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This autobiographical narrative describes many of the activities of the Department of Ophthalmology at New York University Medical Center that took place under the stewardship of Goodwin M. Breinin, who was chairman from 1958 to 2000. The author recalls his 40 years of collaborative research during this period, exploring the visual system with many faculty members at New York University and participating in departmentally sponsored studies elsewhere.

A large population of ametropic scuba divers wear contact lenses. We discuss optics and corneal physiology, as well as the types of contact lenses that are appropriate for underwater activities.We reviewed an extensive body of literature to formulate guidelines to aid the contact lens fitter in satisfying individual sport diver's needs.Optical factors such as image displacement and light wave-length shifts require that contact lenses for underwater use be suitably modified. Underwater images appear nearer and larger (requiring greater accommodation) and are made up almost exclusively of the short wavelength end of the spectrum. Correction of presbyopia, in particular, is influenced by these factors. For example, presbyopic contact lens-corrected myopes require greater near adds underwater than when viewing the same objects in air. In general, presbyopes should consider monovision correction to facilitate underwater visual tasks. Although divers wearing rigid gas permeable contact lenses run the risk of more corneal problems than soft lens wearers if conservative ascents are not adhered to, there are no compelling reasons to change lens types in patients who are already fully adapted. Soft contacts, while very stable on the eye during diving, present a greater risk of lens contamination by sea or fresh water exposure. However, the latter problems are easily overcome by using disposable soft lenses.In this paper, we present several suggestions for lens material, modifications required for underwater ametropia correction, and wearing modalities for the sport divers. An understanding of the dramatic changes that impact the properties of light, corneal physiology, and visual perception which accompany the diver below the surface will enable the contact lens fitter to design a lens appropriate to the needs of the individual patient.

The introduction of a system of classification of color-coded computerized topography has proved of great clinical value but may be misinterpreted by some who assume that the color plots represent actual corneal contour.A three-dimensional system of contour modeling is used to plot equivalents of each category of corneal shape. The round, oval, symmetric bowtie, and asymmetric bowtie of the widely used classification schema are each translated into contour equivalents. Digital subtraction of an appropriate sphere from the contour data is central to the transformation.While round- and oval-type color-coded refractive power plots translate into fairly intuitive contour images, symmetric and asymmetric bowties produce surprising results. We demonstrated that the bowtie appearance is a result of the changing curvatures present between the two principal meridia of the toroidal surface.The shape characteristics of the corneal surface dictate the familiar color-coded dioptric plots.

A young woman presented with recurrent dorsal subluxation of the fifth metatarsal-cuboid joint secondary to trauma. The injury was treated by metatarsal-cuboid fusion without functional residual disability.

Computer-assisted videokeratography holds great promise for the contact lens fitter as well as the refractive surgeon. However, conventional methods of corneal mapping, which present color-coded representations of corneal refractive power, do not provide information about corneal surface contour. We introduce a three-dimensional isomorphic corneal modeling technique that produces a freely rotatable wire-frame image that is infinitely rescalable and open to manipulation such as digital subtraction. As an illustration of this technique, we provide isomorphic representations of corneas with astigmatism induced by large pterygia.

Newer methods of refractive surgery produce their effect by reshaping the corneal surface. It follows that topographic representations, used primarily to map refractive power, should now emphasize morphology and contour features.We introduce a procedure using commercially available instrumentation which provides isomorphic three-dimensional corneal topography. The representations may be displayed either as refractive power, as is conventionally done, or as the more surgically relevant contour configuration. These images contain data points that are continuous rather than stepped as in the familiar color-coded displays.The technique proved easy to execute requiring no special software or mainframe computing. The corneal displays generated were freely rotatable and rescalable.In addition to producing clear and intuitive three-dimensional representations, the digital graphics environment allows manipulation unavailable in the conventional color-coded format; such representations should be particularly valuable for pre- and postoperative evaluation.

