD, which also affects orthographic processing. Furthermore, we found that the functional connectivity between left middle occipital gyrus (LMOG) and left inferior frontal gyrus (IFG) was decreased in the DD group compared to AC and RC for only the lexical task. This suggests a weaker association between orthography and phonology for children with DD. In addition, the children with DD showed decreased functional connectivity between the LMOG and right parahippocampal gyrus for only the visual perceptual task, thereby indicating a weaker association between visual regions for DD during visual symbol processing. Taken together, our findings suggest that the observed orthographic processing deficit in DD might be driven by both a basic visual deficit, and a linguistic deficit.

Extra-axial cavernous hemangiomas (ECH) are rare vascular lesions with a tendency to grow within the medial structures of the middle cranial fossa. This pathological entity lacks specific symptoms, and falls into the category of differential diagnosis of space occupying lesions in the cavernous sinus (CS) with or without sellar involvement, including those of tumoral, vascular and inflammatory nature. Of note, ECH can also be indolent, and is at times discovered incidentally during autopsy investigations. On radiological studies, ECH with sellar extension are frequently mistaken at first for pituitary adenomas. Total removal of intrasellar-CS ECH is technically demanding and burdened by remarkable morbidity and mortality rates, mostly related to the complex neuroanatomy of the CS-sellar region (i.e., peri and postoperative bleeding, and transitory or permanent nerve palsies, hormonal deficits). Consequently, only a few cases of successful total removal have been reported so far in the literature. Surgical debulking with cranial nerve decompression followed by stereotactic radiosurgery is currently considered the best alternative to total removal when the latter carries excessive perioperative risks. We present a rare case of a mainly located intrasellar ECH extending to the left CS discussing its clinical features and focusing on the most relevant aspects of the surgical management along with a review of the pertinent literature.

OBJECTIVEWhile most paraclinoid aneurysms can be clipped with excellent results, new postoperative visual deficits are a concern. New technology, including flow diverters, has increased the popularity of endovascular therapy. However, endovascular treatment of paraclinoid aneurysms is not without procedural risks, is associated with higher rates of incomplete aneurysm occlusion and recurrence, and may not address optic nerve compression symptoms that surgical debulking can. The increasing endovascular management of paraclinoid aneurysms should be justified by comparisons to surgical benchmarks. The authors, therefore, undertook this study to define patient, visual, and aneurysm outcomes in the most common type of paraclinoid aneurysm: ophthalmic artery (OphA) aneurysms.METHODSResults from microsurgical clipping of 208 OphA aneurysms in 198 patients were retrospectively reviewed. Patient demographics, aneurysm morphology (size, calcification, etc.), clinical characteristics, and patient outcomes were recorded and analyzed.RESULTSDespite 20% of these aneurysms being large or giant in size, complete aneurysm occlusion was accomplished in 91% of 208 cases, with OphA patency preserved in 99.5%. The aneurysm recurrence rate was 3.1% and the retreatment rate was 0%. Good outcomes (modified Rankin Scale score 0-2) were observed in 96.2% of patients overall and in all 156 patients with unruptured aneurysms. New visual field defects (hemianopsia or quadrantanopsia) were observed in 8 patients (3.8%), decreased visual acuity in 5 (2.4%), and monocular blindness in 9 (4.3%). Vision improved in 9 (52.9%) of the 17 patients with preoperative visual deficits.CONCLUSIONSThe most important risk associated with clipping OphA aneurysms is a new visual deficit. Meticulous microsurgical technique is necessary during anterior clinoidectomy, aneurysm dissection, and clip application to optimize visual outcomes, and aggressive medical management postoperatively might potentially decrease the incidence of delayed visual deficits. As the results of endovascular therapy and specifically flow diverters become known, they warrant comparison with these surgical benchmarks to determine best practices.

OBJECTIVE: The outcomes of recent endoscopic surgery of nonfunctioning pituitary adenomas (NFPAs) are controversial when compared with traditional microscopic surgery. We aimed to assess the outcomes of endoscopic transsphenoidal surgeries performed by 1 surgeon with 7 years of experience and elucidate the predictive factors for surgical outcomes for NFPAs.
METHODS: We included 331 patients (155 men and 176 women) with clinical NFPAs who underwent transsphenoidal surgery because of visual symptoms by a single surgeon in Seoul National University Hospital from March 2010 to May 2016. We assessed the tumor removal rate, hormonal outcomes, visual outcomes, and complications.
RESULTS: The gross total resection rate of endoscopic transsphenoidal surgery for NFPAs by a single surgeon was 74.9%. Cavernous sinus invasion, a high Knosp grade, large tumor size, previous surgery, and lack of surgical experience in the neurosurgeon elevated the risk for residual tumors. Visual deficits were improved in 73.4% of the patients, which was associated with tumor size, preoperative visual impairment score, previous radiation, and surgical experience. Hormonal status was improved in 15.4% and aggravated in 32.9% after surgery. There were no predictors for hormonal recovery. Transient diabetes insipidus (DI) was the most common complication (9.1%), and among these patients, 3.0% had persistent DI.
CONCLUSIONS: Endoscopic transsphenoidal surgery by a well-experienced surgeon was an effective and safe treatment for NFPAs, but the hormonal outcomes were not changed compared with previous reports of microscopic surgery. Large tumor size and cavernous sinus invasion were still the barriers for achieving total resection.