Wavefront aberrations following laser in situ keratomileusis and refractive lens exchange for hypermetropia

PURPOSE: To compare the magnitude of aberrations in eyes after elective hypermetropic laser in situ keratomileusis (LASIK) and refractive lens exchange (clear lens replacement). METHODS: Forty-nine patients (92 eyes) had hypermetropic LASIK and 28 (48 eyes) had refractive lens exchange; 23 hypermetropic subjects (41 eyes) were the control group. LASIK was performed with the Nidek EC-5000 excimer laser; ablation zones 5.5 to 6.0-mm in diameter with transition zones 7.5 to 8-mm in diameter. For refractive lens exchange, all but four IOLs were made of foldable acrylic. Aberrations and corneal topography were measured with the Nidek OPD-Scan model ARK-10000 more than 12 months after surgery. The higher-order root-mean-square (HORMS) wave aberrations for combined third to sixth Zernike aberration orders and the Zernike spherical aberration coefficient C(0)(4) at both 4.2-mm and 6.0-mm pupil sizes were calculated. RESULTS: For the LASIK group, surgical refractive change correlated significantly with total, corneal, and internal HORMS and spherical aberrations (except with internal spherical aberration for a 4.2-mm diameter pupil). For the refractive lens exchange group, there were no significant correlations of surgical refractive change with any of these factors. Similarly, there were no significant correlations of refraction with any of these factors for the control group. For a 3-diopter change in refraction with 6-mm pupils, LASIK doubled the total HORMS aberrations. LASIK changed the sign of spherical aberration from positive to negative by increasing the negative asphericity of the anterior cornea. Taking age differences between groups into account, refractive lens exchange increased the total HORMS aberrations by 40% compared with that of the control group, but this was not statistically significant. However, refractive lens exchange significantly increased total spherical aberration. CONCLUSION: Refractive lens exchange was a better refractive procedure than LASIK for minimizing total higher order optical aberrations that accompany hypermetropic refractive surgery.     

Relationship between neuropsychological test performance and productivity at 1-year following traumatic brain injury

While there has been strong evidence for the ability of neuropsychological performance at resolution of posttraumatic amnesia to predict later productivity, there has been less conclusive evidence for the relationship of neuropsychological test scores to concurrent productivity status. The purpose of the current study was to evaluate the relationship of neuropsychological test performance at 1 year post-injury to productivity assessed at the same time point. Participants were 518 persons with medically documented TBI who were enrolled in the TBI Model Systems Research and Demonstration Project. Stepwise logistic regression was utilized to determine the contributions of neuropsychological test scores to productivity after accounting for demographic characteristics, injury severity, and pre-injury productivity. Missing neuropsychological test scores were accounted for in the model. Variables that remained in the model and accounted for a significant proportion of the variance included age, duration of impaired consciousness, pre-injury productivity, and scores on measures of GOAT, Logical Memory II, and Trail Making Test, part B. The results indicate that neuropsychological test performance provides important information regarding the ability of persons with injury to return to productive activities. The results also indicate that inability to complete neuropsychological tests at 1 year post-injury is associated with non-productive activity.     

Evidence for interactions between intracellular calcium stores during methylmercury-induced intracellular calcium dysregulation in rat cerebellar granule neurons

