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Anuradha Singh

Publications and source records attributed to Anuradha Singh.

4 recordsLinked to original sources

Phospholipid-assisted synthesis of stable F-containing colloidal particles and their film formation.

This letter illustrates for the first time the preparation of p-methyl methacrylate/n-butyl acrylate/heptadecafluorodecyl methacrylate (p-MMA/nBA/FMA) colloidal dispersions containing up to 15% w/w FMA, which is accomplished by the utilization of biologically active phospholipids (PLs) and ionic surfactants. The use of monomer-starved conditions during emulsion polymerization and the utilization of 1,2-dilauroyl-sn-glycero-3-phosphocholine (DLPC), sodium dodecyl sulfate (SDS), and phosphoric acid bis(tridecafluoro-octyl) ester ammonium salt (FSP) as surfactants, which function as transfer and dispersing agents, facilitate a suitable environment for the polymerization of p-MMA/nBA/FMA colloidal dispersions that exhibit nonspherical particle morphologies. Such nonspherical particles upon coalescence form phase-separated films with unique surface properties.

Biocompatible Materials↗

Is clonidine useful for treatment of clozapine-induced sialorrhea?

Clozapine has shown superior efficacy in treatment of refractory schizophrenia, but its use is limited by emergent side-effects. Among other adverse effects, sialorrhea is a troublesome side-effect, its stigmatizing nature results in poor treatment compliance. Several hypotheses have been put forward in the etiology of clozapine-induced sialorrhea. 2 adrenergic antagonism is hypothesized to be involved in its pathophysiology, based on the response to clonidine and lofexidine. Oral clonidine (50 to 100 g/day) was tried on 12 stable outpatients of schizophrenia maintained on clozapine. Wet area over the pillow as reported by the patients was recorded at baseline and at 4 weeks of treatment along with the subjective response after the treatment. Most of the patients reported a decrease in sialorrhea without any adverse events. We describe encouraging results in an open case series of oral clonidine for clozapine-induced sialorrhea.

Adrenergic alpha-Agonists↗

Postictal laughter following absence status epilepticus.

Acute pathologic neurologic laughter has been described as an ictal phenomenon in epilepsy, as a result of electrical brain stimulation to the cortex and to deep brain structures, in brain tumors, and in stroke. We report what is, to our knowledge, the first report of a case of postictal pathologic laughter. Previously diagnosed with medically refractory complex partial seizures, our patient was admitted to the hospital with phenytoin toxicity. During video-EEG monitoring she experienced multiple brief absence seizures as well as a prolonged episode of absence status epilepticus. Immediately following cessation of the seizure she began to laugh. Her laughter was mirthful and infectious. This lasted several minutes and was followed immediately by several minutes of crying and then a return to normal. We propose that diffuse cortical inhibition led to release of subcortical structures involved in emotional expression. Possible neural substrates of laughter are discussed.

Adult↗

Cognition-induced epilepsy.

Cognition-induced epilepsy comprises a group of loosely tied syndromes characterized by seizures regularly precipitated by cognitive tasks. Linguistic operations (e.g., reading, writing) and decision making associated with visuospatial manipulation are the most frequent and best-characterized triggers. The syndromes reviewed have a high degree of overlap and clinical/EEG variability, suggesting that any of the neural networks subserving these complex tasks may promote seizures on either a topographic basis or a functional/connective basis. Treatment options include typical pharmacological and surgical interventions as well as stimulus alteration, threshold alteration, and avoidance conditioning. We postulate that more commonly encountered epilepsy syndromes also have complex triggers.

Journal Article↗