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Sohan Singh Hayreh

Publications and source records attributed to Sohan Singh Hayreh.

At least 19 recordsLinked to original sources
PubMed2007

Optic disc edema in non-arteritic anterior ischemic optic neuropathy.

We investigated the clinical characteristics, time to resolution and the factors that influence it, and evolutionary pattern of optic disc edema (ODE) in non-arteritic anterior ischemic optic neuropathy (NA-AION). Our study was conducted in 591 consecutive patients (749 eyes) with NA-AION who fulfilled our inclusion criteria. On their first visit to our clinic, all patients had a detailed ophthalmic and medical history, a comprehensive ophthalmic evaluation, and stereoscopic color fundus photography and fluorescein fundus angiography. On each follow-up visit, the same ophthalmic evaluation was performed, except for fluorescein fundus angiography. The effect of steroid therapy on ODE was evaluated in a "patient choice study" in 723 eyes, i.e., patients who voluntarily opted to have (343 eyes) or not have (380 eyes) this therapy. To identify the factors that influence time to ODE resolution, parametric regression models for interval-censored data were fitted by maximum likelihood estimation using an SAS procedure. Our results indicate that the overall median time (25-75th percentile) to spontaneous resolution of ODE from the onset of visual loss was 7.9 (5.8-11.4) weeks. The ODE resolution time was longer in diabetics than in non-diabetics (p = 0.003) in the single factor model. Multi-factor analysis showed that worse initial visual field defects (p < 0.0001) and worse visual acuity (p = 0.04) were associated with a faster resolution of ODE. Those treated with steroid therapy within 2 weeks after onset of NA-AION had significantly (p = 0.0006) faster ODE resolution than untreated cases. Severity of initial visual loss and systemic diseases were identical in steroid treated and untreated patients. A characteristic evolutionary pattern of ODE in NA-AION was observed. In conclusion, our study showed that in NA-AION the time course for resolution of ODE is shorter with greater severity of initial visual field and visual acuity loss, which may relate to the number of axons permanently damaged during the acute stage. Steroid therapy was associated with shorter time to resolution of ODE. Resolution of ODE goes through a characteristic evolutionary process.

Aged↗
PubMed2005

Visual field abnormalities in nonarteritic anterior ischemic optic neuropathy: their pattern and prevalence at initial examination.

OBJECTIVE: To evaluate the pattern of various types of visual field defects and their prevalence at initial examination of nonarteritic anterior ischemic optic neuropathy (NA-AION). METHODS: The data were compiled from 312 consecutive eyes (in 265 patients) that fulfilled our inclusion and exclusion criteria. A comprehensive ophthalmic evaluation was performed, including recording of visual acuity, visual fields with a Goldmann perimeter (using I-2e, I-4e, and V-4e targets regularly), and intraocular pressure; slitlamp examination of the anterior segment; ophthalmoscopy; color fundus photography; and in acute cases, fluorescein fundus angiography. The visual field defects were divided into 2 groups: (1) general field defects and (2) various types of scotoma in the central 30 degrees . The prevalence of various types of visual field defects was estimated for I-2e, I-4e, and V-4e isopters by dividing the total number of eyes with the defect by the total number of eyes that could see that particular target. Exact 95% confidence limits for the prevalence were computed. RESULTS: Of the 265 patients, 169 (63.7%) were male and the mean +/- SD patient age was 55.0 +/- 9.1 years. The median interval between the first visual field test and the onset of NA-AION was 2 weeks. Of the 312 eyes, the I-2e target was seen by 75.3%, the I-4e target by 90.7%, and the V-4e target by 100%. Overall prevalence of general visual field defects was 83.4% with I-2e, 78.8% with I-4e, and 68.9% with V-4e, whereas the prevalence of scotoma(s) within the central 30 degrees was 55.3%, 49.5%, and 36.2%, respectively. Central scotoma was seen in 48.5% with I-2e, 43.8% with I-4e, and 29.2% with V-4e. A detailed prevalence of various types of visual field defects is given. Relative inferior altitudinal defect was most common (34.9% with I-2e and 22.3% with I-4e), but the absolute inferior altitudinal defect was seen in only 8.0%. By contrast, absolute inferior nasal sector visual loss was the most common defect detected in NA-AION (22.4%), but it occurred in only 3.4% with I-2e and 11.0% with I-4e. Overall, loss of the nasal part of the visual field was the most common occurrence. CONCLUSIONS: Our study demonstrated that NA-AION eyes may initially show a variety of optic nerve-related visual field defects. Our study also showed that an absolute inferior nasal visual field defect is much more common (22.4%) than an absolute inferior altitudinal visual field defect (8.0%) in NA-AION and could be considered the most characteristic single field defect in NA-AION. We found that a combination of relative inferior altitudinal defect with absolute inferior nasal defect is usually the most common pattern in NA-AION.