Acute exposure to methylmercury (MeHg) causes severe disruption of intracellular Ca(2+) ([Ca(2+)](i)) regulation, which apparently contributes to neuronal death. Activation of the mitochondrial permeability transition pore (MTP) evidently contributes to this effect. We examined in more detail the contribution of mitochondrial Ca(2+) ([Ca(2+)](m)) to elevations of [Ca(2+)](i) caused by acute exposure to a low concentration of MeHg in primary cultures of rat cerebellar granule neurons. In particular, we sought to determine whether interactions occurred between Ca(2+)(i) pools in response to MeHg. Prior depletion of Ca(2+)(m) using carbonyl cyanide m-chlorophenylhydrazone (CCCP) and oligomycin significantly decreased the amplitude of [Ca(2+)](i) release from intracellular stores, and delayed the onset of whole-cell [Ca(2+)](i) elevations, caused by 0.5 microM MeHg. CCCP alone hastened the MeHg-induced release of Ca(2+) within the cell, whereas oligomycin alone delayed the MeHg-induced influx of extracellular Ca(2+). In granule cells loaded with rhod-2 acetoxymethylester to measure changes in [Ca(2+)](m), MeHg exposure caused a biphasic increase in fluorescence. The initial increase in fluorescence occurred in the absence of extracellular Ca(2+) and was abolished by mitochondrial depolarization. The secondary increase was associated with spreading of the dye from punctate staining to whole-cell distribution, and was delayed significantly by the MTP inhibitor cyclosporin A and the smooth endoplasmic reticulum Ca(2+) ATPase inhibitor thapsigargin. We conclude that MeHg causes release of Ca(2+) from the mitochondria through opening of the MTP, which contributes the bulk of the elevated [Ca(2+)](i) observed during MeHg neurotoxicity. Additionally, the Ca(2+) that enters the mitochondria seems to originate in the smooth endoplasmic reticulum, providing a mechanism for the observed mitochondrial Ca(2+) overload.     

Inflammatory bowel disease and predisposition to osteopenia

The prevalence of osteopenia in children with inflammatory bowel disease (IBD) is unknown. The effect of nutritional state, disease activity, and steroid therapy on bone mineral content (BMC) of whole body, lumbar spine, and left femoral neck measured by dual energy x ray absorptiometry in 32 children with IBD was assessed by comparison with 58 healthy local school children. Using the control data, a predicted BMC was calculated taking into account bone area, age, height, weight, and pubertal stage. The measured BMC in children with IBD was expressed as a percentage of this predicted value (% BMC). Mean (SD) % BMC was significantly reduced for the whole body and left femoral neck in the children with IBD (97.0 (4.5)% and 93.1 (12.0)% respectively, p < 0.05). Of the children with IBD, 41% had a % BMC less than 1 SD below the mean for the whole body and 47% at the femoral neck. Reduction in % BMC was associated with steroid usage but not with the magnitude of steroid dose, disease activity, or biochemical markers of bone metabolism. In conclusion, osteopenia is relatively common in childhood IBD and may be partly related to the previous use of steroids.     

Serum and plasma from patients with Lambert-Eaton Myasthenic Syndrome reduce depolarization-dependent uptake of 45Ca2+ into rat cortical synaptosomes.

The reduction in nerve-evoked release of transmitter at the neuromuscular junction of patients with Lambert-Eaton Myasthenic Syndrome (LEMS) is thought to be caused by a circulating autoantibody to calcium channels of presynaptic motor nerve terminals. Studies were undertaken to determine whether acute application of plasma and serum from patients with LEMS or small cell carcinoma (SCC) would reduce depolarization-dependent uptake of 45Ca2+ into isolated nerve terminals of the central nervous system (CNS). Net potassium-stimulated influx was reduced by sera and plasma from patients with LEMS but not by sera from patients with SCC. Lactate dehydrogenase (LDH) release from synaptosomes incubated with plasma or serum from patients with LEMS was not increased over control. These results are significant because: (1) they demonstrate that acute exposure to a circulating factor in sera/plasma from a patient with LEMS is sufficient to inhibit Ca2+ channel activity in isolated nerve terminals, as opposed to chronic regimens used in other models for the disease; (2) they indicate that the existence of SCC alone is insufficient to trigger a LEMS-like autoimmune response; (3) they suggest that Ca2+ channels of nerve terminals secreting different transmitters may share common epitopes recognized by the LEMS autoantibody; and (4) they suggest that synaptosomes will be useful in determining the neurochemical site and specificity of the LEMS autoantibody.     

The clinical importance of spectacle lens base curves

This paper discusses the importance of spectacle lens base curves to the practice of optometry. The base curve is defined. Principles of spectacle lens design, and the role of the base curve in spectacle lens design, are explained. Current practices of manufacturers and surfacing laboratories concerning base curves are discussed, as is the role of the optometrist in specifying and measuring lens curves