Reliability and validity of surface EMG assessments combined with isometric muscle strength testing in patients with abdominal rectus diastasis and asymptomatic controls.

PURPOSE: Patients with abdominal rectus diastasis (ARD) may have muscular functional impairments, but clinics lack appropriate objective assessment tools. The aim was to establish the relative and absolute reliability, and convergent validity, of muscular activity using Surface Electromyography (SEMG) during isometric abdominal muscle strength testing in patients with ARD and controls without ARD. METHODS: Twenty-six patients with ARD were matched for age, sex and BMI with controls without ARD. Participants were tested twice during isometric muscular contractions using SEMG located on six abdominal sites. Mean amplitude, fatigue, and recruitment order were analyzed. Relative reliability was evaluated with Intraclass Correlation Coefficients (ICC), while absolute reliability was estimated by calculating the Standard Error of Measurement and Minimal Detectable Change. Convergent validity was addressed in relation to participant characteristics, functional ability, and symptoms. RESULTS: Mean SEMG amplitude for all abdominal wall muscle contractions showed moderate to excellent relative test-retest reliability, with ICC values ranging from 0.46 to 0.97. In contrast, fatigue and recruitment order displayed poor to moderate relative reliability in both groups. Absolute reliability measures were generally high. A moderate to high convergent validity (ARD: rho-value 0.41-0.70; Controls: rho-value 0.41-0.75) was observed for mean amplitude in relation to a functional sit-to-stand test, abdominal circumference, BMI, back pain, and quality-of-life. CONCLUSIONS: The results of applying SEMG during isometric abdominal muscle support practicing the method in clinics, although additional development is needed with further standardization and more functional testing. Furthermore, the method demonstrates construct validity in patients with ARD and in age- and sex-matched controls.

Central corneal thickness in the Ocular Hypertension Treatment Study (OHTS).

OBJECTIVE: Central corneal thickness influences intraocular pressure (IOP) measurement. We examined the central corneal thickness of subjects in the Ocular Hypertension Treatment Study (OHTS) and determined if central corneal thickness is related to race. DESIGN: Cross-sectional study. PARTICIPANTS: One thousand three hundred one OHTS subjects with central corneal thickness measurements. INTERVENTION: Central corneal thickness was determined with ultrasonic pachymeters of the same make and model at all clinical sites of the OHTS. MAIN OUTCOME MEASURES: Correlation of mean central corneal thickness with race, baseline IOP, refraction, age, gender, systemic hypertension, and diabetes. RESULTS: Mean central corneal thickness was 573.0 +/- 39.0 microm. Twenty-four percent of the OHTS subjects had central corneal thickness > 600 microm. Mean central corneal thickness for African American subjects (555.7 +/- 40.0 microm; n = 318) was 23 microm thinner than for white subjects (579.0 +/- 37.0 microm; P < 0.0001). Other factors associated with greater mean central corneal thickness were younger age, female gender, and diabetes. CONCLUSIONS: OHTS subjects have thicker corneas than the general population. African American subjects have thinner corneas than white subjects in the study. The effect of central corneal thickness may influence the accuracy of applanation tonometry in the diagnosis, screening, and management of patients with glaucoma and ocular hypertension.

Comparison of once- or twice-daily bimatoprost with twice-daily timolol in patients with elevated IOP : a 3-month clinical trial.

