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Biomedical subjects

V Narayan

Publications and source records attributed to V Narayan.

12 recordsLinked to original sources

Optokinetic and vection responses to apparent motion in man.

Apparent motion was investigated as a stimulus for optokinetic nystagmus (OKN) and self-motion perception (vection). Apparent motion was stimulated by stroboscopically illuminating vertical stripes on the interior of a large drum that rotated about the observer at 20, 40 and 60 deg/sec. We determined threshold stroboscopic frequencies (f) for the appearance of smooth continuous apparent motion and measured responses of pursuit, OKN, optokinetic after nystagmus (OKAN) and vection, to stroboscopic frequencies at, above and below f. Pursuit occurred for all of these stimuli. However OKN, OKAN and vection only occurred for frequencies equal to or greater than the threshold for continuous apparent motion. Our results suggest that pursuit can occur as a response to apparent motion generated by both small and large image displacements, while OKN and vection are responses to apparent motion generated by small image displacements only. These results suggest that different afferent sources are utilized for the control of pursuit and of the slow phase of OKN.

Afterimage

Postnatal development of optokinetic after nystagmus in human infants.

During the first few months of life after birth human infants when tested monocularly move their unoccluded eye nasalward in darkness after viewing a large textured visual field moving either nasalward or temporalward. The eye movements in darkness are optokinetic after nystagmus (OKAN) which is an aftereffect of a reflex horizontal following eye movement, optokinetic nystagmus (OKN). Not until 4-5 months of age did temporalward field motion evoke OKAN with temporalward slow phase. The nasalward slow phase of OKAN that responded earlier to temporalward field motion appears to underlie the delayed development of reflex following eye movements in the temporalward direction.

Adult

Graphical analysis of prism adaptation, convergence accommodation, and accommodative convergence.

A new form of graphical case analysis is described which quantifies static interactions between accommodative convergence, convergence accommodation, and prism adaptation. A clinical gradient measure of the CA/C ratio is compared to haploscopic measures to demonstrate the validity of the new clinical technique for measuring convergence accommodation. Graphical and computational methods are illustrated which predict the quantitative interactions between accommodation and convergence that occur after the phoria is partially corrected by lenses or prisms. Complete correction of convergence accommodation errors with spherical lenses or elimination of the stimulus to convergence accommodation by full correction of the associated phoria with prism will simplify the correction of binocular disorders by preventing the complex interactions of accommodative convergence with convergence accommodation. The new form of graphical analysis quantifies the predicted stress upon binocular vision induced by convergence accommodation.

Accommodation, Ocular

Botulism, type A, and treatment with guanidine.

In a double-blind crossover study in which patients received placebo or active drug for varying periods, we evaluated the ability of guanidine hydrochloride (20 to 35 mg/kg per day perorally) to improve the rate of recovery in patients with moderate or severe botulism, type A, intoxication. Among 14 patients who received conventional botulism therapy, there was no improvement in recovery rate in those who received guanidine compared with the nontreated group. Individual patients in the treated group showed neither an acceleration in their rate of improvement when they received guanidine nor a regression in their progress when the drug was stopped. Individual patients, likewise, noted no subjective improvement when they received the drug compared with the placebo. Treatment with guanidine does not enhance recovery from botulism.

Botulism

Does antibody to mycobacterial antigens, including lipoarabinomannan, limit dissemination in childhood tuberculosis?

Serum immunoglobulin (Ig) G responses to a variety of mycobacterial antigens were measured in children from the UK, in children with tuberculosis from Hyderabad, India and Dhaka, Bangladesh, classified according to whether the disease was disseminated or localized, and in non-tuberculous controls. Anti-lipoarabinomannan (LAM) IgG responses in UK children showed a marked trough between 6 months and 3 years coincident with the reported peak incidence of disseminated tuberculosis. Geometric mean IgG responses to sonicates of slow-growing mycobacteria (rich in LAM) in 36 children with disseminated tuberculosis were markedly lower than in 99 children with localized tuberculous lesions (for Mycobacterium scrofulaceum P < 0.01, for M. tuberculosis P < 0.01, and for M. vaccae P < 0.01). Responses to purified LAM were also lower in the disseminated tuberculosis group (P < 0.05) but there was no difference between the groups in their response to mycobacterial 65 kDa protein. Multiple regression analysis showed that the reduced response to sonicated mycobacterial antigens and to LAM in children with disseminated disease was independent of age, nutritional status, skin test reactivity, duration of previous symptoms, and city of origin. There was no evidence for sequestration of antibody to immune complexes. These findings are compatible with the hypothesis that children with low levels of antibody to sonicated mycobacterial antigen and to LAM, or those who cannot mount an antibody response, are predisposed to dissemination. A role for antibody in preventing disseminated forms of tuberculosis in childhood has implications for the development of improved vaccines and for the optimum timing of vaccination with bacille Calmette-Guérin.

Adolescent

Mortality in diabetes mellitus: experience of a geographically defined population.

A population-based cohort study identified 915 deaths in 4186 patients with diabetes mellitus over a 5-year period. Ischaemic heart disease, cerebrovascular disease and malignant neoplasms were the major causes of death and accounted for 40%, 16%, and 14% of deaths, respectively, compared with 27%, 14%, and 25% of deaths in the non-diabetic population. Diabetic patients had a standardized mortality ratio (SMR) of 1.15 (95% Cl 1.08-1.22) (p less than 0.001). This excess risk of death was largely due to the excess death from ischaemic heart disease (SMR 1.55 (1.40-1.71); p less than 0.001) and the impact was greatest in middle-aged female patients. Stroke mortality was not significantly increased (SMR 1.09 (0.92-1.29)) while cancer mortality was reduced (SMR 0.75 (0.63-0.89); p less than 0.01). Death rates in diabetic male patients (SMR 1.04 (0.96-1.13)) did not differ significantly from those in non-diabetic male patients because the increased risk of ischaemic heart disease deaths (SMR 1.41 (1.22-1.62); p less than 0.001) was offset by the reduced risk of deaths from malignant neoplasms (SMR 0.65 (0.51-0.82); p less than 0.001). The reduction in cancer mortality did not reach statistical significance in diabetic women (SMR 0.82 (0.64-1.05)). Diabetic nephropathy and metabolic disasters were uncommon as causes of death.

Adolescent