Adult↗
PubMed2005

Central retinal artery occlusion: visual outcome.

PURPOSE: To investigate systematically the natural history of visual outcome in central retinal artery occlusion (CRAO). DESIGN: Cohort study. METHODS: At entry, 244 consecutive patients (260 eyes) with CRAO (seen consecutively from 1973 to 2000) had a detailed ocular and medical history and ocular evaluation. CRAO eyes were classified into four categories: non-arteritic (NA) CRAO (171 eyes), NA-CRAO with cilioretinal artery sparing (35), transient NA-CRAO (41), and arteritic CRAO (13). RESULTS: Within 7 days of onset of CRAO, initial visual acuity differed among the four CRAO types (P < .0001). In eyes with vision of counting fingers or worse, it improved in 82% of eyes with transient NA-CRAO, 67% of eyes with NA-CRAO with cilioretinal artery sparing, and 22% of eyes with NA-CRAO. Visual acuity improved primarily within the first 7 days (P < .0001). In the central 30-degree visual field, central scotoma was most common. Central visual field improved in 39% with transient NA-CRAO, 25% with NA-CRAO with cilioretinal artery sparing, and 21% with NA-CRAO. Peripheral visual field was normal in 62.9% of eyes with transient NA-CRAO and 22.1% in those with NA-CRAO. In 51.9% of eyes with NA-CRAO, the only remaining visual field was a peripheral island. Peripheral fields improved in NA-CRAO (39%) and in transient NA-CRAO (39%). CONCLUSIONS: Classification of CRAO is crucial for understanding differences in visual outcome. Marked improvement in visual acuity and visual field can occur without treatment and is determined by several factors. Visual field information is essential to evaluate visual disability in CRAO.

Adult↗
PubMed2005

Prevalent misconceptions about acute retinal vascular occlusive disorders.

