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      Ayurvedic approach in the management of spinal cord injury: A case study

      case-report

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          Abstract

          Spinal cord injury (SCI) is associated with consequences such as full loss of spinal movements, incontinence of bladder functions, bed sores, etc. There is no satisfactory treatment available in biomedicine with only limited treatments only for enhancement of spinal cord function. These treatments have many limitations. Ayurvedic drugs and Pancakarma procedures have been in use to treat such conditions since a long time. We present a case of SCI with lesion at C4 level which was treated for 2 months with an Ayurvedic combined intervention. The combined treatment plan involved Ayurvedic oral medications ( Brhadvātacintāmaṇi rasa - 125 mg, Ardhanāgavātāri rasa - 125 mg, Daśamūla kvātha - 40 ml, Aśvagandhācūrṇa [powder of Withania somnifera DUNAL] - 3 g, Amṛtā [ Tinospora cordifolia WILLD] - 500 mg, Muktāśukti piṣṭi - 500 mg and Trayodaśāṅga guggulu - 500 mg) twice daily. Combined procedures involved such as śāliṣaṣṭika piṇḍasvedana (sudation with medicated cooked bolus of rice) every day for 2 months and Mātrā basti (enema) for first 15 days with Aśvagandhā oil. From 16 th day, Mustādi yāpana basti (MYB, enema with medicated milk) was given for 16 days. After an interval of 7 days, MYB was further repeated for next 16 days. Substantial clinical improvement was reported after 2 months of the Ayurvedic treatment in existing neurological deficits and in quality of life.

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          Most cited references28

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          The ketogenic diet: metabolic influences on brain excitability and epilepsy.

          A dietary therapy for pediatric epilepsy known as the ketogenic diet has seen a revival in its clinical use during the past decade. Although the underlying mechanism of the diet remains unknown, modern scientific approaches, such as the genetic disruption of glucose metabolism, are allowing for more detailed questions to be addressed. Recent work indicates that several mechanisms may exist for the ketogenic diet, including disruption of glutamatergic synaptic transmission, inhibition of glycolysis, and activation of ATP-sensitive potassium channels. Here, we describe on-going work in these areas that is providing a better understanding of metabolic influences on brain excitability and epilepsy. Copyright © 2012 Elsevier Ltd. All rights reserved.
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            The ketogenic diet and brain metabolism of amino acids: relationship to the anticonvulsant effect.

            In many epileptic patients, anticonvulsant drugs either fail adequately to control seizures or they cause serious side effects. An important adjunct to pharmacologic therapy is the ketogenic diet, which often improves seizure control, even in patients who respond poorly to medications. The mechanisms that explain the therapeutic effect are incompletely understood. Evidence points to an effect on brain handling of amino acids, especially glutamic acid, the major excitatory neurotransmitter of the central nervous system. The diet may limit the availability of oxaloacetate to the aspartate aminotransferase reaction, an important route of brain glutamate handling. As a result, more glutamate becomes accessible to the glutamate decarboxylase reaction to yield gamma-aminobutyric acid (GABA), the major inhibitory neurotransmitter and an important antiseizure agent. In addition, the ketogenic diet appears to favor the synthesis of glutamine, an essential precursor to GABA. This occurs both because ketone body carbon is metabolized to glutamine and because in ketosis there is increased consumption of acetate, which astrocytes in the brain quickly convert to glutamine. The ketogenic diet also may facilitate mechanisms by which the brain exports to blood compounds such as glutamine and alanine, in the process favoring the removal of glutamate carbon and nitrogen.
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              Molecular features, regulation, and function of monocarboxylate transporters: implications for drug delivery.

              The diffusion of monocarboxylates such as lactate and pyruvate across the plasma membrane of mammalian cells is facilitated by a family of integral membrane transport proteins, the monocarboxylate transporters (MCTs). Currently, at least eight unique members of the MCT family have been discovered and orthologs to each have been identified in a variety of species. Four MCTs (MCT1-MCT4) have been functionally characterized. Each isoform possesses unique biochemical properties such as kinetic constants and sensitivity to known MCT inhibitors. Several fold changes in the expression of MCTs may be evoked by altered physiological conditions, yet the molecular mechanisms underlying the regulation of MCTs are poorly understood. Post-translational regulation of MCT1 and MCT4 occurs, in part, by interaction with CD147, an accessory protein that is necessary for trafficking, localization, and functional expression of these transporters. Because of the physiological importance of monocarboxylates to the overall maintenance of metabolic homeostasis, the function of MCTs is significant to several pathologies that occur with disease, such as ischemic stroke and cancer. Finally, the expression of MCT1 in the epithelium of the small intestine and colon and in the blood-brain barrier may provide routes for the intestinal and blood to brain transfer of carboxylated pharmaceutical agents and other exogenous monocarboxylates. Copyright 2003 Wiley-Liss, Inc.
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                Author and article information

                Journal
                Anc Sci Life
                Anc Sci Life
                ASL
                Ancient Science of Life
                Medknow Publications & Media Pvt Ltd (India )
                0257-7941
                2249-9547
                Apr-Jun 2015
                : 34
                : 4
                : 230-234
                Affiliations
                [1]Department of Panchakarma, National Institute of Ayurveda, Jaipur, Rajasthan, India
                [1 ]Department of Panchakarma, M.J.F. Ayurvedic College and Hospital, Jaipur, Rajasthan, India
                Author notes
                Address for correspondence: Dr. Sarvesh Kumar Singh, C109, Gole Market, Jawahar Nagar, Jaipur, Rajasthan, India. E-mail: sarveshksingh21@ 123456gmail.com
                Article
                ASL-34-230
                10.4103/0257-7941.160870
                4535072
                26283809
                a0a70033-e7b1-48ad-bb8a-bd179b53c5d5
                Copyright: © Ancient Science of Life

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Categories
                Case Report

                Life sciences
                matra basti,mustādi yāpana basti,patient centered outcome,quadriplegia,spinal cord injury,stem cells therapy

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