青光眼与睡眠

睡眠对于每个人来说都是非常重要的,对于青光眼患者更有极其特殊的意义。睡眠质量对青光眼有很大影响,而青光眼的躯体症状和患者的心理因素又对睡眠产生较大的影响。夜间睡眠时眼压会升高,而眼压是影响青光眼病情最重要的因素,夜间眼压波动对视功能有很大的损害。睡眠期间是青光眼治疗的关键时段,应引起青光眼患者和医生的足够重视。     

The importance of and potential for continuous monitoring of intraocular pressure

Monitoring intraocular pressure (IOP) is a critically important part of glaucoma management; however, clinical tonometry predominantly involves sitting postures and is unable to detect variations in response to posture changes, muscular effort, deep respirations and during a wide range of activities, such as playing high wind‐resistance instruments and wearing swimming goggles in addition to eye touching and rubbing. For example, the usefulness of 24‐hour tonometric phasing may be increased, if nocturnal assessments included side and prone sleeping postures rather than being limited to supine posture tonometry. Continuous monitoring of IOP, which allows unrestricted involvement in a full range of sleep and non‐sleep IOP elevating activities would provide an ideal method of quantifying the frequency, duration and degree of episodes of elevation in addition to physiological and pathological circadian rhythmic variations due to treatment. Apart from the degree of exposure to episodes of elevation of IOP, genetic influences and family history of glaucoma, other factors which are or could be associated with increased susceptibility to develop or progress glaucomatous pathology include age, frailty, race, type and degree of refractive error, systemic hypotension and hypertension, vasospasm, migraine, pigmentary dispersion syndrome, pseudoexfoliation syndrome, obstructive sleep apnoea syndrome, diabetes as well as medication interactions and side effects. Such information, when combined with all details relating to episodes of elevation of IOP, appears likely to be a strong basis for the detection, diagnosis and treatment of glaucoma. This review examines the limitations of methods of longitudinal monitoring of IOP with reference to their validity and the varying degrees of invasiveness involved. Also mentioned is the potential value of knowing the frequency, duration and level of variations of optic nerve subarachnoid space pressure, as the interaction of such changes with IOP and their potential influence on the lamina cribrosa, may help determine pathological significance.     

Hypotensive effect of carteolol on intraocular pressure elevation and secondary glaucoma associated with endogenous uveitis

The therapeutic effects of carteolol hydrochloride were evaluated in the treatment of 44 uveitis patients (51 eyes) with intraocular pressure elevation or secondary glaucoma. Carteolol ophthalmic solutions, either 1% or 2%, were given twice day for more than 4 weeks in glaucomatocyclitic crisis and for more than 8 weeks in other forms of uveitis. Intraocular pressure significantly decreased from week 1 of treatment and persisted within normal limits until week 8 in glaucomatocyclitic crisis. Similarly, intraocular pressure decreased significantly from week 2 in other forms of uveitis. Intraocular pressure was well controlled in patients with open-angle glaucoma, but the control was insufficient in patients with angle-closure glaucoma. No adverse reactions such as systemic hemodynamic effects or exacerbations of intraocular inflammation were observed during this study. Carteolol therefore seems to be effective for the treatment of intraocular pressure elevation and secondary glaucoma associated with endogenous uveitis.     

Risk factors for primary open angle glaucoma progression: what we know and what we need to know

PURPOSE OF REVIEW: Recent literature is reviewed in order to identify possible risk factors leading to primary open angle glaucoma progression and blindness. RECENT FINDINGS: Several risk factors have been suggested to be important for progression of open angle glaucoma. Intraocular pressure appears to be an important risk factor for progression of glaucoma. It is still not clear if intraocular pressure fluctuation and central corneal thickness are related to progression. Myopia might be related to glaucoma progression as well as optic disc hemorrhages. Vascular factors appear to be related to progression also. Genetics seem to play an important role in open angle glaucoma. SUMMARY: Identifying risk factors associated with progression of patients with primary open angle glaucoma is essential to our clinical practices. The level of understanding regarding those risks is suboptimal at this point. Prospective long-term studies are needed if we wish to better understand the disease and help those patients at greater risk of progression and blindness.     