Acute retinal vascular occlusive disorders collectively constitute one of the major causes of blindness or seriously impaired vision, and yet there is marked controversy on their pathogeneses, clinical features and particularly their management. This is because the subject is plagued by multiple misconceptions. These include that: (i) various acute retinal vascular occlusions represent a single disease; (ii) estimation of visual acuity alone provides all the information necessary to evaluate visual function; (iii) retinal venous occlusions are a single clinical entity; (iv) retinal vein occlusion is essentially a disease of the elderly and is not seen in the young; (v) central retinal vein occlusion (CRVO) is one disease; (vi) fluorescein fundus angiography is the best test to differentiate ischemic from nonischemic CRVO; (vii) the site of occlusion in CRVO is invariably at the lamina cribrosa; (viii) clinical picture of CRVO is often due to compression or strangulation of the central retinal vein (CRV) in the lamina cribrosa and not its occlusion; (ix) an eye can develop both CRVO and central retinal artery occlusion (CRAO) simultaneously; (x) every eye with CRVO is at risk of developing neovascular glaucoma; (xi) lowering intraocular pressure (IOP) helps to improve retinal circulation in an eye with CRVO; (xii) every patient with retinal vein occlusion should have complete hematologic and coagulation evaluation; (xiii) the natural history of CRVO does not usually involve spontaneous visual improvement; (xiv) management of CRVO is similar to that of venous thrombosis anywhere else in the body, i.e. with aspirin and/or anti-coagulants; (xv) fibrinolytic agents can dissolve an organized thrombus in the CRV; (xvi) it is beneficial to lower blood pressure in patients with CRVO; (xvii) panretinal photocoagulation used in ischemic retinal venous occlusive disorders has no deleterious side-effects; (xviii) glaucoma or ocular hypertension can cause branch retinal vein occlusion; (xix) branch retinal vein occlusion can cause neovascular glaucoma; (xx) in eyes with CRAO, the artery is usually not completely occluded; (xxi) CRAO is always either embolic or thrombotic in origin; (xxii) amaurosis fugax is always due to retinal ischemia secondary to transient retinal arterial embolism; (xxiii) asymptomatic plaque(s) in retinal arteries do not require a detailed evaluation; (xxiv) retinal function can improve even when acute retinal ischemia due to CRAO has lasted for 20h or more; (xxv) CRAO, like ischemic CRVO, can result in development of ocular neovascularization; (xxvi) panretinal photocoagulation is needed for "disc neovascularization" in CRAO; (xxvii) fibrinolytic agents are the treatment of choice in CRAO; (xxviii) there is no chance of an eye with retinal arterial occlusion having spontaneous visual improvement; (xxix) absence of any abnormality on Doppler evaluation of the carotid artery or echography of the heart always rules out those sites as the source of embolism; and (xxx) absence of an embolus in the retinal artery means the occlusion was not caused by an embolus. The major cause of all these misconceptions is the lack of a proper understanding of basic scientific facts related to the various diseases. The objective of this paper is to discuss these misconceptions, based on these scientific facts, to clarify the understanding of these blinding disorders, and to place their management on a rational, scientific basis.

Acute Disease↗
PubMed2005

Age of retinal hemorrhages by iron detection: an animal model.

Intraretinal hemorrhages have been found in some abusively injured infants and children. Intraretinal hemosiderin has been proposed as an indication of previous injury. The limits of the accuracy of the proposal have not been established. Experimental central retinal vein occlusion (CRVO) was produced in 20 eyes of adult rhesus monkeys as part of ongoing research by one of the authors (SSH). The animal experiments were conducted in accordance with a research protocol approved by the Animal Care Committee, University of Iowa. CRVO produced diffuse intraretinal hemorrhages. Clinical ocular examinations assessed the onset and time course of retinal hemorrhages. Enucleation specimens were used to assess hemosiderin in the retinas. Hemosiderin was detected within 2 days of induction of retinal hemorrhages. It was detected in only 4 of 11 eyes (36%) studied more than 1 week following induction of hemorrhages. In 2 eyes, hemosiderin was found 9 and 16.8 months after development of hemorrhages. Hemosiderin can represent organization of current hemorrhage rather than evidence of prior hemorrhage. This study does not allow specifying the duration of hemorrhages with greater precision than "more than 2 days prior to death," and that, only if there is no survival interval. Failure to detect hemosiderin does not exclude prior retinal hemorrhages.

Animals↗
PubMed2005

Erectile dysfunction drugs and non-arteritic anterior ischemic optic neuropathy: is there a cause and effect relationship?

The recent reports of non-arteritic anterior ischemic optic neuropathy (NAION) occurring shortly after ingestion of erectile dysfunction agents have raised the question of whether these agents have a cause-and-effect relationship to NAION. The nature of optic nerve head blood flow and the various factors that influence it, the systemic vascular effects of these agents, and the clinical features of NAION lead me to believe that these agents are contributory factors. Patients with the appropriate risk factors should, therefore, be warned of this possibility and advised to refrain from using these agents.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed2004

Intraocular pressure abnormalities associated with central and hemicentral retinal vein occlusion.

