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34 results on '"Kannan, Meena A."'

1. Risk of new disease activity in patients with multiple sclerosis who continue or discontinue disease-modifying therapies (DISCOMS): a multicentre, randomised, single-blind, phase 4, non-inferiority trial

Author

Bourdette, Dennis, Yadav, Vijayshree, Goodman, Andrew, Racke, Michael, Fallis, Robert, Tornatore, Carlo, Goldman, Myla, Kannan, Meena, Sriram, Subramaniam, Berger, Joseph, Cross, Anne, Rammohan, Kottil, Xia, Zongqi, Leist, Thomas, Lynch, Sharon, Klawiter, Eric, Amezcua, Lilyana, Bowen, James, Corboy, John R, Fox, Robert J, Kister, Ilya, Cutter, Gary R, Morgan, Charity J, Seale, Rebecca, Engebretson, Eric, Gustafson, Tarah, and Miller, Aaron E

Published
2023
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2. Comparison of switching to 6-week dosing of natalizumab versus continuing with 4-week dosing in patients with relapsing-remitting multiple sclerosis (NOVA): a randomised, controlled, open-label, phase 3b trial

Author

van der Walt, Anneke, Dwyer, Christopher, Buzzard, Katherine, Spies, Judith, Parratt, John, van Pesch, Vincent, Willekens, Barbara, Perrotta, Gaetano, Bartholomé, Emmanuel, Grand'Maison, Francois, Jacques, Francois, Giacomini, Paul, Vosoughi, Reza, Girard, Jean-Marc, de Seze, Jerome, Lebrun Frenay, Christine, Ruet, Aurelie, Laplaud, David-Axel, Reifschneider, Gerd, Wagner, Bert, Rauer, Sebastian, Pul, Refik, Seipelt, Maria, Berthele, Achim, Klotz, Luisa, Kallmann, Boris-Alexander, Paul, Friedemann, Achiron, Anat, Lus, Giacomo, Centonze, Diego, Patti, Francesco, Grimaldi, Luigi, Hupperts, Raymond, Frequin, Stephan, Fermont, Jiske, Madueno, Sara Eichau, Alonso Torres, Ana Maria, Costa-Frossard França, Lucienne, Meca-Lallana, Jose Eustasio, Ruiz, Luis Brieva, Pearson, Owen, Rog, David, Evangelou, Nikolaos, Ismail, Azza, Lathi, Ellen, Fox, Edward, Leist, Thomas, Sloane, Jacob, Wu, Gregory, Khatri, Bhupendra, Steingo, Brian, Thrower, Ben, Gudesblatt, Mark, Calkwood, Jonathan, Bandari, Daniel, Scagnelli, John, Laganke, Christopher, Robertson, Derrick, Kipp, Lucas, Belkin, Martin, Cohan, Stanley, Goldstick, Lawrence, Courtney, Ardith, Vargas, Wendy, Sylvester, Andrew, Srinivasan, Jayshri, Kannan, Meena, Picone, Maryann, English, Jeffrey, Napoli, Salvatore, Balabanov, Roumen, Zaydan, Islam, Nicholas, Jacqueline, Kaplan, Jeffrey, Lublin, Fred, Riser, Emily, Miller, Tamara, Alvarez, Enrique, Wray, Sibyl, Gross, Jeffrey, Pawate, Siddharama, Hersh, Carrie, McCarthy, Lucas, Crayton, Heidi, Graves, Jennifer, Foley, John F, Defer, Gilles, Ryerson, Lana Zhovtis, Cohen, Jeffrey A, Arnold, Douglas L, Butzkueven, Helmut, Cutter, Gary, Giovannoni, Gavin, Killestein, Joep, Wiendl, Heinz, Smirnakis, Karen, Xiao, Shan, Kong, George, Kuhelj, Robert, and Campbell, Nolan

Published
2022
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3. DISCOntinuation of disease-modifying therapies in MS: The DISCOMS extension trial.