Ingestion of the rat poison N-3-pyridylmethyl-N'-p-nitrophenylurea (PNU) produced ocular toxicity in three humans and in an animal model, the Dutch Belted rabbit. The electroretinogram b wave was especially susceptible to the effects of the rodenticide, and the target tissue appeared to be the retinal pigment epithelium. Injection of PNU itself did not produce ocular toxicity. The poison had to be administered orally. Gentamicin administered orally with PNU prevented the ocular toxicity. Presumably this antibiotic killed those gastrointestinal bacteria responsible for PNU's metabolism into an ocular toxin. L-tryptophan, a known antidote for the lethal effects of PNU, was an antidote for the ocular toxicity when administered orally but not when administered parenterally.

Fundus reflectometry of the cat retina showed that under certain circumstances a rapid increase in density may follow intense bleaching exposures. The spectral characteristics of the density changes indicated that neither rhodopsin nor its bleach products could be responsible for this effect. The poor condition of the animals in which the phenomenon was observed and its conspicuous absence in the majority of the experimental runs suggested that the effect was associated with a process other than the resynthesis of rhodopsin. It was shown that an extrareceptoral event, spreading depression (SD) of the retina, is the most likely source of the rapid spectral change. The well-known tissue alterations associated with SD were induced in the retina independently of pigment density change. The resultant difference spectra resembled those produced when the rapid density increase occurred spontaneously. It seems likely that the abnormal physiological condition of those cats in which the phenomenon is more frequently observed primes the retina for the light-induced generation of spreading depression.

In a survey of 546 rhesus monkeys of various ages, 6.1% of the animals showed ophthalmoscopically visible hypopigmented spots in their maculas. There was a statistically significant correlation between the age of the animal and the degree of hypopigmentation. Electroretinographic responses and visually evoked potentials were evaluated in a selected group of monkeys with and without hypopigmented macular spots. No significant change in retinal function as a result of the macular abnormalities could be detected.

The bleaching of rhodopsin by short-duration flashes of a xenon discharge lamp was studied in vivo in the cat retina with the aid of a rapid, spectral-scan fundus reflectometer. Difference spectra recorded over a broad range of intensities showed that the bleaching efficacy of high-intensity flashes was less than that of longer duration, steady lights delivering the same amount of energy. Both the empirical results and those derived from a theoretical analysis of flash photolysis indicate that, under the conditions of these experiments, the upper limit of the flash bleaching of rhodopsin in cat is approximately 90%. Although the fact that a full bleach could not be attained is attributable to photoreversal, i.e., the photic regeneration of rhodopsin from its light-sensitive intermediates, the 90% limit is considerably higher than the 50% (or lower) value obtained under other experimental circumstances. Thus, it appears that the duration (approximately 1 ms) and spectral composition of the flash, coupled with the kinetic parameters of the thermal and photic reactions in the cat retina, reduce the light-induced regeneration of rhodopsin to approximately 10%.

The bleaching and regeneration of rhodopsin in the living cat retina was studied by means of fundus reflectometry. Bleaching was effected by continuous light exposures of 1 min or 20 min, and the changes in retinal absorbance were measured at 29 wavelengths. For all of the conditions studied (fractional bleaches of from 65 to 100%), the regeneration of rhodopsin to its prebleach levels required greater than 60 min in darkness. After the 1-min exposures, the difference spectra recorded during the first 10 min of dark adaptation were dominated by photoproduct absorption, and rhodopsin regeneration kinetics were obscured by these intermediate processes. Extending the bleaching duration to 20 min gave the products of photolysis an opportunity to dissipate, and it was possible to follow the regenerative process over its full time-course. It was not possible, however, to fit these data with the simple exponential function predicted by first-order reaction kinetics. Other possible mechanisms were considered and are presented in the text. Nevertheless, the kinetics of regeneration compared favorably with the temporal changes in log sensitivity determined electrophysiologically by other investigators. Based on the bleaching curve for cat rhodopsin, the photosensitivity was determined and found to approximate closely the value obtained for human rhodopsin; i.e., the energy Ec required to bleach 1-e-1 of the available rhodopsin was 7.09 log scotopic troland-seconds (corrected for the optics of the cat eye), as compared with approximately 7.0 in man.