OBJECTIVE: To compare the safety, tolerability, and efficacy of bimatoprost 0.03% instilled once daily or twice daily with timolol 0.5% twice daily. DESIGN: Multicenter, 3-month, randomized, double-masked, interventional comparison trial. PARTICIPANTS: Patients diagnosed with ocular hypertension or glaucoma (n = 596). INTERVENTION: Patients received bimatoprost 0.03% ophthalmic solution once daily (8 PM, with vehicle control at 8 AM), bimatoprost 0.03% twice daily (8 AM; 8 PM), or timolol 0.5% twice daily (8 AM; 8 PM) in an uneven 2:2:1 randomization. Scheduled visits were at prestudy, baseline (day 0), weeks 2 and 6, and month 3. Intraocular pressure (IOP) was measured at 8 AM (predose), 10 AM, and 4 PM. MAIN OUTCOME MEASURES: The primary outcome measure was reduction in IOP in the eye with higher IOP at baseline. Secondary outcome measures included safety variables (adverse events, ophthalmoscopy, biomicroscopy, iris pigmentation, laser-flare meter, visual acuity, visual fields, heart rate, blood pressure, blood chemistry, hematology, and urinalysis). RESULTS: At month 3, the mean reduction in IOP from baseline at 8 AM was 9.16 mmHg (35.2%) with bimatoprost once daily, 7.78 mmHg (30.4%) with bimatoprost twice daily, and 6.74 mmHg (26.2%) with timolol twice daily. At all follow-up visits, mean IOP reductions were significantly greater in the bimatoprost once daily group than in the timolol group at each time point (8 AM, 10 AM, and 4 PM; P < 0.001). Twice-daily dosing of bimatoprost also provided significantly greater mean reductions in IOP than timolol at most time points but was not as effective as once-daily dosing. Bimatoprost was associated with significantly more hyperemia and eyelash growth than timolol, whereas timolol was associated with significantly more burning and stinging sensation in eyes. Overall, bimatoprost was well tolerated with few discontinuations because of adverse events. CONCLUSIONS: Bimatoprost 0.03% once daily was safe and statistically superior to timolol 0.5% twice daily in lowering IOP in patients with ocular hypertension or glaucoma. Bimatoprost given once daily consistently provided IOP reductions approximately 2 to 3 mmHg greater than those provided by timolol. Once-daily dosing of bimatoprost, 0.03%, demonstrated greater IOP-lowering effect and better ocular tolerability than twice-daily dosing.

Pigmentary dispersion syndrome induced by a posterior chamber phakic refractive lens.

PURPOSE: To report a case of bilateral pigmentary dispersion syndrome (PDS) induced by the implantation of posterior chamber phakic refractive lenses (PRLs). METHOD: Case report. RESULTS: Following bilateral implantation of posterior chamber phakic refractive lenses in 38-year-old woman, unilateral elevated intraocular pressure (IOP) developed within months that was attributable to pigment dispersion within the anterior chamber. Findings consistent with PDS included bilateral transillumination defects of the iris in areas contacting the anterior surface of the PRLs, pigment deposits on the anterior surface of the PRLs, Krukenberg spindles, and bilateral dense pigmentation of the trabecular meshwork. The patient's IOP is presently under control and she has not developed glaucomatous damage. CONCLUSIONS: The development of PDS in this case demonstrates that posterior chamber phakic refractive lenses can make contact with the posterior iris and induce pigment dispersion syndrome in susceptible patients.

How does the trabecular meshwork regulate outflow? Clues from the vascular endothelium.

Although it is well known that the trabecular meshwork plays a central role in regulating the outflow of aqueous humor from the eye, the cellular mechanisms and events responsible for this function are poorly understood. In contrast, the mechanisms by which vascular endothelial cells modulate the permeability of blood vessels have been more thoroughly investigated. It is hypothesized that the cells of the TM employ mechanisms similar to those observed in the vascular endothelium to modulate aqueous humor permeability. Specifically, it is hypothesized that the cells of the TM employ Na-K-Cl cotransport to modulate their intracellular volume and thus the volume of the paracellular pathways through which aqueous humor may travel. The current knowledge about the role of Na-K-Cl cotransport and volume regulation in the regulation of vascular permeability, and evidence that similar physiologic events occur in the TM are reviewed. In addition, the implications for further study of aqueous humor outflow physiology are discussed.

Effects of Na-K-2Cl cotransport regulators on outflow facility in calf and human eyes in vitro.

PURPOSE: Cultured human trabecular meshwork (TM) cells possess substantial Na-K-Cl activity, which is involved in the regulation of TM cell volume. The hypothesis in the present study was that drugs that affect the cotransporter might alter aqueous humor outflow facility (C) in the intact eye. The effects of agents and conditions known to modulate Na-K-CI cotransport activity and/or TM cell volume on C in perfused anterior segments were investigated. METHODS: Human and calf eyes were dissected and perfused, and C was determined according to standard published methods. Perfusates with modified osmolarity were used to cause alterations in TM cell volume. Cl-free perfusate and/or bumetanide (10(-5) M) was used to inhibit Na-K-Cl cotransport activity, and vasopressin (10(-7) M, 10(-8) M) was used to stimulate cotransport activity. RESULTS: In human eyes, hypo-osmotic perfusate decreased C 12%, whereas hyper-osmotic perfusate increased C 44%. These changes lasted approximately 30 minutes, after which C began to normalize. Inhibition of Na-K-Cl cotransport using Cl-free medium or bumetanide resulted in facility increases of 27% and 22%, respectively. There was an additive increase in C with bumetanide plus Cl-free media. Stimulating Na-K-Cl cotransport with 10(-8)M and 10(-7)M vasopressin resulted in 28% and 35% decreases in C, respectively. The results were similar in calf eyes: Cl-free medium or bumetanide resulted in 41% and 52% increases in C, whereas 10(-8) M and 10(-7) M vasopressin resulted in 14% and 19% decreases in C, respectively. CONCLUSIONS: Modulation of Na-K-Cl cotransport results in changes in C that may be mediated in part by cell volume changes.