Author

Corboy, John R, Fox, Robert J, Cutter, Gary, Engebretson, Eric, Miller, Aaron, Morgan, Charity, Gustafson, Tarah, Goodman, Andrew D, Kannan, Meena, Sriram, Subramanian, Xia, Zongqi, Lynch, Sharon, Bowen, James, and Kister, Ilya

Subjects
MAGNETIC resonance imaging, BRAIN damage, LOG-rank test, MULTIPLE sclerosis, CLINICAL trials
Abstract

Background: In the DISCOMS (DISCOntinuation of disease-modifying therapies (DMTs) in multiple sclerosis (MS)) randomized clinical trial, we could not demonstrate that discontinuing MS DMTs in older, stable adults was not inferior to continuing DMTs. Relapses were rare in both groups, and most new disease activity was one to two new brain magnetic resonance imaging (MRI) lesions unassociated with clinical changes. Objective/Aims: Describe results of the DISCOMS extension study. Methods: Among 10/19 of the original sites, we enrolled patients who completed DISCOMS; did not reach the primary endpoint during the original trial; and retained original randomized assignment. Participants completed one study visit and brain MRI at least 30 months after original enrollment in DISCOMS. Primary endpoint was time from entry into the primary study to relapse or new brain MRI activity. Results: Mean (SD) total follow-up was 40 (11.7) months. There were no relapses, and new brain MRI lesions (1/30 continuer, 2/44 discontinuers) were uncommon during the extension. Time from primary trial entry to disease event was significantly shorter for subjects in the discontinue group (p = 0.043 from log-rank test). Conclusions: From entry into DISCOMS extension study, time to new MS activity remained shorter in discontinuers, but relapses were absent and new brain MRI lesions were rare. [ABSTRACT FROM AUTHOR]

Published
2025
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7. HIV Infection

Author

Kannan, Meena, primary, Taylor, Harrison, additional, and Tyor, William, additional

Published
2017
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8. Comparison of switching to 6-week dosing of natalizumab versus continuing with 4-week dosing in patients with relapsing-remitting multiple sclerosis (NOVA): a randomised, controlled, open-label, phase 3b trial

Author

Foley, John F, primary, Defer, Gilles, additional, Ryerson, Lana Zhovtis, additional, Cohen, Jeffrey A, additional, Arnold, Douglas L, additional, Butzkueven, Helmut, additional, Cutter, Gary, additional, Giovannoni, Gavin, additional, Killestein, Joep, additional, Wiendl, Heinz, additional, Smirnakis, Karen, additional, Xiao, Shan, additional, Kong, George, additional, Kuhelj, Robert, additional, Campbell, Nolan, additional, van der Walt, Anneke, additional, Dwyer, Christopher, additional, Buzzard, Katherine, additional, Spies, Judith, additional, Parratt, John, additional, van Pesch, Vincent, additional, Willekens, Barbara, additional, Perrotta, Gaetano, additional, Bartholomé, Emmanuel, additional, Grand'Maison, Francois, additional, Jacques, Francois, additional, Giacomini, Paul, additional, Vosoughi, Reza, additional, Girard, Jean-Marc, additional, de Seze, Jerome, additional, Lebrun Frenay, Christine, additional, Ruet, Aurelie, additional, Laplaud, David-Axel, additional, Reifschneider, Gerd, additional, Wagner, Bert, additional, Rauer, Sebastian, additional, Pul, Refik, additional, Seipelt, Maria, additional, Berthele, Achim, additional, Klotz, Luisa, additional, Kallmann, Boris-Alexander, additional, Paul, Friedemann, additional, Achiron, Anat, additional, Lus, Giacomo, additional, Centonze, Diego, additional, Patti, Francesco, additional, Grimaldi, Luigi, additional, Hupperts, Raymond, additional, Frequin, Stephan, additional, Fermont, Jiske, additional, Madueno, Sara Eichau, additional, Alonso Torres, Ana Maria, additional, Costa-Frossard França, Lucienne, additional, Meca-Lallana, Jose Eustasio, additional, Ruiz, Luis Brieva, additional, Pearson, Owen, additional, Rog, David, additional, Evangelou, Nikolaos, additional, Ismail, Azza, additional, Lathi, Ellen, additional, Fox, Edward, additional, Leist, Thomas, additional, Sloane, Jacob, additional, Wu, Gregory, additional, Khatri, Bhupendra, additional, Steingo, Brian, additional, Thrower, Ben, additional, Gudesblatt, Mark, additional, Calkwood, Jonathan, additional, Bandari, Daniel, additional, Scagnelli, John, additional, Laganke, Christopher, additional, Robertson, Derrick, additional, Kipp, Lucas, additional, Belkin, Martin, additional, Cohan, Stanley, additional, Goldstick, Lawrence, additional, Courtney, Ardith, additional, Vargas, Wendy, additional, Sylvester, Andrew, additional, Srinivasan, Jayshri, additional, Kannan, Meena, additional, Picone, Maryann, additional, English, Jeffrey, additional, Napoli, Salvatore, additional, Balabanov, Roumen, additional, Zaydan, Islam, additional, Nicholas, Jacqueline, additional, Kaplan, Jeffrey, additional, Lublin, Fred, additional, Riser, Emily, additional, Miller, Tamara, additional, Alvarez, Enrique, additional, Wray, Sibyl, additional, Gross, Jeffrey, additional, Pawate, Siddharama, additional, Hersh, Carrie, additional, McCarthy, Lucas, additional, Crayton, Heidi, additional, and Graves, Jennifer, additional