OBJECTIVE: To evaluate the prevalence of ocular hypertension (OHT) and glaucoma in patients with central retinal vein occlusion (CRVO) and hemi-CRVO (HCRVO) and of the fall in intraocular pressure (IOP) secondary to CRVO/HCRVO. DESIGN: Nonrandomized comparative case series. PARTICIPANTS AND METHODS: We investigated 674 consecutive patients who were initially seen with unilateral CRVO (n = 548) and HCRVO (n = 126) at their onset, with a normal fellow eye. The fellow uninvolved eye in each patient acted as a control. Central retinal vein occlusion and HCRVO were categorized into nonischemic and ischemic. At all visits, patients had a detailed ocular history, as well as a thorough bilateral ocular evaluation, including IOP recording with a Goldmann applanation tonometer; when the diagnosis of OHT or glaucoma was initially uncertain, the 24-hour diurnal IOP was recorded. The observed prevalence rates of OHT and glaucoma among patients with CRVO and HCRVO were compared with those in the general population. MAIN OUTCOME MEASURES: The prevalence of OHT and glaucoma, and of ocular hypotension secondary to CRVO/HCRVO. RESULTS: The overall prevalence of glaucoma was 9.9% and of OHT 16.2%. The prevalence of glaucoma/OHT was found to be significantly (P<0.0001) higher in patients with CRVO and HCRVO than in the general population. There was no significant difference in the proportion of patients with glaucoma/OHT among the various types of CRVO/HCRVO (P = 0.156). Forty-eight percent of all patients had lower IOP (>/==" BORDER="0">2 mmHg) in the CRVO/HCRVO eye than in the fellow (uninvolved) eye at their initial evaluation. The prevalence of ocular hypotension was significantly (P<0.0001) higher in patients with glaucoma/OHT not on ocular hypotensive therapy than in patients without glaucoma. Among the patients without glaucoma, the prevalence of ocular hypotension differed significantly among the various types of CRVO/HCRVO (P = 0.007). CONCLUSIONS: Central retinal vein occlusion and HCRVO have a significant association with glaucoma and OHT and with a subsequent fall in IOP in the involved eye. Few patients with CRVO/HCRVO have high IOP in the involved eye, although many of them do have it in the fellow uninvolved eye. It is important to exclude glaucoma/OHT in the fellow eye of any patient with CRVO/HCRVO; if present, elevated IOP should be treated to reduce the risk of that eye developing (1) CRVO/HCRVO and (2) glaucomatous damage. There may be no benefit to prescribing IOP-lowering drops for involved eyes whose IOP is already normal.

Adolescent↗
PubMed2004

Central retinal artery occlusion. Retinal survival time.

PURPOSE: To investigate the retinal survival time following central retinal artery occlusion (CRAO). METHODS: In 38 elderly, atherosclerotic and hypertensive rhesus monkeys, transient CRAO (varying from 97 to 240 min) was produced by temporarily clamping the CRA at its site of entry into the optic nerve. Stereoscopic color fundus photography, fluorescein fundus angiography, electroretinography (ERG), and visual evoked potential (VEP) recording were performed before and during CRA clamping, after unclamping, and serially thereafter. After unclamping of the CRA, the animals were followed for variable lengths of time (median duration 8.14 weeks). Finally, the eyes and optic nerves were examined histologically. The data on ERG changes were analyzed in the following four time frames: (1) baseline before CRA clamping, (2) during CRA clamping, (3) immediately after unclamping, and (4) at the end of follow-up. Duration of CRAO was divided into four groups: 97, 105-120, 150-165, and > or = 180 min. RESULTS: A 'negative ERG' appeared during CRA clamping. With removal of the CRA clamp, there was b-wave recovery, with differential rates of recovery of ERG-eyes with shorter CRAO recovered sooner than those with longer occlusion. On removal of clamp, recovery was seen in scotopic 24 dB b-wave, photopic 0 dB single flash b-wave and 30 Hz flicker, with the b/a ratio of the combined rod and cone response and selective rod response showing statistically significant differences amongst the shorter and longer periods of CRAO. A delayed normalization of the depressed b/a ratio immediately after CRA reperfusion may indicate high-grade ischemic damage. At the final follow-up test session, no clear-cut derangement of any ERG parameter was seen for any group, with subtotal b-wave amplitude recovery for all groups. Longer CRAO produced incomplete VEP recovery. On histology, in the macular retina, eyes with CRAO for 97 min showed practically no damage, but duration of CRAO was found to be significantly associated with the amount of damage in the ganglion cell layer (p = 0.009) and inner nuclear layer (p = 0.017). Outer nuclear and plexiform layers and photoreceptors showed no damage at all with CRAO. There was no significant association of the ERG measures and histologic changes with any of the residual retinal circulation variables. CONCLUSIONS: Our electrophysiologic, histopathologic and morphometric studies showed that the retina of old, atherosclerotic, hypertensive rhesus monkeys suffers no detectable damage with CRAO of 97 min but above that level, the longer the CRAO, the more extensive the irreversible damage. The study suggests that CRAO lasting for about 240 min results in massive irreversible retinal damage.