Na-K-Cl cotransport in normal and glaucomatous human trabecular meshwork cells.

PURPOSE: Previous results from this laboratory showed that intracellular volume of trabecular meshwork (TM) cells is regulated by the Na-K-Cl cotransport system. Other studies suggest that TM cell volume, in turn, is a determinant of permeability across the TM. Given that a decrease in outflow facility across the TM is thought to be the primary cause of elevated intraocular pressure in primary open-angle glaucoma, the present study was conducted to investigate the possibility that Na-K-Cl cotransport function may be altered in glaucomatous TM cells compared with normal TM cells. METHODS: Normal and glaucomatous human TM cells were cultured from donor eyes and trabeculectomy specimens, respectively. Trabecular meshwork cell monolayers were evaluated for Na-K-Cl cotransport activity, assessed as ouabain-insensitive, bumetanide-sensitive K influx using 86Rb as a tracer for K. Cotransporter protein expression was determined by western blot analysis, and intracellular volume was determined radioisotopically using [14C]urea and [14C]sucrose as markers of total and extracellular water space, respectively. RESULTS: Na-K-Cl cotransport activity of glaucomatous TM cells was found to be reduced by 32% +/- 2% compared with that of normal TM cells, whereas western blot analyses showed that cotransporter protein expression in glaucomatous TM cells was reduced by 64% +/- 14% compared with expression in normal TM cells. Also, exposure of normal TM cells to 10 microM norepinephrine or 50 microM 8-bromo-3',5'-cyclic adenosine monophosphate was found to diminish Na-K-Cl cotransport activity, whereas these agents were without effect on glaucomatous TM cell cotransport. Finally, resting cell volume of glaucomatous TM cells was found to be increased compared with that of normal TM cells, whereas intracellular volume of both cell types was reduced after exposure to 10 microM benzmetanide or 10 microM bumetanide. CONCLUSIONS: These findings indicate that Na-K-Cl cotransport function and regulation are altered in glaucomatous TM cells compared with that of normal TM cells. However, the observation that cell volume of glaucomatous TM cells is greater than that of normal TM cells, despite reduced Na-K-Cl cotransport activity, suggests that other volume-regulatory ion flux pathways may be involved in the reduced outflow of glaucoma.

Effects of dexamethasone on sodium-potassium-chloride cotransport in trabecular meshwork cells.

PURPOSE: Previous studies in the authors' laboratory have shown that bovine and human trabecular meshwork (TM) cells possess a robust sodium-potassium-chloride (Na-K-Cl) cotransport system that functions in regulating intracellular volume and may play a central role in modulating outflow facility across the TM. Dexamethasone, which can induce ocular hypertension, has been found to increase resistance to aqueous outflow across the TM. The current study was conducted to investigate the hypothesis that alteration of TM cell Na-K-Cl cotransport function, regulation, or both may be an underlying factor in steroid-induced glaucoma. To this end, the authors evaluated the effects of dexamethasone treatment of TM cells on Na-K-Cl cotransport activity and cotransporter protein expression. METHODS: Cultured bovine and human TM cell monolayers were exposed to dexamethasone (10(-9) to 10(-6) M) for varying times, then evaluated for Na-K-Cl cotransport activity or harvested for cellular membrane proteins. Cotransport activity was assessed as bumetanide-sensitive K influx. Cotransport protein expression was evaluated by Western blot analysis of cellular proteins using a monoclonal antibody to the human colonic T84 epithelial cell Na-K-Cl cotransporter. RESULTS: The authors found that 24- and 48-hour exposures of human and bovine TM cells to dexamethasone stimulates Na-K-Cl cotransport activity (10(-8) to 10(-6) M dexamethasone in human cells; 10(-8) and 10(-7) M in bovine cells). The authors also found that dexamethasone (10(-8) M) stimulates Na-K-Cl cotransport activity of TM cells with exposure times as early as 12 hours and up to 5 days. In addition, the authors found that the level of Na-K-Cl cotransport protein expressed in TM cells is modulated by dexamethasone. When bovine or human TM cells are exposed to 10(-8) or 10(-6) M dexamethasone for 2 to 5 days, cotransporter protein expression is increased. With longer exposures, however, cotransporter protein levels decrease below control levels. Finally, the authors found that TM cells exposed to dexamethasone become unresponsive to regulation by hypertonicity and vasopressin. CONCLUSIONS: The authors' findings suggest that dexamethasone may be exerting its effect, at least in part, through altering Na-K-Cl cotransport function and regulation in TM cells.