Does smoking affect intraocular pressure? Findings from the Blue Mountains Eye Study

PURPOSE: To assess the relationship between smoking and intraocular pressure. MATERIALS AND METHODS: The Blue Mountains Eye Study examined 3654 residents aged 49 years and older in an area west of Sydney, Australia from 1992 to 1994. A trained interviewer collected a detailed history of smoking. Intraocular pressure was measured using Goldmann applanation tonometry; as the correlation between right and left eyes was very high, only right-eye data are presented. Participants using glaucoma medications or who had evidence of previous cataract surgery were excluded. RESULTS: Current smokers (15.8% of participants) had slightly higher mean intraocular pressures (16.34 mm Hg) than nonsmokers (16.04 mm Hg). Intraocular pressure (in the right eye) was significantly associated with current smoking, after adjusting for age and sex (P = 0.03). This association remained unchanged after simultaneous adjustment for other variables associated with intraocular pressure, including blood pressure, diabetes, myopia, glaucoma, family history, and pseudoexfoliation (P = 0.02). CONCLUSIONS: This study identified a modest cross-sectional positive association between current smoking and intraocular pressure.     

Relationship between postural change of the intraocular pressure and visual field loss in primary open-angle glaucoma

PURPOSE: To determine the relationship between the postural changes of the intraocular pressure and the visual field loss in patients with primary open-angle glaucoma. METHODS: Eleven normal subjects and 11 patients with primary open-angle glaucoma were studied. Intraocular pressure was measured in both the sitting and the supine positions. Visual fields were measured with automated perimetry. RESULTS: When patients moved from a sitting to supine position, the intraocular pressure increased by an average of 3.1 +/- 0.4 mm Hg (mean +/- SEM) in normal subjects and 4.0 +/- 0.2 mm Hg in patients with primary open-angle glaucoma. There was a significant difference between the normal subjects and patients with primary open-angle glaucoma (P = 0.049). Intraocular pressure increased by 4.4 +/- 0.3 mm Hg (P = 0.02) in the worse eye for mean deviation and 3.6 +/- 0.3 mm Hg (P = 0.38) in the better eye for mean deviation. There was no significant difference in intraocular pressure in the sitting position between both groups. CONCLUSIONS: The greatest difference in intraocular pressure between the sitting and supine positions was observed in the worse eye of patients with primary open-angle glaucoma. This result suggests that damage to the optic nerve in primary open-angle glaucoma might occur when patients are asleep in the supine position.     

Infections and glaucoma

Glaucoma is an intraocular pressure-related ophthalmic disease with multiple causes that results in an optic neuropathy and vision loss. Intraocular pressure elevation is among its strongest risk factors. While glaucoma is mostly primary in etiology, secondary glaucoma is not infrequent. Recognizing its cause is imperative, since treatment is often different depending on the pathophysiologic mechanism. Numerous clinically relevant ophthalmic infections can result in robust inflammatory responses that may result in pressure elevation or intraocular anatomic configurations that predispose to pressure elevation. Knowing the mechanisms by which these infections can lead to glaucoma is critical in treating, and we consolidate what is currently known in regards to how infectious diseases lead to glaucoma.     

Obstructive sleep apnea–hypopnea syndrome (OSAHS) and glaucomatous optic neuropathy

Obstructive sleep apnea–hypopnea syndrome (OSAHS) is becoming widely accepted as a risk factor for glaucoma. We discuss the proposed mechanism involved in the pathogenesis of glaucoma in OSAHS, and review the published data on the association between these two conditions, as well as papers regarding functional and structural tests related with glaucomatous damage. There is increasing evidence that the prevalence of glaucoma is higher in OSAHS patients, especially in those with severe disease with apnea-hypopnea index (AHI) >30, and also that sleep disorders may be more frequent in patients with glaucoma, especially in those with normal tension glaucoma (NTG). Several ophthalmic signs and symptoms have been associated with this condition. Raised intraocular pressure (IOP), possibly related to increased body mass index, thinning of retinal nerve fiber layer (RNFL), and alteration of visual field (VF) indices has been demonstrated in many studies, in patients with no history of glaucoma or evidence of glaucomatous changes in the ophthalmic examination. A correlation of AHI with RNFL and VF indices has been described in some studies. Finally, corneal thinning, suspicious glaucomatous disc changes and anomalies in electrophysiological tests such as multifocal visual evoked potential have been described in patients with OSAHS, even in patients with normal findings in the optic nerve and VF, suggesting subclinical optic nerve involvement not detectable in conventional ophthalmic examinations. The pathogenesis of optic nerve involvement has been related to vascular and mechanical factors. Vascular factors include recurrent hypoxia with increased vascular resistance, autonomic deregulation, oxidative stress and inflammation linked to hypoxia and subsequent reperfusion, decreased cerebral perfusion pressure and direct hypoxic damage to the optic nerve. Proposed mechanical factors include increased IOP at night related to supine position and obesity, raised intracranial pressure and elastic fiber depletion in the lamina cribosa and/or trabeculum. In conclusion, ophthalmic evaluation should be recommended in patients with severe OSAHS, and the presence of sleep disorders should be investigated in patients with glaucoma, especially in NTG patients and in those with progressive damage despite controlled IOP, as treatment with continuous positive airway pressure may contribute to stabilizing the progression of glaucomatous damage.     

