Publications by authors named "Sudhakar Subramaniam"

Background- Subarachnoid hemorrhage (SAH) is one of the most devastating diseases with a high rate of morbidity and mortality. The heart rate variability (HRV) is a non-invasive method of monitoring various components of the autonomic nervous system activity that can be utilized to delineate autonomic dysfunctions associated with various physiological and pathological conditions. The reliability of HRV as a predictor of clinical outcome in aneurysmal subarachnoid hemorrhage (aSAH) is not yet well investigated in literature.

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Objective: Investigation of onabotulinumtoxinA in a murine model of acute and persistent post-traumatic headache.

Methods: Mild traumatic brain injury was induced with a weight drop method. Periorbital and hindpaw cutaneous allodynia were measured for 14 days.

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An awake craniotomy is a common neurosurgical procedure for excising brain tumor(s) located near or in eloquent areas. The use of benzodiazepine (BZD) for sedation in some patients with neuropathological conditions (e.g.

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Introduction: Intraoperative seizures (IOSs) during awake craniotomy (AC) are associated with significant morbidity. The reported incidence of IOS is between 3% and 30%. The aim of this study was to identify risk factors for IOS during AC for elective resection or biopsy of a space-occupying brain lesion.

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Introduction: Unlike adult gliomas, the utility of combined application of awake anesthesia and intraoperative neurophysiological monitoring (IONM) for maximal safe resection in eloquent region gliomas (ERG) has not been established for pediatric population while it remains unexplored in preadolescents (below 11 years old).

Case Presentation: We report 2 cases of awake craniotomy with IONM in an 8 and 9 year old for safe maximal resection of ERG. In both the cases, repeated preoperative visits of the operating room was performed to familiarize and educate the children about intraoperative communication, comfortable positioning, and neurological assessment.

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Since mitochondrial dysfunction is implicated in the pathogenesis of AMD, this study is based on the premise that repurposing of mitochondria-stabilizing FDA-approved drugs such as PU-91, might rescue AMD RPE cells from AMD mitochondria-induced damage. The PU-91 drug upregulates which is a critical regulator of mitochondrial biogenesis. Herein, we tested the therapeutic potential of PU-91 drug and examined the additive effects of treatment with PU-91 and esterase inhibitors i.

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Re-appearance of trigeminal neuralgia (TN) pain following microvascular decompression (MVD) is a challenging issue. A selective ablation with MVD provides the best response in such recurrences. The absence of intra-operative indicator for immediate correction of sub-optimal decompression is the primary factor for failure.

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In addition to dopaminergic and motor deficits, patients with Parkinson's disease (PD) suffer from non-motor symptoms, including early cognitive and social impairment, that do not respond well to dopaminergic therapy. Cholinergic deficits may contribute to these problems, but cholinesterase inhibitors have limited efficacy. Mice over-expressing α-synuclein, a protein critically associated with PD, show deficits in cognitive and social interaction tests, as well as a decrease in cortical acetylcholine.

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Parkinson's disease (PD) is a chronic and progressive disorder characterized neuropathologically by loss of dopamine neurons in the substantia nigra, intracellular proteinaceous inclusions, reduction of dopaminergic terminals in the striatum, and increased neuroinflammatory cells. The consequent reduction of dopamine in the basal ganglia results in the classical parkinsonian motor phenotype. A growing body of evidence suggest that neuroinflammation mediated by microglia, the resident macrophage-like immune cells in the brain, play a contributory role in PD pathogenesis.

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Aberrant accumulation and self-assembly of α-synuclein are tightly linked to several neurodegenerative diseases called synucleinopathies, including idiopathic Parkinson's disease, dementia with Lewy bodies, and multiple system atrophy. Deposition of fibrillar α-synuclein as insoluble inclusions in affected brain cells is a pathological hallmark of synucleinopathies. However, water-soluble α-synuclein oligomers may be the actual culprits causing neuronal dysfunction and degeneration in synucleinopathies.

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Management of giant intracranial aneurysms presents unique challenges to the neurosurgical team. Various techniques such as adenosine-induced hypotension, rapid ventricular pacing, and inducing deep hypothermia are described in the literature to effect circulatory arrest for the successful obliteration of giant aneurysms. We describe a novel technique of induced hypotension for clipping a giant aneurysm by using an inflatable balloon across the main pulmonary artery with a successful outcome.

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Unlabelled: N-nitrosodiethylamine (NDEA), a nitrosamine compound, is known to cause liver damage through the generation of reactive oxygen species (ROS), resulting in oxidative damage to macromolecules such as DNA, and the consequent development of cancer. The present study examines the protective effects of two antioxidant coumarin compounds umbelliferone (Umb) and esculetin (Esc) against NDEA-induced hepatotoxicity when administered in the diet to male Wistar rats. The results show that treatment with Umb (0.

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Parkinson's disease (PD) is characterized by the progressive degeneration of nigrostriatal dopaminergic neurons leading to motor deficits. The mechanisms underlying the preferential vulnerability of nigrostriatal dopaminergic neurons in PD remain poorly understood. Recent evidence supports a role for mitochondrial dysfunction and increased oxidative stress in PD pathogenesis.

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Parkinson's disease (PD) is a movement disorder that is characterized by the progressive degeneration of dopaminergic neurons in substantia nigra pars compacta resulting in dopamine deficiency in the striatum. Although majority of the PD cases are sporadic several genetic mutations have also been linked to the disease thus providing new opportunities to study the pathology of the illness. Studies in humans and various animal models of PD reveal that mitochondrial dysfunction might be a defect that occurs early in PD pathogenesis and appears to be a widespread feature in both sporadic and monogenic forms of PD.

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The production of reactive oxygen species and mitochondrial dysfunction in the brain are both associated with the progression of several neurodegenerative diseases, including Parkinson's disease. These characteristics are also observed when rodents are exposed to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), a compound that causes nigrostriatal dopaminergic neurotoxicity and that has been used previously for assessing the effectiveness of neuroprotective agents. In this study, the neuroprotective effects of two coumarins, umbelliferone and esculetin, against MPTP-induced neurotoxicity were examined in C57BL/6J mice.

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Identification of mutations that cause rare familial forms of Parkinson's disease (PD) and subsequent studies of genetic risk factors for sporadic PD have led to an improved understanding of the pathological mechanisms that may cause nonfamilial PD. In particular, genetic and pathological studies strongly suggest that alpha-synuclein, albeit very rarely mutated in PD patients, plays a critical role in the vast majority of individuals with the sporadic form of the disease. We have extensively characterized a mouse model over-expressing full-length, human, wild-type alpha-synuclein under the Thy-1 promoter.

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Esculetin (6,7-dihydroxy coumarin), is a potent antioxidant that is present in several plant species. The aim of this study was to investigate the mechanism of protection of esculetin in human hepatoma HepG2 cells against reactive oxygen species (ROS) induced by hydrogen peroxide. Cell viability, cell integrity, intracellular glutathione levels, generation of reactive oxygen species and expression of antioxidant enzymes were used as markers to measure cellular oxidative stress and response to ROS.

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