24小时眼压监测中夜间眼压测量方法的探讨

目的比较24h眼压监测中夜间即刻坐位眼压值和坐起休息10min后测得的眼压值,探讨夜间眼压的不同测量方法对青光眼24h眼压昼夜波动的影响。方法对已确诊且未用药、未做过手术的48例正常眼压性青光眼及17例原发性开角型青光眼患者进行24h眼压监测,每2h1次,其中测量夜间0:00、2:00、4:00眼压时,逐个唤起患者后立即测,后嘱患者坐起休息10min再测,采用SPSS软件以配对t检验分析比较测量结果。结果夜间即刻坐位眼压值和坐起休息10min后测得的眼压值差异有统计学意义(P<0.001),正常眼压性青光眼与原发性开角型青光眼间眼压差值差异有统计学意义(P<0.05)。结论即刻坐位眼压值能更准确反映夜间眼压,对24h眼压测量及青光眼诊断及治疗更有价值,值得临床应用。     

睡眠影响青光眼的发生与发展的研究现状

青光眼是病理性高眼压或正常眼压合并视乳头、视网膜神经纤维层损害及青光眼性视野改变的严重不可逆性致盲眼病。世界卫生组织已将它列为世界范围内的第二大致盲性眼部疾病。睡眠可对青光眼患者的眼压造成一定的影响,从而加剧其病情的发展。反之,青光眼已被列为一种明确的"心理因素影响的躯体疾病"或"心理生理疾病"。青光眼患者的心理特征和躯体症状也会影响其睡眠质量。因此,青光眼与睡眠之间可相互影响。故本文中笔者就青光眼与睡眠之间的相互作用关系做以简要综述。     

急性高眼压发作后眼后节的变化

眼压急进性升高是急性闭角型青光眼的典型表现,也是导致青光眼患者眼部组织损伤,视力下降甚至失明的重要原因。急性闭角型青光眼的短时间内眼压急剧地升高,会对视网膜、脉络膜以及视神经的结构和功能造成特征性的损伤。目前对于青光眼的诊断及病程评估,很大程度上是依赖于高眼压的状态,视神经的变化及视野的损伤,但此时青光眼患者的眼底已经发生了不可逆性的损伤。而眼后节的微结构改变,对于高眼压更加敏感,往往出现在视神经和视野损伤之前,可以更早的提示高眼压对眼部的损伤。通过对眼后节影像学特点的评估,可以从中探索出临床上评估影响青光眼预后的形态学特征,对于青光眼的早期诊断具有重要的临床意义。     

阻塞性睡眠呼吸暂停低通气综合征对青光眼患者眼压波动的影响

目的 探讨阻塞性睡眠呼吸暂停低通气综合征(OSAHS)对青光眼患者24 h眼压波动的影响,评估辅助持续正压通气(CPAP)治疗对患者眼压的控制效果.方法 对可疑青光眼患者166例行24 h眼压监测,对确诊的青光眼患者行7 h睡眠监测.根据呼吸暂停低通气指数(AHI)将患者分成OSAHS+青光眼组与非OSAHS+青光眼组...     

原发性开角型青光眼患者24小时眼压变动规律的临床研究

目的:研究原发性开角型青光眼患者的24h眼压变动规律。方法:选择原发性开角型青光眼患者30人(52只眼,30～60岁),进行24h眼压测量。测量自清晨7∶30开始至第2天清晨7∶30,每2h测1次眼压,共测12次。在7∶00～23∶00时间段测量中,测受检者的坐位眼压和卧位眼压。在23∶00～7∶00时间段测受检者的平卧位眼压。结果:原发性开角型青光眼患者的眼压高峰出现在1∶30,眼压低谷出现在17∶30,24h坐、卧位眼压变动幅度大于24h卧位眼压变动幅度。结论:原发性开角型青光眼患者的眼压高峰大多出现在夜间睡眠时间,夜间眼压控制应引起重视。     