同步监测青光眼患者24h眼压与血压的意义

青光眼是世界范围内致盲和引起视力损害的主要眼病,也是不可逆性致盲性眼病之一.眼压是青光眼发生发展的重要危险因素,但除眼压外,血压在青光眼进展引起的影响也不可忽视.眼灌注压是血压和眼压的差值,可调节视神经的血液供应.眼压、血压、灌注压在青光眼发生发展中有一定相关性.本文通过对眼压和血压在青光眼中的影响以及24 h眼压和血...     

Risk factors of glaucoma progression: intraocular pressure fluctuations

Intraocular pressure is not a fixed value and varies both over short-term periods and periods of several months or years. In healthy subjects, the circadian fluctuations in intraocular pressure are moderate, generally not exceeding 5 mmHg. In patients with glaucoma or ocular hypertension, intraocular pressure fluctuations are greater and circadian rhythms may be inverted. These fluctuations are probably involved in the conversion of ocular hypertension to glaucoma or glaucoma progression. Large observational clinical studies, however, are not unanimous on the role played by intraocular pressure fluctuations on the risk of conversion from ocular hypertension to glaucoma or glaucoma worsening. Nevertheless, it is important for each patient to estimate the short-term and long-term fluctuations and to prioritize a treatment that minimizes these fluctuations.     

Overcoming diagnostic and treatment challenges in uveitic glaucoma

Uveitic glaucoma is a range of disorders that results in optic nerve damage from elevated intraocular pressure secondary to intraocular inflammation. As compared to primary open angle glaucoma, uveitic glaucoma is associated with a more aggressive disease course caused by very high intraocular pressure levels that wax and wane. Diagnosis is often based on clinical presentation, disease course, and associated systemic manifestations. Diagnostic imaging plays an important role in both diagnosis and management. While the mechanisms of uveitic glaucoma vary, treatment requires strict control of the inflammation and may involve additional intraocular pressure lowering techniques. Management often dictates an interdisciplinary approach as systemic association and treatment is common. When topical management does not slow the progression of optic nerve damage and vision loss, surgical intervention is required. A significant portion of patients with uveitic glaucoma will eventually require surgical intervention and the appropriate referrals should be made. By nature, success rates of surgical intervention in uveitic glaucoma patients are lower than non‐inflammatory causes of elevated intraocular pressure and glaucomatous damage. Chronic inflammation, multiple mechanisms, systemic associations, and unpredictable response to treatment make uveitic glaucoma challenging to manage. This review will discuss the pathophysiology, diagnosis, and management of uveitic glaucoma to provide a guide for eye‐care providers.     

Complications of intravitreal steroid injections.

BACKGROUND: Intravitreal corticosteroid injections are a new therapeutic procedure used to treat various retinal edematous and neovascular conditions. They have been used in the treatment of diabetic macular edema, exudative macular degeneration, pseudophakic cystoid macular edema, macular edema associated with retinal vein occlusion, and chronic uveitis as well as other conditions. Because the use of this therapeutic technique is becoming increasingly more common, adverse effects are now being seen. The most common adverse effects associated with intravitreal steroid injection are elevation of intraocular pressure and progression of cataract. Endophthalmitis, pseudoendophthalmitis, and retinal detachment have also been reported. CASE REPORTS: This report describes 2 patients who were followed up at the VA Connecticut Healthcare System Newington Campus Optometry Clinic for steroid-induced elevation of intraocular pressure after intravitreal corticosteroid injection. One patient exhibited elevation of intraocular pressure after his first intravitreal steroid injection for treatment of clinically significant macular edema secondary to diabetes. The second patient did not exhibit a steroid response to the first intravitreal steroid injection utilized as treatment for choroidal neovascularization from age-related macular degeneration. However, he did show a rise in intraocular pressure after a second intravitreal corticosteroid injection. Intraocular pressures, treatment, and frequency of follow-up in both patients pre- and postinjection are discussed. CONCLUSION: Elevation of intraocular pressure after intravitreal steroid injection can commonly be controlled with topical glaucoma medications. Cataract progression is common in patients after intravitreal injection of corticosteroid; however, findings show these patients are at no additional risk for cataract surgery complications. Therefore, these do not appear to be major contraindications. However, because 30% to 50% of patients experience intraocular pressure rise up to a few months postinjection, and patients are at higher risk for complications such as endophthalmitis, optometrists should be aware of appropriate management after this increasingly utilized therapeutic procedure.     