Group dynamics in forensic pretrial decision-making.

This study examines how forensic evaluators' opinions that pertain to diagnosis, competency to stand trial, and criminal responsibility (Maryland's version of the not guilty by reason of insanity plea) are rendered at a state forensic hospital for defendants pleading not criminally responsible. Pretrial evaluations completed independently by a psychiatrist, a psychologist, and a social worker were presented at a forensic staff conference where psychiatrist and psychologists openly "voted" on diagnosis, competency to stand trial, and criminal responsibility. These results were then sent to the court. The purpose of this study was to assess the clinicians' level of agreement and the role that conformity played in the decision-making process. A sample of twenty court-ordered pretrial evaluations of defendants examined at the hospital between March and June 1991, with evaluators' opinions generated by a secret ballot, were compared with a matched control group from an earlier time, when opinions were generated by open ballot. The study was designed to compare the opinions of forensic evaluators in the issues of diagnosis, competency to stand trial, and criminal responsibility between the two samples. The defendants in the experimental group and the control group were matched on the basis of age, race, sex, and offense. It was hypothesized that with secret ballot voting there would be a greater disparity of agreement regarding diagnosis, competency to stand trial, and criminal responsibility opinions compared with the open method of voting. However, the results of this study did not support that hypothesis. There was little disparity on forensic opinions rated either by secret or open voting.

Clinical experience with the Baerveldt glaucoma drainage implant.

PURPOSE: To assess clinical outcomes in patients who were treated with the Baerveldt glaucoma drainage implant. METHODS: The authors performed a retrospective multicenter study of 100 patients (103 eyes) with medically uncontrollable glaucomas who underwent a one-stage implantation with either the 200-, 250-, 350-, or 500-mm2 Baerveldt implant. The authors defined surgical success as 5 mmHg less than intraocular pressure less than 22 mmHg without additional glaucoma surgery and without loss of light perception. RESULTS: With a mean follow-up of 13.6 +/- 0.9 months (range, 4-37 months), 74 eyes (71.8%) had successful outcomes. Cumulative life-table success rates were 90.3% at 3 months (n = 103), 72.6% at 6 months (n = 84), and 60.3% at 24 months (n = 34). Intraocular pressure (IOP) was reduced from a mean of 38.5 +/- 1.4 mmHg with 2.2 +/- 0.1 antiglaucoma medications to 15.1 +/- 0.8 mmHg (P < 0.0005) with 0.5 +/- 0.1 antiglaucoma medications (P < 0.0005). Visual acuity was improved or remained within one line of the preoperative visual acuity in 90 eyes (87.4%). Complications occurred in 74 eyes (71.8%). A significant portion of these complications (45%) was transient, resolving without any intervention. Only 8% were serious sight-threatening complications. The most common complications included shallow anterior chamber or hypotony (32%), choroidal effusion or hemorrhage (20.4%), corneal decompensation or edema (17.5%), hyphema (14.1%), and tube obstruction (12.6%). CONCLUSION: The Baerveldt implant is effective in lowering the IOP in patients with intractable glaucomas. Hypotony and other complications are common, which also have been reported in other nonvalved glaucoma drainage implants. However, the majority of these complications did not affect surgical outcome.

Na-K-Cl cotransport regulates intracellular volume and monolayer permeability of trabecular meshwork cells.