夜间血压下降对开角型青光眼视神经损伤的影响

目的：探讨夜间血压下降与开角型青光眼和正常眼压性青光眼患者视神经损伤进展的关系。

方法：对我院眼科门诊确诊的开角型青光眼和正常眼压性青光眼患者51例51眼分别进行视野、OCT检查,进行平均视神经纤维层厚度、24h动态血压监测、24h眼压监测等检查,分析夜间血压过度下降与视野进展率的关系。

结果：根据夜间血压下降值(dip)进行分组,三组间有显著性差异的数值为平均缺损(MD)差值(P=0.032)、眼压峰值(P=0.003)、视野缺损计分差值(P=0.041)。在视野缺损进展组、视野缺损改善组、视野缺损不变组间,dip有显著性差异(P=0.028)。视野缺损进展组夜间血压下降值明显高于其他两组。夜间血压过度降低组视野缺损进展率明显高于不过度降低组(视野缺损进展率分别为50%,7%)。影响视神经纤维层(RNFL)厚度的相关因素为夜间最低平均动脉压和dip(P=0.011,P=0.032,R²=0.081); 影响MD值的相关因素为眼压波动(P=0.026,R²=0.115); 影响模式标准差(PSD)值的相关因素为眼压波动和dip(P=0.020,P=0.044,R²=0.141)。

结论：与开角型青光眼相比,正常眼压性青光眼患者中夜间血压过度下降的发生率较高。夜间血压过度降低组中视野损伤进展明显。视野缺损进展组夜间血压降低更明显。眼压波动与dip是正常眼压性青光眼和高眼压开角型青光眼的患者视神经损伤与视野缺损高危因素。     

原发性开角型青光眼与24h眼压及眼灌注压的研究进展

原发性开角型青光眼是一类早期无明显临床症状,但随病情进展将导致不可逆的视神经损害及视野缺损的致盲性眼病。眼压是原发性开角型青光眼诊断及评定治疗效果的简单而又重要的指标。临床上,一些治疗中的原发性开角型青光眼患者白天就诊时间所测眼压已达靶眼压,但视神经损害却仍在进展,研究表明可能与夜间眼压的升高、24 h较大的眼压波动及夜间眼灌注压的降低有关。因此,我们对原发性开角型青光眼与眼压及眼灌注压波动的相关文献予以综述,以更好的理解三者之间的关系。     

角膜厚度与青光眼危险性的关系

眼压是青光眼主要的致病因素与诊断指标之一，眼压测量值受中央角膜厚度的影响。中央角膜厚度个体差异较大，导致眼压测量值变异较大。中央角膜厚度与原发性开角型青光眼、正常眼压性青光眼及高眼压症患者的眼压之间存在一定的量化关系。角膜越厚，眼压测量值越高。对于正常角膜厚度青光眼患者，眼压受中央角膜厚度的影响不大。高眼压症患者、正常眼压性青光眼患者应常规作角膜厚度测量以排除角膜厚度的影响。中央角膜厚度，眼压与青光眼之间的关系有待于进一步研究。     