Published
2022
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12. Congenital muscular dystrophy with inflammation: Diagnostic considerations

Author

Konkay, Kaumudi, Kannan, Meena, Lingappa, Lokesh, Uppin, Megha, and Challa, Sundaram

Subjects
Care and treatment, Analysis, Genetic aspects, Research, Risk factors, Muscular dystrophy -- Genetic aspects -- Research -- Risk factors -- Care and treatment, Inflammation -- Analysis -- Risk factors -- Care and treatment, Immunohistochemistry -- Analysis, Genetic disorders -- Analysis
Published
2016

17. Malignant infiltration of peripheral nerves: As initial presenting manifestation of lymphoreticular malignancies

Author

Kannan, Meena, Uppin, Megha, Jabeen, Sheik, Mridula, Rukmini, Challa, Sundaram, and Borgohain, Rupam

Subjects
Diagnosis, Case studies, Health aspects, Peripheral nerves -- Health aspects, Lymphomas -- Case studies -- Diagnosis, Neurologic manifestations -- Case studies -- Diagnosis, Nerves, Peripheral -- Health aspects, Neurologic manifestations of general diseases -- Case studies -- Diagnosis
Published
2014

18. Incidence of malignancies in biopsy-proven inflammatory myopathy

Author

Kannan, Meena, Sundaram, C., Uppin, Megha, Mridula, Rukmini, Jabeen, Sheik, and Borgohain, Rupam

Subjects
Diagnosis, Care and treatment, Research, Risk factors, Cancer -- Risk factors -- Research, Muscular diseases -- Diagnosis -- Care and treatment -- Research, Muscle diseases -- Diagnosis -- Care and treatment -- Research
Published
2013

19. Distal myopathy with rimmed vacuoles and inflammation: A genetically proven case

Author

Kannan, Meena, Challa, S., Urtizberea, Andoni, Krahn, Martin, Jabeen, A., and Borgohain, R.