Various noninvasive test procedures were used to evaluate retinal function in a patient who had become night blind following vincristine chemotherapy. The results obtained were strikingly similar to those reported previously in subjects with recessively inherited stationary night blindness; the dark-adaptation curve was monophasic (ie, no evidence of a scotopic branch), rhodopsin kinetics were entirely normal, and spectral threshold data revealed the presence of residual rod-mediated vision. Also like the heritable condition, the b-wave of the ERG was depressed grossly despite normal a-wave potentials. These findings, and the fact that vincristine is known to disrupt the structural integrity of neuronal microtubules, suggest that the drug-induced defect involves the process of synaptic transmission between the photoreceptors and their second-order neurons.

It is possible to record a pattern electroretinogram (PERG) of near normal amplitude in a situation when the eye containing the active electrode is occluded. Because PERG recording requires high amplification and sensitive signal retrieval techniques, the electrode in the occluded eye records a distant potential from the unoccluded eye. Referencing the active electrode to an ipsilateral ear diminishes, but does not eliminate the referred PERG potential. Such unlooked for interaction may provide misleading data in situations where binocular viewing is used because of poor vision in one eye; therefore, occlusion of the eye not being tested should be undertaken whenever possible.

A psychophysical procedure, the probe-flash paradigm, was used to test explanations of early foveal sensitivity loss in retinitis pigmentosa. The findings suggest that this loss may be due to a decreased responsiveness of retinal elements and not to a decrease in quantum catching ability of functioning photoreceptors.

A gold foil ERG electrode is described. The device is inexpensive and simple to fabricate. Since it is hooked over the lower lid and makes minimal touch contact with the inferior limbal area, it can be used in circumstances which require prolonged testing of retinal function or in eyes with corneal pathology. Because the optics of the eye are not compromised, it is possible, with the use of appropriate stimuli and response-averaging techniques, to record local EFGs from relatively small retinal areas.

Treatment in muscular dystrophy should be prospective and aimed at maintaining maximal function so that the patient can be as independent as possible for as long as possible. DMD must be diagnosed early, not only to enable genetic counseling concerning future pregnancy and screening of female siblings, but also to stage physical therapy to delay muscle contracture. Surgery, when indicated, should anticipate realistic functional goals (standing, walking, transfer), and enable immediate postoperative mobilization. Bracing should be suitably provided and orthoses appropriately constructed to assure maximal support with minimal weight. Spinal deformity must be prevented when feasible and appropriately treated when present. Maximal function in wheelchair-confined patients can be enhanced through the use of an apparatus that encourages proper sitting posture and utilizes residual strength. Complications must be anticipated and vigorously treated. Attention should be paid to the psychic as well as the somatic aspects of this disease. Optimal treatment of the patient with DMD should be multidisciplinary, aggressive, and conducted in an atmosphere of intelligent concern. This approach minimizes the frustrating aspects of DMD while it maximizes the benefits obtained through available care. In this manner, the quality of life for the patient with muscular dystrophy can be significantly enhanced and his life expectancy extended.

The optimal management of muscular dystrophy is multidisciplinary and aggressive in nature. Serial assessment aids in determining the functional stage of the disease and in indicating specific therapies. Physical therapy can augment strength through exercise and relieve contracture through passive stretching. Occupational therapy is employed to help the patient manage his activities of daily living within the restrictions imposed on him by his disease. Progressive disability can be delayed through a variety of physiatric and orthopedic techniques, including surgical release of lower-extremity contracture, repair of foot and ankle deformity, and correction of scoliosis. Appropriate orthoses are available, as are a variety of special devices to facilitate ongoing care for postambulatory patients. Physicians treating the muscular dystrophies should be aware of the complications of these diseases, particularly cardiomyopathy, pulmonary failure, and psychological and social problems.