Role of cerebrospinal fluid pressure in the pathogenesis of glaucoma

The pathogenesis of normal (intraocular) pressure glaucoma has remained unclear so far. As hospital‐based studies showed an association of normal‐pressure glaucoma with low systemic blood pressure, particularly at night, and with vasospastic symptoms, it has been hypothesized that a vascular factor may play a primary role in the pathogenesis of normal‐pressure glaucoma. That assumption may, however, be contradicted by the morphology of the optic nerve head. Eyes with normal‐pressure glaucoma and glaucomatous eyes with high‐intraocular pressure can show a strikingly similar appearance of the optic nerve head, including a loss of neuroretinal rim, a deepening of the optic cup, and an enlargement of parapapillary atrophy. These features, however, are not found in any (other) vascular optic neuropathy, with the exception of an enlargement and deepening of the optic cup in arteritic anterior ischaemic optic neuropathy. One may additionally take into account (i) that it is the trans‐lamina cribrosa pressure difference (and not the trans‐corneal pressure difference, i.e. the so‐called intraocular pressure) which is of importance for the physiology and pathophysiology of the optic nerve head; (ii) that studies have shown that the anatomy of the optic nerve head including the intraocular pressure, the anatomy and biomechanics of the lamina cribrosa and peripapillary sclera, retrobulbar orbital cerebrospinal fluid pressure and the retrobulbar optic nerve tissue pressure may be of importance for the pathogenesis of the highly myopic type of chronic open‐angle glaucoma; (iii) that studies have suggested a physiological association between the pressure in all three fluid filled compartments, i.e. the systemic arterial blood pressure, the cerebrospinal fluid pressure and the intraocular pressure; (iv) that an experimental investigation suggested that a low cerebrospinal fluid pressure may play a role in the pathogenesis of normal (intraocular) pressure glaucoma; and (v) that recent clinical studies reported that patients with normal (intraocular) pressure glaucoma had significantly lower cerebrospinal fluid pressure and a higher trans‐lamina cribrosa pressure difference when compared to normal subjects. One may, therefore, postulate that a low cerebrospinal fluid pressure may be associated with normal (intraocular) pressure glaucoma. A low systemic blood pressure, particularly at night, could physiologically be associated with a low cerebrospinal fluid pressure, which leads to an abnormally high trans‐lamina cribrosa pressure difference and as such to a similar situation as if the cerebrospinal fluid pressure is normal and the intraocular pressure is elevated. This model could explain why patients with normal (intraocular) pressure glaucoma tend to have a low systemic blood pressure, and why eyes with normal (intraocular) pressure glaucoma and eyes with high‐pressure glaucoma, in contrast to eyes with a direct vascular optic neuropathy, show profound similarities in the appearance of the optic nerve head.     

New epidemiologic approach to intraocular pressure in an Antananarivo population

PURPOSE: The Malagasy population is a mixture from many ethnic origins. The Merina population is generally of Asiatic origin. The purpose of this study was to report the main characteristics of Merina intraocular pressure and their risk factors. METHODS: Screening was conducted in 1507 apparently healthy subjects with no known ocular disease (such as glaucoma) living in Antananarivo. Intraocular pressure was measured with a Goldmann tonometer. RESULTS: Males predominated (54.81%). The distribution of aplanation pressure followed an asymmetrical Gaussian pattern. In the Merina population, mean intraocular pressure was low (13.50+/-3.5mmHg, m+/-SD) and increased with age. There was no difference by gender. The prevalence of ocular hypertension was 1.43%. It was slightly higher in females and increased to the age of 50 years, then decreased. Among possible risk factors, only familial glaucoma was significantly frequent. CONCLUSION: The mean intraocular pressure in the Merina population is lower than the accepted statistical mean and is similar in both sexes. The prevalence of intraocular hypertension is also low but glaucoma develops early. Some of our data are similar to those observed in western populations (mean intraocular pressure increases with age). Other points are similar to the Asian population (low mean intraocular pressure and low frequency of intraocular hypertension and its progression after 50 years).     