Subjects
Diagnosis, Care and treatment, Genetic aspects, Case studies, Risk factors, Patient outcomes, Health aspects, Muscular dystrophy -- Genetic aspects -- Risk factors -- Diagnosis -- Care and treatment -- Patient outcomes -- Case studies, Gene mutation -- Health aspects, Gene mutations -- Health aspects
Published
2012

21. MPV17 hepatocerebral mitochondrial DNA depletion syndrome presenting as acute flaccid paralysis - A case report

Author

Kumarasamy Thangaraj, Arumugam Paramasivam, Anjan Pyal, Angamuthu Kannan Meena, and Velpula Bhagya Bhavana

Subjects
0301 basic medicine, Pathology, medicine.medical_specialty, Mitochondrial DNA, Mitochondrial Diseases, Gastrointestinal Diseases, Encephalopathy, Hypoglycemia, Biology, medicine.disease_cause, Quadriplegia, Leukoencephalopathy, Mitochondrial Proteins, 03 medical and health sciences, 0302 clinical medicine, Leukoencephalopathies, medicine, Humans, Point Mutation, MPV17, Child, Molecular Biology, Genetics, Mutation, Membrane Proteins, Cell Biology, medicine.disease, 030104 developmental biology, Failure to thrive, Mitochondrial DNA depletion syndrome, Molecular Medicine, Female, Mutant Proteins, medicine.symptom, 030217 neurology & neurosurgery
Abstract

Mutations in human MPV17 have been reported in patients with severe mitochondrial DNA (mtDNA) depletion manifesting as early childhood onset failure to thrive, hypoglycemia, encephalopathy and progressive liver failure. We describe an 11 year old girl, born to consanguineous parents, who presented with rapidly progressive weakness of all 4 limbs with symmetrical proximal and distal weakness, gastrointestinal disease and leukoencephalopathy. Genetic analysis of the patient revealed a homozygous pathogenic mutation c.121C>T (p.R41W) in the MPV17 gene. Further, screening for this mutation in the parents revealed the presence of heterozygous mutation in both the parents, suggesting the recessive nature of the disease.

Published
2016

23. Novel mutation in C10orf2 associated with multiple mtDNA deletions, chronic progressive external ophthalmoplegia and premature aging

Author

Arumugam Paramasivam, Lalitha Pedaparthi, Shaikh Afshan Jabeen, Angamuthu Kannan Meena, Vuskamalla Jyothi, Challa Sundaram, Megha S Uppin, and Kumarasamy Thangaraj

Subjects
0301 basic medicine, Premature aging, Adult, Male, Mitochondrial DNA, Ophthalmoplegia, Chronic Progressive External, Nuclear gene, Biology, medicine.disease_cause, DGUOK, DNA, Mitochondrial, Mitochondrial Proteins, 03 medical and health sciences, 0302 clinical medicine, medicine, Humans, Point Mutation, MPV17, Molecular Biology, Sequence Deletion, Genetics, Mutation, Base Sequence, Point mutation, DNA Helicases, Aging, Premature, Cell Biology, medicine.disease, Molecular biology, 030104 developmental biology, Molecular Medicine, Chronic progressive external ophthalmoplegia, 030217 neurology & neurosurgery
Abstract

Chronic progressive external ophthalmoplegia (CPEO) is caused by defects in both mitochondrial and nuclear genes, however, the causal genetic factors in large number of patients remains undetermined. Therefore, our aim was to screen 12 unrelated patients with CPEO for mutation/multiple deletions in mtDNA and mutations in the coding regions of C10orf2, which is essential for mtDNA replication. Histopathological study of muscle biopsy revealed cytochrome c oxidase-deficient fibers and ragged blue fibers in all the patients. Long-range PCR of DNA from skeletal muscle revealed multiple mtDNA deletions in all the 12 patients. Further, sequencing coding regions of C10orf2 revealed three variants in three different patients, of which two were novel (c.1964G>A/p.G655D; c.204G>A/p.G68G) variants and one was reported (c.1052A>G/p. N351S). Sequencing of other nuclear genes that are associated with CPEO and multiple mtDNA deletions, such as; POLG1, POLG2, TK2, ANT1, DGUOK, MPV17 and RRM2B did not reveal any pathogenic mutation in patients with C10orf2 mutation. Since in silico analyses revealed p.G655D could be a potentially pathogenic and it was absent in 200 healthy controls, p.G655D could be the causative factor for CPEO. Therefore, we suggest that C10orf2 gene should be screened in CPEO individuals with multiple mtDNA deletions, which might help in prognosis of this disease and appropriate genetic counseling.