日间与昼夜眼压曲线对异常眼压测量能力的比较

目的评价日间眼压曲线与昼夜眼压曲线对异常眼压测量的能力。方法对就诊于北京同仁眼科中心的21例原发性开角型青光眼（POAG）、11例可疑正常眼压性青光眼（SNTG）及24例可疑青光眼患者进行昼夜眼压曲线测量。间隔2 h后,先使用手持式压平眼压计测量24 h的卧位眼压得到昼夜卧位眼压曲线。在9：30、11：30、13：30、15：30,患者完成卧位眼压测量5 min后测量坐位眼压,5 min后再使用非接触眼压计测量眼压,分别得到日间卧位眼压曲线、日间坐位眼压曲线和日间非接触眼压曲线。定义眼压峰值〉21 mmHg时为峰值异常,眼压波动〉5 mmHg时为波动异常。分析日间眼压曲线与昼夜眼压曲线均值、峰值及波动值间是否存在差异。结果不同组别昼夜眼压均值为（20.24±2.45）～（22.32±6.02）mmHg,较日间眼压均值高-0.19～6.37 mmHg;昼夜眼压峰值在（24.17±3.42）～（26.43±6.23）mmHg,较日间眼压峰值高1.75～8.76 mmHg;昼夜眼压波动在（8.00±3.47）～（9.09±3.83）mmHg,较日间眼压波动高3.59～6.00 mmHg。眼压峰值多出现于夜间睡眠时,POAG、SNTG和可疑青光眼患者眼压峰值出现于23：30～5：30的概率分别为57.14%、72.73%和66.67%。日间眼压曲线无法确定昼夜眼压波动的异常,若以昼夜眼压曲线作为金标准,各组的敏感性为10.00%～36.84%。结论56例患者的峰值眼压多发生在夜间睡眠时,日间和昼夜眼压曲线测得的眼压均值、峰值、波动及发现异常眼压的能力存在差异,依靠日间眼压曲线很难对昼夜眼压的情况做出准确判断。     

眼压与头位的关系

一个人从直立到平躺眼压可发生有临床意义的升高，在青光眼患者中这种眼压变化更大。Buys等进行了一项研究，在白天眼压得到很好控制的进展性青光眼患者中，让其睡姿保持头抬高30°，观察其夜间眼压的变化。结果表明，头高30°与平躺相比，眼压平均下降3．2mmHg。     

Nocturnal measurements of intraocular pressure in patients with normal-tension glaucoma and sleep apnea syndrome

BACKGROUND: About half of all normal-tension glaucoma patients and about one third of all primary open-angle glaucoma patients have sleep apnea syndrome. If sleep apnea syndrome causes some cases of glaucoma, the optic nerve damage could result from repetitive nocturnal hypoxias or from repetitive intraocular pressure elevations at the end of the apneas. In this study, we determined the intraocular pressure at the end of long apneas. PATIENTS AND METHODS: In three patients having sleep apnea syndrome and normal-tension glaucoma we recorded in a sleep laboratory during at least six hours of sleep the respiration (oxymetry, nasal and oral air flow, and inductive plethysmography). The intraocular pressure was measured with a pneumatonometer at predetermined times and compared to the values measured at the end of prolonged apneas. RESULTS: The intraocular pressure during normal respiration was in the first patient 19.5 +/- 1.0 mm Hg OD and 19.3 +/- 1.7 mm Hg OS, in the second patient 25.0 +/- 4.2 respectively 25.5 +/- 4.9 mm Hg and in the third one 22 +/- 1.0 respectively 21.3 +/- 1.3 mm Hg. At the end of prolonged apneas the intraocular pressure was in the first patient 19.0 +/- 0.0 mm Hg OD and 19.5 +/- 0.7 mm Hg OS, in the second patient 26.5 +/- 0.6 and 26.8 +/- 0.1 mm Hg and in the third one 20.0 +/- 0.0 respectively 21.0 +/- 0.0 mm Hg. The difference between intraocular pressures during normal respiration and at the end of prolonged apneas was not significant (p > 0.1 for each comparison, paired t-test). CONCLUSIONS: We did not find an increase of intraocular pressure at the end of prolonged apneas compared to periods of normal respiration in patients with sleep apnea syndrome and normal-tension glaucoma. If sleep apnea syndrome causes some cases of glaucoma, it seems more probable that the the optic nerve is damaged by the repetitive hypoxias. Alternatively, an unknown factor might induce both, sleep apnea syndrome and normal-tension glaucoma.     

