Pankaj Vats

Levodopa/Carbidopa in the Treatment of Amblyopia

PURPOSE To evaluate the role of levodopa/carbidopa in the treatment of amblyopia. METHODS Thirty patients with strabismic amblyopia between the ages of 3 and 12 years were part of this double-blind, randomized study. Patients were divided into two groups. Group A received 0.50 mg + 1.25 mg of levodopa/carbidopa per kilogram body weight three times daily after meals, with a protein rich drink, whereas Group B received placebo. Both groups received full-time conventional occlusion until a visual acuity of 6/6 was achieved or for a maximum of 3 months. RESULTS The authors observed more than two lines improvement in visual acuity that was greater in the levodopa group (15 of 15) than in the placebo group (9 of 15) (P < .005). Furthermore, improvement in visual acuity of more than two lines was greater in patients younger than 8 years (100%) than in patients older than 8 years of age (60%) (P = .0026). There was also no significant reversal of the improved visual acuity in up to 6 months of follow-up. CONCLUSION Levodopa/carbidopa improves visual acuity in patients with amblyopia and maintains improved visual acuity, especially in patients younger than 8 years.

Acquired isolated unilateral fourth nerve palsy after ventriculoperitoneal shunt surgery

Ventriculoperitoneal shunt has been the surgical procedure of choice for many years for both communicating and noncommunicating hydrocephalus.(1) High failure rates and complications have been reported, despite major improvements in shunt technology(2); however, fourth (trochlear) nerve palsy has not been reported after this procedure. We describe 2 patients who developed a fourth nerve palsy after shunt surgery. Recovery was incomplete, and strabismus surgery was required.

Vertical synergistic divergence: to be or not to be, that is the quintessential question.

Dear Editor, We do not concur and reiterate that clinical picture cascades down consummately to a hallmark bilateral Brown Syndrome (BBS) presentation.[1–3] Documentation of forced duction test results, ductions, measurements of deviation in prism diopters in nine cardinal gazes with either eye fixing, fundus photographs for torsion, in tandem with findings on neuroimaging/surgical exploration and surgical outcomes would be seminal in sifting the maze, but reports skirt all of that.[1,3] Full bilateral elevation in abduction with gross bilateral limitation of elevation in adduction with down-shoot of adducted eye consistently in side, up and down gazes, with globes nailed in down position and negative head tilt test results, unequivocally cohere to a diagnosis of BBS. An alternative diagnosis can only be entertained in the presence of negative exaggerated forced duction tests, which were not done.[1,3] The report is cryptic as to whether one or both eyes are having 3rd nerve palsy, the extent of involvement, recovery and aberrant innervation, if any present.[1,3] Either eye is dipping in adduction, and the left eye will also dip if the right eye is allowed to fixate and elevate in slight abduction.[3] No light is shed on the plausible location/pathway/mechanism/causation of the expounded synergistic vertical divergence involving only the right eye, in view of the facts that up gaze fibers freely cross in the posterior commissure, whereas down gaze fibers are uncrossed, and the superior rectus (SR) receives crossed innervation through the opposite subnucleus. It follows that proposed synergistic divergence/convergence cannot be conflated via up gaze fibers at the supranuclear level. Neither can it be conflated at the nuclear/infranuclear level. Superior oblique (SO) overactions (not known whether it is primary or secondary) as propounded[1,3] do not produce globes nailed-in down gaze in adduction. In 3rd nerve palsy, as the depressor action of SO is compromised, they instead cause intorsion. Thus, bilateral overdepression in adduction sans intorsion cannot be ascribed to bilaterally overacting SOs due to (right) 3rd nerve palsy as surmised.[1,3] There is nothing proximate to “no significant ocular torsion,” as torsional position of the globe is a state and, therefore, it may only be normal or abnormal.[3] Further, the downshoot is only in adduction, not in abduction, and therefore cannot be explained by aberrant innervation of SR as SRs act in abduction.[1,3] The SR has to be paretic to undergo aberrant innervation; the report does not state so[3] and resultant cocontraction of vertical recti on up gaze will engender convergence retraction instead. Overaction of SOs, downshoot and widening of palpebral fissure in adduction is known in Brown Syndromes, and is the likely cause of asymmetrical underdepression of both eyes in abduction, the hallmark finding militating against BBS as per the report.[1] No perfidy will be committed anyway if congenital 3rd nerve palsy and BBS coexist. In the absence of irrefutable documentary evidence on forced duction tests against BBS and nine gaze deviations fixing with either eye, no meaningful conclusions can be drawn about muscle overactions/underactions and any abstruse synergistic vertical divergence/convergence. Thus, the proposed esoteric expositions about misinnervation and synergistic divergence are bereft of any neuroanatomical substrate at supranuclear/nuclear/infranuclear levels, and are overtly speculative, emanating from a skewed interpretation of a hallmark congenital BBS presentation.[1,3]