Progressive optic neuropathy in congenital glaucoma associated with the Sirsasana yoga posture

The authors describe a case of progressive optic neuropathy in a patient with congenital glaucoma who had routinely practiced the Sirsasana (headstand) yoga posture for several years. Ophthalmic examination included best-corrected visual acuity, anterior segment examination, indirect ophthalmoscopy, ultrasound pachymetry for central corneal thickness, and intraocular pressure before, during, and after maintaining the Sirsasana posture for 5 minutes. Intraocular pressure increased significantly during the Sirsasana posture. Transient elevation in intraocular pressure during yoga exercises may lead to progressive glaucomatous optic neuropathy, especially in susceptible patients with congenital glaucoma.     

Nutritional supplementation in the treatment of glaucoma: A systematic review

Current treatment strategies for glaucoma are limited to halting disease progression and do not restore lost visual function. Intraocular pressure is the main risk factor for glaucoma, and intraocular pressure–lowering treatment remains the mainstay of glaucoma treatment, but even successful intraocular pressure reduction does not stop the progression of glaucoma in all patients. We review the literature to determine whether nutritional interventions intended to prevent or delay the progression of glaucoma could prove to be a valuable addition to the mainstay of glaucoma therapy. A total of 33 intervention trials were included in this review, including 21 randomized controlled trials. These suggest that flavonoids exert a beneficial effect in glaucoma, particularly in terms of improving ocular blood flow and potentially slowing progression of visual field loss. In addition, supplements containing forskolin have consistently demonstrated the capacity to reduce intraocular pressure beyond the levels achieved with traditional therapy alone; however, despite the strong theoretical rationale and initial clinical evidence for the beneficial effect of dietary supplementation as an adjunct therapy for glaucoma, the evidence is not conclusive. More and better quality research is required to evaluate the role of nutritional supplementation in glaucoma.     

Hemodynamic processes in eye models with different levels of intraocular pressure

Intraocular pressure effects on blood flow volumic rate in an eye model were examined in various arterial pressure levels and perfused liquid viscosity values. The findings evidence an exponential relationship between intraocular pressure elevation and blood flow volumic rate reduction. Hypotensive drugs should be prescribed with care to glaucoma patients, with the blood viscosity values monitored.     

No clinically important effects on intraocular pressure after short-term administration of sildenafil citrate (Viagra)

PURPOSE: To assess the short-term effects of sildenafil citrate on intraocular pressure in healthy male volunteers and participants in clinical trials. METHODS: Intraocular pressure and pupil diameter were measured in two placebo-controlled studies. Oral doses of sildenafil citrate (VIAGRA; Pfizer Inc, New York, New York) ranged from 10 mg to 150 mg. RESULTS: No major changes in intraocular pressure or pupillometry were detected at any time (1.0-24 hours) after administration of sildenafil. Additionally, of 36 subjects with a medical history of increased intraocular pressure in the sildenafil safety database, none were reported to have a clinically significant increase of their intraocular pressure. During clinical trials, two glaucoma cases were listed as serious adverse events, but were not considered treatment related.CONCLUSION: No clinical abnormalities were observed in intraocular pressure or pupil diameter in subjects receiving sildenafil. Currently, no evidence suggests that long-term treatment with sildenafil has an effect on intraocular pressure or is associated with the development or worsening of glaucoma.     

DIURNAL VARIATIONS IN INTRAOCULAR PRESSURE Chronic Open Angle Glaucoma: Preliminary Report

Human beings have a diurnal variation in their intraocular pressure and this variation is related to the sleep-wake cycle. Patients with chronic open angle glaucoma have a similar fluctuation in intraocular pressure and, even without medication, may achieve a "normal" intraocular pressure several hours into their sleep period. Two patients with chronic open angle glaucoma, maintained on their usual miotic therapy, also maintained a normal diurnal fluctuation in intraocular pressure as did one patient with a unilaterally transected optic nerve and another with a surgically divided trigeminal nerve.     

Diurnal variation of intraocular pressure in primary open-angle glaucoma.

Intraocular pressure was measured with a Goldmann applanation tonometer in 12 normal individuals (24 eyes), 14 ocular hypertensives (28 eyes), and 14 patients (27 eyes) with primary open-angle glaucoma every hour for 24 hours. In most subjects, pressure was highest sometime during the day and pressure elevation before rising was not demonstrated. The lowest intraocular pressure was most frequently observed early in the morning, whether the patient was normotensive or hypertensive. Fourteen of 27 glaucomatous eyes had intraocular pressure below 20 mm Hg early in the morning.