The significance of intraocular pressure elevation during sleep‐related postures

Intraocular pressure and its fluctuations are associated with the development and progression of glaucoma. This review examines the potential for sleep‐related intraocular pressure elevations to contribute to the onset and progression of glaucoma. Also considered is the potential for patient education and appropriate changes in behaviour as a means of reducing exposure to elevated intraocular pressure. A PubMed search using the combination key words ‘glaucoma and sleep’ was conducted. Information was taken from representative articles from the 187 yielded from the search. Additional papers were found after accessing references in selected papers. Several studies have indicated an association between the progression of glaucoma and both lateral decubitus (side sleep) and supine sleep positions. Evidence that prone sleep positions could raise intraocular pressure to high levels suggests a similar if not stronger association. Intraocular pressure elevation and progression of glaucoma associated with sleep positions suggest that there are similar risks of progression associated with sleep‐related body postures adopted during non‐sleep activities, such as reading, watching television and sun‐bathing. Posture‐related management of patients with glaucoma, which is intended to reduce the risk or degree of progression may include the use of specially designed pillows, bed‐head elevation and recommendations to avoid postures which induce higher intraocular pressure.     

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.     

Posture-induced Intraocular Pressure Changes: Considerations Regarding Body Position in Glaucoma Patients

Although glaucoma is a multifactorial disease, elevated intraocular pressure (IOP) remains the most important known risk factor. Different systemic and local factors are thought to influence an individual's IOP. There can be a clinically significant rise in IOP when going from upright to horizontal or inverted body positions. Although there is a significant interindividual variability, the magnitude of the IOP change is greater in glaucomatous eyes. As patients usually spend a significant portion of their lives in the horizontal position, mainly during sleep, this is highly relevant. In this review we discuss the relationship between postural changes and IOP fluctuation, including changes in both body and head position. The possible mechanisms involved and the main implications for glaucomatous eyes are discussed. Finally, considerations with regard to sleep position in glaucoma patients are made based on evidence in the literature.     

激光原位角膜磨削术在青光眼患者中的应用

激光原位角膜磨削术是否可以应用到青光眼患者是一个重要临床问题,屈光手术所造成角膜厚度和角膜曲度的改变可影响眼压的测量从而影响青光眼的诊断和治疗;在手术过程中一过性但极高的眼压可能引起视网膜神经纤维损害或视网膜中央动脉阻塞,青光眼患者或皮质类固醇敏感者屈光手术后常规应用激素类眼药水可能出现激素诱导性眼压升高。虽然如此,激光原位角膜磨削术并非青光眼手术的绝对禁忌证。本文就激光原位角膜磨削术在青光眼患者中应用的安全性以及影响作出综述。     

Kontinuierliche 24-h-Aufzeichnung von Augendruckschwankungen mittels drahtlosem Kontaktlinsensensor Triggerfish™

Background

For many years researchers have been striving for a non-invasive 24 h continuous method of ambulatory intraocular pressure monitoring. A wireless device with a contact lens sensor is now on the market for clinical use, which is not a quantitative measurement of the intraocular pressure but is at least a recording of qualitative changes. These changes of corneal curvature due to changes of the intraocular pressure result in a distinct profile which gives information about fluctuations of the intraocular pressure, the behaviour during supine sleeping time and the 24 h efficacy of glaucoma therapy. We investigated the practicability and tolerability of this device.

Method

The sensor is embedded in a soft silicone contact lens and consists of 4 strain gauges. Additionally there is an antenna made out of gold and a microchip. A second antenna is fixed around the eye which sends impulses to the microchip and receives data from the microchip. The data are sent to a recorder via a wire. Measurements are made for 90 s every 8.5 min resulting in 144 measurements within 24 h. Of the 4 strain gauges 2 sense changes in the corneal curvature due to changes of the intraocular pressure. This device was used in 11 patients with ocular hypertension or glaucoma.

Results

The result of the 24 h continuous measurement is a pressure profile which may be flat, fluctuating and with no, some or many spikes. We describe 2 examples of profiles from patients with glaucoma. The changes in the profiles were mostly during the sleeping hours in a supine position. Due to the lack of validation of the results it is not known if intermittent spikes are true spikes or artefacts. Practicability was simple and tolerability was reported to be good by all patients.