Retinitis pigmentosa associated with blepharophimosis, blue dot cataract and primary inferior oblique overaction: A new syndrome complex or consummate myotonic dystrophy?

1. Gillies MC, Simpson JM, Billson FA, Luo W, Penfold P, Chua W, et al. Safety of an intravitreal injection of triamcinolone: Results from a randomized clinical trial. Arch Ophthalmol 2004;122:336-40. 2. Thompson JT. Cataract formation and other complications of intravitreal triamcinolone acetonide for macular edema. Am J Ophthalmol 2006;141:629-37. 3. Moshfeghi DM, Kaiser PK, Scott IU, Sears JE, Benz M, Sinesterra JP, et al. Acute endophthalmitis after intravitreal triamcinolone acetonide injection. Am J Ophthalmol 2003;136:791-6. 4. Degenring RF, Sauder G. Vitreous prolapse and IOL dislocation during intravitreal injection of triamcinilone acetonide. Graefes Arch Clin Exp Ophthalmol 2006;244:1043-4. 5. Chen SD, Chen FK, Patel C. Opaque coating of the intraocular lens and regression of iris neovascularization following injection of triamcinolone acetonide into the anterior chamber. Clin Exp Ophthalmol 2006;34:803-5.

Characterizing superior oblique palsies and skew deviations.

B hola et al 1 ascribe bilateral superior oblique palsy (SOP) and dorsal midbrain syndrome to midbrain hemorrhage. We offer the following comments on the cause and diagnosis. Primary position right hypertropia and left hypertropia on head tilt to either side, with no reversal of hypertropia, run counter to a diagnosis of bilateral SOP. A negative head tilt test, acquired comitant esodeviation, oscillopsia, and marked (30°) subjective extorsion suggest an alternate diagnosis of laterally alternating skew deviation with acute acquired comitant esotropia (AACE) due to damage to horizontal and vertical prenuclear vestibulo-ocular reflex (VOR) inputs to ocular motor nuclei. Negative head tilt test and oscillopsia indicating bilateral midbrain stroke, acute hydrocephalus, and surgical trauma from ventriculoperitoneal shunt placement are all present and could be causal. Diffuse midbrain hemorrhage seems to be a chance finding. As for bilateral symmetrical nuclear/fascicular SOP, the insult instead must be focal and selective. Acute acquired comitant esotropia, or horizontal skew, is mediated by abnormalities of translational VOR in the surge plane during fore and aft translation. Laterally alternating skew deviation (adducting/abducting hypertropias) results from anterior or posterior semicircular canal dominance from damage to VOR inputs corresponding to opposite canals. Both AACE and skew deviations may share common etiologies. Laterally alternating skew deviation and pretectal syndrome can coexist, and SOPs can simulate ocular tilt reaction, a type of skew deviation. Laterally alternating adducting hypertropias and bilateral SOPs can mimic and create a diagnostic dilemma, but are distinguished by similar disorders, like Table. Citedness Score and Its Ranking of the Top 30 Articlesa Reexamined by 3 Citation Databases (cont)