The trabecular meshwork (TM) of the eye plays a critical role in modulating intraocular pressure (IOP) through regulation of aqueous humor outflow, although the underlying mechanisms remain unknown. Ethacrynic acid, an agent known to inhibit Na-K-Cl cotransport of a number of cell types, recently has been reported to increase aqueous outflow and lower IOP through an unknown effect on the TM. In vascular endothelial cells and a variety of other cell types, the Na-K-Cl cotransporter functions to regulate intracellular volume. The present study was conducted to evaluate TM cells for the presence of Na-K-Cl cotransport activity and to test the hypothesis that modulation of cotransport activity alters intracellular volume and, consequently, permeability of the TM. We demonstrate here that bovine and human TM cells exhibit robust Na-K-Cl cotransport activity that is inhibited by bumetanide and by ethacrynic acid. Our studies also show that TM cell Na-K-Cl cotransport is modulated by a variety of hormones and neurotransmitters. Inhibition of the cotransporter either by bumetanide, ethacrynic acid, or inhibitory hormones reduces TM intracellular volume, whereas stimulatory hormones increase cell volume. In addition, shrinkage of the cells by hypertonic media stimulates cotransport activity and initiates a subsequent regulatory volume increase. Permeability of TM cell monolayers, assessed as transmonolayer flux of [14C]sucrose, is increased by hypertonicity-induced cell shrinkage and by bumetanide. These findings suggest that Na-K-Cl cotransport of TM cells is of central importance to regulation of intracellular volume and TM permeability. Defects of Na-K-Cl cotransport may underlie the pathophysiology of glaucoma.

Short-wavelength automated perimetry in low-, medium-, and high-risk ocular hypertensive eyes. Initial baseline results.

OBJECTIVE: To examine the relationship between the prevalence of short-wavelength sensitivity losses in the central 30 degrees visual field and risk factors for development of glaucomatous visual field loss in ocular hypertension. DESIGN: A modified Humphrey Field Analyzer was used to perform standard automated perimetry and short-wavelength automated perimetry (SWAP), which is a technique that isolates the activity of short-wavelength-sensitive ("blue") mechanisms. In addition, an assessment of the risk of developing glaucomatous visual field loss was determined, based on a validated model that utilized intraocular pressure, a family history of glaucoma, age, and the vertical cup-to-disc ratio. PATIENTS: Both eyes of 232 ocular hypertensive patients were examined and compared with results from an age-matched control group of normal subjects. Both ocular hypertensive patients and normal subjects had to have normal visual fields on standard automated perimetry, good visual acuity, and no evidence of other ocular or neurologic disease or surgery. Intraocular pressure in the ocular hypertensive patients was 21 mm Hg or greater OU (without medication), and it was less than 20 mm Hg OU in normal control subjects. RESULTS: Less than 10% of the low-risk ocular hypertensive eyes had a SWAP deficit, as compared with 20% of the moderate-risk and 33% of the high-risk ocular hypertensive eyes. Intraocular pressure and a family history of glaucoma showed no meaningful relationship with the prevalence of SWAP deficits, but both age and the vertical cup-to-disc ratio demonstrated a strong association with the SWAP abnormalities. CONCLUSIONS: The SWAP results that were found in the ocular hypertensive eyes were associated with other risk factors that have been reported to be predictive of the development of glaucomatous visual field loss, especially the vertical cup-to-disc ratio and age. These findings support the notion that the SWAP deficits represent early glaucomatous damage and may be related to early changes that occur at the optic nerve head.

Patch grafts of dehydrated cadaveric dura mater for tube-shunt glaucoma surgery.

Human donor sclera is commonly used in glaucoma surgery with a tube-shunt (eg, Molteno, Baerveldt, Shocket, Krupin-Denver) to cover the external portion of the silicone tube and prevent its erosion through the overlying conjunctiva. Common problems with this technique include immune-mediated melting of the graft and the potential for infectious disease transmission by the grafted material. A case is presented of a patient in whom a low-grade iridocyclitis was associated with the gradual melting of a scleral patch graft; the scleral patch was then replaced with commercially available, dehydrated human dura mater. The practical and theoretical advantages of cadaveric human dura mater in tube-shunt glaucoma surgery are discussed.

Blue-on-yellow perimetry can predict the development of glaucomatous visual field loss.