Animals↗
PubMed2003

Influence of arterial hypertension and diet-induced atherosclerosis on macular drusen.

PURPOSE: To evaluate whether development of macular drusen is influenced by experimentally induced chronic arterial hypertension and atherosclerosis. METHODS: The prospective experimental study included 93 eyes of 51 elderly rhesus monkeys. The total study group was divided into groups with experimental arterial hypertension ( n=22), diet-induced atherosclerosis ( n=10), or both arterial hypertension and atherosclerosis ( n=29) and a control group without arterial hypertension or atherosclerosis ( n=32). Using color wide-angle fundus photographs taken at the beginning and the end of the study, age-related macular degeneration was graded by counting the number and estimating the mean size of drusen in the macular region. RESULTS: In the monkeys with arterial hypertension, the count and area of the macular drusen and the change in number and size of macular drusen during the follow-up period were significantly ( P<0.05) higher than in the monkeys of the control group. Correspondingly, the count and size of macular drusen were significantly ( P<0.05) correlated with the duration of arterial hypertension. In contrast, monkeys with only atherosclerosis did not vary significantly ( P>0.10) from monkeys of the control group in number and size of drusen. The macular drusen parameters were statistically ( P>0.20) independent of the duration of atherosclerosis. Similarly, the atherosclerotic monkeys and the monkeys of the control group did not vary significantly ( P>0.30) in the change of the macular drusen parameters during the follow-up period. CONCLUSIONS: Development of macular drusen as part of age-related macular degeneration in rhesus monkeys may be associated with experimentally induced arterial hypertension. It does not seem to be influenced by diet-induced atherosclerosis.

Animals↗
PubMed2003

Visual deterioration in giant cell arteritis patients while on high doses of corticosteroid therapy.

PURPOSE: To report the incidence and extent of visual deterioration in patients with giant cell arteritis (GCA) on high doses of systemic corticosteroids during the early stages of treatment; the various factors that may influence the outcome; and whether intravenous megadose corticosteroid therapy is more effective than oral therapy. DESIGN: Noncomparative interventional case series. PARTICIPANTS: One hundred forty-four patients with GCA (271 eyes) seen initially with visual loss (91 patients) and without visual loss (53 patients). All patients had biopsy-confirmed GCA and were followed while on high doses of systemic corticosteroid therapy for at least 2 weeks. METHODS: Every patient at the initial visit had an ophthalmic evaluation, including visual acuity, visual fields, intraocular pressure, slit-lamp and ophthalmoscopic evaluation, erythrocyte sedimentation rate (ESR; Westergren) and C-reactive protein (CRP) estimation, and temporal artery biopsy as soon as possible. If GCA was either strongly suspected or confirmed by biopsy, they were immediately started in our clinic on high doses of oral (80-120 mg) prednisone daily or intravenous megadose systemic corticosteroids (usually 150 mg dexamethasone sodium phosphate every 8 hours for 1-3 days) followed by oral prednisone. At each visit they underwent all the initial ophthalmic evaluations and had an ESR and CRP evaluation done. Tapering of steroid therapy was not started until both ESR and CRP had reached their lowest stable levels. These showed marked interindividual variation and usually took approximately 2 weeks to stabilize. Then the steroid therapy was gradually tapered, guided primarily by the levels of ESR and CRP. No generalization is possible regarding the period required to achieve the maintenance dosage, because this also varied markedly from patient to patient. MAIN OUTCOME MEASURES: Visual acuity deterioration. RESULTS: While on high doses of steroid therapy during the initial stages of the treatment, only 9 (11 eyes) of the 91 patients seen initially with visual loss developed further visual acuity deterioration in one or both eyes within 5 days after the start of therapy (one of the eyes had normal vision initially), but none of the 53 patients initially seen without visual loss developed any visual deterioration. Six of the 48 patients (13%) who were on intravenous steroid therapy had visual deterioration compared with 3 of 97 patients (3%) who were only on oral steroid therapy (P = 0.060). CONCLUSIONS: Our study shows that although a few eyes can develop visual deterioration while on high doses of steroid therapy, early, adequate steroid therapy is effective in preventing further visual loss in most. When further visual deterioration occurred despite high doses of systemic corticosteroids, it almost invariably started within 5 days after the start of the high-dose steroid therapy. There was no evidence that intravenous megadose steroid therapy was more effective than oral therapy in preventing visual deterioration.