Phosphorus-31 magnetic resonance (MR) spectra of leg muscles in patients with the neuromuscular diseases Duchenne dystrophy, myotonic dystrophy, postpoliomyelitis, Werdnig-Hoffmann disease, and pedal dystonia were recorded. Ratios of beta-adenosine triphosphate (ATP), inorganic phosphate (Pi), alpha-glycerophosphorylcholine (GPC), and phosphomonoesters to phosphocreatine (PCr) were calculated from peak integrals and compared with normal muscle ratios. In all diseases studied, beta-ATP/PCr and Pi/PCr values showed an increase from normal values. The extent of increase in beta-ATP/PCr was related to the clinical severity of the disease, suggesting that this could be a useful noninvasive means of monitoring effectiveness of therapy for neuromuscular disorders. In myotonic dystrophy and Werdnig-Hoffmann disease, GPC/PCr values increased greatly. The intracellular pH in Duchenne and postpoliomyelitis muscles was slightly elevated compared with that in normal muscles. Hydrogen-1 MR images of muscles showed fat infiltration in all patients, more in weaker muscles and less in stronger muscles.

Correction of deformity and maintenance of the upright posture have increased self-reliant skills, thus significantly enhancing the quality of life for the child with muscular dystrophy. In addition, such techniques offer a method of prolonging independent ambulation and, in so doing, forestall confinement to a wheelchair or bed with its inevitable downhill course. Surgery and bracing, accurately indicated and properly timed, play an important role in the total rehabilitation of the patient with muscular dystrophy.

1H MR spectra were recorded from human gastrocnemius muscle at 63.86 MHz using the body coil of the Signa scanner as transmitter and a 3-in. surface coil as receiver. The fat content of the muscle was quantified relative to that of water in a selected volume or slice. The fat/water ratio was 0.05-0.07 for normal muscle but increased to 0.5-6.0 in primary and secondary muscular disorders such as Duchenne and myotonic dystrophy, Charcot-Marie-Tooth and polio muscular atrophy, cerebral palsy, and spina bifida. In Werdnig-Hoffmann spinal atrophy the ratio was above 10. Water-suppressed and slice-selective 1H spectroscopy was used for qualitative analysis of fat. The 1H profile of gastrocnemius muscles between healthy individuals and patients with neuromuscular diseases showed two major differences. In the normal muscle spectra, the resonance from the -(CH2)n- protons at 1.6 ppm was the most pronounced, whereas in the diseased muscle spectra resonances also appeared between 1.1 and 1.4 ppm. Some diseased muscle spectra showed multiple resonances from -CH = CH- in polyunsaturated fatty acids between 5.5 and 7.0 ppm. The corresponding resonances from = CH-CH2-, 1.9-2.0 ppm, and = CH-CH2-CH =, 2.7-2.9 ppm, were also seen. These peaks are usually not detected in normal muscle.

A stimulus consisting of 96 red LEDs mounted in the rear of a ganzfeld bowl was used to elicit focal electroretinograms (FERG) from the central 9 degrees of the retina in human subjects. The luminance of the stimulus was driven sinusoidally at frequencies from 10-60 Hz. The temporal responsiveness and response phase lags of normal subjects and patients with retinal disease were measured. Normal subjects produced maximum amplitude FERG responses to stimuli between 30-40 Hz. Patients with retinitis pigmentosa showed a low-pass pattern of amplitude loss, with an additional frequency independent loss in sensitivity in those with poorer visual acuity. Patients with macular degeneration showed general amplitude loss associated with a relative sparing of the mid-temporal frequencies. The response phase lags in both patient groups were not significantly different from the normals. These findings point to a loss in temporal responsiveness accompanied by a secondary loss of sensitivity in these heredoretinal degenerations.