OBJECTIVE: The purpose of this investigation was to determine whether blue-on-yellow (B/Y) perimetry is capable of predicting the onset and location of impending glaucomatous visual field loss in patients with ocular hypertension. DESIGN: A Humphrey Field Analyzer (Humphrey Instruments, San Leandro, Calif) was modified to perform B/Y perimetry to isolate and measure the sensitivity of short-wavelength-sensitive mechanisms. Participants were tested annually with standard white-on-white (W/W) and B/Y automated perimetry for a period of 5 years. PATIENTS: The study population consisted of 38 patients with ocular hypertension and 62 age-matched normal control subjects. RESULTS: Initially, all 76 ocular hypertensive eyes had normal W/W automated perimetry results, with 67 eyes having normal and nine eyes having abnormal B/Y test results. Five years later, five of the nine ocular hypertensive eyes with initial B/Y abnormal results developed glaucomatous visual field loss measured by standard W/W automated perimetry, while none of the 67 ocular hypertensive eyes with initially normal B/Y results developed abnormal W/W perimetry results. CONCLUSIONS: Blue-on-yellow perimetry deficits are an early indicator of glaucomatous damage and are predictive of impending glaucomatous visual field loss for standard W/W automated perimetry. To our knowledge, this is the first prospective, long-term longitudinal study that demonstrates the ability to predict the onset of glaucomatous visual field loss in patients with ocular hypertension on the basis of psychophysical testing.

Progression of early glaucomatous visual field loss as detected by blue-on-yellow and standard white-on-white automated perimetry.

OBJECTIVE: To determine whether blue-on-yellow perimetry reveals progression of glaucomatous damage before it is evident with standard white-on-white perimetry. DESIGN: A Humphrey field analyzer (Humphrey Instruments, San Leandro, Calif) was modified to perform blue-on-yellow perimetry to isolate and measure the sensitivity of short wavelength-sensitive mechanisms. Participants were tested annually with standard white-on-white automated perimetry and blue-on-yellow automated perimetry for 5 years. PATIENTS: Sixteen patients with early glaucomatous visual field loss in one or both eyes and 62 age-matched normal control subjects. RESULTS: At baseline, 25 (78.1%) of the 32 eyes exhibited larger deficits with blue-on-yellow perimetry, five (15.6%) had equivalent loss with both tests, and two (6.3%) had larger deficits with standard white-on-white perimetry. Seven (21.9%) of the 32 eyes demonstrated evidence of progressive visual field loss with standard white-on-white perimetry in 5 years, while the other 25 eyes (78.1%) were relatively stable. Deficits with blue-on-yellow perimetry were twice as large as deficits with white-on-white perimetry in the stable group and were three to four times as large in the group with progressive field loss. CONCLUSIONS: Blue-on-yellow perimetry is effective in predicting which patients with early glaucomatous visual field loss are most likely to have progressive loss. The rate of progressive loss is greater with blue-on-yellow perimetry than with standard white-on-white perimetry.

The unraveling of a joint venture.

An orthopedic group that recently moved to a new location needed to boost its image. In an effort to gain control of the market, and increase its referral base, the group tried to turn several local health clubs into sports medicine clinics. This case study details the time, money, efforts and, finally, the lessons learned from this unsuccessful venture.

The effect of trabeculectomy on corneal topography.

Trabeculectomy is increasingly being performed earlier in the treatment of primary open-angle glaucoma (POAG). Surgically-induced alterations in corneal curvature resulting from filtering surgery may have a significant impact on patients, especially younger ones, whose vision may already be compromised by visual-field loss. Using data obtained by computer-assisted topographic analysis performed preoperatively and at 12 weeks postoperatively, we longitudinally studied the corneal surface changes induced by primary trabeculectomy in eight eyes undergoing surgery for POAG or normal-tension glaucoma. Additional data collected included refraction, keratometry, axial length, intraocular pressure, and pachometry. Five of eight eyes developed 1.50 to 2.50 diopters of steepening in the 90-degree meridian. One patient developed flattening in the 180-degree meridian without vertical steepening. Two patients had little change in the central optical zone. Of the six eyes with induced with-the-rule astigmatism, keratometry was less sensitive than topographic analysis in detecting the changes induced by trabeculectomy. Our data indicate that changes in corneal curvature are induced by filtering surgery, but may be undetectable without topographic analysis.

Ophthalmology's botanical heritage.

Many of today's important ophthalmic pharmaceuticals have a rich ethnobotanical history. Solanaceous plants, the source of atropine, have contributed to medical therapy since the beginning of Western civilization. The botanical source of physostigmine played a pivotal role as an ordeal poison in the culture of Old Calabar, West Africa. Native peoples of Amazonia treasured plants containing pilocarpine as panaceas because of their impressive diaphoretic effect. Nineteenth century scientists examining these plants because of their folkloric reputations discovered their active compounds and documented their physiological effects. Ophthalmologists such as Argyll Robertson, Laqueur, and Weber built upon this research to bring these pharmaceuticals into therapeutic use. The ongoing loss of the world's tropical rain forests threatens to destroy a vast storehouse of untested biological compounds.