Aged↗
PubMed2002

Hematologic abnormalities associated with various types of retinal vein occlusion.

BACKGROUND: The objective of this study was two-fold: (1) to investigate hematologic abnormalities associated with various types of retinal vein occlusion (RVO) and comparison of their prevalence among those various types of RVO; (2) to review the conflicting literature on the subject, to place the information in perspective. METHODS: In patients with various types of RVO seen in our clinic since 1973, we conducted planned prospective studies on the prevalence of: (1) routine hematologic tests (535 patients) and (2) certain special hematologic parameters (platelet aggregation, antithrombin III, and proportional, variant(2) globulin in 110, 81 and 91 patients, respectively). Patients were categorized into six types of RVO, based on defined criteria: non-ischemic and ischemic central RVO (CRVO), non-ischemic and ischemic hemi-CRVO (HCRVO), and major and macular branch RVO (BRVO). The patients had a detailed ophthalmic, systemic and hematologic evaluation. The data were abstracted and analyzed retrospectively from the detailed information originally collected prospectively in the patients' records. For data analysis, patients were divided into young, middle-aged and elderly. Observed prevalence rates of hematologic abnormalities were estimated. Logistic regression, adjusting for age and gender, was used to compare the observed prevalence of hematologic abnormalities among the various types of RVO. RESULTS: No generalizations about the prevalence of hematologic disorders in all six types of RVO are possible. Ischemic CRVO showed a significantly higher prevalence of abnormal hematocrit ( P=0.044), hemoglobin ( P=0.018), and blood urea nitrogen ( P=0.025) than non-ischemic CRVO, while a significantly higher prevalence of abnormal antinuclear antibody (ANA; P=0.049) was seen in non-ischemic CRVO than in ischemic CRVO. There was a significant ( P=0.011) difference in the prevalence of abnormal uric acid among the three main RVO groups (CRVO, HCRVO, BRVO), highest in BRVO and lowest in HCRVO. There was a higher prevalence of abnormal glucose ( P=0.069) and ANA ( P=0.071) in CRVO+HCRVO than in BRVO. Results of special hematologic studies are given. CONCLUSIONS: Our study showed that a variety of hematologic abnormalities may be seen in association with different types of RVO, and any generalization about these disorders applied to all RVO patients may be misleading. The evidence of our study and in the literature indicates that there is no good reason why all patients with RVO should be subjected to extensive, expensive, special hematologic and hypercoagulability investigations, unless, of course, there is some clear indication; the routine, inexpensive hematologic evaluation is usually sufficient for RVO patients. Treatment with anticoagulants or platelet anti-aggregating agents may adversely influence the visual outcome, without any evidence of protective or beneficial effect.

Adolescent↗