Published
2015

27. Guillain–Barré and Miller Fisher syndromes—new diagnostic classification

Author

UCL - SSS/IONS/NEUR - Clinical Neuroscience, UCL - (SLuc) Service de neurologie, Wakerley, Benjamin R., Uncini, Antonino, Yuki, Nobuhiro, Attarian, Shahram, Barreira, Amilton A., Chan, Yee-Cheun, Créange, Alain, Hsieh, Sung-Tsang, Islam, Badrul, Kannan, Meena A., Kohara, Nobuo, Kokubun, Norito, Lefaucheur, Jean-Pascal, Nascimento, Osvaldo, Shahrizaila, Nortina, Thirugnanam, Umapathi, Bergh, Peter Van den, Wilder-Smith, Einar, Witoonpanich, Rawiphan, UCL - SSS/IONS/NEUR - Clinical Neuroscience, UCL - (SLuc) Service de neurologie, Wakerley, Benjamin R., Uncini, Antonino, Yuki, Nobuhiro, Attarian, Shahram, Barreira, Amilton A., Chan, Yee-Cheun, Créange, Alain, Hsieh, Sung-Tsang, Islam, Badrul, Kannan, Meena A., Kohara, Nobuo, Kokubun, Norito, Lefaucheur, Jean-Pascal, Nascimento, Osvaldo, Shahrizaila, Nortina, Thirugnanam, Umapathi, Bergh, Peter Van den, Wilder-Smith, Einar, and Witoonpanich, Rawiphan

Abstract

Guillain-Barré syndrome (GBS) and its variant, Miller Fisher syndrome (MFS), exist as several clinical subtypes with different neurological features and presentations. Although the typical clinical features of GBS and MFS are well recognized, current classification systems do not comprehensively describe the full spectrum of either syndrome. In this Perspectives article, GBS and MFS are classified on the basis of current understanding of the common pathophysiological profiles of each disease phenotype. GBS is subclassified into classic and localized forms (for example, pharyngeal-cervical-brachial weakness and bifacial weakness with paraesthesias), and MFS is divided into incomplete (for example, acute ophthalmoparesis, acute ataxic neuropathy) and CNS subtypes (Bickerstaff brainstem encephalitis). Diagnostic criteria based on clinical characteristics are suggested for each condition. We believe this approach to be more inclusive than existing systems, and argue that it could facilitate early clinical diagnosis and initiation of appropriate immunotherapy.

Published
2014

28. Mitochondrial disorders: Challenges in diagnosis & treatment

Author

Kumarasamy Thangaraj, Nahid Akhtar Khan, Periyasamy Govindaraj, and Angamuthu Kannan Meena

Subjects
Mitochondrial DNA, Mitochondrial Diseases, Diagnosis - diseases - mitochondrial DNA - mutation - treatment, Mitochondrial disease, lcsh:Medicine, Review Article, mitochondrial DNA, Oxidative phosphorylation, Disease, Biology, Bioinformatics, medicine.disease_cause, DNA, Mitochondrial, Human mitochondrial genetics, General Biochemistry, Genetics and Molecular Biology, diseases, Adenosine Triphosphate, Diagnosis, medicine, Humans, Phosphorylation, Genetics, Mutation, treatment, lcsh:R, General Medicine, medicine.disease, Nuclear DNA, Diagnosis treatment
Abstract