Conclusions

For the first time a practicable, well tolerated, non-invasive device for continuous 24 h monitoring of changes of the corneal curvature due to changes of the intraocular pressure is available. It is not a direct measurement of the intraocular pressure. The resulting profile gives additional information about the behaviour of the intraocular pressure, especially during out-of-office times and night times. Disadvantages are the high cost of the contact lens sensor and the lack of validation of the results and reproducibility in patients.     

Normal tension glaucoma, sleep apnea syndrome and nasal continuous positive airway pressure therapy--case report with a review of literature

BACKGROUND: In the pathogenesis of glaucoma, besides an elevated intraocular pressure (IOP), cardiovascular risk factors, such as arterial hypotension and hypertension, vasospasms, autoregulatory defects, atherosclerosis, and diabetes mellitus are of increasing importance, especially in normal tension glaucoma. Recently, there have been several reports of an additional risk factor: obstructive sleep apnea syndrome. METHODS: Literature review (Medline) and case report. RESULTS: The authors report on a 8 1/2 years follow-up of a 60-year-old patient with normal tension glaucoma. Despite successful pharmacological and surgical lowering of intraocular pressure a progressive glaucomatous damage with optic nerve atrophy and increasing visual field defects occurred. As a result of intensive investigations of possible cardiovascular risk factors, an obstructive sleep apnea syndrome was diagnosed. Since the beginning of therapy with nCPAP (nasal continuous positive airway pressure) more than 3 1/2 years ago, no further progression of glaucomatous optic nerve damage or visual field defects have been observed. CONCLUSIONS: In clinical practice, obstructive sleep apnea syndrome often is underdiagnosed. In patients suffering from glaucoma and obstructive sleep apnea syndrome, intraocular pressure lowering therapy may not be enough, whereas an additional nCPAP-therapy potentially could prevent the beginning/progression of glaucomatous optic nerve damage.     

体位与眼压研究进展

青光眼是受多因素影响的不可逆性致盲眼病,眼压升高是已知最重要的危险因素。研究普遍认为眼压越高,眼压波动越大,青光眼性视神经损害越严重。全身和局部因素变化都可能影响到患者的眼压,而体位是其中重要因素之一。青光眼患者眼压受体位变化的影响普遍大于正常人。体位与眼压的关系在青光眼的日常诊疗和管理中起到重要作用,也越来越得到眼科医生的关注,本文主要就体位与眼压的研究进展及可能机制进行综述。     

Predictive factors for progressive optic nerve damage in various types of chronic open-angle glaucoma

PURPOSE: To evaluate whether various types of chronic open-angle glaucoma differ in predictive factors for progression of glaucomatous optic nerve damage. DESIGN: Observational cohort study. METHODS: SETTING: Prospective observational clinical study. PATIENTS: 517 eyes of 300 Caucasian patients with chronic open-angle glaucoma with elevated intraocular pressure (primary open-angle glaucoma, n = 289; secondary open-angle glaucoma, n = 50) and with normal intraocular pressure (n = 178). OBSERVATION PROCEDURE: During follow-up (median: 49 months, 6 months-130 months), all patients underwent repeated evaluation of color stereo optic disk photographs and white-on-white visual field examination. MAIN OUTCOME MEASURES: Progression of glaucoma was defined as neuroretinal rim loss during the study period. RESULTS: For patients with elevated intraocular pressure, significantly predictive factors for eventual progression were older age, advanced perimetric damage, smaller neuroretinal rim, and larger area of beta zone of parapapillary atrophy. In contrast, in the normal intraocular pressure group, a significant predictive factor was presence of disk hemorrhages at baseline. Within the patients with elevated intraocular pressure, the primary open-angle glaucoma group and the secondary open-angle glaucoma group did not differ in predictive factors for progression of glaucoma. CONCLUSIONS: Open-angle glaucoma patients with normal intraocular pressure and open-angle glaucoma patients with elevated intraocular pressure differ in predictive factors for eventual progression of glaucomatous optic nerve damage. It may have clinical importance and may be helpful in the discussion of the pathogenesis of the glaucomas.     

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.