Mitochondrial dysfunctions are known to be responsible for a number of heterogenous clinical presentations with multi-systemic involvement. Impaired oxidative phosphorylation leading to a decrease in cellular energy (ATP) production is the most important cause underlying these disorders. Despite significant progress made in the field of mitochondrial medicine during the last two decades, the molecular mechanisms underlying these disorders are not fully understood. Since the identification of first mitochondrial DNA (mtDNA) mutation in 1988, there has been an exponential rise in the identification of mtDNA and nuclear DNA mutations that are responsible for mitochondrial dysfunction and disease. Genetic complexity together with ever widening clinical spectrum associated with mitochondrial dysfunction poses a major challenge in diagnosis and treatment. Effective therapy has remained elusive till date and is mostly efficient in relieving symptoms. In this review, we discuss the important clinical and genetic features of mitochondrials disorders with special emphasis on diagnosis and treatment.

Published
2015
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31. Genetic and clinical heterogeneity of mito-neuromuscular diseases in India

Author

Curam Sreenivasacharlu Sundaram, Narayanappa Gayathri, Uppin Megha, Nahid Akhtar Khan, E.M. Elango, N. Dinesh, Govindaraj Periyasamy, G. P. Rajshekher, Ayyasamy Vanniarajan, Angamuthu Kannan Meena, Lalji Singh, Kumarasamy Thangaraj, and Richa Singh

Subjects
General Neuroscience, Clinical heterogeneity, General Medicine, Biology, Neuroscience
Published
2009
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32. Weakness in an Elderly Woman With Asthma and Chronic Sinusitis

Author

Kannan, Meena and Greene, James G.

Abstract

Weakness and sensory changes are common complaints in both the inpatient and the outpatient setting. However, this presentation remains a diagnostic challenge to clinicians due to the many possible underlying etiologies. The initial evaluation of weakness and sensory changes starts a thorough history and physical examination to guide the diagnostic process. In this article, we present the case of an elderly woman with complaints of weakness and sensory changes to highlight a step-wise approach to diagnosis and management.

Published
2016
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33. Incidence of malignancies in biopsy-proven inflammatory myopathy.

Author

Sundaram, C., Kannan, Meena A., Uppin, Megha, Mridula, Rukmini, Borgohain, Rupam, and Jabeen, Sheik Afshan

Subjects
*MUSCLE diseases, *DERMATOMYOSITIS, *MYOSITIS, *UNIVERSITY hospitals
Abstract

Background: Inflammatory myopathy (IM) as a manifestation of paraneoplastic syndrome has been well-documented. However, the prevalence of malignancies reported varies across the studies. There are very few studies reported from Asia, only one from India. Aim: The aim of this analysis was to study the prevalence of malignancy in biopsy-proven cases of IM in India and to study the difference between malignant and non-malignant groups. Materials and Methods: The study was a retrospective review of case records of patients with a biopsy-proven IM attending Tertiary Care University Hospital. Results: Of the total 86 patients with biopsy-proven IM, 22 patients were polymyositis, 63 patients had dermatomyositis (DM) and one was with an inclusion body myositis, not included for further analysis. Associated malignancy was diagnosed in 6 (7%) patients, and five of them were females. Diagnosis of associated malignancy was identified at the time of diagnosis of IM in four (66.7%) patients. All the six patients with an associated malignancy had DM. Only one patient died within 1 year of diagnosis. Creatinine kinase was much lower in patients with malignancy associated IM than in patients with no malignancy (P < 0.0001). Conclusion: The prevalence of malignancy was very low in our cohort as compared to the studies from other countries. Breast cancer was the most common malignancy associated with DM. The type of associated malignancy was quite variable. [ABSTRACT FROM AUTHOR]

Published
2013
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34. An ethical issue at follow-up.

Author

Kannan, Meena A.

Subjects
*NEUROPATHY, *GLUCOSE intolerance, *ELECTROPHYSIOLOGY
Abstract

A response by Meena A. Kannan to a letter to the editor about her article "Prevalence of Neuropathy in Patients With Impaired Glucose Tolerance Using Various Electrophysiological Tests" published in a 2014 issue is presented.

Published
2015

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